Document LK9m6X27BQq42YXJnZd2Yw7mq

, V.. - '.?' r* :,; iJakSi '' '........... .. ' ^4:v Ambient Fugttf .Vinyl Chloride Pflflnthe Class llil of the B.K.K- Laridl West Covina, Califbmitr i. , *?v-stsiif - . ,j!!;.k;,Ti- ilsf April, 1996 Office of Environmental Health Hazard Assessment California Environmental Protection Agency CMA 114305 ADDENDUM HEALTH RISK ASSESSMENT OF AMBIENT FUGITIVE VINYL CHLORIDE EMISSIONS FROM THE CLASS I UNIT OF THE B.K.K. LANDFILL, WEST COVINA, CALIFORNIA APRIL 1996 FINAL Principal Authors: David M. Siegel, Ph.D., D.A.B.T. Lillian J. Kelly, M.P.H. Robert L. Holtzer, M.D. Laurie E. Monserrat Office of Environmental Health Hazard Assessment Hazardous Waste Toxicology Section 601 North 7th Street, MS 241 P. 0. Box 942732 Sacramento, California 94234-7320 (916) 324-2829 CMA 114306 ACKNOWLEDGMENTS The Hazardous Waste Toxicology Section (HWTS) of the Office of Environmental Health Hazard Assessment (OEHHA) expresses appreciation to its colleagues for their contributions to this project: From the Department of Health Services, Division of Environmental and Occupational Disease Control (DHS-DEODC) - Martin Kharrazi, Ph.D., Tim Lomas, and Rachel Broadwin for FIGURES 15, 16, and 17; Rachel Broadwin for Appendix E-FIGURE 1; Michael Armstrong for assisting with the summary of the air dispersion model contained in Appendix F; Joel Swartz, Ph.D., formerly with DHS-DEODC, for the statistical analysis of the 1983-1990 ambient vinyl chloride monitoring data in Appendix D. From the Air Resources Board, Stationary Source Division - Lynton Baker for historical air monitoring and air modeling (Baker and MacKay, 1985) information about the B.K.K. Landfill; and together with Andrew Ranzieri and Anthony Servin for consultation during the development of the air dispersion model contained in Appendix F. This report incorporates comments received during a three-phased review process. The initial review was made by scientists from OEHHA-Air Toxicology and Epidemiology Section, the Department of Toxic Substances Control, the Air Resources Board, the Department of Health Services, and the United States Environmental Protection Agency-Region IX. The second review was made by members of OEHHA's Ad Hoc Advisory Committee for Review of the Draft Addendum Health Risk Assessment. Finally, availability of the report for public review and comment was published in the California Regulatory Notice Register (Register 95, No. 50-Z, December 15,1995). A public workshop, consistent with the Health and Safety Code Section 57003, was held on January 11, 1996 in West Covina to discuss the report. OEHHA-HWTS expresses its appreciation to all the reviewers for their critiques, and wishes to acknowledge members of the Ad Hoc Advisory Committee; Nancy Adin, Ph.D., Resident Jean Ameson, Resident William F. Polich, Ph.D., Resident William Ketteringham, Ph.D., Representative for the City of West Covina Henry Moghtader, M.D., West Covina Physician Jack Yoshino, Representative for the City of Walnut John Froines, Ph.D., Representative for the B.K.K. Corporation Ed Avol, M.S., University of Southern California, School of Medicine Allan H. Smith, M.D., Ph.D., University of California, Berkeley School of Public Health Jay Beaumont, Ph.D., M.S.P.H., University of California, Davis Division of Occupational/Environmental Medicine & Epidemiology OEHHA-HWTS also wishes to thank Vincent James Cogliano, Ph.D.. Acting Chief, Quantitative Risk Methods Group, National Center for Environmental Assessment, United States Environmental Protection Agency, Washington, D.C., for his always gracious discussions and meetings regarding young-age sensitivity to vinyl chloride. The authors express their appreciation to fellow staff members contributing to this report: Julio Salinas, Ph.D. for FIGURE 17; Ed Evans, for computerized data bases; and Sharon Davis, for patient and perfect word processing. Responsibility for the contents of this report resides solely with OEHHA-HWTS. CMA 114307 -i- TABLE OF CONTENTS LIST OF FIGURES....................................................................................................................... iv LIST OF TABLES......................................................................................................................... vi FACT SHEET..............................................................................................................................viii EXEGUTIVE SUMMARY...............................................................................................................x INTRODUCTION........................................................................................................................... 1 Objective, Methodology, and Scope of the Addendum Health Risk Assessment............ 1 Previous Health Risk Assessments of the B.K.K. Landfill................................................ 4 Organizational Changes in the Department of Health Services Since the 1990............. 5 Interim Report Appendices to the Addendum Health Risk Assessment.................................................. 6 HAZARD IDENTIFICATION.......................................................................................................... 9 Vinyl Chloride in the Class I Unit......................................................................................9 Vinyl Chloride Emissions From the Class I Unit............................................................. 10 Other Hazardous Chemicals Detected in Ambient Air.................................................... 12 Regulatory Agencies Involved With the B.K.K. Landfill................................................... 13 TOXICITY ASSESSMENT...........................................................................................................15 Toxicity Values.................................................................................................................15 History of the Assessment of Vinyl Chloride Toxicity...................................................... 15 New Unit Risk Value and Proposition 65.........................................................................19 Sensitivity to Vinyl Chloride From Exposures at a Young Age....................................... 21 EXPOSURE ASSESSMENT....................................................................................................... 23 Ambient Vinyl Chloride Monitoring Data......................................................................... 23 Site Activities..................................................... 40 Odor Complaints Data..................................................................................................... 44 Other Hazardous Chemicals Detected in Ambient Air.................................................... 48 RISK CHARACTERIZATION...................................................................................................... 50 Assumptions Regarding the Beginning of Exposures at Stations A, B, and MY............ 50 Assumptions Regarding Ambient Vinyl Chloride Monitoring Data...................................52 Individual Excess Lifetime Cancer Risk Estimates......................................................... 53 Exposed Population.........................................................................................................56 Estimated Excess Lifetime Cancer Risk Using Different Assumptions and Methodology....57 Limitations and Uncertainties.......................................................................................... 62 Findings of the Addendum Health Risk Assessment...................................................... 64 REFERENCES........................................................................................... 66 -ii- CMA114308 TABLE OF CONTENTS (Continued) APPENDIX A..............................................................................................................................74 Errata APPENDIX B.............................................................................................................................. 76 "B.K.K. Landfill, West Covina, California Fact Sheet, December 1990," California Department of Health Services-Environmental Epidemiology and Toxicology Branch, Emeryville, California APPENDIX C............................................................................................................................... 84 Updated Toxicity Tables from the 1990 Interim Report APPENDIX D............................................................................................................................... 88 Statistical Evaluation of the 1983-1990 Ambient Vinyl Chloride Monitoring Data APPENDIX E................................................. 1990 Population Census Tract Data for the Vicinity of the B.K.K. Landfill, West Covina, California 92 APPENDIX F............................................................................................................................... 96 Air Dispersion Modeling of the 1983-1990 Ambient Vinyl Chloride Monitoring Data APPENDIX G..............................................................................................................................102 Updated Risk Estimate of the 1984 Indoor Air Monitoring Program Evaluated in the 1990 Interim Report APPENDIX H..............................................................................................................................106 Department of Health Services-Cancer Surveillance Section Letter Regarding Review of Recent Tumor Incidence Data APPENDIX I...............................................................................................................................110 Release of the Draft Addendum Report APPENDIX J...............................................................................................................................112 OEHHA's Response to Comments on the Draft Addendum Report CMA 114309 iii- LIST OF FIGURES'1 FIGURE 1 LOCATION MAP, BKK LANDFILL, WEST COVINA, CALIFORNIA................................... 7 (Environmental Solutions, Inc.) 2 WASTE LOCATION INDEX MAP, BKK LANDFILL, WEST COVINA, CALIFORNIA 8 (Environmental Solutions, Inc.) 3 TONS OF HAZARDOUS WASTE DEPOSITED IN BKK LANDFILL................................. 11 WEST COVINA, CALIFORNIA 4 LOCATION OF SOUTH COAST AIR QUALITY MANAGEMENT DISTRICTS ..............25 AMBIENT VINYL CHLORIDE MONITORING STATIONS A, B, AND MY (CH2M Hill) 5 1981-1982 AMBIENT CONCENTRATIONS OF VINYL CHLORIDE NEAR .................... 28 BKK LANDFILL (Air Resources Board) 6 1983-1990 AVERAGE ANNUAL VINYL CHLORIDE CONCENTRATIONS (ppb).......... 31 NEAR BKK LANDFILL, WEST COVINA, CALIFORNIA 7 FREQUENCY OF VINYL CHLORIDE DETECTED AT OR ABOVE 2 PPB, ................... 32 1983-1990, BKK LANDFILL, WEST COVINA, CALIFORNIA 8 FREQUENCY OF VINYL CHLORIDE DETECTED AT OR ABOVE 10 PPB.................... 35 1981-1989, BKK LANDFILL, WEST COVINA, CALIFORNIA 9 MAXIMUM MEASURED VINYL CHLORIDE LEVEL EACH MONTH, 1983-1990........... 36 BKK LANDFILL, WEST COVINA, CALIFORNIA 10 BKK LANDFILL PROPOSITION 65 AMBIENT MONITORING STATION........................39 LOCATIONS (BKK Corporation - ENVIRON Corporation) 11 BKK SANITARY LANDFILL, OCTOBER 20, 1980................................................................ 41 (United States Environmental Protection Agency) 12 BKK SANITARY LANDFILL, SEPTEMBER 2, 1983.............................................................. 42 (United States Environmental Protection Agency) 13 BKK SANITARY LANDFILL, JUNE 15, 1984.......................................................................... 43 (United States Environmental Protection Agency) *A parenthetical notation in the title credits the source of the Table. The full reference is given as a footnote on the Table. CMA 114310 -iv* LIST OF FIGURES* (Continued) 14 TOPOGRAPHY NEAR BKK LANDFILL, WEST COVINA, CALIFORNIA.......................... 45 (Department of Health Services-Division of Environmental and Occupational Disease Control) 15 ODOR COMPLAINTS NEAR BKK LANDFILL, 1980-1982 ................................................. 46 (Department of Health Services-Division of Environmental and Occupational Disease Control) 16 ODOR COMPLAINTS NEAR BKK LANDFILL, 1984-1985 .................................................. 47 (Department of Health Services-Division of Environmental and Occupational Disease Control) 17 TONS OF HAZARDOUS WASTE DEPOSITED, AVERAGE ANNUAL............................51 VINYL CHLORIDE CONCENTRATIONS (ppb), BKK LANDFILL, WEST COVINA/CALIFORNIA *A parenthetical notation in the title credits the source of the Table. The full reference is given as a footnote on the Table. -v- CMA 114311 LIST OF TABLES 1 COMPARISON OF THE 1990 INTERIM AND 1996 ADDENDUM HEALTH...................... 2 RISK ASSESSMENT OF THE CLASS I UNIT OF THE B.K.K. LANDFILL, WEST COVINA, CALIFORNIA 2 RANK ORDERING OF ESTIMATES OF HUMAN RISK BY CATEGORY .......................20 (Office of Environmental Health Hazard Assessment-Air Toxicology and Epidemiology Section) 3 UNITED STATES ENVIRONMENTAL PROTECTION AGENCY'S ESTIMATES ..........22 OF RISK FOR APPORTIONED LIFETIME EXPOSURES TO VINYL CHLORIDE AT VARIOUS CONCENTRATIONS (United States Environmental Protection Agency) 4 1981 VINYL CHLORIDE CONCENTRATION, PPM AT BKK VICINITY........................... 24 (South Coast Air Quality Management District) 5 1981-1982 AVERAGE VINYL CHLORIDE CONCENTRATIONS IN................................. 27 AMBIENT AIR (ppb), BKK LANDFILL, WEST COVINA, CALIFORNIA 6 1983-1990 AVERAGE ANNUAL VINYL CHLORIDE CONCENTRATIONS (ppb)......... 30 NEAR BKK LANDFILL (Ogden Environmental and Energy Services Co., Inc.) 7 NUMBER OF SAMPLES WITH NONDETECTABLE VINYL CHLORIDE ........................34 CONCENTRATIONS PER TOTAL NUMBER OF DAYS SAMPLED, 1981-1990 SCAQMD AMBIENT VINYL CHLORIDE MONITORING DATA, BKK LANDFILL, WEST COVINA, CALIFORNIA 8 BKK LANDFILL PROPOSITION 65 VINYL CHLORIDE MONITORING PROGRAM.... 38 (B.K.K. Corporation) 9 INDIVIDUAL EXCESS LIFETIME CANCER RISK FROM EXPOSURE TO.................... 55 AMBIENT FUGITIVE VINYL CHLORIDE EMISSIONS FROM THE CLASS I UNIT OF THE BKK LANDFILL, WEST COVINA, CALIFORNIA, REASONABLE MAXIMUM EXPOSURE SCENARIO (30 YEARS) 10 ESTIMATED EXCESS CANCER RISK AT STATION A USING DIFFERENT................. 58 ASSUMPTIONS11 11 SUMMARY OF HEALTH RISK ASSESSMENTS OF THE BKK LANDFILL........................61 WEST COVINA, CALIFORNIA *A parenthetical notation in the title credits the source of the Table. The full reference is given as a footnote on the Table. -VI- CMA 114312 BLANK PAGE CMA 114313 -VII- CALIFORNIA ENVIRONMENTAL PROTECTION AGENCY Office ofEnvironmental Health Hazard Assessment HAZARDOUS WASTE TOXICOLOGY SECTION Addendum Health Risk Assessment, B.K.K. Landfill, West Covina, California FACT SHEET APRIL, 1996 This fact sheet summarizes the Office of Environmental Health Hazard Assessment's (OEHHA) "Addendum Health Risk Assessment of Ambient Fugitive Vinyl Chloride Emissions From the Class I Unit of the B.K.K. Landfill, West Covina, California." The addendum report is an update of the 1990 interim health risk assessment conducted by the Hazardous Waste Toxicology Section (HWTS). In 1981, vinyl chloride was found in ambient air in residential neighborhoods adjacent to the B.K.K. Landfill. This is of concern because vinyl chloride is a known human carcinogen and is not normally detected in the South Coast air basin. Emissions of vinyl chloride are clearly associated with thfe Class I Unit of the landfill. Wastes containing vinyl iloride were deposited in the Class I Unit until June 1981. Emissions from the now closed Class I Unit are due to vinyl chloride-containing wastes deposited in the Unit and to the breaking down of other wastes containing chlorinated hydrocarbons. The emissions have been significantly reduced over time. OEHHA's health risk assessment is possible because there were monitoring data collected by a regulatory agency, in residential neighborhoods almost daily, for nearly a decade. The B.K.K. Landfill In 1963 the B.K.K. Landfill, opened on 130 acres in the San Jose Hills in the City of West Covina. In 1971 the B.K.K. Landfill expanded to its present size of 583 acres. In 1972 40 acres of the landfill were permitted as a hazardous waste (Class 1) unit The Class 1 Unit was expanded to 140 acres in 1975. In November 1984, the B.K.K. Class I Unit stopped accepting hazardous waste and in March 1989, was formally closed. The closing process included an extensive landfill gas collection system and the placing of a low-permeability soil cap over 170 acres. tis cap covered the hazardous waste landfill and part of me adjacent Class III (solid waste) landfill. A separate Class III waste area of the B.K.K. Landfill is still permitted and is currently accepting waste. In 1985 the State of California committed to complete three health studies of the B.K.K. Landfill: a cancer study, a reproductive outcomes study and a health risk assessment. In 1990, the cancer study, an initial pregnancy outcomes study and the interim health risk assessment were completed. A more comprehensive reproductive outcomes study is currently being prepared by the Department of Health Services (DHS). At the time the interim report was being released to the public, the cancer potency of vinyl chloride was being reevaluated and a more potent value was expected. This would make the cancer risk estimated in the interim report an underestimate. The final addendum report plus the interim report will complete the health risk assessment of the B.K.K. Landfill promised to the residents by the State of California. Addendum Objective The addendum report estimates the excess cancer risk associated with exposures to vinyl chloride detected at three monitoring stations located south-east and south of the closed Class 1 Unit of the B.K.K. Landfill. Methodology The addendum report uses the four components of a health risk assessment: hazard identification, toxicity assessment, exposure assessment, and risk characterization. Hazard Identification Vinyl chloride is the chemical of primary concern. Although other chemicals have been detected at the monitoring stations, these chemicals are also found in the South Coast air basin. It is not possible to tell how much of these chemicals are from the B.K.K. Landfill and how much are from other sources in the area. Toxicity Assessment To estimate the ability of vinyl chloride to cause cancer, OEHHA evaluated data from studies in humans, exposed at factories that made r used vinyl chloride, and from studies in laboratory animals (rats, mice, and hamsters). viii CMA 114314 The cancer risk is estimated using the cancer potency value for vinyl chloride, 20 x 10'7 per part per billion (ppb). The cancer potency is an estimate of the probability of developing cancer as a result of daily exposure for 70 years to one ppb of a chemical in air. Exposure Assessment The vinyl chloride monitoring data were collected by the South Coast Air Quality Management District (SCAQMD) from June 1981 - March 1990, and by the B.K.K. Corporation from September 1993 September 1994. Station A was located at Marlena & Nogales Streets, Station B at Lynn Court and Station MY at Myra Court. These areas were exposed to the highest detected levels of vinyl chloride. Although other residential areas near the B.K.K. Landfill were exposed to emissions from the landfill, the levels were not as high or as frequent. Risk Characterization Assuming that individuals lived near the monitoring stations for 30 years (1980-2009; a "reasonable maximum exposure scenario"), OEHHA estimates that there is an added 0.006 to 0.009 percent chance of developing cancer as a result of exposure to emissions of vinyl chloride from the closed Class 1 Unit of the B.K.K. Landfill. Addendum Findings There are four findings of the addendum report: 1. For individuals who lived near the monitoring stations during the 1980's, past exposures were higher than current exposures. The majority of the estimated excess cancer risk was incurred by 19831984. 2. The landfill gas collection system and the clay cap covering the closed Class 1 Unit have been successful in lowering vinyl chloride emissions to levels that pose little, if any, risk to nearby residents. 3. Regulatory agencies may want to include past exposures of vinyl chloride near the monitoring stations in subsequent health assessments of emissions from the landfill to ensure future risks do not add significantly to the past cumulative risk. 4. There is uncertainty associated with the assumptions used in the addendum report. The actual excess cancer risk is likely to be lower than these estimates and may be zero. Because the number of people who actually lived or are living near Stations A, B, or MY is small, it is unlikely that excess cases of cancer will occur. Each exposed individual may have an increased risk of developing cancer, however the added risk is small. Questions and Answers Q - What is the difference between the DHS Cancer Study and the OEHHA Health Risk Assessments? A - The cancer study investigated cases of diagnosed cancers for the years 1972-82. The health risk assessments estimate the theoretical probability, or risk, of developing cancer. Q - What is meant by "estimated excess lifetime cancer risk"? A - "Estimated excess lifetime cancer risk" is an estimate of the risk for an individual above the background risk of developing cancer during a 70-year lifetime. An individual living in the United States has a 40 percent (0.4) chance of developing cancer throughout a 70-year lifetime. An individual living from 1980-2009 near Station A, for example, may have an added 0.007 percent chance of developing cancer as a result of emissions of vinyl chloride from the closed class 1 Unit of the B.K.K. Landfill. Q - Has there been an increase in diagnosed cases of cancer since 1982? A - No, the DHS Cancer Surveillance Section recently reviewed the 1988-93 tumor incidence data for a one mile area around the landfill. DHS's review found no indication of increased cancer incidence. Copies of the final addendum report are available at the following address. Office of Environmental Health Hazard Assessment Hazardous Waste Toxicology Section 601 North 7th Street, MS 241 P. O. Box 942732 Sacramento, California 94234-7320 (916) 324-2829 Copies of the cancer study, the pregnancy outcomes study and the health risk assessments are available at the West Covina, Walnut and La Puente libraries. CMA 114315 IX EXECUTIVE SUMMARY This report is prepared as an addendum to the interim report, "Health Risk Assessment of the B.K.K. Landfill, West Covina, California, November 1990" (Department of Health ServicesHazardous Waste Toxicology Section [DHS-HWTS], 1990), and presumes the reader is familiar with the interim report. The format follows the four components of a health risk assessment: hazard identification, toxicity assessment, exposure assessment, and risk characterization. This report is an addendum because at the time the interim report was being released to the public, the carcinogenic potency of vinyl chloride was being reevaluated, and a more potent value was expected to be derived. The interim report stated that an addendum would be prepared which would use the revised potency value and additional ambient vinyl chloride monitoring data. The objective of this addendum report is to quantitatively estimate the excess lifetime cancer risk associated with exposures to vinyl chloride near residential monitoring Stations A, B, and MY, located southeast and south of the closed Class I (hazardous waste) Unit of the B.K.K. Landfill. In May 1981, vinyl chloride was first detected in excess of the state's ambient air quality standard of ten parts per billion (10 ppb) at the landfill perimeter. The interim report and this addendum report primarily focused on exposures to vinyl chloride because vinyl chloride is a known human carcinogen, and it is rarely detected in ambient air of the South Coast air basin. Vinyl chloride has clearly been shown to be associated with the Class I Unit of the B.K.K. Landfill. The health risk assessment, conducted by the Office of Environmental Health Hazard Assessment (OEHHA), is possible because emissions of vinyl chloride reaching the residential community near the B.K.K. Landfill have been quantitatively studied since June 1981. The monitoring data were collected by a regulatory agency in residential neighborhoods almost daily for nearly a decade. Other hazardous chemicals are known to be emitted from the Class I Unit of the B.K.K. Landfill. However, no long-term monitoring of those compounds in air around the B.K.K. Landfill was undertaken, and so evaluation of any exposure to those chemicals is difficult. Those chemicals are also found in background air in the air basin, and it is not possible, with the available data, to distinguish between the amount of those chemicals emitted from the landfill and the amount found in ambient air from other sources. A summary of the sections of this report is given below. HAZARD IDENTIFICATION: The B.K.K. Landfill opened in 1963. Wastes were classified in statute as "hazardous" and "nonhazardous" by the State of California in 1972. From 1972 until December 1984, the B.K.K. Landfill served as the primary commercial hazardous waste disposal site for the Los Angeles area. The Class I (hazardous waste) Unit of the landfill stopped accepting hazardous waste on November 30,1984, and was closed in 1989. The B.K.K. Corporation has been operating a municipal solid waste landfill adjacent to the closed Class I Unit since 1987. Emissions of vinyl chloride from the closed Class I Unit are due to biodegradation of buried wastes containing chlorinated hydrocarbons and deposition of hazardous waste containing vinyl chloride. Other hazardous chemicals detected in ambient air are discussed in this section and in the exposure assessment section. CMA 114316 "X* TOXICITY ASSESSMENT: Information is presented about scientific advances in the understanding of risks associated with exposure to vinyl chloride. Both epidemiologic (occupational) and experimental animal data are reviewed and used in this assessment. Vinyl chloride is classified by both the United States Environmental Protection Agency (USEPA) and the International Agency for Research on Cancer (IARC) as a known human carcinogen. Occupational exposures and doses in experimental animals were in parts per million (ppm). Residential exposures to vinyl chloride from the Class I Unit of the B.K.K. Landfill have been in ppb. (It takes 1,000 ppb to make 1 ppm.) Studies in experimental animals have shown evidence of greater sensitivity in the very young from exposure to vinyl chloride. USEPA interprets the sensitive period seen in animals as relating to children aged 0 to 5. Increased sensitivity from exposures at a young age is discussed in this section and in the risk characterization section. EXPOSURE ASSESSMENT: Three sets of ambient vinyl chloride monitoring data are used in this addendum report: 1981-1982 data collected by South Coast Air Quality Management District (SCAQMD), with a detection limit of 10 ppb; 1983-1990 data collected by SCAQMD, with a detection limit of 2 ppb; and 1993-1994 data collected by the B.K.K. Corporation, with a detection limit varying from 0.005 to 0.010 ppb. SCAQMD's data were collected at three residential monitoring stations located southeast and south of the Class I Unit: Station A, located on the comer of Mariena and Nogales Streets; Station B, located on Lynn Court; and Station MY, located on Myra Court. B.K.K. Corporation's data were collected at three locations in close proximity to the former locations of Stations A, B, and MY. The 1981-1982 data were collected for 16 of the 24 months, the 1983-1990 data were collected almost daily, and the 1993-1994 data were collected every 12 to 14 days. Data collected for less than a 12-month period were assumed to be representative of a 12-month period. Photographs of the landfill operations during the early 1980s show activities such as the changing working face of the Class I Unit and the proximity of residential development. Seventy-two percent of the total 3.4 million tons of hazardous waste accepted at the Class I Unit was liquid hazardous waste, and approximately 85 percent of accepted fluids were disposed of at the working face. Odor studies conducted between 1978 and 1981 show that the most number of complaints came from residents on "M" and "L" named streets, located southeast and south of the Class I Unit, respectively. Residential development near Station A was completed in 1977; near Station MY, in 1979; and near Station B, in 1979. Data on other hazardous chemicals detected at Station A in 1982 are discussed, as are data on the same hazardous chemicals detected in the air basin in 1985. It is not possible, with the available data, to distinguish concentrations of these other hazardous chemicals that are due solely to emissions from the B.K.K. Landfill. RISK CHARACTERIZATION: Assumptions regarding the ambient vinyl chloride monitoring data used in the risk calculations are presented. Exposures are assumed to have begun in 1980, since residential development in the area had been completed in . 1979. A reasonable maximum exposure scenario (30-years) and an average exposure scenario (9-years) are calculated, rather than the worst-case scenario used in the interim report. A "reasonable maximum exposure" is the maximum exposure that is reasonably expected to occur, and is intended to be a conservative estimate, well above the average yet within the range of possible exposures. The unit risk value for vinyl chloride used in the calculations is the current California Environmental Protection Agency (Cal/EPA) CMA 114317 -xi- value of 20 x 10-5 per ppb, rather than the value of 0.69 x 10's per ppb used in the interim ' report. The unit risk is an upperbound estimate of the probability of developing cancer as a result of daily exposure over 70 years to 1 ppb of a substance in air. The Cal/EPA unit risk value was derived from a study in experimental animals (mice). Assuming the reasonable maximum exposure scenario of 30 years with exposures beginning in 1980, and assuming that individuals spend 80 percent of their time at home, the estimated excess (above background) lifetime cancer risk for an individual near the monitoring stations is as follows: at Station A, 7 x 10'5; at Station B, 6 x 10'5; at Station MY, 9 x IQ*5. Assuming an average exposure scenario for a 9-year period beginning in 1981 (covering the years of highest average annual concentrations) the estimated excess cancer risks are: at Stations A, 7 x 10 , at Station B, 5 x 10`5; and at Station MY, 8 x 10". Excess lifetime cancer risks using different assumptions for time spent at home, the average annual concentration of vinyl chloride in 1980, the substituted value for samples with nondetectabie concentrations in the 1981-1982 data, the exposure duration, and the unit risk value are presented using Station A as an example. When values of 62, 76 or 96 percent time spent at home are assumed, estimates of excess cancer risk are between 5 and 8 x 10'5 at Station A. When the value of 5 ppb is substituted for the average annual concentration in 1980 and for samples with nondetectabie concentrations in the 19811982 data at Station A, the estimate of excess cancer risk is 8 x 10's; when the value of 0 ppb is substituted, the estimate of excess cancer risk is 6 x 10'5. When a worst-case exposure duration (70 years; 1980-2046) is assumed, there is no change in the risk estimate at Station A. When unit risk-values derived from studies in male workers exposed to vinyl chloride are assumed, estimates of excess cancer risk are between 0.9 and 1 x 10'" at Station A. The population excess cancer burden (that is, the excess number of cases of cancer that may occur in a defined population who all have the same individual excess lifetime cancer risk) is not estimated because not all of the population around the landfill were or are exposed to the concentrations of vinyl chloride detected at Stations A, B, and MY, and it is not possible to obtain a reliable estimate of exposure to other residential areas. This addendum health risk assessment provides an assessment of past, present, and future risks for individuals living near Stations A, B, and MY from exposures to ambient fugitive emissions of vinyl chloride associated with the closed Class I Unit of the B.K.K. Landfill. There are four findings of this report: 1. From the available monitoring data, the single year of highest detected exposure to vinyl chloride was 1981. The maximum detected concentration of vinyl chloride at Station A in 1981 was 50 ppb, compared to 0.16 ppb in 1994. The average annual concentration at Station A in 1981 is estimated to have been 7.2 ppb, compared to an estimate of 0.05 ppb in 1994. For individuals who lived near Stations A, B, and MY during the 1980's, past exposures to vinyl chloride were higher than current exposures. The cumulative individual excess lifetime cancer risk suggests that for exposures beginning in 1980, the majority of the cancer risk was incurred by 1983-1984, and that there is little change (on the order of 15 to 22 percent) in the cumulative risk after 1986. CMA 114318 -xn- 2. The landfill gas collection system, which was expanded over time, and the cap covering the closed Class I Unit have been successful in lowering the frequency and level of vinyl chloride emissions to levels that pose little, if any, risk to nearby residents. 3. Regulatory agencies with responsibility for remediation or control of the B.K.K. Landfill may want to include past exposures of vinyl chloride near Stations A, B, and MY in subsequent health assessments of emissions from the landfill to ensure future risks do not add significantly to the past cumulative risk. 4. In spite of using best available scientific knowledge, there is considerable uncertainty associated with the estimated exposures, the carcinogenic potency value of vinyl chloride, and young-age sensitivity methodology. The estimated excess cancer risks calculated in this addendum report are upperbound estimates, based on the assumptions, methodology, limitations and uncertainties specified. The actual excess cancer risk is likely to be lower than these estimates and may be zero. Because the number of people who actually lived or are living near Stations A, B, and MY is small, it is unlikely that excess cases of cancer will occur. Each exposed individual may have an increased risk of developing cancer, however, the added risk is small. CMA 114319 -Xlll- INTRODUCTION This report is prepared a$ an addendum to the interim report, "Health Risk Assessment of the B.K.K. Landfill, West Covina, California, November 1990" (DHS-HWTS, 1990), and presumes the reader is familiar with the interim report. The format follows the four components of a health risk assessment: hazard identification, toxicity assessment, exposure assessment, and risk characterization. This report is an addendum because at the time the interim report was being released to the public, the carcinogenic potency of vinyl chloride was being reevaluated by DHS and the Air Resources Board (ARB). The unit risk is a measure of carcinogenic potency and an upperbound estimate of the probability of developing cancer as a result of daily exposure over 70 years to one ppb of a substance in air. It was expected that the reevaluation would indicate vinyl chloride was more potent than previously thought, which would make the cancer risk estimated in the interim report an underestimate and out-of-date. The interim report stated that an addendum would be prepared which would use the revised unit risk value for vinyl chloride and additional ambient vinyl chloride monitoring data. This addendum report is not required by any state or federal statute, regulation, or agency. The original impetus for the health risk assessment of the Class I Unit of the B.K.K. Landfill dates from 1985. At that time, DHS committed to undertake three health studies in response to residents' concerns about potential health hazards associated with living near the B.K.K. Landfill. The health studies were: a cancer study, a health risk assessment, and a reproductive outcomes study. A cancer study investigates cases of diagnosed cancers whereas a health risk assessment estimates the theoretical probability (the "risk") of developing cancer. This addendum report plus the interim report complete the health risk assessment of the Class I Unit of the B.K.K. Landfill in West Covina. Objective, Methodology, and Scope of the Addendum Health Risk Assessment The objective of this addendum report is to quantitatively estimate the "excess" lifetime cancer risk associated with exposures to vinyl chloride at residential monitoring Stations A, B, and MY. "Excess" refers to the risk above the background risk in the United States of developing cancer during a 70-year lifetime. Within the United States, the probability of developing cancer is 4 in 10, or 40 percent (Miller et al., 1993). This addendum report estimates risks above the background level. The methodology of this addendum report follows risk assessment guidelines set forth by USEPA (USEPA, 1989a; 1989b; 1991a; 1991b; 1992a). These guidelines are used so that the addendum report will be consistent with standard methodology, and so that its findings can be compared to findings of other health risk assessments of the B.K.K. Landfill. Changes in USEPA's recommended guidelines followed in this addendum report include the use of reasonably maximum and average exposure scenarios, and use of half the detection limit for samples with nondetectable concentrations. The interim report had used a worst-case exposure scenario, and the value of the detection limit for samples with nondetectable concentrations. TABLE 1 highlights similarities and differences between the interim report and this addendum report. CMA 114320 TABLE 1 COMPARISON OF THE 1990 INTERIM AND 1996 ADDENDUM HEALTH RISK ASSESSMENT OF THE CLASS I UNIT OF THE B.K.K. LANDFILL, WEST COVINA, CALIFORNIA Section Hazard Identification Chemical of Primaiv Concern Other Chemicals Detected in Ambient Air Toxicity Assessment Unit Risk Value Non-Cancer Health Effects 1990 Interim Report Vinyl chloride 7 known or suspected human carcinogens. vinyl chloride (known), benzene (known), trichloroethylene, perchloroethylene, chloroform. *1,1-dichloroelhylene, and 1,2-dichforoethane 0.69 x 10"5 per ppb Estimated using Chronic Reference Doses 1996 Addendum Report Vinyl chloride 6 known or suspected human carcinogens: vinyl chloride (known), benzene (known), trichloroethylene, perchloroethylene, chloroform and 1,2-dichloroethane 20 x 10'5 per ppb Not applicable Exposure Assessment Vinvl chloride momtonnq data * South Coast Air Quality Management District (SCAQMD) * BKK Corporation Samoles With Wondefecfed Concentrations Exoosuie Scenano(s) Risk Characterization Individual Excess Lifetime Cancer Risk O 2 > CO IO "* PoDulation Excess Cancer Burden 1983- 1987 Not applicable June 1981 - December 1982 January 1983 - March 1990 September 1993 - September 1994 Nondelected concentrations given a value equal to the detection limit Worst-Case (70 years) Nondelected concentrations given a value equal to 1/2 the detection limit Reasonably Maximally Exposed (30 years) Average Exposed Individual (9 years) Estimated at Station MV using 1987 ambient vinyl chloride monitoring data Estimated at Station A using 1982 - 1987 ambient vinyl chloride monitoring data Estimated for the 1982 Expanded Monitoring Program (ambient air) Estimated for the 1984 Extended Monitoring Program (indoor air) Estimated using the Air Resources Board model of 1987 vinyl chloride data Estimated for the population within 1 mile of the landfill (40,000 people) Estimated at Stations A, B and MV using SCAQMD and BKK monitoring data (1981 - 1994) . Discussed in Exposure Assessment section Updated risk calculation in Appendix G Modeling program discussed in Appendix F Not applicable * 1, 1-dichloroelhylene is no longer classified asasuspecled human carcinogen by the California Environmenial Protection Agency. -2- Typically, risk assessments required by regulatory agencies estimate current and future risk only. The methodology builds in overestimation of exposures to prevent underestimation of potential risks. Mitigation measures can then reduce current and future exposures if risk estimates are not acceptable. USEPA guidance for Superfund sites notes that `exposure assessments may consider past, present, and future exposures. Current and past scenarios should be based on actual exposure conditions, future scenarios on potential exposure conditions. Typically, Superfund risk assessments focus on current and future exposures, but past exposures may be important for selected sites" (USEPA, 1989b). The guidance recommends the Agency for Toxic Substances and Disease Registry (ATSDR) take the lead in evaluating current health effects from past exposures. ATSDR, created in 1980, is the federal agency authorized to conduct public health assessments at sites subject to the Resource Conservation and Recovery Act (RCRA). ATSDR defines a public health assessment as `an evaluation of environmental contamination data, community health concerns, and health outcome data" (ATSDR, 1994). Of 69 public health assessments completed by ATSDR in 1994, approximately half were for sites with documented past exposure. Th B.K.K. Landfill is not a Superfund site. Between 1980 and 1981, USEPA granted `interim status" to the operation of the Class I Unit (see CH2M Mill, 1988). After subsurface landfill gas migrated from the Class I Unit and triggered the emergency evacuation of 19 homes along the southern border in July 1984, ATSDR evaluated the landfill (ATSDR, 1984). Because the duration of exposure to subsurface landfill gas was determined not to have exceeded seven years (the age of the affected homes), ATSDR concluded that an epidemiologic study was not indicated at that time, and DHS continued as the lead agency for health issues. Of concern regarding the B.K.K. Landfill are the following: Ambient air exposures are to vinyl chloride, a known human carcinogen; vinyl chloride is one of the few chemicals for which there are both human data and experimental animal studies, which indicate carcinogenic potential; Vinyl chloride is clearly associated with the closed Class I Unit of the landfill; wastes containing vinyl chloride were deposited in the Class I Unit until June 1981; Vinyl chloride is without detectable background contribution in the South Coast air basin. OEHHA's health risk assessment is possible because vinyl chloride was monitored in residential neighborhoods (Stations A, B, and MY) almost daily for nearly a decade by SCAQMD. Monitoring in residential neighborhoods eliminates the uncertainty associated with extrapolating from onsite to offsite locations. As technology advanced, the detection limit of . vinyl chloride was lowered, and the data consistently met SCAQMD's internal quality control/quality assurance guidelines. The scope of this addendum report is more refined than was the scope of the interim report. The refinement is due primarily to the iterative nature of risk assessments, and also to some changes in recommended guidance. The interim report was based on the exposure CMA 114322 -3- characterization (CH2M Hill, 1988), and estimated excess cancer risk for individuals living within a one-mile radius of the landfill, using data from four air monitoring programs (collected tietween 1982-1987) and one air modeling program, and a 70-year (worst-case) exposure scenario. Congruent with the iterative nature of risk assessments, this addendum report focuses on exposures associated with detections of vinyl chloride at Stations A, B, and MY because these locations, southeast and south of the closed Class I Unit of the B.K.K. Landfill, have been identified as the most impacted residential neighborhoods, and long-term monitoring data are available. Exposures occurred at other residential locations around the landfill. However, detected concentrations of vinyl chloride at other residential locations around the landfill were neither as high nor as frequent as detected concentrations at Stations A, B, and MY, and long-term monitoring are not available for the other locations. This addendum report assumes exposures at Stations A, B, and MY began in 1980 because residential development near Stations A, B, and MY was completed in 1979. Long-term ambient vinyl chloride monitoring began in June 1981. Only ambient (outdoor) fugitive emissions of vinyl chloride from the closed Class I Unit are evaluated in this addendum report. Complete characterization of the air pathway would also include a consideration of indoor air, reflecting exposure, if any, through subsurface landfill gas migration, and other effects that may make ambient and indoor concentrations differ. Subsurface landfill gas, as indicated by methane, did migrate from the landfill in 1984, and a limited indoor air sampling program for volatile organic compounds was conducted in selected homes. The limited indoor air sampling data is not included in the risk characterization of the long-term ambient vinyl chloride monitoring data because the short-term nature of the indoor monitoring is not compatible with the long-term monitoring. However, an updated risk estimate and more information about the short-term exposure that occurred in 1984 is presented in Appendix G. At this time, there is no evidence that subsurface landfill gas migration is a problem for homes in close proximity to the landfill. However, the B.K.K. Corporation will conduct a subsurface soil gas investigation under USEPA's RCRA Section 3008(h) Corrective Action Order on Consent to determine if a potential could exist for migration of subsurface soil gas even with of the landfill gas collection system. Exposures to additional hazardous chemicals were documented in the first health risk assessment of the B.K.K. Landfill (DHSARB- SCAQMD, 1983). These data and other data are evaluated in this addendum report. Previous Health Risk Assessments of the B.K.K. Landfill The first health risk assessment of the B.K.K. Landfill was conducted as a tri-agency study by DHS-ARB-SCAQMD and released in 1983 (DHS-ARB-SCAQMD, 1983). The study estimated excess lifetime cancer risk associated with exposures to concentrations of seven chemicals detected in ambient air at five locations around the landfill and one background location between July 19 to October 15,1982. Exposures were assumed to have begun in 1976, when the county building inspector began to approve dwellings for occupancy near the landfill (DHS-ARB-SCAQMD 1983). The excess cancer risk for the limited time period was estimated to be approximately 5 x 10 . The second health risk assessment conducted by the state was the interim health risk assessment (DHS-HWTS, 1990). In 1985, DHS initiated three health studies in response to residents' concerns: a cancer study, a health risk assessment, and a reproductive outcomes study. At a public meeting in December 1990, the cancer study, completed in two parts (Mack and Thomas, 1985; Mack and Pinder, 1988), the interim health risk assessment, and an initial CMA 114323 pregnancy outcomes study (Rust et a/., 1988) were released. A fact sheet summarizing the findings of the two-part cancer study and the interim health risk assessment was made available for residents (DHS-EETB, 1990). A copy of the fact sheet is contained in Appendix B. The two-part cancer study investigated cases of cancer diagnosed in residents who lived near the landfill between January 1972 through December 1982. The two-part study found no overall increase in the cancer rate among residents in the 11 census tracts studied, and no consistent pattern of occurrence to suggest that the B.K.K. Landfill was linked to individual types of cancer. Limitations of the study were explained in the fact sheet (see Appendix B). The interim health risk assessment estimated the theoretical probability of developing cancer for residents living near the landfill from exposure primarily to vinyl chloride in ambient air through 1987. The risk was estimated to be approximately 1 to 2 x 10'5. The study of pregnancy outcomes in the 1978-1984 birth cohorts found elevated rates for some pregnancy outcomes (very low birth weight [less than 1,500 grams] and neonatal mortality [death in the first 28 days of life]). The findings of the pregnancy outcomes study stimulated a more comprehensive investigation by DHS, and that study is currently in the process of being completed. The B.K.K. Corporation has completed three health risk assessments of the landfill, and is in the process of conducting one under the directive of the USEPA. The first two were prepared in 1986 as declarations filed in Superior Court of the County of Los Angeles on behalf of the B.K.K. Corporation. Those assessments recalculated the excess cancer risk associated with the seven chemicals detected in the 1983 tri-agency report, for the exposure period 1978-1985. In one report (Crump, 1986), the risk was estimated to be 0.25 x 10'5 (maximum likelihood estimate) and 1.1 x 10'5 (upper 95 percent confidence limit estimate); in the other report (Bogen and Smith, 1986), the risk was estimated to be 1.7 x 10's ("best" [50th percentile] estimate using a Monte Carlo analysis). A copy of each assessment was attached as appendices to the interim report. The third health risk assessment, prepared by ENVIRON Corporation in 1991 in fulfillment of the Air Toxics "Hot Spots" Information and Assessment Act (AB 2588) of 1987, is being reviewed by SCAQMD (ENVIRON Corporation, 1991). The "AB 2588" risk assessment is a regulatory risk assessment, which means that its purpose was to estimate current and future risks associated with the landfill (California Air Pollution Control Officers Association [CAPCOA], 1991). As per the Health and Safety Code Section 44361, OEHHA-Air Toxicology and Epidemiology Section (ATES) reviewed the AB 2588 risk assessment and submitted its comments to SCAQMD (OEHHA, 1993). The current health risk assessment required by USEPA will address evaluations of all environmental media: groundwater, soils, air and if possible, surface water. Evaluation of the air medium will include ambient air and subsurface soil gas pathways. The ambient air pathway will include a one-year sampling program of 19 volatile organic compounds, including vinyl chloride, at onsite and offsite locations (B.K.K. Corporation et at., 1994). Organizational Changes in the Department of Health Services Since the 1990 Interim Report In July 1991, Governor Wilson created Cal/EPA. HWTS, which prepared the interim report, was moved from DHS to Cal/EPA. The Health Hazard Assessment Division of DHS became OEHHA. This addendum health risk assessment is prepared by OEHHA-HWTS. The Environmental Epidemiology and Toxicology Branch (EETB) of DHS is now the Environmental Health Investigations Branch (EHIB), in the Division of Environmental and -5- CMA 114324 Occupational Disease Control (DEODC) of DHS. EHIB is completing the more comprehensive reproductive outcomes study. Appendices to the Addendum Health Risk Assessment Appendices to this report contain the following: Appendix C, updated toxicity tables from the 1990 interim report; Appendix D, statistical evaluation of the 1983-1990 ambient vinyl chloride monitoring data collected by SCAQMD; Appendix E, 1990 population census tract data for the vicinity of the landfill; Appendix F, an air dispersion model of the 1983-1990 ambient vinyl chloride monitoring data; Appendix G, updated risk estimates for the 1984 indoor air monitoring program evaluated in the interim report; Appendix H, a copy of a letter from DHS-Cancer Surveillance Section regarding review of recent tumor incidence data; Appendix I, a copy of the notice of release of the draft addendum report; and Appendix J, OEHHA's response to comments on the draft addendum report. FIGURE 1 and FIGURE 2, from the interim report, show the location of the B.K.K. Landfill and the closed Class I Unit, respectively. CMA 114325 -6- FIGURE 1 2222NMENTAL$OLUTIONS. INC, Souxe*: loviromantal Solution*, Ine., Flura 1.1. -Jnt landfill Sito Aunmat and Mltifa&lon Hoik Flan, Book I, Subauxiaea: Sita CbaiaetatitaLion," Hateb li, 18SS. p. 1*2. 7- CMA 114326 FIGURE 2 01i0 t- r y Ba se vt sm K 3 JH o -fc>. 0to3 ~vl HAZARD IDENTIFICATION This section provides information about vinyl chloride disposal in the Class I Unit, vinyl chloride emissions from the Class I Unit, other hazardous chemicals detected in ambient air around the landfill, and regulatory agencies involved with the landfill. Vinyl Chloride in the Class I Unit While other chemicals are known to be emitted from the B.K.K. Landfill, vinyl chloride is the chemical of concern because it is a known human carcinogen and has clearly been shown to be associated with the landfill. Rarely detected in ambient air in the South Coast air basin, vinyl chloride was monitored almost daily by SCAQMD at residential locations south of the landfill between June 1981 and March 1990. Emissions of vinyl chloride from the landfill are presumed to be due to two processes: biodegradation of buried wastes containing chlorinated hydrocarbons, and deposition of hazardous waste containing vinyl chloride in the Class I Unit. The landfill opened in 1963, approved by the City of West Covina and the Los Angeles Regional Water Quality Control Board (RWQCB). In 1972, the State passed the Hazardous Waste Control Act. The Act required wastes to be classified as "hazardous" or "nonhazardous." From 1972 until November 30, 1984, the B.K.K. Landfill served as the primary commercial hazardous waste disposal site for the Los Angeles area. Records of hazardous waste disposal at the landfill date from 1975 (CH2M Hill, 1988). An estimate of the total amount of waste containing vinyl chloride deposited at the landfill has not been identified. Four facilities in the South Coast air basin handled vinyl chloride, and all four disposed of waste containing vinyl chloride in the Class I Unit at the B.K.K. Landfill (ARB, 1982a). Opening years of operations for the facilities were: Keysor-Century in Saugus, 1958; Stauffer Chemical in Carson, 1959 (closed in 1982); B.F. Goodrich Company in Carson, 1960 (closed in 1985); and Union Carbide in Torrance, 1972. Stauffer Chemical produced vinyl chloride until 1982 (ARB Part A, 1990; SCAQMD, 1983). Stauffer Chemical sent wastes from its ethylene dichloride and vinyl chloride operations to the Class I Unit from at least 1975 to mid-1981; in 1979, Stauffer disposed of approximately 50 tons of waste containing vinyl chloride and larger amounts of waste containing other halogenated compounds (ARB, 1983). Waste from its ethylene dichloride plant contained on the average 45 percent ethylene dichloride and 30 percent 1,1,2-trichloroethane (ARB, 1982b). These two chemicals can biodegrade to vinyl chloride (Vogel et al., 1987). Seventy-two percent (72%) of the total 3.4 million tons of hazardous wastes deposited in the Class I Unit between 1975 and 1984 was liquid hazardous waste (CH2M Hill, 1988). Liquids were disposed of at the working face, buried in drums, or injected into a total of 96 boreholes drilled into buried waste. Injection well (borehole) records identify truckloads of ethylene dichloride waste deposited in 1975, 1978, and 1979 (CH2M Hill, 1988). Approximately 85 percent of accepted fluids were disposed of at the working face and 10 percent in the boreholes (The Janes Network, 1994). CMA 114328 FIGURE 3 is a graphic presentation of the tons of hazardous waste deposited annually in the Class I Unit between January 1975, when records became available, and November 30, 1984, when the unit stopped accepting hazardous waste. Explanations for the dips in the figure are as follows: The dip in the figure for 1981 is attributed to the prohibition in June of waste containing vinyl chloride following the detection at the facility perimeter of vinyl chloride above the California ambient air quality standard of 10 ppb; The decline in 1984 is attributed to regulatory restrictions on the disposal of liquid wastes, and to the halting of hazardous waste disposal (except for asbestos) on November 30, 1984, Vinyl Chloride Emissions From the Class I Unit The landfill gas collection system is one of the ongoing site activities which has reduced the frequency and level of vinyl chloride emissions over time. Gas collection wells and a pilot gas burner and venting system were initially installed at the B.K.K. Landfill in 1975 (CH2M Hill, 1988). In 1980, the system consisted of 15 wells and 2 gas flares. An accelerated gas control program was started in July 1984 after subsurface landfill gas migration triggered evacuation of 19 homes along the southern border of the landfill (see Appendix G). By 1985 the landfill gas collection system included approximately 100 vertical gas extraction wells, 150 perimeter gas control wells, 198 perimeter gas monitoring probes, 4 horizontal gas well systems, and 2 flare stations with a total of 8 gas flares. As of 1994, the system consists of approximately 2,053 vertical gas extraction wells, 317 horizontal gas extraction wells, 170 perimeter gas monitoring probes, and the 2 flare stations with a total of 10 flares. Some of the wells and probes are located on the Class III (nonhazardous) portion of the landfill. The Integrated Waste Management Board (IWMB) and SCAQMD monitor the landfill gas collection system. Maintenance of the cap on the closed Class I Unit is another factor in controlling fugitive emissions of vinyl chloride from the landfill. In 1992, B.K.K. Corporation and the Department of Toxic Substances Control (DTSC) reached a settlement agreement for violations of state hazardous waste laws and regulations found during a 1990 inspection (Cal/EPA, 1992). Failure to properly maintain the cap, designed to prevent rainwater from leaking in and landfill gas from escaping out, constituted one of the violations. On June 28 and 29, 1994, a multi-agency team consisting of 17 representatives from USEPA, DTSC, SCAQMD, IWMB, and the Local Enforcement Agency (LEA, City of West Covina) inspected the closed Class I Unit in response to the LEA's concerns about continuous detections of vinyl chloride in ambient air. Grid sampling on the surface of the closed Class I Unit over the two days found a total of 15 samples with readings of total hydrocarbons in excess of the instantaneous total hydrocarbon limit of 500 ppm (SCAQMD, 1994b). The total hydrocarbon limit was established under SCAQMD's "District Rule 1150.1," adopted in 1985 for the purpose of reducing gaseous emissions from active landfills (SCAQMD, 1985). SCAQMD issued two Notices to Comply to the B.K.K. Landfill for the elevated surface emissions: reinspection by SCAQMD two weeks later found the surface emissions in compliance. Although the B.K.K. Corporation has been working toward improving the vegetative and day cover of the closed Class I Unit, conclusions of the multi-agency inspection included a recommendation for routine and consistent maintenance activities (USEPA, 1994a). -10- CMA 114329 Tons of Hazardous Waste FIGURE 3 TONS OF HAZARDOUS WASTE DEPOSITED IN B.K.K. LANDFILL WEST COVINA, CALIFORNIA 800000 - 700000 600000 500000 400000 300000 200000 x` .*----- 100000 /\ i\ ,____X x \/ \/ x X 1975 1976 1977 1978 1979 1980 1981 1982 1983 1984 Year figure derived from Table 1.4 `BKK Landfill Site Assessment and Mitigation Work Plan, Book I, Subsurface: a Characterization,* Environmental Solutions, Inc., March 15,1988, pgs. 1-22 and 1-23. CMA 114330 -11- Ambient air monitoring at the perimeter of the landfill for concentrations of total organic compounds and any toxic air contaminant (such as vinyl chloride) in the landfill gas control system was also required under SCAQMD's Rule 1150.1. Semiannual monitoring was required of the B.K.K. Corporation. Based on the Rule 1150.1 monitoring, the B.K.K. Corporation published a Proposition 65 Warning for detections of vinyl chloride along the southern perimeter of the landfill on August 29, 1993, in the San Gabriel Valley Tribune (B.K.K. Corporation, 1993b). (Proposition 65 is California legislation [Health and Safety Code Section 25249.5 et seq.] regarding exposures and discharges of known carcinogens and reproductive toxicants. For carcinogens, Proposition 65 requires a warning for exposures in excess of an individual estimated cancer risk of 1 x 10'5. For vinyl chloride, the 1 x 10'5 risk level of 3 micrograms per day under Proposition 65 regulations [California Code of Regulations, Title 22, Section 12705] equates to a concentration in air of 0.05 ppb.) In September 1993, the B.K.K. Corporation began a voluntary ambient air sampling program to collect data that would be used to refine the Proposition 65 warning (B.K.K. Corporation, 1993c). B.K.K. Corporation's Proposition 65 monitoring program evolved to include additional perimeter stations, dilution (residential) stations, and collocated (duplicate) stations, and increased the frequency of monitoring to every 12 to 14 days. The B.K.K. Corporation also sought to lower the detection limit for vinyl chloride (B.K.K. Corporation, 1993a). Since 1993, the B.K.K, Corporation reports achieving a detection limit varying from 0.005 to 0.010 ppb. USEPA has stated that the analytical procedure appears to be acceptable to USEPA for the purposes of ambient air monitoring at the B.K.K. Landfill (USEPA, 1994e). SCAQMD reviewed the modified protocol for vinyl chloride analysis and found it acceptable (SCAQMD, 1994a). USEPA also required control of emissions of vinyl chloride from the closed Class I Unit. Beginning in October 1993, USEPA required the B.K.K. Corporation to develop a Response Action Plan (RAP) which would implement actions within 30 days to reduce vinyl chloride emissions whenever ambient air sampling results showed detections of vinyl chloride equal to or greater than 0.5 ppb (USEPA, 1994f). Response actions included sealing cracks in the cap of the closed Class I Unit, and pumping liquids from gas collection wells. Other Hazardous Chemicals Detected in Ambient Air The earliest ambient air monitoring data of the B.K.K. Landfill is contained in the 1980 report, "Second Interim Report, Investigation of Odorous and Volatile Compounds for BKK Class I Landfill Site in the City of West Covina,'' prepared by the University of Southern California (USC) for the B.K.K. Corporation. Vinyl chloride was not among the more than 20 compounds analyzed; benzene and chloroform were identified as the carcinogens of concern (USC, 1980). The data were collected during active, open-face hazardous waste disposal. They were reviewed by CH2M Hill in the exposure characterization report and found to have limitations and uncertainties in laboratory analytical accuracy and quality assurance which precluded their use as a primary data set to assess human exposure (CH2M Hill, 1988). The 1982 ambient air program conducted by the three agencies (DHS-ARB-SCAQMD, 1983) was designed to monitor nine compounds known or suspected to be human carcinogens. In addition to vinyl chloride, the following chemicals were monitored: benzene, (also a known human carcinogen), chlorobenzene, trichloromethane (chloroform), 1,1-dichloroethene (vinylidene chloride), trans-1,2-dichloroethene, tnchloroethene, perchloroethene, and 1,2-dichioroethane (ethylene dichloride). Trans-1,2-dichloroethene and chlorobenzene were -12- CMA 114331 not detected. Vinylidene chloride is no longer considered a carcinogen by Cal/EPA (Standards - nd Criteria Work Group [SCWG], 1994). The carcinogens detected in 1982 have been detected in landfill gas at the inlets to the landfill flares. Data from flare emissions and source tests were reviewed by CH2M Hill in the exposure characterization (CH2M Hill, 1988). Flare emissions data were determined to be inadequate for use in exposure assessment because of lack of replicate sampling, split sampling, and simultaneous ambient air sampling. The source tests data were found to be inadequate because of limited sampling time (3-hour tests), which may not reflect a full 24-hour period. The carcinogens detected at Station A in 1982 are among 12 selected volatile organic compounds monitored by ARB and/or SCAQMD in the air toxics monitoring program, begun in 1985 (SCAQMD, 1987). The air toxics monitoring program provides information on background levels for the selected compounds in the Los Angeles air basin. Data from ARB's El Monte Station were included in the interim report because the El Monte Station appeared to be more representative of ambient air conditions around the B.K.K. Landfill. However, vinyl chloride and 1,2-dichloroethane were not monitored at the El Monte Station. Monitoring in 1985 at SCAQMD's Azusa Station, located approximately 3.5 miles to the north/northwest of the B.K.K. Landfill, included the six carcinogens also detected at Station A in 1982. These two data sets are discussed in the exposure assessment section of this addendum report. In December 1994, the B.K.K. Corporation began a one-year ambient air monitoring program for 19 volatile organic compounds at onsite and offsite locations around the facility. These data are being reviewed by USEPA for the risk assessment it is requiring the B.K.K. Corporation to conduct. Regulatory Agencies Involved With the B.K.K. Landfill Regulatory agencies involved with activities of the landfill are: the USEPA, for corrective actions at the entire 583-acre facility; DTSC, for the closed 170-acre Class I Unit; SCAQMD, for control of gaseous emissions from the facility; RWQCB, for discharges from the facility affecting groundwater or surface water; IWMB and the City of West Covina, for solid waste issues at the facility. ARB provides technical support to the agencies, as needed. CMA114332 -13- BLANK PAGE CMA 114333 -14- TOXICITY ASSESSMENT This section explains the toxicity values used in the risk characterization, and adds information on how increased knowledge has lead to changes in the assessment of the carcinogenicity of vinyl chloride. Toxicity Values Toxicity values are numerical expressions of a chemical's dose-response relationship, that is, the amount of a chemical (dose) that induces an effect (response). Toxicity values are developed for noncarcinogenic and carcinogenic effects. Reference doses (RfDs) are used when exposure occurs by the ingestion route. Since the 1990 interim report, USEPA developed reference concentrations (RfCs) for exposures by the inhalation route. Both RfDs and RfCs are used as measures of a chemical's noncarcinogenic toxicity. RfDs and RfCs are not expressed as probabilities or risks but rather as thresholds below which it is unlikely that even sensitive populations will experience adverse health effects from exposure to a specific chemical. A slope factor is the upperbound estimate of the probability of a response per unit intake of a chemical over a lifetime, expressed in the units "(milligrams per kilogram per day [mg/kg-d])'1." The unit risk is the probability of a response per unit concentration of a substance in the medium where human contact occurs. Both the slope factor and the unit risk are measures of a chemical's carcinogenic activity. For ambient air exposures, the unit risk is an estimate of the probability of developing cancer as a result of daily exposure over 70 years to 1 ppb of a substance in air. The unit risk is expressed as "(ppb)'1." Updated toxicity information for carcinogens detected in environmental media around the landfill is contained in Appendix C. History of the Assessment of Vinyl Chloride Toxicity Understanding of adverse health effects associated with exposure to vinyl chloride, and the "dose" necessary to induce the effects, has advanced over the years. Vinyl chloride is one of the few chemicals for which there are both epidemiologic studies and experimental animal data. The following chronology is presented to show the change over time of awareness about acute effects, chronic effects, carcinogenic effects, and developmental/reproductive effects. Vinyl chloride, a synthetic organic chemical, is a gas at ambient temperature and pressure, with a density twice that of air. First prepared in 1833, commercial preparation of vinyl chloride in the United States began in 1939 (United States Department of Labor [USDOL], 1974). The primary use of vinyl chloride is in the production of polyvinyl chloride (PVC). The industry is divided into three segments: monomer production, polymer production, and fabrication. Production of the monomer is a large-scale continuous process, involving only a few firms. Conversion to the polymer or copolymer is an incomplete batch process in which not all of the monomer is reacted (Barnes, 1976). Until 1974, high exposures to workers occurred during -15- CMA 114334 evacuation of the residual monomer gas, and during cleaning of the polymerization tank walls. Current regulatory standards and manufacturing processes substantially reduce or eliminate worker exposure to vinyl chloride. Little exposure occurred in the fabrication segment of the industry, where the finished PVC product is made by extrusion, injection molding, and calendering processes. Initially, vinyl chloride was regarded as a material of low human toxicity. In the 1930s, its use as a surgical anesthetic was considered, with narcotic properties being seen at levels around 8,000,000-10,000,000 ppb. However, its high flammability, and the cardiac and circulatory disturbances noted in animals and humans, precluded its use in surgical anesthesia (Patty, 1987). Acute, narcotic effects from exposure to vinyl chloride were the initial toxic end points of concern. The first occupationally associated deaths attributed to vinyl chloride were reported in the literature in 1960 (Danziger, 1960). The deaths were attributed to inhalation of vinyl chloride, presumably at levels above 10,000,000 ppb. In 1961, an indication of a chronic hazard was observed primarily in workers who cleaned polymerization tank vessels. They experienced a wide range of symptoms which became known as "vinyl chloride disease" and included: Raynaud's phenomenon (fingers blanch and experience numbness and discomfort upon exposure to cold), acro-osteoiysis (resorption of the terminal bones of the fingers and/or toes), joint and muscle pain, enhanced collagen deposition (the major protein of the white fibers of connective tissue, cartilage, and bone), stiffness of the hands, and scleroderma-like skin changes (thickening of the skin with adhesions to underlying tissue). These symptoms were observed at exposure levels below 50,000 ppb, Studies in the 1980s identified a role of the immune system in workers with vinyl chloride disease, and determined that susceptibility to vinyl chloride disease was increased in the presence of specific genes; the immunologic effects of vinyl chloride were observed in mice exposed to 10,000 ppb (ATSDR, 1993). No case of vinyl chloride disease has been reported since 1974 (ATSDR, 1990). In 1974, three employees from one PVC manufacturing company in the United States were identified as having died from a rare type of liver cancer, angiosarcoma of the liver (Creech and Johnson, 1974; Falk et a!., 1974). A fact-finding investigation by the Occupational Safety and Health Administration (OSHA) uncovered additional deaths due to angiosarcoma of the liver among workers in three similar companies. Between 1961 and 1977, 23 cases of liver angiosarcoma were reported among approximately 20,000 vinyl chloride workers in the United States (ARB Part B, 1990). Studies were undertaken worldwide (Sweden, England. Italy, Japan, Germany, Canada, Norway, France, and Russia) to assess mortality among workers exposed to vinyl chloride. By 1985, at least 17 epidemiologic studies relating vinyl chloride exposure to the incidence of various cancers had been completed. Most of the studies were a retrospective cohort design in which cases were identified 15 to 29 years after first exposure. Since monitoring of vinyl chloride was not routinely conducted before 1975, exposure concentrations were estimated based on job classification and length of employment, A worldwide registry of histologically confirmed cases of liver angiosarcoma resulting from exposure to vinyl chloride identified 120 cases between 1974 to 1986, of which at least 44 percent (53/120) were employed as polymerization tank wall cleaners (ATSDR, 1990). The worldwide registry, although incomplete, -16- CMA 114335 tabulates information about cases known to have occurred in men xposed to vinyl chloride that ,, have been reported by individual manufacturing companies, trade associations, and occupational health organizations in Europe, North America, and Japan (Forman et at., 1985). Studies in the 1980s examined additional types of cancer and noncancer effects. "Other cancers that have shown a statistically significant increase in mortality among vinyl chloride workers, in at least some studies, included cancer of the brain and central nervous system, the lung and respiratory tract, and the lymphatic/hematopoietic system" (ATSDR, 1993). The earliest experimental animal study on the carcinogenicity of vinyl chloride was reported in 1971 in a study of rats exposed by inhalation (Viola et at., 1971). Subsequent studies have shown that "vinyl chloride is carcinogenic in mice, rats, and hamsters when given orally and by inhalation. Vinyl chloride has been found to cause tumors in a dose-related manner at several sites, including liver, lung and mammary gland. The oncogenic response appears to be a function of the site, vinyl chloride concentration, tumor type, species of animal, and route of administration" (ARB Part B, 1990). In the liver, different types of tumors (liver angiosarcoma, hepatocellular carcinoma) have been seen following inhalation exposures. Hepatocellular carcinomas were observed only in rats, and the incidence of this tumor was significantly elevated when exposures started early in life (Maltoni et at., 1981; Drew et at., 1983; Cogliano and Parker, 1992). Hepatocellular carcinoma was induced in one study when exposures were begun at eight months of age (Drew et at., 1983). A study in newborn and adult rats on the effect of age on induction of pre-neopiastic hepatic lesions showed a well defined period restricted to the early lifetime of the animals (approximately day 7 to 21) during which the liver is most sensitive to carcinogenic effects of vinyl chloride (Laib et at., 1985a; 1985b). Cancer is considered to be a multistage process wherein a healthy ceil is transformed into a malignant one by a series of somatic mutations. The mechanisms by which vinyl chloride exerts its carcinogenic effects have been elucidated from studies in both cultured cells and experimental animals; vinyl chloride is metabolized to 2-chloroethylene oxide, which binds covalently to deoxyribonucleic acid (DNA) causing mutations (ATSDR, 1993; ARB Part B, 1990). Mathematical models derived from the multistage theory of carcinogenesis assist in estimating which stages in the process of tumor development are affected by a particular chemical. Effects on an early stage suggest the chemical "initiates" the cancer process (that is, that the chemical causes the initial event), while effects on a late stage suggest the chemical "promotes" tumor development. Both the epidemiologic (occupational) and experimental animal data indicate that vinyl chloride affects an early stage of carcinogenesis. Epidemiologic studies have found that workers exposed to vinyl chloride before age 25 (Wong et al., 1991) and between the ages of 25 and 34 (Chen and Blancato, 1989; Pirastu et at., 1990) had a higher risk of liver cancer death than workers exposed after age 35. In animal studies, "across all the species and endpoints examined, the evidence consistently suggests that vinyl chloride primarily affects the initial stage in tumor development," and to a lesser degree, contributes to late-stage tumor progression (Brown and Hoel, 1986). Exposure to vinyl chloride in the workplace environment was not controlled by any regulatory program during the 1940s and early 1950s. The first recommendations for an occupational exposure limit in the United States were issued in 1955 at a level of 500,000 ppb (Wu et al., 1989). Concern about the narcotic effects of vinyl chloride and the risk of developing acroosteolysis caused reduction in exposure limits in England in the 1960s (Forman etal., 1985). CMA 114336 -17- One estimate of typical exposures to vinyl chloride monomer among the more highly exposed workers at polymerization plants is: 1,000,000 ppb prior to 1955; from 300,000 to 500,000 ppb during 1955 through 1970; and from 100,000 to 200,000 ppb during 1970 to 1974 (Wu et al., 1989) . In 1974, OSHA promulgated a 1,000 ppb occupational standard (USDOL, 1974). In the late 1970s, several studies were undertaken to determine whether there were any cases of liver angiosarcoma in residential neighborhoods adjacent to vinyl chloride production or polymerization facilities prior to occupational controls (Doll, 1988): a study in Sweden and the former Yugoslavia found none; a study in Great Britain found 1 over a 12-year period but exposure was not attributed to the facility because the individual lived near the plant for only 6 years; a study in New York found 4 cases over an 18-year period in people who lived within 1 mile of fabrication plants or a polymerization plant. The cases in New York were diagnosed between 1958 and 1975, and occurred after 15 or more years of residence, suggesting an association with the facilities (Brady et al., 1977). Doll notes that "This disease [angiosarcoma of the liver] is normally so rare that, in the absence of specific exposure to one of the known causes (vinyl chloride, thorium dioxide, and arsenic in pesticides and medicines), the annual incidence is on the order of 1-2 x 10*7. In these circumstances the discovery of even one case in a man living close to a factory in which vinyl chloride was used in the days before exposure was tightly controlled, may be regarded as presumptive evidence of the effect of environmental pollution." It is reported that concentrations of vinyl chloride within one kilometer of plants handling vinyl chloride in 1975 were on the order of 10 to 40 ppb, which is one-ten thousandth of the estimated concentration that caused the observed occupational incidence (Doll, 1988; Baxter et al., 1977). "Epidemiological studies of families of vinyl chloride workers or communities having vinyl chloride processing facilities suggested the possibility of an increased incidence of birth defects and spontaneous abortions among people at risk; however, subsequent reviews of these studies have concluded that there is inadequate evidence to link environmental or paternal exposure to vinyl chloride with birth defects or spontaneous abortions in humans" (ARB Part B, 1990) . "Vinyl chloride crosses the placenta of experimental animals. Some data indicates it may act as a transplacental carcinogen" (ARB Part B, 1990). Studies in experimental animals have shown developmental toxicity consisting of decreased litter size and fetal weight, delayed ossification, and dilated ureters; however, these effects occurred at levels which also produced maternal toxicity, so it is not clear if the effects on the fetus are due to maternal toxicity or to vinyl chloride (ATSDR, 1993). Reproductive effects reported in male workers exposed to vinyl chloride are decreased sexual function (androgen levels) and libido; exposure levels were not given and concomitant exposure to other chemicals could not be ruled out in those studies (ATSDR, 1993). A study by Bi ef al. of male rats exposed by inhalation to vinyl chloride found a statistically significant increase in damage of testicular seminiferous tubules at concentrations of 100,000 ppb; decreased testicular- and increased liver-to-body weight ratios at 100,000 ppb; and no observed adverse effects at 10,000 ppb (Bi et al., 1985). USEPA, DTSC, and OEHHA developed an action level' of 25 ppb for indoor air exposures to vinyl chloride near Operating Industries, Inc., a Superfund site in southern California, cased on no observed adverse effects in rats at 10,000 ppb (Hiatt ef a/., 1993). ATSDR developed a minimum risk level (MRL) of 2 ppb for inhalation exposures of 15 to 364 days duration, basea on the increased liver-to-body-weight ratio in rats (ATSDR, 1993). Vinyl chloride has been identified as a mutagen in bacteria, yeast, and animal systems. Workers exposed to less than 15,000 ppb, however, did not show higher levels of chromosome breaks or aberrations than those in the control group (ARB Part B, 1990). -18- CMA 114337 New Unit Risk Value and Proposition 65 &EHHA-ATES reviewed epidemiologic (occupational) studies and animal cancer bioassays for the purpose of developing a unit risk value for ARB as required by the Toxic Air Contaminant Program (Health and Safety Code Section 39650 et seq.). The unit risk was derived using the linearized multistage model (described in detail in ARB Part B, 1990). TABLE 2 lists the 95 percent upper confidence limits (UCLs) range of cancer risk estimates for vinyl chloride derived by OEHHA-ATES. Three values are shaded: The high end of the range estimate; the theoretical, upperbound, individual (human) excess lifetime cancer risk of 20 x 10'5 per ppb, based on studies in female mice that developed lung carcinoma; - The low end of the range estimate; the theoretical, upperbound, individual (human) excess lifetime cancer risk of 2.5 x 10`5 per ppb, based on studies in male workers who developed liver cancer only (liver angiosarcoma and primary liver cancer); and - The middle of the range estimate; the theoretical, upperbound, individual (human) excess lifetime cancer risk of 4.5 x 10`5 per ppb, based on combined studies in male workers who developed liver, brain, or lung cancers. A unit risk based only on human studies would range between 2.5 x 10*5 per ppb, for liver cancer only (liver angiosarcoma and primary liver cancer), and 4.5 x 10'5 per ppb, for liver, brain, and lung cancers combined. OEHHA-ATES stated the "Evaluation of animal tumorigenicity data indicates that vinyl chloride's carcinogenic potency is dependent on sex, tumor site, and age of exposure. Taking all these factors into account, staff conclude that the best estimate to use in order to assure the public health is the top of the range of the animal UCLs of risk, 20 x 10-5 (ppb)'1* (ARB Part B, 1990). By using default conversion factors (that is, assuming an individual weighs 70 kilograms and breathes 20 cubic meters of air a day) and assuming daily lifetime exposure, the unit risk is equivalent to a slope factor of 0.27 (mg/kg-day)*1. Low dose extrapolation models other than the linearized multistage model would likely produce lower or higher estimates of cancer potency, depending on the assumptions used in the model (that is, a sublinear model would yield a lower estimate of cancer potency and a supralinear model would yield a higher estimate). Preference for use of the linearized multistage model in estimating the potency of vinyl chloride is consistent with the generally recognized mechanism of action by which vinyl chloride exerts its carcinogenic effects. In December 1990, ARB adopted the unit risk value for vinyl chloride recommended by OEHHA-ATES, and identified vinyl chloride as a toxic air contaminant. In 1992, OEHHA established 3 micrograms per day (p.g/day) as the no significant risk level (NSRL) for vinyl chloride under Proposition 65. Proposition 65 is California legislation regarding exposures and discharges of known carcinogens and reproductive toxicants. For carcinogens, Proposition 65 requires a warning for exposures in excess of an individual estimated lifetime cancer risk of 1 x 10'5. The NSRL represents a daily intake level over a 70-year lifetime that is calculated to result in a risk of 1 x 10'5. The NSRL of 3 pg/day was derived from the unit risk value adopted by ARB, and equates to an ambient air level of 0.05 ppb vinyl chloride. -19. CMA 114338 TABLE 2 (Office of Environmental Health Hazard Assessment Air Toxicology and Epidemiology Section) RANK ORDERING OF ESTIMATES OF HUMAN RISK BY CATEGORY Rank Experiment Straina/Species, Sex Tumor Individuals^ Unit Riskc PPb'1 1. 2 3 4 5 6 7. 8 9 10 11 12 Drew : BT-9,15d Bi Drew BT-9,15 BT-1,2 =: Waxweiier Bi Drew Drew BT-1,2 V Waxweiter ; sw/mouse, female sd/rat, female wi/rat, male fi/rat, female sd/rat, mate sd/rat, female oc/httmao, male wi/rat, male fi/rat, female fi/rat, female sd/rat, female ; oc/humart, mala v ?' king carcinoma =-. liver angiosarcoma liver angiosarcoma liver angiosarcoma liver angiosarcoma liver angiosarcoma jhtep*braln*lung v lung angiosarcbma hepatocellular carcinoma mammary mammary threr . 228 i 380 78 353 298 313 1294 =. 78 353 354 394 1294 . 20-xltr? 18X10 13X10' 8.4x10 6.5x10' 4.9x10 v 45x10" 4.5x10 4 4x10' 4 2x10 3.7x1 O' s 2.5x10" a: sw - CDI Swiss, sd - Sprague-Dawley, wi - Wistar. fi - Fischer, oc - occupational cohort, b: Number of all individuals entered in the analysis, exposed and unexposed. c: Calculated as an upper confidence limit with units (mg/kg-d1) and converted to units of concentration (ppb'1) using default conversion factors. The unit risk is an estimate of the probability of being diagnosed with cancer as a result of daily exposure over 70 years to 1 pg/m^ of a substance in air. d: BT - MaKoni's Bentivoglio (Bologna, Italy) project on long-term carcinogenicity bioassays of vinyl chloride. Source: California Air Resources Board, "Technical Support Document, Part B, Proposed Identification of Vinyl Chloride as a Toxic Air Contaminant," October 1990, Stationary Source Division, Sacramento, California, pages 8-11. CMA 114339 -20- Sensitivity to Vinyl Chloride From Exposures at a Young Age In 1989, V.J. Cogliano of USEPA described in a memorandum a new assessment of the cancer risk from vinyl chloride (USEPA, 1992b), Cogliano identified a public health concern for young-age exposures based on a sensitive period seen in rats exposed by inhalation to vinyl chloride (Maltoni et a/., 1981; Drew et ai, 1983; Laib et at., 1985a, 1985b). The studies in rats showed that the carcinogenic effects from exposure to vinyl chloride depend on both age at initial exposure and duration of exposure, and therefore, suggest that children may face higher risks than adults for exposures of a given duration. USEPA interprets the sensitive period seen in rats as relating to children aged 0-5. The incremental cancer risk from breathing vinyl chloride throughout this age range may be equal and in addition to the cancer risk from breathing vinyl chloride throughout adulthood. This means that, for a given air concentration of vinyl chloride, an individual exposed during the first six years of life (age 0-5) incurs the full conventional (70-year) lifetime of risk, and an individual exposed from birth for 70 years incurs double the conventional lifetime risk. Short-term exposures for adults over 30, however, carry less than the conventional lifetime risk, according to USEPA's interpretation of the experimental animal data. TABLE 3 shows USEPA's estimates of risk for initial 6-year (age 0-5) and subsequent 4-year (age 6-9, etc.) apportioned lifetime exposures to vinyl chloride. The risk values in TABLE 3 are based on USEPA's slope factor for vinyl chloride of 0.29 (mg/kg-d)*1, which equates to a unit risk of 23 x 10'5 per ppb. (Note that the USEPA slope factor is almost identical to the Cal/EPA slope factor of 0.27 [mg/kg-d]'1). USEPA's 1991 interim guidance for Superfund includes a brief note on Cogliano's method of assessing apportioned lifetime exposures to vinyl chloride in the discussion of toxicity values for short-term exposures (USEPA, 1991a). In 1992, Cogliano published his interpretations of the experimental animal data for vinyl chloride (Cogliano and Parker, 1992). The report concludes that vinyl chloride provides an example of a chemical for which both toxicologic and pharmacokinetic evidence exists to override the default assumption of an equal risk over a lifetime under all age exposure conditions. In the 1994 edition of its Health Effects Assessment Summary Tables (HEAST), USEPA emphasizes that the slope factor and unit risk values for vinyl chloride do not reflect state-of-the-art science for vinyl chloride (USEPA, 1994b; 1994c), indicating that they do not reflect sensitivity to vinyl chloride from exposures at a young age, as identified by Cogliano. In 1993, USEPA, DTSC, and OEHHA co-authored a presentation which applied this young-age sensitivity methodology to action levels for relocation criteria at Operating Industries, Inc., a Superfund site in southern California (Hiatt et ai, 1994). There is good evidence that experimental animals are more sensitive to developing cancer as adults when exposed to vinyl chloride at a young age, compared to those exposed only as adults. However, the assessment methodology used by USEPA is relatively new and has not been fully evaluated or accepted for use in this type of health risk assessment. As mentioned, the unit risk value developed by OEHHA (20 x 10'5 per ppb) accounts for age specific sensitivity, and is used in this addendum report. CMA 114340 -71- TABLE 3 (United States Environmental Protection Agency) UNITED STATES ENVIRONMENTAL PROTECTION AGENCY'S ESTIMATES OF RISK FOR APPORTIONED LIFETIME EXPOSURES TO VINYL CHLORIDE AT VARIOUS CONCENTRATIONS Estimated Excess Lifetime Cancer Risk to Humans From a 4 Year Exposure: ________________Apportioned Lifetime Risk___________________ Afle! 0 to 5 6 to 9 10 to 13 14 to 17 18 to 21 1 oom 2.3 E-1 5.8 E-2 4.6 E-2 3.5 E-2 2.3 E-2 ' 100 PDb 2.3 E-2 5.8 E-3 4.6 E-3 3.5 E-3 2.3 E-3 10 DDb 2.3 E-3 5.8 E-4 4.6 E-4 3.5 E-4 2.3 E-4 1 PPb 2.3 E-4 5.8 E-5 4.6 E-5 3.5 E-5 2.3 E-5 0.1 PDb 2.3 E-5 5.8 E-6 4.6 E-6 3.5 E-6 2.3 E-6 0.2 DDb 4.6 E-5 1.2 E-5 9.3 E-6 7.0 E-6 4.6 E-6 * Age range during 4 year exposure period. Source: United States Environmental Protection Agency (USEPA), "Cancer Risk Estimates for Vinyl Chloride." Memorandum dated September 28,1992 from Jim Cogliano, Chief, Carcinogen Assessment Statistics and Epidemiology Branch, Office of Health and Environmental Assessment, Washington, D.C., to Arnold Den, Science Advisor, Region IX, San Francisco, California, with September 26,1989 memorandum attached. Risk estimates are based on USEPA's cancer slope factor for vinyl chloride of 0.29 (mg/kg-d)-1. CMA 114341 -22- EXPOSURE ASSESSMENT This section reviews the types, frequency, magnitude, and duration of residential exposures to vinyl chloride from the B.K.K. Landfill based on ambient vinyl chloride monitoring data, activities at the landfill, and odor complaints from residents around the landfill. In this section, the ambient vinyl chloride monitoring data are divided into four periods: 1981-1982 data, 1983-1990 data, combined 1981-1990 data, and 1993-1994 data. The data collected during the decade of the 1980s are displayed several ways (tables, line graphs, combined graphs, frequency graphs) in order to view exposures from different perspectives. Exposures to other hazardous chemicals detected in ambient air are also evaluated in this section. Ambient Vinyl Chloride Monitoring Data 1981-1982 Data In October 1980, odor complaints from residents living near the landfill prompted SCAQMD to monitor for organic compounds in the vicinity of the facility; in May 1981, vinyl chloride was detected above the ambient air quality standard of 10 ppb (DHS-ARB-SCAQMD, 1983). In June 1981, SCAQMD began monitoring at six locations. TABLE 4 shows the number of days the ambient air quality standard was exceeded at each of the six locations, the maximum concentration detected at each of the six locations, and the number of valid sample days per month (SCAQMD, 1982a). Twenty-four hour integrated bag samples were collected and analyzed by gas chromatograph-flame ionization with a detection limit of 10 ppb (SCAQMD, 1982b; 10 ppb is equivalent to 0.01 ppm). Residence 1 became Station A, located at the intersection of Mariena and Nogales Streets, 450 feet southeast of the landfill property line. Residence 2 became Station B, located on Lynn Court, immediately adjacent to the southern property line. FIGURE 4, from the interim report, shows the locations of Stations A, B, and MY. Monitoring continued at Stations A and B in 1982. The detection limit for vinyl chloride was lowered from 10 ppb to 2 ppb during the 90-day monitoring program conducted by the agencies, DHS-ARB-SCAQMD. The 1981-1982 data were reviewed in the exposure characterization report and deemed not to be useful for exposure assessment because of the detection limit of 10 ppb (CH2M Hill, 1988). They were not included in the interim report because of the change in the detection limit during the monitoring period. However, this addendum report spans long-term monitoring data in which the detection limit for vinyl chloride continues to be lowered as technology advances. Detections at or above the detection limits are assumed to be real detections in each monitoring period. Average annual concentrations in this addendum report are calculated using the arithmetic mean, rather than the geometric mean used in the interim report. USEPA considers "the arithmetic mean is appropriate regardless of the pattern of daily exposures over time or the type of statistical distribution that might best describe the sampling data. The geometric mean of a set of sampling results, however, bears no logical connection to the cumulative intake that CMA 114342 -23- TABLE 4 (South Coast Air Quality Management District) 1981 VINYL CHLORIDE CONCENTRATION, PPM AT BKK VICINITY LOCATION MONTHS DAYS3 Suburban Water Company 163 May June July Aug Septc 0 0 0 0 0 MAXb <01 <01 <01 <01 <01 DAYS OF VALID DATA 1 26 30 29 3 Suburban Water June , 0 <01 21 Company 164 July 0 <01 30 Aug 0 <01 29 Sept 0 <.01 3 Residence 1 June 10 .03 25 July 9 .03 30 Aug 8 .03 29 Sept 5 .01 22 Oct 9 .04 30 Nov 9 .02 24 Dec 12 .02 29 Residence 2 June 14 .05 25 July 9 .02 30 Aug 12 .02 29 Sept 9 03 22 Oct 12 .03 30 Nov 11 .03 24 Dec 7 .02 29 Residence 3 June July 3 .01 25 0 <01 5 Residence 4 July Aug Sept 3 .01 25 9 .02 29 0 <01 3 a) Days Number of days exceeding state standard. VC s .01 ppm, 24-hour average. b) Max - Single highest daily average in ppm. c) Sampling was discontinued on Sept. 3, 1981 at all locations except at Residence 1 and 2. Source: South Coast Air Quality Management District, "Vinyl Chloride in the South Coast Air Basin, May 1982," El Monte, California, p. 18. Note. PPM Parts per million; 1 ppm = 1,000 parts per billion (ppb); 0.05 ppm = 50 ppb. See TABLE 5 for monthly and annual average concentrations of vinyl chloride, Residence 1 = Station A: Residence 2 = Station B. CMA 114343 -24- FIGURE 4 (CH2M Hill) LOCATION OF SOUTH COAST AIR QUALITY MANAGEMENT DISTRICT'S AMBIENT VINYL CHLORIDE MONITORING STATIONS A, B, AND MY FIGURE 7: Air Monitoring Programs, BKK Landfill, West Covina, CA (Based on CH2MHIII Fig. 5-21 and Platt IS) i Source: CH2M Hill, `BKK Landfill Exposure Characterization Report. West Covina, California,' August 15, 1988. Volume I, p. 5-165 (Figure 5.21) and Volume II, Plate 15. CMA114344 -25- would result from long-term contact with the site contaminants, and it may differ appreciably from - and be much lower than - the arithmetic mean" (USEPA, 1992a). Calculating average annual concentrations when a certain portion of the data are below the detection limit requires exchanging samples with nondetectable concentrations for a value. USEPA recommends substituting half the detection limit for samples with nondetectable concentrations (USEPA, 1989b). When more than half the data are samples with nondetectable concentrations, assigned values may result in biased or imprecise estimates (Hornung and Reed, 1990). There is uncertainty associated with the substituted value since nondetected concentrations could range from zero to just below the detection limit. The "true" level cannot be known. TABLE 5 supplements the information in TABLE 4 by providing monthly and annual arithmetic average concentrations of vinyl chloride at Stations A and B during 1981-1982. The data were collected for 16 of the 24 months. SCAQMD's detection limit between June 1981 through September 1982 was 10 ppb, and between October through December 1982, 2 ppb. Results of the data collected between October 16 and December 31, 1982, were reported in terms of the ambient air quality standard (10 ppb) rather than the detection limit (2 ppb). Consequently, the number of samples with nondetectable concentrations in this portion of the data are likely overreported. Approximately 60 percent of the data in 1981 and 80 percent of the data in 1982 were samples with nondetectable concentrations. Substituting a value of half the detection limit (that is, a value of 5 ppb) for samples with nondetectable concentrations in this data set may result in estimated average concentrations that artificially reflect the detection limit. When a value of 1 ppb (half the detection limit for the 1983-1990 data) is substituted in the 1981-1982 data, the estimated average annual concentrations for 1982 are more consistent with the 1983 average annual concentrations. This suggests that 1 ppb is a more reasonable substitution value for the 1981-1982 data. This assumption may underestimate exposures since some samples may have had concentrations of vinyl chloride below 10 ppb but above 2 ppb. In the 1983 data, the percent of samples with nondetectable concentrations at the detection limit of 2 ppb decreased to 53-56 percent. The average values in TABLE 5 were calculated using 1 ppb for samples with nondetectable concentrations. FIGURE 5 shows the percent of days during 1981 and 1982 when vinyl chloride was detected above the ambient air quality standard of 10 ppb at Station A or B (ARB. 1983). CMA114345 -26- TABLE 5 1981-1982 AVERAGE VINYL CHLORIDE CONCENTRATIONS IN AMBIENT AIR (ppb) BKK LANDFILL, WEST COVINA, CALIFORNIA Station A (Residence 1) Annual Average Station B (Residence 2) Annual Average January February March Aphl May June July August September October November December January February March Aphl May June July August September October November December 1981 -- - 10.5 4.4 7.0 7.0 8.2 9.2 4.1 7.2 -- 7.5 4.7 5.0 3.1 6.9 8.4 6.6 6.0 1982 2.0 2.5 2.5 - - 8.1 4.9 3.2 3.1 1.7 2.8 3.4 3.3 3.1 3.4 1.0 2.2 1.9 3.5 2.1 5.0 2.8 Source: Letter regarding South Coast Air Quality Management Distncts continuous sampling and analysis project for vinyl chlonde monomer. Letter dated Aphl 9,1982 from Edward Camarena. Director of Enforcement, Headquarters, South Coast Air Quality Management Distnct, El Monte, to Mr. Joseph Pantalone, California Air Resources Board, Research Division, Sacramento. California. A value of 1 ppb was substituted for samples with nondetectabie concentrations. Detection limits: 6/81-9/82,10 ppb: 10/82-12/92, 2 ppb. CMA114346 -27- FIGURE 5 (Air Resources Board) 1981-1982 AMBIENT CONCENTRATIONS OF VINYL CHLORIDE NEAR BKK LANDFILL RCV (12/C2) Source: Air Resources Board, Figure 1 of "Developments in the BKK Landfill Situation," Memorandum dated January 12, 1983 from James J. Morgester, Chief, Enforcement Division to James Boyd, Executive Officer. Taken from BKK Landfill files, Stationary Source Division, Sacramento, California. CMA 114347 -28- 1983-1990 Data SCAQMD continued almost daily ambient air monitoring for vinyl chloride at residential Stations A and B with a detection limit of 2 ppb beginning in January 1983. On June 27, 1984, SCAQMD established Station MY, located on Myra Court, 150 feet southeast of the B.K.K. Landfill property line (FIGURE 4). SCAQMD continued monitoring for vinyl chloride at these three residential stations through March 1990. The detection limit for vinyl chloride changed during that period as follows: between 1983 through 1987, the detection limit was 2 ppb; from January 1988 through September 1989,1.4 ppb; and between October 1989 through March 1990, 2 ppb. Although SCAQMD's laboratory could achieve a lower detection limit in 1988, the time to process the analysis increased. SCAQMD considered the advantage of a quicker processing time outweighed the small increment in sensitivity, and so returned to using the 2 ppb detection limit. The three residential monitoring stations were dismantled after March 1990 because vinyl chloride was not detected at or above 2 ppb at any of the three stations for two consecutive months. Beginning in 1987, the frequency of samples with nondetectable concentrations was more than 50 percent at all 3 stations. Substituting the value of half the detection limits for samples with nondetectable concentrations beginning in 1987 may overestimate the average annual concentrations. TABLE 6 presents the average annual and maximum concentrations of vinyl chloride detected at Stations A, B, and MY between January 1983 through March 1990. Average annual concentrations ("means") were calculated using three different values for samples with nondetectable concentrations: mean 1 assumed one-half the detection limits; mean 2 assumed zero ppb; mean 3 assumed the detection limits. Although Station MY operated for only the last 6 months of 1984, data collected at Station MY between August through December 1984 show 153 days of vinyl chloride monitoring, for which the average concentration was 5.43 ppb. FIGURE 6 displays the average annual concentrations of vinyl chloride detected at Stations A, B, and MY between January 1983 and March 1990. FIGURE 7 displays on a monthly basis the frequency of vinyl chloride detected at or above 2 ppb at Stations A, B, and MY. Appendix D contains a statistical evaluation of SCAQMD's 1983*1990 ambient vinyl chloride monitoring data. CMA 114348 -29- TABLE 6 (Ogden Environmental and Energy Services Co., tnc.) 1983-1990 AVERAGE ANNUAL VINYL CHLORIDE CONCENTRATIONS (PPB) NEAR BKK LANDFILL 1983 1984 1985 1986 1987 1988 1989 1990(a) Monitoring Station A Max Value Mean 1 Mean 2 190 21 0 16 0 11.0 70 7.4 24 1 0* 2 84 4.17 3 45 1 92 1 67 1.30 0 79 1.00* 2 32 3.76 3.02 1 26 0.94 0.77 003 000 Mean 3 3.37 4 57 387 2.58 2 40 1.83 1.56 2 00 Max Value Monitoring Station B Mean 1 Mean 2 16 0 230 150 80 90 94 24 10* 2.98 3.93 2 29 1 33 1 16 0 76 0 78 1 00* 2 42 3 56 1 74 0 49 0 25 008 001 0 00 Mean 3 354 4 30 2.84 2 18 2 07 1 44 1 56 2 00 Max. Value Monitoring Station MY Mean 1 Mean 2 .__ 20 0 14.0 150 150 36 22 5.36 3 02 2.60 2 48 092 1.04 5.07 2 57 2 04 2 10 0.21 0.07 Means 1,2, and 3 calculated with the following assumptions regarding below detectable vinyl chloride measurements: Mean 1 - assume one-half deteclion limit Mean 2 - assume zero ppb. Mean 3 - assume detection limit. For monitoring periods 1983-1987 and 1990, reported instrument detection limit was 2 0 ppb. For January 1988 through September 1989, detection limit was 1 4 ppb. (a) Data collected only in January, February, and March during 1990 * All nondetecls (asterisks not in original report) Mean 3 . - 566 3 46 3.15 2.87 1 62 2.01 Source: "Table 4-3, Air Quality Modeling for the BKK Landfill Air Toxic Exposure Study," Ogden Environmenlal and Energy Services Co., Inc., November 1992, San Diego. Calitornia . pg. 32. Derived from South Coast Air Quality Management District's daily ambient vinyl chloride monitoring data, January 1983 through March 1990 Although Station MY operated for only the last 6 months of 1984, data collected at Station MY between August and December 1984 show 153 days of vinyl chloride monitoring, with an average concentration of 5.43 ppb. CMA 114349 -30- FIGURE 6 1983-1990 AVERAGE ANNUAL VINYL CHLORIDE CONCENTRATIONS (PPB) NEAR BKK LANDFILL, WEST COVINA, CALIFORNIA 6 Year Source: Figure derived from Table 6 of this draft addendum report *1983-1990 Average Annual Vinyl Chloride Concentrations (ppb) Near BKK Landfill." The source for Table 6 was "Air Quality Modeling for the BKK Landfill Air Toxic Exposure Study," Ogden Environmental and Energy Service Co., Inc., November 1992, San Diego. California. The slight increase in 1990 reflects the fact that 1 ppb was substituted for nondetects in the data, and data was only collected in J~~ ary, February, and March of 1990. No, .detected concentrations were given the value of half the detection limit. Detection limit: 1983-1987, 2 ppb; January 1988-September 1989, 1.4 ppb; October 1989-March 1990, 2 ppb. CMA114350 -31- FIGURE 7 FREQUENCY OF VINYL CHLORIDE DETECTED AT OR ABOVE 2 PPB, 1983-1990 BKK LANDFILL, WEST COVINA, CALIFORNIA 100.0 Station A Frequency (%) Month Source: Figure derived from South Coast Air Quality Management District's ambient vinyl chloride monitoring data, January 1983 through March 1990. CMA 114351 -32- Combined 1981-1990 Data TABLE 7 shows the number of samples with nondetectable concentrations per number of days sampled at Stations A, B, and MY for SCAQMD's combined 1981-1990 ambient vinyl chloride monitoring data. FIGURE 8 displays the frequency of vinyl chloride detected at or above the ambient air quality standard of 10 ppb at Stations A and B between 1981 through 1989. FIGURE 9 shows on a monthly basis the maximum measured vinyl chloride concentrations detected at Stations A, B, and MY between 1983 and 1990. The last year in which detections of vinyl chloride at or above 10 ppb occurred at each station are as follows: - at Station A, in 1986, once in January (10 ppb) and once in February (11 ppb); - at Station B, once in May 1985 (15 ppb); - at Station MY, nine days in 1988. (See also next data group for one detection above 10 ppb in June 1991.) Control measures at the landfill were effective in reducing vinyl chloride emissions over time. By 1989, vinyl chloride was detected at or above the detection limit of 2 ppb only 31 times at Station MY, 4 times at Station A, and once at Station B. During the first three months of 1990, vinyl chloride was only detected three times at or above 2 ppb; all three detections occurred at Station MY and in January. CMA 114352 -33- TABLE 7 NUMBER OF SAMPLES WITH NONDETECTABLE VINYL CHLORIDE CONCENTRATIONS PER TOTAL NUMBER OF DAYS SAMPLED 1981-1990 SCAQMD AMBIENT VINYL CHLORIDE MONITORING DATA BKK LANDFILL, WEST COVINA, CALIFORNIA 1981 1982 1983 1984 1985 1986 1987 1988 1989 1990 # Nondetects 116 181 134 123 137 222 246 240 345 88 Station A # Days Sampled 191 225 254 303 321 337 338 317 349 88 Percent % 60 80 53 41 43 66 73 76 99 100 # Nondetects 125 185 142 113 160 284 305 316 325 81 Station B # Days Sampled 191 224 252 304 289 338 335 327 326 81 Percent % 65 83 56 37 55 84 91 96 99 100 # Nondetects Station MY # Days Sampled Percent % - -- - -- - -- 90 307 29 152 344 44 191 345 55 180 329 55 312 344 91 85 88 97 SCAQMD = South Coasl Air Quality Management District Detection Limits = 6/81-9/82, 10 ppb; 10/82-12/87, 2 ppb; 1/88 -9/89, 1.4 ppb; 10/89 - 3/90, 2 ppb CMA 114353 -34- 60 0 FIGURE 8 FREQUENCY OF VINYL CHLORIDE DETECTED AT OR ABOVE 10 PPB, 1981-1989 BKK LANDFILL, WEST COVINA, CALIFORNIA Frequency Source: Figure derived from South Coast Air Quality Management District's ambient vinyl chloride monitoring data, January 1983 through March 1990 FIGURE 9 MAXIMUM MEASURED VINYL CHLORIDE LEVEL EACH MONTH, 1983-1990 BKK LANDFILL, WEST COVINA, CALIFORNIA Source: Figure derived from South Coast Air Quality Management District's ambient vinyl chloride monitoring data, January 1983 through March 1990 O > CcOn cn -36- 1993-1994 Data Between 1990, when SCAQMD discontinued the almost daily ambient monitoring for vinyl chloride at residential locations, and 1993, when the B.K.K. Corporation began the Proposition 65 ambient vinyl chloride monitoring every 12 to 14 days, data was collected under 2 regulatory programs: USEPA's Site Assessment and Mitigation (SAM) Workplan (Stirrat, 1991) and SCAQMD's Rule 1150.1. - Under an order issued by USEPA in 1986, the SAM workplan required the B.K.K. Corporation to determine the extent of contamination on and off the landfill. In the ambient air monitoring component of the workplan, samples were collected for a total of 33 days between December 1989 and August 1990, and analyzed for 20 volatile organic compounds. The detection limit for vinyl chloride was reported to be 0.1 ppb. Data for the station located at Myra Court showed that of the total 33 samples, vinyl chloride was detected in 21 samples as follows: above 0.1 ppb, 14 times; above 1 ppb, 5 times; above 2 ppb, twice, with a maximum detection of 2.73 ppb in June 1990 (Stirrat. 1990). USEPA's validation of the data concluded that the detected results and quantitation limits for vinyl chloride were, estimates "and usable for limited purposes only"; additionally, "the detected results and quantitation limits for many of the target analytes in ail samples were qualified as the laboratory did not run initial calibration curves" (ICF Technology Incorporated, 1992). - Ambient air monitoring according to SCAQMD's Rule 1150.1 found vinyl chloride south of the landfill as follows; offsite at Myra Court at 10.2 ppb in June 1991; onsite near Nogales Street at 1.38 ppb in January and 1.40 ppb in June, 1992: and onsite at Nogales Street at 0.12 ppb in February 1993. Jased on the ambient air data collected at the perimeter of the landfill under SCAQMD's Rule 1150.1, the B.K.K. Corporation published a warning in the San Gabriel Valley Tribune on August 29, 1993, for detections of vinyl chloride above the Proposition 65 NSRL (B.K.K. Corporation, 1993b). During 1993-1994, the B.K.K. Corporation added several offsite stations to monitor concentrations, collected 24-hour ambient air samples every 12 to 14 days, and updated its Proposition 65 vinyl chloride monitoring data quarterly. TABLE 8 is B.K.K. Corporation's monitoring data for the period September 1993 through September 1994 (BKK Corporation, 1994). USEPA has stated that the analytical procedure appears to be acceptable (USEPA, 1994e), and SCAQMD found the modified protocol acceptable (SCAQMD, 1994a). FIGURE 10 shows the locations of the B.K.K. Corporation's Proposition 65 monitoring stations. Stations #3 ("Nogales End") and #6 ("Lynn Court") are perimeter momtonng stations located on the landfill. They are used to represent the locations of SCAQMD's residential monitoring Stations MY and B, respectively. This may overestimate exposures since some dilution in the ambient air concentration would be expected between the perimeter and the residential locations. Station #10 ("Amar-at-Nogales") is used to represent the location of SCAQMD's residential monitoring Station A. This may underestimate the exposure since Amar is south of Mariena on Nogales, where Station A had been located. (Note: There was no station #8 or #9 in the Proposition 65 monitoring program.) The detection limit for B.K.K. Corporation's data varies from 0.005 to 0.010 ppb. In TABLE 8, only values above 0.005 ppb are detected concentrations. Samples with nondetectabie concentrations are given a value of half the detection limit by the B.K.K. Corporation for each day and station. The number of samples with nondetectabie concentrations per total number of days sampled at each of he three stations is as follows: #10, "Amar-at-Nogales" (Station A), 4 nondetects in 17 days sampled J8 percent); #6, "Lynn Court" (Station B), 13 nondetects in 28 days sampled (46 percent); and #3. "Nogales End" (Station MY), 12 nondetects in 35 days sampled (31 percent). -37- CMA 114356 TABLE 8 (BKK Corporation) BKK LANDFILL PROPOSITION 65 VINYL CHLORIDE MONITORING PROGRAM Cumulative Average Last 12 Months (Parts per billion volume/volume) Sample Station fc Location 1 Sample Date 1 23 Microwave Azusa Nogales Tower Spillway End 4 NW Oats 5 West Borrow 6 Lynn Court 10 11 12 13 14 Amarat Mariana Melissa at Miranda Loraine Nogales Marealla Fence Street Walnut Village 14-Sep-93 15-Sep-93 16-Sep-93 20-Sep-93 22-Sep-93 28-Sep-93 12-Oct-93 21-Oct-93 08-NOV-93 1 S-Nov-93 07-DOC-93 16-Dec-93 29-Dec-93 11-Jan-94 25-Jan-94 03-Feb^94 11-Feb-94 16-Feb-94 01-Mar-94 15-Mar-94 29-Mar-94 12-Apr-94 26-Apr-94 10-May-94 24-May-94 07-Jun-94 21-Jun-94 28-Jun-94 05-Jui-94 19-Jul-94 03-Aug-94 16-Aug-94 30-Aug-94 13-Sep-94 27-Sep-94 0.0025 0.0560 0.0025 0.0030 0.0025 0.0025 0.0025 0.0025 0.0025 0.0140 0.0045 0.0035 0.0045 0.0030 0.0035 0.0045 0.0040 0.0035 00040 0.0040 0.0045 00050 00050 00045 0.0045 0.0040 0.0073 0.0040 0.0150 0.0025 0.0025 0.0025 0.0025 0.0900 0.0025 0.0025 0.0030 0.0025 0.0025 0.0025 0.0025 0.0260 0.0250 0.0190 0.0040 00040 0.0260 0.0040 0.0130 0.0040 0.0030 0.0040 0.0760 0.0045 0.0040 0.0290 0.0055 0.0035 0.0500 0.0660 0.0025 0.0240 0.0025 0.0040 0.0035 1.4000 0.0025 0.0035 0.0025 0.0030 0.0025 0.0025 0.5100 0.7100 0.5800 0.0380 0.3200 0.1400 0.3400 0.2700 0.3300 0.3100 0.0250 0.0170 0.0050 0.5800 1.0000 0.3800 0.0380 0.1800 0.4400 0.1900 0.0045 0.4100 0.5700 0.0025 0.0050 0.0025 0.0025 0.0030 0.0025 0.0025 0.0035 0.0045 0.0030 0.0040 0.0045 0.0140 0.0025 0.0040 0.0090 0.0025 0.0025 0.0025 0.0025 0.0025 0.0150 0.0150 0.0140' 0.0130 0.0035 0.0025 0.0030 0.0025 0.0025 0.0025 0.0025 0.1000 0.0470 0.0660 0.0700 0.0025 0.0720 0.0660 0.0540 0.0360 0.0240 0.0370 0.0040 0.0040 0.0390 0.0040 0.0025 0.0260 0.0125 0.0035 0.0470 0.0610 0.0520 0.1600 0.0250 0.0620 0.0790 0.0035 0.0040 0.0045 0.0160 0.1600 0.0690 0.0590 0.0460 0.0520 0.0030 0.0040 0.0050 0.0770 .0.1500 0.0050 0.0240 0.0580 0.0370 0.0035 0.0840 0.1100 0.0050 0.0650 0.0480 0.0560 0.0035 0.0320 0.0690 0.0580 0.0490 0.0390 0.0210 0.0040 0.0035 0.0030 00940 0.0040 0.0035 0.0340 0.0380 0.0290 0.0035 0.0320 0.0260 0.0600 0.0120 0.0180 0.0180 0.0260 0.0150 0.0040 0.0860 0.0045 0.0640 0 0760 0.0040 0.0050 0.0055 0.0820 0.0035 0.0330 0.0310 0.0340 0.0050 0.0110 0.1000 0.0860 0.0050 0.0240 0.0450 0.0300 0.0590 0.0320 0.0025 0.0035 0.0025 0.0025 0.0025 0.0030 0.0025 0.0025 0.0025 0.0035 0.0045 0.0030 0.0040 0 0030 0.0040 0.0040 0.0045 0.0030 0.0045 0.0035 0.0045 0.0045 0.0030 0.0030 0.0030 0.0093 Avg. 24-hr Avg. ug/day No. Samples Risk 0.0063 0.33 29 1.3E-06 0.0168 0.82 31 3.2E-06 0.2526 13.13 35 5.1E-05 0 0033 0.17 12 6.7E-07 0.0076 0.40 13 1.5E-06 0.0285 1.48 26 5.7E-06 0.0522 2,71 17 1.0E-05 0.0465 2.42 16 9.3E-06 0.0276 1.43 16 5.SE-06 0.0341 1.77 16 6.8E-06 0.0381 1.98 13 7.6E-06 ND ND 25 Source: "BKK Landfill 3008(h) Consent Order, EPA DocKet No. RCRA-09-89-0019. Monthly Progress Report for September 1994. Attachment: BKK Landfill Proposition 65 Vinyl Chlonde Monrtonng Program.' Letter dated October 7.1994. from Julia M. Bussey. Corporate Manager. Regulatory Affairs. BKK Corporation. Torrance. California to Ms. Carmen Santos. United States Environmental Protection Agency-Region IX. San Francisco. California. The detection limit vanes from 0.005 to 0.010 ppb. Only values above 0.005 ppb are detected concentrations. Samples with nondetectable concentrations are given a value of half the detection limit by the B.K.K. Corporation for each day and station. The number of samples with nondetectable concentrations per total number of days sampled at the three stations is as follows: #10. "Amar-atNogales' (Station A). 4 nondetects in 17 days sampled (18%); #6, 'Lynn Court' (Station B), 13 nondetects in 28 days sampled (46%); and #3. "Nogales End' (Station MY), 12 nondetects in 35 days sampled (31%). NOTE: There was no station #8 or #9. -38- CMA 114357 FIGUR. (B.K.K. Corporation-ENVIRON Corporation) CMA 114358 e NV I RON Counsel in lleallh anil [nwonmtnlul Science Proposillon 65 Ambient Monitoring Station Location* Vinyl CMonde Study BKK Landl# Wosl Covina. Caldoinia Source Memorandum dated December 2\. 1994, from ENVIRON Corporation a! the request of Juba M Bussey. Corporate Manager, ftegulaiory Affairs, 8 K K Corporation, Torrance, California, to the Office of Environmental Health Hazard Assessment. Sacramento. Cabforma Note There was no station #8 pr id in the Proposition 65 monitoring program -39- Site Activities Approximately 72 percent of the total 3.4 million tons of hazaraous waste disposed of at the landfill between 1975 and 1984 was liquid hazardous waste (CH2M Hill. 1988). Four disposal methods were practiced between 1972 and 1984 (CH2M Hill. 1988): Commingling: approximately 85 percent of accepted fluids were disposed of by this method between 1972 to May 1984 (The Janes Network, 1994); bulk liquid hazardous wastes were discharged into a cavity prepared in the daily working face and commingled with solid nonhazardous wastes at a ratio of approximately onepart liquid to two-parts refuse; - Solidification: from May 1984 through November 1984. hazardous and nonhazardous liquid wastes were mixed with soil ori approximately 15 acres of the top of the Class I Unit prior to burial: gas condensate generated onsite and contaminated groundwater from extraction wells were air stnpped and then disposed of by this method until November 1987, at which time the leachate treatment plant began operating. - Drum disposal: from 1972 through 1984, closed drums were stacked on pallets then covered with soil to a total height of five feet: drums containing acid, alkaline, or solvent waste were separated from each other by unspecified distances: Injection wells: from 1975 through 1980, waste acids, cyanide solutions, and organic fluids were injected into 96 boreholes ("injection wells") dnlled into the buried waste; these wells were 10 feet wide holes, 120 feet deep; approximately 10 percent of accepted fluids were disposed of by this method. In 1985, USEPA prepared an aerial photographic analysis of the B.K.K. Landfill (USEPA, 1985). Twelve photographs dating from 1964 through 1984 show the expansion of the landfill, and of the residential community around the landfill. The focus of USEPA's analysis was the identification of surface drainage, seepage, leachate, disposal practices, point discharges, and vegetation damage at the landfill. Of the four disposal methods practiced at the landfill between 1972 and 1984, all but the injection well method can be seen in the photographs. Onsite disposal operations seen in the photographs include the working face/active disposal area, standing liquid, and the liquid waste disposal (solidification) area. The following figures are selected from USEPA's aerial photographic analysis: FIGURE 11, October 20, 1980; FIGURE 12, September 2, 1983; and FIGURE 13, June 15, 1984. Residential developments around the landfill poor to 1980, as captured in the aerial photographic analysis, were as follows: 1964, southwest, approximately 1,000 feet from the landfill; 1968, northwest and north; 1970, no new residential development evident; 1973, south of Amar Road; and 1976, north of Amar Road. Residential developments at Marlena and Nogales Streets, location of the future monitoring Station A, were begun in 1976 and completed in 1977; developments at Lynn Court and Myra Court were begun and completed in 1979 (City of West Covina, 1994). -40- CMA 114359 FIGURE 11 ' (United States Environmental Protection Agency) BKK SANITARY LANDFILL, OCTOBER 20, 1980 Source "Aanal Pnotogiaonic Anaiyai* of tha BKK Sanitary Landfill. Wait Covina. California.' January IMS. llnitad Stata* Envwonmwnat Protacaon Agancy, EPA Ragion 9. Envaonmantal Monitomg Syatama Laooratory. Lai Vagaa. Navaoa. pg. 21. TS^MO307ar3eOO. -41- CMA 114360 FIGURE 12 (United States Environmental Protection Agency) BKK SANITARY LANDFILL, SEPTEMBER 2, 1983 Source Aenai Peotoqracntc Analysis of ttif BKK Sanitary Landfill, West Covina. California." January 1985. United States environmental protection Agency, EPA Region 9, Environmental Monrtonng Systems Laboratory, Lit veqat. Nevaaa. pg. 23. T5-AMD-8307a/3$00 Note' incinerator * PIare Station -42- CMA 114361 FIGURE 13 (United States Environmental Protection Agency) BKK SANITARY LANDFILL, JUNE 15,1984 Sown: ~Aom PUMoyoowcmo bkk SonOQfy londW. vne Conoio. Comow.' Jpnuoiy USS. Unpoa Sew enwmmue Pnon<mi igm, EPA ftoen . CmronmtnM Uonoorwy Syworm l mim own Loo vo*o. Novooo. pp, jj. 75 AMO-OX7oOOOO. Now: wmiwer * Plow Moon CMA114362 Odor Complaints Data Complaints of odors emanating from the B.K.K. Landfill were lodged by residents to both SCAQMD and the City of West Covina as early as 1969 (CH2M Hill, 1988). Detection of odors does not necessarily equate to exposure to hazardous substances. Odors do indicate downwind receptors and suggest the potential for exposure when hazardous chemical contaminants are also present (Ziem and Davidoff, 1992). The first odor complaint recorded was in March 1969 to SCAQMD (SCAQMD, 1981). Odor complaints increased from 48 in 1971 to 57 in 1974. In 1974, the B.K.K. Corporation acknowledged complaints from residents situated to the north and northeast of the working face of the landfill (BKK Corporation, 1974). In 1979, B.K.K. Corporation contracted with the USC Environmental Engineering Program to investigate odors from the landfill. The study analyzed complaints received by the City during January 1,1978 through May 16,1979. The objectives of the study were to determine which areas were subject to odors, what climatological factors elicited an increase in complaints, identify sources of odor based on wind data, and select appropriate monitoring and sampling conditions for the next phase of the study. Results of USC's first interim report (USC, 1979) included the finding that of the 521 complaints received during the study period, a larger number were lodged during the initial four months of 1979 as compared to the same period in 1978. The majority of complaints were from residents of the "M" named streets, possibly because those residents were "closer to the working face of the B.K.K. Landfill" and at a `higher elevation consistent with the landfill" (USC, 1979). (It is assumed that the "M" named streets in the USC study included Miranda, Maria, Maureen, and Marlena Streets, developed in 1977. Marlena at Nogales Streets, location of future monitoring Station A, was developed by 1977; Lynn Court and Myra Court, locations of future monitoring Stations B and MY respectively, were developed in 1979 [City of West Covina, 1994].) USC's final report was released in February 1981 and concluded that odor problems were associated with the downslope air drainage into residential areas under nighttime meteorological conditions (USC, 1981). In 1980, the City Council directed city staff to scientifically measure odor emissions from the landfill, so the city contracted with Eutek Inc. Eutek's study included an analysis of odor complaints by month, day of week, and hour of the day. Complaints recorded on Sundays and after-hours suggested a mechanism for odor transport other than the working face. "M" and "L" named streets were more frequently affected by odors from the landfill (Eutek, 1981). DHS-DEODC analyzed odor complaints data in conjunction with its pending reproductive outcomes study. The frequency and distribution of over 4,000 odor complaints made between 1980 and 1985 indicate that topography and meteorology contributed to odor complaints (Kharrazi et al., 1993). FIGURE 14 is a three-dimensional map of the closed Class I Unit and the residential neighborhood one-mile south of the landfill. FIGURE 15 and FIGURE 16 show the location of odor complaints per housing unit for the periods 1980-1982 and 1984-1985, respectively. A 1983 tri-agency study monitored for nine chemicals. Monitoring stations were located onsite at the western and eastern ends of the landfill, and in residential areas around the landfill. The monitoring data indicated that the areas with the greatest frequency of odor complaints, that is the southeastern and southern residential areas, coincided with those areas where highest detections of vinyl chloride occurred. However, odor complaints are not necessarily considered to be an indicator of vinyl chloride exposure, since odors were reported in the residential area north of the landfill, but vinyl chloride was not detected in this area. (DHS-ARB-SCAQMD, 1983). Updated census data for the residential community around the B.K.K. Landfill is presented in Appendix E of this report. CMA 114363 -44- FIGURE 14 (Department of Health Services Division of Environmental and Occupational Disease Control) TOPOGRAPHY NEAR BKK LANDFILL, WEST COVINA, CA Streets Hazardous Waste Area BKK Property lane One Uile Radius Prom Hazardous Waste Area Source- USGS 1978 DEU Data Courtesy of Mafl*n Kharrazi, Ph D . Tm Lomas, and Rachel Broadwin. California Department of Health Services. Division of Environmental and Occupational Disease Control, Environmental Health Investigations Branch. Emeryville, California, April 1994 -45- C M A114364 FIGURE 15 (Department of Health Services Division of Environmental and Occupational Disease Control) -46- CMA 114365 FIGURE 16 (Department of Health Services Division of Environmental and Occupational Disease Control) .dsy of Martin Kharrazi. Ph.D.. Tim Lomas, and Rachel Broadwm. California Department of Health Services, Division of Environmental and Occupational Disease Control. Environmental Health investigations Branch. Emeryville. California, Apnl 1994 -47- CMA 114366 Other Hazardous Chemicals Detected in Ambient Air As discussed in the Hazard Identification section of this report, the 1982 90-day ambient air monitoring program conducted by DHS-ARB-SCAQMD detected five other chemicals that are known or suspected to be human carcinogens; benzene (known), trichloroethylene, perchloroethylene, chloroform, and 1,2-dichloroethane (DHS-ARB-SCAQMD, 1983). Beginning in 1985, these chemicals were also monitored by ARB and/or SCAQMD as part of the air toxics monitoring program in the Los Angeles basin (SCAQMD, 1987). These data are not directly comparable because the data from the two sites were collected during two different years; Station A, in 1982 and Azusa Station, in 1985. Whether concentrations at Azusa Station were higher, lower, or the same in 1982 is not known. Consequently, there is insufficient information to estimate, in a manner similar to analysis of the ambient vinyl chloride monitoring data, risks associated with exposures to the other hazardous chemicals emitted from the Class I Unit of the B.K.K. Landfill. Use of flare data to project concentrations Of the five other hazardous chemicals would involve additional assumptions, including extrapolation from the landfill to residential locations, and would not be consistent with USEPA's recommended guidance that past scenarios be based on actual exposure conditions (USEPA, 1989b). In 1995 OEHHA reviewed limited 1994-1995 ambient air monitoring data regarding potential exposures to future inhabitants of Walnut Village, a residential neighborhood proposed for development east of the B.K.K. Landfill in the City of Walnut. Ambient air levels of benzene, perchloroethylene, chloroform, and carbon tetrachloride monitored at the B.K.K. Corporation's Proposition 65 monitoring stations #1, located at the northeast comer of the facility, and #7, located offsite to the northeast (see FIGURE 10) were compared to levels of the same chemicals found at four of SCAQMD's air toxics monitoring stations (Burbank, Hawthorne, Anaheim, and Azusa). From the available data OEHHA concluded that potential health risks to future inhabitants of Walnut Village would not differ significantly from the potential health risks experienced by inhabitants of other similar areas of the Los Angeles basin exposed to ambient air contaminants (OEHHA, 1995). B.K.K. Corporation's December 1994 - December 1995 ambient air sampling program, required by USEPA, monitored for 19 volatile organic compounds. USEPA is reviewing these data for use in the risk assessment it is requiring the B.K.K. Corporation to conduct. CMA 114367 -48- BLANK PAGE CMA 114368 -49- RISK CHARACTERIZATION This section presents the assumptions used in the risk calculation, the individual excess lifetime cancer risk estimates, the exposed population, estimated excess lifetime cancer risks using different assumptions and methodology, limitations and uncertainties, and the findings of the 1995 addendum health risk assessment. The interim report included risk estimates based on exposure concentrations generated from ARB's modeling of 1987 vinyl chloride concentrations at Stations A, B, and MY (ARB Part A, 1990). In 1991, OEHHA and DHS attempted to refine the air dispersion model used in the interim report. However, the work showed that the B.K.K. Landfill was more complex than could be accounted for in air dispersion models approved for regulatory use in 1991. Appendix F contains information about the air dispersion model developed for this project, and the limitations and uncertainties which precluded its use in this addendum report. This addendum report focuses on monitored data. Assumptions Regarding the Beginning of Exposures at Stations A, B, and MY There are no monitoring data to quantify exposures at Stations A, B, and MY prior to June 1981. Odor complaints data indicate residents were reporting odors from the landfill as early as 1969, and specifically, at "M" and "L" named streets southeast and south of the Class I Unit beginning in 1978. These odor complaints indicate areas of downwind impact and suggest emissions from the Class l Unit were reaching nearby residents. Homes near Station A were built by 1977, and near Stations B and MY, by 1979. Onsite disposal practices at the time included commingling (open-face disposal) of liquid hazardous wastes. It is assumed in this addendum report that exposures at Stations A, B, and MY began in 1980. Ascribing a value to exposures in 1980 at Stations A, B, and MY is done by looking at FIGURE 17. FIGURE 17 juxtaposes FIGURE 3 (tons of hazardous waste deposited in the landfill) with FIGURE 6 (average annual vinyl chloride concentrations in ppb detected between 1983 through 1990). The period of overlap is not long enough to determine if such a lag truly existed. By 1983, the landfill had been receiving wastes for 20 years. FIGURE 17 shows that: No emissions of vinyl chloride could have occurred before 1963, the year the landfill opened; exactly when emissions of vinyl chloride began is not known; - The dip in the graph of hazardous waste deposited in 1981 is attributed to the prohibition of waste containing vinyl chloride after vinyl chloride was first detected above the ambient air quality standard of 10 ppb at the landfill perimeter; - The shapes of the curves of average annual concentrations of vinyl chloride at Stations A, B, and MY in FIGURE 17 and the estimated average annual concentrations at Stations A and B in 1981-1982 from TABLE 5 suggest exposures prior to 1981. CMA 114369 -50- FIGURE 17 TONS OF HAZARDOUS WASTE DEPOSITED, AVERAGE ANNUAL VINYL CHLORIDE CONCENTRATIONS (PPB) B.K.K. LANDFILL. WEST COVINA, CALIFORNIA 800000 700000 600000 | 500000 (0=A 1 400000 zNre 300000 co 200000 - 10 X- - Tons Of HW ---Station A - * -- Station B -.-- Station MY Detection Limit 1981 -1982 data 9 8 7 6S m 5 a 4 2. 100000 r"> tCoT CT> <N r-- 130 Act, BK BKKLlfMM Sllle 51) miMMnOM to MvyAii/WirtlHOWUli Canrw Ad -o----.....- ...... ............... ......-.........-------------------------- 0 i^tor-cocio^rMn^rCOioCtD oC0D^3o0co3D03co aCo>O o& wcommMuting DHS Year ci*i* i untf>" tioepad IHlBPB HW Cui 1 LtndfiO ll ACKIQ *" avail* ClUi 1 CJHHtf and CTQ**d C*yo< WMt CRWowOiC*Ban* 4(K0Wa)oL*jnCat*NUi 1 Juxtaposition of Figures 3 and 6 of this addendum report with the addition of the 1981-1982 average annual concentration This Figure is used to show the shapes of the curves of average annual concentrations of vinyl chloride at Stations A, B. and MY. Detection Limits: 6/81/-9/82, 10 ppb; 10/82-12/87. 2 ppb: 1/88-9/89. 1.4 ppb: 10/89-3/90, 2 ppb. Note: The increase in 1990 reflects the fact that 1 ppb was substituted for nondetects in the data, and that data were only collected for January, February, and March of 1990 CMA 114370 -51- This information suggests that average annual concentrations of vinyl chloride in 1980 at Stations A, B, and MY were not likely zero. This addendum report assumes that average annual concentrations in 1980 at Stations A, B, and MY were 2 ppb. This may underestimate exposures, especially at Station MY. Assumptions Regarding Ambient Vinyl Chloride Monitoring Data Estimates of the individual excess lifetime cancer risk are based on the assumption that ambient air concentrations of vinyl chloride represent indoor air exposures (USEPA, 1989a). The data used in the risk calculations are: SCAQMD's ambient vinyl chloride monitoring data from Stations A, B, and MY for the period June 1981 through March 1990; and the B.K.K. Corporation's Proposition 65 monitoring data from Stations "Amar-at Nogales," "Lynn Court," and "Nogales End" for the period September 1993-1994. The following assumptions are made regarding.the data: 1981-1982 Data 1981-1982 average annual concentrations at Stations A and B are based on data collected for 7 of the 12 months in 1981, and 9 of the 12 months in 1982. The average concentrations for each set are assumed to be representative of a 12-month exposure (see TABLE 5); - Station MY, located 150 feet southeast of the landfill property line, was established in June 1984, Values for the period 1980-1982 are assumed to be equal to the average annual concentrations at Station A, located 450 feet southeast of the landfill property line (see FIGURE 4). This may be an underestimation since Station MY was closer to the Class I Unit than Station A, and the levels and frequency of vinyl chloride detections were consistently higher at Station MY when both stations were in service; - A value of 1 ppb is substituted for samples with nondetectable concentrations. (The detection limit between June 1981 through September 1982 was 10 ppb, and between October through December 1982, 2 ppb.) 1983-1990 Data - The 1983 average annual concentration at Station MY is assumed to be 2.8 ppb, that is, equal to Station A's 1983 average annual concentration (see TABLE 6). This may be an underestimation. For the years 1985 through 1988, TABLE 6 shows that concentrations at Station MY were 1.6- to 1.9-fold higher than concentrations at Station A, and TABLE 7 shows that Station MY had between 25 to 33 percent fewer samples with nondetectable concentrations ; - The 1984 average annual concentration at Station MY is assumed to be 5.4 ppb, that is, the average concentration detected by SCAQMD between August through -52- CMA 114371 December at Station MY. The average concentration of the 5-month period is assumed to be representative of the 12-month exposure; - The detection limit between January 1983 through December 1987 was 2 ppb; between January 1988 through September 1989, 1.4 ppb; and between October 1989 through March 1990, 2 ppb. A value of one-half the detection limit is substituted for samples with nondetectable concentrations. 1993-1994 Data It is assumed that the B.K.K. Corporation's Proposition 65 vinyl chloride monitoring data are acceptable for quantitative assessment; USEPA has stated that the analytical procedure appears to be acceptable to USEPA (USEPA, 1994e) and SCAQMD found the modified protocol acceptable (SCAQMD, 1994a). The detection limit varied from 0.005 to 0.010 ppb (see TABLE 8); It is assumed that the B.K.K. Corporation's Proposition 65 monitoring stations "Amar-at-Nogaies" (residential station), "Lynn Court" (perimeter station), and "Nogales End" (perimeter station) represent SCAQMD's Stations A, B, and MY respectively. Because of the difference in locations, this assumption may lead to an overestimation for Stations B and MY, and may lead to an underestimation for Station A; - Average annual concentrations for the 5-year period 1990-1994 are assumed to be equal to the average annual concentrations detected in the September 1993-1994 Proposition 65 monitoring. 1995-2009 Data - Average annual concentrations for the period 1995-2009 are assumed to remain the same as the September 1993-1994 average concentrations. Changes in site activities, corrective actions, and technological advancements over the 15-year period may invalidate this assumption. Monitoring data collected by the B.K.K. Corporation in 1995 show decreasing vinyl chloride concentrations. Individual Excess Lifetime Cancer Risk Estimates The "individual excess lifetime cancer risk" is an estimate of the risk for an individual above the background risk of developing cancer during a 70-year lifetime. In the United States, a new estimate of the normal background risk of developing cancer has been made since 1990 and it is greater than the value reported in the interim report from approximately 1 in 3 individuals (DHS-HWTS, 1990) to 4 in 10 individuals (Miller et al., 1993); that is, approximately 40,000 in 100,000 individuals will develop cancer during their lifetime. CMA 114372 -53- Exposure Scenario The interim report estimated risk based on a "worst-case" exposure scenario. "Worst-case" represents a hypothetical individual and an extreme set of conditions, which will usually not be observed in an actual population. This addendum report estimates risks assuming a "reasonable maximum" exposure (RME) scenario and an "average" exposure scenario. USEPA defines the RME as "the maximum exposure that is reasonably expected to occur at a site," and is intended to be a conservative estimate, well above the average yet within the range of possible exposures (USEPA, 1989a). Av rage concentrations are used in the risk equation. Use of average concentrations rather than the 95 percent upper confidence limit (UCL) value to estimate the RME is based on the following: 1) the monitoring stations were at the point of exposure; and 2) USEPA guidance states that "data sets with 20 to 30 samples provide fairly consistent estimates of the mean (i.e., the 95 percent UCL is close to the sample mean)....in general, the UCL approaches the true mean as more samples are included in the calculation (USEPA. 1992a)." As shown in TABLE 7, the minimum number of samples collected by SCAQMD in one year was 191. Thus, the 95 percent UCL is represented by the average annual concentrations. USEPA cites national statistics on the number of years an individual resides at one location, and indicates an upperbound (90th percentile) of 30 years and an average (50th percentile) of 9 years. USEPA recommends a 30-year exposure duration when calculating the RME and a 9*year exposure duration when calculating the average exposure (USEPA, 1989a). Risk Equation The equation for the risk estimate is as follows: ECR where ECR Cvc YR EF UR LT = = = - - Cvc x YR x EF x UR x 1/LT Excess lifetime cancer risk Concentration of vinyl chloride in air (ppb) Years of residence associated with exposure Exposure factor, i.e., percent of time at home (80%) Unit risk value for vinyl chloride (20 x 10`5 per ppb) Human individual lifetime in years (70-years) The interim report estimated an individual excess lifetime cancer risk of 1 to 2 x 10"5, based on concentrations of vinyl chloride detected in SCAQMD ambient vinyl chloride monitoring data collected between 1982 through 1987, a worst-case exposure scenario (70 years residence), 80 percent time at home, and a unit risk value of 0.69 x 10'5 per ppb. TABLE 9 is the estimates of individual upperbound excess lifetime cancer risks of this addendum report, assuming a reasonable maximum exposure scenario (30 years, 1980-2009). The estimates are based on concentrations of vinyl chloride detected at Stations A, B, and MY in SCAQMD data (June 1981 through March 1990) and the B.K.K. Corporation data (September 1993-1994), 80 percent time at home, and the unit risk value of 20 x 10'5 per ppb. Exposure values have been rounded to two significant figures, and risk estimates to one significant figure. The individual excess lifetime cancer risk is estimated per a specified period in order to delineate the risk per exposure year(s). Years with higher exposure concentrations are associated with a greater portion of the lifetime risk. The cumulative risk is an estimate of the past risk incorporated into the current and future risk estimate. -54- CMA 114373 TABLE 9 INDIVIDUAL EXCESS LIFETIME CANCER RISK FROM EXPOSURE TO AMBIENT FUGITIVE VINYL CHLORIDE EMISSIONS FROM THE CLASS I UNIT OF THE BKK LANDFILL, WEST COVINA. CALIFORNIA REASONABLE MAXIMUM EXPOSURE SCENARIO (30 YEARS) STATION EXPOSURE PERIOD CONCENTRATION (PPb) DURATION (yrs) EXCESS RISK PER EXPOSURE PERIOD CUMULATIVE EXCESS RISK A 1980* 2.0 1 5x10`6 5x10* 1981 7.2 1 2x10* 2x10*5 1982 3.4 1 8x10`6 3x10* 1983 2.8 1 6x10*6 4x1 O' 1984 4.2 1 1x10'5 5x10* 1985 3.5 1 8x10*6 5x10*5 1986 1.9 1 4x1 O'6 6x10*5 1987 1.7 1 4x1 O'6 6x10* 1988 13 1 3x10*6 6x10* 1989 0.8 1 2x10'6 7x1 O' 1990-1994 0.05 5 6x10'7 7x10* 1995-2009 0.05 15 2x1 O'6 7x10* B 1980* 2.0 1 5x1 O'6 5x10* 1981 6.0 1 1x1 O'5 2x10* 1982 2.8 1 6x1 O'6 3x10* 1983 3.0 1 7x1 O'6 3x10* 1984 3.9 1 9x10* 4x10* 1985 2.3 1 5x1 O'6 5x10* 1986 1.3 1 3xl0*6 5x10" 1987 1.2 1 3x10* 5x10* 1988 0.8 1 2x10` 5x10* 1989 0.8 1 2x10* 6x10* 1990-1994 0.03 5 3x10*7 6x10* 1995-2009 0 03 15 1x10* 6x10* MY 1980* 2.0 1981 7.2 1982 3.4 1983 2.8 1984 5.4 1985 5.4 1986 3.0 1987 2.6 1988 2.5 1989 0.9 1990-1994 0.25 1995-2009 0.25 1 5x10* 1 2x10*5 1 8x10*6 1 6x10* 1 IxlO"5 1 1x10` 1 7x10* 1 6x10* 1 6x10* 1 2x10* 5 3x10* 15 9x10* 5x10* 2x10* 3x10* 4x10* 5x10* 6x10* 7x10* 7x10* 8x10* 8x10* 8x10* 9x10* Calculated by ECR = Cvc x YR x EF x UR x 1/LT where: ECR = Excess lifetime cancer risk Cvc = Concentration of vinyl chloride in air (ppb) YR = Years of residence associated with exposure EF = Exposure frequency, i e , percent of time at home (80%) UR = Unit nsk value for vinyl chloride (20x10*5[ppb]_1) 1/LT = Human lifetime (70 years) Exposure values have been rounded to two significant figures, and nsk values, to one significant digit *1980 concentration = 2 ppb, assumed: no data available. 1981-1982 concentrations = SCAQMD ambient vinyl chlonde monitoring data Nondetected concentrations given the value of 1 ppb. 1983-1989 concentrations = SCAQMD ambient vinyl chloride monitoring data, Nondetected concentrations set at 1/2 the detection limit (detection limit 1983-1987, 2.0 ppb: detection limit 1988-9/89, 1.4 ppb; detection limit 10/89-3/90, 2.0 ppb) 1990-1994 concentrations = B K K Corporations Proposition 65 Vinyl Chloride Monitoring Program, 9/93-9/94 Nondetected values set at 1/2 the detection limit. The detection limit varied from 0 005 to 0.010 ppb -55- CMA114374 Using the assumptions and methodology of this risk characterization, the estimated excess cancer risks are: at Station A, approximately 7 x 10'5; - at Station B, approximately 6 x 10'5; and - at Station MV approximately 9 x 10'5. These excess cancer risks mean that for an individual living from 1980 to 2009 near Station A, for example, the theoretical upperbound risk of developing cancer is increased from 0.4 (the background cancer risk in the United States) to 0.40007 as a result of exposure to emissions of vinyl chloride from the closed Class I Unit of the B.K.K. Landfill. Another way of expressing this excess cancer risk is: an individual living in the United States has a 40 percent (0.4) chance of developing cancer throughout a 70-year lifetime. For an individual living from 1980 to 2009 near Station A, there is an added 0.007 percent chance of developing cancer as a result of exposure to emissions of vinyl chloride from the closed Class I Unit of the B.K.K. Landfill. Assuming an average exposure scenario (nine years) and the average annual concentrations for the years 1981-1989 (the years of highest detected average annual concentrations), the estimated excess cancer risks are: - at Station A, 7 x 10'5; - at Station B, 5 x 10*5; and - at Station MY, 8 x 10'5. The assumptions and methodology of this risk characterization suggest that: - The year 1981 was the year of highest risk, based on available monitoring data; - The majority of the excess lifetime cancer risk was incurred by 1983-1984; Current and future estimates of risk associated with the B.K.K. Landfill which do not incorporate past exposures at Stations A, B, and MY would not fully characterize the risks potentially incurred by individuals who lived near those stations since 1980 (30 year exposure scenario), or during the decade of the 1980s (9-year exposure scenario). Exposed Population In addition to the individual excess lifetime cancer risk, health risk assessments may estimate the population excess cancer burden. The population excess cancer burden is an estimate of the excess number of cases of cancer that may occur in a defined population who all have the same individual excess lifetime cancer risk. This addendum report does not estimate a population excess cancer burden because not all the population around the landfill were or are exposed to the concentrations of vinyl chloride detected at Stations A, B, and MY, and it is not possible to obtain a reliable estimate of exposure to other residents. The number of potentially exposed individuals near Stations A, B, and MY since 1980 or during the decade of the 1980s is unknown, but considered to be too small for the probability that even one excess case of cancer will develop as a result of exposure to emissions of vinyl chloride from the closed Class I Unit of the B.K.K. Landfill. As an example, there would need to be -56- CMA 114375 approximately 14,000 exposed individuals living near Station A between 1980 and 2009 for one excess case of cancer to develop, based on the individual excess lifetime cancer risk as estimated in this addendum report. Because the number of individuals near Station A is much smaller than 14,000, it is unlikely that excess cases of cancer will occur. However, each exposed individual may have an increased risk of developing cancer. Recently, DHS-Cancer Surveillance Section (DHS-CCS) reviewed the 1988-93 tumor incidence data for a one mile area around the landfill. DHS's review found no indication of increased cancer incidence (DHS-CSS, 1995; see Appendix H). Consequently, there is a need for a different way of evaluating the effect of the exposures at Stations A, B, and MY. Stratification of risks by year of exposure, as done in this addendum report (see TABLE 9), accomplishes this by highlighting the different risks associated with exposures in and over time, namely: Risks for individuals who will have lived near Station A, B, or MY from 1980 to 2009 (6 to 9 x 10`5); - Risks for individuals who lived near Station A, B, or MY only during the decade of the 1980s (6 to 8 x 10'5); Risks for individuals near Station A, B, or MY between 1990 and 1994 (3x 1CT6 to 3 x 10`7); and - Risks for individuals near Stations A, B, or MY between 1995 and 2009 (1 to 9 x 10-6). These different risks would not be evident in risk assessments which address only current and future risks. The stratification of risks by year of exposure is consistent with USEPA's position that past exposures may be important for selected sites (USEPA, 1989b). Estimated Excess Lifetime Cancer Risk Using Different Assumptions and Methodology TABLE 10 shows the excess cancer risk at Station A, as an example, using different assumptions for time spent at home, the average annual concentration of vinyl chloride in 1980, the substituted value for samples with nondetectable concentrations in the 1981-1982 data, the exposure duration, and the unit risk value. Time Spent At Home The interim report and this addendum report assumed, individuals spend 80 percent of their time at home. USEPA assumes individuals spend 350 days per year at home, or 96 percent time at home (USEPA, 1991b). Using USEPA's percent time spent at home in the risk equation suggests slightly higher estimates of excess cancer risk: at Station A, for example, 8 x 10`5. There are also California-specific values. ARB funded a statewide survey of activity patterns for the purpose of obtaining representative data for modeling population exposures and designing appropriate monitoring strategies. Activity patterns of residents over 11 years of age were surveyed during 1987-1988 (ARB, 1991; Jenkins ef a/., 1992), and children 11 years and younger, during 1989-1990 (Phillips et al., 1991). Average data rather than frequency distributions were presented. Results showed that, on the average, Californians spend 87 percent of their time indoors, 7 percent in enclosed transit, and 6 percent outdoors. Of the 87 percent time indoors, 62 percent is spent as indoors at home for individuals over 11 years of age, and 76 percent, as indoors at home for children 11 years and younger. Using ARB's percent time spent at home suggests slightly lower estimates of excess cancer risk: at Station A, 5 x 10`5 using 62 percent and 6 x 10'5 using 76 percent. These different assumptions -57- CMA 114376 TABLE 10 ESTIMATED EXCESS CANCER RISK AT STATION A USING DIFFERENT ASSUMPTIONS Time Spent at Home Station A Average Annual Concentration 1980 Substituted Value for Samples with Non-Detectable Concentrations 1981-1982 Data Exposure Duration Vinyl Chloride (years) Unit Risk Cumulative Excess Cancer Risk* Different Time8 Assumptions . 78% , 80% 2 ppb 2 ppb 2 ppb 2 ppb 1 PPb 1 ppb 1 ppb 1 ppb 30 20x10*5 5x10-5 30 20 x 10*5 6 x 10-5 30 20x10-5 7 x 10-5 30 20 x 10-5 8x10-5 Different Substitutedb Value Assumptions 80% 80% 30 20x10-5 6 X 10-5 30 20x10-5 8 x 10-5 Different Duration0 Assumptions 80% 2 ppb 1 PPb 20x10*5 7 x 10-5 Different Unit Riskd Assumptions 80% 80% 2 ppb 2 ppb 1 ppb 1 ppb 30 30 0.9 X 10*5 1 x 10-5 " fiW VV y t v r- - % Assumption* Used In 80% 2PPto 1 Ppb ao aexio- ' 7x10*8 ............................ ............................................................................................ ...................... * Note Cumulative Excess Cancer Risk after replacement of shaded assumptions in column 1, 2 or 3, but retaining all other assumptions for 1983 to 2009 average annual concentrations as shown in TABLE 9. a 62% = for individuals over 11 years of age, taken from the Air Resources Board, `Activity Patterns of California Residents,' Final Report, 1991, Research Division, Sacramento California: 76% = for children 11 years and younger, taken from Phillips, T.J., Jenkins, P.L., and Mulberg, E.J., "Children in California: Activity Patterns and Presence of Pollutant Sources,' 1991, Air Resources Board, Sacramento, California; 80% = Office of Environmental Health Hazard Assessment (OEHHA) value; also assumed in `Health Risk Assessment of the B.K.K. Landfill, West Covina, California, Interim Report November 1990,* Department of Health Services-Hazardous Waste Toxicology Section, Emeryville, California; 96% = United States Environmental Protection Agency value, taken from `Risk Assessment Guidance for Superfund: Volume I - Human Health Evaluation Manual, Supplemental Guidance, 'Standard Default Exposure Factors' Interim Final 1991,* OSWER Directive: 9285. 6-03. Office of Emergency and Remedial Response, Toxics Integration Branch, Washington, D.C. b o ppb = lowest possible value 1 ppb = OEHHA's assumed value for samples with nondetectable concentrations of vinyl chloride in the 1981-1982 data 2 ppb = OEHHA's assumed average annual concentration of vinyl chloride at Station A in 1980, as described in the addendum report 5 ppb = value based on half the detection limit for vinyl chloride in 1980 c worst case duration = for comparison with the 1990 interim report d 2.5 x 10-5 per ppb 4.5 x 10* per ppb 20 x 10* per ppb value derived by OEHHA from a study of vinyl chloride workers who developed liver cancer value derived by OEHHA from combined studies of vinyl chloride workers who developed liver, brain, or lung cancers current unit risk value derived by OEHHA from a study in mice that developed lung cancer -58- CMA 114377 regarding percent time spent at home suggest stimates of excess cancer risk which, at Station A, are approximately 29 percent below or 14 percent above the estimate obtained using the primary assumption in this addendum report for percent time spent at home (see TABLE 10). Average Annual Concentration in 1980 and Substituted Value for Samples With Nondetectable Concentrations in the 1981-1982 Data There is uncertainty associated with the average annual concentration assumed for exposures in 1980, and with the substituted value for samples with nondetectable concentrations. Nondetected concentrations could range from zero to just below the detection limit. The "true" level cannot be known. The reasonable maximum exposure scenario as estimated in TABLE 9 assumes an average annual concentration in 1980 of 2 ppb, and the substituted value of 1 ppb for samples with nondetectable concentrations in the 1981-1982 data. If a value of 5 ppb (half the detection limit achievable in 1980-1982) were substituted for the average annual concentration in 1980 and for samples with nondetectable concentrations in the 1981-1982 data, estimates of excess cancer risks are increased: at Station A, 8 x 10'5. If a value of zero were substituted for the average annual concentration in 1980 and for samples with nondetectable concentrations in the 1981-1982 data, estimates of excess cancer risks are decreased: at Station A, 6 x 10'5. These different assumptions regarding the average annual concentration in 1980 and the substituted value in the 1981-1982 data give estimates of excess cancer risk approximately 14 percent above or below estimates obtained using the primary assumption for the average annual concentration in 1980 and for samples with nondetectable concentrations in the 1981-1982 data (see TABLE 10). Exposure Duration Under a 70-year exposure duration, the average annual concentration at Station A in 1995 is assumed to be constant for the 55-year period, 1995 to 2050. Because the exposure in 1995 is low, there is no change in the risk estimate at Station A assuming either a 30-year or a 70-year duration (see TABLE 10). This estimate differs from that of the 70-year duration risk estimate of th interim report because of the following differences: different assumed year for the beginning of exposures; different exposure concentrations for the years 1980-1982 and the years after 1987; and different unit risk values for vinyl chloride (see TABLE 11). The current 70-year duration estimate is based on updated data and toxicity information. Unit Risk Values The Cal/EPA unit risk value of 20 x 10`5 per ppb is an upperbound estimate of the carcinogenic activity of vinyl chloride in humans, derived from studies in female mice that developed lung carcinoma. TABLE 2 also shows two unit risk values based only on human studies. The unit risk values derived from human data have the advantage that they do not have to incorporate an adjustment for interspecies variation. However, they have limitations which include use of studies of only male workers and use of estimates of exposure based on job descriptions rather than actual exposure monitoring data. The unit risk value 2.5 x 10'5 per ppb is derived from studies of vinyl chloride workers who developed angiosarcoma of the liver; the unit risk value derived from combined studies of vinyl chloride workers who developed liver, lung, or brain cancers is 4.5 x 10'5 per ppb. Assuming the unit risk value 2.5 x 10'5 per ppb, the excess cancer risks (calculated for the period 1980 to 2009, using the average annual concentrations shown inTABLE 9) decrease: at Station A, 0.9 x 10'5. Assuming the unit risk value 4.5 x 10`5 per ppb, the excess cancer risk at Station A is 1 x 10`5. These different assumptions regarding the unit risk value suggest estimates of excess cancer risk approximately 87 percent lower than estimates assuming the current Cal/EPA unit risk value (see TABLE 10). CMA 114378 -59- Sensitivity From Exposures at a Young Aae This methodology suggested by USEPA to estimate risk to vinyl chloride from exposures at a young (0 to 5) age assumes that, for a given constant exposure level, an individual exposed during the first six years of life incurs the full conventional (70-year) lifetime risk, and that an individual exposed from birth for 70 years incurs double the conventional lifetime risk. This increased sensitivity to exposures at a young age does not mean that a child will develop cancer but that when the exposed.child becomes an adult, her or his risk of developing cancer is increased. Although referred to in USEPA's guidance documents, the methodology for assessing risk from exposures to vinyl chloride at a young age is stil! pending final adoption by USEPA. Further discussion is provided in the `Limitations and Uncertainties" section Summary of Health Risk Assessments Conducted To-Date Regarding the B.K.K. Landfill TABLE 11 summarizes results of the health risk assessments conducted to-date regarding the B.K.K. Landfill. Different assumptions, methodologies, and data bases were used. Estimated risks associated with exposures to vinyl chloride range from 0.04 x 10*5 to 9 x 10'5. CMA 114379 -60- TABLE 11 SUMMARY OF HEALTH RISK ASSESSMENTS OF THE BKK LANDFILL, WEST COVINA, CALIFORNIA Report 1 "Ambient Air Monitoring and Health Risk Assessment for Suspect Human Carcinogens Around the BKK Landfill in West Covina* Department of Health Services(DHS}/Air Resources Board(ARB)/South Coast Air Quality Management District(SCAQMD), 1983 2. "Estimates of Carcinogenic Risk in the Vicinity of the BKK Landfill" K S Crump & Co., 1986 3. 'Risk Assessment for Exposure to Ambient Air in the Vicinity of the BKK Landfill in West Covina, 1978-1985' Bogen and Smith, 1986 4 "Health Risk Assessment of the BKK Landfill. West Covina, California, Interim Report* DHSHazardous Waste Toxicology Section (DHSHWTS), 1990 5. 'Risk Assessment in Fulfillment of AB2588 Requirements for SCAQMD Facility No. 55449" ENVIRON, 1991 6. "Addendum Health Risk Assessment of Ambient Fugitive Vinyl Chloride Emissions from Ihe Class Unit of the BKK LandfHI, West Covina, California" Office of Environmental Health Hazard Assessment-HWTS, 1996 Assumptions Methods No dilution in measured concentrations at stations A, B, C, D. E, F Exposure for 24 hrs/day, 365 days/year, for the 7 years (1976-1982) 100% absorption in the lungs Exposure to 7 chemicals: vinyl chloride, benzene, trichloroethylene, perchloroethylene, 1,1-dichloroethylene, 1,2-dichloroethane, and chloroform Unit risk for vinyl chloride 1.3 x 10 s per ppb Individual excess lifetime cancer risk and population excess cancer burden Average air concentrations from 12 SCAQMD stations and 4 University of Southern California stations Exposure for 24 hrs/day, 365 days/year, for the 8 year period 1978-1985 Exposure to 7 chemicals (see above list) Unit risk value for vinyl chloride: 1 x 105 per ppb Maximum likelihood estimate (MLE) and upper 95% confidence limit estimate (UCL) 50% dilution in measured concentrations at stations A, B, D, F Exposure for 15 hrs/day, 365 days/year, for the 7 years (1978-1985) 50% absorption in the lungs Exposure to 7 chemicals (see above lisp Unit risk value for vinyl chloride: 1 x 10 s per ppb Monte Carlo potency analysis method and Monte Carlo procedure, best estimate No dilution in monitored concentrations at stations A, B, and MY; 1982-1987 SCAQMD data Exposure for 24 hrs/day, 292 days/year for 70 years (1976-2046) 100% absorption in the lungs Exposure to vinyl chloride primarily Unit risk value for vinyl chloride: 0.69 x 10 s per ppb Worst case scenario; individual excess lifetime cancer risk and population excess cancer burden -- Under review by SCAQMD -- No dilution in monitored vinyl chloride concentrations at stations A, B, and MY; data sets: 1981-1982 SCAQMD, 1983-1990, SCAQMD; 1993-1994, BKK Corporation Exposure for 24 hrs/day, 292 days/year, for 30 years (1980 to 2009) Exposure to vinyl chloride primarily Unit risk for vinyl chloride: 20 x 10 s per ppb Reasonable maximum exposure scenario; individual excess lifetime cancer risk Excess Cancer Risk 5 x 10 s (all 7 chemicals) 0.25x10 s (MLE) 1.1 x 10 s (UCL) (all 7 chemicals) 0.1 - 0.2 x 10 s (vinyl chloride) 1.7 x 10 5 (all 7 chemicals) 0.04 x 10 s (vinyl chloride) 1 - 2x 10 s Station A: 7 x 10 s Station B 6 x 105 Station MY 9 x 10s CMA 114380 -61- Limitations and Uncertainties The estimated risks calculated in this report are upperbound estimates based on the assumptions, methodology, limitations, and uncertainties specified. Other methods (maximum likelihood estimates, best estimates, Monte Carlo estimates) may yield different risk estimates. Most of the assumptions used in this report tend to overestimate the risk. Normally, the actual risks from a site would be no more than, and likely less than (if not zero), the estimates given in this type of assessment. Limitations and uncertainties associated with the data and methodology of this addendum report are the following: Hazard Identification - Other hazardous chemicals known to be emitted from the B.K.K. Landfill include benzene (also a known human carcinogen), trichloroethylene, perchloroethylene, chloroform, and 1,2-dichloroethane. These chemicals were not quantitated to the same extent as vinyl chloride, and have also been detected in background air in the South Coast air basin. It is not possible with the available data to distinguish between the amount of those chemicals emitted from the Class I Unit of the B.K.K. Landfill and the amount found in ambient air from other sources. Toxicity Assessment - The unit risk value for vinyl chloride (20 x 10`5 per ppb) was estimated using the linear multistage model. This model extrapolates the incidence of the carcinogenic effect observed at high exposure levels, in this case, in the ppm range, to what may be expected at much lower exposure levels, in this case, more than 1,000 times lower (ppb). The unit risk value is the upperbound 95 percent confidence limit of the maximum likelihood estimate. This model may underestimate the unit risk value but is more likely to overestimate it. There is the possibility that the unit risk value is zero at low ppb levels; - The unit risk value is based on an animal study. Other values calculated from data obtained in occupational studies were lower. However, the occupational studies were only of male workers and the exposure levels were not actually measured; There is evidence that very young animals are more sensitive to the carcinogenic effects of vinyl chloride. USEPA recommends age-attributable risk estimations for exposures to vinyl chloride. The unit risk value developed by OEHHA accounts for age specific sensitivity. Exposure Assessment - There are no ambient vinyl chloride monitoring data for the year 1980. It is an assumption of this addendum report that exposures at Stations A, B and MY began in 1980. Residential development near the monitoring stations was completed in 1979, and odor complaints data from 1978 to 1981 suggest that residents on the "M" and "L" named streets were subject to downwind exposures before the residential monitoring program began; CMA 114381 -62- - The 1981-1982 ambient vinyl chloride monitoring data were collected for 16 of the 24 months, and the average concentrations of the available data for each year were assumed to be representative of a 12-month period. This may overestimate exposure; - Results of the data collected between October 16 and December 31, 1982 are available in terms of the ambient air quality standard (10 ppb) rather than the detection limit (2 ppb). Consequently, the number of samples with nondetectable concentrations in this portion of the data are likely over-reported. A value of 1 ppb was substituted for samples with nondetectable concentrations in the 1981-1982 data; this may underestimate exposure; - During the period 1983-1990, ambient air monitoring was conducted only in residential areas to the southeast and south of the landfill. These data may have identified the highest detectable ambient levels of vinyl chloride but they do not provide information for other residential areas around the landfill; - Monitoring at Station MY began in June 1984. Average annual concentrations at Station A for the years 1981 through 1983 are used to represent exposures at Station MY for those three years. This may underestimate exposures at Station MY because it is closer to the landfill than Station A and higher levels were consistently reported for Station MY when both stations were in service; - The majority of samples in SCAQMD's 1981-1990 ambient vinyl chloride monitoring data were samples with nondetectable concentrations (21 of 26 data sets, see TABLE 7). The substitution of 1 ppb for samples with nondetectable concentrations is likely to underestimate exposures in the 1981-1982 data since some of the samples may have had concentrations of vinyl chloride below 10 ppb but above 2 ppb. The substitution of 1 ppb for samples with nondetectable concentrations in the 1983-1990 data is likely to overestimate exposures; - The analytical procedure for B.K.K. Corporation's 1993-1994 Proposition 65 monitoring data has been accepted by SCAQMD and appears to be acceptable to USEPA. Risk Characterization Using a substituted value greater than zero for samples with nondetectable concentrations yields a risk estimate that will always be above zero, whether there were actual exposures or not; - The assumption that 2 ppb is a reasonable estimate for an average annual concentration in 1980 may underestimate exposure because of the average annual concentrations of vinyl chloride at Stations A and B in 1983, and the estimated average annual concentrations of vinyl chloride at Stations A and B in 1981-1982; -63- CMA 114382 - Actual indoor air levels of vinyl chloride are not known. Indoor air monitoring was conducted only in October 1984 and only in ten homes along the southern border of the landfill. The assumption that ambient air and indoor air concentrations are equal may either underestimate or overestimate exposure; - The length of residency and percent time at home are general assumptions which tend to overestimate exposures. They are not based on actual information from residents living near the monitoring stations. 1995 monitoring data collected by the B.K.K. Corporation shows an average annual concentration of 0.12 ppbv onsite at the Nogales End station. This suggests that vinyl chloride concentrations are decreasing, and the associated risk is also decreasing. - There is uncertainty associated with the vinyl chloride unit risk value used in the addendum report. Using USEPA's apportioned lifetime risk estimates to account for increased sensitivity from exposures at a young age (TABLE 3) suggests a 14-fold higher risk at Station A than the estimate obtained in this addendum report. Using a physiologically-based pharmacokinetic model for vinyl chloride (Appendix J, comments from the Chemical Manufacturers Association, article by Reitz at al., 1995) suggests a 140-fold lower risk at Station A then the estimate obtained in this addendum report. Risk estimation is a constantly evolving science and changes as new information and data are accepted by risk assessors. The USEPA apportioned lifetime risk estimate and the physiologically-based pharmacokinetic model for vinyl chloride are proposed newer ways to look at risk from vinyl chloride. This addendum report used a currently established and accepted estimate of risk for vinyl chloride. Findings of the Addendum Health Risk Assessment This addendum health risk assessment provides an assessment of past, present, and future risks for individuals living near Stations A, B, and MY from exposures to ambient fugitive emissions of vinyl chloride associated with the closed Class i Unit of the B.K.K Landfill. There are four findings of this report: 1. From the available monitoring data, the single year of highest detected exposure to vinyl chloride was 1981. The maximum detected concentration of vinyl chloride at Station A in 1981 was 50 ppb, compared to 0.16 ppb in 1994. The average annual concentration at Station A in 1981 is estimated to have been 7.2 ppb, compared to an estimate of 0.05 ppb in 1994. For individuals who lived near Stations A, B, and MY during the 1980's, past exposures to vinyl chloride were higher than current exposures. The cumulative individual excess lifetime cancer risk suggests that for exposures beginning in 1980, the majority of the cancer risk was incurred by 1983-1984, and that there is little change (on the order of 15 to 22 percent) in the cumulative risk after 1986. 2. The landfill gas collection system, which was expanded over time, and the cap covering the closed Class I Unit have been successful in lowering the frequency and level of vinyl chloride emissions to levels that pose little, if any, risk to nearby residents. -64- CMA 114383 3 Regulatory agencies with responsibility for remediation or control of the B.K.K. Landfill may want to include past exposures of vinyl chloride near Stations A, B, and MY in subsequent health assessments of emissions from the landfill to ensure future risks do not add significantly to the past cumulative risk. 4. In spite of using best available scientific knowledge, there is considerable uncertainty associated with the estimated exposures, the carcinogenic potency value of vinyl chloride, and young-age sensitivity methodology. The estimated excess cancer risks calculated in this addendum report are upperbound estimates, based on the assumptions, methodology, limitations and uncertainties specified. The actual excess cancer risk is likely to be lower than these estimates and may be zero. Because the number of people who actually lived or are living near Stations A, B, and MY is small, it is unlikely that excess cases of cancer will occur. Each exposed individual may have an increased risk of developing cancer, however the added risk is small. 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"The rat liver foci bioassay: I. age-dependence of induction by vinyl chloride of ATPase-deficient foci." Carcinogenesis. 6(1): 65-68. Laib, R.J., Pellio, T., Wunschel, U.M., Zimmermann, N., and Bolt, H.M. (1985b). 'The rat liver foci bioassay: II. investigation on the dose-dependent induction of ATPase-deficient foci by vinyl chloride at very low doses." Carcinogenesis. 6(1): 69-72. Mack, T.M. and Thomas, D. (1985). "Methodology for Evaluating Cancer Risk in Small Communities, Evaluation of Cancer Risk in the Residential Neighborhood Near BKK Landfill." University of Southern California, Department of Preventive Medicine, Cancer Surveillance Program. Report to State of California, Department of Health Services. Mack, T.M. and Pinder, R.L. (1988). "Assessment of Cancer Risk to Persons Residing Near BKK West Covina Landfill (Airborne Exposure)." University of Southern California School of Medicine, Department of Preventive Medicine. A report to California State Department of Health Services, Office of Environmental Health Hazard Assessment and Los Angeles County Department of Health Services, Toxics Epidemiology Program. Maltoni, C., Lefemine, G., Ciliberti, A., Cotti, G., and Carretti, D. (1981). "Carcinogenicity bioassays of vinyl chloride monomer: a model of risk assessment on an experimental basis." Environ. Health Perspect.. 41:3-30. Miller, B.A., Ries, L.A.G., Hankey, B.F., Kosary, C.L., Harras, A., Devesa, S.S., Edwards, B.K., (eds). (1993). "SEER Cancer Statistics Review: 1973-1990. "National Cancer Institute, Bethesda, Maryland. NIH Pub. No. 93-2789. Office of Environmental Health Hazard Assessment. (OEHHA, 1993). "Review of the risk assessment for the B.K.K, Landfill (SC-55449)." Letter dated July 16, 1993 from George V. Alexeeff, Ph.D., Chief, Air Toxicology and Epidemiology Section, Berkeley, California to Mr. Mohsen Nazemi, South Coast Air Quality Management District, Diamond Bar, California. 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"California Air Resources Board, Sacramento, California, Presentation at the Air & Waste Management Association 84th Annual Meeting & Exhibition, Vancouver, British Columbia. A Pirastu, R., Comba, P., Reggiani, A., Foa, V., Masina, A., and Maltoni, C. (1990). "Mortality from liver disease among Italian vinyl chloride monomer/polyvinyl chloride manufacturers." Am. J. Ind. Med.. 17:155-161. Rust, K.J., Rust, F.P., and Williams, R.L. (1988). 'Pregnancy Outcomes for Residents Living Near the B.K.K. Landfill: A Study of the 1978-1984 Birth Cohorts." Health Data Research Facility, Community and Organization Research Institute, University of California, Santa Barbara, prepared for the Department of Health Services, Epidemiological Studies and Surveillance Section, Emeryville, California. South Coast Air Quality Management District. (SCAQMD, 1981). "BKK Sanitary Landfill Report.' Prepared by Melvin A. Schreckengost, Industrial Section, Enforcement Division, El Monte, California. 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"The Magnitude of Ambient Air Toxics Impacts From Existing Sources in the South Coast Air Basin." Air Quality Management Plan Revision Working Paper No. 3, Planning Division, Ei Monte, California. South Coast Air Quality Management District. (SCAQMD, 1994a). Letter to update vinyl chloride monitoring in the vicinity of the B.K.K. Landfill. Letter dated March 17,1994 from Dennis Michael Delaney, Meteorologist, Diamond Bar, California to Mr. Steven L. Samaniego, R.E.H.S., Waste Management Enforcement Manager, City of West Covina, California. South Coast Air Quality Management District. (SCAQMD, 1994b). "Report of Surface and Integrated Ambient Air Quality Monitoring Conducted in West Covina in Conjunction with a Joint Agency Inspection of BKK Landfill." Applied Science and Technology-Atmospheric Measurements Division, Diamond Bar, California. Standards and Criteria Work Group. (SCWG, 1994). `California Cancer Potency Factors: Update." California Environmental Protection Agency, Office of Environmental Health Hazard Assessment, Sacramento, California. Stirrat, B.A. & Associates. (1990). `BKK Landfill Ambient Air (Gas) Sampling Program Draft Final Report Volume II, October 30, 1990."Submitted to United States Environmental Protection Agency-Region IX, San Francisco, California. Stirrat, B.A. & Associates. (1991). "BKK Landfill 3013 SAM Workplan Book III Draft, Final Report, January 7, 1991."Submitted to United States Environmental Protection Agency-Region IX, San Francisco, California. The Janes Network. (1994). "Final Interim Remedial Measures Study Scope of Work, BKK Class I Landfill, West Covina, California, May 1994." Prepared for the BKK Corporation by The Janes Network, Santa Cruz, California. -70- CMA 114389 United States Department of Commerce. (1993). "1990 Census of Population and Housing, Population and Housing Characteristics for Census Tracts and Block Numbering Areas, Los Angeles-Long Beach, CA PMSA, Section 1 of 7." Economic and Statistics Administration, Bureau of the Census, Washington D.C. 1990 CPH-3-215B. United States Department of Labor. (USDOL, 1974). 'Title 29-Labor, Chapter XVII, Occupational Safety and Health Administration, Department of Labor, Part 1910, Occupational Safety and Health Standards, Standard for Exposure to Vinyl Chloride." Fed. Reaist.. 1974, 39(194):35890-35898. United States Environmental Protection Agency. (USEPA, 1985). "Aerial Photographic Analysis of the BKK Sanitary Landfill, West Covina, California, EPA Region IX." Office of Research and Development, Environmental Monitoring Systems Laboratory, Las Vegas, Nevada. TS-AMD-83073a/3600. United States Environmental Protection Agency. (USEPA, 1989a). "Risk Assessment Guidance for Superfund: Volume I - Human Health Evaluation Manual (Part A), Interim Final." Office of Emergency and Remedial Response, Washington D.C. EPA/540/1-89/002. United States Environmental Protection Agency, (USEPA, 1989b). "Region IX Recommendations: Risk Assessment Guidance for Superfund Human Health Risk Assessment, Interim Final." San Francisco, California. United States Environmental Protection Agency. (USEPA, 1991a/. "Risk Assessment Guidance for Superfund: Volume / - Human Health Evaluation Manual (Part C, Risk Evaluation of Remedial Alternatives), Interim."Office of Emergency and Remedial Response, Washington D.C. Publication 9285.7-01 C United States Environmental Protection Agency.'(USEPA, 1991b/. "Risk Assessment Guidance for Superfund: Volume I - Human Health Evaluation Manual, Supplemental Guidance. Standard Default Exposure Factors' Interim Final." OSWER Directive: 9285.6-03. Office of Emergency and Remedial Response, Toxics Integration Branch, Washington, D.C. United States Environmental Protection Agency. (USEPA, 1992a). "Supplemental Guidance to RAGS: Calculating the Concentration Term." Office of Solid Waste and Emergency Response, Washington, D.C. Publication 9285.7-081. United States Environmental Protection Agency. (USEPA, 1992b). "Cancer Risk Estimates for Vinyl Chloride. " Memorandum dated September 28,1992 from Jim Cogliano, Chief, Carcinogen Assessment Statistics and Epidemiology Branch, Office of Health and Environmental Assessment (RD-689) Washington D.C. to Arnold Den, Science Advisor, Region IX, San Francisco, California with September 26,1989 memorandum attached. United States Environmental Protection Agency. (USEPA, 1994a). "June 1994 Interagency Steering Committee (ISC) Inspection. " Letter dated August 29,1994 from Carmen D. Santos, Project Manager, Region IX, San Francisco, California to Mr. Paul Neff, Director, Regulatory and Environmental Compliance, BKK Landfill. West Covina, California. United States Environmental Protection Agency. (USEPA, 1994b/. "Health Effects Assessment Summary Tables FY - 1994 Annual."Office of Solid Waste and Emergency Response, Washington, D C. 9200.6- 303(94-1), EPA 540-R-94-020, PB94-921199. United States Environmental Protection Agency. (USEPA, 1994c/. "Health Effects Assessment Summary Tables FY 1994 Supplement Number 2." Office of Solid Waste and Emergency Response, Washington, D.C. 9200.6- 303(94-3). EPA 540/R-94/114, PB94-921102, November 1994. United States Environmental Protection Agency. (USEPA, 1994d). "Integrated Risk Information System (IRIS)." Database access November 1994, and August 1995. CMA114390 -71- United States Environmental Protection Agency. (USEPA, 1994e). "Clarification ofEPA's October 21, 1994 Letter Regarding Ambient'Air Data Validation Reports. " Letter dated October 31,1994 from Carmen D. Santos-Prior, Project Manager, Region IX, San Francisco, California to Ms. Julia M. Bussey, Corporate A^nager, Regulatory Affairs, B.K.K. Corporation, Torrance, California. United States Environmental Protection Agency. (USEPA, 1994f). "BKK's Response Action Plan for Vinyl Chloride - EPA Approval and Errata Sheet." Letter dated August 4,1994 from Carmen D. Santos-Prior, Project Manager, Region IX, San Francisco, California to Ms. Julia M. Bussey, Corporate Manager, Regulatory Affairs, B.K.K. Corporation, Torrance, California. University of Southern California. (USC, 1979). *Interim Report, Odor Investigation and Control for Class I Landfills. * Prepared for the B.K.K. Corporation by the Environmental Engineering Program, Los Angeles, California. University of Southern California. (USC, 1980). `Second Interim Report, Investigation of Odorous and Volatile Compounds for BKK Class I Landfill Site in the City of West Covina. " Prepared for the B.K.K. Corporation by the Environmental Engineering Program, Los Angeles, California. University of Southern California. (USC, 1981). 'Final Report, Investigation of Odorous and Volatile Compounds for BKK Class I Landfill Site in the City of West Covina." Prepared for the B.K.K. Corporation by the Environmental Engineering Program, Los Angeles, California. Viola, P.L., Bigotti, A., and Caputo, A. (1971). `Oncogenic response of rat skin, lungs, and bones to vinyl chloride." Cancer Res. 31:516-522. Vogel, T.M., Criddle, C.S., and McCarty, P.L. (1987). "Transformations of halogenated aliphatic compounds." Environ. Sci. Techno!.. 21(8);722-736. Wong, O., Whorton, M.D., Foliart, D.E. and Ragland, D. (1991). `An industry-wide epidemiologic study of vinyl chloride workers, 1942-1982." Am. J. of Indust. Med. 20:317-334. Wood, J.A. and Porter, M.L. (1987). "Hazardous pollutants in Class II landfills." J. AirPollut. Control Assoc.. 37(5):609-615. Wu, W,, Steenland, K., Brown, D., Wells, V., Jones, J., Schulte, P., and Halperin, W. (1989). "Cohort and case-control analyses of workers exposed to vinyl chloride: an update." J. Occud Med.. 31 (6):518-523. Ziem, G.E. and Davidoff, L.L. (1992). "Illness from chemical "odors": is the health significance understood?" Arch. Environ. Health. 47(1):88-91. -72- CMA114391 BLANK PAGE CMA114392 -73- APPENDIX A ERRATA CMA 114393 -74- ERRATA The following errors were contained in the intenm report, "Health Risk Assessment of the B.K.K. Landfill, West Covina. California, November 1990," prepared by the Hazardous Waste Toxicology Section, Environmental Epidemiology and Toxicology Brancn (EETB), Health Hazard Assessment Division. California Department of Health Services (DHS): Page 8, third paragraph: The B.K.K. Landfill, operated by B.K.K. (Kenneth B. Kazarian) Corporation, is located within the corporate boundary of the City of West Covina. California. 18 miles east of downtown Los Angeles in Los Angeles County (Figure 1)." The reference to Kenneth B. Kazanan as the BKK Corporation is not correct. The text should read: The B.K.K. Landfill. operated by the B.K.K. Corporation, is located within the corporate boundary of the City of West Covina, 18 miles east of downtown Los Angeles in Los Angeles County (Figure 1). Page 80. third paragraph: In 1985, EPA estimated the population within a one~mile radius of the center of the B.K.K. Landfill to be approximately 40.000 persons (LPA. 1985). The reference (LPA. 1985) should read (EPA 1985). CMA 114394 -75- APPENDIX B "B.K.K. LANDFILL, WEST COVINA, CALIFORNIA FACT SHEET, DECEMBER 1990," CALIFORNIA DEPARTMENT OF HEALTH SERVICES ENVIRONMENTAL EPIDEMIOLOGY AND TOXICOLOGY BRANCH EMERYVILLE, CALIFORNIA CMA 114395 -76- FACT SHEET California Department of Health Services Environmental Epidemiology and Toxicology Branch BKK LANDFILL West Covina, California DECEMBER 1990 In-Depth Summaries Of Health Studies Near BKK Landfill This fact sheet contains summaries of two can cer studies and a health risk assessment con cerning the BKK landfill, a hazardous waste site in West Covina, California. These studies were undertaken by the California Department of Health Services (DHS) in response to the con cerns of residents near the landfill. Background In 1963, the BKK landfill, operated by the Ben Kenneth Kazarian Corporation, opened on 130 acres in the San Jose Hills in the City of West Covina in Los Angeles County. Initially, the landfill accepted only municipal waste such as household and commercial refuse and construc tion debris. In 1971, the City of West Covina approved an expansion of the facility to its present size of 583 acres. In 1972, a 40- acre haz ardous waste management unit (a state-desig nated Class I landfill) opened on the existing site and began receiving hazardous wastes. This unit was expanded by an additional 100 acres in 1975. In November, 1984, the landfill stopped accept ing hazardous waste. In March, 1989, the unit was formally closed. The closing process in cluded building a low-permeability soil cap over 180 acres, that is, over the regulated hazardous waste area and some surrounding municipal waste. In 1969, area residents filed their first odor com plaint against the BKK landfill with the South Coast Air Quality Management District. In 1979, 278 odor complaints were reported. Studies have shown that hazardous waste migrated from the landfill into air and water around the site. People living near the landfill have been concerned about possible health effects due to hazardous waste releases in air. surface water runoff, spills and dust from the landfill. Drinking water sup plies are not contaminated. 1. The Cancer Studies What Were The Studies Looking For? Under contract by the California Department of Health Services (DHS), Dr. Thomas Mack, Dr. Duncan Thomas and Richard Pinder from the University of Southern California, Cancer Sur veillance Program, conducted two studies that investigated the distribution of cancer cases m residents living near the BKK landfill between 1972 and 1982. The aim of the first study, completed m 1985, was to determine whether residents living south and west (mostly downsiope) of the BKK land fill had a greater chance of getting cancer than the average resident of Los Angeles County. The second study, completed in 1988, focused on the area to the north and east (mostly downwind during the day) of the landfill. Both studies re lied on data collected by the Los Angeles County Cancer Surveillance Program, and examined cancer incidence from 1972 to 1982. Each study analyzed cancer rates for all childhood cancers, for each of 89 different types of cancers, and for all cancers taken together. In both studies, the distribution of those cancers found to have oc curred at a higher than expected rate was exam ined to determine if the landfill might be a pos sible cause of the increase. (continued on Page 2) -77- CMA 114396 CENSUS TRACTS IN STUDY AREA BKK LANDFILL, WEST COVINA, CA California Department Of Health Services i men > 7.500 *et ---- census Tract 1 Highway The Cancer Surveillance Program collects infor mation on each Los Angeles County resident who has received a microscopically verified can cer diagnosis or for whom cancer is recorded on a death certificate. These two studies focused on persons who were diagnosed with cancer dur ing the 11-year period between January 1,1972, and December 31, 1982. Residents of 11 census tracts (1960 definitions) comprised the popula tion living near the BKK landfill (see map above). In total, about 100,000 people lived in the BKK study area in 1977 (midway through the 19721982 study period), and about 2,000 cancer cases were identified during the 11-year study period. Table 1 shows for each tract the estimated 1977 population (based on 1970 and 1980 census data) and the number of residents diagnosed with cancer between 1972 and 1982. What Did The Studies Find? Among residents of the 11 census tracts, the overall rate of cancer for both adults and chil dren was similar to that for Los Angeles County as a whole. The rate of cancer was not higher for residents living closer to the landfill, nor did the average rate of cancer increase between the ear lier and later study time periods (from 1972-1976 to 1978-1982). Overall sex-specific cancer rates are shown in Table 2 for each census tract, along with a comparison to total Los Angeles County rates. Even though the overall cancer rate in the BKK study area was not higher than the Los Angeles county rate, researchers studied 89 individual types of cancer to determine whether unexpect edly high levels of any one of them appeared in any census tract. A type of cancer was consid ered in excess if; 1) there were more extra cases than could be accounted for by chance alone, 2) cases occurred at least twice as often as usual in Los Angeles County, and 3) that type of cancer met at least one of four other requirements (more than four excess cases; elevated in at least two census tracts; elevated in both sexes; or the rate of that cancer at least doubled over the study (cmtmutd on Ptgt 4) -78- CMA 114397 * Table 1 Total number of cancer cates in 1972-1982 and estimated 1977 population in 11 census tracts around the BKK landfill. West Covina, California. Census Tract Dtraction ef Census Tract from BKK Landfill Eat. 1977 Population Total 1972-82 Canoar Caaas 4080 Tract in Beth Study One and Two Contains BKK landfill 8.565 142 4077 4078 4079 4081 4082 Southwest Southwest West South South and West Other Tracts in Study One 8,652 7,370 4,577 27,280 9.807 209 159 78 380 218 4034 4063 4064 4065 4066 East North and East North North Northwest Other Tracts in Study Two 10,533 3,470 6.720 5.626 8.955 166 111 236 199 277 Total Tract Aggregate 101.555 2.175 Table 2 1972-1982 average annual cancer incidence rates by sex in Los Angeles County and in 11 census tracts around the BKK landfill, West Covina. California. Census Tract Los Angeles County 4080 4077 4078 4079 4081 4082 4034 4063 4064 4065 4066 &*X Male Female Male Female Male Female Male Female Male Female Male Female Male Female Male Female Male Female Male Female Male Female Male Female 1973-1982 Cancer Cases 127,003 148.563 83 59 B7 122 76 83 35 43 176 204 95 123 77 89 56 55 101 135 99 100 118 159 Average IneMenee Rate' 375.6 328.5 368.1 187.9 364.7 362.7 466.1 364.3 297.5 263.5 290.7 245.7 262.5 255.9 343.7 284.2 354.2 290.4 367.7 384.7 477.8 327.8 336.9 345.9 Rata Ralattve To LA CO Rate1 _ - 1.0 0.6 1.0 1.1 1.2 1.1 0.6 0.8 0.8 0.7 0.7 0.8 0.9 0.9 0.9 0.9 1.0 1.2 1.3 1.0 0.9 1.1 ' Average number of cancer cue* per 100.000 population per year. ' A value of 1.0 meant that the cancer raw in the oentut tract it equal to the tate in LA. County. A value greater than 1.0 (e.g,, i .2) meant that the rate in centut pact it greater than rate in L.A. County (e.g.. by 1.2 timet) A value latt than 1.0 (e.g.. 0.8) meant the raw in the oentut pan it lett than the rate in LA. County (e.g.. by 0.8 emet). 3 CMA 114398 -79- period). Ten such types of cancer were identi'fjed: hepatoma, meningioma, tongue, nasophar ynx, larynx, upper colon, pancreas, bladder, melanoma of trunk or scalp, and endometrium (Table 3). Whenever small geographic areas are closely studied as was done here, too many -- and too few -- cases of a few types of cancer are ex pected to appear in some areas by chance alone. Each cancer type listed in Table 3 was scrutinized to determine if any other evidence of a public health risk existed, for example, whether any cancer showed a consistent pattern of increased risk as might be expected from exposure to the landfill. Researchers concluded that excess cases of each of these 10 types of cancer were most likely not due to the landfill, but to other char acteristics of the affected population. First, some types of cancer are known to be related to high income and education. One is endometrial can cer. Risk of endometrial cancer is greater among high-income populations who use estrogen re placement hormones and delay childbearing. When the rates of this cancer in the BKK study area were compared with rates in census tracts of similar socioeconomic status in Los Angeles County, the rates were nearly the same. Second, the increase in some identified cancers disappeared after 1982. In the case of melanoma, its relatively higher rate in one census tract be tween 1972 and 1982 has not continued, and no additional cases appeared between 1983 and 1985. This drop in the rate led the authors to conclude that the 1972-82 rate watftot due to the site. Third, and more significantly, nh cxcess cancer cases were identified in the census tract contain ing the landfill (4080), which covered an area extending approximately one mile from the site. Residents with these 10 types of cancer were more likely to live farther away from the landfill than residents with other types of cancer. If ex posures from the site were causing the cancers, there would be a pattern of more cases near the site, not farther from it. (continued on P*ge S) Table 3 Selected characteristics of 10 specific types of cancers identified ter in-depth analysis in two cancer studies of 11 census tracts around the BKK landfill. West Covina, California. Type of Cancer Hepatoma Meningioma Tongue Nasopharynx Larynx Upper Colon Pancreas Bladder Melanoma. Trunk/Scalp Endometrium Sex F M M M F F F M M M F F M M F F Census Tract 4082 4079 4081 4082 4078 4082 4077 4078 4082 4077 4082 4077 4078 Total Cancer Cases 3 1 5 2 3 3 2 2 6 7 9 6 9 4034 4064 4066 6 23 24 Annual Rate Relative To LA CO Rata* 4.9 3.7 3.5 2.7 10.1 4.6 13.8 9.1 2.0 3.0 1.B 2.8 2.4 2.8 2.0 1.7 Number Excess Cases 2.4 0.7 3.6 1.3 2.7 2.3 1.9 1.8 3.0 4.7 4.1 3.8 5.3 Rate In 197S-SI/1672-76' 2.0 0.0 0.7 1.0 0.5 0.5 Inf3 Inf1 1.0 1.3 2.0 0.5 1.3 3.9 . 11.7 9.4 Inf1 0.8 0.8 ' Value grantor than i.o (e.g.. 1.7) rneens rate m census tact is greater than rate in LA. County (e.g.. by 1.7 smet). > This column is toe rata cf cancer occurrence in 1978-82 divided by the rata dunng 1972-76. Per hepatoma, tor example, the rate in 1978*42 was 2 times die rate in 1972-76. 1 Inf means infinity, and indicates that there ware no eases diagnosed in 1972-1976. 4 -an. CMA 114399 i What May The Studies Have Missed? Although a thorough study has been conducted, all studies have limitations. If there was a rela tionship between the BKK landfill and cancer, there are a few reasons why the study may have failed to find it. First, too small a proportion of the population in the nearby census tracts may actually have been exposed to the landfill. If, for example, only people on the blocks close to the landfill had exposures from the site, then ana lyzing cancer rates for the whole census tract may have been too crude. Census tracts, how ever, were the smallest unit from which the Cancer Surveillance Program could analyze its records. Second, because people moved in and out of the community often, exposed individu als who developed cancer may well have left the area by the time the disease appeared and so were not in the Cancer Surveillance Program's data base. A third reason may be that not enough time has elapsed for cancer to occur the consen sus among scientists is that there is often a 20- to 30-year period between exposure to a cancercausing chemical and the onset of disease. Conclusion These studies compared the rate of cancer occur rence in residents of 11 census tracts adjacent to the BKK landfill to rates in Los Angeles County as a whole. There was no overall increase in the cancer rate among residents living near the BKK landfill. There was no consistent pattern of oc currence to suggest that the BKK landfill is linked to individual types of cancer. The results do not substantiate concerns that there were excess cancers around the BKK landfill between 1972 and 1982. 2. The Health Risk Assessment Introduction In response to residents' requests, DHS con ducted a health risk assessment of the BKK land fill based on environmental monitoring from 1982 through 1987. It provides an estimate of the health risks to individuals living near the BKK landfill from exposure to chemicals found in the air, groundwater and surface water. The assessment is primarily concerned with estimating the risk of developing cancer from exposure to chemi cals found in the air because: 1) monitoring ac tivities indicated that air was the main route of exposure, and 2) it is assumed that no amount of exposure to a cancer-causing chemical is without some risk. A risk assessment is an ongoing process that requires revision as science and technology pro vide new information. The 1990 health risk as sessment of the BKK landfill updates a 1982 risk assessment and will be revised when informa tion about vinyl chloride, one of the cancercausing chemicals found in the air around the BKK landfill, is updated. There were three previous health risk assess ments of the BKK landfill: one by public agen cies and two by private consultants to the BKK Corporation. Previous Cancer Risk Assessments In 1982, the Department of Health Services (DHS), the South Coast Air Quality Management District (SCAQMD), and the California Air Re sources Board (CARB) monitored the air in resi dential neighborhoods around the BKK landfill. The following seven chemicals known or sus pected to cause cancer were identified: vinyl chloride, benzene, perchloroethylene, trichloroethene, 1,1-dichloroethylene, 1,2dichloroethane, and trichloromethane (chloro form). Public health data show that each person has a one-in-three risk of developing cancer during a 70-vear lifetime. This means that 33,000 people in 100,000 will develop cancer sometime during their lifetime. This "one-in-three" risk is referred to as a "background" risk. The 1982 study estimated that for people living near the landfill, and exposed to all seven chemicals, the risk of developing cancer increased to 33,005 in 100,000. In 1986, consultants to attorneys for the BKK landfill performed two separate risk assessments. In the first, the increased cancer risk from the same seven chemicals found in 1982 was esti mated to be much less: between two and 11 in 1 million people. Results in the second assessment were similar an estimated increased cancer risk (continued on Page 6) CMA 114400 -81- from the seven chemicals of two additional cases jin 1 million people. parts of vinyl chloride per billion parts of air (10 ppb). The estimates vary due to differences in the Other chemicals found in the air around the methods and assumptions used by the risk as landfill' are also commonly found in the Los sessors. DHS has used more heaith-protective Angeles air basin at detectable levels. However, methods and assumptions when estimating risk. vinyl chloride is rarely detected in the Los An For example, DHS assumes that 100% of a geles air basin. Therefore, vinyl chloride most chemical detected in the environment is absorbed dearly represents the increased risk of develop by airindividual and that individuals are at home ing cancer associated with the landfill. Liquid 80% of the time. One consultant to BKK used a wastes containing vinyl chloride were buried at method that assumed that 50% of a chemical the landfill until June 1981. -_ found in the environment is absorbed by an in dividual and that individuals are at home less than 80% of the time. Vinyl chloride causes cancer in humans. Health effects other than cancer are seen at levels above 10,000 parts per billion, which is much higher What Did The 1990 Health Risk Assessment Find? than any levels found near the BKK landfill. It is assumed that no amount of exposure to a cancer-causing chemical is without some risk. In 1985, the United States Environmental Protec Therefore, the 1990 health risk assessment fo tion Agency (EPA) hired an engineering firm cuses on the risk of developing cancer from (CH2MH111) to evaluate chemical exposure to breathing the amount of vinyl chloride detected people living close to the BKK landfill. The re by air monitoring around the landfill from 1982 port, completed in 1988, evaluated chemical through 1987. The information used to estimate contaminants in the air, groundwater and sur the risk included the amount of vinyl chloride face water. Chemical analysis of the soil at the detected in the air and the unit risk value for landfill was not done. vinyl chloride. The unit risk value is a measure DHS based the 1990 health risk assessment pri marily on environmental measurements re viewed in the 1988 report. The measurements showed contaminants in groundwater (water found beneath the surface), surface water (water from steams, storm drams or run-offs) and air around the BKK landfill. of the cancer-causing potential of a chemical. It is the estimated excess risk of developing cancer as a result of constant exposure over 70 years to one microgram of a chemical in one cubic meter of air. Unit risk values are determined by EPA and DHS toxicologists based on experimental animal and human epidemiological information. jGroundwater; People living near the BKK land fill are not exposed to the contaminated groundwater because it is not used for drinking water or irrigation. Among people who were exposed to vinyl chloride around the landfill between 1982-1987, the health risk assessment estimates that an ad ditional two people in 100,000 may develop can cer. This means that in every 100,000 people, Surface water People may have been exposed 33,002 of them (rather than 33,000 as in the U.5. to contaminated surface water. However, the average) may get cancer. For the BKK study area, health risk assessment determined that any ex few if any additional cases are expected, too few posure would have involved small quantities, to detect by a health study. Thus the cancer study occurred only once in a while, and lasted only a and risk assessment produced similar results. short period of time. Consequently, the risk to people who may have been exposed to contami nated surface water is considered to be extremely small. What The Health Risk Assessment May Not Shaw Air People living near the BKK landfill may have been exposed to contaminants in the air. In 1981, vinyl chloride was found in the air at the landfill border. From 1982-1987 the amount of vinyl chloride found in residential air monitor ing stations around the BKK landfill was at times above the California air quality standard of 10 As the health risk assessment was being com pleted, DHS also completed a re-evaluation of the ability of vinyl chloride to cause cancer. The re-evaluation suggests that vinyl chloride is more potent than was previously thought. This re- evaluation was not available for use in the health risk assessment. (contnuud on Ptgt 7) -82- CMA 114401 .The health risk assessment used the amount of vinyl chloride that was measured near the landfill between 1982 and 1987, Since 1987, vinyl chloride has rarely been detected near the landfill, so residents' exposure has been reduced. The lower exposure would reduce the risk and the estimated number of additional cancers. Next Steps DHS plans to conduct a new health risk assessment in 1991-92 based on both the new potency information and recent air measurements. DHS also will continue to watch the rate of cancer around the BKK landfill to see whether it in creases. This is because cancer may take a number of years to develop. Residents will be kept up to date as new information becomes available. DHS is conducting a third study at the request of people living near the landfill. This study is ex amining births in the area to see whether there has been any increase in such problems as infant deaths and low weight at birth. Residents vyill receive a summary of that study when it is com pleted in the first half of 1991. Regulation of vinyl chloride by governmental agencies includes the following: The Department of Health Services (DHS/ limits the amount of vinyl chloride in drinking water to 0.5 parts per billion ippb). The California Occupational Safety and Health pro gram (CallOSHA) limits the level of vinyl Moride in the workplaceair to 100ppbaveraged over an eight-hour work period, never to exceed 100 ppb. The California Air Resources Board (CARB) limits the concentration of vinyl chloride in the ambient air to 10 ppb, based on the technology available m 1978. CARB is also proposing to identify vinyl chloride as a toxic air contaminant. A toxic air contaminant is an air pollutant which may cause an increasein serious illness. Identification of vinyl chloride as a toxic air contami nant allows CARB to develop control strategies that reduce vinyl chloride air levels far below 10 ppb. If you have any questions or comments about the studies described in this newsletter, please contact: Elinor Blake Community Relations Coordinator California Department of Health Services Environmental Epidemiology and Toxicology Branch 5900 Hollis Street, Suite E Emeryville, CA 94608 (415) 540-3657 For information about BKK landfill cleanup ac tivities, please contact: Tom Mays Public Participation Specialist California Department of Health Services Toxic Substances Control Program Region 3 1405 N. San Fernando Road. Suite 300 Burbank, CA 91504 (818) 567-3176 Copies of the full epidemiologic studies of cam cer in people living near the BKK landfill, the health risk assessment and other relevant docu ments about the BKK landfill are available at the following libraries: La Puente Library 15920 East Central Avenue La Puente, CA 91744 (818) 968-4613 West Covina Library 1601 West Covina Parkway West Covina, CA 91790 (818) 962-3541 Walnut Library 21155 La Puente Avenue Walnut, CA 91789 (714) 595-0757 CMA 114402 -83- APPENDIX C UPDATED TOXICITY TABLES FROM THE 1990 INTERIM REPORT CMA 114403 -84- UPDATED TOXICITY TABLES FROM THE 1990 INTERIM REPORT In the 1990 interim report. OEHHA-HWTS provided a table showing the USEPA weight-of-evidence classification and site of cancer effect for the carcinogens detected in the environmental monitonng data. Since 1990, USEPA has added cnemical abstract service (CAS) numbers to metals and updated the sites of carcinogenic effects associated with specific chemicals; "Lung" has been added to the site of carcinogenic effects associated with vinyl chlonde (USEPA. 1994b). APPENDIX C-TABLE 1 updates this information. APPENDIX C-TABLE 2 updates the unit risk values for carcinogens detected at the landfill. A side-byside companson of the 1990 and 1994 values shows the changes (increases/decreases or no change) for each chemical. The 1994 values are taken from Cal/EPA's "Critena For Carcinogens" (SCWG, 1994). OEHHA's slope factor for vinyl chlonde is slightly more potent than USEPA's at this time; 0.27 (mg/kg* day)'1 versus 0.29 (mg/kg-day)'1, respectively. The weight-of-evidence classification for the carcinogens has not changed, although USEPA is in tne process of reviewing the weight-of-evidence for tnchloroetnylene. CMA114404 -85- APPENDIX C-TABLE 1a CARCINOGENS DETECTED IN GROUNDWATER. SURFACE WATER, AND AIR BKK LANDFILL WEST COVINA. CALIFORNIA Reported in the 1988 Exposure Characterization Report13 Carcinogen Arsenic (inorganic) Cadmium Chromium(VI)f Lead Nickel(subsulfide) Benzene Bis-2-chloroethyl ether Carbon Tetrachloride Chloroform 1,2-Dichloroetnane 1.1 -Dichloroethylene Methylene chloride (dichloromethane) N-nitrosodimethytamine Perchloroethyiene 1,1,2.2-Tetrachloroethane 1,1,2-Trichloroethane Trichloroethylene Vinyl chloride CAS#0 7440-38-? 7440-43-9 18540-29-2 7439-92-1 12035-72-2 71-43-2 111-44-4 56-23-5 67-66-3 107-06-2 75-35-4 75-09-2 62-75-9 127-18-4 79-34-5 79-00-5 79-01-6 75-01-4 USEPA0 Class A B1 A B2 A A B2 82 B2 B2 C B2 82 C C C B2 A Cancer^ Site lung, skin lung, prostate, breast lung kidney, lung, stomach lung, nasal hematopoietic system (leukemia) liver liver kidnev. liver, rectum, colon, bladder forestomacn, breast, uterus circulatory system, lung, liver kidney, breast, lung liver, breast, lung, leukemia multipfo sites, liver liver liver liver. Dheochromocvtomaa lymph, liver liver, lung a: Update of Table 3. 'Health Risk Assessment of the BKK Landfill. West Covina. California.' Interim Report. November 1990, page 24. Hazardous Waste Toxicology Section. California Department of Health Services, Sacramento. California. Additions are italicized and underlined (i.e., stomach). b: "BKK Landfill Environmental Exposure Characterization Report. West Covina. California." Volume I, August 15.1988. CH2M Hill. Santa Ana. California, c: Chemical Abstract Service number. d: USEPA weight of evidence classification: A. sufficient evidence in humans: B1, sufficient evidence in animals, limited in humans: B2. sufficient evidence in animals, inadequate in humans: C, limited evidence in animals, inadequate in humans. Taken from USEPA's integrated Risk Information System (IRIS), November 1994. and August 1995. Database access August 1995 shows vinyl chloride, perchloroethyiene, and trichloroethylene under review. With the exception of 1,1-dichloroethylene. the above carcinogens are listed as known to the State of California to cause cancer for purposes of the Health and Safety Code Section 25249.5 at sag. e: Additional sites of carcinogenic effects taken from IRIS November 1994 and August 1995, with the exception of vinyl chlonde. Lung site for vinyl chloride listed in "Health Effects Assessment Summary Tables: FY - 1994 Annual." March 1994. Environmental Critena and Assessment Office. U. S. Environmental Protection Agency. 9200.6-303 (94-1) EPA 540/R-94/020; PB94-921199. f: Inadequate evidence to quantitatively evaluate the carcinogenicity of this compound by the oral route. CMA 114405 -86- % APPENDIX C-TABLE 2a INHALATION UNIT RISK (UR) VALUES FOR CARCINOGENS DETECTED AT BKK LANDFILL WEST COVINA, CALIFORNIA Caronoqen Arsenic (inorganic) Cadmium Chromium(VI) Lead Nickel Benzene Bis-2-chloroethylether Carbon Tetrachtonde Chloroform 1,2-Dichloroethane 1,1 -Dichloroethytene Methylene Chlonde N-Nitrosodimethylamine Perchloroethylene 1,1,2.2-Tetrachloroethane 1.1,2-Trichloroethane Trichloroethylene Vinyl Chloride Molecular Weight 74.92 112.40 52 207.2 58.71 78.11 143.02 153.81 119.39 98.96 96.95 84.93 74.10 165.85 167.84 133.40 131.4 62.5 1990 URb (ug/nvV1 4.3E-3 1.2E-2 1.5E-1 . 4.8E-4 5.3E-5 3.3E-4 4.2E-5 2.3E-5 2.2E-5 5.0E-5 1.0E-6 1.4E-2 5.8E-7 5.8E-5 1.6E-5 1.3E-6 2.7E-6 1994 Cal/EPA URC (ug/rrvV1 3.3E-3 4.2E-3 1.5E-1 8.0E-5 2.6E-4 2.9E-5 7. IE-4 NCf 5.3E-6 NCf NL9 NC* 4.6E-3 5.9E-6 NCf 2. IE-5 2.0E-6 7.8E-5 1994 Cal/EPA URd (ppb)*1 1.0E-2 1.9E-2 3.2E-1 6.8E-4 6.2E-4 9.3E-5 4.2E-3 2.6E-4 2.6E-5 8.9E-5 - 3.5E-6 1.4E-2 4.0E-5 4.0E-4 1.1E-4 1.1E-5 20E-5 USEPA Class A B1 A B2 A A B2 B2 B2 B2 C B2 B2 C C C B2 A a: Update of Table 10, "Health Risk Assessment of the BKK Landfill, West Covina, California," Intehm Report, November 1990. page 47. Hazardous Waste Toxicology Section. California Department of Health Services. Sacramento. California. b: Values listed were derived by the United States Environmental Protection Agency (USEPA) or the California Department of Health Services. Health Hazard Assessment Division. Air Toxics Section (DHS) and were taken from Table 3.15, "Air Toxics Assessment Manual." California Air Pollution Control Officers Association. October 1987 pgs. 3.5-24 to 3.5-28. c: Taken from Standards and Critena Work Group. (1994). "California Cancer Potency Factors: Update.' California Environmental Protection Agency (Cal/EPA), Office of Environmental Health Hazard Assessment, Sacramento. California. NOTE. 1,1-Dichloroethene is no longer considered a carcinogen in California and has been deleted from the California Cancer Potency Factors. Changes in the unit risk values are due to increased knowledge about the inherent toxicity of the chemicals. d: (ppb)"1 = ((jig/m3 x molecular weight) / [24,45m3/umole]). e: USEPA weight of evidence classification: A, sufficient evidence in humans; B1, sufficient evidence in animals, limited in humans: B2. sufficient evidence in animals, inadequate in humans: C. limited evidence in animals, inadequate in humans. Taken from USEPA's Integrated Risk Information System (IRIS), November 1994. Database access August 1995 shows vinyl chlonde. perchloroethylene, and trichloroethylene under review. f; NC * No Change. g: NL = Not Listed by Cal/EPA: no change in unit risk value or classification by USEPA per IRIS. November 1994, CMA 114406 -87- APPENDIX D STATISTICAL EVALUATION OF THE 1983-1990 AMBIENT VINYL CHLORIDE MONITORING DATA CMA 114407 STATISTICAL EVALUATION OF THE 1983-1990 AMBIENT VINYL CHLORIDE MONITORING DATA When estimating the average concentration of an environmental contaminant over time, a certain proportion of the data is often reported to be below the detection limit. Companng two groups of data, such as site data and background data, requires summary statistics including means and standard deviations. Calculating means for samples with nondetectable concentrations requires exchanging nondetects for a value. There are three methods of estimating summary statistics for data that include samples with nondetectable concentrations: distributional, robust, and substitution methods (Helsel. 1990). Use of these methods when more than half the data are samples with nondetectable concentrations may result in biased or imprecise estimates (Homung & Reed, 1990). Distributional methods use the characteristics of known distributions to estimate summary statistics. A critical assumption when using distributional methods is how well the data can be expected to fit the assumed distribution. Commonly used distributions include the normal, lognormal, and Weibuil. Estimates of summary statistics are computed that best match the observed concentrations above the detection limit and the percentage of data below the limit. A frequently used method for fitting points to a distribution is the maximum likelihood estimation (MLE). Robust methods combine the observed data above the detection limit with below-limit values extrapolated in order to compute the mean and standard deviation. The robustness results primanly from the use of observed data rather than a fitted distribution above the detection limit. Substitution methods for nondetects include using the detection limit, half the detection limit, or zero. The substitution of zero produces estimates that are biased low, and the substitution of the detection limit results in estimates considered to be above the true mean. USEPA recommends substituting half the detection limit (USEPA, 1989b). In generating values for samples with nondetectable concentrations in the SCAQMD data. HWTS requested statistical evaluation of the data by DHS-DEODC. The fit of the air monitoring data to normal, lognormal, exponential, and Weibuil distributions was evaluated using data from Stations A. B, and MY for the years 1983 through 1989. To evaluate each distribution, Gibbs technique was used to estimate the value of samples with nondetectable concentrations as follows: first, the value of half the detection limit was substituted for samples with nondetectable concentrations; then, the MLE was used to estimate the parameters for the entire distribution: then, a random number generator was used to generate new values for samples with nondetectable concentrations. The data were generated using the given distribution and the most recent parameter estimate. The process was then iterated until a convergence cnterion was met. The Gibbs method differs from other algorithms in that it requires no numencal integration. The integration is replaced by the random number generation. CMA 114408 -89- The lognormal distribution showed the best fit. Arithmetic means of the lognormal distribution for vinyl chtonae concentrations at Stations A, 8, and MY for the years 1983 through 1989 are gitn in APPENDIX D - TABLE 1. Blanks in the table indicate insufficient data to compute the algonthm. These concentrations are similar to the concentrations reported in TABLE 6 of this addendum report. When substituted into the nsk equation, average annual concentrations using the Gibbs technique result in risk estimates per year that are similar to the risk estimates using the simple substitution method for samples with nondetectable concentrations. Since the substitution method can be more easily reproduced and the results are comparable to a more sophisticated method, the substitution method was used for samples with nondetectable concentrations. '***&. CMA114409 -90- APPENDIX D - TABLE 1 AVERAGE ANNUAL CONCENTRATIONS OF VINYL CHLORIDE BASED ON GIBBS TECHNIQUE* FOR SAMPLES WITH NONDETECTABLE CONCENTRATIONS Station A Station B Station MY 1983 2.84 2.98 - 1984 4.08 3.88 5.38 1985 3.34 2.20 5.36 1986 1.77 1.24 2.97 1987 1.51 1.12 2.45 1988 1.25 1.87 2.32 1989 * 0.83 'The Gibbs technique was used to estimate the value of samples with nondetectable concentrations as follows: first, the value of half the detection limit was substituted for samples with nondetectable concentrations; then, the maximum likelihood estimate was used to estimate the parameters for the entire distribution; then, a random number generator was used to generate new values for samples with nondetectable concentrations. The data were generated using the given distnbution and the most recent parameter estimate. The process was then iterated until a convergence criterion was met. The Gibbs method differs from other algonthms in that it requires no numerical integration. The integration is replaced by the random number generation. NOTE: Values computed by Joel Swartz, Ph.D.. California Department of Health Services-Environmental Epidemiology and Toxicology Section. Emeryville. California. 1992. using South Coast Air Quality Management Distnct s ambient vinyl chlonde momtonng data. January 1983 through December 1989. CMA 114410 -91- APPENDIX E V 1990 POPULATION CENSUS TRACT DATA FOR THE VICINITY OF THE B.K.K. LANDFILL WEST COVINA. CALIFORNIA CMA 114411 -92- APPENDIX E-FIGURE 1 (Department of Health Services, Division of Environmental and Occupational Disease Control) Courtesy of: Rachel Sroadwin, California Department of Health Services, Division of Environmental and Occupational Disease Control, Environmental Health Investigations Branch, Emeryville, California, April 1994. CMA 114412 -93- 1. AlG<ouos Total ChHdten{0-4| CNhfcen (5-9) CNkfeen (10-14) CMdran (IS-19) Adults (20-64) Adults (65*) Median Age N. Females Total Females (0-14) Females (15-44) Females (45-64) Females (65*) APPNOIX E-TABLE 1a 1990 POPULATION CENSUS TRACT DATA TOR THE VICINITY OF THE BKK LANDFILL, UEST COVINA, CALIFORNIA6 Contains BKK 4080 01 4080 02 4079 4075 Census Tract to the North of the BKK Landfill 4074 4067 4055 4056 4065 4068 02 4066 01 4064 11 4064 12 4064 02 4063 6 871 582 546 484 545 4.281 433 29 9 7.051 643 610 524 520 4.353 401 29 4 5.455 458 465 506 502 3.217 307 28 7 8.851 706 688 568 565 3,845 479 27 6 1,464 106 119 its 141 874 109 30 2 8,332 760 646 596 644 4.833 853 30 5 5,954 481 453 406 424 3,588 602 32 4 4.748 334 364 347 J39 2.753 611 34 0 5.634 455 417 424 410 . 3 529 599 31 5 4.316 369 339 318 304 2,570 415 31 1 3.473 786 1,859 602 228 3.489 815 1.853 599 222 2.751 722 1,341 512 176 3,449 970 1,688 524 267 719 4,314 2.988 159 951 646 351 2.069 1.386 155 755 613 54 539 343 2,441 504 1,086 502 349 3.002 634 1.474 532 362 2,206 523 1,024 438 223 4 571 313 305 314 310 2,731 598 36 2 2,341 468 961 577 335 2006 173 143 192 160 1,192 146 28 9 1,020 262 486 186 86 2,209 121 131 159 143 1,374 281 37 6 1.129 222 441 313 153 1.999 133 95 131 125 1.213 302 3B0 4.G5S 237 336 358 369 2 899 456 35 7 1,030 174 418 266 170 2,333 443 1,115 541 234 CMA 114413 94 APPENDIX E-TABLE 1a(continued) 1990 POPULATION CENSUS TRACI DATA FOR THE VIC1N1TT OF THE BKK LANDFILL, UEST COVINA, CALIFORNIA11 1 All Groups Total Children (0 4) Children (5 9) Children (TO T9) Children (15-19) Adults (20 64) AduHs (65) Median Age It Females Total Females (0-14) Females (15-44) Females (45-64) Females (65*) 4034 40B1 31 408 1 32 409102 Census Tracts to the South of the BKK Landfill 4081 01 4082 11 4092 12 4078 4077 4082 02 4072 4073 26.792 2.471 2 660 2.766 2 464 17.327 1.104 31 3 13.346 1.256 1.073 1,062 1 178 8.213 542 28 1 9.281 952 931 873 992 5.087 446 24 4 0,082 786 737 711 891 4,525 432 25 4 7 792 627 609 614 677 4.921 344 29 2 5.519 428 481 368 455 3.225 562 30 5 4.032 262 269 346 364 2.501 291 32 7 7.438 66 5 673 686 740 4 289 385 27 5 11 642 1 196 1 090 308 1 047 6.761 640 26 0 2.308 207 192 182 204 1,317 206 28 1 6.865 570 608 657 675 3 872 483 27 3 7.438 596 641 668 724 4,353 436 28 4 4076 7,441 724 671 655 687 4.251 453 26 6 14.501 3.907 7,627 2 336 631 6,000 1.723 3.747 1.011 328 4.628 1.3B7 2.243 741 257 3.992 1,096 2.009 624 283 3.970 906 2,134 729 199 2.751 591 1.355 464 339 2,057 438 974 457 188 3.760 1.019 1.903 649 2Q9 5 681 1,534 2864 883 400 1.068 283 506 153 126 3.384 839 1.652 639 254 3,715 945 1,761 770 239 3.634 1,030 1.796 576 232 a Update ol Table 4. "Health Risk Assessment ot the BKK Landfill. West Covina. California." Interim Report. November 1990. page 34. Hazardous Waste Toxicology Section. California Department ol Health Services. Sacramento. CaMomia Taken from "BKK LandFill Environmental Exposure Characterization Report, West Covina. CaMomia. "Volume I. August IS 1998. CH2MHM. Santa Ana, CaMomia b "United Stales Department ol Commerce. 1990 Census ol Population and Housing, population and Housing Characlenshcs foe Census 11acts and Bloch Numbering Areas. Los Angeles-long Beach CA PMSA Secbon 1 ol 7 " August 1993 Economic and Statistics Admmislralion. Bureau of the Census. Washington D C 1990 CPHT2I5B CMA 114414 -95- APPENDIX F AIR DISPERSION MODELING OF THE 1983-1990 AMBIENT VINYL CHLORIDE MONITORING DATA CMA 114415 -96- -as.' AIR DISPERSION MODELING OF THE 1ti3-1990 AMBIENT VINYL CHLORIDE MONITORING DATA Ogden Environmental and Energy Services Co.. Inc. (Ogden) was contracted by DHS-DEODC and OEHHA-HWTS in February 1991 to select an air dispersion model ana develop a data base which would be used to model estimates of histonca! vinyl chionde concentrations in ambient air around the landfill. The modeled estimates were to be used in the pending DHS-OEODC reproductive outcomes study and in the present addendum health nsk assessment. ARB provided technical consultation for the project and assisted staff from OEODC in refining the emission rates. In November 1992. Ogden submitted its report "Air Quality Modeling for the B.K.K. Landfill Air Toxic Exposure Study" (Ogden, 1992). The modeling was conducted using the Fugitive Dust Model (FDM), a Gaussian air dispersion model developed by USEPA and similar to USEPA's Industnal Source Complex (ISC) model. The ISC model is an approved model for regulatory purposes. The FDM model was selected over the ISC model because at the time the study was initiated, the FDM model was considered to estimate air concentrations close to large area sources, like the B.K.K. Landfill, better than the ISC model. The version of ISCST available at the time of the project represented an area source by a single line source segment. Consequently, estimated concentrations for receptors close to a source ("near-field") could be under- or over-predicted. Near-field concentrations have been associated with highest detected values of vinyl chionde in momtonng around the landfill. The inability of ISCST to capture near-field concentrations was considered to be a serious limitation for this project Although intended primarily for the calculation of particulate concentrations, FDM is equally suited for any pollutant from non-buoyant sources. FDM uses the standard Gaussian plume formulation for computing downwind concentrations from an emission point line, or area source. The area source algonthm was used for the B.K.K. Landfill. The algonthm provides a uniform distribution of emissions from the area source, represented as a series of line sources (rectangles) oriented perpendicular to the wind. For the purposes of this project the area source for the model was considered to be the 170-acre closed Class I Unit Neither ISCST nor FDM can account for terrain influences on the direction of plume travel. Studies conducted in the 1980s around the landfill document a nighttime wind flow from the landfill down the hill to the residential community adjacent to the landfill. All of the available Gaussian complex terrain models are designed to simulate impacts on terrain elevated above the source; none are intended to simulate impacts on nearby receptors below the emission point, as exists at the B.K.K. Landfill. Meteorological data required for the model were obtained from three sources. The primary source was SCAQMD's meteorMttnfstation located at Station A. Wind speed and wind direction data were collected hourly bet^Hg$83 and 1985 at Station A. Data missing from Station A were replaced with corresponding dattSHKjAQMD's meteorological station at Walnut Additional meteorological data used in the modefin^^wTobtained for the same time penod using hourly data collected by the National Climatic Data Center at Ontario Airport in Ontano. All three years of meteorological data were combined to represent average annual meteorological conditions at the B.K.K. Landfill during the modeled time periods. To predict annual average concentrations for the years after 1985, the three years of hourly meteorological data were run through the stability array (STAR) program. STAR is a statistical meteorological program which produces a composite wind direction frequency distribution, stratified by wind speed and stability class. Wind speed and wind direction determine both the location of pollutant impacts and their magnitude. Station A wind data were considered to be the most representative available histonca! information on the transjsort of pollutants from the landfill because vinyl chionde was monitored almost daily at Station A from June 1981 through March 1990. Walnut Station is located approximately .. -97- CMA114416 three Kilometers south-southeast of the landfill and is influenced by different terrain features. Walnut data were not deemed as representative as the primary data source but were considered acceptable to fill in gaps missing in Station A data. Stability class is a measure of the dispersive capacity of the atmosphere. It is not measured directly but derived from otner measurements. USEPA developed a data processing package called RAMMET which uses concurrent sky cover measurements and wind speed to derive stability class. Hourly stability categories were developed using the RAMMET program and sky cover data from Ontario Airport Mixing height determines the depth through which pollutants can disperse in the atmosphere. Modeling for ground-level sources such as the B.K.K. Landfill are mostly insensitive to mixing height Hourly mixing heights were calculated using the RAMMET program and average, seasonal mixing heights interpolated from values published for the contiguous United States. Annual vinyl chloride emission rates were estimated from continuous 24-hour average vinyl chloride concentrations measured at SCAQMD's three residential monitoring stations south of the landfill, Stations A, B, and MY. Average annual concentrations were then determined for each monitoring station, with the nondetected samples set at one-half the detection limit (1983 through 1987, 2 ppb; January 1988 through Septemoer 1989,1.4 ppb; October 1989 througn March 1990, 2 ppb). To calculate emission rates, the FDM model was run with a nominal emission rate for each year at each momtonng station when monitoring data were available. All of the vinyl chtonde was assumed to have onginated homogeneously from a rectangle approximating the Class I unit The emission rates were then scaled so that the modeled concentrations equaled the measured concentrations. The highest average annual emission rata from the three stations for each year was selected as representative of vinyl chloride emissions for that year. For all years except 1988, the highest emission rate was obtained from Station A. For 1988, the highest emission rate was obtained from Station MY. ARB provided technical consultation to the project. ARB recommended running tests to estimate the difference that would be predicted using different meteorological data sets (SCAQMD's Station A and walnut Station) and different models (USEPA's regulatory models, ISCST and SCREEN; and FDM). To test the effects of using Station A meteorological data versus Walnut data, FDM was run twice; first using hourly Station A data for the time penod October through December 1984, then using the wind data from Walnut for the same time period. In both tests, the model was run with a unit emission rate, and the landfill emission rate was then back-calculated from the measured concentrations at Station A, B, and MY. The results showed that significant differences in emission rates were obtained, with smaller emission rates obtained using Station A data. The conclusion for this project was that the site-specific data from Station A would more accurately reflect the micrometeorology around the B.K.K. Landfill. Compansan of the FQMand ISCST models was made using the estimated emission rates for JanuaryMarch 1983. The reatjjte showed similar isopleth contours and a similar point of maximum impact, located on the landfill boundary However, the maximum concentration predicted by FDM was almost three times higher than that predicted by ISCST. The conclusion for this project was that FDM would not underpredict near-field receptors, such as Stations A, B, and MY. All air dispersion models are designed to be health protective. SCREEN is a worst-case model which, rather than using actual meteorological data, calculates hourly concentrations from a matrix of wind speeds and stability conditions, and reports the maximum. Comparison of the FDM and SCREEN models was made using emission rates for Station A for the time period January-March 1983. Results showed that SCREEN predicts concentrations three- to ten-fold greater than FDM. The conclusion for this project was that the order of health protective conservatism built into the three models is; SCREEN > FDM > ISCST. as desired. CMA 114417 -98* APPENDIX F-FIGURE t is an isopleth of vinyl chloride at 2,1, and 0,05 ppb modeled concentrations around trie B.K.K. LandUfri 1989 generated by FDM, Trie purpose of the isopleth is to show the general direction of the plume. Confidence in the extent of contamination depicted in the isopleth is low for the following reasons: All of the vinyl cfilonde was assumed to have onginated homogeneously from a rectangle approximating the Class I Unit. This assumption may overestimate concentrations at residential locations on the eastern side of the landfill and underestimate concentrations at residential locations on the western side of the landfill since vinyl chloride may have been released from other areas of the landfill. Similarly, the assumption does not estimate potential localized "hot spot" areas of vinyl chloride emissions; Vinyl chloride monitoring data and the meteorological data were solely from the southern boundary of the landfill. Less confidence can thus be placed on modeled estimates at other areas around and away from the landfill; Emission rates were developed from average annual vinyl chloride concentrations calculated with nondetected measurements set at one-hatf the detection limit Between 37 and 100 percent of the measurements in any given year were below the detection limit. This assumption may produce overly conservative concentration estimates. In 1989, 99 percent of the data from Station A was non-detects; The emission rate estimated for each year was the highest emission rate back-calculated from the data at the three stations. Emission rates calculated using Station A data were on the average 139 percent higher than emission rates calculated using Station B data. This assumption will overestimate concentrations near stations which were not used to estimate a given year's emission rate, and may result in higher concentration estimates in other areas as In addition to data and methodology limitations given above, there are uncertainties and limitations inherent to ail Gaussian air dispersion modeling, the extent of which, regarding the B.K.K. Landfill, were not apparent until after working with the model: Gaussian models cannot calculate concentrations accurately when wind speeds fail below one meter per second (m/s). As recommended by ARB, all wind speeds which fell below one m/s were adjusted to one m/s. At the B.K.K. Landfill, wind speeds below one m/s occurred 60 percent of the time. Setting a lower wind speed boundary at one m/s would tend to overestimate the back-calculated emission rates. The effect is somewhat offset by the fact. that emission rates were back-calculated from measured data near the landfill. . Gausajidfrla cannot factor in complex, topographical terrain, as exists around the B.K.K. Lmkthat is, models cannot account for an emission source which is at a higher elevatiarFfflPtme receptors. * CMA 114418 -99- APPENDIX F-FIGURE 1 (Department of Health Services, Division of Environmental and Occupational Disease Control) Note: Confidence in the extent of modeled vinyl chloride concentrations is low because of the assumptions used in, and limitations and uncertainlies of the Fugitive Dust Model. In the figure, the 2 ppb vinyl chloride isoplelh is on the landfiif, the 1 ppb vinyl chloride isopleth extends to Amar Road, and the 0.05 ppb vinyl chloride isoptelh extends to the three mBe radius southwest and easl of the landfill. The purpose of Ihe isopleth is lo show the general direction of the estimated modeled ptume. .y -100- CMA 114419 BLANK PAGE CMA 114420 101 APPENDIX G UPDATED RISK ESTIMATE OF THE 1984 INDOOR AIR MONITORING PROGRAM EVALUATED IN THE 1990 INTERIM REPORT -102- CMA 114421 UPDATED RISK ESTIMATE OF THE 1984 INDOOR AIR MONITORING PROGRAM EVALUATED IN THE 1990 INTERIM REPORT This Appendix revises the risk estimate for the USEPA-DHS 1984 indoor air momtonng program using updated unit risk values. On July 17, 1984, 19 homes along the southern and southeastern border of the B.K.K. Landfill were evacuated when methane, from lateral subsurface landfill gas migration, was detected at concentrations above the lower explosive limit (50,000.000 ppb). The Southern California Gas Company detected the methane gas dunng a routine (every four years) survey of residential gas distribution piping system. Methane gas migrating from a landfill can serve as a earner gas for nonmethane hydrocarbons, such as vinyl chlonde, which are deposited or generated at landfills. On July 18,1984. a team from SCAQMD, USEPA, and DHS collected grab air samples in 2-liter bulb containers from inside the evacuated homes. The samples were analyzed for methane, nonmethane hydrocarbons, vinyl chlonde and selected volatile organic compounds. Ten of the evacuated homes were designated 'Priority I* based on the concentrations of vinyl chlonde detected. The highest detection of vinyl chloride in the 2-liter bulb containers was 990 ppb. (Five cays later, analysis inside the same home showed 160 ppb vinyl chlonde, and on August 1. 1984. vinyl chlonde was not detected at or above the detection limit of 2 ppb.) In October 1984. the ten Prionty I homes and one control" home were resampled. Samples were collected in Tedlar bags over 24-hours. The purpose of the indoor air momtonng program was to determine the safety of reoccuDying the homes. There was a discrepancy regarding the concentrations of benzene detected in the Prionty I homes. CH2M Hill reported laboratory contamination. However, no documentation or explanation was provided, and .the benzene data were included in the appendices of the exposure characterization (CH2M Hill, 1988). To estimate the duration of exposure for the risk characterization in the interim report. HWTS reviewed the records of the Southern California Gas Company. According to the records reviewed, elevated `field gas' (combustible gas onginating from natural decomposition of organic material and not the company's metered gas) was detected at one residential location near Station B in May 1984. The detection was determined to be not hazardous. Beginning July 3,1984, other residential locations in the vicinity of Station B were surveyed. Detections of field gas were determined by the gas company to pose a hazard to people or property. The gas company continued to monitor the area, leading to the evacuation on July 17, 1984. HWTS estimated that the duration of exposure to landfill gas contaminants in indoor air of the evacuated homes was no more than 1-year. This assumption may underestimate or overestimate the exposure. An article published in 1987 desenbed the gas migration as "fresh" and "new." and stated that "it may not have been going on long enough for steady state conditions to have been achieved" (Wood and Porter, 1987). jm&> The limited scope ofjKniidocr air program (grab samples in July and 24-hour samples in October) precludes its usefuMMr&fthe long-term assessment of this addendum report APPENDIX G-TABLE1 updates the risk estimate associated with the five carcinogens detected in the evacuated homes in October 1984. The individual excess lifetime cancer risk associated with an assumed one-year exposure to the concentrations detected in the homes is estimated to be approximately 2 x 10*5. Vinylidene chloride (1.1-dichloroethene) is no longer considered a carcinogen in California and has been deleted from the list of California Cancer Potency Factors. Consequently, it is not included in the revised nsk estimate. n -103- CMA114422 APPENDIX G-TABLE 1* INDIVIDUAL EXCESS LIFETIME CANCER RISK*) USEPA-OHS 1984 EXTENDED MONITORING PROGRAM (INDOOR AIR. EVACUATED HOMES) BKK LANDFILL. WEST COVINA. CALIFORNIA Carcinogen Vinyl Chloride Perchioroethyiene Trichtoroethene 1,2-Oichioroetnane Benzene Medianc ppb ug/m3 4 10.2 2.5 170 1.5 3.1 3 12.1 7 22.4 Unit Riskd (ug/m3)-l 1990 1994 2.7 E-6 5.8 E-7 1.3 E-6 2.2 E-5 5.3 E-5 .7.8 E-5 5.9 E-6 2.0 E-6 2.2 E-5 2.9 E-5 Total Excess Lifetime Cancer Risk Including Benzene Total Excess Lifetime Cancer Risk Excluding Benzene Cancer Risk 1990 1994 3.1 E-7 11 E-7 1.2 E-7 3.0 E-6 1.4 E-5 9.1 E-6 1.1 E-6 1.9 E-7 3.0 E-6 7 4 E-6 1.8 E-5 3.5 E-6 2.1 E-5 1.3 E-5 USEPAO Class A C B2 B2 A a: Update of Tabla 16. 'Healtn Risk Assessment of the BKK Landfill. West Covina, California, Interim Report, November 1990.* pg. 68. Hazardous Waste Toxicology Section, California Department of Health Services, Sacramento. California, b: Calculated by ECR * C x YR x EF x UR x 1/LT whore ECR 9 Excess lifetime cancer nsk C 3 Concentration in ug/m3 YR 3 Years of residence associated with exposure (1) EF = Exposure factor, i.e. percent of time at home (80%) UR = Unit risk value LT 3 Human individual lifetime in years (70) c: Median values taken from Table 6-13. 'BKK Landfill Environmental Exposure Characterization Report, West Covina, California." CH2M Hill, 1988, volume I. p. 6-*5. d: 1990 values were derived by the United States Environmental Protection Agency (USEPA) or the California Department of Health Services. Health Hazard Assessment Orvisron. Air Toxica Section and were taken from Table 3.1S. 'Air Toxics Assessment Manual.' California Air Pollution Control Officers Association, October 1987 pgs 3.5-24 to 3.5-28. 1994 values were taken from the Standards and Criteria Work Group, 'California Cancer Potency Fsctors: Update 1994*. California Environmental Protection Agency (Cal/EPA. Office of Environmental Health Hazard Assessment), Sacramento. California. NOTE: 1,1-Oiehtoroethene is no longer considered a carcinogen in California and has been deleted from tne California Cancer Potency Factors. Consequently, it is not included in the table update. Changes m the unit risk values are due to increased knowledge about the inherent toxicity of the chemicals, e: USEPA weight of evidence classification: A. sufficient evidence in humans; B1, sufficient evidence in animals, limited in humans: B2. sufficient evidence in animals, inadequate in humans: C. limited evidence in ammals. inadequate in humans. Taken from USEPA's Integrated Risk Information System (IRIS), November 1994. -104- CMA 114423 BLANK PAGE -105- V* CMA 114424 APPENDIX H DEPARTMENT OF HEALTH SERVICES-CANCER SURVEILLANCE SECTION LETTER REGARDING REVIEW OF RECENT TUMOR INCIDENCE DATA -106- CMA 114425 fE OF CAUFOftNlA--HEALTH ANO WflFARl AGENCY ;PARTMENT OF HEALTH /744 9 STWET BOX 943733 J!ANIO. CA 94314-7330 SERVICE 10'* 540-2711 Novemner 16, 1995 PfTf WILSON. Cmiiw Robert L. Holtzer M.D. Hazardous Waste Toxicology Section Office of Environmental Health Hazaras Assessment 601 North 7th Street/MS 241 P.O.Box 942732 Sacramento. CA 94234-7320 RECEIVED VlGV 10 aha. Hazardous waste Toxicology Section Dear Dr. Holtzer. In response to your request, the Cancer Surveillance Section of the Department of Health Services, in collaboration with the Cancer Surveillance Program of Los Angeles, has examined the incidence of invasive cancer in the six census tracts (see enclosed map) around the BKK landfill in West Covina. We have compared the observed cancer incidence in the area with the incidence expected on average if the residents had the same cancer rates as Los Angeles County as a whole. As you know. California has had a statewide cancer reporting system since 1988. The California Cancer Registry (CCR1 has information on every cancer case diagnosed in a California resident after January 1, 1988. with the exception of squamous and basal cell carcinomas of the skin, which are very common and usually treated in doctors' offices. The information gathered includes addresses at the time of diagnosis, which are allocated to the appropriate census tracs. Data for Los Angeies County are collected by the Cancer Surveillance Progranvof Los Angeies. University of Southern California. These oa*a enabled us to obtain the observed number of cancers, that is the number of invasive cancers of all anatomical sites combined that were actually diagnosed among residents of the area of the six census tracts during the sixryear period 1988-93. We estimated the expected number by applying the average annuai incidence rates of invasive cancer for Los Angeies County, specific for five-year age group, race, and sex. to the corresponding 1990 population data for the census tracts. Assuming the population either to be stable or to have increased lineariy between 1988 and 1993. multiplying the expected numbers for 1990 by six. produces estimates of the cases expected during the six years. 1988-93. The table below shows the numbers. -107- CMA114426 THE INCIDENCE OF INVASIVE CANCER IN THE BKK LANDFILL AREA ALL RACES. ALL ANATOMICAL SITES COMBINED LOS ANGELES COUNTY. 1988-93 Census Tract 4034 4078 4079 4080.01 4080.02 4081.31 Expected No. 1222 56.3 17.0 12.6 18.7 16.8 23.7 Expected No. 1988-0? 338 102 76 112 101 142 Observed No. 198?-3 333 114 85 114 81 128 Total 145.1 871 855 As the the table shows, the observed number of cases in the entire area. 355. was actually lower than the number expected, on average, during this time period. 371. Neither this difference nor the differences between the oDserved and expected numbers tor the individual census tracts are statistically significant: the differences are within the bounds of what can be expected to occur, in either direction, by chance alone. No cases of hemangiosarcoma of the liver were reported among residents of these six census tracts during the years 1988-93. Of the 27 hemangiosarcomas diagnosed in California during this time period, seven occurred in Los Angeles County, a proportion roughly equivalent to the population proportion in Los Angeies. Only one case occurred within five miles (neither downwind nor aownwaten of the BKK landfill. This was in an elderly person who moved into the area in 1989. and was diagnosed a few years later. Thus there is no indication of an increase in hemangiosarcoma of the liver m the area around the BKK landfill durin this ume period. In summary, for the six-year period. 1988-93, there is no indication that the incidence of invasive cancer among residents of the area around the landfill has been different than cancer incidence among residents of the entire Los Angeies region. -108- CMA 114427 If there are any questions, piease caii me at (5101 540-2711. Sincereiy. Eva R. Glazer. M.D., M.P.H. Cancer Surveillance Section 2151 Berkeley Way, Annex 2 Berkeley, CA 94704 John L. Young Jr.. Dr.P.H., CTR Cancer Surveillance Section P.O. Box 942732 MS 592 Sacramento. CA 95814 Wendy Cozen D.O., M.P.H. USC Cancer Surveillance Program 1540 Alcazar St., CHP-204 Los Angeles. CA 90033 Phil Jacobs Toxics Epidemiology Program Los Angeles County Department of Health Services 510 S. Vermont. Room 215 Los Angeles. CA 90020 Richard Kmiiger. M.D. Environment Health Investigations Branch 5900 Hollis Street. Suite E Emeryville. CA 94608 -109- CMA 114428 APPENDIX I RELEASE OF THE DRAFT ADDENDUM REPORT -110- CMA 114429 CALIFORNIA ENVIRONMENTAL PROTECTION AGENCY OFFICE OF ENVIRONMENTAL HEALTH HAZARD ASSESSMENT NOTICE TO INTERESTED PARTIES DECEMBER 15. 1995 NOTICE OF AVAILABILITY OF DRAFT ADDENDUM HEALTH RISK ASSESSMENT OF AMBIENT FUGITIVE VINYL CHLORIDE EMISSIONS FROM THE CLASS I UNIT OF THE B.K.K. LANDFILL. WEST COVINA. CALIFORNIA and NOTICE OF PUBLIC WORKSHOP The Office of Environmental Heaitn Hazara Assessment (CEHHA) reieaseo tne "Draft Aaaenaum Heeltft Risk Assessment of Ambient Fugitive vmvt Chlonae Emissions From tne Class i Unit of tne S.K.K. Landfill. West Covina. California' for a 60-day puotic comment oenoa oegtnnmg Deeemoer i, 1995. The 1995 draft aaaenaum neaitn nsx assessment uoaates tne 1990 mtenm -Health Risk Assessment of the B.K.K. Lanatiil. West Covina. California.* The aran aaaenaum neaitn nsx assessment wui oe tne suotea c; a ouonc worxsnoo to oe neia on Thutsaay. January 11 1996. tram 7.20 o.m. to 10:00 o.m.. at tne City of West Covina Council Chamoeis. locateo on tne First Floor ot City Hall. 1444 west Garvey Avenue. West Covina. California. Comments may oe oresentea aunng tne worxsnoo. or suomrttea in writing to tne aaaress oeiow. wnaen comments must oe received oy OEHHA on or oetare Fedruary 12. 1996. At tfte eno of tne comment oenod. the final reoon will be oreoareo ana released. The aaaenaum reoert plus tne mtenm reoon will camoiete the neaitn nsx assessmem at tne B.K.K. Landfill oramtsea to tfte residents oy tne State of California. Please Street any Questions regarding tne wonesnoo or tne draft aaaenaum neattft nsx assessment to Lillian Kelly at tne aaaress ana teieonone numoer maieatea oeiow Coates of tne aran aaaenaum neattft nsfc assessment mav oe ootamea ay suommtng a wmten reauest. Lillian Ketlv. M.P.H. Office 01 Environmental neaitn Hazara Assessment Hazardous Waste Toxicology Section 601 North Seventh Street. MS 241 P. O. Box 942732 Sacramento. California 94234-7320 PHONE No. (9161324-2829 FAX NO. (916132Jtf705 Cootes of tne oraft aaaenaum ana mtenm neaitn nsx assessments ano other neaitn stuoies regarding tfte B.K.K. Landfill are avauaote to oe reaa on tne oremtses at tne following uoranes: West Covina Library 1601 Wes: Covina Pancwav West Covina. California 9179C (8181 962-3541 Walnut Library 21155 La Puente Avenue Walnut. California 91789 (9091 595-0757 La Puente Library 15920 East Central Avenue La Puente. California 91744 (818 968-4613 *111- CMA 114430 APPENDIX J OEHHA'S RESPONSE TO COMMENTS ON THE DRAFT ADDENDUM REPORT -112- CMA 114431 =s; OEHHA's Response to Comments From Regulatory Agencies United States Environmental Protection Agency - Region IX -113- CMA 114432 OEHHA'S RESPONSE TO COMMENTS FROM USEPA Response to Comments From Gerald F.S. Hiatt, Ph.D., Senior Risk Assessment Advisor 1. Cal/EPA has participated with USEPA in the evaluation and presentation of USEPA's assessment of increased sensitivity of infants and children to inhaled vinyl chloride. USEPA's October 20, 1995 policy statement says that "the Agency will develop a separate assessment of risks to infants and children.' To date, quantitative assessments of young-age sensitivity to inhaled vinyl chloride have not been used extensively in assessments such as the addendum report. OEHHA's unit risk for vinyl chloride is derived from the Drew et al. studies in female mice, and includes consideration of increased sensitivity of young animals to vinyl chloride induced carcinogenicity. In selecting this value OEHHA noted: "The animal studies demonstrate a relationship between tumor formation and the sex and age of the animal at first exposure. Fetuses, newborns, younger animals, and females exhibited the highest carcinogenic sensitivity (Drew et al., 1983). In the epidemiological studies of vinyl chloride workers, who were predominantly male, the average age at first exposure was 29.7 years. Thus, to protect all members of the general population, it is more appropriate to base risk assessment calculations on the animal inhalation studies, which because of their use of more sensitive categories, the young and females, reflect a wider range of population sensitivity.' Utilizing the USEPA's approach to evaluate the theoretical upperbound excess lifetime risk for exposure to vinyl chloride at a young age suggests a risk estimate at Station A that is approximately 14-fold higher than the estimate obtained in the addendum report This qualitative estimate has been added to the Risk Characterization, Limitations and Uncertainties. 2. USEPA's guidance states that `Sampling.data from Superfund sites have shown that data sets with fewer than 10 samples per exposure area provide poor estimates of the mean concentration (i.e., there is a large difference between the sample mean and the 95 percent UCL), while data sets with 10 to 20 samples per exposure area provide somewhat better estimates of the mean, and data sets with 20 to 30 samples provide fairly consistent estimates of the mean (i.e., the 95 percent UCL is close to the sample mean). Remember that, in general, the UCL approaches the true mean as more samples are included in the calculation (USEPA, 1992a).' TABLE 7 of the addendum report indicates that the minimum number of samples collected by SCAQMD in one year is 191. Thus, we believe that the average annual concentrations used in the addendum report are justified. 3. Discussion of the underestimation of exposure at Station MY for the years 1980 through 1983 has been expanded in Risk Characterization, Assumptions Regarding Ambient Vinyl Chloride Monitoring Data. For the years 1985 through 1988, concentrations of vinyl chloride at Station MY were 1.6- to 1.9-fold higher than concentrations at Station A, and Station MY had between 25 to 33 percent fewer samples with nondetectable concentrations. Response to Comments From Carmen D. Santos-Prior, Project Manager, B.K.K. Landfill 1. The sentence has been corrected. 2. Information about the subsurface soil gas investigation USEPA is requiring the B.K.K. Corporation to conduct has been added. 3. The scope of the risk assessment required of the B.K.K. Corporation under the USEPA Order has been expanded. 4. Please see Exposure Assessment, Other Hazardous Chemicals Detected in Ambient Air. 5. Information about the Response Action Plan for Vinyl Chloride has been added to the Hazard Identification section, Vinyl Chloride Emissions From the Class I Unit. 6. Correspondence from SCAQMD (SCAQMD, 1994a) has been added as the reference for SCAQMD's acceptance of B.K.K. Corporation's contract laboratory protocol for vinyl chloride. -114- CMA 114433 ENCLOSURE 1 UNITED STATES ENVIRONMENTAL PROTECTION AGENCY REGION IX 75 Hawthorn* StrMt (H-9-3) San Francisco, CA 94105 MEMORANDUM February 13, 1996 Subj ect: BKK - Cal/EPA Draft Risk AMeBW-- From: Gerald F.3. Hiatt, Ph.D. Senior Risk Assessment Advisor To: Carmen Santos Project Manager - BKK Site Per your request, I have reviewed the Draft Addendum Health Risk Assessment of Ambient Vinyl Chloride Emissions from the Class I Unit of the 3.K.K. Landfill, west Covina, California, prepared by the Office of Environmental Health Hazard Assessment of Cal/SPA and dated December 1995. In general, the risk assessment is well written and represents a thorough analysis of the relatively extensive data collected by the various airborne vinyl chloride monitoring efforts over a number of years at the BKK site. I was especially impressed by the various approaches the authors used to incorporate non-detects from the earlier years of vinyl chloride monitoring (when limits of detection were in the 2 to 10 ppb range) and the various different ways that risks are apportioned over the entire period of time covered by the draft risk assessment. There are two specific issues on which the Cal/EPA approach used in this risk assessment differs from the procedures used by U.S. ERA and these are worthy of comment, as is one of the vinyl chloride exposure assumptions used by Cal/EPA: 1. Vinyl Chloride Risks in Children: under U.S. EPA risk assessment policy and guidelines, the risk assessment should quantiC&tlvely address the sensitivity of young children to the carcinogenic action of inhaled vinyl chloride for lessthan-lifeeime exposure scenarios. It is U.S. EPA policy to explicitly assess risks to children whenever possible: "It is the policy of the U.S. Environmental Protection Agency (EPA) to consider the risks to infants and children consistently and explicitly as a part of risk assessments ... the Agency will develop a separate assessment of risks to infants and children ... * (Browner: New Policy on Evaluating Health Risks to Children (memo), October 20, 1995). -115- CMA114434 -2- Consistent with this policy, and with reports in the scientific literature documenting the enhanced sensitivity of neonates to the carcinogenic action of inhaled vinyl chloride, the U.S- EPA Region 9 Office and Office of Research St Development derived a procedure for assessing enhanced risks to infants and children from inhaled vinyl chloride. This procedure has been adopted as risk assessment guidance within Region 9, has been presented and discussed at a number of national SPA and independent conferences on risk assessment, has been presented in a number of scientific publications (including peer-reviewed journals) and has been incorporated quantitatively into risk assessments at three hazardous waste sites in Region 9 (including the on-going ambient air study at BKK) . This issue is especially important in light of the fact, as detailed in the draft report <pp. xii, 63), that most of the exposure (and hence risk) during the entire period covered by the risk assessment accrued during the early 1980's - vinyl chloride levels detected by the monitoring program decreased significantly after this period. Because of the childhood sensitivity, this disproportionate accrual of risk will be further enhanced for anyone who was an infant or young child in the community during chat period. 2. Exposure Concentration Term: The draft risk assessment uses the mean (arithmetic average) of the monitoring data as the vinyl chloride concentration term in the exposure equations (first- paragraph, p. 54), U.S. EPA risk assessment guidance for the Office of Solid Waste and Emergency Response (OSWSR) is explicit on this point - the concentration term in exposure equations should be the 95% upper confidence limit on the arithmetic mean (95% UCL): ' -. the concentration term ... in the intake [exposure] aquation is an estimate of the arithmetic average concentration for a contaminant based on a set of sice sampling results. Because of the uncertainty associated with estimating JThe true average concentration at a siS^. the 95 oer cent upper confidence limit fUCL) of__SSfiarithmetic mean should be used for this, variable.* (Supplemental Guidance to RAGS: Calculating the Concentration Term. OSWER Publ 9285.7-081. May 1992.) Please note that the 95% UCL is used as *an estimate of the arithmetic average", not as an 'upperbound* estimate as implied by the draft 3KK risk assessment (p. 54). 3. K5f Area - 1983 vinyl Chloride concentration: For the draft risk assessment "[t]he 1983 average annual concentration at CMA 114435 -116- 3 Station MY is assumed to be 2.3 ppb, that is at least equal to Station A's 1933 average annual concentration ..." (p. 32) - this results in an assumed exposure during 1983 which is almost one-half of chat during 1984 (5.4 ppb) . This assumption probably underestimates actual vinyl chloride levels in the MY area by a significant amount. As is apparent from the graph on page 31, for all of the years monitored prior to 1989. vinyl chloride levels in the Station MY area were significantly greater than, not equal to, those at Station A. Also, the overall trend in the monitored areas is for vinyl chloride levels to spike in 1983 and then generally decrease over the rest of the monitoring period (p. 31). These two. trends indicate that the assumption of equivalent exposures in the MY and A areas probably understates the actual exposure levels for the farmer area. It may not be possible to Incorporate this consideration into the risk assessment in a quantitative fashion, but a more thorough discussion would highlight the uncertainty this assumption brings to the risk calculations. If you have any questions or need any clarification on c^ese comments, I can be reached by voice at (415) 744-2319 or by fax at (415) 744-1916. 0313MM.WPS 5SaS- -117- CMA 114436 enclosure 2, Page 1/2 OEHHA's Draft AOOenaum tietltti RISK Assessment 5KK Lanatin, West Covina, Caiitoma U,$. Environmental Protection Agency Additional Comments February 12. 1996 The U.S. Environmental Protection Agency has the following additional and general comments on the OEHHA Draft Addendum Health Risk Assessment of Ambient Fugitive Vinyl Chloride Emissions from the Class I Unit of the B.K.K. Landfill, West Covina, California dated December 1S95. Additional Comments 1) Objective, Methodology, and Scope of the Draft Addendum Health Risk Assessment, Page 3, Second Paragraph: The closed Class I Unit is not under a RCRA permit as stated. BKK is seeking a post closure permit which is now being drafted by Cal-EPA DTSC. The Class i unit is currently regulated under interim status. 2) Objective, Methodology, and Scope of the Draft Addendum Health Risk Assessment, Page 4, Second Paragraph: The report states that "At this time, there Is no evidence that subsurface landfill gas migration is a problem for homes in close proximity to the landfill*. EPA recommends that this sentence be deleted because BKK still needs to conduct a subsurface soil gas investigation to determine if a potential could exist for migration of subsurface soil gas to occur despite the gas collection system. BKK will conduct this investigation under the RCRA Section 3008(h) Corrective Action Order on Consent, U.S. EPA Docket No. RCRA-09-89-0019 (Order). EPA is currently reviewing BKVCs subsurface soii gas investigation work plan. 3) Previous Health Risk Assessments of the B.K.K. Landfill, Page 5, Last Paragraph: The report states that "The current health risk assessment required by USEPA wili be based on a one-year ambient air sampling program of 19 volatile organic compounds, including vinyl chloride at onsite and offsite locations (B.K.K. Corporation et a!., 1994)." As to the scope of the health risk assessment that BKK is required to conduct under the EPA Order, the cited statement provides a limited description of the scope for this risk assessment. -118- CMA 114437 OEHHA's Drift Aaaancum Httit)i RIsA Assessment 9KK LanaltH, West Catena, Catfoma U.S. Environmental Protection Agency Additional Comments (Continued) February 12, 1996 Enclosure 2. Page 2/2 The risk assessment required of BKK under the Order will address evaluations of all environmental media: groundwater, soils, air and if possible, surface water. The air medium will be evaluated for the ambient air pathway and the subsurface soil gas pathway m order to achieve a complete evaluation of the air medium. Please expand on the scope of the risk assessment required under the EPA Order. 4) Hazard Identification, Vinyl Chloride in the Class I Unit, Page 9, Paragraph 1: EPA agrees that vinyl chloride is one of the chemicals of concern and a . very important one. However, data from previous ambient air sampling studies were not sufficient to demonstrate the potential contribution of the other chemicals to the risk calculations. EPA recommends that these limitations of previous sampling programs be discussed in this context. 5) Hazard Identification, Vinyl Chloride Emissions from the Class I Unit Page 10-12: This Section does not make mention of the BKK Response Action Plan for Vinyl Chloride (RAP) dated July 21,1994 which EPA approved on August 4, 1994 (EPA letter to BKK corporation, August 4, 1994, Re: BKK's Response Action Plan for Vinyl Chlonde - EPA Approval and Errata Sheet). BKK submitted and implemented the RAP under the Order. Under the RAP, BKK took actions (e.g., increase maintenance of the Class I landfill cap by sealing cracks; pumping of liquids from gas collection wells to increase gas collection capatityyv the purpose of reducing vinyl chloride emissions whenever ambient air sanqpip^restiits showed vinyl chloride at concentrations equal to or above 6) Hazard Identification, Vinyl Chloride Emissions from the Claaa I Unit, Page 12: The report states at the bottom of the paragraph that 'USEPA has stated that the analytical procedure appears to be acceptable to USEPA and SCAQMD for the purposes of ambient air monitoring at the B.K.K. Landfill (USEPA, 1994e)". EPA recommends that OEHHA cite SCAQMD correspondence directly regarding SCAQMD's opinions about the BKK vinyl chloride analytical procedure with 0.005 ppbv detection limit instead of EPA correspondence. -119- CMA114438 OEHHA's Response to Comments From Interested Parties Jean Ameson B.K.K. Corporation Chemical Manufacturers Association William F. Polich, Ph.D. -120- CMA114439 OEHHA'S RESPONSE TO COMMENTS FROM JEAN ARNESON 1. ARB's records (ARB 1982a) indicate that vinyl chloride was deposited prior to 1981. There could very well have been exposures for residents near Station A from the period 1977 to 1981 since residential development near Station A was completed in 1977. However, it is not possible to quantitatively estimate that exposure. The report has been modified to reflect that 1981 was the single year of highest detected exposure to vinyl chloride. 2. More information has been added to Appendix G concerning the 1984 indoor air sampling for vinyl chloride. 3. Although other hazardous chemicals were emitted from the B.K.K. Landfill, it is not possible with the available data to state that emissions of other hazardous chemicals from the B.K.K. Landfill were significant. Because these other chemicals typical pollutants found in the ambient air of the South Coast air basin, determining the significance of any specific source is not possible with the available data. -121- CMA 114440 February 9, 1996 David M. Siegel, Ph.D. Chief Hazardous Waste Toxicology Section California Environmental Protection Agency 601 N. 7th St. MS-241 P.O.Box 942732 Sacramento, Calif. 94234-7320 Dear Dr. Siegal, I have some concerns about the Draft Addendum Health Risk Assessment of Ambient Fugitive Vinyl Chloride Emissions from the Class I Unit of the BKK Landfill, West Covina, California. The assumption is made that because no monitoring data is available for the years 1978-1980, that 1981 was the single year of highest ex posure to vinyl chloride. Since vinyl chloride dumping stopped in June 1981, isn't it logical to assume that more vinyl chloride was dumped in the years prior to 1981 and there could very well have been years of higher exposure. Therefore if this is to be a truly conser vative estimate, shouldn't the report state that the actual excess cancer risk might be higher for any residents living near StationsA, B, and MY since 1978. Especially if the report is to be a guide to ensure future risks do not add significant cumulative risk, we need to consider all those people impacted since vinyl chloride was dumped at BKK.. Also Appendix G-Table la has a fdotnote(c) that median values of 4ppb. were taken from Table 6-13 "BKK Landfill Environmental Exposure Cha racterization Report, West Covina, Calif." CH2MHill, 1988, Volume 1, page6-45. The Table is of the Sxtended Monitoring Program from Aug ust to October. However on page 1-8 of the same CH2MHill Report it states that on Julyl8 levels inside two of the evacuated homes ranged from 5 to 990 ppb. It makes me wonder the value of including the chart without mentioning the levels in the homes prior to the chart date Also at the end of paragraph 5 on page x of the executive summary I think it should say,"However it is expected that signifigant emis sions from other hazardous chemicals have occurred. Thank you for considering my comments. Jean Arneson 1116 Donna Beth Ave. West Covina, calif. 91791 (818) 919-3304 -122- RECEIVED FEB 151996 Hazardous Waste Toxicology Section CMA 114441 OEHHA'S RESPONSE TO COMMENTS FROM B.K.K. CORPORATION Response to Comments From Julia Bussey, Director, Corporate Regulatory Affairs 1 There are no data to show that dilution in the concentration of vinyl chloride occurs with distance from the site, although it is reasonable to assume. B.K.K. Corporation's 1995 average annual concentration has been added in the Risk Characterization, Limitations and Uncertainties. 2. The lower average annual value in 1995 is noted in the Risk Characterization, Assumptions Regarding Ambient Vinyl Chloride Monitoring Data and in the Limitations and Uncertainties. The typical landfill gas generation curve has distinct, timed phases. The production of methane gas follows lag-log-steady state-decline curve. The steady state phase begins approximately three years after initial acceptance of waste and continues up to 40 years (Farquar and Rovers, 1973). ARB's report Suggested Control Measures for Landfill Gas Emissions, August 1990, notes that `The gas generation rate depends on several site specific factors including: the amount of moisture present, composition of the waste, temperature, age of the refuse, pH, and quantity and quality of nutrients. Most of California has a dry climate which tends to reduce the amount of moisture in landfills. This slows the gas generation rate, but it also tends to extend the period of time during which a landfill actively generates gas.' SCAQMD's review of the TeraMeth Industries, Inc. Landfill Gas to Methanol Project notes `The BKK Landfill is currently expected to reach its design capacity by 1995. At that time existing operational activities are expected to cease, although landfill gas emissions could continue for an estimated 20 to 40 years into the future" (Letter from Jack Broadbent Director of Planning, SCAQMD to Mr. Jeffrey Collier, Director of Planning, City of West Covina, dated October 4,1994). 3. OEHHA has attempted to discuss fully the strengths and limitations of the 1981-1982 data in the addendum report. Response to Comments From Robert Scofield, D.Env. and Shari Ublckl, Ph.D., ENVIRON 1. Comments based on Community Meeting, first paragraph: The second and third paragraphs of the Introduction explain the purpose of the addendum report 2. Comments based on Community Meeting, second paragraph: The report is organized to provide risk information in three ways, with increasing technical language: the first is the Fact Sheet, the second is the Executive Summary, and the third is the report with Appendices. We believe Finding #4 adequately communicates the added risk. 3. Comments based on Community Meeting, third paragraph: Occupational exposure concentrations are presented^ the Toxicity Assessment, History of the Assessment of Vinyl Chloride Toxicity. Risk estimates using unit risk values derived from the epidemiological (occupational) studies are presented in TABLE 10. Appendix H updates tumor incidence information. 4. Comments based on Community Meeting, fourth paragraph: Please see Exposure Assessment, Other Hazardous Chemicals Detected in Ambient Air. 5. Specific Comments on the Report and Fact Sheet Document Title: While it is technically correct that emission rates perse are not actually measured, it has been clearly established that vinyl chloride emissions are associated with the closed Class I Unit of the B.K.K. Landfill. -123- CMA114442 6. Specific Comments, Page 3, paragraph 1: The 8.K.K. Landfill assessment is based on detections of vinyl chloride, a known human carcinogen, in ambient air in a residential area. This chemical is known to be emitted from the landfill. Reliable information on potential past exposures to specific chemicals is generally lacking for other landfill, Superfund or RCRA sites. The ambient vinyl chloride monitoring data collected by SCAQMD and others allows for the quantitative estimation of risk at this site. 7. Specific Comments, Page 44, paragraph 5: Clarification has been added to the Exposure Assessment, Odor Complaints Data. 8. Specific Comments, Page S3, paragraph 2: This comment has been added to the fourth paragraph regarding the 1995-2009 data. 9. Specific Comments, Page 58, TABLE 10: See response to ENVIRON #3. 10. Specific Comments, Page 62, paragraph 1: The phrase has been deleted. 11. Specific Comments, Page 63, Finding 2 and 3: There is no intention to imply that any additional environmental control may or may not be required. We recognize that this would be a risk management decision by the appropriate regulatory agency. 12. Specific Comments, Page 63, Finding 4; We believe that the addendum report adequately states that the risks are associated with detections of vinyl chloride at the three monitoring stations, and that detections of vinyl chloride in other neighborhoods were not as frequent or as high. The discussion on odors complaints data has been clarified. -124- CMA 114443 SENT BYiENVIHON-E.neryvi I le 2-13-36 : 4-'43PM 510555951 7-* 9153229705:# 2 corporation Ms. Lillian Kelly, M.P.H. Office of Environmental Health Hazard Assessment Hazardous Waste Toxicology Section 601 N. 7th Street, MS 241 PO Box 942732 Sacramento, CA 94234*7320 2$SO 237th SlfM Tonnes. ClITsm* >0908 (310) MS-T-SC F (310)MM#33 February 13, 1996 Subject: Comments on Draft Addendum Health Risk Assessment of Ambient Fugitive Vinyl Chloride Emissions from the Class I Unit of the BKK Landfill, West Covina, California Dear Ms. Kelly: This letter is to convey our comments on OEHHA's risk assessment Comments prepared by ENVIRON on behalf of BKK are attached to this letter. First please let me express our appreciation for OEHHA's work on the completion of the risk assessment. We believe thin OEHHA attempted to objectively and fairly portray the risks at the site. This Is very difficult because of the competing concerns and sensitivity regarding the site. While we do not agree with ail of the assumptions that were made, we do appreciate the time and effort which were evident In OEHHA's choices. As noted in the letter from ENVIRON, we are pleased that Dr. Holtzer added some perspective to the public meeting and hope that his comments and information will be Included in OEHHA's revisions to the risk assessment In addition to ENVIRON's comments, BKK has one technical comment BKK believes that the risk is overestimated based on the future estimated ambient air concentration assumed in the risk assessment BKK has three bases for this comment: 1. The current annual average is 0.12 ppbv at the Nogales End station. OEHHA used the estimate of 0.25 ppbv at Myra Court The estimate 18 twice as high as the currently measured concentration. In addition, the location of Nogales End Is on the BKK property line whereas the Myra Cout location is offsite more than one hundred fleet from the BKK property line. The experience of BKK In drawing its Proposition 65 isopleth is that sir concentrations decrease radically with distance. Data from the ambient air site sampling program suggest that the concentrations drop by one-half every 200 feet from the source. Therefore, the actual concentration at Myra Court must be lower than the Nogales End station. 2. The risk assessment bases the 30-year reasonable mtximum exposure end risk In part on 15 years of future exposure to vinyl chloride at 0,25 ppbv (fnom 1986 to 2009). The exposure due to vinyl chloride la acknowledged in the risk assessment to be derived from the Class I landfill. The Class I landfill's emissions are due to CMA114444 NT SY'SMVlRON-s.-s.-yvi i i e 3PM ; 510SS55517-- 3163229705:3 3 Ms. Ullian xsily January ic, 1396 Page 2 the aeqraaanan cr wastes into mstnana gas wnicn tnan camea vinyl chlonde into tna amciant air. it is wait estaotisheo that lanoni gas procucdor trom oagraoation raaucas over time in a oraaicsaoia lancnii gas asenna curve. This is founa in many texts oy dcm the SPA ana ctnar scientists ivno study landfills.1,2 SKICs gas prooucaon naa tnus far foitowea tna praoied lanofifl gas generation curve as moaaieo using a first order aacay rate at 7% par year of gas amissions. This means that mstnana gas production and ccrrssocnang emissions nave oeen decreasing and will continue to decrease over time. Therefore, a future risk scanano based on a single estimate wnicn does not decrease is an unreasonable overesttmation of tna hsk because it does not take into account me real decreases In future emissions. 3. As noted by Or. Jcnn R. Froines in his comments issued in May 1995, the amciant air data from :SS1 to 1982 Is unreliable, we understand mat you nave the data ana wisn ts use it. However, noth tna CH-MHill risk evaluators working tor (USEPA on an exccsure assessment for the BKK LanafiHf ana Or, Friaries nave considered the use of me data in a Quantitative nsk assessment inapcrconare for many technical reasons. This data represents me majority or me risk estimate for the 30 year reasonable mawmum' axocsura. we would encourage you to raevaiuaB the aaermfic merits of use cf this aata. it contributes to an unreasonable overesttmation of risk and increases the scarmflc uncertainty or the risk estimate. Thank you again for completing the risk assessment Our technical staff is avaiiabio to answer arty questions you might have and to provide additional technical information to you, if you would like. Pfaaae call me at (310) 533*7150 if you would like more information. Julia Bussay, Director Corporate Regulatory Affairs ca stave Samaruagc, uHA. City of West Covina Carmen Samos. US SPA Region 9 Steve Lavmgar, QTSC Region 3 Dennis Oelaney, SCAQMD Rick Vergets. RWQCS 1 ePMOO/tWm LANaPtL aw EMISSIONS MTIMATION MOBIL. Ban-- Umnmmm, Cmw. 13IMIWW wm 2 Bntm ri**e few-- NO. 44 landfill MCTHANS aeegvBwr sfumm*. Out 0--. iso. -126- CMA114445 SENT 5V: sMVIROiN' yv iiis : 13S533 ENVIRON 3153229705)3 i February 13, 1996 Ms. IiUiati Kelly, .VLPii Office or Haviroszsssisi Health Hazara Assessment Hazardous Waste Toxicology Section. oOl N. 7th Street. MS 241 P.O. Box 942732 Sacramento. CA 94234-7320 Re Comments on Dtaanoer 1995 Draft Addendum Health Risk Aiusxmem or Ambient Fugitive Vinyl Chloride Emissions ttom the Clas* 1 Unit of the BEK Laflll. Weet Covina. California Dear Ms. Kelly; On behalf of the BKK Corporation. ENVIRON is providing comments on the December 1995 Draft Addendum Health Risk Assessment of Ambient Fugitive Vinyl Chloride Emissions tram the Cass Unit of the RRK 7 West Covina, California. These comments are based on our review of the report and observations we made during the community meeting held in West Covina on January 11,1996. We appreciate the opportunity to provide these comments. We think the OEHHA staff should be commended for doing a very good job of responding to diffitr.lt questions from the comxmmny at the January 11 mrenng. It was our perception that many of the answers direcnv responded to speone concerns expressed by peopie woo live in the vtamty of dm provided by the OEHHA staff. We beiieve the effeeaveness of the OEHHA risk assessment report as a risk cnmrrnrxrci-tfln^ toci would be ***>*" by some ox the information provided by the OEHHA staff during ms community m**nng to the report. In addition, we believe the eueedvexuss of the report as a risk comsmmcasan tool would be enhanced by clarifying a few poms addressed in the report. These comments are ciscnsscri in more detail below. Comment* Baaed on Cammmrtrr M~rtnT At least one person attending the noted differences in methods (e.g^ exposure assumptions) between the most recent OEHHA report and past risk assessments (e.g* the lost OEHHA nsk assessment). The reason for these changes were not apparent to him and clearly had diminished his wm in the conclusions presented in the OEHHA report Dr. Siegel and Ms. Kelly responded to his question; and we believe the report would be strengthened by an ^rnariA^A discussion of their response that deficit CMA114446 Mi/urroiic, Tow,, . - jjfl ShtUmwuM itrrer ism* /OO EmmWtt. CtUiaflU* *4SO USA 7:i: .110) 655*`WO Fw li 10) SJVS17 -127- 3163229705:* 5 Liman Kelly 2 February L3, 1996 assnnrpuoas ana other aspects of risk assessment methodology vary between regulatory programs ana change over urns. In addition. BKK has been required to perform several different nsk assessments unoer various reguiaiory programs (e.g, Proposition 65, AB 2588. RCRA 5008(h)). Some of ese other nsic assessments are mendoned in the QEHHA nsx assessment reoon. but the reiationshio between these other nsic assessments ana the QEHHA repan is not dear. It may be worth clarifying in the report that the QEHHA ;epon is being performed in addition to the other risk assessments that BKK must perform to satisfy their regulatory obligations. As was dear tram same of die questions asked at the community meeting, many peopie want to know if die site poses a reai health risk, as opposed to a hypothetical upperbouna risk basea on RME ana other atnTmwTrnn< In other wards, there is a risk communication need in aridjp'nn to needing to know how the risks calculated under the varying assumptions of various regulatory programs compare against risk levels that trigger acson (e.g,, nonricauoru remeaiadom under sp^dne regulations. At the community meeting. Dr. Hoimer. from QEHHA. provided some responses that directly addressed many of the community's expressed concerns. Spccmroily, Dr. Haitzer compared die concentrations measured in the worrpiaces that were studied in the epidemiology studies of workers g*p<n**i to vinyl to the amcenaarions m the vidmty of die 3SK TamtfTt. as mentioned below, we believe it would be useful to present the risk results that axe currently provided is tne report using epidemioiogy- basea CSFs along with some of the informadan Dr. Haitzer provided. Someone from the audience at the community *i* noted that the most recent risk assessment report only addressed vinyl ehi<mdc, while die previous report had addressed several other volatile organic chemicals. Dr. Siegel noted that the other chemicals had been shown to pose de risks. Adding this point to the report would enhance die credibility of the State's analysis. Specific rommenta on the Rw>nrr and Fa Sheet Document 111101 This title refers to "Ambient Fugitive Vinyl Chloride Emissions''. Hie report should refer to "Ambient Vinyl Q>inr>^ Concentrations11, as emissions per se, are never mentioned. Page 5, Paragraph I This paragraph cites E?A Region DC as noting that past exposures msy be important at selected sites but does not explain what feature of selected sites warrants conaideraaaa of past exposures. It does not what is unique about past exposures at the BSX Tanner warrants any different treatment would be given to pan exposures at any other landfill, Superfund Site, or RCRA site. Page 44, Paragraph 5: The discussion of odor ` notes that the detection of odors suggests the potential for exposure. The aisauson does not explain that a large -128- CMAT14447 NT ev-=MVInCN-=rsryviiie 5PM : 5195:33:17- 9153223705:* 5 Lillian Kdlv 3 February 13,1996 number or odor complaints mm* rfom areas (e.g., to the north of the lanrifjfO where monitoring has consistenzly failed to detea vmyi chloride. The ooar complaints discussion does not attempt to describe the correlation between the location of the odor complaints noted on Figures 16 17 ana the mannaring resuits from the same areas. By ozmthng such an analysis, the report trusses an opportunity to communicate turn the detection of odor in some areas near the does not necessarily correspond to exposure to vinyl Ey restating and confirming the common concern tfra* odor chemical exposure without discussing the specific lack of correlation between the two in the neighborhoods near the BXEL landfill the discussion of odor complaints now in the OEHHA report is in fact misleading Clarification of this poms is would hgfa prevent unwarranted concerns. Page 53. Paragraph 2i Current monitoring 1994 data. This shornd be mentioned. show decreasing concentrations over Page 53. Table 10 The reporrs vaiue as a nsic communication vehicle would be further enhanced by giving greater emphasis to some of the epidemiology information already in the State-! report. In particular, the risks eimln*d cancer slope moon based on epidemiological data could be given a more prominent presentation. Perhaps, the risks calculated on the basis of the human-oased CSF could be more explicitly described as being based on tinman data, rather than merely being a "Different Unit Risk Assmupriari' (&, in Table 10). We believe that adding a separate section of the report, with is own yj which ail the infaiwiiirinw is presented would whann: the tisk consummation aspect of the report. This section could include the points Dr. Holtzer made along with the quantitative estimates of risk based on the human-based CSF this is already presented in the report. Page 62. Paragraph l: Text states that the 1993-1994 Proposition 65 daza have not been fully validated by e regulatory agency; neither has the agency data. Either both, or nether should be meunoneo. Page *3. Finding 2 and 3 In Finding 2, OEHHA notes that the gaa collection system and cap put in place over the dosed Class l unit, "have been successful in lowering the frequency and level of vinyi chloride to leveis that pose little, if any, risk to nearby residents-. In spite of this Finding 3 is pr*****^* anrf in-Tpi** that aWftiWnnai environmental consol may be required to "`ensure future risks do not add significantly to the pan cumulative risk". Finding 3 is also presented in spite of the results presented in Table 9 showing that future risks add little to oo cumulative risk. The only potential tigtrifanr coosibunon to future contribution was estimated in the OEHHA report for the MY station. As in the accompanying letter front Julia Bussey and based on 1995 data, projected future concentration of <X25 ppo at Mvra Court is approximately 50%, or more, faghg* than we would ppw. -129- CMA 114448 iENT 5v:NVIR0N-;-spyvil !e 2-'2--55 ::i7PM 135555517- 3163229705:# 7 Lillian Kelly February 13. 1996 Page &3, Finding 4 While the report clearly states teat tie results presented are applicable to people who live in tie vicinity of Stations A, B, ana AfY, these three monitoring stanons oniv represem --c exposures of a small fraction of the peopie who live in the vicinity of the la'nrfgi. We believe tee ns* comrimmeacon value of the report would be greaav by a more direct statement regarding toe fact that vinyl chloride levels at other locations are substantially lower than at A B, ann MY. A rfitiiKtin-p 0i the lower ieve15 detected at other monitoring stanons and the faa that VC was never nm**?** at stations needs to be added elsewhere to the report to support this statement. We beiieve a brief summary discussion of mannarmg results at other stanons is parneniariy important to address the Questions and concerns ct the peopie who live distant from the A3, and MY stanons. These peopie may get the tmfwmnrt that the risks at these three stanons apply to their location as welL This rtnRrnnnn is parneciaitv imoortant in light of the impression created that odor deteenon equates to vmyi chloride exposure. We appreciate the opportunity to nave provided these comments ana would be happy to discuss them with you. Sincerely, v Principal RSdf -130- CMA 114449 BLANK PAGE -131- CMA 114450 OEHHA'S RESPONSE TO COMMENTS FROM CHEMICAL MANUFACTURERS ASSOCIATION Chemical Manufacturers Association submitted three articles for consideration. The "EPA Facts About Vinyl Chloride, June 1992" provides a brief summary of information about vinyl chloride. The other two articles describe an alternate method of deriving a cancer potency factor for vinyl chloride ("Predicting Cancer Risk from Vinyl Chloride Exposure with a Physiologically-Based Pharmacokinetic Model," Reitz et al., 1995, and "Considering Pharmacokinetic and Mechanistic Information in Cancer Risk Assessments for Environmental Contaminants: Examples with Vinyl Chlonde and Trichloroethylene'', Clewell et al., 1995). The physiologically-based pharmacokinetic (PBPK) model described by Reitz et al. predicts for humans that continuous exposure to 0.869 ppb of vinyl chloride would increase lifetime cancer risk by one in a million. The carcinogenic potency of vinyl chloride estimated using this PBPK model is approximately 137 times less than Cal/EPA's unit risk value used in the addendum report. Assuming the PBPK value for vinyl chloride suggests an estimate of risk at Station A that is approximately 140-fold lower than the estimate obtained in the addendum report. This qualitative estimate has been added to the Risk Characterization, Limitations and Uncertainties. -132- CMA114451 m Chemical Manufacturers Association February 9, 1996 David M. Siegei, Ph.D.. Chief California Environmental Protecnon Agency Office or Environmental Health Hazard Assessment 601 North 7th Street, MS-241 P.O. Box 942732 Sacramento. CA 94234 Dear Dr. Siegei: RECEIVED FEB 13 1996 Hazardous Waste Toxicology Section The CMA Vinvi Chloride Health Committee submits the following reports to aid the California Office or Environmental Health Hazard Assessment in its cancer risk assessment tor vmvi chionde using pharmacotcinenc and mecnamsnc: (1) Common Chemicals Found at Supemmd Sites, Office of Emergency and Remedial Response, C.S. EPA, 1994: (2) Predicting Cancer Risk trom Vinvi Chionde Exposure with a Physiologically Based Pharmacokinetic Model. Reitz et ai. Toxicology and Applied Pharmacology (In Press); and, (3) Considering Pharmacokinetic and Mechanistic Information In Cancer Risk Assessments for Environmental Contaminants: Examples with Vinyl Chloride and Trichloroethylene, Cleweil et ai. Chemosphere, 1995. The Committee looks forward to receiving the final "Addendum Health Risk .Assessment of Ambient Fugitive Vinvi Chionde Emissions From the Class 1 Unit of the BBK Landfill, West Covina, California.' when completed and released. Thank you for vour consideration of the enclosed information in preparing a final risk assessment addendum for vinyl chloride. Please call me at 703-741-5637 if you have any questions or need additional information. My fax number is 703/741-6091. Sincerely, cc: Lililian Kellev (with enclosures) Enclosure Hasmukh C. Shah, Ph.D. Manager, Vinyl Chloride Panel -133- CMA 114452 1300 Whson Boulevard. Arlington, va 22209 Telephone 703-741-3000 Fa* 703-741-6000 UIKc nitM SUMS .lUBlMIIIWtllll faiBLum Aoancv Otlie* oi Emaroancv ana 3voa*snnomaatioRneja;s;ons* 3203.1-17 a 9-9mta SM 540/044/0*4 *01*011994 Common Chemicals -134- CMA 114453 4 E?A Facts About Vinyi Chloride * jMtiS What is vurvi chloride? t | Vinvt cntonae u a colorless ens wun a mild. ; | sweet oaor. L is a man-maae cr.cmteji ir.ai does not occur naturally. Most at the vmvt chloride produced in the United Slates is used to make polyvinyl chloride fPVC). This maienat is used to manutaciure a vunerv at plastic and vinyl produas including pipes, wire and caale coatings, - packaging materials, furniture and automomte upnolsterv, .all coverings, r.ousewares. and automotive parts. Mucn smaller amounts at vinyl cnionoe arc | used as a cooling gas and in tne manmacturc o: other cumpounas. Emissions from vinyl chloride and PVC manuiacturers are responsible far the majority of vtnyt chloride released 10 the environment* i How might exposure to vinyi chloride occur? Vinvt cnlortde has been found in approximated a i s 01 me I.-DO ha.aaraous waste sues on the X.wuntu Pnnrttws l.:: ts'PLu Vinyl chlonde is matnlv released into tnc air and discharged in wastewater trom tnc plastics industry. Most of the vinvt chloride that enters the air gradually breaks down into less harmiul substances. Levels of vinyl chloride found m the environment are usually more than a thousand times below levels found in occupational settings. Elevated i -uidoor levels arc usually expressed in terms ot parts oi vinyl chlonue present in a billion pans of air or water (ppoj. The term `pans per billion'' is a way of ^pressing trie concentration ot a contaminant in a ii.iuid or air. One pan per billion is cuuui to one men .a a distance ot about sixteen thousand miles lur a pennv in icn million dollars!, a very small amount. Qutduor levels of vinyl chloride rcsmi from tne discharge of exftaust eases from tactoncs nut manutuemre or process vinyl chlonde. or evaporation from areas where chemical wastes are stored. The highest outdoor levels have oeen measured in air near \ tnvt chloride lactones or over cnemicai waste storage areas. Vinyl chlonoe that enters drinking water domes from factories mat release vmyi chlonde wastes into riven and lakes, and from leacntn? into groundwater m areas wiick chemical wastes are stored. Small amounts of vinyl chlonde cun enter drinking water from with polyvinyl chlonde pipes, in the past, higher than r^p*^** amounts were present in foods packaged in pmstie that contained vinyi chloride. Currenuy. the U.S. Food and Drag Administration (FDA! regulates the amount of vinyi rhlaitde allowed m food packaging in order to limit the make of vinyi chlonde. How can vinyi chloride affect human health? Short-term exposures to very high levels of vinyl chloride In air can cause dizziness, lack of muscle coordination, headaches, unconsciousness, or death. Long-term exposure to tower amounts in factories which produce or use vinyl chlonde has caused `vinyl chlonde disease*. This dhrasr is characterized by severe damage to the liver, effects on the lungs, poor circulation in the fingers, changes in the bona of the fingers, thickening of the skin, and changes in the blood. An increased risk of developing cancer of the liver and possibly several other tissues has been linked with breathing air tn factories containing vmvi chloride. Some nealth effects observed tn humans have also been seen in laboratory animals. Effects on the nervous system of animals have occurred following snort-term exposure to very high levels of vinyl chloride in air. Animals exposed to high levels for a short period of time, as well as to low levels tar a tong period, developed liver damage. Kidney effects nave also occurred following exposure to high levels. Animals developed cancer tn several tissues after eaiiag food or breathing atr that contained vinyi chloride. How can vinyi chloride enter the body? The most likely way that vinyl chlonde can enter the body is by inhalation. This exposure route is of concern for penons employed in vtnyt chloride manufacturing or processing, tar people living in communities where vinyi chloride plants are loaned, and for individuals living near hazudous waste disposal sites. Vinyi chloride can also enter the body thrauen ingestion. Absorption of vinyl chloride through the skin is not likely to be an important exposure route. -T3F' CMA 114454 's there a medicai to identify vioyi :air'^Qe exposure? Vinvl chtonae can be measured in unne ana body tissue. out these tests annot be used to determine tne evei at vtnvt chionae exposure. Measuring tne amount of the ma\OT breatiaown oroauct of vinyl chionde m the inne mav give some indication of recent exposure: However, the quantity of this breakdown oroauct may ary tor different people. Neither of these tests is rounueiv available at a doctors office. Laboratory tests commonty used by doctors to evaluate liver damage ana liver tunaton are usually not helpful in determining whether liver damage aas milted from vinyl chloride exposure. What are the methods of treatment and Hfoprweni of viuyi chionde? The recommenced metnod of disposal of vinyl chloride is ioaneration. following mixing with another combustible fuel. Complete commotion mum be ensured to prevent the formation of photteste, a poisonous gas. An aad scruober s also required to remove nvdrocnionc aad produced during inattention. EPA has classified vinyl chionde as a fmrdoos component of solid waste* in order to control the handling ot this chemicaL All releases greater than one pound must be reported to the National Response Center. /hat levels of exposure have resulted in armful health effects' invl cnionae is regaraed worldwide as a cnemioi that causes cancer tn humans, but exposure levels necessary ' to ouse cancer ..re not known. The L\. Environmental Proteaton Agency (EPA), aicreiorc, use antnui dau to estimate rat in humans. According to this data, u is estimated that breaming air containing 1 p- tnyl chloride for 70 years may place as many as ^Revaeio persons in a population of 100000 at risk of ping cancer. Eating food containing 1 ppm vtnyi chloride every day for 70 yean may place as many as 6,440 persons in a population of 100U000 at risk of developing cancer. Similarly, drinking water containing 1 ppm vinyl chionde every day for 70 yean may place as many as 9^570 persons in a population of 100.000 at nsk-- of developing cancer. What r^f*fTWWTW*w*i***T*rt ha frHfflli government mane to ptotca human health? EPA requires that community drinking water systems that regutariv serve the same 25 persons for at least 8 months of the year must limit vinyl chloride in the .making water to 2 ppb. Recently, the FDA changed .is regulations regarding the vinyl chloride content of anous plastics used in food packaging and to cany *ater used in food processing in order to limit the intake of vinyl chionde tn food to levels considered to ne sate. Limits range nom a to SO ppm depending on -he nature of the plastic and its use. GLOSSARY Brtakaown Produce Mast contaminants are combinations of specific substances. Contaminants are degraded, or separated, into these individual substatics through chemical or physiol means. Exposure Route: The way in which people come into comas with a substance. The main routs are ingestion, inhalation, aad absorption through the skin. Leach: The process by which suhstancs an released from the soil by dissolving in fluids, usually rain and surface water, and are anied down thiougn the soiL National Priorities List (NPLU EPA's list Of uncontrolled or abandoned hazardous waste sits identified for possible long-term clean-up under the Superrsnd Program. For more information about Vinyl Chloride, please contact EPA at the following address: US Environmental Protection Agency ATTN: Superfund Hotline 401M Streep S.W. Washington, D.C. 20460 1400-424*346 or 1-8004334202 L. -ubtion conn-- in tiw tag iWb nappwed (nom Hie Tommowcal Profile for VmW Oilonde. Awrr far T_ wz' U-S, Public Hmin lovn a axiaborcuoa wnn me Ui. Eavmimiiciim Proiacuoo Aacy. Auyou. 199V. Thufaa PA dam iwtuam tame tmaaea an tat uiwwik. mnutmf ptmtm -136- CMA 114455 Predicting Cancer Risk from Vinyl Chloride Exposure with a Physiologically-Based Pharmacokinetic Model November 19,1995 Richard H. Reitz' Michaei L. Gargas3 Meivm E. Andersen3 W. M. Provan4 Trevor L. Green4 Corresponding Author Dr. Richard H. Reitz RHR Cunsuiting Services 4105 Chelsea Ct. Midland. MI 48674-3361 U. S. A. Tel (517) 631-7089 Fax (517) 631-7089 Manu a.IVS (Revision) -137-Reitz et al. CMA 114456 liSLi Abstract Predicting Cancer Risk from vinvi Chloride Exposure with a Phvsioioeicailv-Based Pharmacokinetic Model. Reitz. R.H.. Gargas, M.L.. Andersen. M.E.. Provan, W.M-, and Green. T.L. 119961 Toxicui. Aupl. P'innmcai.. 000. 000-000. A Phvsioiogically-Basea Pharmacokinetic (PBPK) model capable or describing the metabolism or vinvi chloride iVC) in rats. mice, and humans has been developed and validated by comparison with experimental data from experiments not used in model development. This PBPK model has been used to predict measures of delivered dose treactive VC metabolites produced in the livers of the affected species) hypothesized to be involved in the induction of liver angiosarcoma in rats, mice, and human populations exposed to VC. Measures of delivered dose in rats were fit to an empirical Jose response modei (the linearized muiti stage model of Crump et al.) ana usea to make predictions of liver angiosarcoma incidence in mice and human populations exposed to VC. This procedure gave a good prediction of angiosarcoma incidence m mice. Predictions of angiosarcoma incidence in humans were more than two orders of magnitude lower than risk estimations which did not utilize pharmacokinetic data (HEAST, 1995), but were still almost an order of magnitude higher than actually observed in exposed human populations. Introduction Vinyl chloride (1-chioroethylene, VC) is a colorless, explosive gas. VC is only slightly soluble in water but dissolves readily in fats and organic solvents. VC is most commonly used as a precursor for the production of polyvinylchloride (PVQ plastics, and the highest potential for human exposures exists at the sites where PVC's are manufactured. Because this material has relatively low acute toxicity, occupational exposure standards for VC (OEL) were typically 500 ppm fECETOC, 1988) until 1970 when Viola discovered that rats exposed to VC vapor developed an increased incidence of tumors (Viola, 1970; Viola et al., 1971). Violas results were confirmed by Maltom et al. in 1974, and Maltoni also reported that a rare form of liver cancer (angiosarcoma) was induced in rats by VC (Maltoni et al., 1974). In that same year Creech Sc Johnson (1974) reported that a search of the medical files of employees exposed to VC at a Goodrich plant in the USA revealed three cases of death from the same rare type of liver cancer (angiosarcoma). Since that time, VC has been the subject of numerous animal studies and epidemiological surveys, and it is clear that VC induces angiosarcomas of the liver in both animals and humans (see ECETOC, 1988 for a review). Other types of tumors (non-liver) have been associated with VC exposure in animals, but the epidemiological data |Manu a.198 (Revisioni Reitz et ai. CMA 114457 Page 2 I have not linked exposure to VC to induction or other types of tumors in humans (ECETOC. 1988). VC is metaboiicaiiy activated to a reactive species tprobabiv cnloroethyieneoxide) which is capabie or bindinc to DNA ana causing genotoxiciry in vivo (ECE" C. 1988). This activation is catalyzed bv Cytochrome P450 enzymes, and there : good evidence that the metaboiism or VC is saturabie in vivo and in vitro (Kappus et aL. 1976; Gehring et al.. 1978; Guencerich & Watanabe. 1979). A large body of data relating the tumongenic response in the livers of animals and humans to biochemical events taking piace m the various species is available. The purpose of this paper is to discuss methods for using this database to prepare estimates of cancer risk for human populations exposed to VC. VC is worthy ot consideration for another reason. In most cases where estimations of the human cancer risk have ceen basea on animai studies, it is not possible to know wnethcr rr.e crbiections of risk are realistic or not (epidemiological data are not precise enoueh to either confirm or deny the risk projections). In the case a rather iarge body or epiaemioiogicai data indicates that significant increases in human cancer have occurred as a result of past practices which resulted in high human exposures to VC. This provides a unique opportunity to test the ability of current risk assessment practices to provide reliable estimates of human cancer risk from animai data. Qfrteflivw; Physiologically-based pharmacokinetic (PBFK) models of chemical disposition have been developed for a variety of chemicals, including the chlorinated ethylenes (NAS, 1987). These models are particularly weii suited for risk extrapolations because they are based on specific physiological and biochemical properties of the different species and dose routes as well as physical chemical information about the solubilities and vapor pressures of the different compounds (Andersen et aL, 1987). Our objectives in this project were; 1. To develop a PDTK model capable or predicting the metabolism of VC in both rodents and humans. 2. To validate this model with existing data sets for rodents and humans. 3. To develop a quantitative risk assessment procedure based on the predictions or the validated POTK model for VC. 4. To compare the TCTK based risk assessment procedure with the existing PA risk assessment procedure iHEAST. 1995) 5. And finally, to compare the results from this PDPK based risk assessment with the actual incidence of liver angiosarcomas in human populations exposed to VC in the workplace. (Simonato et al., 1991) CMA 114458 |Manu a3VS (Revisioni -139- Reitz et al. Page 3 1 Methods Construction of the PBPK Model: The PBFK model for VC was based on a PBPK model developed by Ramsey & Andersen 11984) to describe tne kinetics or inhaled styrene in rats and humans. In this model a senes or simultaneous differential equations describing the distribution, elimination, and metabolism of chemical was incorporated into a computer program using an integrated software package containing routines for numerical integration, optimization, sensitivity analysis, and graphical display. This software package (Simuoolv5) is commercially available from Mitchell U Gauthier Associates. ZOO Baker Ave, Concord MA 01742-0013, USA. The VC model contains four tissue grouos (fat, muscle, rapidly perfused tissues, and liven and assumes that all metabolism takes place m the iiver where the rate of metabolism is descrtoea cv tne Michaeiis-Menten equation. Detailed descriptions of this type of modei are given elsewnere (Ramsey and Andersen, 1984; Andersen et al.. 1987). An annotated copy of the source code for this model is available from the corresponding author (Reitz).'1 Physiological parameters in the model (blood flows, ventilation rates, organ sizes) appropriate for rats, mice, and humans were identical to those used by Andersen et al., (1987) in a multispeeies PBPK model for methylene chloride with two changes; (1) the size of the liver compartment for rodents was based on historical data for control animals from the Toxicology Laboratory of the Dow Chemical Company and (2) the ailometric constants for alveolar ventilation and cardiac flow in rats used by Andersen et al. (1987) were increased from 15 to 18 in order to provide a more consistent description of the gas uptake data sets. Blood/air partition coefficients for rat, mouse, and humans and tissue/air partition coefficients for rat liver, rat muscle, and rat fat were determined using the vial equilibration method of Sato and Nakajima (1979) as modified by Gargas et al. (1989). Tissue/blood partition coefficients for rats were obtained by dividing the tissue/air partition coefficients by the blood/air partition coefficient. Mo direct measurements were available for the tissue/'air partition coefficients in the rapidly perfused group of tissues m this model, so this partition coefficient was set equal to the partition coefficient for iiver. a technique that has proven successful in the development of PBPK models for other nalogenated, volatile materials (Andersen et al., 1987; Reitz et al., 1988; Reitz et ai., 1990a.b). Tissue/blood partition coefficients for mice and humans were estimated by dividing the tissue/air partition coefficients for rats by the blood/air partition coefficients for mice or humans respectively. All of the partition coefficients used in the PBPK model for VC are listed in Table 1. Manu X3V81Revision) -140Reitz et al. CMA 114459 Page 4 \ Mefahoiir C'-?n*tang **r R^ts: Metabolic parameters tor maie and femaie Sprague - Dawiev rats (body weients 2C0-40Q gramsi were obtained by computer optimization of gas uptake data sets ifour e>:periments for each sex) according to procedures previously described by Careas et ai. (1986). Basically, given the physiology of the ammais and the soiubiiities or VC in rat blood and tissues, the metabolic rate constants VMaxC and Km were varied until a satisfactory description of data gathered in severai indepenaent gas uptake experiments was obtained for both maie and female rats (Figures la. lb). Metabolic Constants for Mice .and Humans: Vinyl chloride belongs to a large class of low molecular compounds (including -benzene, styrene. CCLt, CHCLi, CH^CI^ CH3CI. CHtCCh, 1-2 dichlorooropane. ethylene dichioriae. ethylene dibromide, vinyl bromide, acrylonitrile, vinyl carbamate, ethyl carbamate, and trichloro ethylene) which are reaaiiv metabolized by Cytochrome P--ISO. IIE1 (P450 2E1). Guengerich et ai. (1991) uDservca that metabolism or these substrates by microsomal preparations from liver :aj showed the same relative activity for different preparations of microsomes with all the substrates, (b) was sensitive to inhibition by known inhibitors of P450 2E1 metabolism such as diethvidithiocarbamate and disuifiram with all the substrates, and (c) showed inhibition by specific antibodies to P450 2E1 raised in rabbits, but was not sensitive to addition of antibodies specific for other forms of P450 such as P450 UIA or P450mp- Guengerich also reported that purified preparations of P450 2E1 were also active on all these substrates. Based on these and other studies, oxidation of this broad group of substrates by P450 2E1 has been identified as the primary means of biotransformation in both animals and man (Nakauma et al., 1990; Guengerich et ai., 1991; Raucv et at, 1993). Consequently, the extensive m vivo and in vitro studies carried out with CH2CI2 (Andersen et al., 1987. 1991) ana CHCI3 (Corley et ai.. 1990; Reitz et al.. 1990a) provide a reliable basis for estimating m vivo metabolic rates for other members of this class (including VO in humans. The process by which these data were used to estimate in vivo metabolic rate constants for humans and mice for VC is outlined below: 1. in vivo maximum rates ot metabolism < VMax s) in rats are obtained by experimentation (VC) or from tne literature (CH^C^ CHCI3). These vaiues are listed in Table 2. 2. The weight of the liver in animals used in the in vivn studies is calculated for each chemical and each species from the percent liver and the body weight (Table 2). 3. The VMax for each species is divided by the weight of liver to give an m vivo rate per gram for each chemical. These VMax/gs are normalized to the rat for each chemical, and the "Ratio to Rat" is listed in the last row oi Table 2 for each chemical. 4. For chloroform and methylene chloride, the in vivn "Ratio to Rat" is nearly constant (2.570, 2.707) suggesting that alter normalization, the "Ratio to Rat" does not depend upon the chemical being studied (at least within this limited senes of chemicals ail metabolized by P450 2E1). Manu a398 f Revision 1 -141Reitz et ai. CMA 114460 MJ 5 In vivo studies bv Andersen et al (1991) with CH2CI2 provjde a basis for calculating the "Ratio to Rat" for humans ot 0.2CS: Table 2. (Camparanie in vivo studies tor CHCI3 in humans were not available.) * Finailv. the experimentally determined in vivo VMax inr VC in rats and the `Ratio to Rat' for mice and humans were used to calculate in viv* VMax s tor VC by multiplying VMax/g (rat) by the Ratio to Rat" ana weicnt of liver in eacn species. For example the in vivo V Max tor VC in humans is calculated as: iU.968/5.69) x 0.208 x 2198 * 77.7 mg/hr (Table 2) Results Model Validation Validation in Rats As noted in the Methods section, metaboiic rate constants were obtained from in vilfl gas uptake experiments previously at Wright Patterson AFB (Gargas et al., 1990). To verify that the model using these metaboiic rate constants was broadly descriptive of metabolism m the rats, independent experiments performed by Watanabe et al. (1976) were evaluated. Watanabe and coworkers exposed rats to a series of concentrations of radiolabeled VC for six hours, and then collected radioactive excreta from these animals for up to 72 hrs. These studies allowed the estimation of the total amounts of VC metabolized by the rats (Watanabe et at, 1976; Gehring et al. (1978). The amounts of radioactive metabolites observed by Watanabe et al. were compared to the predictions of the PBPK model for rats. Other than changing the body weights and exposure concentrations to reflect the different experimental conditions, no changes were made in the model developed from gas uptake experiments. The results are shown m Figure 2. The model gave an excellent simulation of Watanabe et al.'s data. Over a range of concentrations from 1.4 ppm up to 4,600 ppm, the PBPK model accurately predicted the levels of radioactive metabolites produced and successfully identified the region where saturation of VC metabolism occurs (200-S00 ppm; Figure 2). Validation in Mice Metaboiic rate constants for BaCjFi mice were estimated by extrapolation from in nilfl. results in B6C3F1 mice obtained with model substrates as outlined in the Methods section. In order to test whether these estimated rate constants accurately reflected the in vivo metabolism of VC in mice, an independent set of gas uptake experiments conducted in male and female B6C3F1 mice was used for validation. For this validation, the basic PBPK model for rats was adapted to mice by (a) incorporating the known physiological differences between rats and mice (see | Manu aJ98 (Revision! _________ Reitz et al. CMA 114461 Pa--1> I Andersen et ai.. 1987), (b) changing the biooa/air partition coefficient for VC to that measured in the laboratory with samples or BaCjF-, mouse blood (Gargas et al., 1989), and ic) setting the aiiometnc constant describing the maximum rate or metabolic oxidation or VC to the vaiue estimated from ip V-iV-0 studies with other volatile, low molecular weight, halogenated hydrocaroons (Table 2). Other than these changes, the structure of the moriei was not altered. Simulated and actual data rrom tour exoeriments with maie B6C3F1 mice (initial concentrations of 345. 570, 1065. and 3190 ppm) and four experiments with female B^CjFt mice (initial concentrations of 280, 550. 975, and 2950 ppm) are shown in Figures 3a and 3b. As can be seen from inspection of these figures, the model gives a reasonable (but not perfect 1 simulation of the gas uptake data. The highest concentrations of VC (-3000 ppm where metabolism is probably saturated) were weii descrmed bv the PBPK based on me metabolic rate constants estimated from model suDstrates. These data depend primarily upon the vaiue chosen for VMax in the model and suggest that tne extrapolation procedure employed for estimating the maximum in vivo rate of metabolism in B6C3F1 mice was successful. The low concentrations (.--300 ppm. where metabolism is presumably first order) are also well described by the model. For rapidly metabolized substances, the uptake is largely flow-limited (i.e. depends upon how rapidly the material is delivered to the liver rather than the specific values of VMax and Km). Correspondence of model simulations with experimental data at low concentrations suggests that the physiological parameters for mice (flow rates and partition coefficients) used in the PBPK models for B^CsFi mice are appropriate. However, for the experiments involving intermediate concentrations of VC (550-1065 ppm) the model predicts slightly more metabolism (uptake from the chamber) than was experimentally observed. These results were obtained in the region where metabolism of VC changes from flow-iimited conditions to zero order (enzyme saturation), and the simulation of these concentrations is sensitive to the value chosen for Km in the Michaeiis-Menten equation. To explore the possibility that a different value of Km might give a better simulation of the experimental results, a computer optimization was conducted with 5imuSolv. The results of this optimization tin which the computer varied both VMaxC and Km) are shown in Figure 3c. In this optimization, it was found that a Km of 0.28 gave a much better simulation of the gas uptake data than the Km obtained from the rat experiments (Km = 0.04 in rats). However, the optimum value for VMaxC remained relatively constant (the optimum value of VMaxC was 8.13; quite close to the extrapolated value of 9.04). | Menu a398 (Revision t -143-_________ Reitz et at. CMA114462 ! Given that the same enzyme t P450--2E11 is responsible tor oxidation of VC in both species, it may seem surprising that the apparent Km's differ dv this amount. However, based on studies of deuterium isotope effects on CH7CI2 metabolism, Andersen et al. (19941 have suggested that the apparent Km's for oxidation of P4502E1 substrates likely reriect a more compiicated senes of events than simple "binding of a substrate to an enzvme s active site. Andersen speculated that the apparent Km's for P450 2E1 suDStrates may be "... a measure of reactivity of activated oxygen species with available C-H bonds '. If this hypothesis proves to be correct, then the Km for VC oxidation in humans would be expected to be mqtte like the Km of rats than the Km or mice, since the mouse iiver has an usually high capacity for oxidation of these substrates (Andersen et al., 1987; Coriev et al.. 1990). The preceding validation exercise indicates that the procedure used to estimate in yivn metabolic rare constants for VC should give accurate representations of human VC metabolism at either high or iow concentrations of VC. The extrap olation procedure would be less Drecise in identifying the region where transition from first order to zero order kinetics with VC occurs when extrapolating to species other than the rat. Validation in Humans We also attempted to locate independently gathered human data for validation of the human PBPK model for VC. Validation of human models for other solvents (CH7CI2, 1,1.1-trichloroethane. styrene) has been previously reported (Andersen et al., 1991; Reitz et al., 1988; Ramsey and Andersen, 1984), providing support for the techniques for estimating partition coefficients and physiological constants in humans. Consequently, the primary emphasis was on evaluation of the metabolic rate constants for VC estimated bv the techniaues outlined in the Methods section. #A No attempt was made to 'curve fit" experimental data by adjustment of model parameters in validating the human PBPK model. Ideally, we hoped to find measurements of the rate of production of VC-specific metabolites m human subjects (e.g. excretion of VC-specific metabolites in the urine of humans exposed to VC similar to data gathered in humans exposed to trichloro ethylene; Muller et al., 1974) Unfortunately, we were unable to locate this type of dataset for VC. However, we did locate a dataset in which exhaled air concentra tions of VC were reported for human volunteers following VC exposure and this dataset was evaluated with the human PBPK model. In these studies. Baretta et al. (1969) exposed groups of human volunteers to 59, 261, or 492 ppm VC for 7.5 hrs in a carefully controlled laboratory setting. Workers entered the chamber and were exposed to VC at the indicated concentrations for approximately 3.3 hrs. Then they left the chamber to have lunch in an area free of |Mmi a398 1 Revision 1 Reitz et ai. CMA 114463 Paws VC fur acproximateiv 0.3 hrs. roiiowing which they returned to the chamber for , another 4 hrs 17.3 hrs exDosure to VC). This exposure pattern was simulated by the PBPK moaei durinc the validation exercises. Samples of exhaled bream were coiiectea from these volunteers U-7 subjects in each exposure! at different times post-exposure for up to 20 hrs. The sampling procedure involved giving eacn person several glass tubes t20 mm diameter, approximately 23 cm in ienetn) capped with screw cap septa. Each worker was asked to inhale through his nose and exhale by mouth into the giass tube four times. After the fourth breath, the workers quicklv capped the giass tubes with impermeable septa and returned the tubes for analysis. A comparison of observed and simulated results for these exposures is presented in Figure 4. The model for VC gave an good simulation of expired air data tor ail three concentrations over the period from i hr post exposure to 20 hr post exposure. It is noteworthy that these experiments included exposures at concentrations up 500 ppm. a region where metabolic saturation occurs m rats (Figure 1). A sensitivity analysis was conducted to determine whether this fit was dependent upon selection of the proper values for the metabolic rate parameters (Vmax and Km) or whether other model parameters were more influential in the prediction of expired air concentrations of VC (CEX) as described elsewhere (Reitz et al., 1990b). Predicted values of CEX one hour and ten hours post exposure were compared to the same values predicted with "baseline" values for ail model parameters with VC concentrations of 59 ppm and 492 ppm (the lowest and highest VC concentrations studied by Baretta et ai., 1969). The sensitivity analyses revealed that model parameters associated with flow rates (fraction cardiac output directed to fat compartment, aiveoiar ventilation and cardiac output) and parntiorung within the body (blood/air, fat/air, and. at the 1 hr post exposure period, muscie/air) had 3-30 fold more influence on the predicted values of CEX than the metabolic rate parameters Vmax and Km. In fact, doubling or halving the values of Vmax or Km did not appreciably change the fit to the data collected by Baretta et al. (simulations not shown). Buchter et ai. (1978) also studied the pharmacokinetics of VC in human subjects. Human volunteers inhaled VC vapor from tand exhaled back to) a closed system containing 10 ppm and the removal of VC from this system for periods up to 20 minutes was evaluated. In other studies, volunteers inhaled a constant conct 'tra* tion of VC (-2.5 ppm i for 15-30 minutes. Data reported by Buchter et al. were also well simulated by the PBPK model (simulations not shown), but a sensitivity analysis revealed that simulations of these data were even less sensitive to the values chosen for Vmax and Km than the data of Baretta et ai., (1969). Manu a39B (Revision t -145Reitz et al. CMA 114464 rage* 1 It is reassuring that the limited human data tor VC are consistent with the PBPK -v model developed here. However, it must be conceded that the validation procedures described above neither support nor refute our procedure for estimating VC metabolic rate constants in humans. Unfortunately, since VC is a known human carcinogen, u is considered uniikelv that definitive studies of VC metabolism capable or rigorousiv establishing metabolic rate constants for the human PBPK model wiil be conducted in the foreseeable future. Risk Estimation The carcinogenicity of VC in animals has been studied extensively (in fact it may be the most extensively studied of any of the animal carcinogens known). Exposure paradigms include single exposures, high exposures for short periods (days or weeks), exposures eariv in the natural lifespan versus late in the natural lifespan, etc. Given the wealth or data available for preparation of risk estimations, we were forced to select a subset of the data tor lilustrative purposes. We have chosen to focus on studies in which VC was administered for a substantial fraction of the animal's lifetime 112 months exposure in each of the cases evaulated) with follow up until the ammais' death wherever possible. The reader is referred to the publications of Maltoni, Drew, and Lee for further details of these and other studies. We are aware that the pattern of exposure (i.e., whether a given exposure occurs early or late in life) may influence the carcinogenic potency of VC, but we have not attempted to consider this factor in our analyses. Similarly, we are aware that the life expectancy of mice (but not rats) exposed to VC in the first 12 months of their life is significantly shorter than the life span of control mice (c.f.. Drew et al,, 1983 who reported a mean survival time of 780 days for control female mice compared to 301 days in the group exposed to 50 ppm VC for o hr/day). However, we have not attempted to apply any "less than lifetime' correction factors to the cancer potencies obtained from the mouse studies. Deriving Rat Potency Estimates Maltoni conducted a series of inhalation bioassavs of VC in male and female Sprague Dawlev rats at concentrations ranging from 1 ppm to 30,000 ppm (Maltoni, 1974). These animals were exposed to VC for 4 hr/day, 5 days/week, with exposures beginning in young adult animals and continuing until the animais reached one year of age. After the first year of exposure, animals were held until they died and then examined for the presence of tumors. Survival of the animais was compromised at the highest concentrations, so these results were not employed in derivation of a rat potency for VC. Results from exposures conducted at 0,1,5,10, 25.50,100,150,200,250,500,2500, and 6000 ppm were selected as the basis for fitting a dose response curve for induction of liver angiosarcoma by VC metabolites. Tumor incidence data used in constructing this curve are listed in Table 3. |Manu X398 (Revision) -146Reitz et al. CMA 114465 Pa-- iO I The dose surroeate' (measure or dose delivered to the target organ) chosen for "risk analysis was the average daiiy amount of metabolite produced per day per liter of liver tissue. This tvpe or dose surrogate is appropriate for risk analysis when the metabolite :s highiy reactive las the cnloroethylene oxide formed from VC would be) and either reacts with DNA or water m the target organ with a very short halflife (i.e. wouid not be exoectea to persist long enough to circulate to other organs in the body >. Rationale for tne seiection of dose surrogates from PBPK models have been discussed exrensiveiv elsewnere (Andersen et al., 1987) and the reader is referred to this publication ror further details. The PBPK model for VC in rats was then used to caiculate the amount of metabolites produced during a typical dav of exposure (4 hr exposure to the selected VC concentration). Maltoni exposed rats to VC for 5 days/ week and for 1 year, so the lifetime average dailv doses i LADD) were calculated by multiplying the values obtained from the computer bv 5/7 (to correct for less man daiiv exposure) and 1/2 (to correct :or less tnan lifetime exposure). Results from male and femaie rats were combined and empirically fitted to a metabolic dose/tumongenic response curve with the computer program GLOBALS3 (Howe and Crump, 1982; Howe, 1983). The predicted (maximum likelihood estimate) and observed results are depicted graphically in Figure 5. The risk estimation based on the PBPK model (curved, heavy line in Fig 5) describes the tumor incidences observed by Maltoni over a broad range of doses, showing the ability of the PBPK model to compensate for the effects of metabolic saturation in the activation of VC. For illustrative purposes, a hypothetical risk estimation based on administered dose tppm VC) at the two highest concentrations (2500, 6000 ppm) is also shown with a dotted line m Figure 5. This represents the type of risk estimation that EPA might have conducted if the VC data were from a "typical" bioassay (i.e. the only tumor incidences reported were for MTD and MTD/2), and it is noteworthy that such a procedure wouid have significantly UNDERPREDICTED the tumor incidences seen in rats by Maltoni at lower concentrations (e.g. 10-100 ppm). This line does not correspond to the actual EPA risk assessment for VC (HEAST. 1995) For the purposes of illustration m this paper, the dose-response model relating tumor incidence in rats and levels of VC metabolites in liver was obtained from the GLOBAL83 computer program. Other mathematical models reiating tumor incidence to doses of carcinogenic species have been developed and could certainly have been employed in addition to or instead of the multi-stage model. However, since the extrapolation range evaluated was relatively small, it was not considered necessary to explore these other models (they ail give basically the same results when used for regions where experimental data is available as is the case here). Manu aJV8 /Revision) -147- Reitz et al. CMA 114466 Pa-- li~l Extrapolation from me fittea dose/response curve in rats indicates that a LADD of 0.177 mg equivalents or VC metabolites/ day/ iiter of liver is associated with a lifetime increase of 1 x 10*4 in the cancer incidence of rats (MLE estimate). This Risk Specific Dose lRSDl may now be used to esnmate the excess risk of cancer in mice and humans exposed to VC under the assumption that equai average concentrations of VC metacoiites m the liver of these species produce equal lifetime risks of cancer. This assumption is precisely the same as that used by most U.5. cejjgjkatory agencies when performing risk assessments based on administered L^9& (e.g. doses in mg/kg/day) except that an interspecies scaling factor related to body surface area is also employed by those agencies. Andersen et al. (1987) suggested that since the PBPK model already contains provisions for considering metabolic and physiological differences between species, the body surface area factor should be eliminated from risk assessments based on PBPK models. As will be seen later, comparisons of predicted ana observed incidences of angiosarcoma in humans exposed to VC are consistent with the proposal of Andersen et al (19871. Estimation of Risk to Mice from Rat Data Maitoni also reported the effects of exposure to VC on the incidence of angio sarcomas in Swiss albino mice exposed to VC 4 hr/day, 5 days/week for 30 weeks with the experiment terminated at 81 weeks (Maltoni's experiment BT 4 summar ized in ECETOC, 1988). This experiment contained exposure groups of 0,50,250,500, 2500. 6000, and 10000 ppm VC with approximately 30 male or female animals/group (approximately 60 total mice/group) except for the control group which contained 150 male and female mice. VC was seen to increase the incidence of angiosarcoma of the liver (and angio sarcoma at other sites) in exposed mice in a dose-related fashion (Table 4). As with the rats, the tumor response at very high concentrations of VC reached a plateau and then declined. It is presumed that the decrease in tumor incidence is related to the fact that the animals in the highest dose groups showed very poor survivaL Lifetime average daily dose surrogate measures (LADD) were calculated for the mice and these doses and the tumor incidences were subjected to processing by GLOBAL83 to determine the parameters for the LMS, with the MLE and extra risk options selected. When this was done, the R5D (MLE estimate of dose associated with a lifetime increase in risk of 1 x 1(H to mice) was found to be 0.0797 mg equiv alents of metabolite per iiter of liver per day, in fairly good agreement with the RSD previously calculated for rats (0.177 mg equivalents/liter liver/day). Two other studies of the effect of VC exposure on development of liver angiosarcoma have been reported. Lee et al. (1978) exposed CD-I mice to VC for 6 | Menu AjyH (RevmonT 44ft Reitz et al. CMA 114467 rwi2 i hr/day. 3 days/week for 12 months, at which time the experiment was terminated Tno holding period after exposure!. Lee resorted combined incidences of hepatic angiosarcoma of 0%, 4.3%. 36.5%. and 44.9% after exposure to 0. 50. 250. and 1000 ppm or VC respectively. '.Vhen subjected to GLOBAL83 calculations, the R5D associated with a iifetime increase in risk or 1 x 10-4 to mice (based on Lee et al.'s studies) was found to be 0.120 mg equivalents of metabolite per liter of liver per day, intermediate m potency between the RSD previously calculated for rats (0.177 mg equivalents/liter iiver/dayi and the RSD based on Maltonis experiments in Swiss albino mice (0.0797 mg equivalents of metabolite per liter of liver per day). Thus these two mouse studies and the rat studv gave quite consistent estimates of the RSD for VC metabolites. However, when a bioassav of VC in B*C3Fi and Swiss CD-I femaie mice (and F344 rats and Syrian Golden Hamsters! conducted bv the Nationai Toxicology Program (NTT; Drew er al.. 17331 was evaluated, quite different results were seen. In these studies, oniy one exposure concentration was studied (30 ppm. b hr/dav, 5 days/week), but exposures were begun at different points in the animals life spans and were conducted for different durations (6 months, 12 months, etc.). One of the exposed groups of mice was subjected to an exposure paradigm similar to that employed by Maitoru et al. (1974) in that exposure began when the animals were 9 weeks old. they were exposed for almost 12 months. Drew et al. reported that none of the treated animals survived more than 1 year, and the cause of death in the treated animals was frequently considered to be "... due to the development of neoplasms...". In this group of femaie EUC3F1 mice VC increased the incidence of angiosarcoma in the NTP study from 5.3% in controls (4/69 animals) to 76.7% (69/90 animals). In contrast, at this exposure concentration and paradigm, Maitoru et al. (1974) and Lee (1978) observed a 2-3% incidence of angiosarcomas in treated mice with no angiosarcomas seen in control animals. Thus the NTP has reported a considerably higher incidence of angiosarcomas in both control and treated animals than either Lee or Maltoni and this difference is not due to differences in survival, since the treated mice studied by Lee and Maltoni all survived longer than in the NTP study. The RSD lor VC In B^C^Fi mice (calculated in the same manner as the RSD's for Maltoni s and Lee's studies) was 0.0032 mg equivalents of VC metabolites/day/Iiter of liver. This RSD is significantly lower (25-55 fold, implying more risk associated with a fixed concentration of VC) than the RSD's calculated from the Lee and Maltoni studies. The discrepancy in the carcinogenic potency of VC appears to be laboratory rather than strain specific, because NTP also studied another strain of mouse (CD-I mice) and again observed a much higher incidence of angiosarcomas in the liver (63.8% in treated versus 1.4% in controls) than seen by either Maltoni or Lee. It is noteworthy Manu a398 (Revision) -149Reitz et ai. CMA 114468 rage 13 that the incidence of iiver aneiosarcomas reported by NTP (Drew et al.. 1983) in rats exposed to 100 ppm v'C (20%) was aiso siemricantiv higher tnan reported by Maltoni il-2% incidence). Estimation of Human Risk Risk estimates for humans occupationaiiv exposed to VC were prepared by the Following procedure: 1. The validated PBPK model for humans was used to constructortable of lifetime average daily doses (LADD) expressed in the same terms as used in the rat model: mg VC metabolites formed/day/liter or liver tissue for conditions thought likely to have been present in the workplace m past years (i.e. TWA's of 50 - 2.000 ppm and employment for 10 - 20 years). In performme these calculations, mg equivalents of metabolites were adtustea for tne traction or the aav tnat workers were exposed (S/24), the davs/week that the workers were at their jobs (5/7), and the fraction of a lifetime that exposure took place (years/TO). 2. Once these estimates of dose had been prepared, the GLOBALS3 program was used to estimate the likelihood that tumors would be produced, based on the potency number derived from rats (RSD = 0.177). The results of these estimations are presented in Table 5. The predictions range from about two hundred cases per 100,000 (for workers empioyed 10 years at a plant where the TWA was 50 ppm) to almost 4,000 cancers per 100,000 in workers employed for 20 years in a plant where TWA's were 2,000 ppm. The predictions of human risk may be compared with results reported by Simonato et ai. (1991) based on the worid-wide vinyl chloride tumor registry. Simonato s results are based on the evaluation of 12.706 individuals selected from a population of 14,351 subjects from 19 factories where VC was used industrially. The completeness of followup in this study was stated by the authors to be 97.7%, and the average iength of followup was 17 years (with 36% of the population followed for >25 years). The total number of person years at risk in this study was 222.746. Simonato et al. (1991) reported a clear association between both duration of employment and ranked level of exposure. They estimated the absolute risk of angiosarcoma in exposed population with >25 years since first employment to be between t>.2 cases/100,000 for exposures less than 2,000 ppm.years to 280 cases/100,000 for individuals with more than 10,000 ppm.years. Relative risks in highly exposed populations were as high as 45.4:1. Absolute risks observed in the VC cohort with >25 years since first employment are listed in Table 5 for comparison with risks predicted by the linearized multistage model (LMS) using maximum likelihood estimates (MLE) from the PBPK model. 1 Manu aJ98 (Revision! -150Reitz et al. CMA114469 In eacn case, the estimates rrom the procedure employing the PBPK model are substantial' higher tnan actuaiiv observed in humans. For exampie, based on the PBPK prediction, workers exposed to 200 ppm TWA VC for 20 years (4,000 ppm years) wouid be expected to develop i.465 cases of angiosarcoma/100,000. However, the incidence of angiosarcomas oDserveri in the group with >25 years since first employment and 2,000*5.999 estimated ppm.vears was reported by Simonato etaL to be 42.2, wmch is about 35 foid iower than the PBPK prediction. At higher levels of human exposure te.g. 6,000-9.999 ppm.vears. > 10.000 ppm.vears) the PBPK predictions are higher tnan tne observed rates by a factor of ten or so tTableS). Potency factors derived from the studies of Drew.et al. (1983) were aiso used to predict human risk (data nor shown i. When these potency factors were used, the discrepancy between predicted risk and observed incidence was much greater. Predictions based on the Drew studies were aimost three orders of magnitude (1,000 fold) higher than tne actual (observed) incidences or iiver angiosarcoma in exposed workers, so these studies are cicartv less consistent with human experience than the studies conducted by Maltoru ana Lee. It is noteworthy that we did not empiov the "body surface area factor ' employed by the U. S. Environmental Protection Agencv for cancer risk extrapolation between rats and humans in our risk estimations. If the surface area factor had been employed, the predicted risks wouid have increased by a factor of approximately 5-6 fold for rat to human extrapolations (or 12-13 fold for mouse to human). Inclusion of the surface area factor in the PBPK based risk estimation for VC wouid dearly have made the risk estimations we produced less consistent with the reported" incidences of angiosarcomas in the exposed workers. Discussion A multispecies PBPK model capable of quantitatively describing the metabolic activation of inhaled VC was developed from pharmacokinetic principles and then validated with independent data sets for rats, mice, and humans. Only minor modifications of the model described bv Ramsev and Andersen (1984) for inhaled styrene were necessary to accomplish this. VC is metabolized in mammais by the cytochrome P450 enzymes (likely by the 2E1 subclass) to produce reactive, short-lived intermediates (chioroethvlene oxide). These reactive intermediates aikylate DNA and are genotoxic (mutagenic) to both bacterial and mammalian ceils. The reactive metabolites of VC are generally assumed to be responsible for the induction of angiosarcomas and other tumors in mammals exposed to VC. Since these intermediates are too short-lived (reactive) to circulate in the blood stream very far from the organ of their formation, the carcinogenic effects of VC on a particular organ svstem is assumed to be related to _____________________ -151- Manu A398 (Revision i________ ___________ Reitz et ai. CMA114470 Pawls I the rates of metaboiic activation occurring m that organ. We estimated, the rates of induction of liver cancer in various species under different exposure regimens by using the PBPK moaei to predict the rates or metabolism m the iiver of the treated animals. Tumor induction in Rats The resuits presented in Figure 5 indicate that accurate predictionftof. the risk of developing angiosarcoma must consider the dose dependency of VQJjpetaboiism. When risk assessments are based on the concentration of VC inhaled^ky the animals (instead of the amount of reactive metabolite formed by the animals) the predictions deviate widely from incidences observed by Maltoni and others. For example, ::' a risk assessment were prepared from a cancer study which contained only high doses or VC (i.e. doses where metabolic activation was saturated), extrapolation to low doses wouid significantly underestimate the incidence of tumors in rats (shown by the dotted line in Figure 5). On the other hand, if risk estimations were based doses of VC below the level of metaboiic saturation, linear extrapolation to high doses wouid greatly overestimate the incidence of tumors in rats exposed to high concentrations of VC. .\s Gehring et al. (1979) pointed out, basing risk estimation on VC metabolites instead of VC ifself produces a consistent estimate of carcinogenic potency across the entire dose range (Figure 5). Tumor Induction in Mice In addition to increasing the reliability of high dose/low dose extrapolations, PBPK models provide an scientific basis for extrapolations between different species, considering pnvsioiogicai as weil as metaboiic differences. Since VC has been extensively studied in the mouse as well as the rat, this provided an opportunity to test the ability of the PBPK model to accomplish interspecies extrapolations. Mice, are generally known to contain higher levels of the cytochrome P450 enzymes than either rats or humans and this is reflected by the higher rates of in vivo metabolism seen in mice versus rats for the substrates listed in Table 2 (CH7CI2, CHCI3, VC). Based on this knowledge, mice wouid be expected to be more sensitive to the tumorigenic effects of exposure to a given concentration of VC than rats, and this has been widely verified (Maltoni et al.. 1974; Lee et al., 1978; Drew et al., 1983; ECETOC. 1988). The RSD's (1 x 10*4 lifetime risk) calculated for the different species/strains of mice were: [Manii a398 (Revision i -152Reitz et al. CMA114471 sin Maltom irar potency)................................................................... ........... 0.177 Maltom (Swiss mouse potency)....................................................... --0.0797 LeetCD-1 mice;........................................................................................ 0.120 Drew iB^C'.ri mice).......................................................................... --0.0032 It is noteworthy that the duration or the mouse experiments differed from those or the rat; Maltom s experiments in rats were entire lifespan" (generally > 100 weeks), while Maltom s experiments m mice were terminated at 81 weeks of age. In the case of mouse studies conducted by Lee ec al. and Drew et al.. all animals had either been sacrifiea or had died by 52 weeks of age tLee et al., 1978; Drew et aL, 1983). Thus it might be argued that if the mouse experiments had been of longer duration, higher cancer potencies ror mice might have been calculated for that application of a "less than lifetime correction tactor was warranted, reducing the similarity of the RSD values in rats and mice). However, since the aumors or at least one study (Drew et al.) attributed theeariy mortality to ... induction or neoplasms <tn the treated animais> it is not dear that application of a factor intended to correct for ioss of animals from nonnepplastic causes before they had a chance to develop cancer would be appropriate. In any case, the incidence of angiosarcoma was very high in the Drew et al, and Lee et al. studies [7710 and 45% respectively), so holding the animals for another year could not have increased the tumor incidences by more than a factor of two. The mouse studies of Maltom. bv contrast, were nearly lifetime studies (81/104) so that only a small "less than iifetime correction factor would have been required (-2 fold). Thus, with the exception or the RSD estimated from the Drew et al, (1983) data set, the estimated cancer cotencies in rats and mice are remarkably close. This * suggests that when the pnvsioiogicai and biochemical differences in rats and mice are property considered, these species have similar sensitivities to the carcinogenic action of VC metabolites and provides support for the hypothesis that reliable estimates of human iiver cancer can be produced by this technique. The reason for the discrepancy in potency factors derived from the Drew et al. study is not dear, since even within the same species (mouse) and experimental paradigm 112 months exposure, tumors evaluated at or before 12 months; Lee et aL, 1978, and Drew et al.. 1983) dramatically different potencies were obtained. One possibility is that diagnostic criteria in this bioassav may have differed from those employed by other investigators, since angiosarcomas of the liver (a rare tumor) was not reported in any of the control mice from other groups but were reported in 2-5% of the control animais at NTP. This possibility could be evaluated by an expert committee of veterinary pathologists with access to slides from the archives of the different organizations. Manu a398 (Revision) -153Reitz et al. CMA 114472 rate 17 1 It is aiso possible that the reiativeiv high background incidence of liver tumors in the B<sC3?i mouse has maae it abnormaiiv sensitive to the influence of liver carcinogens such as VC. This suggests that rodent strains with high background tumor incidences may not ce good moaeis to use when estimating human risk (if humans nave much lower background incidences). In any case, as wiil be discussed later, the results from Maitom s and Lee s grouDs appear to be much more consistent with the data from numans exposed to VC than the results of Drew et al. (19831. Comparison t)f Potency Factors (PBPK and Conventional) Maitom s studies on VC carcinogenicity in rodents probably are the most extensive animal carcinogenicity data set in the world and were chosen as the most appropriate basis for estimations of human risk. Using the potency factor previousiv calculated for rats, u is possible to calculate the "unit risk" for humans continuously exposed to VC. The fitted dose response curve indicates that lifetime exposure to 1.77 x iU'-5 mg equivalents of VC metabolites /day/liter of liver tissue is associated with an increase in iiver cancer risk of 1 x IQ*6 (maximum iikelihood estimate: MLE). The 95% lower confidence limit on dose far this risk would be 1.40 x 10-3 mg equivalents of metabolite per day per liter of liver tissue. It may be calculated with the PBPK model for humans that continuous exposure to 0.869 ppD of VC would be predicted to increase lifetime cancer risk by one in a million (MLE), or that continuous exposure to 1 jig VC per cubic meter would increase lifetime cancer risk by 4.51 x 10*7 (MLE). The corresponding 95% upper confidence iimits (UCL) obtained from CLOBAL83 are 0.687 ppb (for one in a million risk) or 5.70 x 10-7 increase m lifetime excess risk for continuous exposure to 1 jig VC/cubic meter. The numbers calculated with the PBPK model may be contrasted with the value reported in HEAST (1995). In each case the caiculations represent the UCL for excess lifetime risk associated with continuous inhalation of 1 jig/m^ of VC; HEAST Value .......................................................................8.4 x 10'5 risk PBPK Based Value................................................................5.7 x 10*? risk Thus the value calculated from the PBPK based approach described here suggests that the potency factor currently listed in HEA5T should be reduced approximately 147 fold. In performing a risk estimation such as this one, there are many points where use of different assumptions/data (e.g., type of tumor modeled, selection of most sensitive species/bioassav as sole source of data, application of "less than lifetime correction factors, etc.) can impact the cancer potency factor. Nevertheless, since PBPK modeling predicts roughly an order of magnitude less VC metabolism in humans than rodents at equivalent atmospheric concentrations and does not ________________________ Ntanu *398 (Revision) -154Reitz et al. CMA 114473 - inciude a surface area correction' factor predicting that humans are always more * sensitive than rodents bv another order or magnitude, changes in these two factors appear to account for most of the differences itwo orders of magnitude) in the two risk estimations. The HEAST value is taken rrom a current issue of the EPA publication, but the entry for VC bears the note that the recommended values "... do not incorporate considerable information tnat is now available." The Office of Health and Environmental Assessment goes on to state that "One unpublished physiologicallybased pharmacokinetic model prediction results in a 100-fold increased risk (emphasis added)." If the EPA were to increase the value in HEAST by 100 fold, then the procedures outlined here wouid differ from those in HEAST by 14,700 fold (more than four orders or magnitude). Comparison with Human Epidemiology It was noted above that considerable variation exists in the potency factors available for estimating the incidence of angiosarcomas in human populations exposed to VC. One of the most important questions, therefore, is: "Which of the alternative potency factors gives the most accurate description of the actuai human experience?" To answer this question, we have consulted the epidemiological literature generated on VC during the past 30-10 years. AU of these studies, share, to some extent, the common problems of not having complete follow-ups for the total lifetimes of the individuals, the possibility of missing a tumor when another cause of death is present, imprecise measures of exposure, etc. ,\fter surveying the avilable literature, ive chose to compare our predicted risks to data gathered by Simonato et al. (1991). This epidemiology study was chosen because we believe that it represents one of the most robust analyses available, both with regard to the number of individuals followed and the quality and length of follow up procedures employed. A weakness in this database is the absence of a precise measure of the magnitude of VC exposures in the workplace. However. Simonato et al. (1991) have attempted to characterize the magnitude of occupational exposure by subdividing workers into groups based on their ppm.vears of exposure (calculated as years on the job times TWA ppm levels estimated to be present in the occupational setting during hours of work = ppm.vears). This grouping permited simulation of worker exposures with the PBPK model. The reader is reviewed to Simonato's manuscript for further details of the exposure estimations. Manu a398 (Revision) -155Reitz et at. CMA 114474 PW19 | Simonato et al. had 21 cases or liver cancer m rheir cohort. The overall incidence of liver cancer was statisticaiiv different than expected, and the odds ratios as high as 45:1 were observed in some of the groups with the longest duration of exposure and highest exposure concentrations iTable 9 in Simonato et al., 1991). For the purpose of this comparison, we selected a suDgrouo of workers with more than 25 years since first exposure, subdivided by Simonato et al. into four exposure categones: (1) < 2,000 ppm.vears. (2) 2,000-5.999 ppm.vears, (3) 6,000-9.999 ppm.years, and (4) >10,000 ppm years. Although this exposure information is obviously imprecise, it allowed the caicuiation of a roughly equivalent exposure paradigm in Table 5 so that we could predict the approximate tumor incidence in the groups studied by Simonato to compare with the results he reported. For example, in the subgroup estimated to have the lowest exposures by Simonato (0*2.000 ppm.vears!. the "reported" incidence of angiosarcoma was 6.2 per 100.000. In contrast, the risk assessment procedure described m this manuscript gave a maximum likelihood estimate i.MLEj of between 138 and 736 cases per 100,000 for ppm.vears between 500 and 2.000 (Table 5). Thus the PBPK model predicted almost two orders of magnitude more cancer cases than actually occurred. Similarly, individuals with 2,000-5,999 ppm years had a "reported" incidence of 42.2 cases per 100,000, while the PBPK based procedure estimated the incidence in this group to be from 700 to 1.500 cases per 100,000. A similar disparity existed for the two most highly exposed groups from Simonato et al. (153-280 cases per 100,000 versus 1,500 to 4,000 cases per 100,000 predicted by the PBPK based extrapolation. It is noteworthy that in the higher exposure group, the degree of overprediction by the PBPK procedure seems to decrease (from almost two orders of magnitude overprediction to approximately one order of magnitude: Table 5). It also appears that the degree of overprcdiction (excess conservatism) is greatest at the iowest'rates of VC exposure (below o,000 ppm.vears m Table 5). It should be noted that a large fraction of the cohort from Simonato is still alive, so it is possible that more tumors may be added to the 24 already reported. Nevertheless, in view of the long follow up time in the subgroup selected for comparison, it is considered extremely uniikelv that the incidence will double even when ail the workers are followed to the end of their natural lives. Consequently, it appears that risk assessments based on estimates of the amounts of reactive metabolites of VC delivered to the liver of the target species (calculated with a PBPK model) still significantly overestimate the potential of VC metabolites to induce iiver cancer m humans. Since the PBPK has been well validated in several species, we do not believe that this is because the PBPK model has overpredicted the formation of VC metabolites m human liver. Rather, it appears that the livers of humans are less sensitive to the carcinogenic effect of reactive VC metabolites tne livers of the commonly used inbred laboratory rodents. Manu a398 (Revision) ________________-156-_________________ Reitz et al. CMA 114475 Page20 | The reasons for this lower sensitivity of human livers to reactive metabolites are not dear, out it has been notea that ionger lived species such as humans have higher ieveis of DNA repair enzvmes than rodents. Thus production of a genotoxic lesion m humans may not nave me same adverse consequences as in the relatively DNA repair-deficient rodents. A vanetv of other explanations are also possible, and cleariv further researcn wiii be required before it is possible to choose between the different possibilities. In summary, the proceaures we have described here (based on a quantitative description of the metabolism of VC in different species and a well characterized oncogenic response to VC in different species ) suggest that current estimates of the carcinogenicity of VC basea on rodent studies significantly overestimate its oncogenic potential in humans. Furthermore, there nas ocen considerable discussion as to whether it is appropriate to inciude a -unace area factor ' when using a PBPK moael to extrapolate the results or roaent cancer studies to humans. We believe that the resuits of these studies suggest that inclusion of such a factor m a PBPK based risk assessment cannot be justified on either pharmacokinetic or pharmacodynamic grounds. References Andersen. M E., Cargas, M L. and Ramsey. j.C. (1984V Inhalation Pharmacokinetics: Evaluating System Extraction. Total m Vivo Metabolism, and the Time Course of Ensvme induction for Inhaled Styrene in Rats Based on Steaov-State BIoodiAir Concentration Ratios. Toxicol Ann! Pharmacol a 176-187. Andersen. M E., Cleweil. H.f, Careas, M L.. Smith. F A., and Reitz, R.H. (1987) Thysioiogically-based pharmacoicinetics and the tisk assessment process for methviene chloride. Toxicol A opt. Pharmacol 87 185-205 Andersen, M'E, Cleweil. H.J., Cargas, M L.. MacNaughton. M.G.. Reitz. R.H., Nolan, R.J., and McKenna. M.J. (1991). rhvsioiogicallv based pharmacokinetic modeling with dichlofomethane, its metabolite. Carbon Monoxide, and blood Carboxvhemogiobin in Rats and Humans. Toxicol. Aopl Pharmacol.. 108. 14-27. Andersen, MI, Cleweil, H.J. III. Mahle. D.A., and Gearhart. j.M. (1994) Gas uptake studies of deuterium isotope eifects on dichioromethane metabolism in female B^CjFi mice In Vivo. Toxicol. Appl. Tharm., 113, 15S-165. Baretta. E.D.. Stewart. R.D., ana Mutchler. J.E. (1969) Monitoring exposures to vinyl chloride vapor Breath analysis and continuous air sampling. Amw Inrluxt Hygiene Asor loumal. jSL 537- 544. Buchter. A . Bolt. H M,, Fiiser, | . Coereens. H.W., Laib, R J, and Bolt, W. (1978). Tharmakokinetik and karztnogenese von vmvichlond abreitmedizinische nsikobeurteilung. Verh Dtsch Ges. Arbeitsmed.. 18. 111-124. Manu x398 (Revision) -157-__________ ____ Reitz et ai. CMA 114476 nm 2H Corlev. R.A.. Mendraia. A M.. Smith. F.A.. Staats, D A.. Cargas. M L., Conollv. R.B. Andersen, M.E.jna Reitz. R.H. (1990) Development m a pnysioioeicailv-basea pharmacokinetic based model for cnlorotorm i~Pxiroi. Amt Pharmaroi. 103. 512*327. Creecn. I.L.. It M.N. lohnson i 1974), Aneiocarcoma or the liver in the manufacture or PVC. I Dmm. Med.. 150-151. Drew. R.T., C.A. Doorman, i K. Haseman. E.E. McConnell. VV M. Busev. it I.A. Moore < 1983) The effect of age and exposure duration on cancer induction by a known carcinogen in rats. mice, and hamsters. Toxirm Acpt Pharm.icoi, ^ 120-130. ECETOC (1988), Technical Report No, 31 The mutacenicitv and carcinogenicity of vinyl chloride: A historical review and assessment. ISSN 0773-8072-31, Orussets. Belgium. Cargas, M.L, Andersen, M E. ana Clewell. H.|. III. (1986). A physiologicallv-based simulation approach for determining metabolic constants from gas uptake data. Toxicol Ann! Pharmaml. flfi, 341-352. Cargas, M L., Durgess. R I, Voisara, D.E., Cason. C.H., and Andersen. M E. (1989) Partition coefficients of low molecular weient volatile chemicals in various liquids ana tissues. Toxicol Ann!. rhar.imr. 25.'87-00 Cargas, M L.. Clewed. H I III. ana Andersen. M E. il000) Gas uptake inhalation techniques and the rates or metaoolism oi chloromemane. chloroetnanes. and ehloroetnvlenes in the rat. Inhalation Toxicology 2 295-319. Gehnng, P J. r.C. Watanaoe. it C.N. Park (1978) Resolution of dose-response toxicity data for chemicals requiring metabolic activation. Toxicol. Arpl Pharmaeool. 44. 581-591. Guengerich, FT. Sc P.C. Watanabe (1979) Metabolism of (14C) and (36Q)-labeied vinyl chloride in ma and io_VUrg Piorhem Pharmacol. 21 589-596. Guengerich. FT., Kim. D.H., and Iwasaki. M. (1991) Role of human cytochrome P-4501IE1 in the oxidation of many low molecular weight cancer suspects. Chem Res. Toxicol.. 1 168-179. Health Effects Assessment Summary Tables (HEA5T. 1995) United States Environmental Protection Agencv. Office ot Solid Waste and Emergency Response, 9200.6*303 (95*1), ETA/540 R-95/036, rB95-92I199, May, 1995. Howe. R.D., (1983) GLOOAL83: An experimental program developed for the U.S. Environmental Protection Agency as an update to CLOBAL82. Howe, R.D., and Crump, K.S., (1982) GLODAL83: A computer program to extrapolate quanta! animal toxicity data to low doses (May, 1982). OSHA Contract No. 41USC252C3. International Commission on Radiation Protection (1975). Report of the task group on Reference Man, ICRr Publication 23, (W. S. Snyder etai. eds), Pergamon Press, New York. Kappus. H , H.M. Dolt, A. Ouchter. Sc W Dolt (1976) Liver microsomai uptake of 14C-VC and transformation to protein aikyiating metabolites in vitro. Toxicni. Ann!. PharmarnnL 2Z 461. Lee, C.C. Bhandari. 1C, Winston. j.M., Jouse. W.B., Dixon. R.L., and Woods, I S. (1978) Carcinogenicity of vinvi chloride and vinyiidene chloride. I Tnxirol Fnvir. Hlth . 1 15-26. Maltom. C. (1974) "Vinyl Chloride Carcinogenicity: An Experimental Model for Carcinogenesis Studies.", monngrapn from the Institute of Oncology and Tumour Center, Bologna, Italy 40138. Maltoni. C, C. Lefemtne. P Chieco, Sc D. Carrettu (1974), Vinyl chloride carcinogenesis: Current results and perspectives. Med I tv.. 5,421. Muller. C., Spassovski. M., and Henschier, D. (1974) Metabolism of trichloroethylene in man. 11. Pharmacokinetics of metabolites. Arch T.'xirnt 22, 283-295. |Manu a398 (Revisioni .is*. Reitz et at. CMA114477 HEID National Acaaemv or Sciences 119871 Tharmacorcinetics in Risk Assessment '. Veil 8 Drinirtrur Wmw and Hv'iith. National Academv Press. vVashington. DC. Nlakauma. T . Wane, R S.. Muravama. N . and Sato. A., (19901 Three torms of trichloroethylene* metabolizing enzvmes in rat liver induced bv ethanoi. phenoparbital. ana 3-methvicholanthrene. Taxicm lant. Pharmnco*, 6449-6455. Raucv. j.L.. ! C. Kraner. k I.M Lasker (19931 Bioactivation or haloeenated hydrocarbons by Cytochrome P4502E1. OirirM Rpyaw* in Tpvirntpnv. 23. 1-20. Ramsey. J R. and Andersen, M E. (19841. A physioioeicailv based description of the inhalation pharmacoxinetics or styrene m rats and humans. T.>ximl. Ann! Pharamcnl 21139*175. Reitz. R.H.. McDougai, J.N.. Himmeistein. M.W., Nolan. R.J. and Schumann. A.M. (1988V Phystnlogicailv-based pharmacokinetic modeling with methvichloroform: Impiicattara far interspecies, high dose/low dose and dose/route extrapolations. Toxicol Arpl. Pharmxrr^ <M. 1SS199. Reitz. R.H.. Mendraia. A.L ana Guengench. F.P. (19891 In Vitro Metabolism of Methviene Qilonde m Human and Animat Tissues: Use in Phvsioioeicaiiv-Basea Pharmacokinetic Models. XoiicnL Anpl. P-^rmaroi 2, -0-246 Reitz. R.H.. Mendraia. A M.. Guriev, R A.. Quast. I P , Cargas, M L. Andersen. M E.. Staats, D.A., and Conotlv. R.D.. (1990al Estimating tne risk of iiver cancer associated with human exposures to chlorororm using physiological Iv based pharmacokinetic moaeiing. Toxicol. Vnc^f Pharmacol lQi 44A-459 Reitz, R.H., McCroskey, r.S,, Park. C.N., Andersen. M.E., and Cargas. M.L, (1990b) DeveiopiMnt of a physiologically based pharmacoxinetic model for risk assessment with 1,4-dioxane. Toirimt. Appl. Chaimacoi, lfll 37-54. Simonato, L,, L'Abbe. K.A., Andersen, A., Belli. S., Comba. T., Enghoim. G.. Ferro, C., Hagmar, L, Langard. Lundberg, 1., Terastu. R., Thomas. P., Winkeimann, R.. and Saracci, R. (1991) A collaborative study of cancer incidence and mortality among vinvl chloride workers. SeandL L Work Environ Health. 17. 159-169. Sato. A , k Nakajima. T. (19791 Partition coefficients of some aromatic hydrocarbons and ketones in water, blood, and oil. Drit. I !nd MpH 231-234. Viola. r.L. (1970), Pathology or vinvi chloride. Med I .v/.. 61. 174. Viola, P.L.. A. Bigotti. and A. Caputo (1971) Oncogenic response of rat skin, lungs, and bones to vinyl chloride. Cancer Be 2\, 516-522. Watanabe. P G., C.R. McGowan. E.O. Madrid, k P.J. Gehring (1976) Fate of 14C-vinyi chloride following inhalation exposure in rats. T.ndmi Appi Pharmxrnnl 1?. 49-59. [Manu a398 (Revision! -159Reitz et at. CMA 114478 Page 23 FiCUTCF LEGENDS Figure i: Predicted (solid line) and observed (open symbols) concentrations of vinyl chionae in a 9.1 liter recirculating exposure cnamDer containing 3 maie rats (Figure ia) or 3 female rats (Figure lb). .Figure 2: Predicted (solid line) and observed (open symbols 1 amounts of radioactive metabolites derived from exposure of maie rats to the indicated concentration of 14C-vinyl chloride gas tor o hours. Data taken from Watanabe et al. (1976). Figure 3: Predicted (solid line) and observed (open symbols) concentrations of vinyl chloride in a 9.1 liter recirculating exposure chamber containing 14 maie mice (Figure 3a) or 14 female mice (Figure 3b) with vaiues of VMaxC and Km calculated from in vitro studies (VMaxC 9.04, Km * 0.04). Figure 3c shows the same data for 14 male mice after computer optimization of VMaxC and Km (VMaxC - 8.13, Km - -.).2S). Figure 4: Predicted (solid line) and observed (open symbols) concentrations of vinyl chloride exhaled by human subjects following 7.5 hours of exposure to vinyl chloride concentrations of 59, 261, or 492 ppm. Data are taken from Baretta et aL, (1969). Figure 3: Predicted (solid line) and observed (open symbols) incidences of liver angiosarcoma in rats following exposure to various concentrations of vinyl chloride for 4 hr/ day, 5 days/week, for 12 months (animals held until death for observation of tumor incidence). The dotted line represents the type of risk extrapolation that might have been prepared by EPA if the only data available for VC had been from two high VC concentrations but does not correspond to the actual EPA risk assessment (HEAST, 1993). Data are taken from Maltoni et aL, (1974b). |Manu x398 (Revision i -160Reitz et ai. CMA 114479 Footnotes 1 RHR Consulting durvices. Midland. MI. ** McLaren/Hart. ChemRisk Division. Cleveland. OH. ^ 1CF Kaiser, K. S, Crump Division, Research Triangie Park, NC. 4 Zeneca Central Toxicology Laboratory, Macciesfield. ENGLAND 5 Simuoolv is a registered trademark of the Dow Chemical Co. 6 To receive a copy of the source code, please send a self-addressed stamped envelope. If a copy on magnetic media is desired, please include a formatted 3.5* DOS diskette with vour reauest. I Menu A398 (Revision) -161Reitz et at. CMA 114480 Paw 25 1 Table 1 Parameters used in the pnvsioiogicailv basea charmacokinetic model for vinyl chloride for Humans. Rats, and Mice. Aiveoiar venniation and cardiac output are calculated from the aiiometric constants bv muitioivmg the constant bv the body weight i.kg) of the ammai raised to the 0.74 power. \rMax is calculated from the aiiometric constant VMaxC by multiplying the constant bv bodv weight raised to the 0.70 power. WEIGHTS (or Body Weiahc) Liver Rapidly Perf. Slowly Perf. rat "LOWS 'Mlcmecno 'Tcnscnr.cO: Aiveoiar VentiiuEtcn Cardiac Output HUMANRAT MOUSE 3.14% 3.71% 62.1% T2 .1% 2.53% 5.0% 76.47% ^ 0% 5.86% 5.0% 76.14% 4 . 0% IS 18 28 15 13 28 Liver Rapidly Perfused Slowly Perfused Fat PARTITION COEFFICIENTS Blood/Air Liver/Air Rapidly Perfusea/Air Slowly Perfused/Air Fet/Air METABOLIC CONSTANTS vmexc (Allomuici Km (ma/liter*- % nf Oardij? C'-itPUt 24.0% 52.0% 19.0% 5.0% 24.0% 52.0% 19.0% 5.0% 24.0% 52.0% 19.0% 5.0% 1.16 1.60 1.60 2.10 20.0 1.68 1.60 1.60 2.10 20.0 2.41 1.60 1.60 2.10 20.0 3.97 0.04 2.75 0.04 8.13 0.28 -162- CMA 114481 Table 2 In vivn metabolic rate constants tor the PB-PK model for vinyt chloride were estimated from data reported by Andersen et al. (1987 rats 6c mice: 1991 humans; for metnytene cnioriae and Coriev et al. (1990) for chloroform. Published in vivo maximum rates t\Maxi of oxidative metabolism icataivzea bv P450 enzymes) and histone organ weight data from subchronic studies at Dow Chemical Co. were used to calculate the VMax/ kg or liver i VMax/ VL). Then me characteristic interspecies ratios of VMax/VL for oxidative metabolism of these typical halogenatea hydrocarbons were used to estimate the in vivo VMax s for VC in mice and humans. Methviene Chloride: Body Wt (kg; Percent Liver Liver Wt (gj VMax tmg/hr) Ratio to Rat Chloroform: Body Wt (kg) Percent Liver Liver Wt (g) VMax (mg/hr) Ratio to Rat Vinvi Chloride: Body Wt (kg) Percent Livet Liver Wt (fljjpgT Ratio to Rat (AvIfP* VMax (mg/hr) VMaxC (aiiometric) Rat 0.233 2.33% 5.895 1.500 i.ooo- 0.230 2^3% 5.819 2.431 1.000 0.225 153% 5.69 1.000 0.968 2.75 Mouse Human 0.0275" 5.86% 1.612 1.054 Z570 83.0 3.14% 2606 138 0.208 0.0285 5.86% 1.670 1.889 2.707 0.0285 5.86% 1.67 2.639 0.749b 9.04 70.0 3.14% 2198 0.208 77^ 3.97 4 Andersen et ai. (1987) listed 34.5 g as the body weight for mice in their Table 1 since this was the body weight for the mice in the NTT bioassay of methylene chloride and their PB-PK model was used for risk assessment. However, the average body weight of the mice used in the gas uptake studies was actually 273 grams and this body weight is used to calculated the VMax/VL ratio. b Calculated by multiplying the average mouse or human RATIO of VMax/VL's to rat (methylene chloride ana chlorotormi, the ia vivn VMax/VL value for VC in rats, and the VL for mice or humans. -163CMA 114482 Incidence or angiosarcomas or the liver observed in Sprague Dawiev rats. Data are from Experiments BT1, BT2, BT9. = BT15 conducted by Caseare Maltoru 11974a,b). Data are given ns # angiosarcomas/ ff animais examined for maies. femaies. and combined males and females. Control arumais from several exDenments are combined in the 0 4 ppm group. Animais were exposed 4 hr/ dav, 5 days / week for 52 weeks and then held until they died (typically at ieast another yean. Tumors were scored at the time of death. Exposure Concentration iPPM) 0 1 5 10 25 50 100 150 200 250 500 2500 6000 Males 0/173 0/58 0/59 0/59 1/60 2/174 0/60 1/60 7/60 1/29 0/30 6/30 3/29 Females Males + Femaies 0/239 0/60 0/60 1/60 4/60 13/180 1/60 5/60 5/60 2/30 6/30 7/30 10/30 0/412 0/1181 0/119* 1/119 5/120 15/354 1/120* 6/120 12/120 3/59 6/60 13/60 13/59 i Eliminated from CLQBAUU analysis because of mathematical limitations of the I'C version of the computer fitting program (only 10 dose/ response groups alloweal -164- CMA114483 Incidence of angiosarcomas or the iiver observed in Swiss aibino mice. Data are from Experiment BT 4 conducted by Caseare Maitoni 11974a,b) and summarized in ECETOC. 1938. Data are given as * angiosarcomas/# animais examined for maies. females, and combined maies and females. Animais were exposed 4 hr/day, 5 days/ week for 30 weeks and then neid unni tthev reached 81 weeks of age. To calculate the dose surrogates for mice, the PB-PK model was configured according to Table 1 and a 4 hr exposure with 20 hours exposure free was simulated by the model. The simulated values of the dose surrogate were converted to lifetime average daily doses by multiplying by 5/7 (days / week) and 30/104 (fraction or lifetime exposed). Potency values were estimated with GLOBALS3 as described in the Methods section. * Exoosure Concentration iPPM) 0 50 250 500 2,500 6,000 10,000 Males 0/80 1/30 9/30 6/30 6/29 2/30 1/26 Femaies Males + Females 0/70 0/30 9/30 8/30 10/30 11/30 9/30 0/150 1/60 18/60 14/60 16/59 l3/60> 10/56 PB-PK LADD 0 38.4 173.1 265.2 331.0 -- -- J Eliminated from dose response regression because of the likelihood of poor survival at this dose. -165- CMA 114484 Table 5 Lifetime Average Delivered Doses < LADD's) of VC metabolites in humans exposed to VC for 5 davs/ week, 50 weeKS/ vear. tor the indicated numbers of years. The LADD's are calculated from the PB-PK moael for humans constructed as outlined in Methods, correcting tor the fraction of a vear exposed (50/521 and the fraction of a lifetime exposed f 10,20, or 30/70), Estimated lifetime risks (incidences/100,000) predicted for these exposures based on the rat potency factor are obtained from the GLOBALS3 computer program (specifying the Maximum Likelihood Estimate, NOT the 95% upper confidence limit). Observed cases per 100,000 at different levels of exposure (cumulative ppm.vears) for the grouts having more than 25 years since first employment are obtained from Table 10 of Simonato et al,, (1991). Years PPM Exposed Ten Years Exoosure 50 100 200 -- 500 -- 1000 -- 2000 10 10 10 -- 10 -- 10 -- 10 Twenty Years Exoosure 50 100 200 -- 500 -- 1000 2000 20 20 20 -- 20 -- 20 20 PPM Years 500 1,000 2,000 4,000 5,000 8,000 10,000 >10,000 20,000 1,000 2,000 4,000 8,000 10,000 15,000 20,000 40,000 PB-PK LADD 333 6.63 13.06 -- 26.68 -- 3138 -- 36.03 6.66 1336 26.11 -- 5335 -- 6237 72.07 PB-PK Prediction per 100.000 Observed Cases per 100,000 188 374 736 -- 1.497 -- 1,753 -- 2332 -- (63)' -- 423 -- 1523 -- (280.0)b -- 376 747 1,465 -- 2,971 -- 3,476 3,993 (63)* -- 423 1523 (280.0)6 J Croup listed as having <2,000 cumulative ppm years by Simonato et al,, entered at 1,000 ppm.yean for comparison. b Croup listed as having >10,000 cumulative ppm.years by Simonato et ai,, entered between 10,000 and 20,000 ppm.vears for companson. -166- CMA 114485 'I a. Chamber Cone (ppm) -167- CMA 114486 n lh Chamber Cone (ppm) -168- CMA 114487 b -) 1 Mg Equivalents -169- CMA 114488 f *\ 7 a fl Chamber Cone (ppm) TImo ihr) -170- CMA 114489 Chamber Cone (ppm) 7 fl ; J CMA 114490 -171- Chamber Cone (ppm) -172- CMA 114491 1T Tumor incidence 10 100 1000 PPM Vinvi Chloride 10000 -174- CMA114493 ItUUU V 1-u fflUniW H.S./.A CONSIDERING rEARMACaSKTHC AND MECHANISTIC CtTORMATTON IN CANCER SISK ASSTSSMBflS FOR ENVIRONMENTAL CONTAMINANTS: HCAMFLES WTTH VINYL CHLORIDE AND TEICHLOROETEYLEffi H. J. Ckweii*. P. R. Gentry, J. :.L Garnn. 2. C. Alien. K. S. Ciwno Gratis. iCT Raiser iraermriond Ruson. Louisiana 7IT70 USA Anassa ABSTRACT Risk assessments tor vinyl -nnfi (VC) ana tndtiorectnviene iTCEl as presented a examples of appimeass tor tnesrmaoay ehaaicu-speaxis -mri information into a mate tcanttnally plausible cancer risk assessment. For VC, tbs ragawiag ittooc of action moan of a meaoaiite wits DMA. reauidag in DMA and misaanscnotion. and ernss- of a me minor type. Risk at mutes for human to VC prammed with a ptipinbuinll) onaiTTUcnJunsik (PBPK) mead and the tiaarsad (IMS) tnedd wets lower than those amd in environmental dcrision-maxiiiy by a factor of 10 to iQ. and were mote consistent with hTMTM epdcmiotoyicai data. For TCE. iDae is oitlcace of tneBssd ceil pretiiemxion due to receptor i"1'""" or eymtoxieity in every irmaaea in which tumors axe omciveu. and the tumors typicallv 111 sn inasa in the - incidenee of a commonly observed, ipscies-ioeeiftc lemon. vimmiiy sate enaosuis estloiniss for human 10 TCS craaicicP with a PBPk mood and a marysn of exposure fMCE) approach were hifher tnan thorn oamiaed by the conventional UUS appmaen py reuyniy a laanr of 100. The MCE asomaen is resetmessssd ax aa slternauve to tne LM5 aopioacn for enemiots wnn a eaismosetue moae of action wmch entails ineteasao edl prati/cration. isaamt to the asnesuen of a highly rtotuinsr INTRODUCTION Assessing me ootemiai risk associated with human uoosura to caratnoyente environmental contaminants represents an uneomtonahie admixture of tricntiric evaluation ana political policy, with the potential for enormous impact on ootn the puoik health ana the economic weii-beint of the nation.- Tlis pnneioal challence fades canor risk assessors toaay is to realistically consider tne unotteaimns of the cnemicoi's tnecnanismis) of eatdaoteddiy -175-- CMA 114494 ceveiootng 2 nix assessment icrrcirr. for 3 camcuar cz.Tru3trr.1c cffsss- i: if becoming maosmgty amkuh to justify ms use gt she mas sianaarn nix assessment anprcacn vitn cnemtcai* mst set utrausn a otrretr naiomtmetic. gssotoxic maerunism. as weti as witn ehemieau for wmeh eannogemcity is mauled by inmsxsl cell protttertion secondary to cvtotoxicity or rcsestar mteraeusn. Mcehanumuceenoem nsk assessment inpreacac are me omy alternative tor maintaining me creatoiiity at gnetrr ootertCY estimates m the face at ,neiBiint tcorustisuse in the undemanding of the meeanums or etrcaiogenieitY. The new atari revutou to me U.S. ZnYironmeauj Protection Agency (U5EFA) guidelines ior carreer nsk (i] waid apperr to provide die fleaibiiity necessary to move forwam m this area. Risk jTMwigm for eitsasicsi carsinogens muss neeeuahiy be iterative in nature. It is in me tunare of setestiitc ineurry mat unaei iisnoing acveioes slowly, as enerncsBai ittformauoa tutumulaics and theories su bo testa and refined. Risk assessments, however, sseot be Mpyuwi indefinitely until an attentate unaerxaaaeg of the earstnogentettY of a parueitar cnemial has oea aenieva. Thoerdre. it is necessary to attestor to periaf me most tcismtncaiiv aefensiotc assessment oosstnie. given tne mtormatton available st mat time, ana to be may to revise tne estimate, reyuiteflly, wnenever important new iruormauon is developed- In dm last few yean idem has ben a signified improvement tn the tevei of unustjuamag regaining cnsmual cueinogenesis in general 2nd the mecnanisms of araaogmueiiy of vinyi ehfance (VC) aaa uissioraeuiyteae (TC3 in parttctiiar. The pmpam '{ the sstey reported here waa to attempt to perform mrr nf the tnrnrr risk assessmems for VC and TCE. using .0 as gist an sot as postsie the itudnuaitoo esmssiy available on metabolism, and arenagents meetantstn of action. . VTNYL C3L0R3PE Whn it oesme evtceni mat VC was oismogenie both in and in- humans, many of its tries nti atsantmuea: me current use of VC U limited to serving as a precursor in the proaucton of such materials as polyvinyl chloride (PVQ ana caooiymer tains. However. VC is ala p--"1--* from tne binrleguaticn of tnriiiorocmytene by bameiia in the mil. Titts past spiiis of cnehietoetnylene may lea to current or future exsanra of the paolie to VC in drinking nte or other mvitonmami media. The tuna potenev csttmates for VC puelithrri by the USEPA do not ouanuzaiiveiy incorporate phanttacokinettc informatma on VC Into tne risk calculations (2]. To provide 3 more agr-n-u* assessment of human risk from exposure to VC, a ptiysiatogicaiiybascd nharmacaemetic <PSPK) model was aavetooed which demriba the uptake, dtsuibtnim tnd meooolism of VC in tne moose, mi. hamster, and hmn following innalauon or oral exposure. Hie PBPK model was used to credit: the total oreoucuon of reactive meoaotites from VC bath in the animat bioasssyt and m human exposure scenarios. These measures of internal exposure were uten used in the linsrized muitisiags (LMS) moeet (31 to predict tne risk annelined with lifetime exsasure to VC in sir or drinking water. -176- CMA 114495 S.-.dence tor ecranefemcim The eareurosenieity at VC has seen weti ciuolithen in iwaa aaiam icecies av i numoer of routes of exposure fl]. C.r the many different tumor types wnich have seen ` m animai bioassays of VC. four are of neater conecrn oecausc tnsy have oeen seen repreoudbly at low concentrations (220 epm ana below i: liver angiosarcoma. hsatoceduiar eremama. neonreoiastoma. ana ciMioar/ >tand adcooearemopra. Of these, two are oaiueuiariy noaoie in mat tnev are teresy sees in umoesa ammau: liver angiosarcoma ano ncc.-.reoiastoma. Grater man exoeetes tncmrnrrt of angiosareoma of the liver have aico been regoneo in a numoer or canons of women oceuoatmtally exoosea to VC Ul* Anytosaicaoa of the liver is conatoem to oe a very rere type of cancer, with otuy 20-30 esses per year rrpotreo in the UJ. (4]. Increased dash due to aTMTM with human VC exposure has also bens leuunea for brain. lung, hematoootettc systems, as well as for outer tissues, out seven! analyses have concluded that liver ingtoaamm show the deatea evidence for sure! assoentidn ana also the highest relative risk (5]. The eotresoonoence across rests: for liver ncmangrooredma is quite smiting ano has made this tumor tns primary foeus for VC risk asscssnents in resent veers. Weraoousm: Eased on tnc enmimuon of VC obzrvso following aoministnooa oy vartous routs of exposure, the mcaoctism of VC appears to oe a cote-cajotoem. tamable process. The ptonerv route of metaoolism of VC Is by the action of the mixed function (MFOI system, now refsren to as Cytodnoare P430 or CYP. os VC to form cniotoetnylene oxide. Gdareeutytene oxide (CEO) is a highly reactive. tI--i liiril emde that rapidly arranges to form ehlornarrialdchyde (CAA). a rsezive o-haiocarnonyi compound (6). The sain detoxifistion of three two meaoolites is conjugation binding with giuoduone (GSH). as by the observenan of demised non-protein sul/hydryl concentraosas at high VC exposure eoneemntions (7], Meeheioim ofearonoyemdrr It has long been a wq of memogenic risk < that the i of carcinogenicity for *;gaotoxic` earemogctu (sometuns raijjrea to as initiators) involves reaction with OKA, lading to misiraassrmiea daring suosemtent edl division, causing a toss or change in henraOic infotmanan whies results in a neoplastic daughter cod. As any as 1971. it was demonstrated that binding of VC to brer maeremoteculs following inhalation exposure of rats ea-m-d wed with both total mcsaOoiism and the i * incidence of angtuvutuma ffl. It was suggested that the oreutogeaictrv of VC was dtts to binding of a : maabolite with DMA iQ^^nmijBem miscoding during eed reproduction. The in vivo formation of fear i DNA sdducts have snm^pb demonstrated following exposure of animals to VC: l..M'-ethreoguaaine: N*J- ethenoguamne: ! ,.*C-etheno-x'-deaxyaaenosine. and 3.N*-heno2*-dcoeyeytidine (9], Three aOfao-addaee are highly persistent and eaa lead to defective tnnsenotion f 10]. Selection of a risk assomtem ooenecn: Based on me information desenBad above on the metabolism snd meenantsm ot earcmogemcixv of VC. it is fleeesary to deteRnine the appropriate appraeh for conouriiitg a human nth assessment. The evidence is strong mat me carcinogenicity of VC is related to the preouetion of -177- CMA 114496 reactive metasouc inermeaiatss. .,-.s most aooruorraie otunnacoKinetic case mesne tor a i" 11 in> mi i imien is :he total amount of the msiaoome senerateo atvioed by tne volume ot' the tissue into wnich it is promt, cU (I IT- 1 :nc cn*e or' VC, . reisonaoie cos: metric for ansiosareams would be oravioed by the total amount ot mcrmolrtm divided by tne votums of the over. The sssumotton unaertvinf tns use of this oose metric is that die concentration of the actual siemosentc motetv. or the extern of the crucial event issnrimai with the cellular transionratton. is imam resales to tms osssioo-concentiauan of reactive intermediates. and that the ii'lmiuiihip of the aouai cammogenic motetv or crucial event to tne dose metric is constant across concentration and spedta. Specifically, the avenge amount generates in a single day is usco. avenges over the lifetime (i.e., the bfeurnu avenge daily dose, or LADD). Tl-.s use of a dose rate, sued as the LADD, raider than total lifetime ntm. has bora found ernotrioily to provide a better cross-ioetnea extnoolation of chemical caisaotenic coteney (12J. Subsequent stem in the earemogeme msenanism rented to specific ***"* formation, detection, and n psir. as well as to the consecuenca of DMA mmnnsenotion ana the potential imoact of inerravri cell oroiifenaoa. taw not yet rsecned me oomt wnere tncy car. oe mcorooratea into a nsk assessment in any quantitative fonts. However, mere coocars to oe sufficient eviaence to iusury the assumotion mat VC sets as a classic initiator, ptoaucing jrretre transformations trupugn direct rooion of its metaoolitss with DMA. There:ore the tradhtaml sssumotton of low-uose iinority of risk appears to be warranted, and the LMS model would seem to be tta mot appropriate approach for low-aose extiaoatatian. Dtser.prion of F5PK maati: The PSFK model for VC in this study is an adaptation of a prerioniy desenoed PSFK mooei for vinyiidene cnioride (13]. Fur a poorly soluble, volatile chemical like VC. only fear tissue compartments are required: a richly perfused tissue compartment which indudes all of the organs t ti |* tta liver, a slowly perfused tissue comeartment which includes ail or the muscle and skin tissue, a fat anpumta which includes ail of the tarty tissues, ana a liver compartment. The pnysioiogical parameters used in tta motal are the current USa?A reference values (U], The mooei assumes tlow.timited kinetics, or venous equilibrating that is. that the tnnsoort of VC between olood and aim is fast enough for steady state to be reached within tae time it is transported througn the tissues in the blood. The partition coefficients are based on in vitro studio whb tisane susoensions (13]. All moaoolism is assumed to "* in the liver, which is a good assumption in OB of the overall kinetics of VC. but wnich woutd have to be revised to target-tissue-specifie metabolism if a serious attemot were to b* mams to perform a VC risk assessment for a tissue other than the liver (l l]. Metabolism of VC is mooclcri by two saiunote oautways: one nigh affinity, low capacity. representing P-*30 2E1. ind one low affinity, high eaoacuv. representing the other P-130 isotvmes <e.g.. ICIl/6 and IAI/T). The parameter; for the two oxidative oatnways in the mouse. hamster, and human were estimated by fitting tta model to oats from etosed-chamoer inhalation exoosutes witn each of the soeexes and streins of interest f 161. In the mooei. the reactve metaoolites praduesd bv these oathways (whether CSO. CAA. or other imermemaissi may then eitner be metabolized further, leading to CO- ream with OSH. or react with other -178- CMA 114497 :;:iular maienats. DNA. 3-nausc exposure to VC lus seen snown to aeoiete ctminimg levels a* CSH. i stmnte asicnouon of G5H kinetics was aiso ineuioed in tns mooei (13]. Initial estimates tor me mntrrnrm maaootum of me reasnver meaoatites ana for me gmtatntone suomooei in the rat were taken from tnc mood far vtnyitdene emoride (13]. These parameter estimates were men refines for me case of VC wire data on ttutahinne dsnietton (17,7], total metaooiism (13], ana CC. dimmauon (19]. The paratneten ootameo for this ooruoe at the mood in me rat were used for the outer spceies wim aepraptuie ailotnetns sealing (i.e.. the fttsi-oraer sue constants were scaled by body werent raiscn to me >1/4 power . Phamaadnerie risk assessment: The mood just aemhded was useo to calculate die pharmacokinetic dam meshes for angiosarcoma in the mast informative of the animal biaassays (20.21,22]. as well as far human inhalation exposure. The 95 % upper confidence limits (UCL4 on tns human risk cuprums for lifetime to I pan per pillion tppb) VC were then oloitotcd on the basis of each of the sets of binassay data, using the LM5 mood, ace the resnuing rtsx estimates are mown in Table 1. Table 1: Human risk estmutes tper mtliion) for tifi-iw... exposure to 1 ppo vinyl chloride in air bund on me incidence of liver angto&reoma in animal btoasssys Antroai Bioassay Study Mahoni a aL Mouse Inhalation (20,211 Maitoni of. Rat Inhalation (20.21] Peren ei at * Rat Diet (22] Maitoni a ai. * Rat Gavage (20.21] 95% UCL Risk / million / ppb Males Fmmues IJ2 307 5.17 2.24 3.05 1.10 S.6S 15.70 The has estimates based on inhalation studies with mica (UxlO* and 3.3x10*) agree very weil with thorn based on inhalation studies with rats (5.17x10* sad 2.24x10*7 . demonstrating the ability of phannaeakinetics to imepjpldcsc-responsc infoimauon across species. The risks estimated from me dietary administration of VC (Urenv and 1.1x10*) are also in good agreement with those ooiaiocd from me innataiion biaassavs. showing good tixue-to-route corresoonaenee of [*" based on the pharmacokinetic dose metrie. However, the estimates based on oral gavage of VC in vegetable oil (5.65x10* and 15.7x10*) are about o*fold higher than either dietary or inhalation exoosure. Incorporation of com oil iota the dies increased the yield of aflamem 3.-induced tumors in rats (23]; a similar pnenomsnon could be responsible far the apparently higher potency of VC when atuninistereo by oil gavage cornearea to incorporation in the diet. -179- CMA 114498 Zpidemtmaticai otanisi in oroef to evaluate tne Plausibility of tne nsns predates on me basis at the intmat asa. nsx calsatmcna were aiso oenormea on tne oasts of the seat available eoioemtoiogieai baa pnarmatsiunetie. numan-oasea rise estgist--. me PSPK mocet was run tor me exposure scenario apprnpiare to seen of the tetecisa itiocanarts from sen of the stuaies,. The resulting internal dose manes were mutimlkti by me acumuimc nutations to oatam me eantuative tntenm dates, wnieb were men moot into tne motive nsx monel, along wim the ootsrvea ano egoar.es liver oaor deaths tor eess subeoboR. to obtain an cuimarr of die carexncrente ootencv. Thee, to eeterenne me mx sssocritrti with a continuous lifetime exposure to l ppb for comoamon with the ansuai resuni. the PSPK moosl was nm for a l ppb continuous exposure and the average daily vaiue of the internai dose marie was raintlurri Using we PS X upper oouno on the irttinatn tor the potency provings a 93X upper eoaridenen limit os the lifetime risk per ppo of vinyl chlariPe for comparison with the anuiui-bateo resits obaisss with the LMS mood. Table 2: Human rtsx aumates iser million} for lifaints mnalstion of 1 ppo vinyr chlonne in air based on tne incidence or liver angiosarcoma in human roteesmotogreal studies Epidffitioio'id Saidy 95% UG. ?isk / million t ppo Fox <k Chllier {14] 0.71 4.22 Jones a aL (251 0.97 - 3.60 Simwotn a aL (251 0.40 0.79 A asmosnson of the remits of the analyses of the litres of data, shown in Table 2,. gives some indication of the conintcncy of the human remits, even before tne campanson wuh the animal prentsttons. It if encouraging mat tne lifetime nsk of liver cancer oer ppm VC exposure *** from tne three snwiies only ranges over about one other of magumioe: from 0.4x10* to 4.2x10*. Moreover, these murrain are in remarkable agreement wuh the cstmatea based on saiaol daa shown in Table 1. However, any confidence produced by this agramee should be temocrea by tbe kvbim4 that raisciassiftotioa of exposure in the human studies tenas to unurrmimate the tree risk at lower oases. .V-ivutrnciess. the agreement of the proratacakmcic animal-based risk estimates with the onarntaeoxinsiic huraan-ossed risk estimates provides strong suppon for the assumotion uses in this study; that crcss-iococs sealing of lifttiree cancer risk can be performed on a dirrex basis of lifetime average daily dose i without applying a body sutxaae area adiussmem) when the risks are based on biologically appropriate dose manes calculated with a validated PSPK model. Canamtonr. Giving priority to tne animal studies most closely approximating the human route of posurn. the pest conservative caimaie of the carcinogens nsk of angiosarcoma from lifetime exposure to 1 pph -180- CMA 114499 VC in ur u i.lxiO*. cr 2.0x10* fug/nvT*. based on mnaiation imoiei in mate mis (20.21]. This vans is consistent -vitn tne onto or estimates from eotoontotogtm suoies or' 0.4xt(7* ro 4.2x10* nil: per ppm VC. but is \ mugnty i ncxar of 20 below me currently puotishea imsistion unit risk of 3.4xl(7* The stood was also uses co mimaie tns oaiiv internal aose for human onnxin- water consumption. The resulting bed conservative a!me of the caicmcssnte ~ix of angtoaieoma from lifetime enoosute to 1 ug/L VC in miiifctog Yater is 1.14x20* Gig/W*. bases on studies wun mare ns of the dietary xoministcuron of VC (22]. This vatoe is rougnly a racer of 50 below tne currently puotishea unit risk of 5.4x10' (mPW- Althcuxn VC has often oest cited as a csamtm for which saainnie metaoolism would be eamiiifimi is the mt *-- conation sopors to become unporaet only very rush exposure levels (poor Oca 230 ppm ov inhalation or 25 mg/kg/day oraiiv) ccmearco to the lowest aimorigcnic levels, ana thus las link on the suaauauve risk estimates. The important camnnation of phaimacnxincuc mooeiing is to provide a t oioloetstiv ptsustnte estimate of the ertesuve aosc: cocai proauatan of reesuve mr-inotices at the target ass The ratio or this bioiottmiv effective boss to tne aamtnisarss aose is not unuoim scross routes ana ipoac There:ott any estimate of sdtntnistersa cose is iess for performing rouie-io-route ana intuiuoLwo exmoatauon of risk. The nsx ifstanaics ootainca for VC hm; tne onannacokineaa aosc metric ass tower i chase ootatnim with eanvenuoaai extsRai dose mediations oy a facar of 30 to 50. ana sopor to oe mas ffonstnrnt with human epidsmtoiogisi data. ISIOLOROEISYLSNE TCS has seen widely uses in inaustry tor many yeats *--*" of its --"yiT" salvem properties and its nomlammaotiity. The ACCS has ie_uuiy announced its intention of classifying TCS into1 a new camatoccsicxcy Siouo. A5 (not nnomm as a nuiuan meinoxen), oases on a weti-conoumso. negative estacmtoiogisl study pemrmea tn an ximrxrt maintenance fasiiity at Hill Air Fetes Ease oy the National **'"---- institute (27.23], Tbs USEPA. on the other head, has for a numoer of yean tegtoatai TC on tns basis of its carewoscarcity, xlthosgb it has wavered berwesa peep 2S (sufficient evidence in inimais) and C (Umned evideoee) in trying to classify the likelihood of rauiiuguiiuiy from TCS (29.3QJI]. However, to 1989 the Intcnrtttonal Agency for Rcsmsh on Comr ctaaified ii_s as a group j astmei eustnogea (limited evidence) (32], ana the USE?A has stoB *3*_' withdrawn me rlatuficatinn of TCS ftsni its SIS dstaoase for consideration. Nevenmtoss. regainless of toe formal clsssifiotien toe USEPA cancer nsk esimates for TCE (30J I], m pm basis of metaooiixcd dose wttn the LMS aodd. have continued to be used for environmental plosion-making since 1933. tn contraa co the ease of VC. toe must ream potency estimates for TCS puoitshed by the USEPA da aaempt to incatpatstc phannacoiunstc information on TCS into tne nsk calculations (30.31 ]. Tlicxunem USEPA unit risks for TCE. 1.7x10* US'1"1)** 2mi 0.32x10* (ng/LJ**. 4re based on total metaooiixcd data m mgfkg/day. adjusted oy body surtacs area t i.c-- by toe ratio of the body weights raised to the negative 1/3 power), which provides a i iianunhln -181- CMA 114500 approximation to me internal cosure tarea linear tn; car -piwn curve) for the emasotes. Ha wow. it is aueoocemn; 10 note urn these pnaimacouinsucaiiv basso potencies tor TCS are very simitar to m sw aoove tor VC. if. roue of the urong eptaemiotosicai evmsnee majnittne mat VC it a mote txxent mmiae carcinogen true 7CC. Clearly, ptarmacsKinsucs close u in*""""'* to orovtoe a r~ff~innrtr cuatumoo oi the hums mu for casaar from mess two cnesnaii. Jus; aj me oturmacorincitca ot a cnemial sum always he conttaerea m amer to octxin a rcausus reassure ot interim exoosure to toe chemical. the pnanmmoynimai of the cnemial.(that is. the meesasttzn oy wmch the etiauai causes cajsscn must also be cnmihriiu ia araerm obtain a resiisue measure at the tEroanse to toe ehesimi. Sevenu stees are involved ia penbrmmg a hah """ tor TCS that roittirieia both phanTV'ni'rrwin tab meessnism. infbmmsisn must fust be garnered oa me pnarmaccuinetia and mmooiism of TCS. as wii as an ease of ia key metinoHtrr asienl (C5L1. tnsaisrmeetic acid (TCA1, tnshisreetoaaoi CTCOH), dichloreaeaue acid CA1. ana diehiarevinvieysieme (CCVO, This ptunnacmrinctic ana mermniine bats can then oe urea m a ?HPK mood ta oravtae a oraateuoa ot the esnsssoeuoa pretties for TCS am us rnnaoaities os earn of the target -- wneuter rgneatsa wtm exposure to TCS In uw nnimai bioassays or ia potemui fauesaa exposure reaearies. Mechanistic information toastie ta earn of the turnon of caaeern must that be iiv uiywratab ta provioe a iiak between urget tissue enarnmi exposure anb bioiogioi or bicchrmhal efreas in the target tiaae lending to the observed oncer response. The sppifls mode of action **"*< with the pmdurunn of a pantcuiar tumor provides the basis for expeeauons regaining both the dose*response for tumor incidence and the (enure of cross-species tojin;. These expeetattoe*. in turn, should drive --* conccnung the mm appropriate risk atfftnmmt appreaen and the assumptions ta be made where ehsmicai-ipeeulc the are licking. Eridtnct for asnsiwyttuarr. By far the most common catenafente outcomes assncbrnl with TCS exposure are itver and king tumors in several luams see both sexo of mice (33]. Sutisucaily inermrd tumor omonies oaserves in only a stagis may include malignant lympsoma tn KANlNMXX mice mposrrt by mhaiatirm. renal mhotar cal adenoma ana ormnoma ia main r3<U rats exposed by oral savage, and bemga nuuratar (leydig cefO utmoo ia Spague-Oawley tea g*p--* by "* Of (hate, the kidney turnon hoe. mind the grams ware aim tney were not abserree in eamrei antmaii. Oirea human evidence of cuneoremcnv from TCS exposure is equivocal at fag- asidemioicgieai hare generally ben negative, aliheege most are Irmacd by preeiema aue to small eahena. uudeeuam iaicacy and co-exposure to other onQimnana (33J. The larges may, mentioned above (17.23]. was unable to link TCS exposure with iuereuad cancer incidence m aoy tissue. A few epiecmieieeicai T""*irr have. However, temauvely linked TCS expoccre wtta increases incidence of urinary tract tumors and tympnoma m woneen. as well as with childhood Imhcmii (331. -182- CMA 114501 Metaooasne. on ootn tn wro ana m vivo sinniss. tr.e meunoiiitn af 7CS has scan suggested b fwipn of .mw.im. ih^hbm oi TC2 to CHI. by me WFO system. (oUoweo oy either oxiaatian si CHL to TCA by zn aldehyde or reduction 10 TCCH by ttconai dehydrogenase (ADffl wn suoseauenr tuomndaosK oxidation ot' TCCH id TCA was aiso oroposeo (34]. ECA has seen isestiiles as a minor unnary meaoolne at TCS (on tne oreer of l S) in corn mu ass miss, but has not oeen aetscaa as a mcaooiiie of 7C is me hml Signiilcanuy. the -Ham** ot DCA in numans aooon to oe muea mom rapid than would be eaaemen (ran aliaaoRS at /nw me extremsty aigh rate si eienxanee of DCA in humans is prasabiy icapuuibto for the failure of invesugazcia to sens it as a mtaaonihr of TCC. MrrhmrT*, of atranajeman in me liver. It has seen suggested that both TCA aaa DCA play a ajar mis in thejp-.-i-- oeservee in mice *''*** with TCS (3TJ. Both compounds have been snowe to pimhmc focal hyperproiiferative trsiims. irtrnrmus. and camnumis on chronic mmiiuttraiicn The typtol tr.nimri of evens for nimongtaicity cut oe amended as follows: miiiaily upon treatment with DCA or TCA. them is evidence of s tii^hfr put geaexauxaa liver nypereiasta. eoesisient wttn the mauiaion of a mitogenic signal by the ehemscai. However, this inmessn esil proliferation soon remrns to a normal liver turnover raze in sow of camnurri exposure to the mitogen, praunaniy in rmuoasr to the exoimsien of endogenous negative growth fsocr (TG?nT) by suumai ceils. Upon reseated exposure for about 30 weexs. however, tfisrs is a sudden appearance of hypetpnatie noontin, wnich evenmaUy pragma to neoplastic lesions. This inpitnec of evens is tody consistcm whh a 'suppression escape' for promotional carainogcnicny [36]. The suodsa appertain, c of rapidly dividing esiis. raprerguiag an escape from eytasstie rupprmtion. producer a {tody increases pmtnbiiiiy of irmranonsl eveau leading to an tumoogemerty. Tim ooservarion that litmus concentration-time profiles of DCA and TCA produce the hyperplastic aed tumengentc resoesex in the mouse but not in the tat apparently reflect a difference in the susespubtiuy ot the two rpeeics to the cruet of hyperpusia. Since tn mra auniei with tat oepatoeytes have demenstnied the mitogenic mnnaiii. the mas liiteiy possibility for the ooserved difference in murmibility is a differemni (nsie pntitxoosuioe for the weape from suppression. The materoal imprinting of the gene for a negative growth hoar imxpiui1 in the mae [37] provides aaa sued possible explanation, if the tat is not tintiiariy prodtsposrt geoctiaUy. Since urn heemn appears to have ooth alieirn tor this gens (37], it is possible that the mueh tower potency of TCA and OCA in urn tar provides a mom roiistic -<> of the patency that couid be npound in Mechanism of cainncfereerv in ute lung: Turnon have airo been ooserved in the lungs of mice expose to TCE by inhalation. The wrnamtm tn this csss appears to oe entirely di/Terant tram mar just described for the liver. In a weU-di'iignrrt exoerunauai effort (33], wnieh provtees an excellent example of the kind of undies nested to support 0ialogKiUy-based halt inrnnanu. investigators at ICl eomoincd in vivo and in wro expeni ** -183- CMA 114502 ctuciaatc meaaaum of TCS carainegsmeuv in tna mouse tune. in the in * female miss and su were cssosm to TCS at a range of inhaieo concentrations it ana octow me conesssrations a wnich cumco are observes m mice, zsa the effects of TCS in me tun* were aessrmmed. A spoaiic lesion, chajactarasd by vaatoussuan of iung Clara ceus. w ooservea in mtcc. out not rats. Thera was evidence 01 a thns&ald for the Clara eetl effects a incut 20 opm. Mice caoosca to 100 opm CHL by mnaiaison oisolayea Clara cal lessons similar to tnose ooservea with 1000 oom TCS. in gqntn" to these reams, only niiid effeca wera eoservtd with TCQH inhaled at 100 ppm. ana none were ooservea with 500 mg/kg TCA given muMcrnoneaiiy (the micas tad twee ooservea with inuaoentonesuiy sdrainuierea TCS a 2000 mg/cg). These ressits suggesea that CHL was responsiole for the taxsehy. In the ut wire studies, mouse lung Clara ceils wera xnown to mcaooiize TCS to CHL TCQH. and TCA. with CHS bera^ the major metabolite. Sigaifismiy, no TCCH giueurentde was nnmna. In comasiaee with moose Clara eais. moose hemtoevtes were mown to srintahiy TCCH and its giucaremoe. In both cell praparations. a stsaey tote concentration of CIS. was acnievea. -coarate m wire stuaies acatoasmtaa that moose Clara ceils possess a ratativety low acuvity for the giucurenthation of TCCH as comiarea either to the glueutomdatioa of other suntTTjiar in the lung or to the giucuronicaiion of TCQH in me liver. I: has also bram determtneo that ADR. the exsyme wnich converts to TCQH. has a low activity in the mouse lung, consistent with the reaiireiy low production oarer nl is the Clara ceils. Oa the basis of this evidence, the inventgators concluded that the observed acute toainty in the lung was a rand of accmnolaiion of CBL ia Clan osUs resulting from a iitnioiion in the formation of TCQH and its 'iucurenide. The spcaficity of this lesion for the Clara cells can be rauonaiged in terms of their relatively high Cytaestome PJ50 aeavity. counted with limited ASH me LTD? ;ltteeioBosyi transferase (UGT1 aamties. The imouations of these results for the lung turnonconguv of TCS are twofold. rim. me ji-uirneiiiinn of CHL. if it doss oeesr * wre. lias elor earautogeius impueaiisns. since CHL has been mown to be teaeesne in a numoer of studies pS]. Sraonoly. the reairruu toseity ooserred with iwesmiaem esposure is likely W produce eempeesuory ceil preiifcmion. csasereatsng the --?* cfTes. The fas that the lung tumors were generally benign is also umfusm: me prediction of primarily benign tumors is more conshteat with a nongenotoxic. ccil-pretiferauvu meenanism. Mtehanum of uuuwjninrr m mo iddnrr. While botn of the tumors discussed thus far are observml in the mouse out not m the rat. the reverse is true for the kidney tumors produced by TCS. A mechanism for the induction of these tumors has been proposed, in wnich direct conjugation of TCS witn glutathione (GSH) in the liver is followed by further mesaaoiism in the kidney to a cysteine conjugate which can then be cleaved id a reasttve tmermeeiaie m the kidney tueular cells p9J. Tha cysteine conjugate formed from TCS. dichioravtnyicysreinB (DCVC1, has been mown to he highly ncsmotoxic is weii as mutagenic in the Ames teat. -184- CMA 114503 Detoxification ina -Ittni"** af DCVC ukas Dues oy urinary excreuon at the N-*eryl derivative. q- jo ms **sca*vl-DC/C his -- laeniitted in me unoe at humans exoosea to TCS oceusansasily (39], ) inoiota ms exoosurc at the Sidney to DC/C does occur ui tne humaa. As with the two previous rasas. :uu proliferation aiso appeals to oay a roie in tnis tumor iTM* la the 'otuy bioassay mat leportsa a urnuiam mmsss in kidney tumors from TC5. syrotamciry was Deserved to Ad kidney at ooth the to* ana high oases, whiie mmon were egib*m oruy at the high dost. Kidney cytomncky was also teconea in association with a non-staunieailY-signiiireni tndneacs 0/ Iddney turnon in the only nthm study ocmonstnmg the tumor response. ScUaton of a risk assessment approear. With lEjJlu ID U USE U1 highly nonlinear cose-response expected for the promotional mechanism suggested for 1 eaigmoeerueitv 01 TCC argues against me use of the usual linrer exusooiatioa to low-nose tux *---** use of the 1315 mood ]. in the oss of the lung ana kidney, auhnagn genotaiicity may lead to a snali b finite residual risk com00mint wnieh is linor at low aose. use is also evidence tor cytotoxicity at the high where tumors are actually obsenreo. Cm eausne noaiieamy of the impact of cytotoxicuy driven eeU-ptoiifenaan on risk at use doses wncre tuisofs are an*--TM is tmmpabeie with the behavior and 11mmnoons of the IMS model, even if a ptnrmii nlr inriir dose TM'i* is used. It has frequently that the 1315 mood may sinroly be iiuopniptute for use with whose oretsogmucity is changes in ceil ptelifensiaa. and that a premising aitemriu in if* is a bioiogiaily based (BBDR) model of renrrr whiefa incorporates cell preiifessdao: it is also to link sued models to PBPK desenpdons of target tissue exposure to provide a --"p*-- deseription of the earanogemc preee for cytotoxic or mhagenie ehemiais (40,41], However, there are at tost two difficulties with the of these alternatives to the LMS moaeL Fiat, toe pTM-- for the eel1 proliferation moods are ofn not available from aura experiment, put must be -- by fitting oiauay data. Unfortunately, it has brea shown that the therefore the (42], Seconoly. in the BBDR mood are not mdcpeooeatiy uaoer such conditions. and of risk at low aose could vary widely on the spoeifte panniriniation choa data on hyperplastic nodules or altered hepatic foci permit a more mooel parameters, low-dor* nsx TMTM with the typical 2-stage SHDR model are espuuiteiy lensuive to tne estimated dose-response for the mood prr1 (43], Another litsxmxrve wnieh has been suggested for risk assessments with non-gcttotaiic carcinogens is the use of a threshold aopreacn based on the uneerlying process which is tcputiea for catciaotemeity (-U), The muonale for the cstri utirtn of a thresooid in non-fenmaate csremogemeity is that, unlike the ase for direct rsetion with ONA, the nonlinear process uneerlying ordnogenteity in these cases (e.g.. cytotoxicity or response to mesator binding) is not one which would be to be active at very tow The gtretest di/ltarity in -185- CMA 114504 raining acetones ter me thrssnotd aosroacn is mat, sinalY speaxing. it imoties mat no merased risk is in imcii from exoosures oeiow me mresnoic. but ontv an aooarcm texocnmemaiiy ooservaote) idresnoid can oe * determines. Sxsiduai carcinogenic activity oelow me apparent tnreenold for tne nonlinear orecess could result from miumcicnt exoerimenoi oower to aetsst tne effect at tower incioensc. from secondary m--rnnirmi (c.;. from tne mutagenic activity of a cnemtmi wntch is atso cytotaate at niftier concentrations), or from me iniieiam nature of the sose-resotmse for the effect te.g. for m'.utufmnnnieo effects oassessuf a iinar case-reason* m the iow-oose tcgimci. Tile marfis of exposure (MOE) approaes is simitar in pneucs to the threshold approach, but the assumottons uederiyinf its use are not as corutraiain;. Father than estimating a human exposure threshold below which 22 nsk is eiprrrrri. the MOE approach merely i the human exposure oreducing a dose-mezne valet which is a specified factor < "margin*) below the value of the marie at which a minimal tumor rrmwnw (tg. I0S -- me ED*) was ooservea in animats. Tie MOE anpreacn admits the possibiiity tnat in tone of the presaee of a hifhly norunrsar uose-reroonsc m tne eaocnmrmal refime mere may tttil be residual risk, ana even Ice dom linear oshamor. below tne apparent mresnoid far me notuimr process. However, it relies on the nomineanry of (he process uederiyinf the earemogenic moee of action to assure tnat the margin of risk between me human and ansnai exposures is tnuen greater than me MOE. That is. an MOE of 100 mifm be expected to provide a risk reduction of gister than 1000, while an MOE of 1000 mifst be 1 [-- lBii to provide a risk reduction of gramer than 100,000 (since it is * that risk falls off at a reach faster rate than exposure). Dcunmien of PBPK moati: The PSPK mooei for TCE usea in this study is an expansion of a previously published model of TCE and its metabolite TCA {451, to *<-< the other key metabolites: OCA. TCOH (which # is the ortnbpal source of DCA). DCVC In the kidney, and CHL in the lung. The parent ehanioi ponton of the model includes individual tissue commitments far the liver, gut tissue, fat. ana tncheo-oipncttial region of the lungs. All other tissues are lumpen into rapidly perfused (kidney, brain, aivcoiar region of lungs, ete) and slowly perfused (muscle, skin, ete) esresaronems. The mood both ---"" and oral routes of exposure. Oral gavage is modeled using z twolcoaipunmcre description of the GI tram. Allemctnc sealing is used througnoot the madd (flows and capaeiiies sealed by body weight to the three-quarters power, rate constants scaled by body weight to the negative one-quarter oower) to ssmpitfy iroasoccics and intetspecies extrapolation. The mood includes three target tissues: lung, kidney, and liver. The dose metrics provided in the lung are the tnttanuneons concentration ana arm unaer the curve (AUQ for CHL in tne trosbeo-broncnuJ region, whieh is assumes to be produced by saturable oroouction ana ciammre of CHL in Clara cells. Tie dose metric in the kideey ts total praeuoion of the thioacctytating imermeoiate from DCVC divided by the volume of the kidney. The mooei implieitly assumes that all glutathione conjugation of TCE leads eventually to the appearance of DCVC in the kidney. Clearance of TCE by N-icctyMiansierase into the urine is also modeled. Two dose metrics are -186- CMA114505 includes in ms ossetration of the liven AUC Ter OCA un AUC far TCA. The moaei anm uni all oddative meaoaiism orocesos mrodgn CKL. wnich is further meoooiizca ts TCA ana TCOH. TCOH ican lutaeousnily be oxidizes to TCA. ccnnigatea with siucurmuc zetd. or reduced to OCA. DCA ii alio produces front tne tsdaoioa of TCA. Binary exaction of TCCH ;lueuronioe arts enteroneoatic recirculation of free TCOH ii nrimaeri. with only ms ctnanoruse eeing extrsss in the unne. The moaei is able to reproduce data on TCC. TCOH and TCA longues in tte mouse, tat. and human, as well as OCA Ravage. in mice, for both inhalation exposure and oral Table 3: Companion of virtually sate lifetime exposure levels (ppb in air or ng/L in water) for TS baaed on the Matgm of Exposure (MOE) approach and the Linearized Multistage (LMS) approach MQF * 1000 J ED*/MOE MOE Level 10- Risk Level* | Inhalation (ppb): Midsey 1 | Ur | 0.009 9.02 3-39 6000 (9)* 13000 (36) 81 (IZJ) 41 (0.06) 300 (0.64) 0JS (0.03) Drinking Water Oig/L): urn Kidney 1 0.009 | 9.02 | L39 600.000 (900) 223.000 (340) 390 (36) 4000.(6.0) 4300 (9.6) 3.6 (0.8) ' Margin of exposure oclow ED,, (dose mwinniiiiM to an extra risk of 10%) * LifctPTT- extra oncer nsk bases on the Multisage Model * Altciiuia (wais-ase) ealmtation -- see totI *I M iMWMw- The rouits of the doae metric oleulattons with the PBPK model are lummanzat in Table JITMthis table, the mast plausible " of acespodle exposure levels are shew* for each target tome and Mm opesure semano of concern. The numoert in patemheses represent alterative, wont-case risk estimates. The purpose for mehuting these aitentative " is to demonstrate the broad uncertainty in the current nsk estimates. In every ose the discrepancy between the best estimate and wont-ease estimate could he gtoily reduced by experiments wtnch are well within the of the science. In the ease of lung tumors, tne numbers in patontteses itatiuem the calculations which assume that the cross-species seating for the clearance of CHL id the lung parallels that of P450 (which falls off dramatioily) rather than following alloeietnc expoctationt. In the ose of kidney turnon, the numoert in parentheses represent the calculations whieh -187- CMA 114506 ssume an ext:r-tY ioy GST eatawav proauetton in me rat ssnsua to tee human tbasad on one trninl study) outer man assuming a proouction more in keeotns wun iliomsnc esoeesuons (bases on anouier ammai mar}. Both ot mese unesauuies on merrily be addresses ov in vtm iruaies similar to uiose wnieh have oese perrormsa wim memvtene cnioriae 1471. in the see ot liver tumors, the numnen in oaremneses rtureseix the calculations wnicn assume us: ins human luseeeoaiiiiv to rnuoyentc oremogma is similar to that of the mourn. is opposes to me most plausible esumates. wnieh assume teat me numan suscssubilttv is more simitar to toe tax. The stuaies neseso to resolve this suestion are moot oifftcuit to define. out the imoonance of this avesuon foes well beyona TCZ. ana the benefits ot sues strata would be signifiaat. Table 3 also deawtmrores two di/Terrat aopnaencs for ai.i rmable exposure levels for the public. In the traaitiorei quartnmtive risk estimate anprosea, the LMS moael is uses to obtain qttamintTvt essimates of the nsk with a given human exposure sesano. based oa the bioassav aose-resootsss dasL Typieadv, USE?A considers an increases lifetime risk of cancer on the enter of 10* to be acceptable for the puotie 12?.30.31'. Deoaiomg on tne target tissue, me TG sxooautg tsveia with an ""'`i iif-- risk of 10* range from 0.13 to 300 opo tn air or 5.6 to 4500 upL in water. far comcanson. the ores ^ll*) published nsk from USE?A would emote to lifasme 10* risk czoenure icrcis of 0.11 ppa and 3.1 pgil~ A seeono approach for estimating accsoals levels is to simply relate the human exposure level to the snanal bioaxsay results by tne ratio between the ED* its the ""* (caicuiaied from the bioassy htl using the muiiisogo model) and the dose marie for the human exposure. Alternatively, in rasa, or MOE, san oe set and the corresponding human exposure can be direedy from tne ED* sad the MOE. This is me approach shown in the left side of Table 3. In oat rose, the acespohle dose marie terete were calculated by dividing the appropriate ED* by the desired MOE. The model was then used to translate the iceeptaoic dose mane level into an acessosie exposure level. By*** on an analogy between noogeaotsxs careinogemcitv ana noneaneer toxicity, a minimum MOE sf 100 would teem to be on tne basts of 10 Gar human vsnaoiiity (paroealariv for vanaoillty in the salaried of the key moboitzieg enzymes! and (0 for uneenaimy in the anneal to human extrapolation, for m|www. a{ tfce p^wiw it mtyw miwuiwi he -nynyAie to add an additional margin of 10 hminc of the potentially Urge number of individuals exposed, far the puipuw of this illustration an MOE of 1000 was used in renaming the public exposure levels in Table 3. Dapcnoing on the targa ussue. the TS exposure teveu which provide an MOE of 1000 range from S3 to (3000 ppe in air or 390 to 600.000 upL in water. In general, the MQE appraaca results in levels whieh are higher man those ooaineo by the LMS appreaen by roughly two omen of Conclusions: The basis tor determining wnieh of the two apprmcaea is the mast appropriate is the node of action of the chemical oremogentcity being considered, for exampa, it would <--* clar that the use of the LMS appreaen is both justisied ana orerersbte in tne sse of a mresnogen suea as vinyl chloride for which the 'denes regareme morn of action includes (a) direct reaction of a metaoeilin with SNA that results in DNA -188- CMA 114507 afi0 mmxansertonon; lb) no evtosnso =f snhancee oil proufcraoon. rejector interaction. or eyntozncr at :larly cumongenic ana (e) crea-socems target-tissue ecrresoonoence of a nrs tumor grpe. The cancer rtjJe ;ram a gsnotoxie r~*' lie vtnyi cfllortee is very tikeiy 10 tall off iinearty *'i dose, even to very low exposure isvets. On the otcsr eaad. cr.s MO srstoaca seems quits applicable. sad more aepreprute than ids LMS acpreaea. for i oranegcn sucn as T~ far wtuen (a) there a no similar evidence of direct tnteraerien with ONA. (b) there a evidence of enxnncse cad premciatioa atte to reesoisr mtereeuoa or cytotoxicity stioriimrt wild every target,iw,w jjp* (e) there a dale evteeaee ox auB*iwiti cottespoflaeucc or tite pnmutiiaa of tare tumor types (the kidney turnon providing tne ooxhble exasdoa). The cancer task from a cnewiwMi like i<--L for which the **; of TM sapors to involve the highly noniiaear rntoact of cahaaeea ceil proliferation, is very Ukdy to fail off muea asier man dose, prexaicag an iimcinrau.il reauction in risk thr rrmraing tne reduction in exposure. 4 ctotoiwea gemenu This stuay was supponeo by tne USE?A Office of Health ana Environmental Assessment ana the (/.. Occupational Safety ana Hoith Agency QUSOSHA) Department of Healtn and Environmental Policy. However, the views preseated in this paper are stnctiy those of the aiixsors sad do not Mcesariiy refleet the position of either of the agencies. The atiuwn are greatly indebted to the U5EFA ana 17SQSHA prefect officers. Lares Rtemoerg and Christine Whlsaker. for their gumanm. support, and thoughtful discussions. REFEHETfCZE 1. U.S. Eavirenmeual Protection Agency. 1994. Daft revisions to tne guidelines tor cancer risk assessment. EPA/60Q/BP-92/Q03. QfTlec of Rcaoscn sad Devwoomem. Washington. DC 2. U.S. Atviiunmenal Protection Agency. 1933. Kokh and envirenmenal effeos profile for chioreetnena. ECAO-CIPf-PIJJ. Ea^wanoeanl Criteria sad Assessment Office. Caewaaii. OH. 3. Cntmp. K.S. 19>^tc bnpioven oroceoure for low-oose carcinogenic risk asosssment from stttaui data. I Environ Path Taxied a?Si9-34g. A Purchase. I.5.H.. Staffed. J., ano Paddle. C.M. 1933. Vinyl chloride - a i sneer ease study, In; Toxieologtcai Risk Assessment. Vol. Q. Clavson. D.. ei at., eds. CSC Press. Soea Room FL. pp. 167-193. 5. Agency for Tosie Substances and Disease Registry. 1993. Taxtcoiogtcai Profile for vinyl chloride. TP-92/19. U.S. Depanmem of Health ana Human Services. Atlanta. GA. 6. Pltxgge, H. sad Safe. S. 1977. Vinyl chloride msaeoiism A review. ChciaospBcra 6:309-313. 7 Wataaaee. P.G.. Hefner. Jr., and Gehring. P.J. t?76. Vinyl efttorida-tndueed depression of hepatic non-protem sutftiydryt content and effects on bremosutpaalein elesrence in rets. Toxicology 6:1 -S. CMA 114508 -189* 3. Watanaoe. Genteei. J.A.. ?xc;, D.Z.. ano Gehnn;. P.L 197S. Hssatic macmunninasar tecta; following excasure to vtnyi cnionoe. Tj.ticoi Add! Pharmacol -U:57I-579. 9. I -vn p ' 1986. The rote of cyclic oasc aaducis in vmyi-chionde-inauees ccrcinogsitesis: Studies 03 nueicic acta aikylauon in vivo. IARC Zz: Publ 70; 101 -103. 10. Swenoerg. j.A.. Fedtke. N., Ciroussci. Harbin. A., sr.a flartscn. H. 1992. Frhcnn Minuets turned in DNA ot vinyl chloridc-exoosea rcu are mshiy persistent ir. liver. Carcinogenesis 13:737-729. 11. Andersen. M.. Gswell. K.. Gzrgas. M., Smith. F.A.. and Reitz. R.H. 1937. Physioiogiaity baaed pharmacokinetics and the nik assessment orocess tor metnyiene enioride. Toxicol Appt Pharmacol 37:133*202. 12. U.5. Environmental Protection Agency. 1992. Hastiest tor comments on arart .moon at anmpda traitn; factor for sneer risk assessment. U.5. Fed. Rs-.. 57 (1992) 24152. 13. D'Souza. R.W.. and Andersen. M.. 1983. Phyiioioeicaily based oharmarnkinetic model for vtayiidene chioriae. Toxical Appi Pharmacol 95:220-240. 14. U.S. Environmental Protection Agency. 1983. reference snysioiosieai parameters m oraimaeokiosie modeling. EPA/6QQ/6-88/004. Q.Tice ot Health ana Environmental Assessment. Washington. DC 15. Garzas, M.!_. Harness. P_2.. Yaisara. D.E.. Cascn. G.H.. ana Andersen. M.E. 1989 Partitiontactileirnts of Iow-moiecuur-wci$nt volatile cncaticais in various iipuids ana Toxicol Appi Pharmacol 98:37*99. 16. Clement International. 1990. Development and Validation of Methods for Applying Pharmacokinetic Data in Risk Assessment. Final Report. Volume V: Vinyl Chloride. AAMRL-TR-90-072. Armstrong Aerospace Medical Research Laboratory, wright-Panenon Air Force Rase, Ohio. 17. Jcdrychowski. R.A.. Sakai, I.A., and Chaieinida. i. 1985. Campamon of the impact of iroiainunut aad iiuetimncnx exposure to vinyl chloride, indudin; pnsnooarbitai effects, J Hy; Epidemiol Microbiol Immunol 23:111-120. IS. Watsnaoe. P.G. and Gehnn;. p.J. 1976. Cose-depeneent fate of vinyl chloride and its possible relationship io oneocemeity in rats. Environ Health Pcrspeex 17:145-132. 19. Gehnn;. Watanaoe. P.G.. ana Park. CM. 1973. Resolution of dose-response toxicity data for chemicals requiring metabolic activation: example - vinyl chloride. Toxicol Appi Pharmacol 44:531-591. 20. Maitom. C.. Lefentine. G.. CHibeni. A., e: at. 1981. Caretnogentcity bioassay of vinyl chloride monomer: a model of risk mrtsmrm on an experimental basis. Environ Health Penpect 41:3-29. 21. Maitoni. C.. Letenine. G.. Cilibeni. a., er at. 1934. Experimental researen on vinyl chlonde carcinogenesis. A(drives of Researcn on industrial Carcinogenesis. Voi. 2. Malum. C. and Mehlmaa. M.A. (eds.1. Princeton Sciamirlc Publishers, inc.. Princeton. New Jersey. 22. Feron.- V.J.. Hendnksen. C.F.M.. Speck. AJ.. a at. 1931. Lifespan oral toxicity study of vinyl chloride in rats. Food Cosmet Toxicol 19:317-333. 23. Newbcree, P.M.. Weigcrt. J.. and Kula. N. 1979. Effects of dietary tat on hepatic mixed function oxidases and hepatocellular carcinoma induced by ailauxtn 3. in rats. Cancer Res 39:3986-3991. -190- CMA 114509 Fox. a.j. ana Collier. r.F. 1977. Mortality exueriense or worsen exsosura :o vinvi chloride sane cue manufacture of potyvinyi chloride in Great Britain. 3r J Ind Mod 3-: 1 -10- 1 33. Janes. R.W.. Smith. D.M.. ana Thomas. P.G. 1983. A monatity sway ot' vinvi chlonae monoroar emoioyea in the United Kingaom in i940-1974. Scaup i Work Environ Health 14:133*160. 36. Sunoiuto. L., I.'Abbe. k.A.. Andersen, a.. Belli. 3.. Combs. Enghoim. C.. Ferre. G.. Hagtnsr. L.. Ungain, 3.. LundOerg, L. Pirasm. ?... Thomas. P.. Winkeinnnn. R.. Zzsasa. R. 1991. AeoUaborative study of cancer incidence and mortality iroon; vinvi ehlohde omn. 3sand J Work Environ Health 17:139*169. 27. Spinas. R.. Siewsrt. P.A.. Lee. J.S.. Msnno. D.S.. Forbes. C.D.. Gtansan. DJ.. Pettigrew. HJiL. Blair, a.. Hoover. R.N.. aad Cohen. i.I_ 1991. Retnspeertve conon morality stray of women at an aimm& maintenance fadlity. I. EpidemtoiogrraJ results. Br J lad Med 48:315'530. 28. Stewan. P.A.. Lee. J.S.. Maano. D.E.. Spans. R.. Forbes. C.3.. and Blair. A. 1991. Rctraspceovc codon monaiitv smdy of workers at an airman manuenanee facility. C. Exposures and their assessment. Be I lad Med 48:531-537. 29. U.S. Environmental Protection Agency. ! 983. Health Assessment Document for Triehloreeuiytene. E?A/600/3-82-006B. Office of Health and Environmental Asseasment. Washington. DC. 30. U.S. Environmental Proteetion Agency. 1983. Health Assessment Document for Triehiotoetnyiene. rtral Report. EPA/60Q/8-82/006F. Office of Holth asp Environmental Assessment. Washington. DC 31. U.S. Environmcmai Prelection Agency. 1987. Addendum to the health document for tridtloroenyiene: updated asetaegenieity asscssmetu for trshloroethylene. EPA/600/8-S2/006FA. 32. International Agnqr for Reseaica on Cancer. 1919. 1ASC caidnogcnkity evaluations of vinylidew ehtoride. methylene dichloride aad uiefaioroetnytsae. Environ Res 49:333*334. 33. Davidson. I.W.F.. aad Belilcs. R.P. 1991. Consideration of the target organ toxicity of triehteraeshyino in terms of metaootite toxicity and pharmacokinetics. Drag Mead Rev 23:493*399. 34. Muller, G.. Spassevski. M.. aad Heruenter. D. 1973. Mceahoiism of inehloroetnvlenc in eon. L Interaction of triehloroemylene and ethanol. Ardl Toxikol 33:173. 33. Bull. R.J.. Tempitn. M.. Lanon. J.I_. and Stevens. D.KL 1993. The rate of diehtotoaeaate in the hapasoeaicnogcnieity of trichloroethylene. Toxicol Lea 68:203-211. 36. Andersen. JJ.. Jinie. R.L.. and Greouee. W.F. 1993. Negmive selection in hepatic tumor ptmnotioti in relasioojmieBr risk airwanent. Toeieowgy. in pres. 37. Kalscheucr. V.hfe-Mhtiman. E.C. Schepeas. M.T.. Redder. H.. and Ropers. H.-H. 1993. Tlie martin* like growth factor type*2 remnur gene is imprinted in the moose but not in **"-"* Nature Genetics 5:74-71. 33. Odum. 1.. Foster. J.R.. and Grain. T. 1992. A mechanism for the development of Clara cell lesions in the mouse lung after exposure to tnchloroetnyiene. Chcm-Bioi Interact S3:133*153. 39. Sinter, G.. Vamvaxas. S.. Dekam. W.. mp Heascnler. O. 1993. Nephraroxid and gcnatoxic N*aeayl*S* diehlotovinyt-L-cyneme is a urinary metabolite after regupatimtai t. i.2 -trichloroethylene exposure in humans: imptiattons for the risk of triehloreetnyiene exposure. Environ Health Psrspea 99:281 -2S4. -191- CMA 114510 0. Conolly. R.3., Reis. R.H., Clawed. K.J.. via Andersen. M.H. 1933. Biologically siruaurea models and computsr simulation. Comments in Toxicology 2:205-319. 41. Conolly. R.3.. Sail*. R.H., Clewed, H.J.. and Andersen. M.E. 198S. Pharmacokinetics, biochemical mecnanism ana mutation accumulation: A comprenenstve model of chemicai carcinogenesis, Tox Lett 43:159-200. 42. Portier. C.J. 1990. Utilizing biologically based models to estimate carcinogenic risk. In: Scientific Issues in Quantitative Cancer Risk Assessment. . Moolgavkar fed.). Birfchauscr. Boston. MA. pp. 252-266. 43. Crump, K.5. 1994. Use of mecnanmic models to iow-dose cancer risks. Risk Anal 14:1033-1033. 44. Reitz. R.H.. Mendtaia A.L.. Corley, R.A.. Quail. J.F., Gargas. M.l_, Andersen. M.E.. Stasis. D.A., and Conolly, R.B. 1990. Estimating the risk of liver cancer associated with human exposures to chloroform using physiologically based pharmacokinetic modeling. Toxicol Appt Pharmacol 105:443-459. 45. Alien. B.O., and Fisher. J.W. 1993. Pharmacokinetic modeling of trichloroetnylene and trichloroacetic acid in humans. Risk Anal 13:71-56. 46. Fisher. J.W., and Alien. 2.C. 1993. Evaluating the risk of liver oncer in humans exposed to [riehioroetnylene using physiological models. Risk Anal 13:37-95. 47. Reitz. R.H., Mendtaia. A.I_ and Guengertch. F.P. 1989. In vitro metabolism of methylene cnioride in human and animal tissues: Use in physioiogicaily-based pharmacokinetic models. Toxicol Appl Pharmacol 97:230-246. 192- '- - CMA 114511 OEHHA'S RESPONSE TO COMMENTS FROM WILLIAM F. POUCH, PH.D. 1. For a pathway of exposure to humans to be complete there needs to be a source of release, a route of exposure, and a point of human contact. While the Class I Unit was the source of vinyl chloride emissions from the B.K.K. Landfill, and air is a route of exposure, the point of human contact is not clearly established until the development of homes north of Amar near Nogales beginning in 1977. According to the USEPA aerial photographic analysis of the landfill dated July 28, 1964, the nearest residential development in 1964 was approximately 1,000 feet to the southwest of the landfill. Concentrations of gases emitted into the air will decrease with distance from the landfill. Residential areas other than the southeast and south either have not been impacted at all or by as high and as frequent detections of vinyl chloride. The "Scope' section of the Introduction states the refined nature of the addendum report This is summarized in the second paragraph of the Executive Summary. 2. Please see Risk Characterization, Exposed Population. 3. A worst-case (70-year 1980-2050) exposure estimate has been added to TABLE 10 to facilitate comparison with the interim report 4. Please see Hazard Identification and Exposure Assessment, Other Hazardous Chemicals Detected in Ambient Air. 5. a) Please see TABLE 10 for risk estimates using 5 ppb as the substituted value for samples with nondetectable concentrations in the 1981-1982 data set. b) Please see TABLE 10 for risk estimates using 5 ppb as the assumed exposure concentration in 1980. c) Discussion of potential underestimation of the exposure concentration at Station MY for the years 1980-1983 has been expanded. d) We assume an exposure concentration for 1980 because the 1981-1982 data suggests concentrations at Stations A, B, and MY were not likely zero. However, there is no way of knowing quantitatively what exposures were prior to monitoring data. 6. We recognize your concern regarding past exposures. The inability to use flare data has been discussed in the addendum report Manifest data is categorical data, as was shown in Table 1 of the interim report There is no generally accepted scientific method to convert such categorical data to specific chemical concentrations in air at a receptor location for use in exposure assessment and quantitative risk estimation. "4 -193- CMA 114512 t-eoruarvv. i wo 12 i o riollencrest unve West covina. la vt 7vi umce or Environmental rieaim .Assessment Hazardous vvaste faxicoiogy section 0O1 Norm 7th street P O Box V42732. .SliS 241 Sacramento. lA V4224-7 jiu Attention: Dr Davia M. Siegei Subject: Review ot'Adaenaum Healtn Risk Assessment ot .Ambient Fugitive Vinyl Chlonae Emissions trotn tne Llass i Unit or tne BKX Lanotni. ^est Lovrna. Laiitorma Dear L)r Stegei. 1 he suo.tect document nas Deen reviewea ana a list or comments ana sugeestea moamcattons is attacneo. Please contact me at 313-9 19-3272 it there are any questions on my comments. Sincerely, William f Policn, Ph D FEB AJ73SS Haza:~:. egy -194- CMA114513 bratt Addendum Assessment or Ambient Fugitive Vinyl Chloride Emissions From tne Class i Unit ot the BKK Landfill. West Covina. California Comments and Suggested Modmcanons I The rationale given tor assuming 1980 as tne start or the exposures Decause no one was then living wnnm a tew nunorea reet or the location or the monitoring stations sounds ridiculous. There were more than 30.000 people living within a mile or the landtill m 1979 and many wnnm a tew hundred yards or the monitoring locations. Wtth this line ot reasoning, if the monitoring locations nad been located a few hundred feet to the north on BKK property, no exposures would have occurred to date and the nsK would be zero regardless of the magnitude of the emissions or the number ot people living nearby The real reason tor selecting 1980 was the lack ot emission data prior to 1980 that met hPA analysis standards. Surely, if adequate emission data were available, the assessment would have staneo m 1963. The analysis should not assume tne exposure to residents living near Ukk started in m i80 because that is not true, it should say that tne assessment started ui 1980 because adequate Oata to evaluate tne nsx tor tne period from 1963 througn 1979 are not available. The report should dearly state tn the Executive Summary that the carcinogenic exposures to the residents living within a mile ot the landfill started tn 1963 but adequate data to esnmate the risk was not available for the years prior to 1980. 2.The report is very misleading. It gives the impression that the total cancer risk for ail residents who ever lived near the landtill has been estimated and shown to be less than the values given in the report. The scope and limitations of the assessment should be dearly defined m the report The dimensions of the areas surroundmg the monitoring stations tor which the assessment results are applicable and the number of residences included within these areas should be precisely defined. The report should state residents living m other areas near the landfill could have received greater exposure levels and acrued higher risks because ot higher annual emission levels m previous years or the cumulative erfects of exposures since 1963. An esnmate of the number of people living within a nrule of the landtill as a tunenon of nme since 1963 should be made and induded in the report. This would help show how the analysis had to be limned in scope because of the lack of data. 3 The report shoul&otm out that the use of the 30 and 9 year exposure durations when calculating the tht^Bcer risk is not adequate for a substantial portion of the people living near BKK Many pmpie living within a mile of BKK have already been exposed to carcinogenic emissions tor 33 years and sureiv some now young adults will be exposed for more than oO years. 4 The cancer risk due to carcinogens other than vinyl chloride present in the landfill gas at BKK is minimized and quickly dismissed in the report. .Analyses of the of the composition of the landfill gas at the mlet to the flares consistently show enough carcinogens other than vinyl chloride at high enough concentrations to cumulatively equal or exceed the cancer risk due to vinyl chlonde. There is no mechanism by which these chemicals will not enter into the neighborhoods m roughly the same ratio to vinyl chlonde as present in the inlet -195- CMA114514 gas. The presence or some or rhese carcinogens m me background is not important. The enuttea concentrations wni alwavs oe higher man the background near the source. The Executive Summary snould contain rne inxormanon that carcinogens other than vinyl chlonae are present in the ianariil gas out were not included in the assessment. It should also contain tne inxormanon mat. oasea on concentration measurements or'the iandhil gas at the hare iniets. the presence or these otner carcmogens cause a cancer risk similar in magnitude to vmyt chlonae. The esrimatea cancer nsx would be at least twice that reponea if the otner carcinogens were included in the assessment. 5. The report claims that the estimated excess cancer nsks are upper bound and actual excess cancer nsks are likely to dc lower. Actually, the opposite is true. The analysis contains many assumptions which substantially minimize the nsk. These include the Ibtlowing: a. The use of 1 ppo for the samples with nondetectable concentrations for rhe 19811982 data. The reason given is tnat by using tppb, the average annual concentrations tor 1981 ana 1982 ire tnen more consistent wnn the 1983 annual average, rhe average annual concentration was lower in ty83 because or improvements m the gas collection and incineration system. It is not reasonaole to assume that the daily and day to day variations mthe measurements were as rush as 10 to l. A more reasonable assumption is 1/2 of the detection limn {5 ppb for tins data ) for the samples with nondectabie concentrations as was done tor all the other measurement data b. The assumption of 2 ppb as the annual average concentration of vinyl chloride in 1980 unaeresomates the actual value. The plot of average vinyl chloride in figure 17 should have included the 1981 and 1982 data If it had. entirely different conclusions would have had to be drawn since the average concentrations rapidly increased tfom 1983 threugn 1981 A concentration value tor 1980 which was lower than 1983 never could have been selected. The implied correlation Between the tons of hazardous waste deposited and the measurea average annual coneentrattons.in addition to ignoring the 1981 ana 1982 data, does not include the erect of emission control measures implemented at the landfill wmcn substantially altered the emxsstons data. The average annual vinyl chlonae concentration in 1980 had to be much larger than the average or the concentrations measured from June through December of 1981 from November 1980 to June 1981. the gas collection system was expanded, vinyl chlonae was banned and a maintenance program muated to add till and groom the slopes to reduce escaping gases. The USC report of September 1980 tbuna the working race at BKK to be the major source of voianle organic compound emissions. A conservative assumption would be that the banning or vinyl chloride reduced the emissions by at least 15 to 20 percent. In December 1980 the operating gas collection and incineration system had 15 wells ana 2 Hares. By June 1981. the system had 55 wells ana 4 hares: a 3.67 fold increase m capacity The January 1981 Eutek report states that the existing gas recovery system ot 1S wells and 2 hares nad the capability or extracting 2200 ctm of landliil gas. The report also states that BKK estimated that the total gas production at the site in January 1981 was bbOO ctm. The expanded gas collection system of 55 wells and 4 hares completed by -196- CMA 114515 June t981 had the capaowtv or extracting a 100 ctm wmch is 1500 ctm more than wnar was estimates: to oe proaucea by tne landiiil. Thus, since the banning or vinyi chloride dinunatea emissions rrom tne wonting race, u the gas control system was 100 percent efficient, the vinyi chionae emissions would have oeen reaucea to zero in june 1931. To estimate tne actual reauction. a gas contoi system efficiency or 50 percent m 1980 ana 55 percent tn 1981 was assumea. A lugner efficiency was used for 1981 because or' improved maintenance ot the slopes ana the aaaition ot 2 new more efficient dares. Using these assumptions, a ol percent reauction in the 1980 vinyi chlonae emissions was achieved by the expansion oi the gas control system installed between January and June 1981. Euteic in their January 30. 1981 report esnmatea that the installation of a plannea gas control system expansion which would increase the capacity to 5500 ctm would reduce the odor emissions by 68 percent which is general agreement with the above estimate. Combining, the emission reductions aue to tne gas control system expansion and the enmmanon of working race emissions gives a total reducnon of 76 to 81 percent rrom 1980 to June 1981 Thus, tne average annual vinyi chloride concemranons in 1980 are about 4 times greater man tne average or the concemranons measurea from June tnrougn Oecemoer 1981 There oovtousiy was a lot ot vinyi chlonae brougm to BKK in 1980 since banning it in 1981 reaucea the total amount ot hazaraous waste deposited in 1981 by 180.000 tons. c. The assumption that the average annual concentration for Station MY for the penod 1980-83 was equal to the Stanon A values is not reasonable and lowers the estimated risk for Station MY. Since the measured concemranons at Station MY are consistently higher thin at Stanon A tbr the years prior to 1983, it is reasonable to assume the concentration values were higher at Stanon MY than at Station A in 1980-83 when no measurement were made at Stanon MY. A comparison of the 1984 -1987 measurements shows that the Stanon A data are on average 49 percent higher than Station MY. Theretore. the average annual vinyl chlonae concemranons at Stanon MY are assumed to be 49 percent greater than mose at Stanon A for the years pnor to 1984 d. Tables 1 and 2 were prepared to show what the 1981 and 1982 monthly vinyl chlonae concemranons for Stations A and B and the 1980 through 2009 average annual vmvl chionae concemranons would be if the change* m assumptions discussed in a. b. and c above were lmplcmmtqd Table 1 was developed by substituting a value of 5 ppb ( as discussed in Commcn^l a > tor the samples with nondeteatable concemranons for the momns or June 198 liiihougn September 1982 for Stanons A and B. The 1980 average annual concentrations ror Stanons A and B were obtained by multiplying the average of the concemranons for the months June i 981 through December 1981 by 4 ( tbr the reasons given m Comment 4 b ) to give 38.4 (4x9.6) tbr Station A and 34 4 (4x8.6) tbr Stanon 8 A linear decrease m concentration rrom 1 January 1981 to 1 June 1981 (tfom 38.4 to 9 6 tor Stanon A and 34 4 to 8.6 for Station B ) was assumed to determine the concemranons tor January tnrougn May. Hus is a reason able assumption since the changes m the gas collection system were incrementally added from January through May in 1981 The average annual vinyl chlonae concemranons tor Stanon MY were obtained by increasing the corresponding Stanon A values by 46 percent as discussed in Comment4 c. -197- CMA 114516 Using me average annum concentrations rrom fable 2. jsnmates or the excess cancer risk were maae tor Stations A. S ana MY The results are snown in Tables 4. 5 and o. The nsks are seen to De 2 to J times rusher wnen tne effect or emission control measures implemented at BKK prior to June 1931 are consiaerea in the analysis. 6 What is reauy neeaed are cancer nsk estimates ror ail the residents living within a miie or so or the lanotill. The resiaems nave a ngnt to know wnat tney have been exposed to. The hsk should be determinea as a runction or' time since i 963 and should include ail' ot' the carcinogens known to be present at BKK. This was the original request at the residents and the original objective or this study Perhaps this is relt to be impossiole to do because of a combination or lack ot' data ana analysis requirements dictated by EPA. However, there snouid be enough information to make reasonable estimates of the nsks since 1972 when all toxic lanatiils and government agencies had to start maintaining records of ail toxics aepositea in lanatiils. Water Quality should have records of the amount or waste deposited since 1963 from wmch the amouni of landtill gas proaucea eacn vear can oe esttmatea. Documentation snouid be available at AQMD on tne development ot the gas colletion system ana other controls to reauce emissions to estimate me amouni oflandiill gas leaving BKK. AQMD should also have measurements ot the composiuon at the landtill gas at the inlets of the tlares since the experiments with the small test ilare in 1973 from which the concentrations of the carcinogens can be determined. The waste producers manifests provide information on the amount oftoxics deposited each year and their general composition. If all the tiubrnianon available at the landfill monitoring agencies was used, a reasonable estimate satisfying EPA requirements could probably be accomplished. The report should be expanded to include an assessment of the excess cancer risk starting in 1972. Kor tne years prior to 1972, hazardous waste was not defined nor controlled so that no data are available for cancer nsk evaluation. However, all Class 2 landfills accepted tndustrtal waste some of whtcn was later classified as hazardous. Most of the Class 2 landtills. wmch never accepted toxics alter 1972, are now emitting vinyl chloride. Operating Industries Landfill has been round to be emitting enough vinyl chionde to exceed the air quality standard of 10 ppb for a 24 hour average in the summding neighborhood although it never accepted toxics. Carcinogens were obviously deposited at BKK prior to 1972 and nsk estimates starting in 1972 will underestimate the nsk to residents living near Bkk m pnor years. The report should also be expanded to contain a discussion of the prooable carcinogmc exposures and cancer nsks from living near the landtill from 1463 to 1972. Estimates ot the excess cancer nsks acrued since 1972 at Stations A. B and MY are presented m Tables 5. 6 and 7 These estimates were derived by estimating the average annual vinyi chionde concentrations tor the years 1977 -1979 based upon the development of the gas control system. In Comment 4 b. it was determined that the 1980 average annual concentranon was higher than in 1981 pnmaniy because of the expansion of the ]as control system. Similarly, the concentration was probably higher in 1979 than in 1980 because the numoer or gas extraction wells was increased from 9 to 15 in 1980. In 1979 -198* CMA114517 the capacity was tripled by me addition or a new dare and 5 gas wells so that the 1973 concentration was probably higher man ine 1979 value. .Also, the concentration m 1977 could have oeen ragher man 1978 because a gas control system ot 4 wells and 1 flare were installed in 1978. Thus, the concentrations m 1980 were higher than in 1981 ana each prior year could have oeen mgher unni 1977 because ot' the reductions m emissions acnievea by an expanding gas control system, in the analysis* the concentrations tor the years 1977 -1980 were assumed equal because the amount ot landhll gas would prooabty be increasing and compensate tor the increased gas collection. A linear extrapolation to a concentration ot zero on 1 January 1971 was used to determine the concentrations tor the yean 1971-1976. The estimated excess cancer risks are about 10 times greater than those shown in the report. -199- CMA114518 **z TABLE l At/^-A6ir CHLodu coWceNT(Ar(^i n Ah^r^iu flKK I-AMFilL / ivnsr CtJV/*/* , t-AiiFafiH/A ppt-, Moi rti J'. b Mh April JVtH< Aitju.SC tcJ m br D*-r A/ l) l/t-rti b-**' D b*V Ahhit< 1 A u> *. -----...5 TA rim.} A -- ___ MttJ. *w . o 3u . L 2* .1 lo. a .1 s-.i. *.e 0.1 7.1 *i.J l.-i to.i H. 1 1.1 to.-t 7.V j.) 1.1 lit t(..k S.5 -- j re rioh.- `A ____ |< a, ---- jtX6 tBini 3i.u j?. 7 3U /7 /a i / 1*. u 7S 7. *i C.& 17 ^7 *. i. I C. j iT -To i~. 7 S. 1 3.7 7/ r.t> Y. V r.i CMA 114519 r/UJLt 2 A V f: A-A C li. A AJN U A 4- I'lNlL C Jll.U4.iO l CoMLC^iraAriJHi U l Aft U Kit. {.AtbFii-i- V Js * * STVSJjO a/ A $ f Af IUH (i jrApQAj 21 y J *1 bo 14 111 14 HI 3 J40-3 l4BiT 1401 I 4H I too /40iI /ftfi I44o- iff* I- AuiW Jd. i /t. 2 r. a H V.2 55 /'I A7 1.1 6.fi 0.0* ff.OJ /-/.v 5. 3 3b 34 2. 3 l. J i. 2. Oft oe 0 0J O.u l 17.2 2*7. I t!. * */. 2 r. */ r-i 3t J. L 2.1 C,*f o.i> O.xs CMA 114520 !f TAZLc 3 04 A-/ Oi A. At $ Z/AfC/Si ?e'o 3 T"A no*4 IzxPQ SUX.S 0 COHCGur/lA TlJU Qua AnctJ XC-Si p f* 4 YA4.S 3lSfv JMd S C*/ XCS? &I&K. * lfli A ifdo 14 eft 1 9 82 30. *< /2 J7 j / 9*3 f 1 9ts l / *7 i.a V.2 5. 3 , 4r 1.7 / ffi* >.3 o. / / `rtV I99S~ l^UT A.Of 0 .of i G,7<7 8,7 9 / 3. 7/ IX. So 1 /.XL. ii. 7L 1 Ai /V. Vo i /i.JC i .90 tL.lL t . H ib.Za 1 . if IC.99 i . J3 n.& i , /g / ?. V7 i* n.a IS* ,/0 /27f 5 / fd Si.9 /< rt. / f2/f 3 r.i Vo / /f4* a.y 2.3 IV7 /tab tin* t 776-/79* / <r?3- -J*jo7 t.i 1 .X .3 ,,r .03 . 03 i 7.07 7.87 i 3. 3o tl.17 i /.ii IX. 3 A i >*? (1.07 1 .07 IX.7L 1 .iJ /v.vf i 17.77 i . 17 /S.0<- i .'0 A-.iV i .18 /r?fi S .03 />". IS .10 /sr./s* -202- CMA 114521 TA S "5, C CauD H U/Zb') /.rc./&.SS CA N uA AiSK Sl*<-(Z. I` I5.X f> O > U *<5. /VAiKta ZiJ'lGA'AJ il? pas ue, pRus C.\?WC^rXAT7flW \jUATUJ *J PPS V AAA Sk <-$ d\ska, j *" o/t OiS* *<#f 1 Itt0 I *8 1 / f 82 1 48,3 i 4* / 48 / 4ec. 1 <rH 7 /4* / 4fi <4 i Ho-trt* / f^y - iixiy -T7. 1 -IV. 1 tf,2. v.z 3*,*V r* 1.0 -A A5 U.V 42* . AZf t /3 . /<J 1 f.Sl 1 /.S ( .4C ( /.A*/ l /. 4* 1 UV 1 .40 t . 5*7 1 .2.1 S* .X4 /S / 3./ o f(|.42 20<io 21. TO a*.v* J-S.12 IS. SC 14.01 24. Jo JUT./1 -203- CMA 114522 llX .15. SS _____ TA BL(= H CL /Ita. l 5 fA S / A/ C^rS- <"?7Z /rA *S j ATf 4^A/ a 'I* OljiU/llS - i./ii'Y A A*4 *J z *3 v /s a.a_ Puiu A. -iSJLtfS CJA/CAirATj>l PP R 0uA*rwu V/?A#.4 iSXCCZSS /?i&a *./ *" Cu'H srcejs /9 1 4 A .. c a" / 9 *ri '9 73 /4 7Y / 775 / f 7t /f 77 / Y 7tf 'Y?f /4S- tW (7m t le* /Y4 / 7 f?7 /7tt /ret l 77*.- <*7y / 7**-*- 1**< 3.9 // .. / 9,1 17./ 37 .4, it.i iC.7 33.7 its f /. .1 -To' At* 7.a. 3.3* M /. 7 /.3 ,ti .05 1 1 t < 1 t / / / / 1 / < / 1 1 < 1 S* 7 . rf 1. ** *y.7<? 6.1/ 7. 71 5.79 ,7? S. 79 7f 3 7/ /.it .frV .71 .tso .n .37 Jo ./a .*** .u* .e* 3 . >*i ?. fr ixoe 3*j. tt7 37. -va.Y3* -TlUt At 73* 1.2.XI Y 1ST *** OY.fc/ A*o-3 6CYY 0*77 Y 4*" 726>*7V 4>t/i -204- CMA 114523 r/v Bi. cr CA-uc.iXiK a.ii*. ^/a/c/T /f 7: ^"O /z /'u ii;A/l ; j jt/SAA. JC/j^AA.- -5 * ^osu^.i? Cjw Cn/Wr^ATlOW &U(tATfOM ,-*C<^4S r* r /? J c 0 P A <3 V?AAA PliK. AlO S CtJM ^ce^s i9 r$ mji 19 71 Ja 1 . S7 . 7 . S -7 5 /w. s 1 1. 7 J 3 .17 / 9 *7 f / 9 7? <7,*l 2-t, 1 i.4? 7. 15 1 /.J4 ,2. ill i 4 74 3/. 2. ) 7. /# /4. 4` 17 77 34. V l 7. 57 *7 02 -77 - t 7. tf7 3 f, 70 / 47 7 i 4j JT 37.- J 7,*7 V3. 7c I 7, g7 37. <7-i' / //.*# 1 3. J<3 3*4.7 4 / 4e2 r. 3 l /. U i?.9i /4s 2 3.o 1 .frf (*4 1 49*7 3.4 1 .af j7.f3 / 40 S' 2.3 / .5*3 ". OL i 4ei 1.2 1 Ji 1 4 07 t.Z. 1 ,17 re. 43 / 403 . d 1 . /*S 40. B( ! 404 .0 . <a . iv i 4?u - / 44* . 4>3 jT .03 cf.ca /9r J 3> 7 .off J7.0 7 CMA 114524 -205- /Sr 1~A ftu.CZ is, i CAW C/S. A. /I i 4 rV l 9 72. /-jA. SrA-7~itJ*i M V /.XPt> i-'/Lii 5 Oi-.VArt./ o 3 c 1 /IXPoiuA/* ^OA/CiEWrAAT-tUU O^a Arrow rsr ecu P A < J ii yAtts. R lih. xiij^ . C/./7 5ci ft iSk a a 19-72 / *773 / 977 <97!/ f 7C. / 9 7? 7 7 7b 7 1 7V / 7ttc; / fa/ / 9 SI /7S3 /9tt V /73` /7ac 7767 /<rfc rn9 /9fo - /ff* / *TiS~- 2*J 4". 7 / 7. a 1ft. U Vt>. o SV. 39*7. 2. 5*7. 2. 5*7,2. 4*7.2 iy.f 9.2 V. 2 r.7 r.v 1.0 1C JLr .7 .-is* .it 1 I l i i 1 1 i l 1 t l l 1 l t l ) 5* 7 1 ,3J 3.7t 6.iY 9.5C 5/. 7* / a./o /3,io /3.i* / i /o f.n /.ea H t.xi I.XH >9 >o .5*7 .W . 19 /.l? s'-tfS' // .6a 26.76 31. Sf *?.IS 3*8.7S' ea.tr 9*. 97 9J-35 .3i f v.rj 9X79 fM <r?Mt r>.u* ?&*? -206- CMA114525