Document 6RRxKmG3QnGMM0aj6BVj639ao

DRAFT 0171 D/0158W State of California AIR RESOURCES BOARD Staff Report: Initial Statement of Reasons for Proposed Rulemaking r Public Hearing to Consider the Adoption of a Regulatory Amendment Identifying Asbestos as a Toxic Air Contaminant Agenda Item No.: 86Scheduled for Consideration: March 27, 1986 Release Date: February 10, 1986 (This report has been reviewed by the staffs of the California Air Resources Board and the California Department of Health Services and approved for publication. Approval does not signify that the contents necessarily reflect the views and policies of the Air Resources Board or the Department of Health Services, nor does mention of trade names or commercial products constitute endorsement or recommendation for use.) D 004-192 OVERVIEW AND RECOMMENDATION I. INTRODUCTION The Air Resources Board {"ARB" or "Board") identifies toxic air contaminants and develops regulations for the control of their emissions according to the requirements of state law. A toxic air contaminant (TAC) is an air pollutant that the Board or the Department of Food and Agriculture finds may cause or contribute to an increase in mortality or an increase in serious illness, or which may pose a present or potential hazard to human health. Health and Safety Code Section 39655 specifies that substances identified by the U.S. Environmental Protection Agency as hazardous air pollutants (Section 112 of the Clean Air Act) shall be identified as toxic air contaminants by the Air Resources Board. This report recommends that the Board find asbestos (in the following forms: chrysotile, actinolite, amosite, anthophyllite, crocidolite, and tremolite) to be a toxic air contaminant. Section II of this Overview to the report presents the technical and toxicological information that supports the staff's recommendation. Section IIA is a summary of Part A, which presents data on the uses of asbestos, its emissions, and the concentrations of asbestos in the ambient air. Section IIB sunmarizes the Department of Health Services' (DHS) analysis in Part B of the health effects of asbestos. Section III presents the regulatory background and reviews the procedures by which the Board considers substances for the TAC designation. Section IY of this Overview discusses potential environmental effects of the recommended action, and Section V contains the staff's recommendation to the Board. D 004193 II. EVALUATION OF ASBESTOS The ARB and the DHS prioritize candidate substances for evaluation and regulation as toxic air contaminants pursuant to Health and Safety Code (HSC)* Section 39660(f). That section states that the selection of a substance for consideration as a TAC is to be based on the risk to the public posed by the substance, the amount or potential amount of emissions from use of the substance, its manner of usage In California, Its atmospheric persistence, and Its concentration In the ambient air. Under these guidelines, we selected asbestos for the Board's consideration as a TAC because it has been identified by the International Agency for Research on Cancer as a human carcinogen, It Is emitted from many sources in the state. It Is persistent In the atmosphere and in the environment at large, and its presence In the ambient air is documented. Asbestos has also been listed as a hazardous air pollutant by the U.S. Environmental Protection Agency and National Emission Standards have been promulgated. The standards are applicable to asbestos mills, roadways, manufacturing, demolition and renovation of buildings, spraying, fabricating, insulating materials, and disposal of asbestos containing waste. A. EMISSIONS, PERSISTENCE AND AMBIENT CONCENTRATIONS OF ASBESTOS The principal sources of asbestos emissions In California are a) mining and milling, b) manufacturing of asbestos products (both primary and secondary), c) automobile braking, and d) quarrying. Except for quarrying, these emission estimates include total asbestos fibers emitted into the atmosphere. For quarrying, the emission estimates are for asbestos fibers that have an effective aerodynamic diameter of 7 microns** or less. Other * HSC; all statutory references are to the Health and Safety Code, except otherwise stated. **A micron is 1 x 10" meters. -2- D 004194 sources of emissions are demolition and renovation of buildings, roads surfaced with gravel containing asbestos, landfills, and natural weathering or human disturbance of serpentine (asbestos-containing mineral) deposits; however, emissions from these sources were not estimated due to lack of available information. Information on the emissions, persistence, and ambient concentrations of asbestos are summarized on Table I. Asbestos supply and demand data for the United States from 1973 through 1984 shows a general decline in production and consumption. The demand for asbestos Is expected to remain below the 1980 use through 1990. Asbestos is exceptionally resistant to thermal degradation and chemical attack and fine fibers can remain airborne for long periods of time. Settled fibers are easily re-entrained back into the atmosphere. Atmospheric transport involves dispersion and reentrainment of asbestos fibers with deposition occurring due to wash-out and gravitational settling. The deposition and eventual burial of fibers in soils and sediments are the major.- Jr" f processes by which asbestos fibers leave the atmosphere. Asbestos has been documented in the air at several locations statewide by various studies. However, one study* was chosen for use in this report because the staff believes it provides the most suitable and most recent ambient data available for showing exposure to asbestos at several locations in California. The study found that in general, the highest concentrations (average 50 to 500 fibers/cubic meter)** of asbestos were measured at sampling Science Applications, Incorporated, 1983. Ambient Asbestos Concentrations in California - Volumes I and II Although measurement of ambient asbestos fibers is currently performed using transmission electron microscopy (TEM), cancer risk in this report is expressed in terms of phase contrast microscopy (PCM) fiber counts. Therefore, all concentrations in the Overview has been converted to PCM fibers per cubic meter to allow easier comparison of the health risk and exposure data. See Table III for sample calculations.. Note: 100 to 1,000 TEM fibers/PCM fiber. -3- D 004195 table I Summary of Data for Asbestos Emissions Statewide Source Mining Milling Manufacturing Source Type Point Point (Ton Per Year) 120 340 Inventory Year 1984 1984 Primary Point 4 1982 & 1984 Secondary Automobile Brakes Quarrying Total* Point 2 Mobile Point 0.8 JLJi 470 Atmospheric Fate 1982 8 1984 1984 1981 Asbestos can be readily subdivided into fibers of submicron diameter, which can remain airborne for long periods of time. In addition, asbestos is exceptionally resistant to thermal degradation and chemical attack, therefore settled fibers are persistent in the environment and subject to re-entrainment into the atmosphere. Ambient Concentrations Range of Total Asbestos Fibers Measured at Ten Sampling Locations (average of all samples analyzed by transmission electron microscopy and converted to PCM fiber concentrations). Averaged asbestos concentrations range from 8 to 80 PCM fibers per cubic meter at Sonora to 50 to 500 PCM fibers per cubic meter at South Gate. Generally, the highest concentrations were measured at sampling locations influenced by localized and industrial sources; the lowest concentrations were found at sites isolated from asbestos emission sources. * The total emission estimate has been rounded off to one significant figure. -4D 004196 locations Influenced by localized (where asbestos is processed, refined, or otherwise used) and industrial sources (areas with high density clusters of asbestos users). The lowest concentrations (average 8 to 80 fibers/cubic meter) were found at sites isolated from asbestos emission sources. In some of the locations with high concentrations, the population within ten kilometer grids is significant. The samples collected during the referenced study represent short averaging times thus, we are uncertain of how representative these concentrations are of annual averages. In Part A, we also discuss an asbestos contamination problem in Alviso, California that DHS staff has been investigating. The contamination is thought to be caused by asbestos waste disposal and flooding in the area during the past 30 years. Ambient air monitoring studies by OHS have shown significant concentrations of asbestos fibers in the air throughout Alviso. B. HEALTH EFFECTS AND RISK In response to the.ARB staff's request (Appendix A) and according to HSC Section 39660, the Department of Health Services (DHS) evaluated the health effects of asbestos and the risks from exposure to asbestos. To assist DHS, we provided DHS with a bibliography (Appendix B) of literature concerning the health effects of asbestos. The bibliography was obtained from the Toxline, Medline, and Blosis data bases available from NLM and Dialog Information services. Also, we sent a letter (Appendix B) to all Interested parties to request additional information. The Information so obtained was forwarded to DHS. D 004197 -5- In meeting the requirements in Section 39660 for OHS' evaluation, the DHS addresses these issues in Part B: 1) Is asbestos a carcinogen for animals and humans? 2) May health problems other than cancer occur from exposure to ambient concentrations? 3) Is there a "threshold" exposure level below which asbestos will not cause cancer? 4) What is the range of added risk of cancer during a lifetime of exposure to typical ambient concentrations of asbestos? 5) Should some particular fiber types (e.g., chrysotile, amosite) be considered more likely to cause cancer than others? 6) How does the relationship between fiber dimensions and carcinogenic potency affect the appropriateness of extrapolating health effects observed in occupational exposures to ambient air exposures? In response to these Issues, the OHS makes the following conclusions and recommendation in Part B: 1} Asbestos is an undisputed human and animal carcinogen, and has been documented to cause cancer In humans in both occupational and nonoccupational settings. 2) Ambient asbestos levels in California are not expected to cause any acute health effects nor to result In asbestosis, a frequently disabling lung disease. 3) Although the mechanism of asbestos carcinogenicity is unknown, there is no compelling evidence that this process is characterized by a threshold. 4) The Department of Health Services has recommended the use of excess lung cancer lifetime risk values between 11 and 110 cases per million for each 100 PCM (phase contrast microscopy) fibers per cubic meter of asbestos exposure, and for mesothelioma a range of lifetime risk between 38 and 190 cases -6D 004198 for each 100 PCM fibers per cubic meter of asbestos exposure. Selection of these ranges was based on several health conservative assumptions. One effect of these assumptions is to produce estimated ranges of potential risk from exposure to ambient asbestos which, consistent with the health-conservative intent, include the highest, but not the lowest, reasonable projections. Estimated lifetime risks of lung cancer and mesothelioma by exposure group are shown in Table II. To calculate the risk estimates in Tables III and IV, DHS used average mean asbestos concentrations that have been measured in California. The concentrations used for exposure levels were 8 3 "3 to 80 fibers/m for the lower range and 50 to 500 fibers/m for the upper range. Because of differences in counting methods, the average mean asbestos concentrations which were analyzed and counted by the transmission electron microscopy (TEM) method had to be converted to phase contrast microscopy (PCM) concentrations for DHS to do their risk analysis for those concentrations (see Table III). These values are consistent with the results of air sampling in a variety of locations in the United States (NRC, 1984).* As shown in these tables, risk estimates were also developed for a concentration of 2,000 fibers/m3, chosen by the NRC (1984) as representative of the 90th percentile of ambient asbestos concentrations, usually indicative of a local source of asbestos contamination. For Information on the references cited in the Overview, see the Part B reference listing beginning on page R-l. -7- D 004199 Table II Estimated Lifetime Excess Risks of Lung Cancer and Mesothelioma Due to Continuous Exposure to 100 Fiber/m3 of Asbestos (Expressed as Cases per Million Population)!/ Exposure Group Male Smokers Female Smokers Male Nonsmokers Female Nonsmokers Lung Cancer 11 (110) 5 (50) 2 (15) 1 (6) Mesothelioma 24 (120) 32 (160) 32 (160) 38 (190) )_/ Numbers in parentheses represent approximate upper confidence limits. The analysis corrected for competing causes of death using lifetables constructed from recent California vital statistics. Since risks for lung cancer and for other causes of death are dependent on smoking status, the lifetables were modified to account for age- and gender-specific smoking prevalence. Thus, risks are presented by gender and smoking status. -8D 004200 TABLE III Estimated Lifetime Excess Lung Cancer Risk Due to Continuous Exposure to Asbestos (Expressed as Cases per Million Population)* Exposure Level {fibers/m3) Exposure Group 8 50 80 500 2,000 Male Smokers 1(0-9)** 6(0-55) 9(0-88) 55(0-550) 221(0-2,210) Female Smokers 1(0-5) 2(0-25) 5(0-41) 25(0-250) 101(0-1,010) Male Nonsmokers 1(0-1) 1(0-8) 1(0-11) 8(0-75) 29(0-290) Female Nonsmokers 1(0-1) 1(0-3) 1(0-5) 3(0-28) 11(0-110) * Calculated with Ci = 0.01. Ranges in parentheses were estimated with a lower limit of zero and an upper limit calculated with C] = 0.1. This upper bound is an approximate upper confidence limit. ** Sample Calculation For Excess Lung Cancer Risk - Male Smokers Coversion from TEM = (7.700 TEM fibers) (1 PCM fiber) to PCM concentrationsiP (1000 TEM fibers) = 7.7 or 8 fibers/nr* Estimated lifetime excess* (PCM concentration) x (Lung cancer estimated lung cancer risk-lower (Estimated lifetime lifetime risk) confidence limit risk exposure concentration) =(8 fiber/m3) v n (lOO fibers/m3} = 0.88 or 1 Estimated lifetime =(8 fibers/m^) y 110 excess lung cancer (100 fibers/nr) risk - higher confidence 1 imit = 8.8 or 9 D 004201 -9- TABLE IY Estimated Lifetime Excess Mesothelioma Risk Due to ~ Continuous Exposure to Asbestos (Expressed as Cases per Million Population)* Exposure Group Male Smokers Female Smokers Male Nonsmokers Female Nonsmokers Exposure Level (fibers/m8) 8 50 80 500 2(0-9)* 11(0-59) 19(0-95) 120(0-590) 2(0-12) 16(0-81) 26(0-120) 160(0-810) 2(0-12) 16(0-79) 25(0-120) 160(0-790) 3(0-16) 19(0-97) 31(0-160) 190(0-970) 2,000 470(0-2,400) 640(0-3,300) 630(0-3,200) 780(0-3,800) * Calculated with Cm = 2.4 x 10"8, P * 3.0, 20-year lag. Ranges in parentheses were estimated with a lower limit of zero and an upper limit calculated with Cm = 1.2 x 10"*7, which is the highest estimated value for the proportionality constant C^ (from Finkelstein, 1983). -10- D 004202 5) Risk assessment should not be segregated by fiber type. 6) DHS staff members believe that it is appropriate and reasonable to extrapolate from occupational exposure measurements to ambient air exposures. The Department of Health Services' conclusions and recommendation were based upon the following: o Asbestos has been consistently demonstrated to be carcinogenic in animals and humans and Is recognized as a human carcinogen by the International Agency for Research on Cancer. o In occupational cohort mortality studies, exposure to the three principal commercial forms of asbestos has been repeatedly linked with increased risks for lung cancer, mesothelioma and, to a lesser extent, other neoplasms. o Other than cancer, the most serious adverse health outcome ascribed to asbestos exposure is asbestosis, a consequence of extensive fibrosis of the lung due to the presence of asbestos fibers. However, DHS staff members concur with the Consumer Products Safety Commission (CPSC) (1983) panel that knew of Hno reports of disabling asbestosis occurring among persons whose maximum exposure to asbestos was of the order of 1 fiber/ml (by PCM) or less". The reserve capacity of the lung is sufficiently large that exposure to ambient asbestos levels does not yield asbestosis symptomatology. o Chronic exposure to asbestos can also result in pleural changes (thickening, plaque formation, and/or benign effusions), which are generally asymptomatic. o' Lung cancer and mesothelioma are the outcomes of interest for the purpose of a quantitative risk assessment, since both are considered -H- D 004203 to be nonthreshold processes posing potential population risks at ambient concentrations of asbestos. The risk assessment utilized the work done by the CPSC (1983), the National /Icademy of Sciences (NRC) (1984), Nicholson (1985), and the Ontario Royal Commission (1984). o DHS adapted models developed and/or used by earlier investigators to estimate risks of mesothelioma and lung cancer to the general population, and extrapolated risks observed in occupationallyexposed cohorts to lower levels of asbestos to which the general population may be exposed. o In estimating the maxmlum excess lifetime risks, DHS has used health conservative assumptions. Some of the more significant health conservative assumptions can be classified as relating to pathophysiology, to exposure or to the models used. These assumptions are listed below: Pathophysiology. The carcinogenic effects of asbestos fibers are assumed to be exerted by short ( <5 microns in length) fibers as well as long ( >5 microns) ones, at doses substantially lower than those in past occupational settings (see Sections 9.b and 9.d of Part B). Chrysotile is assumed to be as potent as the amphiboles in causing mesothelioma (see Section 9.f of Part B). Exposure. Exposure to ambient levels of asbestos is assumed to occur 24 hours/day at ambient levels for a lifetime (see Section 9.f of Part B). , Models. The risk assessment models are nonthreshold and are linear with dose. The lung cancer proportionality constant -12- D 004204 "C-j " used by DHS was derived omitting the results from the nwning and milling epidemiologic studies (see Section 9.a.i.5 of Part B ). The upper bound in DHS risk assessment was calculated with Cj set at 0.1, which was the highest 95% upper confidence limit estimated for any of the epidemiologic studies under consideration (See Section 9.2 of Part B). o DHS* estimated lifetime risks of lung cancer and mesothelioma dje to continuous exposure to 100 fibers/m3 of asbestos are compatible with the range of risks derived from the reports by NRC (1984), CPSC (1983) and Nicholson (1985). Mesothelioma risk estimates are also consistent with tne recent incidence data obtained from the Bay Area Surveillance Epidemiology and End Results Program for 1973-1983. o Although some epidemiologic evidence suggests that the risk of mesothelioma from exposure to chrysotile may be lower than that from exposure to the amphiboles,* DHS concludes that there is no compelling reason to differentiate between fiber types in risk assessment. Mixed exposures, lack of good quantitative exposure data, and the physical effects of different industrial processes on asbestos fibers make the comparison of epidemiological studies problematic in this respect. Furthermore, in animal studies chrysotile has been shown to be at least as potent as the amphiboles in inducing mesothelioma. o The generally accepted hypothesis that longer and thinner fibers have greater carcinogenic potency than shorter and/or thicker fibers was based on Stanton's study in which animals exposed to large Anphibole asbestos is a general term for all varieties other than chrysotile. -13- D 004205 numbers of long, thin fibers produced the highest incidence of mesotheliomas. However, DHS staff members have found limitations with the experimental b_asis for this hypothesis. These limitations are: 1) The experimental model can be directly applied only to mesothelioma; 2) The range of fiber dimensions used in the study is incomplete or uncertain due to the Inherent problem of accurately measuring asbestos fibers and the difficulty of obtaining the exact distribution of fiber dimensions; 3) Further analysis of the experimental data indicates that carcinogenicity appears to be a continuous, increasing function of the aspect ratio of fiber dimensions; 4) Although the clearance of shorter fibers is more efficient such clearance is neither instantanous nor complete; 5) Most asbestos fibers found at the pleura are short ( < 5 microns), fine chrysotile, as opposed to the mixed fiber populations found In the lung parenchyma; and 6) The relationship of physical dimensions of fibers and their translocation and final deposition to target organs In humans has not been well characterized. III. REGULATORY BACKGROUND AND PROCEDURES Division 26, Chapter 3.5 of the HSC and Food and Agriculture Section 14021 et seq. set forth the procedure for identifying and controlling toxic air contaminants in California. (These provisions were enacted in September 1983 as Assembly Bill 1807, Stats. 1983,' ch. 1047). The Department of Food and Agriculture is responsible for identifying and controlling TACs in their pesticidal uses. The ARB has authority over TACs in all their other uses. -14- D 004206 HSC Section 39650 sets forth the Legislature's findings about substances which may be TACs. The Legislature has declared: "TTiat public health, safety, and welfare may be endangered by the emission into the ambient air of substances which are determined to be carcinogenic, teratogenic, mutagenic, or otherwise toxic or injurious to humans." The findings also include directives on the consideration of scientific evidence and the basis for regulatory action. With respect to the control of TACs, the Legislature has declared: "That it is the public policy of this state that emissions of toxic air contaminants should be controlled to levels which prevent harm to the public health." The Legislature has further declared that, "while absolute and undisputed scientific evidence may not be available to determine the exact nature and extent of risk from toxic air contaminants, it is necessary to take action to protect public health." In the evaluation of substances, the Legislature has declared that the i best available scientific evidence, gathered from both public agencies and private sources, including industry, should be used. The Legislature has also determined that this information should be reviewed by a scientific review panel and by the public. The Board's determination of whether or not a substance is a toxic air contaminant includes several steps specified by HSC. First, we request the OHS to evaluate the health effects of a substance (Section 39660). The evaluation Includes a comprehensive review of all available scientific data. Upon receipt of a report on health effects from DHS and in consideration of -15- D 004207 their recommendations, we prepare and submit a report to the Scientific Review Panel (SRP) for its review (Section 39661). The report consists of the OHS report (Part B), and material prepared by the ARB staff on the use, emissions and ambient concentrations of the substance (Part A). It serves as the basis for future regulatory action by the Board. The report is also made available to the public, who may submit comments on the report to the SRP. After receiving the SRP's written findings on the report, the Board issues a public hearing notice and a proposed regulation which include the proposed determination that a substance is a toxic air contaminant. If, after a public hearing and other procedures to comply with Government Code Section 11340 et seq., the Board determines that a substance is a toxic air contaminant, its findings must be set forth in a regulation (Section 39662). The HSC also sets forth procedures for developing and adopting control measures for substances identified as TACs (Sections 39665-39667). IV. ENVIRONMENTAL EFFECTS The identification of asbestos as a TAC will not In itself have any environmental effects. If the Board lists asbestos as a TAC, the staffs of the ARB and the air pollution control districts will evaluate the need for, and appropriate degree of controls for emission sources. After this evaluation, the Board and the districts may adopt emission control measures which will result In the reduction of asbestos concentrations in the ambient air. Any environmental effects associated with control measures will be identified when such control measures are considered pursuant to HSC Sections 39665 and 39666. -16- D 004208 V. RECOMMENDATION Because asbestos is a known animal carcinogen and human carcinogen, has been listed by the U.S. Environmental Protection Agency as a hazardous air pollutant, and is known to be anitted in California, the ARB staff recommends its listing as a toxic air contaminant. In making this recommendation, we note that there is not sufficient available scientific evidence to support the identification of an exposure level below which carcinogenic effects would not occur. -17- D 004209 State of California AIR RESOURCES BOARD TECHNICAL SUPPORT DOCUMENT PUBLIC HEARING TO CONSIDER THE ADOPTION OF A REGULATORY AMENDMENT IDENTIFYING ASBESTOS AS A TOXIC AIR CONTAMINANT Agenda Item No.: 86Scheduled for Consideration: March 27, 1986 Release Date: February 10, 1986 D 004210 Part A Part B Part C TABLE OF CONTENTS A Review of Asbestos Uses, Emissions and Public Exposure Health Effects of Asbestos Public Comments and Responses D 004211 PART A - A REVIEW OF ASBESTOS USES, EMISSIONS AND PUBLIC EXPOSURE Prepared by the Staff of the Air Resources Board January 1986 (This report has been reviewed by the staffs of the California Air Resources Board and the California Department of Health Services and approved for publication. Approval does not signify that the contents necessarily reflect the views and policies of the Air Resources Board or the Department of Health Services, nor does mention of trade names or caimercial products constitute endorsement or recommendation for use.) D 004212 PART A - A REVIEW OF ASBESTOS USES, EMISSIONS AND PUBLIC EXPOSURE LIST OF TABLES AND FIGURES TABLE OF CONTENTS I. NATURAL OCCURRENCE, PRODUCTION, USAGE, AND EMISSIONS A. NATURAL OCCURRENCE B. PRODUCTION C. USAGE D. ESTIMATED STATIONARY AND MOBILE SOURCE EMISSIONS II. PERSISTENCE IN THE ATMOSPHERE A. CHEMICAL AND PHYSICAL PROPERTIES B. FATE IN THE ATMOSPHERE III. EXPOSURE TO ASBESTOS A. ASBESTOS MEASUREMENT TECHNIQUES B. ASBESTOS MEASUREMENTS C. AMBIENT ASBESTOS CONCENTRATIONS D. SOURCE OF ASBESTOS CONTAMINATION E. EXPOSURE THROUGH OTHER MEDIA APPENDIX A - DEPARTMENT OF HEALTH SERVICES HEALTH EFFECT EVALUATION REQUEST APPENDIX B - INFORMATION REQUEST AND PUBLIC RESPONSES APPENDIX C - EMISSIONS CALCULATIONS APPENDIX D - DOCUMENTS CONTAINING ASBESTOS MEASUREMENTS TAKEN IN CALIFORNIA APPENDIX E - AMBIENT ASBESTOS MEASUREMENTS IN CALIFORNIA page No. 1-1 1-3 1-3 1-5 II-l II-7 II1-1 III-3 III-IO I11-21 III-21 A-l B-l C-l D-l E-l D 004213 APPENDIX F - SAI SAMPLING, SAMPLE PREPARATION, ANALYSIS AND QUALITY CONTROL TECHNIQUES APPENDIX G - MEMORANDUM REGARDING ASBESTOS CONTAMINATION IN ALVISO, CALIFORNIA APPENDIX H - CALCULATIONS AND DISCUSSION OF ESTIMATES ON YEARLY INTAKE OF ASBESTOS FIBERS F-l G-1 H-1 D 004214 LIST OF TABLES AND FIGURES TABLES 1-1 1-2 1-3 1-4 SUMMARY OF ESTIMATED ASBESTOS EMISSIONS SUMMARY OF ASBESTOS EMISSIONS FROM PRIMARY MANUFACTURING LOCATIONS OF PRIMARY MANUFACTURING FACILITIES IN CALIFORNIA SUMMARY OF ASBESTOS EMISSIONS FROM SECONDARY MANUFACTURING PAGE 1-8 1-12 1-13 1-14 1-5 LOCATIONS OF SECONDARY MANUFACTURING FACILITIES IN CALIFORNIA 1-15 II-l MINERALOGY OF COMMERCIAL ASBESTOS 11--2 11-2 11-3 CHARACTERISTICS OF THE MAIN TYPES OF ASBESTOS FIBERS SUMMARY OF AVERAGE DIAMETERS AND LENGTHS OF SAMPLES COLLECTED BY SAI DURING 1981 11-6 11--8 III-l NAMES, CLASSIFICATION CATEGORIES AND POPULATION NEAR THE TEN SITES CHOSEN FOR THE SAI ASBESTOS SAMPLING STUDY III-7 111-2 SUM1ARY OF INDIVIDUAL ASBESTOS SAMPLES COLLECTED BY SAI DURING 1981 III-ll 111-3 SUMMARY OF AVERAGED AS8EST0S CONCENTRATIONS SAMPLED BY SAI DURING 1981 III-16 111--4 MEAN ASBESTOS CONCENTRATIONS CALCULATED BY THREE AVERAGING METHODS III-19 111--5 YEARLY INTAKE OF ASBESTOS FIBERS FROM VARIOUS MEDIA FOR AN OFFICE WORKER, HOUSE PERSON, AND CHILD II1-22 111--6 ASBESTOS CONCENTRATIONS FOUND IN CALIFORNIA WATERS II1-25 III-7 SUMMARY OF INDOOR ASBESTOS SAMPLES II1-26 111-8 INDOOR ASBESTOS MEASUREMENTS TAKEN IN A CALIFORNIA BUILDING I11--28 AND THREE HOMES FIGURES 1-1 PRINCIPAL ASBESTOS DEPOSITS IN CALIFORNIA 1-2 1-2 ASBESTOS PRODUCTION AND CONSUMPTION IN THE UNITED STATES 1-6 1-3 FLOW DIAGRAM OF ASBESTOS MINING AND MILLING 1-9 D 004215 II1-1 II1-2 CALIFORNIA MAP SHOWING LOCATIONS OF THE TEN SAMPLING SITES USED IN.THE SAI STUDY RELATIONSHIP BETWEEN DETECTION LIMIT AND SAMPLING TIME USED IN SAI ASBESTOS STUDY 111-8 II1-17 D.004216 I. NATURAL OCCURRENCE. PRODUCTION. USAGE, AND EMISSIONS A. NATURAL OCCURRENCE The word "asbestos" is not a mineral name, but a term applied to a group of naturally occurring mineral silicate fibers of the serpentine and amphibole series. Serpentine minerals are "layered silicates" and only one of these, chrysotile, is an asbestos mineral. The amphibole asbestiform minerals are "chain silicates" and the five varieties of commercial importance are commonly known as actinolite, amosite, anthophyllite, crocidolite and tremolite (Chronic Hazard Advisory Panel on Asbestos, 1983). Chrysotile occurs only in serpentine, a fine-grained rock composed almost entirely of hydrous magnesium silicate minerals similar to chrysotile in chemical composition. Serpentine Is a secondary rock, derived by alteration of several magnesium-rich types of Igneous rocks, principally peridotite, and is abundant in the Coast Ranges, Sierra Nevada, and Klamath Mountains of California (California Department of Conservation, 1963). Amphibole asbestos Is a general term for all varieties other than chrysotile. Only a few of the amphibole minerals, primarily those that are aluminum poor, become sufficiently fibrous to be used as asbestos. Of these, tremolite and actinolite are the only ones that have been of significance in California. Amosite has not been found in California, and crocidolite and anthophyllite have not been found here in commercial quantities (California Department of Conservation, 1963). Figure 1-1 shows the principal asbestos deposits in California and the location of the two operating mines. 1-1 D 004217 Figure i-i SOURCE' CALIFORNIA DEPARTMENT OF CONSERVATION, 'CALIFORNIA ASBESTOS INOUSTRT*, SEPTEMBER ISS5 1-2 D 004-218 A M ItO N A B. PRODUCTION Only three mines produce asbestos in the United States, two of these are in California: The Calaveras Asbestos Corporation which operates a mine in Calaveras County, and KCAC, Inc. which operates a mine in San Benito County. Both mines produce chrysotile asbestos by open pit mining (Burnett, 1982; U.S. Department of the Interior, 1976-1984; Versar Inc., 1984). Prior to 1980 as many as five asbestos mines were in operation in California (Roberts, 1980). In 1984, California mines and mills produced 57,308 tons of asbestos. C. USAGE Before asbestos from a mine can be used, it must be processed into fiber at a mill. Milling is a complex operation which separates the fiber from the mined rock by repetitively crushing the rock and then screening out the fiber. The fiber is then separated into various grades based on length. The processed asbestos fibers are then utilized by either primary or secondary manufacturers to produce various products for end users (U.S. Department of the Interior, 1980). The longest fibers are used for spinning and are woven into fabrics while the shorter fibers, nonspinning grades, are used in such products as cement or paper stock. Primary manufacturers are companies that process raw asbestos fiber into either intermediate products (to be further processed or fabricated) or into finished products. Intermediate products from primary manufacturers include gasket paper, electrical insulating paper, textiles, packings and gaskets, and asbestos-cement sheets. Typical examples of finished products from primary manufacturers Include coating mixtures, adhesives and sealants, floor covering, roofing felts, and asbestos-cement pipes. Some primary products 1-3 D 0042^9 such as asbestos cement pipe, vinyl asbestos floor tile, and asbestos coatings and sealants undergo little or no secondary processing. Other products such as asbestos packings.-, gasketing materials, asbestos textiles, asbestos reinforced plastics, asbestos papers, and asbestos cement sheets must undergo further fabrication or modification before the product is finished (Versar Inc., 1984). Secondary manufacturers are companies that further process the intermediate asbestos product to produce either another intermediate product or a finished product. Some examples of finished products from secondary manufacturers Include tapes, spacers, washers and electrical component boards fabricated from electrical insulating paper; brake pads riveted or bonded to brake shoes; fume hood liners and laboratory table tops (Versar Inc., 1984). Although processed asbestos fiber has more than 2000 uses, its major use has been in products connected with the construction Industry (U.S. Department of the Interior, 1980). In 1984, the end use consumption of asbestos in the U.S. was as folldws: friction products, 22 percent; flooring products, 21 percent; asbestos cement pipe, 12 percent; coatings, adhesives and sealant compounds, 11 percent; asbestos cement sheet, 8 percent; packings and gaskets, 6 percent; roofing products, 3 percent; paper and textiles, 1 percent; and other, 16 percent (U.S. Department of the Interior, 1985). Of the total asbestos consumed in the United States in 1983, 97 percent was chrysotile and three percent was crocidolite. Small amounts of amosite were reported used (U.S. Department of the Interior Minerals Yearbook, 1984). A more recent breakdown of the types of asbestos used is not yet available. Asbestos supply and demand data during the last 10 years shows a general decline in production and consumption. Figure 1-2 depicts the general 1-4 D 004220 decrease in production and consumption of asbestos from 1973 to 1984 (U.S. Department of the Interior, 1965-1974; U.S. Department of the Interior, 1976-1984). The demand for asbestos is expected to remain below the 1980 use through 1990 (U.S. Department of the Interior, 1985). Consumption of asbestos could decrease at a greater rate if the U.S. Environmental Protection Agency (EPA) pursues a draft proposed asbestos ban under the Toxic Substances Control Act. On June 15, 1984, EPA submitted to the Office of Management and Budget (0MB) a draft proposed rule that would have banned the use of asbestos in asbestos cement pipe, roofing tiles, floor tiles, and sealant compounds beginning in 1985. EPA submitted a second draft proposed rule on August 15, 1984 that would have banned the use of asbestos clothing immediately and would have banned all uses of asbestos by 1995. EPA's regulatory impact analysis of the proposed rules attributed 87 percent of the benefits to reduced exposure in the workplace. The other 13 percent were attributed to reduced ambient exposure. The EPA dropped its proposal to ban asbestos in February, 1985 based on OMB's legal analysis which concluded that it was appropriate for EPA to refer regulatory authority to another agency if that agency can reduce or prevent the risk associated with the substance. It is unclear at this time if EPA will pursue this again in the future. D. ESTIMATED STATIONARY AND MOBILE SOURCE EMISSIONS The principal sources of asbestos emissions in California are a) mining and milling, b) manufacturing of asbestos products (both primary and secondary), c) automobile brakes, and d) quarrying. Other sources of emissions are landfills, renovation and demolition of buildings, roads 1-5 0 004221 CO 00 eo 00 00 z o CM 00 CzL CO zo CO z oo o o 00 Q OO 00 cm cm c\j o o o oo CMI 00 <U i_ C3TI 00 r>. < vOI UJ > oo u_ -*Z hZO3(0<ZQ HOZCO GO <0 OO uo roo T Z o GO HCOO) CO OZ) chcchn a oo a O CL CL a zx Q. *- bJ I I l I I I surfaced with gravel containing asbestos, and natural weathering or human disturbance of serpentine (asbestos containing mineral) deposits. A summary of estimated asbestos emissions is shewn in Table 1-1. Except for quarrying, the emission estimates include total asbestos fibers emitted into the atmosphere. For quarrying, the emission estimates are for asbestos fibers that have an effective aerodynamic diameter of 7 microns or less. 1. Mining and Milling Mining and milling by the Calaveras Asbestos Corporation and KCAC, Inc. account for most of the estimated emissions of asbestos in the state (refer to Table 1-1). These emissions arise from activities such as drilling, blasting, gathering and loading of ore, transportation of the ore, milling, and the removal of waste dust (Archer and Blackwood, 1979; Versar Inc., 1984). Figure 1-3 shows a typical flow diagram of mining and milling operations. Available asbestos emission factors for mining operations range from 5 to 8 pounds per ton of processed ore if emission control methods are used and from 9 to 10 pounds per ton if no control methods are used (Archer and Blackwood, 1979; Meylan, et al., 1978; Rajbans and Bragg, 1978; Versar Inc., 1984). Emission control methods for mines include spraying the ore and/or roadways to reduce dust, as well as fitting drilling equipment with cyclone dust collectors. Generally, it is difficult to completely control mining operations because many activities are carried out in the open. Since California mines are required to use control methods in order to comply with the National Emission Standard for Asbestos and to wet exposed ore, the lowest emission factor of 5 pounds per ton was used to estimate mining emissions. 1-7 D 004223 Table 1-1 Summary of Estimated Asbestos Emissions Source Source Tvoe Mining Point Mi11ing Point Manufacturing Primary Point Secondary Point Automobile Brakes Mobile Quarrying Point Total Emissions* (tons/vear) 120 340 Inventory Year 1984 1984 4 2 0.8 0.5 470 1982 A 1984 1982 A 1984 1984 1981 Reference 1/ 1/ y y 3/ 4/ * The emission estimates may not total due to rounding. 1/ Archer and Blackwood, 1979; Roberts, 1980; U.S. Department of the Interior, 1976-1984; Yersar Inc., 1984. y California Air Resources Board, 1985; Yersar Inc., 1984; Zwiacher et al., 1983. y California Air Resources Board, 1984; Williams and Muhlbaier, 1982. y Air and Industrial Hygiene Laboratory, 1981; Blackwood, Chalekode, and Wachter, 1978; U.S. Environmental Protection Agency, 1981. 1-8 D 004224 OKU AREA Figure 1-3 FLOW DIAGRAM OF ASBESTOS MINING AND MILLING Source: Versar Inc., 1984. 1-9 D 004225 Asbestos emissions from mining operations are therefore estimated to be approximately 120 tons in 1984. Reported milling-emission factors range from 12 to 80 pounds per ton if controlled and 100 pound per ton if uncontrolled (Archer and Blackwood, 1979; Meylan, et al., 1978; Rajbans and Bragg, 1978; Versar Inc., 1984). A number of control methods are used for milling operations. Cyclones are used first to concentrate and collect the fibers. Figure 1-3 shows the typical locations where cyclones are used. Baghouses are then used to control the air emissions of asbestos from such processes as crushing, screening, fiberizing, product bagging, and conveying of waste rock material to the tailing pile (Harwood and Blaszak, 1974; Meylan, et al., 1978; Versar Inc., 1984). Engineering estimates of collection efficiency for baghouses are about 99.99 percent for fibers greater than 1.5 urn and about 98 percent for fibers less than 1.5 urn in length (Harwood, C. F., et al., 1974). However, the overall reduction in asbestos emissions should be greater when cyclones and baghouses are used in series. Tailing emissions also arise from the milling operation. These are usually controlled by spraying with water and chemical stabilizers. The Calaveras Asbestos Corporation uses baghouses or cyclones combined with baghouses to control emissions during ore preparation, drying, at the dryrock storage building, and on the milling facility. They also apply chemical stabilizers and water to control emissions from mill tailings . Assuming that both milling facilities in the state control asbestos emissions to the lowest reported level, an emission factor of 12 pounds per ton of processed asbestos was used to calculate emissions. The estimated emissions from California milling operations in 1984 is 340 tons. 1-10 D 004226 2. Manufacturing Emissions ~a. Primary There are 42 identified primary manufacturers of asbestos products in the state. Of these, 33 are in the South Coast Air Basin. About three-fourths of the manufacturers produce coatings, adhesives and sealants. The rest are producers of asbestos cement pipe, asbestos reinforced plastic, floor tiles, paper, packings and gaskets or friction products. Reported emission factors for primary manufacturing of the various asbestos products range from 0.14 pound to 1.1 pounds asbestos per ton of asbestos used (Versar Inc., 1984). Applying these factors to the data derived from surveys of asbestos product manufacturers, asbestos emissions from primary manufacturing are estimated to be about 4 tons per year. Table 1-2 presents estimated emissions by product category for the primary manufacturing facilities and Table 1-3 shows where the facilities are located. Although most of the manufacturers produce coatings, adhesives or sealants, over 70 percent of the estimated emissions come from the production of asbestos cement pipe. Emissions occur during the mixing of asbestos fiber with cement and silica, and during the receiving and storage of asbestos. Baghouses are typically used to control emissions where possible. The overall emission factor for the process was estimated to be 0.30 pound per ton (Meylan, et al., 1978; Versar Inc., 1984). b. Secondary There are 48 Identified secondary manufacturers of asbestos products in California. About half are engaged In the fabrication of friction products, 27 percent in packings and gaskets and the rest in paper, coatings, adhesives and sealants, plastics, textiles and chlorine manufacture. The combined 1-11 D 004227 Table 1-2 Summary of Asbestos Emissions from Primary Manufacturing!/ Friction Products Packings and Gaskets Coatings, Adhesives and Seal ants Cement Pipe Paper PIastics No. of Facilities 2 2 32 2 1 2 Floor Tile Total 1 42 Total Tons Processed 350 3 4,080 16,700 30 9,300 30 30,493 Emission Factors (oound/ton) Emissions* (ton/vear) 0.60 0.60 0.20 0.1 . < 0.1 0.4 0.30 1.10 0.14 0.34 3 < 0.1 0.7 < 0.1 4 * The emission estimates may not total due to rounding. U References used to develop this table were: Air Resources Board, 1985 and Zwlacher, 1983. Emission factors used were taken from Versar Inc., 1984. 1-12 D 004228 Table 1-3 Locations of Primary Manufacturing Facilities in California Product Los Angeles Countv Orange Countv Other 1/ South San Coast Diego Counties County Contra Costa Countv A1ameda County Other/ Bay Area Counties San Joaquin Countv Total Friction Products 2 2 Packings and Gaskets 1 1 2 Coatings, Adhesives and Sealants 19 2 3 12 3 2 32 Cement Pipe 1 12 Paper 11 Plastics 11 2 Floor Tile J_ -- J_ Total 24 4 4 1 3 3 2 1 42 y Riverside County and San Bernardino County tJ San Francisco County and San Mateo County 1-13 D 004229 Table 1-4 Summary of Asbestos Emissions from Secondary Manufacturing!/ Friction Products Packings and Gaskets Coatings, Adhesives and Sealants Paper Plastics Textiles Chlorine Manufacturing Total No. of Facilities 25 13 1 5 1 2 1 48 Total Tons Processed 12,500 80 0.2 13 0.1 0.6 30 12,624 Emission Factors (Dound/ton) Emissions* (ton/vear) 0.31 0.53 2 < 0.1 0.024 <0.1 1.08 0.14 0.28 0.14 < 0.1 < 0.1 < 0.1 <0.1 2 * The emission estimates may not total due to rounding. }/ References used to develop this table were: Air Resources Board, 1985 and Zwiacher, 1983. Emission factors used were taken from Versar Inc., 1984. 1-14 D 004230 Table 1-5 Locations of Secondary Manufacturing Facilities in California Product Los Angeles County Friction Products 20 Packings and Gaskets 6 Coatings, Adhesives and Sealants Paper 3 Plastics Textiles 2 Chlorine Manufacturing Total 31 Orange County 2 3 2 1 8 Other 1/ South Coast Counties 1 1 1 3 Contra Costa Countv 2 3 Alameda Countv Total 2 25 1 13 1 5 1 2 J_ 3 48 1/ Riverside County and San Bernardino County 1-15 D 004231 asbestos emissions from these secondary facilities is estimated to be about 2 tons per year. Table 1-4 presents a summary of asbestos emissions by product category from secondary manufacturing and Table 1-5 shows where the facilities are located. As in primary manufacturing, baghouses are the major emission control device used by secondary manufacturers. 3. Automobile Brake Emissions The major constituent of automobile brake linings is chrysotile asbestos which makes up about 35-60 percent of the brake liner. The rest of the ingredients are binders which are phenolic type resins and modifiers such as carbon black, graphite, aluminum and silica (Meylan, et al., 1978). Braking causes the brake lining to wear away and creates dust particles. These particles are first entrained around the brakes, but eventually settle onto the roadway or become airborne. Although the brake material contains about 50 percent asbestos, the emitted particles contain only about 0.029 percent asbestos. Apparently, most of the original asbestos fibers are broken down into nonfibrous materials (magnesium silicates) during the braking process (Lynch, 1968; Rowson, 1978; Williams and Muhlbaier, 1982). On a statewide basis, emissions from automobile brakes are estimated to be a minor fraction (less than 1 ton/year) of the asbestos emissions. This emission estimate is based on an emission factor of 2.6 ug/km/vehicle (California Air Resources Board, 1984; Williams and Muhlbaier, 1982). However, in high braking areas such as toll booths, some researchers reported a noticeable increase in asbestos levels. Air concentrations of asbestos in an area adjacent to a toll booth has been reported to be 3-5 times higher than areas where little braking is expected to occur. 1-16 D 004232 Other possible sources of asbestos emissions related to brake linings occur during the maintenance and repair of the liner. There are no available estimates for emissions from these activities. However, the concentration of asbestos may be significant due to the cloud of dust that is generated in the work area when loose dust is blown from the brake drums and back plates with compressed air (Meylan, et al., 1978). 4. Other Sources of Emissions Other sources of asbestos emissions include 1) emissions related to rock quarrying operations In serpentine deposits and 2) natural weathering or other types of human disturbance of serpentine deposits (e.g., off-road vehicle use, road building). Eight rock quarries in the state are located in serpentine deposits and operate on a continuous basis. The chrysotile concentration in these quarries ranges from trace amounts to 20.0 percent by weight (Air and Industrial Hygiene. Laboratory, 1981; U.S. Environmental Protection Agency, 1981). The number of quarries by county as identified by EPA are as follows: Santa Clara (2), Alameda (1), Marin (1), Tuolumne (3), and Shasta (1). Two of the quarries in Tuolumne County (Six Bits Quarry and Woods Creek Quarry) produce crushed gravel which is used for surfacing unpaved roads. Using the emission factor of 0.012 pound per ton of crushed stone produced (Blackwood, Chalekode and Wachter, 1978), the respirable asbestos emissions from the quarrying of serpentine was estimated to be 0.5 tons per year. According to an EPA report, there are only 5 miles of county roads surfaced with serpentine material in the state. The ARB staff believes there may be a higher number of roads in California surfaced with serpentine material. Information from the Siskiyou County Air Pollution Control District indicated that a temporary rock quarry in Siskiyou County supplied serpentine 1-17 D 004233 rock for use by the U. S. Forest Service In the building of roads in the Shasta-Trinity National Forest. Tests by the National Institute for Occupational Safety and Health (NIOSH) showed asbestos ranging from 1 to 30 percent by volume in the serpentine rock. The U.S. Forest Service hired Radian Corporation to obtain airborne samples of asbestos near the roadways. The study showed asbestos in the samples ranging from 0.01 to 0.27 fibers per cubic centimeter (see Part C). The ARB staff has not determined how the samples were analyzed and has requested a copy of the Radian study from the U.S. Forest Service. The Radian study points out the need to consider, in future inventories, the fugitive emissions from roads surfaced with serpentine rock. At the present time, emission factors are not available to estimate these emissions. Some other potential sources of asbestos emissions for which emission factors have not been established are demolition and renovation of buildings, maintenance and installation of insulating materials, landfills and natural sources of asbestos. An EPA report and survey estimated that 95,556 public and private schools and 700,000 commercial, residential apartments, and federal buildings in the United States contain friable asbestos materials (Greenblatt, 1984; Zurer, 1985). If these buildings were demolished or renovated, the potential emissions to the atmosphere can be significant; however, there is no information available to allow one to estimate the emissions from the demolition and renovation of buildings. The ARB staff recognizes that emissions from this source and others for which emission factors have not been established can contribute to ambient levels of asbestos. As new information becomes available, these emissions should be added to the inventory. 1-18 D 004234 It has been reported that about 90 percent of asbestos scrap (baghouse dust and product wastes) are eventually disposed of in landfills (Meylan, et al., 1978). The Department of Health Services considers waste materials containing asbestos as hazardous waste and has issued specific guidelines for asbestos handling and disposal. The Department's guidelines state that the asbestos waste should be wetted and sealed in non-returnable containers or in closed vehicles for handling and transport. For disposal, the guidelines specify that advance arrangements be made with the disposal site operator to assure that the asbestos containing waste is covered quickly with six inches of compacted soil. Landfill operators are also cautioned to take actions that ensure the compacting equipment does not become contaminated with asbestos dust. Appendix C contains the calculations used for the emission estimates given in this chapter. 1-19 D 004235 REFERENCES FOR CHAPTER I Air and Industrial Hygiene Laboratory Reports - Study Identification No. C81-014, 1981. Archer, S. R. and T. R. Blackwood, 1979. Status Assessment of Toxic Chemicals: Asbestos. Final report prepared by Monsanto Research Corporation for the U.S. Environmental Protection Agency. PB 80-146327, EPA-600/2-79-2100. Blackwood, T. R., P. K. Chalekode and R. A. Wachter, May 1978. Source Assessment: Crushed Stone. Final report prepared by Monsanto Research Corporation for the U.S. Environmental Protection Agency. EPA-600/2-78-004L. Burnett, J. L., 1982. Mining Review - California Geology. California Department of Conservation. California Air Resources Board, 1984. "BURD1984M, Computer Printout Dated September 2, 1983, Emission Inventory Branch, Technical Support Division. California Air Resources Board, 1985. Survey of Asbestos Manufacturers, Stationary Source Division. California Department of Conservation, September 1963. "California Asbestos Industry." Yolume 16, Number 9. Chronic Hazard Advisory Panel on Asbestos, July 1983. Report to the U.S. Consumer Product Safety Commission. Greenblatt, J., 1984. Evaluation of the Asbestos-In-Schools Identification and Notification Rule, rinal report prepared by Westat, Inc. 'tor the U.S. Environmental Protection Agency. EPA 560/5-84-005. Harwood, C. F. and T. P. Blaszak, 1974. Characterization and Control of Asbestos, Emissions from Open Sources. Prepared by ITT Research Institute for the U.S. Environmental Protection Agency. EPA-650/2-74-090. Harwood, C. F., P. Siebert, and T. P. Blaszak, 1974. Assessment of Particle Control Technology for Enclosed Asbestos Sources. Prepared by IIT Research Institute for the U.S. Environmental Protection Agency. Contract No. 68-02-1353, EPA-650/2-74-088. NTIS PB 239-926. Lynch, J. R., 1968. "Brake Lining Decomposition Products." Journal of the Air Pollution Control Association. 18(12)524-526. Meylan, W. M., et al., 1978. Chemical Market Input/Output Analysis of Selected Chemical Substances to Assess Sources of Environmental Contamination III - Asbestos'/ IPA''55(T/y-78'-l)UgrWS'Tr^53r.--------------------------------------------- Rajhans, G. S., and G. M. Bragg, 1978. Engineering Aspects of Asbestos Dust Control. 1-20 D 004236 Roberts, R. M., 1980. An Inventory of Carcinogenic Substances Released into the Ambient Air of California, Hnal Report Task II and IV. KVR. Inr. for-- Science Applications Inc. Rowson, D. M., 1978. - "The Chrysotile Content of the Wear Debris of Brake Linings." Wear. 47:315-321. U.S. Department of the Interior, 1980. Asbestos: A Chapter from Mineral Facts and Problems. 1980 Edition, Bureau of Mines. U.S. Department of the Interior, 1985. Mineral Comnodlty Sunroaries, 1985. Bureau of Mines. `~ U.S. Department of the Interior, Minerals in the U.S. Economy: Ten-Year Supply-Demand Profiles for Mineral and Fuel Commodities, 1965-1974. Bureau of Mi nes. U.S. Department of the Interior, Minerals Yearbooks for 1976, 1978, 1979, 1980, 1983, and 1984. Bureau of Mines. U.S. Environmental Protection Agency, 1981. Assessment and Control of Chrysotile Asbestos Emissions from Unpaved RoaHsI EPA 450/3-81-006. Versar Inc., 1984. Exposure Assessment for Asbestos. Draft final report prepared for U.S. Environmental Protection Agency. EPA contract no. 68-01-6271, Task No. 49. Williams, R. L. and J. L. Muhlbaler, 1982. "Asbestos Brake Emissions." Environmental Research. .29:79-82. Zwiacher, W. E., et al., 1983. Emissions of Potentially Toxic Hazardous Air Contaminants in the South Coast Air Basin. South Coast Air Quality Management District, Engineering Division. Zurer, P.S., 1985, "Asbestos". Chemical and Engineering News. March 4, 1985, pages 28-41. 1-21 D 004237 II. PERSISTENCE IN THE ATMOSPHERE A. CHEMICAL AND PHYSICAL PROPERTIES Unlike many substances that are discrete entities definable by a fixed chemical structure, asbestos fibers comprise a group of materials that are less easily defined. They have a broad range of chemical compositions, crystal structures, sizes, shapes, and properties. They have also been described with diverse terminology (Committee on Nonoccupational Health Risks of Asbestiform Fibers, 1984). The term "asbestos" is not a mineral name, but a commercial-Industrial term applied to a group of naturally occurring mineral silicate fibers of the serpentine and amphibole groups. Serpentine minerals are "layered silicates" and only one of these, chrysotlle. Is an asbestos mineral. The amphibole asbestiform minerals are "chain silicates" and the five varieties of commercial importance are known as actinolite, amosite, anthophyllite, crocidollte and tremolite (Chronic Hazard Advisory Panel on Asbestos, 1983). Table II-l lists the names of the minerals Included In the term asbestos. The crystalline structure of chrysotile consists of a layer of magnesium oxide-hydroxide octahedra bonded to a layer of silicon dioxide tetrahedra in a somewhat mismatched fashion that produces a curvature In the sheet. The sheet, consequently, tends to roll Itself Into a hollow tube or possibly a tight spiral with the magnesium hydroxide on the outer surface. This hollow tube constitutes the basic fibril of chrysotile. Fibrils, bonded together, constitute fibers and the fibers.in turn may be banded together to build up the macroscopic material. Theoretically, chrysotile can be successively split until the ultimate fibrils are reached, but the ease of fiberizatlon varies with the particular ore (Selikoff and Lee, 1978). II-l D 004238 Table II-l Mineralogy of Comnercial Asbestos^ Commercial Name Chrysotile Crocidolite Anthophyllite Amosite (No common commercial name; sometimes called amosite) Mineral Name Chrysotile Riebeckite Anthophyl11te Cummingtonite- gruneriter/ Actinollte- tremol 1 ter' Mineral Group Serpentine Amphibole Amphibole Amphibole Amphibole 1/ This table was taken from the report, Asbestiform Fibers Nonoccupational Health Risks, by the Committee on Nonoccupational Health Risks of Asbestiform Fibers, 1984. Page 27. 2/ Hyphenated mineral names, such as cummingtonite-grunerite, represent mineral series. The minerals in the series are structurally identical but can contain variable proportions of two or more different cations in the same structural site. Thus, these mineral series may be regarded as solid solution series. The variable cations in the cummingtonitegrunerite series are magnesium and iron; most minerals in this series have both elements. The end members are identified by the unhyphenated names, e.g., cummlngtonlte, and grunerlte. Sometimes the name of the end member Includes the cation, e.g., ferroactlnolite. y Although asbestiform tremolite and actlnolite occur in nature, large commercially mined deposits are rare. However, actlnolite asbestos is found as a contaminant of amoslte from South Africa, and tremolite asbestos is found as a contaminant of some talc and chrysotile deposits. II-2 D 004239 In contrast with the chrysotile crystal, amphiboles consist of double chains of linked silicon-oxygen tetrahedra lying parallel to the vertical crystallographic axis and bound laterally by metallic ions. There is no tendency for such layers to roll in tubes. The Si-0 bonds along the chain are much stronger than the metallic ion bonds between chains, so that the amphiboles break lengthwise with ease, giving a fibrous appearance (Selikoff and Lee, 1978). The best known chemical quality of all types of asbestos fibers is their heat resistance. All types of asbestos progressively break down to simpler structures through dehydroxylation or dehydrogenation when heated to temperatures between 400*C and 1000*C. It should be noted that asbestos fibers as such do not have melting points but the decomposition products formed on heating will themselves eventually melt. The reactivity of asbestos towards acids and alkalines is fairly well known. Strong acids rapidly decompose chrysotile but amphibole fibers show various degrees of resistance against attack by strong acids. Strong alkalines have little Influence on all asbestos fibers. In particular on chrysotile which makes the latter fiber a likely reinforcing agent in cement. Since the biologically relevant physical properties of asbestos are described by the Department of Health Services staff in Part B, only the physical properties of asbestos that resulted In Its widespread commercial use will be described here. 1. Tensile Strength Tensile strength Is the most important physical property of asbestos. Asbestos fibers with sufficiently small diameters have great strength and are used in many industrial-commercial products. Maximum tensile strength values 11-3 D 004240 have been obtained for chrysotile and crocldolite of about 60,000 kg/cm2, however, the tensile strength varies with length and diameter of fibers. These values are of the same order as those given for glass fiber and carbon steel and are somewhat greater than those for cotton and rock wool (Selikoff and Lee, 1978). 2. Surface Area In industrial terminology, surface area means degree of openness or degree of fiberization. Each process involving asbestos fiber requires a degree of fiberization which, within limits, is critical for Its purpose. For example, chrysotile fibers prepared for inclusion in moulded brake linings will have a different degree of fiberization from those prepared for the carding process which brushes, cleans and straightens fibers in the first stage of textile manufacture (Michaels and Chisslck, 1979). 3. Thermal Insulatlve Value The insulative value of asbestos has in the past been widely utilized. The asbestos fiber itself does not have low thermal conductivity, but when fibers are separated they trap air which has a very low conductivity and so provide insulation that, for heat flows In a constant direction, is comparable to that provided by similar materials made from other fibers. For heat loads that take place in alternate directions, such as on a roof exposed to the sun, the moderately high density of the material combines with the low thermal conductivity to give one of the lowest values for thermal diffusivity, the governing physical attribute under these conditions (Selikoff and Lee, 1978). Table I1-2 shows chemical and physical characteristics of the main types of asbestos. Note that the chemical composition of the amphiboles are 11--4 D 004241 Ufcl* l!-<! CHARACTERISTICS OF THE M IN TYPES OF ASBESTOS FIBERS^' ft a --5 S 5V 0 * o~ 3*5 3 0SSS wm 1 *001 0I 0 0B 91 0 M *M S zz l 3> k V* ss?srss~2 s si j 2 i i *4 3 -?5 ' J=C N o~ 1 w o_^o- -- -- *2 900^0 0*10 JOB# B OO0K^O0 *N* -T5 3 1 M M W a Mk O ^ 0<M0#00<*0 ^iootAooo 0 ^ 0 w w ^5 -ff M 3 55 5 -- J3 m -+ m -- m--* --+ m 0M*WM000 1 t B 1 T s m N I * ~" w k> 3 -- - 1 B m I 5 am m 1 m * l I m mi 0N000N0RM 3 jr 3- e i <i i i i i t 3* asesass- 5k 5 | JVI 1 ^ 3b mm 1 a t i ; < i i H j 3* 4 m me R m I ** 3c 12 2 3 I 2 4 8 Jk * 1 8 5 S S 5 Jk i M3 N 9 I 0 N fm M 1 f zC a #Q 30 AN 3 2 a I aA al Mm c 4 CVJ <N ^T O O Q similar, therefore, fiber identification during analysis is difficult unless proper laboratory equipment and techniques are used. Some of these equipment and techniques are discussed in Section III-A. 4. Fiber Dimensions in Ambient Air and Occupational Settings Available data on asbestos fiber dimensions In the ambient air indicate that ambient fibers tend to be smaller than fibers found in occupational environments. For example, the Committee on Nonoccupational Health Risk of Asbestiform Fibers estimated that for equal mass, there would be approximately 35 times more ambient air fibers than occupational air fibers. In the SAI report, the mean diameter and length for each sample analyzed by SAI is given. Table II-3 summarizes the SAI data in terms of average mean values for the samples taken at each location. There was only one location. South Gate, where the average mean length was greater than 5 microns. Occupational asbestos samples are usually analyzed by phase contrast microscopy (PCM) and counted by a method prescribed by the U.S. Occupational Health and Safety Administration (OSHA). Only fibers greater than 5 microns and having an aspect ratio greater than 3:1 are counted. Therefore, small fibers are not counted. Because of this, it is not possible to characterize occupational samples in terms of mean diameter or length. The OSHA counting method has lead to problems when attempting to compare ambient air concentrations and occupational air concentrations. DHS Included a detailed discussion In Appendix A of the Part B report on the ratio of fibers longer than 5 microns to total fibers counted in ambient air samples. DHS concluded that there are between 1 and 10 long fibers per 1,000 total fibers counted in ambient air samples. 11--6 D 004243 Table II-3 Summary of Average Diameters and Lengths of Samples Collected by SAI During 1981 Sample Site King City San Jose Napa Sonora Century City San Fernando Valley Bakersfield South Gate San Diego Stockton Chrysotile AverageH) Average Mean Mean Diameter Length (Microns) (Microns) 0.4 4.6 0.14 1.3 0.12 1.1 0.14 3.0 0.06 0.9 0.05 1.1 0.08 0.7 0.43 5.1 0.12 1.2 0.05 0.71* Amphiboles Average Average Mean Mean Diameter Length (Microns) (Microns) ---- 0.14 2.0 0.18 1.1 0.20 1.3 0.30 1.1* 0.08 0.6 0.17 2.1 0.13 1.5 0.18 1.0 0.15 1.4* H) For each sample taken by SAI, the mean diameter and length were reported. These values are the averages of the mean dimension found at each location. * Only one sample was reported. 11-7 D 004244 B. FATE IN THE ATMOSPHERE Transformation processes associated with the fate of asbestos In the environment are generally Insignificant; the material is relatively inert. Degradation has been observed in the laboratory under extreme conditions of heat, mechanical stress and acidity. These conditions, however, are not normally observed or encountered in the ambient environment (Versar Inc., 1984). Winds are capable of dispersing asbestos fibers from industrial sources and naturally occurring sources. Once in the atmosphere, the fibers are subject to removal by gravitational settling (dry deposition) and atmospheric washout by precipitation (Versar Inc., 1984) but are also easily reentrained from ground surfaces (U.S. Environmental Protection Agency, 1978). In a study conducted by Harwood and Ase (1977) in the vicinity of asbestos waste piles in Denison, Texas, nearly equal upwind and downwind concentrations of asbestos fibers were theorized to result from upwind resuspension of previously settled fibers. The deposition and eventual burial of fibers in soils and sediments are the major natural processes by which asbestos leaves the atmosphere. Asbestos fibers could be reentrained if soils or sediments are disturbed by anthropogenic or natural activities. 11-8 D 004245 REFERENCES FOR CHAPTER II Coitim'ssion of the European Communities, Directorate - General for Social Affairs, Health and Safety Directorate, 1977. Public Health Risks of Exposure to Asbestos. Committee on Nonoccupatlonal Health Risks of Asbestiform Fibers, 1984. Asbestiform Fibers - Nonoccupationl Health Risks. Harwood, C. and P. Ase, 1977. The Control of Fugitive Emissions from Asbestos Waste Piles. Draft final report prepared for the U.S Environmental Protection Agency. EPA Contract No. CA-6-99-3380-A. Michaels, L. and S. Chissick, Editors, 1979. Asbestos Volume 1 Properties. Applications and Hazards. Selikoff, Irving J. and Douglas H. K. Lee, 1978. Asbestos and Disease. Timbrel!, V., 1965. The Inhalation of Fibrous Dust. Annuals of. the New York Academy of Science. 255-273. U.S. Environmental Protection Agency, April 1978. Dispersion Model Analysis of the Air Quality Impact of Asbestos Emissions From Iron Ore Benefication Plants. EPA Contract No. 68-02-2507.--------------------------------------------------- Yersar Inc., 1984. Exposure Assessment for Asbestos. Draft final report prepared for the U.S. Environmental Protection Agency. EPA Contract No. 68-01-6271, Task No. 49. II--9 004246 D III. EXPOSURE TO ASBESTOS A. Asbestos Measurement Techniques Ambient asbestos air samples are usually analzyed by either optical (light) microscopy or electron microscopy methods. In some cases, the fibers must have an aspect ratio* of 3:1 or greater to be counted. Each microscopy method has its advantages and limitations and some of these are discussed in this section. In optical microscopy, there are two methods used to analyze asbestos fibers: phase contrast microscopy (PCM) and polarized light microscopy (PLM). PCM enhances the visibility of fibers under low magnification powers of the phase contrast microscope, but cannot distinguish between asbestos and non-asbestos fibers. In addition, the poor resolution power of the microscope limits the detection of fibers to those larger than 0.3 microns. However, PCM Is widely used for asbestos screening and counting since this Is the prescribed method by U.S. Occupational Health and Safety Administration (OSHA) for determination of asbestos emissions in occupational settings. This method involves counting fibers with acceptable aspect ratios and greater than 5 microns in length; therefore, the smaller fibers are not counted. There are two disadvantages with PCM. First, the count includes fibers within a specified size range, whether the fibers are asbestos or not. Second, due to the poor resolution power of the phase contrast microscope, fibers less than 0.3 microns will not be detected (Hayward 1985, Versar Inc., 1984). Aspect ratio means that the length of the fiber must be at least 3 times longer than the width of the fiber. III-l D 004247 PLM can be used to identify and characterize asbestos and non-asbestos fibers based upon the crystal structure of the fibers. When used with dispersion staining, PLM may be able to distinguish different types of amphiboles within the sample. However, PLM has the same limitation as PCM which is poor resolution powers in detecting the smaller fibers. To analyze and identify smaller asbestos fibers, electron microscopy (scanning electron microscopy (SEM) and transmission electron microscopy CTEM)) should be utilized. SEM has a resolution limitation In that it can only detect fibers larger than 0.1 microns. With respect to fiber identification, SEM equipped with an energy dispersive X-ray spectroscopic (EDXS) system can identify asbestos fibers by providing elemental analysis of the fibers, but it does not provide structural Information to identify specific fiber types. The preferred analytical method is TEM because of Its ability to analyze and detect the smaller asbestos fibers that are found in the ambient air. A transmission electron microscope has the resolution capability of detecting fibers that are 0.2 nanometers in diameter. TEM can be used with selected area electron diffraction (SAED) which provides crystallographic (structural) information of the fibers being analyzed. TEM-SAED can identify chrysotile fibers, although X-ray diffraction analysis can be used for confirmation. To Identify amphiboles, TEM-SAED must be supplemented by EDXS analysis in order to obtain elemental Information. Although TEM is the preferred analytical method, there is no standarized procedure for laboratories to use. Due to different Instrument capabilities, operator proficiencies, and procedures, it is difficult to compare the results from various laboratories. In recognition of this problem, the EPA evaluated 111--2 D 004248 the TEM/SAED method and procedures of different laboratories and developed a TEM/SAED provisional methodology manual to minimize the variability of results. The provisional methodology is found in Electron Microscope Measurement of Airborne Asbestos Concentrations, A provisional Methodology Manual by A. V. Samuda, Colin F. Harwood, and John 0. Stockman which was published in June 1978. At the present time, EPA Is revising the manual, but the changes have not been finalized. B. ASBESTOS MEASUREMENTS Several documents containing asbestos measurements taken In California were reviewed to show asbestos exposure to the general population (Appendix D). Only the report entitled Ambient Asbestos Concentrations in California: Volumnes I and II, prepared by Science Applications, Incorporated (SAI) under contract to the Air Resources Board, contained asbestos measurements from several populated locations in the state. The samples were prepared and analyzed using EPA's provisional TEM methodology with only a minor modification which consisted of using a smaller pore size filter for better collection of smaller fibers. With one exception, the remaining studies were older, had used different sample collection methods, sample preparation techniques and analytical techniques and were concerned with specific sources such as freeways, art asbestos mill, and off-road vehicles. Since different sample collection and analytical techniques were used for these studies, the results are not directly comparable. However, the measurements are useful for documenting that asbestos is present in the ambient air. Appendix E contains a table listing some of these measurements. In Section D of this chapter, a discussion of ambient asbestos monitoring data collected In Alviso, California 111--3 D 004249 Is presented. This area is contaminated with asbestos fibers as a result of disposal of asbestos waste in a nearby landfill. We believe the asbestos data contained in the SAI report represent the most recent and suitable data that are available for evaluating ambient asbestos concentrations in California. Therefore, we are limiting our discussion to this study. (Science Applications, Inc., 1983). Samples were collected and analyzed by SAI at ten sites located throughout California. As with most asbestos data, samples represent very short averaging times and were collected over a very limited time period. Although ambient levels determined over the short-term are discussed, no method has been developed to extrapolate from short-term averages to long-term averages. Because of the nature of the measurements and the unknown variability of concentrations over time, annual average concentrations and associated population exposures cannot be determined for asbestos. The samples were collected using a single-point filter sampler with a cyclone inlet providing a collection efficiency of 50 percent for 3.5 microns (urn) aerodynamic diameter particles. This particular sampler was chosen because of its ease of use in the field, ability to selectively sample particles In the respirable range, and a design which allows for uniform particle deposition on the filter. After the collection phase, samples were taken to the laboratory for analysis. All sample analyses were completed using a transmission electron microscope (TEM) with a resolution of six angstroms and equipped with selected-area electron diffraction (SAED) instrumentation. Chrysotile asbestos-fibers can be identified using the SAED 111-4 D 004250 technique, however, amphibole asbestos fibers cannot be differentiated. Appendix F presents more detailed sampling, sample preparation, analysis and quality control information. In addition to measurement of asbestos concentrations, monitoring of meteorological conditions and of temporal variations in particulate matter concentrations were conducted at each site. The overall accuracy and precision of the data collected by SAI are not documented In the final report. The reason for this is that the actual number of samples collected and analyzed were too limited to statistically validate the precision and accuracy of the numbers reported for each site. However, It is now known that the high flow rate used for sampling in this study can result in significant fiber loss (20-50% of the total) probably as a result of electrostatic charging of the plastic filter holder (Hayward, June 1985). Asbestos sampling sites were chosen based on emission and exposure potential. The project's goal was to measure airborne asbestos In areas known or suspected to have elevated levels as well as in areas isolated from asbestos sources. Six factors related to source type and potential population exposure guided site selection: 1. Localized Sources: Locations at or near which asbestos ore is processed, refined, or otherwise used, and at which asbestos can potentially be released Into the air at elevated concentrations; 2. Natural Deposits: Areas where soil provides a source of asbestos fibers; 3. Non-Urban Locations: Rural areas with low population and which are located away from metropolitan asbestos emissions and natural deposits; III--5 D 004251 4. Urban Locations: Areas of potentially high population exposure to elevated particulate matter; 5. Industrial Sources: Metropolitan areas with high density clusters of asbestos users, as identified In the Environmental Protection Agency's register of sources regulated under the National Emission Standards for Hazardous Air Pollutants; and 6. Vehicular Braking: Areas where asbestos emissions from automobile brake and clutch friction materials are expected to be high. Ten sites were selected for study. The site names, classification characteristics and population within a five kilometer and ten kilometer grid area of each are listed in Table III-l. The relative locations of the sites throughout the state are shown in Figure III-l. Two rural/suburban sources, a mill near King City and the asbestos cement pipe manufacturing plant in Stockton, were chosen to represent the localized source category. The mill is an asbestos processing plant and Is the only asbestos source in this study located in a rural area; chrysotile asbestos ore is both refined and packaged at the King City mill. The asbestos pipe manufacturing plant is located at the border of the Stockton urban area; no other asbestos sources were identified in the vicinity of this plant. Sonora In Tuolumne County was selected as a natural source site. Sonora is the only one of three serpentine-rich deposit areas within the state that does not have active mining nearby. Population surrounding the Sonora site is low, with a seasonal (summer and fall) influx of tourists. 111-6 D 004252 Table III-l Names, Classification Categories, and Population Near!/ the Ten Sites Chosen for the SAI Asbestos Sampling Study Site Name Classification Category Population at Population at 5 Kilometers 10 Kilometers King City Stockton Sonora Napa Oil dale San Diego Sherman Oaks San Jose South Gate Century City Localized Source Location Localized Source Location Natural Deposit Location Non-Urban Background Location Non-Urban Background Location Urban Background Location Urban Background Location Industrial Source Location Industrial Source Location Vehicular Braking Location 8,200 15,000 7,700 48,000 4,300 10,000 6,400 180,000 150,000 130,000 8,200 34,000 19,000 66,000 23,000 100,000 120,000 620,000 680,000 460,000 Population estimates were made by summing the population of census track centroids located within a 5 kilometer and 10 kilometer radius of each monitoring site. II1--7 D 004253 Figure II1-1 California Map Showing Locations of the Ten Sampling Sites Used in the SAI Study III--8 D 004254 SAI chose two non-urban background sites at Napa and Oil dale (near Bakersfield) as being located in non-serpentine areas. These two sites represent differing climatological settings, especially with respect to dominant wind patterns. However, Napa County does have natural serpentine deposits (chrysotlle) throughout the county as shown In Figure 1-1. The Oil dale site had the second highest concentration measured In the study. SAI was not able to explain this value. The ARB staff believes that It Is important to note the presence of asbestos fibers in an area that was not suppose to have Identifiable asbestos sources. Sites In San Diego and Sherman Oaks (San Fernando Valley) were selected as urban background exposure sites. The sites were chosen to reflect dissimilar climatological conditions and are located away from both serpentine deposits and heavy automobile traffic. There were fewer than three sources using asbestos in each of the two communities. San Jose and South Gate (Los Angeles County) were chosen to represent industrial source sites. Eighty-six asbestos users were identified in the San Jose area in 1981. Also in 1981, 147 users were identified in the Los Angeles area; the South Gate location represents a dense cluster of these asbestos users. One of the major historical uses of asbestos has been as frictional material in vehicle braking and clutch facings. Therefore, Century City was chosen as a location representative of emissions from vehicular braking. In order to duplicate meteorological-conditions at the Century City site and also quantify the affect of varying traffic volumes, samples were collected on an adjacent Sunday (low traffic volume) and Monday (high traffic volume). 111--9 D 004255 Traffic counts between the two days were anticipated to vary by at least an order of magnitude. C. AMBIENT ASBESTOS CONCENTRATIONS All asbestos samples referenced in this discussion were collected during 1981. Samples were collected at each site during a single day except at Century City, where samples were collected on two consecutive days (Sunday and Monday) in an attempt to quantify the effect of traffic related sources on ambient asbestos concentrations. Two asbestos samplers were operated at each site location. Original sampling plans called for collection of at least four four-hour samples at each site between the approximate hours of eight o'clock in the morning and four o'clock in the afternoon. Because of ordinarily high particle concentrations, and therefore possibly high asbestos levels, samples at several locations were collected over shorter time Intervals to preclude overloading the filters. Short-term (single sample) results are summarized in Table II.I-2. Information given for each individual sample includes date of sample, sampling time, sampling duration, and concentrations of chrysotile and of amphibole asbestos( separately and combined) In fibers per cubic meter of air. Only valid sampling data are included in the summary. Concentrations listed include values below as well as concentrations at and above the analytical detection limit. The analytical detection limit is a function of the total area of collection filter scanned during analysis and also of the volume of air sampled. At the time of sample analysis, only those fibers with a length to diameter ratio of at least three to one were counted. When only one chrysotile or amphibole fiber was counted on the sample scanned, the concentration value based on that single fiber was used to define the III-10 D 004256 detection limit for the specific fiber type. Samples that were analyzed and not having any fibers counted during analysis were classified by SAI as being below the detection limit (DL). Nearly all fibers were less than to five microns in length. Three samples contained asbestos fibers greater than five microns in length and only one sample had a mean fiber diameter of one and a half microns. The remaining samples had mean diameters less than one and a half microns. Table II1-2 suggests that asbestos sampling results from the ten sites are variable. In addition, individual samples collected at each of the sites are also highly variable. Overall, fiber-specific and combined concentrations range from levels below the analytical detection limit to a maximum 3 concentration of 140,000 fibers per cubic meter (f/m ). In addition, several samples collected at the same location had concentrations ranging from below the detection limit to. quantifiable concentrations. SAI did not have an explanation for this, but they believe that meteorological conditions and humidity can influence the sampling results. The highest asbestos concentration measured was near the mill at King City. The site represents a source-specific area In that it is located in a rural area with high levels of asbestos emitted from an isolated industrial source. All fibers sampled at the King City mill were chrysoti^e asbestos; this Is not unexpected since the milling operation processes chrysotlle ore. 3 The maximum concentration, 140,000 f/m , was measured In the early morning under reduced airflow conditions. This was Intended to represent an upwind sample from a localized source. However, the data did not Indicate this. Although it Is generally thought that wind conditions determine the amount of asbestos which can be picked up into the air, concentrations measured at this site indicate higher levels under reduced air flow conditions than under III-12 D 004258 Table III-2 Sunnary of Respirable Asbestos Samples Collected by SAI During 1981 Sampling Sampling Sampling unrysotllei/ Amphlbolel/ Total Sample Site Date Ml dpolnt Time (min) (f/m3) (f/m^) Asbestos!/ King City Q9/2U&1 (Local Source) Stockton 07/23/84 (Local Source) Sonora 09/24/81 (Natural Deposits) Napa 09/23/81 (Non-Urban) Oil dale 10/21/81 (Non-Urban) San Diego 12/17/81 (Urban) Sherman Oaks 10/20/81 (Urban) San Jose 09/22/81 (Industrial) South Gate 10/22/81 (Industrial) Century City 10/18/81 (Vehicle Braking) (Sunday) Century City 10/19/81 (Vehicle Braking) (Monday) 09:46 11:07 14:03 15:45 10:25 11:43 10:05 10:40 14:40 14:39 09:48 10:06 14:01 14:20 10:10 10:40 13:30 14:35 09:40 09:38 13:05 13:28 15:30 10:05 10:17 13:37 14:30 10:15 10:31 14:30 14:43 09:30 09:50 12:04 14:25 09:10 09:20 13:45 14:05 07:30 09:10 14:43 15:30 219 140,000 <DL 240 9,400 cDL 240 4,700 < DL 239 2,400* <DL 227 <DL 2,500 214 18,000 3,700* 240 12,000 2,400* 247 6,900 2,300 240 2,400* 2,400* 239 <DL <DL 240 4,700 -=DL 240 < DL 4,700 240 9,400 <DL 239 4,700 7,100. 177 < DL <DL 179 6,300 9,500 182 3,100* <DL 169 52,000 52,000 195 = DL 2,900* 190 3,000* 8,900 210 2,700* 2,700* 248 4,.500 23,000 69 <0L 16,000 241 = DL < DL 241 16,000 -=DL 119 14,000 4,800* 180 28,000 .*=DL 240 21,000 2,900 241 14,000 9,400* 240 9,400 2,400* 240 14,000 7,100 54 < DL 11,000* 99 18,000 18,000 59 9,600* 58,000 59 56,000 <DL 158 < DL <DL 137 4,100* <DL 204 15,000 <DL 86 46,000 20,000 61 56,000 <DL 69 < DL <DL 164 < DL =DL 60 28,000 9,400 for the sampling period. 1/ 11 out of 43 (261) were below the detection limit. l! 19 out of 43 (441) were below the detection limit. ?/ 6 out of 43 (141) were below the detection limit. 140,000 9,400 4,700 2,400 2,500 21,700 14,400 9,200 4,800 < DL 4,700 4,700 9,400 11,800 <DL 15,800 3J00 104,000 2,900 11,900 5,400 27,500 16,000 < DL 16,000 18,800 28,000 23,900 23,400 11,800 21,100 11,000 36,000 67,600 56,000 = DL 4,100 15,000 ' 66,000 56,000 < DL <DL 371,400-u-- III-ll D 004257 higher wind conditions. Later in the afternoon, concentrations were much lower. Results of sampling at this site emphasize the importance of changing meteorological conditions and temporal variability on ambient asbestos concentrations. Asbestos concentrations measured at the other two source-specific locations, Stockton (point source) and Sonora (natural source), are low in "comparison to the King City site. The high concentration at King City is approximately six to ten times greater than the highest total asbestos level measured at the other two sites. Concentrations measured at the Sonora site were all relatively low. During the day on which samples were collected, there was no measurable wind and visibility was clear. These types of meteorological conditions are atypical for the site, and measured asbestos concentrations were lower than expected. Consequently, it Is difficult to draw arty conclusions from the data and may be misleading to compare the Sonora results with those from other sampling locations. As was true of the King City location, samples collected at both the Stockton and Sonora sites Indicate the Importance of meteorological Influences on resulting levels of airborne asbestos. The remaining sites considered In the SAI stu<(y represent a variety of conditions statewide, designed to Identify more normal ambient conditions than those influenced by specific sources. Included among the other sites were background sites which are located away from natural asbestos deposits, industrial sites located among a* number of commercial asbestos users, and a site designed to Identify the potential contribution of vehicle braking In an urban area. III-13 D 004259 Other sites chosen by SAI were located at Napa, Oildale, San Diego, and Sherman Oaks. A single observation of 104,000 f/m3 was measured at Oildale in the afternoon. This is the second highest concentration measured at any of the ten sites. SAI was unable to explain this high value. Other concentrations measured at these locations range from levels below the 3 detection limit to a concentration of 28,000 f/m . Eight of the seventeen 3 observations are less than 10,000 f/m . Total asbestos concentrations measured at the two industrial locations, San Jose and South Gate, are all above the analytical detection limit suggesting a more constant presence of airborne asbestos at these sites. Concentrations range from 11,000 f/m3 to 67,000 f/m3 with the majority of 3 values above 20,000 f/m . Asbestos levels measured at the industrial sites are less variable than those observed at background and localized source sites. Asbestos samples collected at the Century City location span a two day period. Samples collected on Sunday represent light traffic conditions while Monday samples represent heavy traffic conditions. Values for the two days 3 range from below the detection limit on both days to maximums of 66,000 f/m and 56,000 f/m on Sunday and Monday, respectively. Comparison of the high value measured on each of the two days does not show any significant difference related to light traffic versus heavy traffic conditions. Of the total samples taken at Century City, only the two samples taken on Sunday and Monday, early In the morning, show a significant difference. The chrysotile asbestos level was higher by a factor of ten on Monday. SAI staff states in their report that conclusions from these data should be cautiously drawn because the sample with the higher level could be a result of a series of emergency brakings at some point during the sampling. 111-14 D 004260 Averages of, all concentrations measured at each of the sampling sites are summarized in Table III-3. In calculating these averages, concentrations reported as below the detection limit were assigned a value of one-half the detection limit as determined using Figure II1-2.* For example, a sample collected over four hours and analyzed as below the detection limit was assigned a concentration value of (0.5 x 2,400 f/m3) or 1,200 f/m3 for inclusion in the averaging calculation. The averaging process tends to smooth out the variability present among Individual observations due to meteorological and source related parameters and gives a more representative Indication of daily average concentrations and potential differences among the sites. As noted, individual concentration measurements include levels below the analytical detection limit as well as values at and above this limit. In the previous discussion, asbestos concentrations below the detection limit were so identified; in the following discussion of site averages, these values are treated differently. All samples analyzed in the SAI stuc(y were collected at the same flow rate (15.5 liters of air per minute) and counted in an identical manner. Therefore, the analytical detection limit Is a function only of sampling time. A graph of detection limit versus sampling time is shown in Figure II1-2. Since sampling times in the SAI study ranged from one hour to four hours, net detection limits range from 9,100 f/m3 to 2,400 f/m3 , respectively. Concentrations presented in the SAI stu<iy are reported as below *This averaging method was used to strike a balance between other averaging methods that provide estimates lower than actual averages. If the non-detectable values are assumed equal to zero, or estimates higher than the actual average If the non-detectable values are assumed to equal the detection limit. III-15 D 004261 Table III-3 Summary of Averaged Respirable Asbestos Concentrations - Sampled by SAI During 1981 Chrysotile Total # Sampl es Peak Mean Site Name Samples DL (f/m3) (f/m3) Amphibole Samples Peak DL (f/m3) Mean (f/m3) Total* Mean (f/m3) King City Stockton Sonora Napa Oil dale San Diego Sherman Oaks San Jose South Gate Century City Sunday Monday 4 2 4 4 4 5. 4 4 4 4 4 0 140,000 39,000 4 1,200 1 ,200** 40,000 1 18,000 9,600 0 3,700 3,100 13,000 1 12.0U0 5,600 1 2,400 2,000 7,600 1 9,400 5,000 2 7,100 3,500 8,500 1 52,000 16,000 2 52,000 16,000 32,000 2 4,500 3,200 0 23,000 11,000 14,000 1 28,000 15,000 3 4,800 2,200 17,000 0 21,000 15,000 0 9,400 5,500 1 56,000 22,000 1 58,000 23,000 21,000 45,000 1 46,000 17,000 3 20,000 6,300 2 56,000 22,000 3 9,400 5,000 23,000 27,000 * The total mean concentrations may not total due to rounding. **For consistency, the averaging method was used for all locations. We would not expect to find amphiboles at this location because the mill processes chrysotile ore. III-16 D 004262 Figure III-2 RELATIONSHIP BETWEEN EEMECTION LIMIT AND SAMPLING TIM2 USED IN SAI ASBESTOS STUDY SAMPLING TIME (HOURS) III-17 D 004263 the detection limit if less than one fiber was counted on the portion of filter scanned. Simply because no fibers were counted, one cannot eliminate the sample from consideration or assume the asbestos concentration present in the sample is zero. Some asbestos could be present, but were not analyzed. Average asbestos concentrations for the ten sites sampled range from 7,700 f/m3 at Sonora to 45,000 f/m3 at South Gate. Comparison of the average values in Table II1-3 is similar to the comparison of individual values presented in Table 111-2. South Gate shows the highest average concentration while King City had the second highest average concentration. Total asbestos concentrations tend to be higher at the industrial and localized sources than the other sampling sites. In the discussion above, we have presented an analysis of the asbestos data by assigning a value of one-half the detection limit for each sample result that was reported below the detection limit. For comparative purposes, in Table II1-4, we present mean asbestos concentrations for each sampling site that were calculated using three methods. The three methods are: 1) assuming non-detectable values are equal to zero, 2) assuming non-detectable values equal one-half the detection limit, and 3) assuming non-detectable values equal the detection limit. Results of the SAI sampling study Indicate that measurable airborne asbestos concentrations are present at a number of locations throughout the state. Quantifiable single sample concentrations vary by a factor of nearly sixty, ranging from 2,400 f/m3 to 140,000 f/m3 total asbestos. The variation of mean concentrations from site to site is nearly a factor of six (7,700 f/m3 to 45,000 f/m3 total asbestos). Generally, the highest concentrations were measured at sites influenced by localized and 111 -18 D 004264 Table I I I - 4 Hean R e sp ira b le Asbestos C o n ce n tra tio n s C a lc u la te d By Three A ve ra g in g Methods < P ib e rs/*3)* 004265 0 i-3 2Q 3 A a i 0A4 44J 4J O 9 sH U 0 C 0 z & 0 JuC 8 < JP o o o n u*i % s o 9 9 9 9 9 9 9 9 <N r> 9 <n n m04 094 CON 9 ** o m fM CN cn o o o O o o 9 #4 r9- 9 O 9 9 O o o 9 9 9 o% cn cn *4 rt n ^4 t*o4 C9N cn 9 9 a n CN o o o 9 9 r* 9 9 9 o 9 9 O 9 9 9 O 9 9 9 9 9 9 o m --4 r* 9 <N n --4o P ^4 OCN in 99 9 9 m r* n 9 4 > H 0 *3 u 09 *8 I1 G 0 z jjj s Q 2 JP 9 > *aum94 s O 2; c u 5 ,s. -O ->l i 9 8 3 09 o o o *4 9 9 (9N 9 9 O 9 O 9 9 9 <N O 9 in 9 9 9 CN r* 0*4* <n m n 9 99 in n* r* r* o o 9 9 9 9 9 9 9 o o 9 9 cn 9 *4 9 <n e m 04* H CN H in in * N CN 9 9 9* m o9o999 9o 9 o CN s9-4 9H 9 o 99 99 C9N 9 m 9 9 *4 n % r* m 91 0044 CN in cn n 9 m9 9 9 to in 9 % 9 9 9 9 9 9% 9 9n 9 9 9 9 9 m 9k 9^4 in n to *4 99 9 9 9* m04 m*4 9 9 9 n 9 W8 9 9 r* H CN o o 99 9 9% 9 n 9 9 P* 9 9 9 9 9 9 9 9 9 o 9 9 (A in N m in cn 9 8 9 O 99 t0o4 p4 CN o 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 O 9 <** 9 9 9 9 oi n in 9 cn m m04 CN n o9 99 99 r* CN H CN Mm >4 * o M*coj cOk H g *oj Ka 4 V 0 G 0 03 m 4 Q 4 *V404 Zo 0 0o 0 -H e Q u1 e 4 jG 03 03 4 0 *3 ea 0) 4J 4 u 5 03 u >4 > >4 4 4 M 43J e a G 0 e CO 2 ` * H G S 0u 0 TJ 04 4 0 u 0 G a 6 -0c 4 b C jj o g 4 0 60 os u 0A4 4 U c 4 0. I a SQ (t Q a% I Industrialized sources; the lowest concentrations were found at sites isolated from asbestos emission sources. Although SAI's measured asbestos concentrations suggest these conclusions, individual measurements represent a very short averaging time, one hour to four hours. In addition, comparison of asbestos data with simultaneously collected meteorological data indicate ambient asbestos concentrations are greatly influenced by changes in parameters such as wind and humidity. The effect of changing meteorological conditions on resulting average asbestos concentrations over a longer timeframe cannot be extrapolated from the one day samples that are available. In conjunction with asbestos sampling, SAI also monitored site-specific particle concentrations. The intent of these measurements was to determine whether asbestos and particle levels are related and consequently, if particle measurements could be used to predict ambient asbestos concentrations. SAI found no relationship between measured asbestos levels and concentrations of total suspended, inhalable, or fine particulate matter. The ability to determine annual average concentrations is essential to the evaluation of population exposures and the associated risk of ambient levels of potentially toxic compounds. At the present time, however, no long-term asbestos sampling data are available and no method has been developed to extrapolate long-term average concentrations from limited short-term observations. Consequently, no estimate of annual average concentrations and associated population exposures can be made. However, in some sampling locations, a significant population resides In the area. In Table III-l, we presented the population within five and ten kilometer areas for each of the sampl1ng 1ocations. II1-20 D 004266 D. SOURCE OF ASBESTOS CONTAMINATION The DHS staff has been investigating an asbestos contamination problem in Alviso, California which is a small community located near San Jose (see Appendix G). The population in a 5 kilometer area surrounding central Alviso is approximately 31 ,000. Population located within a 10 kilometer radius of Alviso is approximately 270,000. During the 1950's and 1960'$, waste from an asbestos cement pipe manufacturing plant was disposed of in a landfill near Alviso. Subsequent flooding of the landfill at various times in the past 30 years have caused contamination of the soil in Alviso. Ambient air monitoring studies by DHS have indicated significant concentrations of asbestos fibers in the air throughout Alviso when compared to upwind concentrations (910,000 total fibers/m versus 12,000 total fibers/m ). This area has been designated as a federal and state superfund clean-up site. E. EXPOSURE THROUGH OTHER MEDIA Although the primary focus of this report is exposure to asbestos from the ambient air, asbestos can be taken into the body by either inhalation or ingestion of asbestos in other media. This section summarizes available information on exposure through other media. Table III-5 expresses asbestos exposure from various media in terms of the intake of fibers per year for an office person, house person, and child (see Appendix H for details). The relative amount of time a person spends in each exposure environment has a major impact on the levels of asbestos fibers taken into the body. For example, although there was no significant difference in the asbestos concentrations found in the home and the ambient air, the difference in yearly intake of asbestos fibers into the body from these two environments was significant, (see Table 111-5) III-21 D 004267 Table III-5 Yearly Intake of Asbestos Fibers From Various Media For An-Office Worker, House Person, ana Child Exposure Route Inhalation Ambient Air Indoor-Schools with asbestos Inaoor-Otfice buildings with asbestos Indoor-Homes with asbestos Total** Ingestion Treated Water System Child (10 fibers per year) 20-100 50-4,000 0 House Person (10 fibers per year) 6-30 0 10-200* Office Worker (10 fibers per year) 6-30 0 60-1,500 1-200 70-4,300 1-300 20-500 .1 -200 70-1 ,700 400-90,000,000 500-140,000,000 500-140,000,000 Accounts for time in stores, banks, and other similar types of buildings. ** Intake levels have been rounded off. Note: The estimates presented in Table 111-5 are based on limited data and should not be considered absolute. This data was tabulated to illustrate the combined effect of assumed exposure times and concentrations on the intake of asbestos fibers. II1-22 D 004268 Indoor concentrations in office buildings and schools can exceed anfcient air concentrations when asbestos has been used in buildings for specific purposes such as insulation and as a fire retardant on structual components. The asbestos intake levels in Table II1-5 for exposures in buildings (home, office buildings, and schools) include estimates for buildings with asbestos present in the surrounding materials. The upper levels, therefore, may not be representative of the concentrations one would find in an "average" home, school, or office building but for the group of individuals affected, the intake levels can be significantly higher than those from ambient air. Although intake of asbestos from drinking water can be thousands of times the intake from inhalation, DHS has concluded that experimental studies were not conclusive in determining the relationship of ingestion and various types of cancer. Therefore, the relative intakes of asbestos fibers for inhalation and ingestion should not be compared for risk assessment purposes. 1. Drinking Water Exposure According to work done by Dr. Steven Hayward of the California Department of Health Services (Hayward, 1984), levels of asbestos in California drinking water can vary from one to 260,000 MFL (million fibers per liter) observed in a storage tank in the Klamath River Basin. In general, higher levels were found after storms occurred in areas with asbestos-containing serpentine rock formations. In the American River at Sacramento, from which drinking water is drawn, concentrations varied from 53 to 5600 MFL, depending upon season and recent storm history. In the California Aqueduct, levels of 300 MFL have been found at the head, compared to 15,000 fFL found just south of Coalinga. These 111--23 D 004269 concentrations can be lowered through water treatment. However, a report done by EPA's Health Effects Research Laboratory in 1979, "Exposure to Asbestos from Drinking Water in the United States" (600/1-79-028), states that in the San Francisco Bay area, concentrations greater than 100 MFL have been found in treated water systems. In San Francisco's Crystal Springs Reservoir, a concentration 130 MFL has been found . These concentrations have been attributed to erosion of naturally occurring serpentine deposits. In contrast, Los Angeles water was found to contain less than 1 MFL. Another source of asbestos in drinking water is from asbestos cement pipe; however, there is insufficient information to estimate the amount of asbestos that is contributed by the asbestos cement pipe. Table II1-6 summarizes the asbestos concentrations found in California water systems. 2. Indoor Exposure Table II1-7 shows a summary of indoor asbestos exposure samples collected in public and private schools and federal buildings. According to the report, "Indoor Pollutants", 1981, by the National Research Council's Committee on Indoor Pollutants, friable sprayed asbestos insulation on structural surfaces is the major source of airborne asbestos. Sprayed material has been applied for building Insulation and fire proofing. The EPA has now banned spray-on application of asbestos-containing materials, except where the fibers are encapsulated with a binder during spraying and are not friable after drying. Some estimates are that over half the buildings In the United States contain asbestos In a form that could give rise to indoor airborne exposures. In these buildings, the sprayed asbestos material Is friable and susceptible to damage and disintegration by hand pressure. Most contamination from these sources is dependent on human activity, by contact disruption, and by re-entrainment of settled fibers. In addition, airborne exposure may result II1-24 D 004270 Table II1-6 Asbestos Concentrations Found In California Water Treated Water Los Angeles San Francisco Klamath River Asbestos Concentrations (106 fibers/liter) 1 100-130 260,000 Untreated Water American River California Aqueduct 53-5,600 300-15,000 II1-25 D 004271 Sample Set Table III-7 Summary of Indoor Asbestos Samples!/ N_o. of Measured Concentration Equlvalent,,Coqcentration S'ampl es (ng/m3) (fibers/m3 )zJ 1/ Median 90th Percentile Median 90th Percentile Air in U.S. school rooms without asbestos 31 Air in U.S. build ings with cementi tious asbestos 28 Air In U.S. build ings with friable asbestos 54 Air in U.S. school rooms with asbestos surfaces 54 Air in U.S. schools 27 with damaged asbestos surfacing materials 16.3 7.9 19.2 62.5 121.5 72.7 19.1 96.2 550 465 540 260 640 2,080 4,050 2,420 640 3,210 18,330 15,500 1/ Table adapted from Committee on Nonoccupational Health Risks of Asbestiform Fibers, 1984. Page 220. 2J Based on a conversion factor of 30 ug/m3 = 1 fiber/cm3. V Equivalent phase contrast microscopy measurement. II1-26 D 004272 from breakdown of a hard asbestos surface such as vinyl-asbestos floor tiles (Sebastien, et al.( 1982). Dr. Steven Hayward also provided the information regarding indoor asbestos exposures at four locations in the San Francisco Bay area (Hayward, May 1985). Measurements were provided in fibers per cubic meter and in nanograms per cubic meter, as analyzed by transmission electron microscopy. Table III-8 shows the results of the indoor measurements taken at four locations. 3. Other Nonoccupational Exposure Routes In 1977 the Consumer Product Safety Commission banned production of patching compounds and artificial fire logs that contained asbestos. In a series of regulations issued between 1972 and 1975, the Food and Drug Administration banned the interstate commerce of asbestos-containing garments and disallowed the use of asbestos In food, food additives, drugs, and drug components. Manufacturers have voluntarily curtailed the use of asbestos In other consumer products such as hair-dryers. Nonoccupational exposures attributable to the use of manufactured asbestos products have often been assumed to be relatively low, because almost all these products contain asbestos In a binding matrix, such as cement, plastic, rubber or resin. However, exposures can occur if fibers are liberated from these matrices (Committee on Nonoccupational Health Risks of Asbestlform Fibers, 1984). Exposures to asbestos may also result from the use of products made from asbestos contaminated substances. An example is talc, which Is widely used as a pigment, extender, or processing aid In ceramic tile, paint, paper, and plastics. In smaller quantities talc is used as a component of cosmetic powders, foods, drugs, pesticides, and many other products (Committee on Nonoccupational Health Risks of Asbestlform Fibers, 1984). II1-27 D 004273 Location Table II1-8 Indoor Asbestos Measurements Taken in a California Building and Three Homes - Flbers/m^ Nanograms/m^ Description DHS Laboratory!/ Room 1 DHS Laboratory!/ Room 2 34.000 2,600 18.000 93,000 Menlo Park Home!/ <11,000 (asbestos ductwork) Berkeley Home!/ (front of heat register) 6,000 63 .06 .003 .02 2.5 -- .14 1.1 Day one Day two Day one Day two (after maintenance activity above celling) No fibers detected Indoor-small fibers Indoor-large fibers Corte Madera Home!/ (before asbestos paper removal) (after asbestos paper removal) 56,000 32,000 4,000 .3 2.1 29 All fiber sizes Indoor-small fibers Indoor-large fibers 1/ Asbestos had been sprayed on girders above the ceiling. 2/ The ductwork was made of asbestos paper. ?/ The ventilation system ductwork was made of metal but was lined inside and out with asbestos paper. / The ventilation system ductwork was made of metal but was lined on the outside with asbestos paper. II1-28 D 004274- REFERENCES FOR CHAPTER III Beaman, D. R. and D. M. File, 1976. "Quantitative Determination of Asbestos Fiber Concentrations." Anal. Chem. 48:101-110. Committee on Nonoccupational Health Risks of Asbestiform Fibers, 1984. Asbestiform Fibers - Nonoccupatlonal Health Risks. Hayward, Dr. Steven B., March 1984. "Field Monitoring of Chrysotile Asbestos in California Waters." Journal of the American Water Works Association. 66-73. Hayward, Dr. Steven B., May 31, 1985. Research Specialist, Air and Industrial Hygiene Laboratory, California Department of Health Services. Personal communication with Ralph Propper of the Air Resources Board. Hayward, Dr. Steven B., June 18, 1985. Research Specialist, Air and Industrial Hygiene Laboratory, California Department of Health Services. Personal communication with Janette Munson of the Air Resources Board. Hayward, Dr. Steven B., October 26, 1985. Research Specialist, Air and Industrial Hygiene Laboratory, California Department of Health Services. Personal communication with Todd Wong of the Air Resources Board. Ontario Ministry of the Attorney General, 1984. Report of The Royal Commission or Matters of Health and Safety Arising from the Use of Asbestos in Ontario. ' Science Applications, Incorporated, December 1983. Final Report Ambient Asbestos Concentrations In California: Volumes I and~TT^ Sebastien, P. J. Bignon and M. Martin, June 1982. "Indoor Airborne Asbestos Pollution From the Ceiling and the Floor." Science. 216:1410-1413. U.S. Environmental Protection Agency, June 1978. Evaluating and Optimizing Electron Microscope Methods for Characterizing Airborne Asbestos. EPA-600/2-78-038. Versar Inc., January 9. 1984. Draft Final Report - Exposure Assessment For Asbestos. Prepared for the U.S. Environmental Protection Agency, Contract No. 88-01-5211, Task 49. II1-29 D 004275 Appendix A Department of Health Services Health Effect Evaluation Request D 004276 Memorandum : Stanley Cubanski, Acting Director Department o Health Services 714 P Street Dote : February 19, 1985 Subject: Evaluation of Asbestos I am writing to formally request that the Department evaluate the health effects of asbestos (e.g., actinolite, amcsite, anthophyllite, chrysotile, crocidolite and tremolite) as a candidate toxic air contaminant in accordance with Assembly Bill 1807 (Tanner). According to Health and Safety Code Sections 39660-62, your Department has ninety days to submit a written evaluation and recommendations on health effects of asbestos to' the Air Resources 3oaj.d. If required, your Department may request a thirty-day extension of the deadline. Attached fcr your staff's consideration in evaluating asbestos are: Attachment I - A list of references on asbestos health effects which were identified in an Air Resources Board letter of public inquiry and received in response to the inquiry letter; Attachment II - Suggested issues which should be. considered in preparing the health effects document on asbestos fibers; Attachment III - Ambient asbestos concentration data which should be used to estimate the range of risk to California residents as required in Health and Safety Code Section 39660(c), sources of asbestos emissions and emission trends; and Attachment IV - Descriptions of the sampling and analytical methods used to determine the ambient asbestos concentrations. My staff is available for consultation in conducting this health effects evaluation. We look forward to continuing to work closely with you and your staff in carrying out this A-1 D 004277 Stanley Cubanski, Acting Director -2- legislative mandate. If you have any further questions regarding this matter, please contact me at 445-4383 or have your staff contact Peter D. Venturini, Chief of the Stationary Source Division, at 445-0650. Attachments cc: Gordon Duffy Alex Kelter, DHS w/attachments Raymond Neutra, DHS w/attachments Emil Mrak, Chairman and Scientific Review Panel Members w/attachments Peter D. Venturini, ARB John Holmes, ARB Assemblywoman Sally Tanner Senator Ralph Dills Senator Art Torres Claire Berryhill, DFA A-2 D 004278 Attachment I ASBESTOS REFERENCES (11/9/84) 1 Aches on E D , Bennett. C . Gardner. M J and Vinter, p Q (l?81) Mesothelioma in a factory using amosite and chrysotile asbestos Lancet 2CS260-41):1403-1406 2 Acheson, E Dand Gardner, M J <1980) Possible synergism between chrysotile and amphtbole asbestos (Letter) Lancet 1(8170)704 3 Acheson. E 0and Gardner, M. J (1981) Dose-response relations froa epidemiological studies Proc R Soc London, (Ser ) A. 374 <1744): 79-85 4 Acheson, E D , Gardner, M J , Pippard, C and Criae, L P (1982) Mortality of two groups of women who aanufactureed gas Basks from chrysotile and crocidolite asbestos a 40-year follow-up Br J Ind Med 39( 4 ):344 - 348. 3 Acheson. E D . Gardner, M. J., Vinter, P. D, and Bennett, C. (1984) Cancer m a factory using aaosite asbestos Int J Epideaiol. 13(l>:3-10. 4 Aisner, 242 J and Viernik, P H. (1981) Asbestos-re1 ated neoplasm Seain Oncol. 8(3) :241- 7. Archer, V. (1979) Carcinogenicity of fibers and filas: a theory. Med Hypotheses. 5(11) 1257-1242 8 Archer, V E and Roa, V. N. (1983) Trends in mortality of diffuse malignant mesothelioma of pleura (Letter) Lancet. 2(8341) 112--113. 3 Armstrong, B K. et al (1984) Epidemiology of malignant aesothelioaa in Vestern Australia Med J Aust 141(2):84-88. 10 Artvinli. M and Baris, Y. !. ( 1 982 ) Environaenta 1 f i bar - induced pleuro-pulaonary diseases in an Anatolian village: an epideaio1ogtc study Arch Environ Health. ' ' ' 3 > 17 7-181 11 Artvmli, M. and Baris, Y I ( 1 982 ) Environmental fiber induced pleuro pulmonary diseases in an anatolian Turkey viltage-an epidemiologic study Arch Environ Health 37 C3) 177-181 12 Arul. K j and Holt, P. F. (1980) Clearance of asbestos bodies from the lung: a personal view Br J Ind Med 37(3>.273-277 17 Barry, B E. et al ' 1 98 3 > Reaction of rat lungs to inhaled chrysotile asbestos following acute andsubchronic exposures Exp Lung Res 3(l):l-22. 14 Beck. B Konetxke. G V and Strum, V (1982) Asbestos and mesothelioma in east Ctrmany Arch Immunol Ther Exp 30(3 -- 4>.229-234 15 Beck, E C 1980) Eipeiimental pathology-in vitro studies-related to asbestos and other mineral fibers 1ARC Sei Publ 1(30) 385-400 Is Becklake. 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C. and MaDonald, A D (1981) Mesothelioma as an index of asbesto impact Banbury Report 9.73-84 108 Mcnchaux, C et al (1981) mesothelioma m rats following inoculation with acidleached chrysotile asbestos and other mineral fibers Carcinogenesis 2(3)229-234 1C 9 Morgan, A. ( 1 980 ) Effect of length on the clearance of fibers from the lung and on body formation. IARC Sci Publ 1(30)-329-335 110 Mossman, B , Light, V. and Wei, E (1983) Asbestos: mechanisms of toxicity and carcinogenicity m the respiratory tract Annu Rev Pharmacol Toxicol 23 395-413 A-8 D 004284 111 Mossaan, B T and Craighead, J. E (1981) Mechanisms o( asbestos care 1 nogentsis Environ Res 25(2) 289-280 112 National Research Council (1984) Non-occupattonal esposure to asbestiform fibers NAS Report 113 Newhouse. M L ( 1 983 ) Asbestos-related diseases. Practitioner 227 < 1 383 > 1 399-H11 114 Newhouse. M t (1981) Epidemiology of asbestos-re1 ated tuaors. Seam Oncol 8(3) 230 257 115 Newhouse, M. L. and Berry, C (1979) Patterns of mortality m asbestos factory workers in London Ann NY Acad Sci. 330:33-40 116 Newhouse, M l.. Berry, G. and Skidaore, J. V. (1982) A mortality study of workers manufacturing friction aateriils with chrysotile asbestos Ann Occup Hyg. 24(1-41:89?909 117 Nicholson, V J ct al (1981) Cancer froa occupational asbestos esposure projections. 1980-2000 Banbury Report 9:87-111. 118 Nicholson, V. J. (1984) Asbestos Health Assessaent Update. EPA Report (Revie draft) EPA-600/8-84-003A:131. 119 Nicholson, V. J et al (1979) Long-term mortality eiperience of chrysotile miners and aillers in Thetford Mines, Quebec. Ann NY Acad Sci. 330:11-21. 120 Nicholson. V J , Perkel, G. and Selioff, I. J (1982) Occupational esposure to asbestos: population at risk and projected aorta 1ity--l980-2 0 30. Am J lnd Med. 3( 3 ) :259-3 1 1 . 121 Norseth, T. (1980) Asbestos and metals as carcinogens J Tosicol Environ Health. 6(56 >:l0 2 1 - 10 2 8 . 122 Ordonet. N C and Smith. J. L. Jr <1983) Peritoneal malignant mesothelioma with multiple distant skin metastases. Arch Dermatol. 119(101:827-830. 123 Peto, J (1980) The incidence of pleural mesothelioma in chrysotile asbestos testile workers. IARC Sci Publ 2(30)703-71 1 . 124. Peto, J (1979) Dose-response relationships tor asbestos-related disease, implications for hygiene standards. Part 11. Mortality. Ann NY Acad Sci. 330-195-203 125 Peto. J (1980) Lung cancer mortality in relation to measured dust levels m an asbestos testile factory IARC Sci Publ 2(301.829-836. 126 Peto, J., Henderson, B. E. and Pike, M. C. (1981) Trends m aesothelioma incidence m the USA and the forcast epidemic due to asbestos esposure during Vorld Var II Banbury Report 9:51-72 12' Peto, J . Seidaan, H and Selikotf, I. J. (1982) Mesothelioma mortality in asbestos workers implications for models of carcinogenesis and risk assessaent Er J Cancer 43(1' 124-135 12? Pott, F <1982) Aniaal experiments on biological effects of mineral fibers IARC Sci Publ 1 ( 30 ) .24 1-272. 125. Price-Jones, M J., Cubbings, G. and Chamberlain, M. (1980) The genetic effects of crocidolite asbestos comparison of chroaosome abnormalities and sister chromatid eichanges Mutat Res 79(4) 331-336. Q D 004285 130 Pylev, t N *t *1 (1982) Pleural mesothelioma in the Rhtsus monkey Macaca-mulata induced by intri tracheal injections o( chryasotile asbestos. Eksp Onkol. 4(41.34-38 131 Pylev, LN (1980) Pretumorous lesions and lung and pleural tumors inductd by asbestos in rats. Syrian golden hamsters and Macaca mulatta (rhesus) monkeys. IARC Sc i Pub 1 1 ( 30 ) 343-3 55 132 Rahman, Q , Das, 8 and Viswanathan, P N. (1983) Biochemical mechanisms in asbestos tcsicolcgy Environ Health Perspect 51 299-303 133 Reiss, 8 et al (1983) Absence of mutagenic activity of three forms of asbestos in liver epithelial cells Environ Res 3 1 ( 1 ):1 00-1 04 . 134 Robock, K (1979) Based on available data, can we project an acceptable standard for industrial use of asbestos' Absolutely. Ann NY Acad Sci. 330.205-210 135 Rogol, P R , Ryu, J H. and Ginns, l. C. (1983) Reduced natural killer cell activity in asbestos workers Am Rev Respir Dis. 127(4 part 23:73 134 Rom, W. N et al (1983) Sister chromatid exchange frequency in asbestos workers. J Nat! Caner Inst 70(P 45-48 137 Rubino, G F et al (1979) Mortality of chrysotile asbestos workers at the Balangero Mine, Northern Italy Br J Ind Med. 36( 3 ):1 87-1 94 . 138 Scansetti, G et al (1981) Pleuat mesothelioma after a short interval from first exposure in the wine filter industry. Am J Ind Med 5(4) 335-339. 139 Schenker, M B , Garshick, E and Speiter, F. E. (1984) A case control study of incident mesothelioma deaths among railroad workers Am Rev Respir Sis. 129(4 s u p p 1 ) A14 6 140 Seidman, H.. Selikoff, I. J and Hammond, E. C. (1979) Short-term asbestos work exposure and long-term observation. Ann NY Acad Sci. 330 61-90 141 Seidman, H , Selikoff, 1 J and Hammond, E C. (1982) Mortality of brain tumors among asbestos insulation workers in the United States and Canada. Ann NY Acad Sci 38! 140-171 142 Selikoff. I J., Churg, J and Hammond, E. C (1984) Classics in oncology: Asbestos exposure and neoplasia CA 34(1)'48-S6 143 Selikoff, I. J , Hammond, E C. and Seidman, H. (1980) Latency of asbestos disease among insulation workers in the United States and Canada Cancer 46(12) 2.736-2740 144 Selikoff, I. J , Hammond, E C and Seidman. H. (1979) Mortality experience of insulation workers m the United States and Canada, 1943-1976. Ann NY Acad Sci 330 91-114 145 Selikoff. I J., Lilis, R and Nicholson, V J. (1979) Asbestosdisease in United States shipyards Ann NY Acad Sci. 330-295-311. 144 Selikoff, I J , Seidman. H and Hammond, E. C. (1980) Mortality effects of cigarette smoking among amosite asbestos factory workers. JNCI. 65(3):507-5l3. 147 Selioff I J (1981) Constraints in estimating occupational contributions to current cancer mortality in the USA Banbury Report 9 3-.18 A- 10 o 004286 H8 Stanton M, F ft al <1?S1> Relation of particle dimension to carcinogenicity in amphibole asbestoses and other fibrous minerals JNCI 47(5>.943-973 H? Stevens. J B it al (1984) Asbestos metabolism in-vivo, Am Rev Respir Dis 129(4 suppl) A148 130 Stuaphius, J (1979) Mesothelioma incidence in a Dutch shipyard Ann NY Acad Sci 330 317-322 131 Styba. K and Lange. A (1982) Effects of asbestos on benso(a)pyrcne mutagenicity Mutat Res 97(3) 227-228 132 Taylor. R A. and Johnson, L P (1981) Mesothelioma: current perspectives. Vest J Med 134(3) 379-383. 133 Teta, M J. et al (1982) Occupational asbestos exposure and mesothelioma in Connecticut USA. "Occupational lung disease" edited by Gee, JB et.al. Raven Press, New York 249pp 134 Teta, M J et al (1983) Mesothelioma in Connecticut, 1935-1977. Occupational and geographic associations. J Occup Med. 25(10.) 749-754. 15S Thomas, H F et al (1982) Further follow-up study of workers from an asbestos cement factory Br J Ind Med 39(3>-273-234 . 154 Topping. D. C. and Nettesheim, P. (1980) Two-stage carcinogenesis studies with asbestos in Fischer 344 rats JNCI. 45(3):427-430. 157. Topping. D C , Nettesheim, P and Martin, D. H. (1980) Toxic and tumortgenic effects of asbestos on tracheal mucosa. J Environ Pathol Toxicol. 3(3-4):241-273 158 Valerio. F. et al (1983) Chromosomal aberrations induced by chrysotile and crocidolite in human lymphocytes in vitro. Mutat Res. 122(3-4):397-402 139 Vicent, J H et al (1981) Static electrification of airborne asbestos- a study of its causes, assessment and effects on deposition in the lungs of rats. Am Ind Hyg Assoc J 42(10)'711-721 UQ Vagner. J C (1979) Diseases associted with exposure to asbestos dusts Practitioner 223(13331.28-33 -- 14! Vagner, J C. (1982) Experimental studies and the pathology of asbestos induced lung diseases Arch Immunol Ther Exp. 30(3-4) 221-228 142 Vagner. J C.. 8erry, G and Pooley, F D (1982) Mesotheliomas and asbestos type in asbestos textile workers a study of lung contents. Br Med J 285(4342) 403-404. 143 Vagner. J C - Berry, G and Pooley, F D. (1930) Carcinogenesis and mineral fibers Br Med Bull 34(1) 33-34 144 Vagner. J C , Berry, C., Skidmore, J V. and Pooley, F. D (1980) The comparative effects of three chrysotiles by injection and inhalation in rats. IARC Sci Publ 1! 3 0 ) 3 4 3- 372 143 Vagner. J C , Griffiths, 0 M and Hill. R. J. ( 1984) The effect of fibre sire on the in vivo activity of UICC croeidolite Br J Cancer 49(4).453-458 Uc Vagner. M H (1980) Immunology and asbestos IARC Set Publ 1(30) 247-251 A-11 D 004287 147 Vagner, M M and (1783) HLA-A and B antigen frequencies and mesothelioma in relation to asbestos exposure Br J Cancer, 8S( 5). 727-730 168 Walker, A M. et al~(l83> Projections of asbestos related disease 1980-2009. J Occup Med 25(5) 808-825 149 Varnock. M L , Kuwahara, T J and Volery, C. (1883) The relation of asbestos burden to asbestosis and lung cancer Pathol Annu. 18<pt 2) 107-185 17C Whitaker, 0., Shilkin, K. B and Valters MNI (1888) Cytologic and tissue culture characteristics of asbestos induced mesothelioma in rats Acta Cytol. 28(2) 185-117 171 Winkler, C C. and Ruettner, J R. (1882) Penetration of asbestos fibers in the isceral peritoneum of nice a scanning electron microscopic study. Etp Cell Biol 50(8) 187-178. 172 Voitowitx, H. J et al < 1982) Asbestos related diseases in Vest Germany. Arch Immunol Ther Exp 30 ( 3-8 ) . 1 83- 1 88 173 Voitowitx, H J et al (1781) Asbestos-related diseases in the Federal Republic of Germany An J Industr Med 2(1). 71-78. A- 12 O 00A288 [NORTH AMERICA ASBESTOS INFORMATION ASSOCIATION 1745 Jefferson Davis Highway. Crystal Square 4, Suite 509 Arlington. Virginia 22202 (703) 979-1150 January 17, 1985 William V. Loscutoff, Chief Toxic Pollutants Branch Re: Asbestos California Air Resources Board P.0. Box 2815 Sacramento, CA 95812 Dear Mr. Loscutoff: I am writing in response to the Air Resources Board's request for information regarding asbestos. I have had the opportunity to review the ARB's bibliography and to discuss the program with Mr. John Batchelder. The greatest omission in the ARB's bibliography appears to be in not listing a number of large, overview studies of asbestos which are valuable for their scope and for the many individual references assembled in them. I would, therefore, recommend that the ARB collect and consider the following studies: Acheson, E.D., Gardner, M.J. (1983) Asbestos. The Con trol Limit for Asbestos. Her Majesty's Stationery Office, London. British Advisory Committee. (1979) Asbestos. (The Simpson Report). Her Majesty's Stationery Office, London.- CPSC. (1983) Chronic Hazard Advisory Panel on Asbestos. U.S. Consumer Product Safety Commission, Directorate for Health Sciences. Report of the Royal Commission on Matters of Health and Safety Arising from the Use of Asbestos in Ontario. (1984). On the issue of ingestion of asbestos, there is a recent animal bioassay from the National Toxicology Program: NTP. (1983) Lifetime carcinogenesis studies of amosite asbestos in Syrian golden hamsters. NIH publication number 84-2505. A-13 D 004289 Page 2 I am also enclosing a copy of the EPA's response from the December 19, 1984 Federal Register regarding the use of asbestos in brakes. Mr. Batchelder noted that this is one area which may be a concern of the ARB. Finally, I am enclosing a copy of a paper by Wagner and Elmes en titled "The Mineral Fibre Problem." As the use of asbestos de clines, the use of other fibrous materials increases. The Wagner and Elmes paper cautions, on the basis of animal and human evidence, against the indiscriminant and uncontrolled use of these fibrous materials. The purpose of sending this paper is to make the point to the ARB that these fibrous materials constitute an area of in vestigation which has received scant attention, as oppossed to asbestos, which has been very thoroughly studied and regulated. Yet another survey study of asbestos, as is presently contemplated by the ARB, has a certain aura of "reinventing the wheel" about it, whereas, with the exception of the Danish government, there has not been a regulatory body which has addressed the issue of fibers generally. I would appreciate being kept informed of the progress of this project of the ARB, and if there is a mailing list established, please include my name on it. If I may be of any assistance, please feel free to contact me. Very truly yours. A-14 D 004290 Fedotil Register / Vol. 49. No. 2*5 / Wednesday. Deccmlnr IS. ISO* / Proposed Rultt *9311 *0CFRPrt7tJ cummenos a civil action in a district lom.juots. tsh-tri. tm-ii court of lha United Sietes lo compel KPA to Initiate e rulemiVlng proceeding Asbestos; Rtsponse to Cltlssne' * requested In the petition Any such Petition. civil tcllon musl be (lied within 90 deys AOtMCtr. Environmental Protection Agency (EPA). action: Response to Ottzena' Pelllion. efier ERA'S denial of Ihe petition or.lt EPA fells lo grant or deny the petition w ithin 90 days after Iht petition Is filed, within 90 days following sxplrstlon of suuuxar: The Envirenmenlel Protsctloa the 00-dsy responaa period. - Agency (ETA) li (Tinting petition filed under iictlon 2! of thi Toxic < tl. Evaluation of the Petition Substance* Control Act (TSCA) by thi Natural Rtiourcii Defense Council. Incto prohibit tha use of sebiitos In automobile end truck brakci. EPA hae commenced an epprcprieje proceeding to addrese Ihe risks which may be poied by this uae of asbestos. ....... oxn; Submit written comment! on or before March 19.1995. ' address: Submit written comments la triplicate Identified by the document control number (OPTS-21101S) to: TSCA Pubtlc Information OfficelTS-793), Office of Toxic Subitancei. Environmental Protection Agency, Rm. E-107. *<n M. SU SW. Washington. D.C. 20460. A copy of the petition end related Information (with any confidential business Information deleted) Is located In. Room E-107, Environmental ' ' Protection Agency, *01 M SU SW;' . Washington. DC 20*90. ' This material is available for viewing and copying from 9 aun. to 4 pan. Monday through Friday, excluding legal holidays. A Introductioa On September ti'l96*. EPA re'cslred a petition from Iht Neturtl Resources, Defsnse Council. Inc (NRDG). - . requesting that EPA prohibit ths further use of asbestos tn automobfls and truck brakes under section 6 of TSCA Tbs petition requested s prohibition of sabeitos In both bracts for new sin and trucks and In replacement brakes for existing vehicles. Tha ptUUon argued that the nsks posed by asbestos In brakes are unreasonable and thdt . . economically and technically fessfbla substitutes art available. - In order to promulgate any rules under TSuA section 9. the Agency must consider s number of factors. Including, among other things, the effects of i chemical substance on human health and the magnitude of exposure: the benefits of utilizing Ihe substance and the availability of substitutes for the trie or uses of the substance being assessed. 15 U.S.C. 2905(c)(1). Tha Agency has conducted a review of the available Information pertaining to the use of * SOA FURTHER INFORMATION CONTACT! Edward A. Klein. Director. TSCA -- Assistance Office fIS-799), Office of . Toxic Substances. Environmental Protection Agency. Rm. E-543. *01M SU SW. Washington. D.C 20*90. Toll-free: [800-424-0065). In Washington. D.C: (554-1*0*).' asbestos* in brakes. Including the information In NRDCs petition. A * summary of that review, including tn evaluation of the risks posed by Ala use and the availability of substitutes. Is presented below. B. Ttisk Presented by Asbestos Outside the USA' (Operator--202-554140*). SURRlEMEXTARY INFORMATIOSC Asbestos It a demonsCratsd human carcinogen that causea lung cancer and mesothelioma (s cancar of the cheat and L Introduction abdominal linings), aa wall as otherlung Section 21 of the Toxic Substances Control Act (TSCA). IS U.S.C. 2620. . provides that any penon may petition the Administrator of Q>A to initiate a . proceeding for the issuance, amendment, or repeal of a rule under, various sections of the Act. ETA may disorders. People ere exposed lo tsbestos throughout the life cycle of the substance--when tsbestos is mined, mQJed. processed.fabricated into Industrial end consumer products, and .. when those products art used repaired, end disposed of. .' . . . hold a public hearing or may conduct an Wiib regard to the uae of-atbestos in appropriate investigation to determine brakes, it has been estimated that about w hether the petition should be gristed. 2.750 people are potentially exposed EFA must either grant or deny the.. during primary manufacturing of brake petition within 90 days. If EPA pants, friction materials, and that abovt.5S0.cn> the petition, EPA shall promptly ' people are potentially exposed to. commence tn appropriate proceeding*. If asbestos during servicing and repair of EPA denies the petition, the reasons for vehicle brakes {Ref. 9). For example. . denial must be published in .the Federal persons In brake service and repair Regiatar, and the petitioner may shops typically aft exposed to asbestos A- 15 whea dust W blows mi ot brska drums being rsplsced. sthro brskr Itekig* are roufnrnrd to Incrvaae hXBvei properties and when braie ahnrs are rrliiwd Uae of aabealus In vehicle brain may Iss result In Inerrand asbestos tbor concentrations In the smblras air Pm eiampls. EPA bat rv.denes dial motor vehicle braking most Hkaly contribstes between 0 23 to U percent of Iht concentrsilon of siBestoi In the ambient sir (Ref. 7). Both general popoleboo tod workplace exposures to tsbestos Bben from Its etc In brakes may retch Is tn Increased number of asbestos-related Illnesses, including cancer. ; C. Availability ofSubstitute* Tha petitioner assarts that economically and technically kaiible substitutes, moal prominently iemimetalllc friedoo materials and iramid fibers, are available to reptacr asbestos In brakes. EPA has analyzed the availability of aabetihrtej for many asbenlof products, fcidudiag brakes, sad that tnslytis It summarized In Appendix A of the "Regulatory Impact Analysis of Commit on Asbestos Product*" (Rai Ik which Is included ia the public record established lor NRDCs section 21 petition. EPA acknowledges that naw substitutes for asbestos use 1st brakes are betag developed and that BA'i analysis (summarized below) may cot include reant developments. 1. Heavy vtbide brake block*. Brake blocks art components of brakes that are riveted or bolted to the insides of brake shoes lo provide protection sgainst the heat and wear anted by braking Heavy vthicia brake block* are used on heavy duty trucks, buses, sod other heavy duty vehiclas-Abost 14 percent of *Q asbestos used in brakes is in this category of ase. Albertos busy vehicle brake blocks account for about 99 percent of ths market for heavy vehicle brake blocks.' . Until recently, (he only commerdaSy available substitute tor asbestos heavy vehicle brake block* was a semimetaQic brake block using brats end zinc chips la an organic binder,b not "considered at good si isbeitoe beesore tt performs erratically at different temperatures. It I* also considered inferior to the tsbestos brake block In resisting wear sod minimizing brake fade. Recently, eramid fiber products, sock ts Kevlar, here been introduced. but aramid fiber products are eow more expensive Sian asbestos products, and (here fa do* sufficient evidence to determine . whether eramid fiber products will be as effective as atbestoa Gi (hie application. Information eoggrets that tod products may last longer than asbestos-based D 004291 producta. but verttlcattofl l (Ni dlere bitkrt hi the original equipment Informettoa M wrk a* lofomellcn a* price and efficacy o( the product* r needed hrfoc* DA can arlmJna whether continued uir of etkeelo* In broke block* pranenta on anrastonebl* rtlk. ^UnktnnJamdiua rvhiclt+vm broke Unlngt, Oner* brk liflint* era *wd* of fclcUon motartah which now ml motet shoe* ta * dram ink*. About 40 percent el oB etbesto* *etd ta brokt* bitbli category *f tm. I%t0 rwhiata ihia4bta Itanp meg b* v**d Ib both A* boot tod mr > broket adlghiaad medium vehldev . primarily tb* fcuol wheah. Ibwim moat yj*eager vehicle* etiB am irm brokt Unlng* oo lb* war wtnck-At ItaatOBptroaotoI drum beak* taring* . in Hill aibetto*. . Until racially tbo only eubetltute* tec i otbcita* brokt Qnlna which appeared ts hart oay poleatlu wart eemlmetalBc - broke Union. However. (bote prodirata tend la perform initially it uUcraal. temperature*. fide, end produce mara" nota* tbaa eebeetoe-breed fining*. Mara racially, brake fining* madf wiib oriraJd Ober hivi been developed. ' However, the** era non exposedve tbta tbe asbestos product and Him it market era eehrhtu* end SO percent irr ermlmfletlk tn Ihr frptarrmrnl brake* fire market approximately Mrcml of ditc brakee ere etbcelo* end 31* pcrcret era eeadraeuUte Scmlmetellle dtac broke* cnet approximately S Has et much a* lb* sibettaa ditc brain pad*, but to; ta* about 40 pameat longa ikutk* * aibcitoi pads. ScmimeUltk dtac bmka path cannot aubeUluta toe tab**to* Aac brake pads la ovary appttcaflaa tecaaa* ol Inlartor parformanc* ch*r*ctariatk*> ETA keo kifomadon Indicating that oestlmatalUc disc brake* thotue ba seed only la can with power brake tyetara* because otherwtaa'tha aemlaiataUle brake* may not ptovlda enough elopping power. EPA tlio hat InfnnaaUoo tail the itmlmelalltc brakee era iRghtly Inferior becauia'Bit uier hai (o putl harder on (hem before they art wanned up to |et (he tame performance at with ibeetoi brake*. ,. , . EPA la aware that a food dear nI * prodod rrecardi to beJnf done ta developefbetiva anbadtetaa lv * - eebeetoe la brake* EPA la mklny additional Infamatloaon enbaEMaa tor eebeetoe in brake*. . not currently enough InTorsudoa DLConduoloa -j.-- -- available to Judge tbe performance of eramid fiber briki Bnmga. rtirthermor*. EPA'o tvldene* Indicate* tbit ttrg* EPA he* decided fo granl NKDC* petifton becaaec tfia Ayency beffrvt* velum* produetlon of inndd fiber ' * that the uet of eebeetoe la brake* doe* broket any rmjutr* lubitentief rrloofbtg pnoeatriokalobumaa health. EPA I*. by bnki mimrficluran. Therefor*, aramid fiber breket any not be Initialint a procaadlnf to tithor Information oo tho duiiabllUy end vitUbb hi tubaUnOal qienOtflca for ' rntnlnra, fttsibilily of raducin| rlaka aiaadatad with the ui* of eebeetoe t* brake*. DA *. Heavy eeAfcfc Ac brat* pacta - wtD analyxa the expoeura boa uatt aI Plot brake pndi era steel yllha fetid eibeotoe, (he riek pnaanltd by (boar with friefioa metertak ika rub agitatt un*. and lb* icbefttulre ba eoch otca. I * rotor. Heavy lahlctat rarely era diee DA will el*o f*ther brformotion af tba brake* About ai percent ad el oebcotee 1 price, efficacy, end aeaflabAy ad teed tebnfcet letatafccatageeytf **: eubatSWe* tar aobeate* (a bruaa. Altar 8--drKiHlc dtecbrala pedo tea analytic ad dita Informha DA *4 iboat 20 percent ainre txpatuiv* tan tbe itbettoe diae brake podidrat they let! about 30 percent longer. Tki determine whel further acU ta ' appeopnet* toaddma lha riaka which may b* posed by tbta oaa ad a*be*aa. eemimataUtc* ditc bnki pitle era not Baaad an tafermtlcB tratavead W considered to b good genxnd ' data. DA I* ant praperedlo make n replacement* for aabaetoa dbcbreki unraaaontblt riik Rndlpt for aa pede for heavy Yiblrdee because Immediate baa olell uaaa od aabeala* ta oearimeteBIc* perform batter (bea brakee el this Kma Effective rubetltulee atbeetoe only la bootSi, hlgh-Mcflon. ' may aoi ba evallibla for certain bl*b-bet environment*. epplicatlona of ubraloe ta brakes ead A- Ughl and arrJiiui reAnnta the eubeatuue Cor ether epplicebooa era apt - brain podt. Tit*** era (hi time n dioc ' avtilebi* la eudllciaat qaanllly becaiw* brake pedo hr beery v*bfcf**. except of United production capacity. RelooUnft- they an aotDer. Ararat 20 percent of all may be rtqulrad lo make euballtulet oabettai ued in brakes I* m tale avilltble la larje voleroc*. . . categoryof**. fata*tfl*cbrake-' Tba Afancy lavlta* the public ho iriak Moihnrtillic brakeo kera submit comment* on treat* nlalfnf to Inedy mtd* larger faroedu and te ta the petition. EPA h partSenlcHp tbe Iria brake Ueb|i market eramid* tnlueitad tajecelvla* Information oa bated brake* era foot beginning to be "* both (ha currant availability od Introduced. Approximately SO peicent at iubatllulaa for asbeslda In brake* and A- 16 on flew eubillluit prodicii ihel era cumnlly belni drvtloped. The Ayancy hat an or^olnt w*tk|roup, whkh will review these comment*, will cantina* ta lnv*all|*ia the availability of affactiv* ibeeloe-be* tubadtula* tar asajn \ vablcl* brahat, and cnaaidar i approprlata optkraa la addraee Ih* h*k prvunled by atbe*toe ta brakee, IV. Record ' DA ha* lelablUhed record tar InformtUoa nltdaf to the NRDC peUtloa The racord tadude* Information coraldoad by DA ta developing tala ttapons* and coniUte ad Iht followln* e*lt|Orie* of InformsUoa: (t) The NRDC petition. (2) Appendix A of the "Rendelory Impact Aaalyito ad Controls on Asbeeloe Producta.* (3) Other information on lobetltotia ' for aibeatoa In bnkt*.' (4) Infocmatloa received from tho public eoncernlni th* patlttrak (5) Memoranda innunartzlnt m**lln|* and telephone conversation* with tb* public cone*mlng (ha paUUon. (#) Appendix | of tho Hefaletory Impact Analyst* ef Control* oa Aibeltos Produet*.' (7) Appendix N of the Hejulatory Impact Anelysle of Control* oa Aebeeto* Producta.* A public - eralsn od Iht record, without any uonfldantlal buelneee. lnformalloo. Ip available lo th* pobUe ta th* Office of Toxic Substance* PubUc Information Offlea, horn I an. to 4 p.m. Monday through Friday, except legal holidays. Th* PubUc Information Oflica 1a located la Ra. B-107.401 M SU SW. Waehlngton. O.C Dated: December IV1M4. WUSeea D. luekeiehem. Admielttntnr. IFR Doc. *4-33120 Tiled 13-17-44:1:14 pa) enuea cect <iee e e D 004292 FROM: RECENT ADVANCES IN OCCUPATIONAL HEALTH, Ed.: McDonald, j.c. Churchill Livingstone, Edinburgh, 1981: Pages 1-13.; 1. The mineral fibre problem J. C. Wagner P. C. Elmes IOEH 5723 Code 43 44 45 46 48 52 53 90 82 For many years interest in the biological effect of mineral fibres was mainly confined to the commercial types of asbestos. Recently many other fibrous minerals have been recognised as potentially dangerous pollutants of the environment. The majority of these materials are naturally occurring, others are synthetic. The natural fibres are either specifically exploited for commercial purposes or else occur as atmospheric contaminants which are released during mining or tunnelling operations. Industry has been developing other mineral fibres as a substitute for asbestos to meet an increasing need for cheap and reliable materials for reinforcement, friction products and insulation. The latter drmand has been emphasised by the present fossil fuel crisis. Minerals being exploited for a variety of purposes other than insulation and reinforcement are known to consist of fibres or elongated crystals, for example, wm, clays and some zeolites. Thus, these minerals can be considered under the following groups: 1. Asbestos minerals a. Of commercial value b. As potential environmental contaminants 2. Synthetic mineral fibres 3. Other naturally occurring fibrous minerals ASBESTOS r Asbestos of commercial value Practically all the knowledge that is available about hazards associated with the inhalation of fibrous mineral dusts has been obtained in studies of asbestos. Asbestos consists of six naturally occurring minerals: chrysotile, croddoiite, amosite, anthoph* yilite, tremoiite and acrinolite. Chrysotile is a member of a group of minerals referred to as the serpentines and is composed almost exclusively of magnesium in cembina- tion with silica. It has a sheet structure which curls to produce hollow tube-like fibres. The other five are members of one mineralogies] group referred to as the amphiboles. They are very similar in crystal structure, being chain silicates, but they vary in chemical composition. Croddoiite and amosite are iron-rich varieties, antbophyilite is a magnesium rich mineral, while tremoiite and acrinolite contain a large amount of caldum together with magnesium. The annual world production of asbestos in 1976 was 5 x 10* kg, of which 97 per cent was chrysotile and the remainder croddoiite and amosite. The commercial production of the other three amphiboles has been on a small scale in the past, but they are important as contaminants of other minerals and agricultural soil. Chrysotile is widely distributed, with the largest production from the Ural es--- A-17 D 004293 THE MINERAL FIBRE PROBLEM 3 With the development of more sophisticated techniques it is now obvious that t correct estimation of the number of fibres in tissue or environmental samples can only be obtained by examination under > transmission electron microscope, otherwise the large number of fibres of less than O.S /an in diameter will not be observed. The crucial question of the amount, size and type of fibre found in tissue which can be related to the diseases which will be described later, cannot be stated with confidence at this stage. In macerated specimens of dried lung 106 fibres per gramme can be found without evidence of disease; in cases of asbestosis the count is usually over 10*. With a light microscope seldom less than 2S0 000 fibres per gramme lung tissue are found in cases of asbestosis. 2. PLEURAL PLAQUES AND DIFFUSE PLEURAL FIBROSIS The presence of circumscribed areas of fibrous thickening below the mesothelium on the lower portion of the chest wall, over the diaphragm or on the pericardium are characteristic of exposure to fibrous mineral dusts. These plaques may be extensive, are leaf-shaped, often bilateral and have an irregular embossed surface. They consist of woven collagen fibres and as they mature become acellular and avascular. This avascularity leads to necrosis and sometimes to the gradual deposition of calcium in the lesions (Meurman, 1966). It can take 2D years or more for sufficient calcium to be deposited for the plaques to become radio-opaque and visible on chest radiography. Therefore, the plaques are seen much more frequently by the pathologists at necropsy than by the radiologist. In some cases there is generalise! pleural fibrosis, leaving the lungs en adrasse completely sheathed in a thick layer of fibrous tissue. Unlike plaques, generalised pleural thickening can restrict the expansion of the lungs and cause breathlessness. 3. ASBESTOSIS Asbestosis is a slowly progressive and persistent interstitial fibrosis of the lung associated with the inhalation of asbestos dust and characterised by asbestos bodies and fibres in large numbers in the tissue. If sufficient dust has been retained, the individual lesions in the alveoli join up until the individual acini become linked in a fibrous mesh, the process starting at the base of the lung and gradually spreading upwards. This process is fairly well established before there is recognition on radiological or by physiological examination, the latter often being obscured by the effects of cigarette smoking. If exposure has been sufficient the disease will progress after the worker has left the industry (Becklake et al, 1979). 4. CANCER OF THE LUNG Carcinoma of the bronchus is a frequent cause of death among workers with radiological evidence of asbestosis (Liddell and McDonald, 1980). The risk of a cigarette smoking worker heavily exposed to asbestos developing lung cancer is 25 to 50 times greater fhan an age matched non-smoker who has not worked with asbestos (see J. C. McDonald, 1980). Initially the carcinomas reported in the asbestos workers were peripherally situated, with adenocarcinomas being the most common (Bucha nan,' 1965). With the increase in cigarette smoking, all types of endobronchial tumours are being seen, but the number of adenocarcinomas is sriU more frequent than in non-exposed cigarette smokers (Kannerstein and Churg, 1972). A-18 D 004294 THE MINERAL FIBRE PROBLEM 5 of fibre; apart from mining areas, pure exposure is rare. South African experience with crocidolite has been repeated on a smaller scale at Wittenoom in Western Australia, where mesotheliomas have occurred, both in those employed in the mine* and in the environmentally exposed population (Hobbs et al, 1980). Nothing comparable has been reported for chrysotile, amosite or anthopyllite mining The gas mask workers investigated by Jones et al (1976) and some of those by McDonald and McDonald (1978) appeared to have had a pure exposure. Pooley's analysis of the lungs of the Nottingham cases also showed significant amounts of chrysotile, but not more than is found in autopsy material generally. The technique developed by Pooley (1975) for the idendficadon of asbestos and other mineral fibres in lung tissue is the most useful method available for identifying individual exposures and the complexity of the situadon gives emphasis to the need for the parallel examinadon of appropriate controls. The comparisons made between the fibres in the lungs of the mesothelioma cases and controls in Britain by Jones et al (1980) when compared with those obtained by A. D. McDonald (1980) in the United States and Canada has shown that chrysotile fibres are found in considers r.s quantity equally in raw and controls. In Britain, crocidolite and to a lesser extent .nosite were associated with mesothelioma, whereas in the USA it was predominantly amosite and less often crocidolite. Selikoff et al (1972) found a considerable excess of mesotheliomas in factory workers exposed to amosite but has not reported on the fibre content of their lungs. The Advisory Committee to the Secretary of State for Employment (Health and Safety Commission, 1979) concluded that in the causadon of mesotheliomas, crocidolite was more dangerous than chrysotile but that amosite might be intermediate between the two. Experimental evidence has complicated the situadon by showing that many types of mineral fibre can cause mesothelioma. This evidence has come in the main from intrapleural implantation studies which were initiated by Wagner (1962) and conti nued in collaboration with Stanton and Wrench (1972); Pott et al (1972) undertook similar intraperitoneal investigations. This work has indicated that the size of the fibres was more important than their nature. IMPORTANCE OF FIBRE SIZE The significance of the physical characteristics of fibres in explaining the biological effects of asbestos was first emphasised by Timbrell (1965). He demonstrated that diameter was the most important factor in determining whether a fibre would be inhaled. The finer the fibre the more easily would it reach the lung parenchyma. Later, Timbrell et al (1970) showed that this could be applied to the amphiboles and that the ultimate diameter of crocidolite was less than that of amosite. Although the individual fibres of chrysotile have a diameter less than that of crocidolite, they occur in a woven coil formation, the total diameter of which affects its aerodynamic behaviour. Thus chrysotile behaves as a coarse fibre and finds difficulty in reaching the pleura] surfaces through the peripheral airways. However, chrysotile fibres in aqueous solution can divide longitudinally into fibrils which under some circum stances are straight and have similar properties to very fine amphiboles. The typical electron microscopic appearance of asbestos fibres is shown in Figure 1.1. Calculations and experiments with casts of the lower respiratory tract showed that fibres up to 3.0 fim in diameter would reach the respiratory bronchioles. The length of fibres most likely to cause fibrosis would appear to be greater than 10 /im (Timbrell A-19 D 004295 THE MINERAL FIBRE PROBLEM 7 At this stage we must assume that all mineral fibres of similar sue range are potentially hazardous^ man, whether of asbestos or other type. Asbestos minerals as potential environmental contaminants Under this heading the following situations will be considered: 1. asbesdform minerals contaminating banded ironstone 2. tremolite as a contaminant of other mineral deposits 3. possible contamination of agricultural soil. Asbesdform minerals contaminating bonded ironstone Although it has been known for many years that banded ironstone deposits frequently contain small seams of fibrous silicates, occasionally the fibrous deposits are large, and may then be the source of amphibole asbestos as exploited in South Africa and Australia. Other deposits occur which are of qo commercial value, for example, there are the tacooite fibres in the Mesabi Range on the shores of Lake Superior. Although it has been shown that iron ore mining in this region is causing both contamination of the atmosphere and the water of the lake, no evidence of a hazard to man has been established. All the fibres axe below 5.0 ftm in length. In a large South Dakota gold mine the ore-bearing rock was cummingtonite -- grunerite (a dose relation of amosite) and some fibres were found in the dust. It was suggested that these fibres were associated with an increased incidence of carcinoma of the lung, but these findings were not confirmed by the investigations of McDonald et al (197S). Nevertheless, the possibility that hazardous fibres may sometimes be released from iron deposits in the vicinity of amphibole mines remains. Tremolite as a contaminant of other mineral deposits The fibre dimensions of tremolite vary even more between deposits than the other amphiboles. A coarse flake-like tremolite occurs as a contaminant of talc in California; this material does not cause tumours when implanted intrapleuially in rats, and there is no published evidence of disease among the miners. A coarse fibrous tremolite is found as a contaminant of the chrysorile deposits in Quebec Province in Canada. This fibre has been found in the lungs of miners and millers from these mines (Pooley, 1976); whether h plays any part in the etiology of pleural plaques and pulmonary fibrosis is still mMwwin. In the talc mines in the northern part of New York State there is contaminadon by a finer fibrous tremolite, and a few mesotheliomas and carcinomas of the lung have been reported among the miners (Kleinfeld et al, 1967). Practically pure tremolite of a coarser type has been used in Eastern Turkey for stuccoing houses. Yazidoglu (1976) found a significant incidence of pleural plaques among the inhabitants. Tremolite with very fine long fibres has been mined in South * Korea (see Fig. 1.1); this fibre has been shown to produce a high incidence of mesotheliomas in experimental animals. We have been informed that the mining operations have now been suspended because of suspected cancer among the workers. Possible contaminadon of agricultural soil A further source of fibrous mineral exposure only recently appreciated, may prove of consequence. Evidence is still fragmentary, and the only confirmed situation is in Bulgaria, where Burilkov and Michailova (1970; 1972) found pleural plaques in A-20 D 004296 THE MINERAL FIBRE PROBLEM 9 GLASS FIBRE (CODE 100) ii 10 nm particularly on factory floors, and occasionally for agricultural and pharmaceutical purposes. Information is scanty concerning the size and shape which particles of these fibrous minerals assume under a range of potentially relevant natural and artificial conditions; nor is much yet known about their biological activity in various in vitro tests. Animal experiments have been recently initiated in which scpiolite and attapuigite fibres are inhaled or implanted intrapleurally; the results will not be A-21 D 004297 THE MINERAL FIBRE PROBLEM 11 TURKISH FIBRE ERIONITE FROM USA Fig- 1-3 Electron micrographs ofdispersed samples of synthetic tad naturally occurring fibrous erionite To date, synthetic substitutes for asbestos (the man-made vitreous and ceramic fibres) do not appear to have caused lung fibrosis, lung cancer or mesothelioma in man. However, animal experiments indicate that it would be unwise to create materials which include fibres smaller than 0.5 /an in diameter if the risk of mesothelioma is to be avoided. Experimental work suggests that both synthetic and natural non-asbestos mineral fibres of less than 0.5 pan in diameter and greater than 8 pan in length may be hazardous. Some fibrous clays have already been shown to cause mesothelioma experimentally while epidemiological evidence suggests that fibrous erionite may well have been responsible for a very high incidence of mesotheliomas in man. Changes in industry and commerce are leading to human exposure from a variety of natural and synthetic mineral fibres. Further research is urgently needed to avoid replacing the hazard of asbestos with others as serious. REFERENCES Arrvinli M, Buis Y11979 Malignant mesotheliomas is s mull village is tbs Anatolian region of Turkey: sa epidemiological study. Journal of the National Canes Institute 63:17-22 Baris YI et al 1978 An outbreak of pleural mesothelioma and chronic fibrosing pleurisy m the village of Karain/Urgfip in Anatolia. Thorax 33:181--192 BotVlakc M R, Liddell FDR, Manfreda J, McDonald J C 1979 Radiological changes after withdrawal from asbestos exposure. British Journal of Industrial Medicine 36:23-21 Buchanan 97 D 1965 Asbestosis and primary thoracic neoplasms. Annals of the Hew Yock Academy of Sciences 132:507-511 Burilkov T, Mkhailora L 1970 Asbestos content of the soil and endemic pleural asbestosis. Environmental Research 3: 443-451 Burilkov T, Michailova L1972 Uber den Sepiolitgehah des Bodens in Geheta ch Endemischem Fleuraverkaikungen. Internationales Archir fur Arbestsmedizin 29:93-101 A-2 2 D 004298 THE MINERAL FIBRE PROBLEM 13 faserfenniger Stsube usd But Deutung im Hinblick auf die Tumorenutenhung Me&scben. ZentralbUn fur Bakteriologie, Parasitenkunde, Infektionskrankheiten usd Hygiene: ente Abeteiluof Ongusale, Reihe B: Hygiene, Preventive Median 162: 467-505 Poa F, Huth F, Friedrichs K H 1972 Tumoren der Rine nich up. Injektion von gtmihknem Qsrysocfl und Benzs (t) pyren. Zentrmlblstt fur Baktericlogit, Pinsteakunde, Infektionskrankheiten uad Hygiene: ente Abeteiluag: Originate, Robe B: Hygiene, Praeventive Medina 155:463-469 SelikoffI J, Hammond E C, Churg J 1972 Cardnogeaiary of imodu asbestos. Archives of Environmental Health 25: 133-186 Stanton M F, Layird M, Tegeris A, Miller E, May M, Rent E 1977 Cardsogenidry of fibrous glass: pleural response in the rat in relation to fiber dimension. Journal of the National Cancer Institute 51: 517-603 Stanton M F, Wrench C 1972 Mechanisms of mesothelioma induction with asbestos tnd fibrous glass. Journal of the National Cancer Institute 46:797-621 Stell P M, McGill T 1973 Asbestos and laryngeal carcinoma. Lancet 2:416-417 Thomson J G, Kaschula ROC, MacDonald R R1963 Asbestos as a modem urban hazard. South African Medical Journal 37: 77-81 Timbrell V 1965 The inhalation of fibrous dusts. Annals of the New York Academy of Saenees 132: 255-273 Timbrell V, Pooley F D, Wagner J C 1970 Characteristics of respirable asbestos fibres. In: Shapiro H A (ed) Pneumoconiosis: Proceedings of the International Conference Johannesburg 1969. Cape Town Oxford University Press, London, pp 120-125 Timbrell V, Rendall REG 1971/2 Preparation of the UICC standard reference samples of asbestos. Powder Technology 5:279-267 Timbrell V, Skidmore J W1966 Significance of fiber length in experimental asbestesis. In: Holstein E (ed) Internationale Konferenz der biologische Wtrkungen des Asbates, Dresden. Dtsch. Zentralinst, Arbeianted, Berlin, DDR pp 52-56 Wagner J C1962 Experimental production of mesotbelial tumours of the pleura by implantation of dusts m laboratory animals. Nature 196: 1 SO-ltl Wagner J C1979 Diseases associated with exposure to asbestos dusts. The Practitioner 223:26-33 Wagner J C, Berry G, Pooley F D 1980b Carcinogenesis and mineral fibres. British Medical Bulletin 36: 53-56 Wagner J C, Berry G, Skidmore J W 1976 Studio of the carcinogenic effects offiber glass of different diameters following intrapleural inoculation in experimental animals. In: Occupational exposure to fibrous glass -- proceedings of a symposium. (DREW Publication no (N10SH) 76-151.) U.S. Department of Health, Education and Welfiue, Washington DC, pp 193-197 Wagner JC,SkggsC A, MarchandP 1960 Diffuse pleural mesothelioma and asbestos exposure in the North Western Cape Province. British Journal ofIndustrial Medicine 17:260-271 Wagns J C, Berry G, Skidmore J W, Timbrell V1974 The effects of the inhalation of asbestos in no. British Journal ofCancer 29: 252-269 Wagner J C, Berry G, Kill R J, Munday D E, Skidmore J W 1960a Animal experiments with man-made mineral fibres. In: Wagner J C (ed) Biological effects of mineral fibres. WHO/IARC, Lyon, pp 361-362 Webster 1 1973 Asbestos and malignancy. South African Medical Journal 47:165-171 Yazidogiu S1976 Pleural calcification associated with exposure to ehrysotile asbestos in south east Turkey. Chest 70:43-47 Yazidogiu S, Dcsyto, R, Bald K, Sayli B S, Yorulmaz B 1980 Pleural calcification, pleural mesotheliomas and branchial cancers caused by tremolite dust. Thorax 35:564-569 A-23 D 004299 DEPARTMENT OF THE ARMY U. S. ARMY ENVIRONMENTAL HYGIENE AGENCY ASEROEEN PROVING GROUND. MARYLAND 21010-W22 ftCPLT TO attention 0* JAN 3 0 1985 Occupational and Environnental Medicine Division William V. Loscutoff Chief, Toxic Pollutants Branch California Air Resources Board P.0. Box 2815 Sacramento, California 95312 Dear Mr. Loscutoff: This Agency does not have data on asbestos per your request. However, we are aware of a document or. the health effects of asbestos which you may want to review. The title is: Asbestos - An Update of Epidemiology and Pathology since 1976. This document was published by the USAF Occupational and Environmental Health Laboratory, Aerospace Medical Division, Brooks Air Force Base, Texas in February 1984. A copy can be obtained by requesting report number 84-125C011 BOB from either the National Technical Information Service or the Defense Technical Information Center. Any questions concerning this reply should be directed to Major Robert W. Petzold, M.D. at telephone number 301-671-2464. Sincerely Colonel, Medical Corps Director, Occupational and Environmental Health A-24 D 004300 Attachment II SUGGESTED ISSUES WHICH SHOULD BE CONSIDERED IN PREPARING THE HEALTH EFFECT DOCUMENT ON ASBESTOS FIBERS Three publications may be useful for providing the background information on the health effects of asbestos {IARC, 1977; EPA review draft, 1984; and NRC, 1984; see attached reference list for full references). The IARC publication (1977) provides an adequate summary of asbestos health effects through 1976. The other two publications provide summary reviews on more recent health information and quantitative risk estimates of lung cancer and mesothelioma. Based on its evaluation of the health effects of asbestos, IARC has found "sufficient evidence" for carcinogenicity to humans and animals. Evidence for activity in short-term tests has been found to be "inadequate" (IARC, 1982). The following is an outline of issues in the format desired by the SRP: I. Asbestos As a Toxic Air Contaminant A. Asbestos is a generic name for a category of fibrous minerals that are used commercially. In EPA's National Emission Standard for Asbestos, the minerals defined as asbestos are actinolite, amosite, anthophyllite, chrysotile, crocidolite and tremolite. Because of the provisions of Article 39655 of the Health and Safety Code, it will be important to include at least those minerals in the California definition of toxic air contaminants. B. The physical properties of fibers such as respirability, size and aspect ratio, durability, flexibility and tensile strength, surface area and surface charge have been considered in relationship to observed health effects- of asbestos minerals. A discussion of these relationships of fiber* characteristics to health effects of asbestos will be very useful in eventually establishing control approaches. C. Evidence of carcinogenicity of several asbestiform fibers has been demonstrated in occupational studies, in studies of other human populations and in animal studies. Because the evidence of carcinogenicity is so strong in humans and animals it is unlikely A-25 D 004301 that other toxic effects need to be considered in order to list asbestos as a toxic air contaminant. II. Threshold Determination of Asbestos A. There is no strong positive experimental or epidemiological evidence that asbestos has a carcinogenic threshold. Therefore, it should be treated as a substance without a threshold. B. Because of the evidence that asbestos is not directly genotoxic, it might be argued that asbestos is likely to have a threshold. Therefore, the possibility that a single fiber of asbestos is capable of producing cancer would appear to need discussion. III. Dose-Response Estimates of the Carcinogenicity of Asbestos Choices and related considerations are as follows: A. The choice of using data from human epidemiologic studies or animal studies or both. B. The choice of using lung cancer or mesothelioma or both as the biological endpoints for the carcinogenic effects of asbestos. C. The choice of using one or more of the different types of asbestos as the causative agents. D. The choice of using one or more of the indices for quantifying the dose. For example: mass or number of fibers or fibers at specific size distributions or total surface areas. . The establishment of a method or factor to relate the fiber counts and size distribution obtained from optical and electron microscopy measurements. F. The establishment of a method or factor to relate fiber counts to mass measurements. A-26 D 004302 G. The synergistic effect of asbestos fibers and cigarette smoke or benzo(a)pyrene may be considered as an additional risk. H. An estimation of the potential risk related to indoor air exposure to asbestos. I. An estimation of the potential risk associated with asbestos exposure via drinking water. References: EPA Review Dra.ft (1984) Asbestos Health U.S.E.P.A. report (EPA-600/8-84-003A), 133pp. Assessment Update. IARC (1982) IARC Monographs on The Evaluation of The Carcinogenic Risk of Chemicals to Humans. IARC Monography Supplement 4, P.52-53. World Health Organization. IARC (1977) IARC Monographs on The Evauation of Carcinogenic Risk of Chemicals to Man--Asbestos. Vol. 14, 106pp. World Health Organization. NRC (1984) Asbestiform Fibers--Nonoccupational Health Risks. Committee on Nonoccupational Health Risks of Asbestiform Fibers, National Research Council, National Academy Press, 334pp. A-27 D 004303 Attachment III Ambient Asbestos Concentrations, Asbestos Sources and Emission Trends Data from a study done under contract to the Air Resources Board, entitled Final Report - Ambient Asbestos Concentrations in California, Volume 1, (December 1983), show mean concentrations of total asbestos fibers in the range of 9,500-66,000 fibers/cubic meter. The study also shows mean concentrations of chrysotile fibers in the range of 4,500-51,000 fibers/cubic meter, and mean concentrations of amphibole fibers in the range of below the detection limit to 31,000 fibers/cubic meter. As further discussed in Attachment IV, the sampler used has a collection efficiency of 50 percent for 3.5 um aerodynamic diameter particles. Of the reports containing measured ambient asbestos concentrations in California, we used the results from the above referenced study because it was the only one containing measurements from several populated locations in the State and because the samples were analyzed by transmission electron microscopy. Although we believe this data represents the best available, it is not possible to estimate an annual average concentration from these measurements with an acceptable degree of accuracy. Sources that lead to conmunity exposure to asbestos are: A-28 D 004304 o asbestos mining and milling operations; o floor: tile production; o gaskets and packing production; o manufacturing of friction products; o paints, coatings and sealants production; o asbestos reinforced plastics production; o asbestos cement pipe production; o asbestos textiles production; o asbestos paper production; and o asbestos cement sheet production. We are currently investigating the asbestos mining/ milling and manufacturing/fabricating source categories in California in order to estimate asbestos releases to the atmosphere. Other potential sources contributing to community exposure to asbestos are: o Natural weathering or human disturbance of mineral deposits (off-road vehicles, road-building); o Reentrainment of asbestos fibers that have settled out by dry deposition; o Transportation (consumption of brake and clutch 1inings); A-29 D 004305 o Demolition operations; and o Fiber loss from unpaved roads surfaced with crushed serpentinite (contains chrysotile) as a result of vehicular traffic. Asbestos fiber production at the mines and mills in California decreased from 1979 to 1983.--^ National consumption of asbestos decreased from 1977 to 1982.-^/ We are determining whether this trend has occurred in manufacturing/ fabricating source categories in California. At the present time, we are unable to assess the emission trends of the potential sources. 1/ Telephone conversation with Fred Carrillo, U.S. Bureau of Mines, January 1985. y Draft Final Report-Exposure Assessment For Asbestos prepared by Yersar Inc. for the U.S. Environmental Protection Agency, January 9, 1984, pg. 24. II Asbestlform Fibers-Nonoccupational Health Risks by the Committee on Nonoccupational Health Risks ot Asbestiform Fibers, National Research Council, National Academy Press, 1984, pg. 56. A-30 D 004306 Attachment IV - Sampling and Analytical Methods The goal of Science Applications, Inc. (SAI) project was to establish "worst case" respirable asbestos concentrations in a representative cross-section of California locations. Given the project objective, sampling and analysis methods focused on applying state-of-the-art sampling and analysis techniques to a cross-section of geographical sites based on emission/exposure potential. To examine maximum asbestos level conditions, sampling was done during the dry period of the year. Sampling methods adopted for the study followed protocols established by Dr. Walter John of the Air and Industrial Hygiene Laboratory in 1976, 1978, and 1980. The samples were analyzed by transmission electron microscopy according to the measurement and verification procedures specified by the U.S. Environmental Protection Agency (EPA) in their provisional method (1978). Since previous SAI surveys using electron microscopy showed that 90 to 95 percent of asbestos fibers in the ambient environment are shorter than 5.0 urn, a single-point cyclone sampler with a collection efficiency of 50 percent for 3.5 urn aerodynamic diameter particles at a flow rate of 15.5 1/minute was chosen for all filter sampling. An 8.0 urn pore size 47 irni diameter Millipore backing filter was used in conjunction with a Nuclepore 0.2 urn pore size collection filter. The backing filter A-31 D 004307 was used to ensure even distribution of particles across the filter face. The project was intended to measure airborne asbestos concentrations in areas that are known or are suspected to have elevated levels and in those that are isolated from asbestos sources. An additional site criterion was to co-locate, where possible, field measurements with existing particulate matter monitoring stations. Ten sampling sites were chosen: Napa, San Jose, Stockton, Sonora, King City, 8akersfield, San Fernando Valley, San Diego, South Gate and Century City. Original sampling plans called for collection of at least four four-hour samples at each site. Paired replicate samples were taken morning and afternoon at King City, San Jose, Napa, San Fernando Valley, and Sonora. Century City, Bakersfield, South Gate and San Diego normally have high particulate concentration levels, so samples were collected at these locations over shorter time intervals to preclude overloading the filters. At these sites, SAI took five to nine samples per day. Sampling time was based on prior calibrations of filter loading, as a function of suspended particle count levels, by scanning electron microscopy. A JEOt 6C transmission electron microscope (TEM), with a resolution of six angstroms and equipped with selected area A-32 D 004308 electron diffraction was used for all sample analyses. Calibration of instrument magnification was performed using a 21,400 lines/inch carbon replicate standard against a scale etched on the fluorescent screen of the TEM. In reporting the analytical results, values shown as zero are below the detection limit. Detection limit is defined as a function of the total area of the filter scanned and the volume of air that is sampled. When only one fiber was found on the sample scanned, the value obtained was used to derive the detection limit. Samples having less than one fiber found during analysis were defined as being below the detection limit. All the samples analyzed were counted in an identical manner and had been collected at the same flow rate, therefore, the detection limit was a function only of the duration of sampling time. Since sampling times ranged from one to four hours depending on mass concentration, net detection limits ranged from 9100 to 2400 3 fibers/m of air, respectively. To fulfill quality assurance requirements, the University of Washington Transmission Electron Microscopy Center was provided with replicate filter samples for an interlaboratory comparison. The samples were analyzed according to the EPA provisional method and the data returned to SAI for computer reduction. In addition to a background control (Napa site). A-33 D 004309 sites selected for inter-comparison analyses were King City, Sonora, Century City, and San Diego. The Napa sample was done in duplicate by both laboratories to provide or measure reproducibility. The detection limit for TEM asbestos analysis in this study was approximately 2400 fibers/m , the result of counting only one fiber in the filter area analyzed. The greatest difference between comparative samples was for the duplicated background control samples done by the University of Washington. Although values for these two replicates are a factor of 11 apart, the difference represents the counting of four fibers vs. one fiber per total counting area, respectively. Differences between the two laboratory's analytical results for the other replicate samples are in all cases less than the variation in the single duplicate analysis. A-34 D 004310 Appendix B Information Request and Public Responses STATE OF CALIFORNIA AIR RESOURCES 1102 O STREET F.O. BOX 2813 SACRAMENTO. CA 93812 BOARD - GEORGE DEUXMEjIAN, Smn<or December 7, 1984 Dear Sir or Madam: Subject: Request for Information Regarding Asbestos I am writing to request information on the health effects of asbestos (e.g., chrysotile, crocidolite, actinolite-tremolite, amosite, anthophyllite, etc.) as part of our toxic air contaminant program. This program is based on Health and Safety Code Sections 39650, et seq. which require the ARB to identify compounds as toxic air contaminants and once identified to develop and adopt control measures for such compounds. After consultation with the staff of the Department of Health Services (DHS), we have selected asbestos as a candidate toxic air contaminant to be evaluated in accordance with the provisions of Health and Safety Code Sections 39650, et seq. Before the ARB can formally identify a compound as a toxic air contaminant, several steps must be taken. First, the ARB must request the Department of Health Services to evaluate the health effects of candidate compounds. Second, the ARB staff must prepare a report which includes the health effects evaluation and then submit the report to a Scientific Review Panel for its review. The report submitted to the Panel will be made available to the public. Information submitted in response to this request will be considered in the ARB report to the Panel. Although any person may also submit information directly to the Panel for its consideration, I urge you to submit all information at this time for our consideration in the development of the report for the Panel. The, Panel reviews the sufficiency of the information, methods, and data used by the DHS in its evaluation. Lastly, after review by the Scientific Review Panel, the report with the written findings of the Panel will be considered by the Air Resources Board and will be the basis for any regulatory action by the Board to officially identify a compound as a toxic air contaminant. Prior to formally requesting the DHS to prepare a health effects evaluation of asbestos, we are providing, pursuant to the provisions of Section 39660(e) of the Healtn and Safety Code, an opportunity to interested parties to submit information on the health effects of asbestos which they believe would be B-l 0 004312 -2- December 7, 1984 important in DHS's evaluation of asbestos as a candidate toxic air contaminant. In late October 1984, ARB staff received a reference search on health effects of asbestos using the Taxline, Medline, and Biosis databases available from NLM ana Dialog Information Services. The search was limited to material available to the public between January, 1980 and July, 1984. The attached bibliography lists the references from this information search. We are requesting pertinent information on the health effects of asbestos, including any material that may not be available to the public, that is not included in the attached bibliography. Pursuant to the provisions of the Public Records Act (Government Code Sections 6280 et seq.), the information you provide will be a public record and subject to public disclosure, except for trade secrets which are not emission data or other information which is exempt from disclosure or the disclosure of which is prohiDited by law. The information may also be released to the Environmental Protection Agency, which protects trade secrets and confidential information in accordance with federal law, and to other public agencies, which are also required to protect such information. To expedite the review process, we ask that any information which you believe should be regarded as "trade secret" be clearly marked and separated from other infon.iation. You may identify portions of the information you submit as "trade secret" in accordance with Health and Safety Code Section 39660(e). The claim of trade secrecy must be supported upon the request of the Air Resources Board. Other information claimed to be trade secret and information otherwise claimed to be exempt from disclosure may be identified as confidential in accordance with Section 91011, Title 17, California Aaministrative Code. Section 91011 requires that the claim of confidentiality be accompanied by specified supporting information. I would appreciate receiving any relevant information you wish to submit by January 21,1985. Your help in expediting our review will be greatly appreciated. Please send the information to the attention of: William Y. Loscutoff, Chief Toxic Pollutants Branch Re: Asbestos California Air Resources Board P. 0. Box 28T5 Sacrament o,'CA 95812 If you have any further questions regarding health effects information, please contact Mr. John Batchelder at (916) 323-1505. For any other questions, please contact Mr. Robert Barham at (916) 322-7072. B-2 D 004313 -3- December 7, 1984 If you are not the person to when this request should be addressed, please forward it to the appropriate person in your organization. Also, please let us know whether you would like to continue to receive Information Inquiries for other candidate compounds, and if not, if there is anyone in your organization to whan such requests should be sent. Sincerely, cc: Alex Kelter, DHS Lori Johnston, DFA Wayne Morgan, President, CAPCOA Jan Bush, Executive Secretary, CAPCOA David Howekamp, EPA Region IX Assemblywoman Sally Tanner Senator Ralph Dills APCOs Emil Mrak, Chairman, and Scientific Review Panel Members Attachment B-3 D 004314 ASBESTOS REFERENCES (11/9(84) 1. Acheson, E. D.* Bennett, C., Cerdner, M. J. end Vinter, P. D. (1980 Mesothelione tn 4 fectory using eaosite nd chrysotilc esbestos. Lencet. 2<8240-41):1403-1404 . 2. Acheson, E. D. end Cirdner, M. J. < 1 980> Possible synergism between chrysotilc end eaphibole esbestos (Letter). Lencet. 1(8170:704. 3. Acheson, E. D. end Cerdner, M. J. (1781) Dose-response reletions (roa epideaiologicel studies. Proc R Soe London, (Ser.) A. 374(1744): 79-83. 4. Acheson, E. D., Cerdner, M. J., Pipperd, E. C. end Crime, L. P. (1982) Mortelity of two groups of women who aer.ufectoreed ges aesks froa chrysotilc end erocidolite esbestos: e 40-yeer follow-up. Br J Ind Med. 39 (4>: 344-348 . 3. Acheson, E. D., Cerdner, M. J., Vinter, P. D. end Bennett, C. (1984) Cencer in e fectory using eaosite esbestos. Int J Epidemiol. 13(0:3-10. 4. Aisner, J. end Viernik, P. K. (1981) Asbestos-releted neoplesa. Semin Oncol. 8(3):2412 42 . 7. Archer, V. E. (1979) Cereinogenicity of fibers end films: e theory. Med Hypotheses. 5 ( 1 1 ) : 1257-1242 . 8. Archer, V. E. end Rom, V. N. (1983) Trends in nortelity of diffuse aelignent aesotheliome of pleure (Letter). Leneet. 2 ( 8340:112-113. 9. Armstrong, E. K. et el (19.84) Epidemiology of aelignent aesotheliome in Western Austrelie. Med J Aust. 1 4 1 ( 2 ) : 84-8 8 . 10. Arteinli, M. end Beris, Y. 1. (1982) Entironaentel fiber-induced pleuro-pulaonery diseeses in en Anetolien tillege: er. epidemiologic study. Arch Enriron Keelth. 37 ( 3 ) : 1 7 7- l 8 1 . 1. Arteinli, M. end Beris, Y. 1. (1982) Enrironaentel fiber induced pleuro puiaonery diseeses in en enetolien Turkey viliege-en epideaiologic study. Arch Eneiron Keelth. 37 ( 3 ) : 1 77- 1 8 1 . 12. Arc 1 , K. J. end Holt, P. F. ( 1980 ) Cleerence of esbestos bodies from the lung: e personel eiew. Er 0 Ind Med. 37(3):273-277. 13. Berry, B. E. el el ( 1 983) Seection of ret lungs to ir.heled chrysotilc esbestos following ecute endsubchror.ic exposures. Exp Lung Res. 5(0:1-22. 14. Beck, E., Xonetike, C. V. end strum, V. (1982) Asbestos end mesothelioae in eest Cermer.y. Arch Immunol Ther Exp 30 (3-4 ) : 229-234 . If Beck, E C. ( 1 980 ) lrperiaer.ee: pcthelogy-ir. ritro studies-releted to esbestos end ether minerei fibers IARC Sci'Publ. 1 (30:385-4 00. It Beckleke, K r. (1982: Exposure tc esbestos end huaen dtseese (editorieL:. N Engl J Med 314(24):1480-148: 1' Beckiekt M ?. '082: Asbestos-releted d:seeses of the lungs end pleure current c 1 : r.: c l 1 issues Ac. ?. e v Rest:: Cts 134(3 lt'-lc4 B-4 D 004315 18. Begin- R. ct *1 (1981) Early long events following low-dose asbestos exposure. Environ Res. 24(2):392-40 1 . 1^- Berry, C. and Newhouse, M. L. (1983) Mortality of workers manufacturing friction material using asbestos. Er J Ind Med. 40(l):l-7. 20. Bignon, J. et al. ( 1 979) Human and Experimental Data on Translocation of Asbestos Fibers through the Respiratory System. NT Academy of Science. 745-50. 21. Bignon, J. and Jaurand, M. C. (1983) Biological in vitro and in vivo responses of chrysotile verse aaphiboles. Environ Health Perspect. 51:72-80. 22. Blot, V. J. et al. (1980/September 1980) Lang and Laryngeal Cancers in Relation to Shipyard Employment in Coastal Virginia. JNCI. 45(3):57l-5. 23 . Bolton, R. E. et al (1982) Variations in the carcinogenicity of mineral fibers. Ann Occup Hyg. 24(1-4):549-582. 24 . Bolton, R. E. et al (1982) Variations in the carcinogenicity of mineral fibers. Ann Occup Hyg. 24 ( 1-4 ):549-582 . 25. Boman, C. et al (1982) Malignant mesothelioma in Turkish immigrant residing in Sweden. Scand J Vork Environ Health. 8(21:108-112. 24. Briselli, K., Mark, E. J. and Dickersin, C. R. (1981) Solitary fibrous tumors of the pleura: eight new cases and review of 340 eases in the literature. Cancer. 47 ( 1 1 ):2478-2689 . 27. Brody, A. R. and Hill, L. K. (1981) Deposition pattern and clearance pathways of inhaled chrysotile asbestos. Chest. 80(1 Sapp 1 ):44-47 . 28. Brown, R. C., Poole, A. and Fleming CTA ( 1 983) The influence of asbestos dust onthe oncogenic tranformation of C-3H-10T-1-2 eells. Cancer Lett. 18(21:221-228. 29 B r owne, K . (1983) The -pidecielogy of mesothelioma. J Oecup Med. 33(4) .190-194 30 B r owne, X . (1983) Asb est os-r e1 a t ed mesothelioma: epidemiological evidence for asbestos as a promotor. Arch Environ Health. 38 (5 ): 24 1 -24 4 . 3 ; . B,r own t, F.. and Goffe, 7. ( 1 9 84) Mesothelioma due to domestic exposure to asbestos ("letter). Er Med J (Clin Res). 2 89 ( 4437 1:1 1 0-1 1 1 . 32. Browne. X. and Smither, V. J. (1983) Asbestos-related mesothelioma: factors discriminating between pleural and peritoneal sites. Br J Ind Med. 40(2) .`145-152. 23 Casey, C. (1963) Sister-chromatid exchange and cell kinetics in CHO-Kl cells, human figroblasts and 1ymphob1 asto i d eells exposed in vitro te asbestos and glass fiber.' Mu tat Res. 116(3-4): 349-377. 34 Chovii, A and Stewart, C. (1979) latency period for mesothelioma (Letter). Lancet. 2 ( 8 1 47 ) : 853 2! Churg, A K tnc Varnock, M L (1981/March 1981) Asbestos and Other Ferruonous Bodies, Their Formation in: Clinical Significance. At C Pathol. 1 02 ( 3 ):447-5i it Churg. A and Colder.. disease Paths! A nr v *:*:* Current crobiems'tr. the pathology oc isbestos-relate: 3 33-et B- 5 D 004316 37 . Char 9 B. ( 1784) Fiber sire end nuaber in eaphibole isbestos induced ntiothe 1ioai. Aa J Pethol. 1 15(3 ): 437-442 . 38 . Churg, A. end Vood, F. (1783) Observetion on the distribution o( esbestos fibers in huemn lungs. Environ Res. 3 1 (2) : 347-380 . 37 . Cook, P. M., Peleker, l. D. end Coffin, D. 1. ( 1782) Interprelet ion of the cercinogenicity of emosite esbestos end ferro ectinolite on the besis of reteined fiber dose end eherecteristics in vivo. Toxicol Lett. 13(3-4):151-158. 40. Creigheed, J. E. end Mossaen, B. T. (1782 Associeted Diseeses 308(24) :1448-55. ) The Pethogenesis of Asbestos. New Englend Journel of Medieine. 41. Devis, J. M. ( 1777) The Use of Animel Models end Priaery Prevention of Ceneer. NY Aeed of Science. 330:775-8. 42 . DiFeolo, J. A., DeMerinis, A. J. end Doniger, J. (1783) Asbestos end Benxo(e)pyrene Synergisa in the Trensforaet ion of Syrien Heaster Eabryo Cells. Pheraeco1ogy. 27(2):85-73. 43 . Dodson, R. F. et el ( 1 78 4 ) Asbestos Content in Lungs of occupetione 11y exposed individue 1. JAMA. 252 ( 1 >:88-71. 44 . Donhea, X. J. et el (1780) The effects of long-tera ingestion of esbestos on the colon of F344 rets. Ceneer. 45(5 Suppl):1073-1084. 45 . England, A. end Engholn, C. (1782) Asbestos releted ceneer in Swedish construction workers. Arch Iaaanol Th'er Eip. 30 ( 3-4): 157-180 . 48 . Enterline, P. E. (1783) Risk essessaent of esbestos cercinogenicity in nonoecupetioneiIy exposed populetions. VDI-Ber.' 475 :l?7-303 . 47 . Enterline, F. E. (1783) Ceneer produced by nonoeeupetionel esbestos exposure in the United Stetes. J Air Fetlut Control Assoe. 33(4):31t-322. 48 interline. P. E. (1781) Proportion of ceneer dae to exposure to esbestos. Benbury Report. 7:17-38. 47 . Epler. C. R., Mcloud, T. C. end Ceensler, E. A. (1782) Prevelenee end incidence of benign esbestos plecrel effusion in e working populetion. JAMA. 247(5):8 17-422. 50 . Findley, M. E. et el (1783) An essessaent of the Environaentel Protection Ageneys (USA) esbestos heterd eveluetion elgoritha. Aa J Publie Heelth. 73( 10):1177-11*1 . 5 1 . Finklestein, M. V. (1763) Mortelity eaon; long-tera eaployces of en Ontirio esbestosceaent feetory. Br J Ind Med. 40 (2 ) : 136-144 . s:. Finklestein. K. V. (1784) Mertelity eaong eaployces of en Onterio esbestos-ceaent feetory AcRevRespirDis. 127(S):754-78i. Fischbein. A. end Rohl , A K. ( 1 764 ) Pleue! aesothelioae end neighborhood esbestos exposure Findings iron a: c: ocheet ce i er.elysis of lung tissue. JAMA. 25 2 ( 1 ): 88-87 . "leury. J et el (!*S3) I r.; e r ec t i ons of esbestos fibers with hepetocytes in vitro: er. uit restructure! study. Toxicol Lett 1 7 c; - 2 ): 15 - T2 rrer.k A L : 1 C ftrscet: 3 4 Z`-3C ebservetior.s fe B-6 owing esbestos exposure Lnviron Keelth D 004317 34. Gardner. M. 3., Acheron, . D. end Vinter, P. D. (1962) Mortality from mesothelioma of the pleural during 1948-78 in England end Vele*. Br J Cencer. 46(l):81-88. 37. Gledfelter, T. ( 1 982 ) Melignent mesothe 1ione: an occupation disease (clinical conference). 3 faa Prtct. 14 (3 ): 827,830-832 . 58. Glickman, L. T. et al ( 1983) Mesothelioma in pet dogs associated with etposure of their owners to asbestos. Environ Res. 32(2 ): 303-313. 39. Goldsmith, 3. R. (1982) Asbestos as a systemic carcinogen: the evidence from eleven cohorts. Am J Ind Med. 3 (3): 341-348 . 40. Goschicki, 3. V. and Indulski, J. A. (1982) The polish studies on occupational exposure to asbestos and its biological effects. Arch Immunol Ther Exp. 30(3-4):149174 . 41. Griffia, L. C. et al (19S3) Deposition of erocidolites asbestos and glass microfibers inhaled by the Beagle dog. Am Ind Kyg Assoc J. 44(3):214-222. 62. Hallenback, V. H. ( 19 83 ) Asbestos PENETRATION OF THE GASTROINTESTINAL TRACT. Environ Health Ferspect. 33:133-154. 43. Hallenbaek, V H., Markey, D. R.- and Dolan, D. G. (1981) Analyses of tissue, blood, and urine samples from a baboon gavages with chrysotile and erocidolite asbestos. Environ Res. 25 (2 ) :349-36 0. 64. Hamilton, J. A. (1980) Maerophage stimulation and the inflammatory response to asbestos. Environ Health Perspect. 34:69*74. 65. Karinaton, 3. S. (1981) Fiber earcinogenesIs: epidemiologic observations and the Stanton hypothesis. JNCI. 67 (5 ): 977-989 . 66. Harvey, &., Page, K. and Dumas, L. (1984) Binding of environmental carcinogens to asbestos and mineral fibers. Er 3 Ind Med. 41(31:396-400. 67. Haugen, A. and Harris, C. (1982) Asbestos careinogenesis: asbestos interactions and epithelial lesion m cultured human tracheobronchial tissues and cells. Recent Results Cancer Res (Germany, Vest). 82:32-42. 68. Henderson, D. V. ( 1982 ) Asbestos-re1 ated p1euopclmonary diseases: asbestosis mesothelioma and lung eaneer. Pathology (Australia). 1 4 (3 ): 239-243. 69. Henderson, V. L. and Enterline, P. E. (1979) Asbestos exposure: factors associated with excess cancer and respiratory disease mortality. Ann NY Acad Sci. 330:117-124. 70. Hesterberg, T. V. et al (1982) Asbestos induces morphological transformation in Syrian hamster embryo cells in culture. 3 Cell Biol. 95(2 part 2):449A. 71. Hi 1 Ierdal , C. ( 1 983 ) Malignant mesothelioma 1962: review of 4170 published cases Br J Die Chest . 77 ( 4 ) : 32 1 - 3 43. 72 Holt. F F. (1982) Translocation of asbestos dust through the bronchiolar wall. Enviror. Res 27 ( 2 ) .235-2 60 . 73 Hopkins J (1984: Epidemiological studies on ingested asbestos. Food Chem Toxicol 2 2 ' Z ' "C-1S1 ? i Huir.: z 1 : Amos : *. e . chrysotile and crecicd:*. t asbestos are mutagen:: ir. !h:r.ef t r.i:is : e l u cells Mu:a: Res 6 : 1 3> . 241-2"< D 004318 B-7 75. Humphrey, E. V. et el (1981) The production of aelignent tenors of the lung end pleurel in dogs Iron intretrecheel esbestos instillition end cigerette saoking Cencer. 47(8 ): 1974-1999 . n. Huukonen, M. S. (J 980) Asbestos end eencer in Finlend. J Toxicol Environ Heelth 8(5 8):1281-1285. 77 . Huukonen, M. S. (1982) Asbestos end cencer. Eur J Respir Dis. 123:145-152. 78 . Jones, J. S. ct el (1980) The pethology end ninerel content of lungs in eeses of aesotheiioae in the United Kingdom in 1978 . 1ARC Sci Pubi. 1 (30): 187-199. 7? . Joseph, L. B. et el (1983) Morpho1ogice1 trensformetion in vitro of norael huaen fibroblests by chrysotile. Environ Heelth Perspeet. 51:17-22. 80 . Kegen, E. (1981) The elveoler meerophege: innune derengenent end esbestos-releted neligneney. Seain Oncol. 8 (3 ): 258-247 . 8 1 . Kehn, E. 1. et el (1980) Fri&ery peticerdiel mesothelioae following exposure to esbestos. Environ Res. 23(21:270-281. 82 . Kennerstein, H. (I960) Recent edvenees end perspectives relevent to the pethology of esbestos-releted diseeses in men. IARC Sei Fubl. 1 (30>: 149-142 . 83 . Kennerstein, M. end Churg, J. (1980) Kesotheliome in men end experiaentel eniaels. Environ Heelth Perspeet. 34:31-34. 84 . Kew, J. L., Tilkes, F. end Beck, E. C. (1982) Reeetion of cells cultured in vitro to different esbestos dusts of equel surfeee eree but different fiber length. Br J Exp Pethsl. 4 3 ( 1 ) : 1 0 9-1 1 5 . 85 . Kolev, K. (1982) Experiaente11y induced aesotheiioae in white rets in response to intre peritoneel edainistretion of emorphous crocidolite esbertos prelininery report Environ Res. 29< 1 ):123-133 . 88 . Kolev, K. (1982) Experiaente11y induced aesotheiioae in white rets in response to in t r eper i t oneel edair.istret ion of emorphous crocidolite esbestos: preliainery report Environ Res. 29 ( 1 ) : 1 23- 133 . 87 . Lefuae, J. et el (1980) Mesothelioae induced by intrepleurel injection of different types of fibers ir. rets; synergistie effect of other cercinogens. IARC Sei Fubl. 1(30) :3ll-320. Eenger, A. K. et el (1980) Asbestos es e eofeetor in cereinogenesis eaong nickel processing workers. Science. 209 < 4454 ): 420-422. 8? . leaen, R. A., Dement, J. M. end Vegener, J. (1980) Epideaiology of esbestos-releted diseeses. Environ Heelth Perspeet. 34:1-11. 90 . Lewmsohn. K. C. et el (198C-) The influer.ee of oceupetienel end environments! esbestos exposure on the incidence of aelignent aesotheiioae ir. Connecticut. IARC Sc Fubl 2(30):55-440 1 i:: s. ?.. et e! (!*??) Asbestos diseese ir. meintener.ee workers of the ehcmicel industry. Ar.r. KY Aced Sci. 330:1 27- 1 25 2: p i:: r., L E (i8t< Cellule: effects of esbestes er.d other fibers- ccrreieticns wit ::. v:vc induction ef piecre! secroae Envirsr heeith rerspec: 3 4 9 1 -1 C 2 B-8 D 004319 ?3. Lirmgston, G. K.. Rom, V. K. and Morris MV (1780) Asbest os-indueed saister chromatid exchanges in cultured Chinese hamster ovarian fibroblast cells. J Environ Pathol Toxicol. 4(2-31:373-382. 94. Lopex-Areal Del Amo L -(1980) Diseases associated with asbestos in Spain. IARC Sci Pub 1. 1(301:201-2 08. 95. Maltoni, C., Minardi, f. and Korisi, L. (17821 The relevance of the experimental approach in the assessment of the oneogenie risks from fibrous and nonfibrous particles. The ongoing project of the Bologna Institute of Oncology. Med Lav. 73(43:374-407. 98. Mancuso, T. F. (17831 Mesothelioma among machinists in railroad and other industries. Am J Ind Med. 4(41:501-513. 77. Masse, R. et al (17801 Experimental demonstration of the penetration of asbestos fibers into the gastrointest ina1 tract. IARC Sci Publ. 1 (301 : 321-328. 98. McConell, E. E. et al (1983) Chronic effects of dietary exposure to amosite and chrysotile asbestos in Syrian golden hamsters. Environ Health Perspect. 53:11-25. 97. McConell, E. E. et al (1983) Chronic effects of dietary exposure to amosite asbestos and tremolite in F344 rats. Environ Health Perspect. 53:27-44. 100. MeCullagh, S. F. (1980) Amosite as a cause of lung eaneer and mesothelioma in humans. J Soc Occup Med. 30(41:153-158. 101. McDonald, A. D. et al (1984) Dust exposure and mortality in an American ehrysotile asbestos friction products plant. Br J Ind Med. 41(21:151-157. 102. McDonald, A. D. et al (1983) Dust exposure and mortality in an American factory using chrysotile, amosite, and crocidolite in mainly textile manufacture. Br J Ind Med. 46 ( 4 ) : 3 6 8-37 4 . 103. McDonald, A.. D. et al (1983) Dust exposure and mortality in an American chrysotile textile plant. Br J Ind Med. 40(41:381-387. 104 McDonald, J. C. ( 1980 ) Asbestos-re1 ated disease: an epidemiological review. IARC Sc: Publ. 2 ( 30 ) :587-8 0t. 105. McDonald, J. C. et al (1980) Dust exposure and mortality in chrysotile mining, 17101975. Br J Ind Med. 37(1):ll-24. 108. McDonald, J. C. and Liddell, ?. D. (1777) Mortality in Canadian miners exposed to ehrysotile. Ann KT Acad Sci. 230:1-9. 107 McDonald, J. C. and MaDonald, A. D. (1711) Mesothelioma as ar. index of asbesto impact. Banbury Report. 7:73-88. ICE Menehaux, C. et al (1981) mescthelioma in rats following inoculation with acidleached chrysotile asbestos and other mineral fibers. Carcinogenesis. 2 ( 3 ) : 22 9-2 34 1C4 Me: ear., A. (1980 Effect clength on the clearance of fibers from the lung and or. body formation IARC Sci Pub I . 1 (30 ): 329-335 . 11C Mrssmar.. E , light V. and e: Z ( 1 9 83 ) Asbestos- mechanisms of toxicity tnc carcinogenic:tv :r. the resxiratcry tract Annu Rev Pharmacol Toxicol. 22:595-813 B-9 D 004320 111. Hossman, B. T. and Craighead, J. E. <1781) Mechanisms of asbestos carcinogenes Is. Environ Res. 23 (2) :247-280 . 112. National Research Council (1784) Non-oceupationa1 exposure to asbestiform fibers. NAS Repor t. - 113. Newhouse, M. L. (1783) Asbestos-related diseases. Practitioner. 227< 1 383 ): 1398-1411. 114. Newhouse, M. L. <17 81> Epidemiology ot asbestos-related tumors. Semin Oncol. 5<3):230 257 . 115. Newhouse, K. I. end Berry, C. (1779) Patterns of mortality in asbestos factory workers in London. Ann NY Acad Sei. 330:53-80. in. Newhouse, M. 1., Berry, C. and Skidmore, J. V. ( 1782) A mortality study of workers manufacturing friction materials with ehrysotile asbestos. Ann Occup Hyg. 26(1-41:877 90? . 117. Nicholson, V. J. et al (1781) Cancer from occupational asbestos exposure projections 1780-2000. Banbury Report. 9:87-111. ns. Nicholson, V. J. (1784) Asbestos Health Assessment Update. EPA Report (Revie draft). EPA-600/8-84-003A:13l . 117. Nicholson, V. <J. et al (1777) Long-term mortality experience of ehrysotile miners and millers in Thetford Mines, Quebec. Ann NY Acad Sci. 330:11-21. 120. Nicholson, V. J., Perkel , C. and Selioff, I. J. ( 1 782 ) Occupational exposure to asbestos: population at risk and projected mortality --1780-2030 . Am J Ind Med. 3(3):259-311. 121 . Norseth, T. (1780) Asbestos and metals as carcinogens. J Toxicol Environ Health. 6(54):1021-1028. 13 2. Orconer, N. C. and Smith, J. L. Jr (1783) Feritoneal malignant mesothelioma with multiple distant skin metastases. Arch Dermatol. 1 17( 1 0 ):827-830. 123 . Peto, J. (1780) The incidence of pleural mesothelioma in ehrysotile asbestos textile workers. IARC Sci Publ. 2(30):703-7l1. 124. Peto, J. (1777) Dose-response relationships for asbestos-related disease: implications for hygiene standards. Part II. Mortality. Ann NY Acad Sci. 330:175-203. 123 reto, J. (1780) Lung eaneer mortality in relation tc measured dust levels in an asbestos textile factory. IARC Sci Publ. 2(30):827-836. 12 . Pete, J., Henderson, B. E. and Pike, M. C. (1781) Trends in mesothelioma incidence in the USA .and the foreast epidemic due to asbestos exposure during World War 11. Banbury Report 7:51-72. 127 Pete. J., Seidman, K. and Selikoff, I. J. (1782) Mesothelioma mortality in asbestos workers; implications fe: models of carcinogenesis and risk assessment. B; J Cancer. <:(::.i24-13s. Fett. F (! 7 6 2 '< An:nal experiments on biological effects of mineral fibers. IARC Sc: Pcbl 1(301.261-272 ?: :ce-Jcr.es r: o : : c c 1 : : t et M .* Cuttings. C i s; t; : : ::c;i: :sct. : l : ?.* and Chamberlain. K of chromosome a'onerma b-10 !8C'< The :: its and genet i effects of sister r.r omi 11 c D 004321 130. ^ N. * t al C1 ? 8 2 ) Pleural meso the 1 iota in the Rhesus monkey Macaca-mulatta induced by intri tracheil injections of ehryisotile asbestos. Eksp Onkol. 4(45:34-3*. 131 . Pyletr, L. N. <1?80) Pretumorous lesions and lung and pleural tumors Induced by asbestos in rats, Syrian golden hamsters and Maeaea mulatto (rhesus) monkeys. IARC Sci Pub 1 . 1 ( 30 ): 343-3SS . 132 . Rahman, Q., Das, B. and Viswanathan, P. N. (1983) Biochemical mechanisms in asbestos toxicology. Environ Health Perspect. 51:299-303. 133. Reiss, B. et al (1983) Absence of mutagenic activity of three forms of asbestos in liver epithelial cells. Environ Res. 31(1): 100-104. 13 4. Robock, K. ( 1 979) Based on available data, can we project an acceptable standard for industrial use of asbestos? Absolutely. Ann HY Acad Sci. 330:205-210. 135 . Rogol, P. R., Ryu, <7. H. and Ginns, t. C. (1183) Reduced natural killer cell activity in asbestos workers. Am Rev Respir Dis. 127(4 part 2) :73. 134 . Rom, V. N. et al (1983) Sister chromatid exchange frequency in asbestos workers. J Natl Caner Inst. 70(l):45-48. 137 . Rubino, C. F. et al <1979) Mortality of chrysotile asbestos workers at the Balangero Mine, Northern Italy. Br J Ind Med. 36(3):187-1S4. 138 . Seansetti, C. et al <19813 Pleual mesotheliona after a short interval from first exposure in the wine filter industry. Am J Ir.d Med. 5 (0:335-339. 13? . Schenker, M. 3., Carshick, E. and Speiser, F. S. (1984) A ease control study of incident mesothelioma deaths among railroad workers. An Rev Respir Dis. 129(4 supp1):Al4 4. 140 . Seidman, K., Selikoff, I. J. and Hammond, Z. C. (1979) Short-term asbestos work exposure and l^ng-term observation. Ann KY Arad Sci. 330:41-90. 141 . Seidman, H., Selikoff, I. J. and Hammond, Z. C. (1912) Mortality of brain tumors among asbestos insulation workers in the United States and Canada. Ann NY Acad Sci. 38 1 :1 4 0 -17 1 . 142 . Selikoff, I. J., Churg, J. and Hammond, l. C. (1984) Classics in oncology: Asbestos exposure and neoplasia. CA. 34(l>:4&-54 143 . Selikoff, I. J., Hammond, E. C. and Seidman, K. (1980) latency of asbestos disease among insulation workers in the United States and Canada. Cancer. 44(12):2734-274C. 144 . Selikoff, 1. J., Hammond, E. C. and Sei-dnan, H. ( 1 979 ) Mortality experience of insulation workers in the United States and Canada, 1943-1974. Ann NY Acad Sei. 330:91-114. 1 4 S . Selikoff, ! . J. , Lilis, R. and Nicholson, V. J. ( 1 979 5 Asbestos disease in United States shipyards. Ann NY Acad Sci. 33C.295-311 . 144 Seiikcff. I. J., Seidman. K. and Hammond, S. C. (1980) Mortality effects of cigarette smoking among amosite asbestos factory werktrs. UNCI. 45 ( 3 5:507-5 . 14" Seiicff 1 U (1981) Constraints ir. estimating occupational contribulions te currer.: cancer mertaiitv ir. the USA Sanbury Reucrt *:3-l8 B-ll D 004322 148. Stanton, M. F. t *1 (1781) Relation of partial* dimension to carcinogenicity in amphibole asbestoses and other fibrous minerals. JHC1. 47(5):?45-?75. 147. Stevens, J. B. *t suppI):Al68. (1784) Asbestos metabolism in-vivo. Am Rev Respir Dis. 127(4 ISO. Stunphius, J. (177?) Mesothelioma incidence in a Dutch shipyard. Ann MY Acad Sei. 330:3 1 7-322 . 151. Ssyba, K. and Lange, A. (1782) Effects of asbestos on b*nso(a)pyren* mutagenicity. Mutat Res. 77 (3): 227-228 . 152. Taylor, R. A. and Johnson, t. F. (1781) Mesothelioma: current perspectires. Vest J Med. 134(3):37f-383. 153. Teta, M. J. et al (1782) Occupational asbestos exposure and mesothelioma in Connecticut USA. "Occupational lung disease" edited by Gee, JB et.al.. Raven Press, Hew York:24?pp. 15 4. Teta, M. J. et al (1783) Mesothelioma in Connecticut, 1755-1777. Occupational and geographic associations. J Occup Med. 25( 1 0 ):747-756 . 155. Thomas, K. F. et al (1982) Farther follow-up study of workers from an asbestos cement factory. Br J Ind Med. 37 ( 3 ) : 273-236. 156.' Topping, D. C. and Hettesheim, P. (I960) Two-stage carcinogenesis studies with asbestos in Fischer 344 rats. JNCI. 65<3):627-630. 157 . Topping, D. C., Nettesheim, ?. and Martin, C. K. (1780) Toxie and tumorigenic effects of asbestos on tracheal mucosa. J Environ Pathol Toxicol. 3(5-6):261-275. 158 . Valerio, F. et al (1783) Chromosomal aberrations induced by ehrysotile and croeidolite in human lymphocytes in vitro. Mutat Res. 122(3-4):377-402. IS? . Vicent, J. H. et al (1781) Static electrificition ef airborne asbestos: a study of its causes, assessment and effects on deposition in the lungs of rats. Am lnd Hyg Assoc J. 4 2 ( 1 0 ) : 7 1 1-72 1 . 1(0. Vagner. J. C. (177?) Diseases associted with exposure to asbestos dusts. Practitioner. 223 ( 1333):21-33 . U 1 . Vacner, J. C. (1782) Experimental studies and the pathology of asbestos induced lung diseases. Arch Immunol Thar Exp. 30(3-4):221-228. 162 . Vagner. J. C., Berry. C. and Pooley, F. D. (1762) Mesotheliomas and asbestos type in asbestos textile workers: a study of lung contents. Br Med J. 285 ( 6341 ): 603-606. 163 Vagner, J. C., Berry, C. and Pooley, F. D. (1780) Carcinogenesis and mineral fibers. Br Med Bull 36 ( 1 ) : 53-56 . 16 4. Vagner- J C., Berry, C , Skidmore, J V. and Pooley, F. D. (1780) The comparative effects of three chrysctiles by injection and inhalation ir. rats. 1ARC Sci Publ . 1'3C< 365-372 165 Vagner. J C , Griffiths D K and Kill. ?. J. (1*84) The effect of fibrt site or. the : r. :* activity e f U1 CC cr oci oe i: t e :: ; Cancer <(4):<53-456 ; c c Vagner M K 1?s* imsur.eiegy ar.d asoesics B-12 I Ar.C Sc: Put: 1 ( 3 c:. 2 <" - 25 l D 004323 147. Vagner, K. M. and < 1 9 8 3 ) HLA-A and B antigen frequencies and mesothelioma ia relation to asbestos exposure. Br J Cancer. 48(S):727-730. 188. Valker, A. H. et al (1783) Projections of asbestos related disease 1780-2007. J Oceup Med. 25(5 ) :407-425 . - 149. Virnock, M. L., Kowahara, T. J. and Volery, C. (1783) The relation of asbestos burden to asbestosis and lung cancer. Pathol Annu. 18Cpt 2) : 107 -- 145. 170. Vhitaker, D., Shilkin, K. B. and Valters KKI (1784) Cytologic and tissue culture characteristics of asbestos induced aesothelioaa in rats. Acta Cytol. 21(2):185-117. 171. Vinkler, G. C. and Ruettner, J. R. (1782) Penetration of asbestos fibers in the visceral peritoneum of alee a scanning electron aicroscopic study. Exp Cell Biol. 50 ( 4): 187-174 . 172. Voitowitx, K. J. et al (1782) Asbestos related diseases in Vest Germany. Arch Immunol Ther Exp. 30(3-4):143-144. 173. Voitowits, K. J. et al (1781) Asbestos-related diseases in the Federal Republic of Ceraany. Am J Industr Med. 2(1):71-7I. B- 13 D 004324 UNITED STATES ENVIRONMENTAL PROTECTION AGENCY WASHINGTON. O.C. 20460 MAR 4066 OFFICE OF RESEARCH AND DEVELOPMENT Mr. William V. Loscutoff, Chief Toxic Pollutants 3ranch Re: Asbestos California Air Resources 3oard P. 0. Box 2815 Sacramento, CA 95812 Dear Mr. Loscutoff: A copy of your request for information regarding asbestos, dated December 7, 1984, has been forwarded to my office. The Office of Health and Environmental Assessment has published a document entitled, .Asbestos Health Assessment Update. The document is a First External Review Draft, dated February 1984, and we plan to revise it later this year. Unfortunately, we have run out of copies, but the document is available from: National Technical Information Service 5285 Port Royal Road Springfield, VA 22161 The order number is PB-84-186832. I hope the information will be useful to you. If you have questions, please feel free to call me at 202/382-7345. Sincerely yours M_.____ Technical Information Staff Office of Health and Environmental Assessment B-14 D 004325 u Ford Motor Company The American Road Dearborn, Michigan 43121 February 18, 1985 . Mr. William V. Loscutoff, Chief' Toxic Pollutants Branch Re: Cadmium and Asbestos California Air Resources Board P.0. Box 2815 Sacramento, CA 95812 Subject: Response to Mr. P. D. Venturis's Requests for Information Regarding Cadmium and Asbestos Dear Mr. Loscutoff: The Ford Motor Company has not undertaken independent scientific studies to evaluate the health effects relating to either cadmium or asbestos. Rather, the Company quantitatively measures the ambient concentrations within the plant environments of regulated and suspected toxic air contaminants. These concentrations are evaluated with respect to the current Occupational Safety and Health Administration permissible exposure limits, National Institute of Occupational Safety and Health recommended standards, and American Conference of Governmental Industrial Hygienists Threshold Limit Values. We regret that we are unable to submit information pursuant to your inquiries concerning health effects but we would like to continue to receive information on your progress in regulating toxic air contaminants. 10:DKJ7/L F. P. Partee Principal Staff Engineer Air/Noise Compliance Stationary Source Environmental Control Office B-15 D 004326 DEPARTMENT OF THE ARMY U. S. ARMY ENVIRONMENTAL HYGIENE AGENCY A8EROEEN PROVING GROUND. MARYLANO 210108422 ATimTErNTtIoON 0# JAN 3 0 1985 Occupational and Environmental Medicine Division William V. Loscutoff Chief, Toxic Pollutants Branch California Air Resources Board P.0. Box 2815 Sacramento, California 95812 Dear Mr. Loscutoff: This Agency does not have data on asbestos per your request. However, we are aware of a document on the health effects of asbestos which you may want to review. The title is: Asbestos - An Update of Epidemiology and Pathology since 1976. This document was published by the USAF Occupational and Environmental Health Laboratory, Aerospace Medical Division, Brooks Air Force Base, Texas in February 1984. A copy can be obtained by requesting report number 84-125C011 BOB from either the National Technical Information Service or the Defense Technical Information Center. Any questions concerning this reply should be directed to Major Robert W. Petzold, M.D. at telephone number 301-671-2464. Sincerely Colonel, Medical Corps Director, Occupational and Environmental Health B-16 D 004327 m A' ASBESTOS INFORMATION ASSOCIATION 1745 Jeffersen Davis Hignway. Crystal Square 4, Suite 509 Arlington Virginia 22202 (703) 979-1150 January 17, 1985 William V. Loscutoff, Chief Toxic Pollutants Branch Re: Asbestos California Air Resources Board P.0. Box 2815 Sacramento, CA 95812 \ Dear Mr. Loscutoff: I am writing in response to the Air Resources Board's request for information regarding asbestos. I have had the opportunity to review the ARB's bibliography and to discuss the program with Mr. John Batchelder. The greatest omission in the ARB's bibliography appears to be in not listing a number of large, overview studies of asbestos which are valuable for their scope and for the many individual references assembled in them. I would, therefore, recommend that the ARB collect and consider the following studies: Acheson, E.D., Gardner, M.J. (1983) Asbestos. The Con trol Limit for Asbestos. Her Majesty's Stationery Office, London. British Advisory Committee. (1979) Asbestos. (The Simpson Report). Her Majesty's Stationery Office, London. CPSC. (1983) Chronic Hazard Advisory Panel on Asbestos. U.S. Consumer Product Safety Commission, Directorate for Health Sciences. Report of the Royal Commission on Matters of Health and Safety Arising from the Use of Asbestos in Ontario. (1984). On the issue of ingestion of asbestos, there is a recent animal bioassay from the National Tqxicology Program: NTP. (1983) Lifetime carcinogenesis studies of amosite asbestos in Syrian golden hamsters. NIH publication number 84-2505. B-17 D 004328 Page 2 I am also enclosing a copy of the EPA's response from the December 19, 1984 Federal Register regarding the use of asbestos in brakes. Mr. Batchelder noted that this is one area which may be a concern of the ARB. Finally, I am enclosing a copy of a paper by Wagner and Elmes en titled "The Mineral Fibre Problem." As the use of asbestos de clines, the use of other fibrous materials increases. The Wagner and Elmes paper cautions, on the basis of animal and human evidence, against the indiscriminant and uncontrolled use of these fibrous materials. The purpose of sending this paper is to make the point to the ARB that these fibrous materials constitute an area of in vestigation which has received scant attention, as oppossed to asbestos, which has been very thoroughly studied and regulated. Yet another survey study of asbestos, as is presently contemplated by the-ARB, has a certain aura of "reinventing the wheel" about it, whereas, with the exception of the Danish government, there has not been a regulatory body which has addressed the issue of fibers generally. I would appreciate being kept informed of the progress of this project of the ARB, and if there is a mailing list established, please include ray name on it. If I may be of any assistance, please feel free to contact me. Very truly yours, Nicholes J. '"Jfiuchyj , E^c^ Government Affairs Councvt- B-18 D 004329 Federal Register / Vol. 49. No. 245 / Wednesday, December 49. 1964 / Proposed Rul 493H 40 CFRPart 7*2 cummanoa a civil action In a district l0FTV2t1014. T5M-TRI TI%r| court of the United States to compel ETA to tnlltstr s rulsmsklng proceeding Asbastoa; Response to Citizen*' es requested In the petition Any such Petition civil ectlon must be filed within 80 dev* AotHcr. Environmental Protection Agency (EPA). Acnorc Response to Citizens' Petition. fttr EPA'i denial of !h* petition or. If EPA falls to grant or deny the petition within 90 day* aftsr ths petition Is filed within 80 days following tspirsUon of tonMAAr: Th* Environmental Protection the 90-day ratponit period n. th*Agency (ETA) li granting petition flltd under taction 21 o( th* Toxic Evaluation of Petition Substances Control Act (TSCA) by th* A. introduetia* ' * Natural Resources Deftni* Council Ino. to prohibit th* us* of aibaitol in automobile *nd truck br*k*(. EPA h** commenced an *pprapri4l* pracatdlnt to address th* riik* which may b poi*d by thli uic of asbestos................ OATt Submit writlsn comment* on or before March 18.1985. 1 soonest: Submit written comment* la triplicate Identified by the document control number (OPTS-21J015) to: TSCA Public Information Office (TS-793). Office of Toxic Substance*. Environmental Protection Agency. Rm. -107.401 M. SL SW. WaibingtoD. DC 20460. A copy of the petition and related information (with any confidential business information deleted] la located ire Room -107, Environmental ' Protection Agency, 401 M Sl_ SW; . Washington. DC 20160. This matenal is available for view mg and copying From 8 a.m. to 4 pro. Monday through Friday, excluding legal holiday*. FOR FURTHER IMF0RI4AT10N CONTACT: Edward A. Klein. Director. TSCA - - Assistance Office (TS-799). Office of Toxic Substances. Environmental Protection Agency. Rm. -542. 401 M SU SW. Washington. D.C 2048a ToO-frem (800-424-0085). .. On September 12.*1964, EPA racalved a petition Erom th* Natural Resources Defense Council Inc. (NRDC). - . requesting that EPA prohibit ths further uie of asbestos th automobile tnd truck brakes under section 6 of TSCA. Tb* petition requested s prohibition of asbestos In both brakes for new can and trucks and In replacement brakes for existing vehicles. The petition argued that the risks posed by asbestos in brakes are unreasonable and that economically and technically feasible substitutes are available. * tn order to promulgate any rules under TSCA lection 8. the Agency must consider a number of factor*. Including, ar'w.g other things, th* effects of i chemical substance on human health and the magnitude of exposure: the benefits of utilizing the substance: and the availability of substitute* for th* us* or uses of the substsnee being assessed IS U.S.C 2605(c)(1). The Agency has conducted a review of the available information pertaining to tha us* of ' asbestoe th brakes, including the Information tn NRDCi patidoh. A ' summary of that review, including an evaioation of tha risks posed by this use and the svailabilily of substitutes, la presented below. In Washington. D.C.-(554-1404). - B. Hoi Pnseattd by Atbaio* Outside th* USA: (Operator--282-5541404). ' tuaaiEuexTARV inforhatmhc Asbestoa is a demonstrated human carcinogen that causes lung cancer and mesothelioma (a cancer of the chest and L Introduction abdominal linings), as wall as othsr lung Section 21 of the Toxic Substances disorder*. People are exposed to Control Act (TSCA), 15 U.S.C. 2620,. asbestos throughout the life cycle of th* provides that any person may petitioo substance--when asbestos la mined the Administrator of EPA to initiate a . milled processed fabricated into . proceeding for the issuance, Industrial and consumer products, and amendment or repeal of a rule under when IboK products art used repaired various sections o( the Act EPA may and disposed of, ` hold a public heanng or may conduct an With regard to the use of-asbestoa in appropriate investigation todatermint brakes, it has been estimated that about whether the petition should be granted. 2.750 people are potentially exposed EPA must either graat or deny the. during primary manufacturing of brake petition within 90 days, if EPA grants fnction material*, and that sbovt.550000 the petition. EPA shall promptly people are potentially exposed to commence an appropnata proceeding If asbestos during servicing and repair of EPA dentes the petition, the masons for vehicle brake* (Rtf. 81 lj>r example, . . denial must be published is .the Federal persona In brake service end repair Register, and the petitioner may shops typically are exposed to asbestoa B-19 wlit* dust V* blew* owi ot brake drum* being replaced, when bn hr hobs* are rougnened to Inovaae hkbusi prupertte* and whrn braha ahrvx arv rellfwd Us* of t*br*tu* tn eohsck brain my lio result In tncraaasd ttbesto* Sbcr cancenlrttlon* In tha ambtror air. Pw example. EPA baa rv-dwc* that rotor vehicle braking moat Ukaly eeaUribarr* between 0 23 to U percent of the concentration of aioeito* in the ambient Ir (Ref. 7). Both general prynUtkvo tod workplace exposure! to aabeatoa fiber* from It* oat In brake* may reault tn tn Increaaed number of atbeftot-rrlated Hlneatta. Including carterr. - C. Availability af SubtUtatoM Th* petitioner a atari* that economically tnd technically lettibl* aubahtute*. moat prominently acmimetallle friersoo materials tod iramid fiber*, are available to replace aabcato* to brake*. EPA has analysed the availability of aabttihrte* for many asbestos products, kvdudiag brakev and that analysis Is summarized ki Appendix A of the "Regulatory Impact Analytlt of Controls on Asbestos Product*" (Ref. 21 which la included us the public record esta biiabed ice NRDCt section 21 petition. EPA acknowledges that new substitute* for asbestos ui* lrr brakes are being developed and that EPA'i asalysis (summarized below) may oot tocludl recent developments. 1. Htavy vehicle broke block*. Brak* blocks are components of brake* that are riveted or bolted to tb* (raids* of broke shoe* to provide protection against tb* beat and wear caased by braking. Heavy vehicle brake block* at* used on heavy duty trucks, buses, and other heavy duty vehicles.Aboat 24 percent of aD aabestos used in brakes is in this category of as*. Asbestoa heavy vehicle brake blocks tccount for about 99 percent of tha market for heavy vehicle hrake block*. - Until recently, the only commercially available substitute Tor asbestos heavy vehicle broke blocks waa semimetaOic brake block using brass and zinc chips to tn orginic binder. V (s not considered as good as asbestos because It performs rrattcaDy at different temperatures, ft la also considered inferior to the asbestos brake block in resisting westr tnd minimizing brake fade. Recently, aramid fiber peodocta. sikA as Kevlar, bsva been introduced, but aramid fiber prodoct* art now more expensive Aan aabeatoa product*, and there fa oot sufficient avtdeoc* to determine . whether aramid fiber products will be as effecSv* as asbestoa in this application. Information suggests (hit soch products may )aal longer than asbestos-based -- o\j<r- D 004330 product*. bet verification l (Ms dtsra hrakrs In the original equipment Information * wl as iafennMtai *o market ere ashrktu* end 30 percent ire price and rfTicacy of the products are simUm'lsIHc In Ihr rrplarrmrnt brakr* needed hrfore EPA can drteraWns llrt merit! apprevfnretrly 71> Poncrnt whrther continued use of asbestos In of disc limits sit esbesto* tno 3b brake blocks presents an unreasonable penrat ere semlaetelUc risk. Semlaietalllc disc brake* coal - 1 Util end amdiva vehicle +*m - spprualmateti 1 time* ss much a* the broke iMeg*. Drum brake lining* are asbestos disc bnko pads, hot they bat asada of Mate aSsrlsb arhfch cover about 40 poroaaC longas than tko oartred Mai toe** to a drem toaka. asbcitoi pad*. SeadmotalUc dloa hraka About 4* parani of aB aabaaaaa met bs pad* cannot substitute Ur aabeato* dm brakes is as fids category of to*. Light Irak* pad* to every appttcsOs* haciaaa vehicle aabastaa hero heat* Bofags may of tofartoe performance characteristics be used be both dse boat sod M . ETA has Information Indicating that brakes af tghl sod medium vehide* . semimttelllc disc brake* should bo used primarily mm tba bast wheels. lhiwsias. only to care arlth power brake systems aioat passenger vehicles atIS aaa deni because olherwtae Ike semlmelaUlc brake linings on the raaT vriweta. At brakes may not provide enough slapping least 90 percent of drua hraka Mctug* . power. EPA also has Information last _ art still asbestos. _ . Until recently lbs only substitutes Coe the aunlmetalllc brakes are slightly Inferior because (he user has to push asbestos brake Gnlnn which appeared to have any potential war* aemiaetalBs herder on them before they ere warmed up to get the same performance at with brake Unlnga. However, these products tend to perform trratlcaOy at dillerea*. . temperatures, fade, and produce mors * noise than asbestos-based finings. Mott recently, brake Dnfngs made with steroid fiber have been developed. However, these are room expeoaiva than tha asbesfot product and there la asbestos brakes. ,,. , EPA Is iwirt that a good deal of prodact research b being dona ta develop effective iwbstihites tar - asbestos In brake*. EPA Is sacking sdditioaa) Information on sabs6tte* for asbestos to brake*. not currently enough Information DL Conclusion -- availabla to (udge tha performance of armmid fiber brake linings, furthermore. EPA's evidence Indicates that Urge volume piorfucflon of aremid fiber brakes may require substantial retooling by brake manufacturers. Therefore, erarold fiber brakes may not bo available to substantial qaantitfles Ur ' several yeot*. EPA has dedtUd to grant NRDCs petition beccaae tha Agency befirvet that the us* of asbestos to brake* doc* present risks to human health. EPA Is. initiating a proceeding Vo galbro information on tha desirability and feasibility of reducing risk* associated with the ui* of aabeato* to brake*. EPA X lltovj rWucJlr <fiac broke pooh. - will analyse the exposure bom uaaa of Disc brake pade are sSeoi ptosaa had with bitotao meterish whte nih against a rotor. Heavy vahidaa rerely asv disc brakes. About 0.1 percent mlel sobcsSoa . aabeato*. tha riak presented by thoer uses, end (be sobtlttotes Ur such cacti EPA wtti also gather informetion af the pries, efficacy, and avollabOty of seed In beaks* la to tela cstogmy af aaa. substitute Ur asboitos to brake*. Altar Seitoroelallte disc beak* pad* sea analytes af this toformeOoa. EPA *41 about 20 percent more expensive dte delerciin* what furthae ocSiaa Is ' tha aibeato* dioc breka podstel they appropriate to address the risk* which Uat about 30 percent longer. lbs aemlmetalllcs disc beaks pads are not may b* poaad by ltd* o*a of asbestos. Based an toformotte reviewed w considered to bo good genera? dele. EPA la sot prepared to meka an replacements for asbestos disc brake unreasonable risk finding for an pads for haovy vehicle* becanaa semimetafiles perform batter than Immediate baa of alt use* of asbestos to brakes al this Km*. Effective substitutes asbestos only (n bostfle. hlgb-fifctfon. may rest be arcGable for canals blgh-beat environment*. application* of asbestos to brake* and 4. Light and medium re/ride dlec substitutes for *tb*r application* are ant brake pode. These are the same as disc available to sufficient quantity because brake pads Ur heavy vtWdev. except of limited production capacity. Retooling- they are areaDcr. Aboot 20 percent of all may be required to maka substitute* asbestos need to brake* Is to thJa avatiabla to large voiaroea. categoty of aae. to the <fl*c brake ' The Agency Invites the public To market, scmfmetallfc brakes bat* submit comments oo Issaet relating to altaady made Urger hroads. and as b tha petition. EPA Is portfcolarty tb* dram brake linings market aramfd- Interested Inreceiving Information am beaed brakes are foal beginning to bo ~~ both the current availability of Introduced. Approximately SO percent of substitutes for ssbestos tit brakes and B-20 on new substitute products that are currently being developed The Agency has sn ongoing workgroup, which te(0 review these comments, will contine* to investigate the ivsilsblhtir of effect!%h asbestos-ire* substitute* tor tsssjn \ vshicl* brakes, sad coaster s t spproprUts optloos to address the risk presented by ssbestos to breka*. It jt || Ij ;; |i IV. Record H EPA bes ttUbUahad a record toe < Information relsttof to tb* NROC petition. The record includes ']j Information considered by EPA ta j developing Us response and consists of | the following categories af Information: (1)ThtNRDC petition. (2) Appendix A of the "Regulatory Impact Analysis of Controls on Asbestos Products.' (3) Other Information on substitutes ' | for ssbestos to brakes.' (4) Information ncalvtd from tha public concerning the petition. ; (3) Memoranda somrairixlng meetings ! and telephone conversations with the j public concerning tha petition. j (8) Appendix) of the "Regulatory ; Impact Analysts sfControls on Aibeatot Product*.* (7) Appendix N id the "Regulatory Impact Analysis of Controls oo Aabeato* Products.* A public version of the record, without any confidential business information, (g available to the public to tire Office of Toxic Substance* Public Information Office, boo ( ajb. to 4 p.m, Monday through Friday, except legal holiday*. The Public Information Office 1* located to Ra. -107. IDIMSU $W. Washington. D.C Dated: Decambw IS. 1M. WAdtnekiirnaitDtn.ttourc.kekkeea. int Doc. SS-33130 Filed 13-I7-S4:1:3* pm| ams coos lie ss o D 004331 FROM: RECENT ADVANCES IN OCCUPATIONAL HEALTH, Ed.: MCDONALD, J.C. Churchill Livingstone, Edinburgh, 1981; Pages 1-13. 1. The mineral fibre problem J. C. Wagner P. C. Elmes IOEH 5723 Code 43 44 45 46 48 52 53 90 82 For many years interest in the biological effect of mineral fibres was mainly confined to the commercial types of asbestos. Recently many other fibrous minerals have been recognised as potentially dangerous pollutants of the environment. The majority of these materials are naturally occurring, others are synthetic. The natural fibres are either specifically exploited for commercial purposes or else occur as atmospheric contaminants which are released during mining or tunnelling operations. Industry has been developing other mineral fibres as a substitute for asbestos to meet an increasing need for cheap and reliable materials for reinforcement, friction products and insulation. The latter demand has been emphasised by the present fossil fuel crisis. Minerals being exploited for a variety of purposes other than insulation and reinforcement are known to consist of fibres or elongated crystals, for example, some clays and some zeolites. Thus, these minerals can be considered under the following groups: 1. Asbestos minerals a. Of commercial value b. As potential environmental contaminants 2. Synthetic mineral fibres 3. Other naturally occurring fibrous minerals ASBESTOS t Asbestos of commercial value Practically all the knowledge that is available about hazards associated with the inhalation of fibrous mineral dusts has been obtained in studies of asbestos. Asbestos consists of six naturally occurring minerals: chrysotile, croddolite, amosite, anthoph- yllite, tremolite and actinolite. Chrysotile is a member of a group of minerals referred to as the serpentines and is composed almost exclusively of magnesium in combina tion with silica. It has a sheet structure which curls to produce hollow tube-like fibres. The other five are members of one mineralogical group referred to as the amphiboles. They are very similar in crystal structure, being chain silicates, but they vary in chemical composition. Croddolite and amosite are iron-rich varieties, anthophyilite is a magnesium rich mineral, while tremolite and actinolite contain a large amount of caltium together with wupwinm. The annual world production of asbestos in 1976 was 5 x 10* kg, of which 97 per cent was chrysotile and the remainder croddolite and amosite. The commercial production of the other three amphiboles has been on a small scale in the past, but they are important as contaminants of other minerals and agricultural soil. Chrysotile is widely distributed, with the largest production from the Ural D 004332 THE MINERAL FIBRE PROBLEM 3 With the development of more sophisticated techniques it is now obvious that a correct estimation of the number of fibres in tissue or environmental samples only be obtained by examination under a transmission electron microscope, otherwise the large number of fibres of less than 0.5 /im in diameter will not be observed. The crucial question of the amount, size and type of fibre found in tissue which can be related to the diseases which will be described later, cannot be stated with confidence at this stage. In macerated specimens of dried lung 10* fibres per gramme can be found without evidence of disease; in cases of asbestosis the count is usually over 10*. With a light microscope seldom less than 250 000 fibres per gramme lung tissue are found in cases of asbestosis. 2. PLEURAL PLAQUES AND DIFFUSE PLEURAL FIBROSIS * The presence of circumscribed areas of fibrous thickening below the mesothelium on the lower portion of the chest wall, over the diaphragm or on the pericardium are characteristic of exposure to fibrous mineral dusts. These plaques may be extensive, are leaf-shaped, often bilateral and have an irregular embossed surface. They consist of woven collagen fibres and as they mature become acellular and avascular. This avascularity leads to necrosis and sometimes to the gradual deposition of calcium in the lesions (Meurman, 1966). It can take 20 years or more for sufficient calcium to be deposited for the plaques to become radio-opaque and visible on chest radiography. Therefore, the plaques are seen much more frequently by the pathologists at necropsy than by the radiologist. In some cases there is generalised pleural fibrosis, leaving the lungs en adrasse completely sheathed in a thick layer of fibrous tissue. Unlike plaques, generalised pleural thickening can restrict the expansion of the lungs and cause breathlessness. 3. ASBESTOSIS Asbestosis is a slowly progressive and persistent interstitial fibrosis of the lung associated with the inhalation of asbestos dust and characterised by asbestos bodies and fibres in large numbers in the tissue. If sufficient dust has been retained, the individual lesions in the alveoli join up until the individual acini become linked in a fibrous mesh, the process starting at the base of the lung and gradually spreading upwards. This process is fairly well established before there is recognition on radiological or by physiological examination, the latter often being obscured by the effects of cigarette smoking. If exposure has been sufficient the disease will progress after the worker has left the industry (Becklake et al, 1979). 4. CANCER OF THE LUNG Carcinoma of the bronchus is a frequent cause of death among workers with radiological evidence of asbestosis (Liddell and McDonald, 1980). The risk of a cigarette smoking worker heavily exposed to asbestos developing lung cancer is 25 to 50 times greater than an age matched non-smoker who has not worked with asbestos (see J. C. McDonald, 1980). Initially the carcinomas reported in the asbestos workers were peripherally situated, with adenocarcinomas being the most common (Bucha nan, 1965). With the increase in cigarette smoking, all types of endobronchial tumours are being seen, but the number of adenocarcinomas is still more frequent than in non-exposed cigarette smokers (Kannerstein and Churg, 1972). B- 22 D qq4333 THE MINERAL FIBRE PROBLEM 5 of fibre; apart from mining areas, pure exposure is rare. South African experience with crocidolite has been repeated on a smaller scale at Wittenoom in Western Australia, where mesotheliomas have occurred, both in those employed in the mines and in the environmentally exposed population (Hobbs et al, 1980). Nothing comparable has been reported for chrysodle, amosite or anthopyllite mining. The gas mask workers investigated by Jones et al (1976) and some of those by McDonald and McDonald (1978) appeared to have had a pure exposure. Pooley's analysis of the lungs of the Nottingham cases also showed significant amounts of chrysodle, but not more than is found in autopsy material generally. The technique developed by Pooley (197S) for the identification of asbestos and other mineral fibres in lung tissue is the most useful method available for identifying individual exposures and the complexity of the situation gives emphasis to the need for the parallel examination of appropriate controls. The comparisons made between the fibres in the lungs of the mesothelioma cases and controls in Britain by Jones et al (1980) when compared with those obtained by A. D. McDonald (1980) in the United States and Canada has shown that chrysodle fibres are found in considerable quandty equally in cases and controls. In Britain, crocidolite and to a lesser extent amosite were associated with mesothelioma, whereas in the USA it was predominantly amosite and less often crocidolite. Selikoff et al (1972) found a considerable excess of mesotheliomas in factory workers exposed to amosite but has not reported on the fibre content of their lungs. The Advisory Committee to the Secretary of State for Employment (Health and Safety Commission, 1979) concluded that in the causation of mesotheliomas, crocidolite was more dangerous than chrysodle but that amosite might be intermediate between the two. Experimental evidence has complicated the situation by showing that many types of mineral fibre can cause mesothelioma. This evidence has come in the main from intrapleural implantation studies which were initiated by Wagner (1962) and conti nued in collaboration with Stanton and Wrench (1972); Pott et al (1972) undertook similar intraperitoneal investigations. This work has indicated that the size of the fibres was more important than their nature. IMPORTANCE OF FIBRE SIZE The significance of the physical characteristics of fibres in explaining the biological effects of asbestos was first emphasised by Timbrell (196S). He demonstrated that diameter was the most important factor in determining whether a fibre would be inhaled. The finer the fibre the more easily would it reach the hing parenchyma. Later, Timbrell et al (1970) showed that this could be applied to the amphiboles and that the ultimate diameter of crocidolite was less than that of amosite. Although the individual fibres of chrysotile have a diameter less than that of crocidolite, they occur in a woven coil formation, the total diameter of which affects its aerodynamic behaviour. Thus chrysotile behaves as a coarse fibre and finds difficulty in reaching the pleural surfaces through the peripheral airways. However, chrysotile fibres in aqueous solution can divide longitudinally into fibrils which under some circum stances are straight and have similar properties to very fine amphiboles. The typical electron microscopic appearance of asbestos fibres is shown in Figure 1.1. Calculations and experiments with casts of the lower respiratory tract showed that fibres up to 3.0 pim in diameter would reach the respiratory bronchioles. The length of fibres most likely to cause fibrosis would appear to be greater than 10 fxm (Timbrell 8-23 D 004334 THE MINERAL FIBRE PROBLEM 7 At this stage we.must assume that all mineral fibres of similar size range are potentially hazardous to man, whether of asbestos or other type. Asbestos minerals as potential environmental contaminants Under this heading the following siruadons will be considered: 1. asbestiform minerals contaminating banded ironstone 2. tremolite as a contaminant of other mineral deposits 3. possible contamination of agricultural soil. Asbestiform minerals contaminating banded ironstone Although it has been known for many years that banded ironstone deposits frequently contain small seams of fibrous silicates, occasionally the fibrous deposits are large, and may then be the source of amphibole asbestos as exploited in South Africa and Australia. Other deposits occur which are of no commercial value, for example, there are the taconite fibres in the Mesabi Range on the shores of Lake Superior. Although it has been shown that iron ore mining in this region is causing both contamination of the atmosphere and the water of the lake, no evidence of a hazard to man has been established. All the fibres are below 5.0 pm in length. In a large South Dakota gold mine the ore-bearing rock was cummingtonite -- grunerite (a close relation of amosite) and some fibres were found in the dust. It was suggested that these fibres were associated with an increased incidence of carcinoma of the lung, but these finding* were not confirmed by the investigations of McDonald et al (197S). Nevertheless, the possibility that hazardous fibres may sometimes be released from iron deposits in the vicinity of amphibole mines remains. Tremolos as a contaminant of other mineral depones The fibre dimensions of tremolite vary even more between deposits than the other amphiboles. A coarse flake-like tremolite occurs as a contaminant of talc in California; this material does not cause tumours when implanted intrapleurally in rats, and there is no published evidence of disease among the miner*. A coarse fibrous tremolite is found as a contaminant of the chiysodle deposits in Quebec Province in Canada. This fibre has been found in the lungs of miners and millers from these mines (Pooley, 1976); whether it plays any part in the etiology of pleural plaques and pulmonary fibrosis is still uncertain. In the talc mine* in the northern part of New York State there is contamination by a finer fibrous tremolite, and a few mesotheliomas and carcinoma* of the lung have been reported among the miners (Kldnfeld et al, 1967). Practically pure tremolite of a coarser type has been used in Eastern Turkey for stuccoing houses. Yazidoglu (1976) found a significant incidence of pleural plaques among the inhabitants. Tremolite with very fine long fibres has been mined in South Korea (see Fig. 1.1); this fibre has been shown to produce a high incidence of mesothelioma* in experimental animals. We have been informed that the mining operadons have now been suspended because of suspected cancer among the workers. Possible contamination of agricultural soil A further source of fibrous mineral exposure only recently appreciated, may prove of consequence. Evidence is still fragmentary, and the only confirmed situation is in Bulgaria, where Burilkov and Michailova (1970; 1972) found pleural plaques in B-24 D 004335 THE MINERAL FIBRE PROBLEM 9 GLASS WOOL ROCK WOOL Fig. 1.2 Electron micrographs a(synthetic vitreous fibres GLASS FIBRE (CODE 100) ii 10 jim particularly on factory floors, and occasionally for agricultural and pharmaceutical purposes. Information is scanty concerning the size and shape which particles of these fibrous minerals assume under a range of potentially relevant natural and artificial conditions; nor is much yet known about their biological activity in various in vitro tests. Animal experiments have been recently initiated in which sepiolite and attapuigite fibres are inhaled or implanted intrapleurally; the results will not be B-25 D 004336 THE MINERAL FIBRE PROBLEM 11 TURKISH FIBRE ERIONITE FROM USA FI*. 1J Electros miaotnphs of dispersed samples of synthetic and naturally occurtis* fibrous eriooite To date, synthetic substitutes for asbestos (the man-made vitreous and ceramic fibres) do not appear to have caused lung fibrosis, lung cancer or mesothelioma in man. However, animal experiments indicate that it would be unwise to create materials which include fibres smaller than 0.5 fan in diameter if the risk of mesothelioma is to be avoided. Experimental work suggests that both synthetic and natural non-asbestos mineral fibres of less than 0.5 fan in diameter and greater than 8 fan in length may be hazardous. Some fibrous days have already been shown to cause mesothelioma experimentally while epidemiological evidence suggests that fibrous erionite may well have been responsible for a very high incidence of mesotheliomas in man. Changes in industry and commerce are leading to human exposure from a variety of natural and synthetic mineral fibres. Further research is urgently needed to avoid replacing the hazard of asbestos with others as serious. REFERENCES Anviali M, Buis Y11979 Malignant mesotheliomas in a small village in the Anatolian region ofTurkey: an epidemiological study. Journal of the National Cancer Institute 63:17-22 Bans YI et al 1971 An outbreak of pleural mesothelioma and chronic fibrosing pleurisy in the village of Karain/Orgtip in Anatolia. Thorax 33: ltl-192 Becklake M R, Liddell F D K, Manfreds J, McDonald J C1979 Radiological changes after withdrawal from asbestos exposure. British Journal of Industrial Medicine 36:23-21 Buchanan VP D 1965 Asbestosis and primary thoracic neoplasms. Annals of the New York Academy of Sciences 132:507-51S Buhlkov T, Michailova L1970 Asbestos content of the soil and endemic pleural asbestosis. Environmental Research 3:443-451 Buhlkov T, Michailova L 1972 Uber den Sepiolitgehalt des Bodens in Gebieten mit Eademischem Pleuraverkalkungen. Internationales Archiv fur Axbeitsmedian 29:95-101 B-26 0 THE MINERAL FIBRE PROBLEM 13 faserformiger Suube und ihre Deurung un Hinblick auf die Tumorcntstenhung hnm Meascfaen. Zenoalblan fur Baktenologie, Pamitenkunde, Infekuonskrankheuen und Hygiene: ente Abeieiluag: Onjuule, Reibe B: Hygiene, Praevc&uvc Medina 162: 467-SOS Pon F, Hutb F, Fnedrichs K H 1972 Tumorcn der Riae nach i.p. lniekdon von gemahknem Chrysoti] und (i) pyren. Zentralblatt fur Baktenolope, Pamiteakunde, Infektionskmkbeiten und Hygiene: ente Abeteilung: Originals, Reibe B: Hygiene, Praevennve Median 1SS: 463-469 Selikoff IJ, Hammond C, Chur) J 1972 Cardnogeaidry of unosite asbestos. Archives of Environmental Health 25: 183-186 Stanton M F, Layard M, Tegeris A, Miller E, May M, Kent E1977 Caronojenicity of fibrous {lass: pleural response in the rat in relation to fiber dimension. Journal of the National Cancer Institute 58: 587-603 Stanton M F, Wrench C 1972 Mechanisms of mesothelioma induction with asbestos and fibrous {lass. Journal of the National Cancer Institute 48:797-821 Stell P M, McGill T 1973 Asbestos and laryngeal carcinoma. Lancet 2: 416-417 Thomson J G, Kaschula ROC, MacDonald R R 1963 Asbestos as a modem urban hazard. South African Medical Journal 37:77-81 Timbrel] V 1965 The inhalation of fibrous dusts. Annals of the New York Academy of Sciences 132: 255-273 Timbrell V, Pooley F D, Wagner J C 1970 Characteristics of respirable asbestos fibres. In: Shapiro H A (ed) Pneumoconiosis: Proceedings of the International Conference Johannesburg 1969. Cape Town Oxford University Press, London, pp 121M25 Timbrell V, Rendail REG 1971/2 Preparation of the U1CC standard reference samples of asbestos. Powder Technology 5:279-287 Timbrell V, Skidmore J W 1968 Significance of fiber length in experimental asbestosis. In: Holstein E (ed) Internationale Kocferenz der biologische Wirfcungen des Asbestes, Dresden. Dtsch. Zentralinst, Arbcitsmed, Berlin, DDR pp 52-56 Wagner J C1962 Experimental production of mesothelial tumours of the pleura by implantation of dusts in laboratory animals. Nature 196:180-181 Wagner J C 1979 Diseases associated with exposure to asbestos dusts. The Practitioner 223:28-33 Wagner J C, Berry G, Pooley F D 1980b Carcinogenesis and mineral fibres. British Medical Bulletin 36: 53-56 Wagner J C, Berry G, Skidmore J W 1976 Studies of the carcinogenic effects of fiber glass of different diameters following intrapleural inoculation in experimental animals. In: Occupational exposure to fibrous glass -- proceedings of a symposium. (DHEW Publication no (NIOSH) 76-151.) U.S. Department of Health, Education and Welfare, Washington DC, pp 193-197 WagnerJC, SleggsC A, MarcbandP 1960 Diffuse pleural mesothelioma and asbestos exposure in the North Western Cape Province. British Journal ofIndustrial Medicine 17:260-271 Wagner J C, Berry G, Skidmore J W, Timbrell V1974 The effects of the inhalation of asbestos in rats. British Journal of Cancer 29: 252-269 Wagner J C, Berry G, Hill R J, Munday D E, Skidmore J W 1980a Animal experiments with man-made mineral fibres. In: Wagner J C (ed) Biological effects of mineral fibres. WHO/1ARC, Lyon, pp 361-362 Webster 1 1973 Asbestos and malignancy. South African Medical Journal 47:16V171 Yizirioglu S 1976 Pleural calcification associated with exposure to chrysodle asbestos in south east Turkey. Chest 70:43-47 Yazidogiu S, Bcayto, R, Bald K, Sayli B S, Yorulmaz B 1980 Pleural calcification, pieural mesotheliomas and bronchial cancers caused by pemolite dust. Thorax 35: 564--569 B-27 D 004338 OCAW Oil, Chemical & Atomic Workers International Union, AFL-CtO f. / Joph Mi>br*nr. Pt tidant -- Miehitl Rictgliino.Scfttirv Ttturt L. Calvin Moof. v>c P'<dnt Robert E. Waget. v<c Pr,,a*nt international Officit 255 Unon 8ivd . Lakewood, CO 80228 303/987 2229 Mail P O 8o* 2812. Denver. CO 80201 December 17, 1984 Peter D. Venturini, Chief Stationary Source Division State of California Air Resources Board P. 0. Box 2815 Sacramento, CA 95812 Dear Mr. Venturini: Reference is made to your recent request for information regarding Asbestos. Please be advised that we have no additional Information or materials that you do not already have. Thank you for your inquiry. Dan C. Edwards, Director Health and Safety Department DCErpl cc: R. Wages, Vice President J. Foley, Dir Dist. # 1 D V L'- B-28 D 004339 DEPARTMENT OF HEALTH AND HUMAN SERVICES Division of Health Services COUNTY OF MARIN HALL OF JUSTICE CIVIC CENTER SAN RAFAEL. CALIFORNIA PHONE 499-6879 3^ December 13, 138 4 received Peter D. Venturini, Chief Stationary Source Division Air Resources Board 1102 Q Street Sacramento, CA 35812 oiohina.-y Sourca Division Air Resources Board Re: Your letter 12/7/84 requesting Information Regarding Asbestos Dear Mr. Venturini: This is not a response to your request, but is a heartfelt plea for clarity and accuracy. In accord with the dictum, "Do no harm," bureaucratic agencies should strive always not to pollute the English language. Asbestos cannot be a "toxic air contaminant," not even if Ronald Reagan and the Congress say it is. Asbestos is not a toxin. It is not even a poison. Here is Borland's Medical Dictionary definition: TOXIN -- A poison; frequently used to refer specifically to a protein or conjugated protein substance produced by higher plants, certain animals, and pathogenic bacteria that is highly toxic for other living organisms. Such substances are differentiated from the simple chemical poisons and the vegetable alkaloids by their high molecular weight and antigenicity. Now that we have moved into the era of industrial toxins, we are merely adding chemists to the list (plants, animals, bacteria) of things that pro duce toxins. We should not be changing the meaning of the root word. Asbestos is virtually inert in all the forms you mentioned. It cannot be a toxin. It is not even a "simple chemical poison." Look at the confusion and tremendous cost engendered by bureaucratic and media repetition of the phrase "deadly toxic PC3s." PCBs are not deadly -- they were handled quite casually by thousands of workers for many years, with no reported deaths, just chloracne. Neither are PCBs toxic, being relatively inert, like asbestos. There is absolutely no reason for any per son to react with fear to the presence of small quantities of PCBs in urban soil. B-29 D 004340 2 All that I say here is not meant in any way to lessen the legitimate concerns this society must have for keeping harmful, potentially carcinogenic (or mutagenic, or teratogenic) substances out of the air we breathe (like micro scopic asbestos fibers) and out of the food we eat (1 ike bioconcentrated PCBs), and out of the water pipes. My plea is only for accuracy and preservation of the language upon which accuracy depends. With accurate thinking it becomes obvious that a PCB-filled transformer atop a pole is no more dangerous than a room filled with polyvinyl furniture where people smoke cigarettes. Ignition of either one will seriously endanger fire fighters or anyone else who might breathe the smoke. And the same is true of encapsulated asbestos. Yet this society spends billions of dollars clean ing up certain PCB - contaminated soils that don't need to be "cleaned up," and removing asbestos materials that don't yet need to be removed. The re moval itself generally causes more danger to workers, the public, and the biosphere than would exist if the material were left alone. It seems to me that both public and private funds should be spent more wisely in working toward a total prohibj tion of continued corporate contamination of the earth, air and water that make up our common heritage. Sincerely. Theodore 0. Hiatt, M.D. Marin County Health Offi'cer TDH:jm CC: William V. Loscutoff, Chief Toxic Pollutants Branch California Air Resources Board Assemblywoman Sally Tanner Senator Ralph Oil Is Alex Kelter Dept, of Health Services David Howekamp EPA Region IX P.S. DHEW Publication Number (NIH) 78-1681 May 1978 "Asbestos: An Informa tion Resource" has a bibliography even more extensive than the one supplied by you. There are few, if any, hazardous substances more extensively documented. B-30 D 004341 STATE Of GAUFOCNIA AIR RESOURCES 1102 Q SHEET 9.0. SOX 2815 SACXAMENTO. CA 95812 BOARD - OEO OtUKMSjIAN. Go January 7, 1985 Theodore D. Hiatt, M.D. Marin County Health Officer Department of Health and Human Services Hall of Justice - Civic Center San Rafael, CA 94903 Dear Dr. Hiatt: Thank you for your letter of December 13, 1984, responding to our request for information regarding asbestos. With respect to the question of whether or not asbestos can be a toxic air contaminant, we are constrained to follow the language of California Health and Safety Code Section 39655, which includes the following: "...toxic air contaminant means an air pollutant which may cause or contribute to an increase in mortality or an increase in serious illness, or which may pose a present or potential hazard to human health." Substances whictThave been identified as hazardous air pollutants pursuant to Section 7412 of Title 42 of the United States Code shall be identified by the state Air Resources Board as toxic air contaminants (asbestos has been so identified pursuant to the cited U.S. Code). In addition, the intent of the legislation establishing our toxic air contaminant program was to protect the public from "...the emission into the ambient air of substances which are determined to be carcinogenic, teratogenic, mutagenic, or otnerwise toxic or injurious to humans." Although the definition for a toxic air contaminant may be inconsistent witn the definition of toxin found in a medical dictionary, I do not believe that the intent, as stated in the statute, is in disagreement with your concerns. The intent of the law is to protect public health. Please be assured that I share your concern with proper usage of the English language in government work. Thank you again for your letter. If you have B-31 D 004342 Theordore D. Hiatt, M.O. -2- January 7, 1985 any further questions concerning our toxic air contaminant program please feel free to contact me at (916) 445-0650 or William Loscutoff, Chief of tt Toxic Pollutants Branch, at (916) 322-6023. Sincerely, Petei.u. venujnni, t/nef--- Stationary Source Division cc: W. Loscutoff Assemblywoman Sally Tanner Senator Ralph Dills Alex Kelter, DHS David Howekamp, EPA B-32 0 004343 Appendix C Emissions Calculations* * sample calculations in this Appendix contains more significant figures than were used In the Part A of the report. All differences between estimates here and In Part A are due to rounding. D 004344 Mining Asbestos Emission Calculations for Mining and Milling, 1984 Process Rate In 1984, 57,308 tons of asbestos Mere produced; 36,000 tons by Calaveras Asbestos and 21,308 tons by KCAC Corp. (formerly Union Carbide Corp.) Mining emissions from Calaveras Asbestos: Process Rate: 36,000 tons asbestos produced Emission factor: 5 lb/ton at 501 control Drilling A Blasting Loading____________ Hauling____________ Uni oadl ng__________ Emission Factor at 501 Control 2 1 1 1 Total 5 lb/ton 36,000 tons (5 lb/ton) Emission --------------------------------------- 90 tons 2,000 lb/ton Mining Emissions from KCAC Corp. Process Rate: 21,308 tons asbestos produced Emission factor: 3 1b/ton at 501 control frcm the following activities only: loading, hauling and unloading D 004345 C-l For 1984, KCAC obtained Its ores from existing stockpiles. Mining Is done every 2 or 3 years by stripping Material fra the asbestos deposit with push scrapers; no drilling or blasting Is required. 21.308 tons (3 1b/ton) Emissions * --------------------------------- 32 tons 2,000 lb/ton Total Mining Emissions * 90 tons + 32 tons * 122 tons 2. Milling Process Rate Asbestos produced in 1984 = 57,308 tons Emission Factor*: 12 lb/ton Emission * 57.308 tons (12 lb/ton) ---------------------------------- * 344 tons 2,000 lb/ton emission factor assumes best controls on dry process, KCAC uses a wet process for which no emission factors are available C-2 D 004346 3. Manufacturing a. Primary Process Rate Data on process rate (amount of asbestos used) was obtained from: 1) 1983 South Coast Air Quality Management District's Toxics Survey and 2) 1985 asbestos survey conducted by the Stationary Source Division, Air Resources Board (ARB) (see Table C-l). ARB surveyed the manufacturing facilities identified by the U.S. Environmental Protection Agency (EPA) that were not included in the 1983 South Coast survey. Overall response to both surveys was about 70 percent. To calculate the total emissions from all manufacturing facilities surveyed, it was assumed that those that responded are representative of the whole population. Emission Factor The emission factors for primary manufacturing of the various asbestos product categories range from .14 lb/ton of asbestos used to 1.1 lb/ton of asbestos used (see Table 1-2). The emission factors were cited from an EPA report (Versar, 1984). Emission * Process rate x emission factor Sample calculation: 50 tons asbestos used x .2 lb/ton = .005 ton/year in manufacturing sealants ----------------- 2000 lbs/ton C-3 D 004347 Table C-1 ASBESTOS EMISSIONS FROM THE MANUFACTURING OF ASBESTOS PRODUCTS Product Type Average Process Rate (ton) Range of Process Total Primary Rate Emission* (ton) (ton) Average Process Rate (ton) Range of Process Rate (ton) Total Secondary Emission* (ton) 1. Friction 2. Packings & Gaskets 3. Coatings, Adhesives 4 Sealants 4. Cement Pipe 5. Paper 6. Plastics 7. Textiles 8. Floor Tile 9. Miscellaneous (Chlorine) Total 175 - 127.50 8350 - 4650 0 - 0 150-200 1.67 0.1 <0.1 0.025-1202 0.4 7500-9212 3 30.3 < 0.1 0.548-18,283 0.7 00 29 <0.1 00 4 500 0.1-1775 2 6.15 0.025-40 < 0.1 . 0.18 <0.1 00 0 2.60 0.25-5.00 <0.1 - 0.13 <0.1 - 0.32 < 0.1 00 0 - 30 <0.1 2 * Emission estimates may not total due to rounding. C-4 D 00434-8 b. Secondary Process Rate Data on process rates were obtained from the 1983 South Coast Toxic Survey and the 1985 asbestos survey by ARB. Emission Factor The emission factors for secondary manufacturing are estimated from the emission factors used for primary manufacturing. The equation used for calculations is as follows: Emissions = Emfac x process rate Where: Emfac = (EF) x W EF = asbestos emission factor for primary manufacturing W * asbestos content of the Intermediate product used in producing another product 4. Automobile Brakes Process Rate Total vehicle miles traveled in 1984 456,857 x 103-miles per day Emission Factor 2.6 ug/km {Williams and Muhlbaler, 1982) C-5 D 004349 Emission (2.6 x 10"g/km)(456,857 x 10^ miles/day)(365 days/year) (454 g/lb)(.62 mile/km1(2000 Ibs/ton) = .77 ton/year 5. Quarrying Table C-2 contains estimated asbestos emissions from quarries. Asbestos Emissions = Amount of respirable particulate x % chrysotlle asbestos content by weight. Sample calculation for George Reed, Inc.: Process Rate = 274,000 tons of crushed stone produced Emission factor * 0.012 lbs respirable particulate per ton of crushed stone 0.20 lb of chrysotlle asbestos per lb of respirable particulate Emission: 274,000 tons x (0.012 lb/ton)(0.20} = 658 lbs asbestos Reference for emission factor for respirable particulate: Blackwood, T.R. and P.K. Chalekode, 1978. Source Assessment: Crushed Stone. Prepared by Monsanto Research Corporation for the U.S. Environmental Protection Agency. EPA-600/2-78-004L. C-6 D 004350 Table C-2 Asbestos Emissions from Quarrying, 1984 Quarry 1. George Reed Inc, Tuolumne 2. Woods Creek Rock, Tuolumne 3. Raisch Products Santa Clara 4. Ghilotti Bros. Maria 5. Dumbarton Quarry Assoc., Alameda 6. Hillsdale Rock Santa Clara Production of Crushed Stone/Year 274,000 231,894 435,000 156,000 1,000,000 250,000 Respirable Particulate (lb) 3,288 Chrysotile Asbestos ContentU) 20 2,783 1 5,220 1.6 1,872 1.4 12,000 0.5 3,000 2.7 TOTAL Asbestos Emissions (lb) 658 1) reference 28 2) 84 1) 26 2) 60 1) 81 1) 937 lbs or 0.468 tons References for 1984 production of crushed stone: 1) ELLEN LINDER, BAAQMD for quarries located in the Bay Area. 2) JERRY BENICASA, Tuolumne County for quarries located in Tuolumne. D 004351 C-7 REFERENCES FOR APPENDIX C 1. U.S. Environmental Protection Agency, 1981. Assessment and Control of Chrysotile Asbestos Emissions from Unpaved RoactsT EPA 450/3-81-006. 2. Versar Inc., 1984. Exposure Assessment for Asbestos. Draft final report prepared for U.S. Environmental Protection Agency. EPA contract No. 68-01-6271, Task No. 49. 3. Williams, R. L. and J. L. Muhlbaier, 1982. "Asbestos Brake Emissions," Environmental Research. 29:79-82. C-8 D 004352 Appendix D Documents Containing Asbestos Measurements Taken in California D 004353 An Inventory of Carcinogenic Substances Released into the Ambient Air of California. Final Report Task it and IV. March 1980. KVB, Inc. Inventory of Carcinogenic Substances Released into the Ambient Air of California: Phase Ii. November 1982. Science Applications, Inc. Ambient Asbestos Concentrations in California, Volume 1. Final Report. December 1983. Science Applications, Inc. Ambient Asbestos Concentrations in California - Field Number and Mass Concentration Summaries, Volume 2. december 1983. Science Applications, Inc. An Inventory of Carcinogenic Substances Released into the Ambient Air of California: Volume 1. final Report - Screening and Identification of Carcinogens of Greatest Concern. February 19, 1979. Science Applications, Inc. 2 "Chrysotile Asbestos in a California Recreational Area.11 Cooper, VI.C., J. Murchio, W. Popendorf, and H.R. Wenk. Science 206:685-688, November 9, 1979. Assessment and Control of Chrysotile Asbestos Emissions from Unpaved Roads. May 1981. U.S. Environmental Protection Agency. Experimental Determination of the Number and Size of Asbestos Fibers in the AmDient Air. January 1976. Air and Industrial Hygiene Laboratory, Laboratory Services Branch, Department of Health Services. AIHL/SP-1. Asbestos in the California Environment. June 1975. Air and Industrial Hygiene Laboratory, Laboratory Services Branch, Department of Health Services. Asbestos Fibers in Ambient Air of California. March 1973. School of Public Health, University of California, Berkeley. Report of Seasonal Variations in Asbestos Aerosols In The Clear Creek Recreational Area (1979). University of California, Berkeley. "Sunmary of Airborne Asbestos Data - Alvlso, California and Control Sites". April 15, 1985. Memorandum from. Dr. Steven Hayward of the Air and Industrial Hygiene Laboratory to Ralph Propper of the Air Resources Board. D-l q 004354 Appendix E Ambient Asbestos Measurements In California D 004355 Ambient Asbestos Measurements In California Location In California Number of Flbers/m^ King City, downwind of a milling plant King City, upwind of a milling plant San Jose Berkeley Los Angeles (Downtown) Emeryville, near asbestos manufacturer White Mountain (desert) Santa Monica Freeway, upwind (at 4th) Santa Monica Freeway, downwind (at 4th) Harbor Freeway, upwind Harbor Freeway, downwind (at 146th) San Diego Freeway, up- wind (at National) San Diego Freeway, down- wind (at National) San Diego Freeway, up- wind (at 122nd) San Diego Freeway, down- wind (at 122nd) Los Angeles Freeways, upwind (four sites) Los Angeles Freeways, downwind (four sites) San Lucas Berkeley 6,000 to 1,600,000 200 to 11,000 0 to 3,500 o to 4,000 0 to 5,700 238,000 20 to 100 700* 700* 1,100* 1,600* 200* 800* 900* 500* 800** 900** 1,000,000 .700,000 References John et al., 1976 John et al., 1976 Murchio et al., 1973 Murchio et al.. 1973 Murchio et al.. 1973 Murchio et al., 1973 Murchio et al.. 1973 Murchio et al.. 1973 Murchio et al.. 1973 Murchio et al., 1973 Murchio et al.. 1973 Murchio et al., 1973 Murchio et al.. 1973 Murchio et al.. 1973 Murchio et al.. 1973 Murchi et al.. 1973 Murchio et al.. 1973 ` Wesolowski, 1975 Wesolowskl, 1975 *Mean values ** Mean value of 60 samples Source: Science Applications, Inc., February 19. 1979. An Inventory of Carcinogenic Substances Released Into the Ambient Air of California. Volume I - Final Report Screening and Identification of Carcinogens of Greatest Concern. Page 357^ ' E-l D 004356 Appendix F SAI Sampling, Sample Preparation, Analysis and Quality Control Techniques D 004357 SAI Sampling, Sample Preparation, Analysis ~ and Quality Control Techniques for the 1983 Asbestos Study I. Introduction Given the project objective of providing an inventory of respirable airborne asbestos in California, the technical approach focused on applying state-of-the art sampling and analysis techniques to a cross-section of geographical sites based on emission/exposure potential. Sampling method adopted for this study followed protocols established by John et al. (1976, 1978, 1980). No exceptions were taken to the measurement and verification procedures specified by the U.S. Environmental Protection Agency (U.S. Environmental Protection Agency, 1978). Discussions with California Air Industrial Hygiene Laboratory (AIHL), the U.S. Environmental Protection Agency and the National Bureau of Standards (NBS) staff resulted in a number of minor changes and improvements. To accomplish the program objective for quantifying asbestos fibers in the respirable range (less than 3.5-um aerodynamic diameter), a single-point filter sampler with a cyclone inlet providing a collection efficiency of 50% for 3.5-um aerodynamic diameter particles at a flow rate of 15.5 liters per minute was used for all filter sampling. An 8.0-um.pore size backing filter was used in conjunction with a 0.2-um pore size collection filter. Although original protocols specified the use of a 0.4?*um pore size collection filter, the 0.2-um pore size filter was chosen for better collection efficiency of smaller fibers. No other significant changes were incorporated. The cyclone sampler shown in Figure F-l was developed for ambient air size-selective monitoring. This sampler will collect particles as small as D 004358 F-l 2.5-um (21.7 liters per minute flow); Figure F-2 (from John et al., 1978) indicates the particle deposition efficiency, relative to 50% cutoff, of the cyclone design showrf in Figure F-l. Design criteria for the sampler include: o A vertical cone with cap at bottom and outlet on top. This configuration minimizes loading and re-entrainment. o The after filters are 47 ran diameter which will allow the use of membrane filters, if chemical analysis is desired. o The cyclone is intended for 24 hour sampling at average flows of 15 to 20 liters per minute. o Both liquid and solid particles can be sampled with this device. The cyclone was selected for use over other samplers for this study because of its ease of use in the field, its ability to selectively sample because of its ease of use in the field, its ability to selectively sample small particles and the design which allows for uniform particle deposit on the filter. II. Sampling Procedures Preparation and Handling of Filters To reduce contamination from handling in the field. Individual polyethylene cassettes were constructed to hold the backing and collection filters for each sample. These cassettes consisted of two rings that F-2 D 004359 Figure F-l ALUMINUM ///*///f///i/t///*//>/.. STAINLESS STEEL CUP ASSEMBLY DRAWING OF THE CYCLONE SAMPLER DEVELOPED FOR AMBIENT AIR MONITORING (John and Reischl, 1980). F-3 D 004360 FRACTION DEPOSITED IN CYCLONE Figure F-2 Fraction of Methylene Blue Particles Deposited in the Cyclone as a Function of the Aerodynamic Particle Oiameter. The curves are labeled with the flow rate (from John et al., 1978). F-4 D 004361 press-fit together to provide a rigid support for the filters. Before loading the filters, the cassettes were pre-washed in an ultrasonic bath of 0.1-um filtered, de-ionized water and allowed to dry in a "particle-freeu clean room (class 100 certified). The filters were loaded into the cassettes inside the laminar flow bench of the clean room, using vacuum tweezers. Before sampling, an 8.0-um pore size, 47 mm aiameter Mi Hi pore backing filter was placed under the Nuclepore 0.2-um pore size collection filter to insure even distribution of particles across the filter face. After being loaded, each cassette was placed in a separate, clear plastic box (50mm x 80mm), which had been treated with Zerostat anti-static charge reducer. A secondary box specially constructed to reduce contamination and filter tipping was used to transport the filter boxes. Vibration during transportation was minimized by placing this secondary box containing a plastic bag full of water and styrofoam pellets. Filter cassette loading was done on a damp-wiped table in the mobile laboratory; the entire cyclone was disassembled and rinsed with Freon 113. Cassettes and cyclone components were handled with polyethylene gloves, reducing possible contamination time to that required to remove the sample from its box and transfer it to the head of the cyclone (approximately ten seconds). Air Sample Collection Procedures Original sampling plans called for at least four four-hour samples at each site. Paired replicate samples were taken morning and afternoon at King City, San Oose, Napa, San Fernando Valley and Sonora. Century City, Bakersfield, South Gate and San Diego ordinarily have high particle D 004362 F-5 concentration levels, so samples were collected at these locations over shorter time intervals to preclude overloading the filters. Sampling time was based on prior calibrations of filter loading as a function of suspended particle count level, by scanning electron microscopy. Sample filtering was carefully done, as described earlier in this section, with plastic gloves worn to transfer filter cassettes to the pre-cleaned cyclone assembly. The sampling pumps were operated at 15.5 liters per minute under a vacuum of six to seven inches of mercury. The pump and filter train were pre-tested to assure that there were no leaks in the six to seven-inch (mercury) vacuum range. III. Analytical Techniques Sample Preparation Procedures Upon return to the laboratory, the plastic filter cassettes were wiped clean with a damp, lint-free cloth and placed in clean room facilities. Everything relating to filter handling was cleaned with 0.2-um pore size filtered water and blown dry with Freon dusting spray. Direct handling of the filter cassettes was done with plastic gloves under a class 100 (fewer than 100 particles per cubic foot of air) laminar air flow. Particulate matter levels under the laminar air flow were maintained at 1 ^ss than 5 particles per cubic foot in the 0.3-um diameter range; particulate matter in the clean room was kept at less than 10 particles per cubic foot in the 0.7 um size range. Mass levels measured by the RAM counter in the center of the room were 1 ug/m^. Sectioning of Filters Sectioning of Nuclepore filters with the least disturbance to the membrane surface was a critical step in sample preparation. The Nuclepore F-6 D 004363 filter with 8.0.-um pore size Millipore backing filter was removed from the cassette and transferred to a 2 inch x 2 inch plexiglass plate. A new razor blade (cleaned with dusting spray) was slowly pressed on the filter pad using a downward vertical motion to cut the filter in half. The Nuclepore filter section from each half filter was carefully slid off the Millipore backing filter onto a clean piece of plexiglass. The filter was then tacked in place and a series of polyvinylchloride (PVC) cement beads were placed around the edges of each filter section. The tacked filters were allowed to dry under plastic petri dish covers. The plexiglass square containing the tacked filter section was placed in the bottom of a petri dish with a minimum clearance of 1.5 cm and fastened with double stick tape. One section was saved as an archive and for sub-sectioning for replicate analysis by the University of Washington. The other section was reserved for carbon coating as required by the EPA method. Carbon Coating Procedures Carbon coating was done with a Denton rotating stage carbon evaporator. The filters were carbon coated at 1 x 10-5 torr in short bursts with 30 to 40 nm of carbon. To minimize fiber dislodgement on the sampler filters, evacuation of the carbon coating chamber was performed slowly over a period of five minutes. Modified Jaffe-Wick Grid Preparation The filters were extracted using a modified Jaffe-Wick technique outlined in the provisional U.S. EPA methodology (EPA, 1978). All petri dishes and utensils were precleaned and spray-dusted. The foam supports and filter paper sections were ultrasonically cleaned with three washes of analytical grade acetone. Although the provisional method calls for the use of screens to F-7 D 004364 support Formvar sample grids, Whatman 42 filters papers were used because they produce more uniform grids. Another difference in the methodology was the use of 300-mesh instead of 200-mesh grids (300-mesh grids provide more support for the Formvar grid layering, as well as more accurate tracking of particle location within each grid hole by electron microscopy). A clean section of 0.25 inch x 2 inch x 2 inch polyurethane foam with a 2 inch x 2 inch filter paper on top was placed in a 6 cm diameter petri dish. Approximately three to six 300-mesh sample grids were placed on top of the filter paper, Formvar side up. Three square sections (4 mm x 4 mm) of the sample filter were excised with a clean razor blade and placed against the Formvar side of the grid with the particle side facing against the grid. Each of the grids was then saturated with 5 to 8 ul of analytical grade chloroform by filling the petri dishes to a level that just covered the filter paper support, using a long-needle, 50 ml syringe. Each dish was transferred to a glass dessicator with a reservoir of chloroform below the support plate. The chloroform level in the petri dish was carefully raised to the top of the filter paper, the petri dish covered, the dessicator lid replaced and the filters allowed to dissolve for 24 hours. An outside light source just above the dessicator kept it at a temperature of about 26.7 C. After 24 hours, the chloroform from each dish was removed with a syringe and the grids were allowed to dry before being transferred to a grid storage box. Sample Analysis Procedures A JEOL 6C transmission electron microscope (TEM), with a resolution of six angstroms and equipped with selected area electron diffraction (SAED), was used for all sample analyses. Calibration of instrument magnification was F-8 D 004365 performed using a 21,400 lines/in carbon replicate standard against a scale etched on the fluorescent screen of the TEM. The scale etched on the screen contained divisions of 1 cm, with a mm-division scale near the center. Both scales were set so that magnifications of 10,000X and 20.000X were accurate within 5%. All diameter measurements were done under the 10X viewing microscope on the TEM. At a magnification of 10,OOOX, 1 mm on the screen is equal to 0.1 urn; at 20.000X, 1 mm is equal to 0.05 urn. The counting magnification ranged from 15.000X to 20.000X. Each lot of grids was calibrated in two ways. First optical calibration was performed on a Leitz Dialux 20 light microscope using a standard with divisions of 0.01 mm. Second, the area of the grid holes was checked by scanning electron microscopy (SEM: International Scientific Model III-A }. Calibration of scanning electron microscope magnification was performed using latex sphere standards of 2.02 um diameters, respectively. Optical microscopy was not selected for analysis of the samples, since the optical technique is not able to measure fibers less than 5 um in length. Quantitation Techniques The count data from each sample were analyzed by a modified version of the computer program outlined in the U.S. EPA provisional methodology (EPA, 1978). The reported data included fiber concentrations (by fiber type: chrysotile, amphibole, indeterminate, non-asbestos) as fibers/m^ of air. 3 Mass concentrations of asbestos (pg/m air) were calculated, although these data are subject to error accumulated from squaring particle radii in the computation*. In addition to the standard EPA reporting format, an additional F-9 D 004366 category to distinguish chrysotile fibers in the occupational exposure size range (length 5.0 um) has been provided. In reporting data, values shown as zero are below the detection limit (DL: a function of the total area of the filter scanned and the volume of air that is sampled). When only one fiber was found on the sample scanned, the value obtained was used to derive the detection limit. Samples having less than one fiber found during analysis were defined as being "below the detection limit" ( DL). All the samples analyzed were counted in an identical manner and had been collected at the same flow rate (15.5 liters per minute), therefore, the detection limit was a function only of the duration of sampling time. A graph of detection limit vs sampling time is presented in Figure F-3. Since sampling times ranged from one to four hours, net detection limits ranged from 9,100 to 2,400 fibers/m'* of air, respectively. IV. Quality Assurance To fulfill the project's quality assurance requirements, the University of Washington Transmission Electron Microscopy Center was provided with replicate filter samples from different locations as part of an interlaboratory comparison. To insure proper handling in transit, the samples were carbon coated at SAI's laboratory and hand-carried to Sea.cle. The samples were analyzed according to the EPA provisional method and the data returned to SAI for computer reduction. In addition to a background control (the Napa site)* sites selected for inter-comparison analyses (Table F-I)' were King City, Sonora, Century City, and San Diego. The Napa sample was done in duplicate by both laboratories to provide a measure of reproducibility. F-10 D 004367 Figure F-3 fib e rs / cu. meter SAMPLING TIME (HOURS) Relationship Between Minimum Asbestos Detection Limit vs. SamDl Time F-1I D 004368 The detection limit for TEM asbestos analysis in this study was approximately 2.4QG fibers/m , the result of counting only one fiber in the filter area analyzed. The greatest difference between comparative samples was for the duplicated background control samples (Napa) done by the University of Washington. Although values for these two replicates are a factor of 11 apart (41,000 vs 3,600 fibers/m ), the difference represents the counting of four fibers vs one fiber per total counting area, respectively. Differences between the two laboratories1 analytical results for the other replicate samples are in all cases less than the variation in the single duplicate analysis. F-12 D 004369 Table F-l Interlaboratory Comparison of Asbestos Measurement by Transmission Electron Microscopy Sample SAI TEC Laboratory Chrysotile Amphibole (fibers/m3) (fibers/m3) A-14 King City A-24 Napa A-27 Sonora A-100 Century City A-202 San Diego 9.4 x 103 4.7 x 103 2.4 x 103 2.4 x 103 1.5 x 104 3.0 x 103 < DL 7.1 x 103 4.8 x 103 2.4 x 103 < DL 8.9 x 103 University of Washington Chrysotile Amphibole (fibers/m3) (fibers/m3) 1.5 x 104 3.6 x 103 4.1 x 104 3.6 x 103 2.1 x 104 7.2 x 103 < DL 1.2 x ID4 1.7 x 104 2.1 x 103 2.5 x 104 4.5 x IQ3 F-13 D 004370 REFERENCES FOR APPENDIX F 1. John, W., A. Berner, G. Smith and J.d. Wesolowski, 1976. Experimental Determination of the Number and Size of Asbestos Fibers in Ambient Air. California Air Industrial Hygiene Laboratory Report, AIHL/ SM. 2. John, W., G. Reischl, and J. Wesolowski, 1978. Size-Selective Monitoring Techniques for particulate Matter in California "RTF. California Air and Industrial Hygiene Laboratory feeport. AIHL/SP-12. 3. John, W. and G. Reischl, 1980. "A Cyclone for Size-Selective Sampling of Ambient Air." JAPCA. 3:872-876. 4. U.S. Environmental Protection Agency, 1978. Electron Microscope Measurement of Airborne Asbestos Concentrations, A Provisional Methodology Manual. U.S. Environmental Protection Aqency Report. Ef>A-600y2-77-176, Revised June 1978. F-14 D 004371 ZLt00 a os}.aIV u} uo|.qeu}uiequ03 soqsaqsy 6a}pjp6sy uinpuejouiaw $ x}pu9ddv Sample_ Calculations of the Amount of Asbestos Fibers Ingested or Inhaled into the Body l.UiALATIUis OF ASBESTOS A. AMBIENT AIR EXPOSURES Assumptions of exposure for office worker 1. Mean asbestos concentrations range from 7,700 to 45,000 fibers/ 3 as measured by`TEM (see Table III-3). m 3 2. Breathing rate of air is 0.83m /hr. 3. Time outside (10%) for 365 days/yr. Sample calculation Yearly intake of fibers = 7,700 fibers x 0.83m^ x m 3 hr. 24 hr x 0.10 x 365 days day year = 5.6 x 10 or = 6 x 10^ yearly intake of fibers (estimates are rounded off) B. INDOOR AIR EXPOSURE - SCHOOL Assumptions of exposure for school children 3 1. Breathing rate of air is 0.75m /hr. 2. Time in school (15%) - normalize to 365 days/yr. 3. Concentrations are in PCM units. Convert to TEM units by using the conversion factor of 100 to 1000 TEM fibers/PCM fiber. 4. The median asbestos concentrations in schools range from 540 PCM fibers/ni to 4,050 PCM fibers/m (see Table III-7). The low value for the estimated yearly fiber intake uses the 540 PCM concentration and the 100 TEM fibers per PCM fiber conversion factor, while, the upper value uses the 4,050 PCM concentration and the 1000 TEM fibers per PCM fiber conversion factor. D 004373 Sample calculation Yearly intake of fibers = 540 PCM fibers x 0.75m^ x - m 3 hr. 100 TEM fibers x 24 hr x 0.15 x 365 days PCM fiber day year = 53.2 x 106 or = 50 x 10^ yearly intake of fibers (estimates are rounded off) INDOOR AIR EXPOSURE - OFFICE BUILDING Assumptions of exposure for office worker 3 1. Breathing rate of air is 0.83m /hr. 2. Time in office building (33/o) - normalize to 365 days/yr. 3. Concentrations are in PCM units. Convert to TEM units by using the conversion factor of 100 to 1000 TEM fibers/PCM fiber. 4. The median asbestos concentrations in office buildings range from 260 PCM fibers/ni to 640 PCM fibers/ni (see Table III-7). The low value for the estimated yearly fiber intake uses the 260 PCM concentration and the 100 TEM fibers per PCM fiber conversion factor, while the upper value uses the 640 PCM concentration and the 1000 TEM fibers per PCM fiber conversion factor. Sample calculation Yearly intake of fibers * 260 PCM fibers x 100 TEM fibers x m 3 PCM fiber 3 0.83m x 24 hr x 0.33 x 365 days hr day year = 6-2 x 106 or = 60 x 106 yearly intake of fibers (estimates are rounded off) D 004374 D. INDOOR AIR EXPOSURE - HOMES Assumptions of exposure for houseperson 3 1. Breathing rate of air is 0.83n /hr. 2. Time in office building (85>;) - for 365 days/yr. 3. Concentrations are in TEM units and range from 63 fibers/tn to 56,000 fibers/mJ (see Table III-8). Sample calculation Yearly intake of fibers * 56,000 fibers x m3 0.83m^ x 24 hr x 0.85 x 365 days hr day year = 347.3 x 10 or = 350 x 10^ yearly intake of fibers (estimates are rounded off) II. INGESTION OF ASBESTOS A. TREATED WATER Assumptions of exposure from drinking of water for children 1. Consumption rate is 1 liter/day (children) for 365 days/yr. 2. Asbestos concentrations in water range from 1 x 10 fibers/liter to 260,000 x 10 fibers/liter (see Table III-6). Sample Calculation Yearly intake of fibers * 100 x 10 fibers x 1 liter x liter day 365 days year - 36,500 x 106 or 3>7 x 1Q10 yearly intake of fibers. D 004375 III. DISCUSSION OF ESTIMATE A. Only exposures by the same route, either inhalation or ingestion., should be compared. It is not possible to compare health risk exposures of ingestion or inhalation because the health risk associated with ingestion have not been conclusively determined in animal and epidemiological studies (see DiiS Part B report). Also, the fraction of asbestos fibers that is retained by the body has not been determined for the different exposure routes (Committee on Nonoccupational Health Risks of Asbestiform Fibers, 1984). B. Exposure estimates were calculated for three different lifestyles: office worker, houseperson, and school children. The amount of time that an individual is exposed to and at any given asbestos concentrations may vary considerably from the values that were assumed; however, because of the uncertainty in the measurement methods and concentrations, the range of exposures given should cover most individuals. Table H-l lists the amount of time the office worker, houseperson, and child was expected to be in each environmental setting. The breathing rate was assumed to be 0.75 in /hour for a child and 0.83 ra /hr for an adult. For drinking water, the consumption rate was assumed to be 1.0 liter/day for a child and 1.5 liter/day for an adult (Committee on Nonoccupational Health Risk on Asbestiform Fibers, 1984). Table H-l Annual Percentage of Time in Various Environments Ambient Air Indoor-Home Indoor-Office Building Indoor-Schools Office Worker (%) 10 . 57 33 ___0 100% Houseperson ( /o ) 10 35 5* ___0 100% Child (Z) 35 50 0 1,5 100% Accounts for time shopping and inside of other office complexes. D 004376