Document 8O2xwZXzM7xzz176RQrdQR5na

Drift Report VALUING THE BENEFITS OF THE NEW SUBSTANCES NOTIFICATION REGULATIONS Prepared for Environmental Protection Service Environment Canada Prepared by. Lara B. Sheer, Anne P. Downey, Mark D. Ewen, Timothy B. Petenen (Project Manager) and Brian G. Morrison (Project Director) Industrial Economics, Incorporated 2067 Massachusetts Avenue Cambridge, MA 02140 Project Steering Committee: Elaine DuWors National Wildlife Research Centre Environmental Conservation Service Environment Canada Jim Frehs Water &. Habitat Conservation Branch Environmental Conservation Service Environment Canada Rj*l (Sandy) Matheson Commercial Chemicals Branch Enviiommental Protection Service Environment Canada Danny Guay Regulatory and Economic Assessment Branch Environmental Protection Service Environment Canada Jacqueline Sitwell Bureau of Chemical Hazards Environmental Health Directorate Health Canada Scientific Authority: Paul De Civita Regulatory and Economic Assessment Branch Environmental Protection Service Environment Canada (819) 997-7061 September 1996 CMA114630 Author: STEWARTTeepndce.nci.nih.gov at internet Date: 11/22/96 9:32 AM Priority: Normal TO: robert venezia at CMAHQ Subject: RE: .......... -.................................................................................................... Message Contents Dear Mr. Venezia: I think something got lost in the message. NCI is not following up a cohort of vinyl chloride workers, nor do I know of anyone who has, other that those who have published in the occupational hygiene literature. I'm not sure what I said to Dr- Lewis (I did talk with him), but I may have mentioned that at one time I had wanted to get measurement data on vinyl chloride workers to do a methodologic study; I was not successful. I'm sorry I cannot provide you with more data. Trish Stewart CMA 114631 TABLE OF CONTENTS EXECUTIVE SUMMARY............................................................................................ CHAPTER 1 Introduction............................................................................................................................ -1-1 Selection of Substances Analyzed ......................................................................................... 1-1 Overview of Methods .............................................. *........................... .......................... -1-2 Identification and Screening of Benefits............................................. 1-3 Developing Annual Benefits Estimates ..................................................... 1-7 Developing Total Benefits Estimates..................................................................... 1-11 Results......................................................................................................... 1-11 Vinyl Chloride (VQ................................................................................................ 1-11 Dichloromethane (DCM) ....................................................................................... 1*12 Polychlorinated Biphenyls (PCBs)..........................................................................1-12 Limitations................................................................................................................1*16 Organization of Report...................... 1-16 References for Chapter 1 ..........................................................-.............................,......................1-18 Appendix 1A Supplemental Information on Health Risk Assessment ..................................... 1-19 VINYL CHLORIDE........................................................................................................CHAPTER 2 Overview of Chapter......................... .2-1 Summary of Benefits..............7................................................................................2-1 Limitations...................................... ^2-1 Organization of Chapter...................... 2-2 Background Information on Vinyl Chloride......................................................................... 2-3 Description of the Compound.............................................. 2-3 Information on Manufacture in 2-3 Releases to the Environment.................................................................................... 2-4 Human and Ecological Exposures to Vinyl Chloride....... ................................................. 2-6 Human Exposures......................................................................................................-2-6 Ecological Exposures............... 2-7 CMA 114632 TABLE OF CONTENTS (continued) The Benefits of Controlling Vinyl Chloride Releases: Overview................................... 2-8 Mortality from Cancer............................................................ ............. '..................2-8 Morbidity.............................. ^................................................................................. 2-8 Estimating Human Health Effects............................................................ .2-9 Cancer Cases Resulting from Exposure to Vinyl Chloride .............. .................. 2-9 Noncaidnogenic Effects Resulting from Exposure to Vinyl Chloride........................................................................................................... 2-15 Valuing Human Health Effects: Annual Values.............................................................. 2-18 Carcinogenic Effects: Mortality.............................................................................. 2-19 Noncardnogenic Effects: Morbidity ..................................................................... 2-21 Valuing Human Health Effects: Total Values...................................................................2-22 References for Chapter 2.................................................................................................................2-25 Appendix 2A: General Population Exposed to VC Emissions from Point Sources..............................................................................................2-29 Appendix ZB: Estimating General Population Cancer Cases: Detailed Example.................................................................................................... 2-32 Appendix 2C: Estimates Used to Generate Proposed Distribution of Value of Life....... ....................................................................................2-33 DICHLOROMETHANE.................................................................................................. CHAPTERS Overview of Chapter......................................... .........................J....................................... 2-1 Summary of Benefits.................................................................................................. 3-1 Limitations of Analysis ............................;...............................................................3-1 Organization of Chapter.................................................... 3-2 Background Information on Dichloromethane ...................................................................3-2 Description of the Compound.................................................................................. 3-2 Information on Use in Canada ................................................................................ 3-3 Releases to the Environment.....................................................................................3-3 CMA 114633 TABLE OF CONTENTS (continued) Human and Exposures to Dicfaloromethanc ................... ...............................3*4 Human Exposures..................................................................................................... *3*5 The Benefits of Controlling DCM Releases Overview.....................................................3-d Carcinogenic Effects from Chronic Exposures .................... 3*7 Noncardnogenic Effects from Chronic Exposures ............................... 3*7 Acute Health Effects.................................................................................... 3*7 Ecological Effects..................................................................................................... -3-8 Estimating Human Health Effects......................................................................................... 3*8 Annual Cancer Cases Resulting from Exposure to Dichlorometbane ...................................................................................................................3-8 Noncardnogenic Effects Resulting from Exposure to Dichlorometbane...................................................................................................... 3-10 Acute Health Effects................................................................................................3-11 Valuing Human Health Effects: Annual Values..............................................................3-12 Carcinogenic Effects: Mortality..............................................................................3-12 Other Health Effects................................................................................................3-13 Valuing Human Health Effects: Total Values...................................................................3-14 References for Chapter 3..................................................................................................................3*16 Appendix 3A: Estimating the Average Daily Exposure of Individuals Exposed to DCM in the Workplace............................................................................................ .3-17 POLYCHLORINATED BIPHENYLS (PCBs).............................................................CHAPTER 4 Overview of Chapter .............................................. 4-1 Summary of Benefits.......................................................................................... .4-1 Limitations..................................................................................................................4-1 Chapter Organization ............................................................................................... 4-2 CMA114634 TABLE OF CONTENTS (continued) Background Information on PCBs .......................................................................................4-3 Description of PCBs.................................................................................................. 4-3 Information on Use in Canaria ................................................................................ 4-3 Releases to the Environment.....................................................................................4-4 Ecological and Human Health Exposures..................... .......... .................................. .4-5 Ecological Exposure to PCBs.................................................................... 4-5 Human Exposure to PCBs......................................................................................... 4-9 The Benefits of Controlling PCB Exposures: Overview................................. .............. 4-9 Benefit Categories................ 4-9 Methods of Estimating PCB-Related Benefits..................................................... 4-11 Annual Benefit Estimates.....................................................................................................4-13 Extractive Use Value Benefits.................................................................................4-14 Non-Extractive Use...................................................................................................4-27 Passive Use................................................................................................................ 4-28 Human Health ......................................................................................................... 4-32 Total Benefits Estimates....................................................................................................... 4-32 References for Chapter 4 . .............................................................................................................4-35 Appendix 4A: Distribution of PCBs in Use and Storage in Canada ........................................ 4-39 CMA 114635 ACKNOWLEDGEMENTS The authors gratefully acknowledge the guidance and assistance offered by Paul De Civita and the members of the Project Steering Committee in preparing this report. Additional assistance in its development was provided by Stephen MacDonald, Andy Atkinson, Lawrence Fedoruk, Birgit Biaune, Francois Lavalee, Arthur Sheffield, Jeff Harris, Art Stelzig, Andre Jacquemot, and Chuck Cox. Copies of the draft report were also furnished to John HOborn and Uwe Shneider. CMA 114636 EXECUTIVE SUMMARY CHAPTER 1 INTRODUCTION The New Substances Notification Regulations ("the NSNR* or "the Regulations") were developed to ensure "that no new substances will be manufactured in or imported into Canada on a commercial scale before an assessment has been carried out to determine the risks posed to the environment and human health by the substances (Canada Gazette 1994)." To characterize the potential benefits of the Regulations, this report analyzes the benefits that would have resulted had the Regulations been implemented in time to control or prohibit the use of three- substances currently or previously manufactured in or imported into Canada: vinyl chloride (VC), dichloromethane (DCM), and polychlorinated biphenyls (PCBs). This approach is analogous to evaluating the human health and environmental damages incurred due to the release of these substances into the Canadian environment, assuming that these damages would not have resulted had the Regulations been in place at the time the substances were introduced. This type of approach is often referred to as an "avoided damages" approach. This executive summary describes the process Environment Canada (EC) and Health Canada (HC) employed to select the substances analjaed. It then outlines the benefits typology used in this report, summarizes the methods used to estimate annual and total benefits, and presents a summary of the results for each substance. It also cites the major limitations of the analysis and provides an overview of the structure of the remaining chapters. SELECTION OF SUBSTANCES ANALYZED In the course of developing the NSNR, EC and HC committed to a mult-stakeholder review of regulatory impacts, including an analysis of the Regulations' environmental and health benefits. This analysis is to be submitted to the New Substances Notification Impact Working Group (NSNIWG), which is comprised of representatives from EC, HG Industry Canada, and the Industry Coordinating Group for the Canadian Environmental Protection Act (CEPA). The analysis is to be completed by September 1997, approximately three years after the rules' promulgation. Ideally, the impact analysis would focus on benefits attributable to regulation of new substances under the NSNR. The data required to conduct such an analysis, however, are currently unavailable, and unlikely to become available by 1997. Therefore, EC and HC chose to characterize the Regulations' potential benefits through case studies of three CEPA toxic substances that in all 1-1 CMA 114637 likelihood would have been prohibited or controlled had they been evaluated through the new substance notification program. EC and HC selected the three substances analyzed in this report using a screening approach to narrow the list of CEPA toxic substances (substances subjected to regulatory control under CEPA and identified as toxic under the Priority Substances Program). First, to ensure a focus on commercially manufactured or imported products, substances that generally would be classified into one of the following categories were eliminated from consideration: FJfhients and wastes. Effluents and wastes are not notifiable under the. Regulations, and therefore are not affected by them. By-products ofmanufacturing pfrw^jny Manufacturing and processing by-products are also not directly notifiable under the regulations. Elements and natmaDv-occumng compounds. Elements and naturallyoccurring compounds were eliminated from consideration due to the inherent difficulty in distinguishing anthropogenic impacts from natural impacts. The remaining substances were reviewed to determine: the completeness of data on human health and ecological effects; their suitability as surrogates for the NSNR analysis (i.en solely or primarily anthropogenic in origin); and whether they had been determined to be CEPA toxic by both EC and HC The result of this effort was the selection of VC DCM, and PCBs as the most appropriate candidates for analysis. These substances are anthropogenic in origin and have been determined to be CEPA toxic by the two Departments. In addition, the data available on the impacts of these substances is relatively substantial, facilitating the development of a benefits assessment. OVERVIEW OF METHODS We evaluate the benefits of the NSNR using an approach resource economists commonly refer to as the damage function approach.1 As generally applied, this approach includes the following steps:* , 1 The term damages refers to negative environmental or human health effects. The benefits of a particular policy (e.g, a pollution control regulation) are the reduction in damages th?t result frou? the policy's implementation. ' 1-2 CMA 114638 (1) Estimating the r*te*t to which a regulation would change the quantity of a pollutant or toxic substance released to the environment; (2) Employing dispersion modeling techniques to characterize changes in the concentration of pollutants in environmental media; (3) Applying concentration* or dose-response functions to estimate changes in physiol impacts (c.g^ human health impacts or impacts on species abundance) attributable to pollution; (4) Valuing the change in physical impacts, thereby creating an economic benefits estimate; and . (5) Aggegating benefits estimates across all relevant categories and time periods. The broad scope of this analysis and the limited time and resources available for the effort have necessitated some simplification of this approach. For example, we assume that control or prohibition of a substance under the NSNR would eliminate all associated health or environmental impacts; as a result, the benefits of the Regulations are simply the absolute value of the damages attributed to unregulated manufacture and/or use of each substance. In addition, we have not undertaken any original pollutant dispersion modeling, choosing to rely instead on previously developed information to characterize concentrations of VC, DCM, and PCBs in the environment Nonetheless, the approach employed here is consistent with the underlying theory of scientific injury assessment and environmental impact valuation, and provides a reasonable characterization of the benefits of three hypothetical applications of the NSNR. The following discussion notes key methodological issues in our implementation of the damage function approach to analyze the benefits of controlling VC DCM, and PCBs. As described below, implementation of the methodology includes the following major elements: A preliminary evaluation of each substance to identify major benefit categories and to determine if sufficient data arc available to quantify key benefits; Use of this information to develop a detailed evaluation of the effect of each substance on human health and/or the environment; and Valuation of human health and ecological effects, including the incorporation of simulations to address uncertainty in the underlying estimates. Identification and Screening of Benefit A number of different classification approaches have been developed to structure assessments of the benefits of environmental protection. This report employs a benefits classification framework that Environment Canada itself recommends (EC 1996). The Environment 1-3 CMA 114639 Canada framework, which is similar to many of the classification schemes in the published literature, is summarized in Exhibit 1-1. | Exhibit M ECt FRAMEWORK FOR CLASSIFYING BENEFITS Category Human Health Extractive Uses Benefits resulting from decreased mortality and/or morbidity. Benefits resulting from the increased use of natural resources that arc used directly for commercial recreational or subsistence needs (e.g, increased recreational fishing opportunities). Non-Extractive Uses Ecological Functions Passive Uses Benefits resulting from the increased use of environmental services that are not consumed (e^, activities such as hiking and canoeing). Benefits resulting from a wide range of ecological services that are dependent on a healthy ecosystem (e^, benefits that humans receive from the ability of soil to filter impurities from groundwater). Benefits resulting from the knowledge of the continued existence of natural resources and the desire to leave natural resources to future generations. Built Environment Benefits resulting from reduction in materials damage and soiling. Optional Uses Benefits resulting from potential future uses (in the above categories), including insurance against unknown future events. As the preceding exhibit shows, the benefits of environmental regulations can take a variety of forms. Exhibit 1-2 illustrates the process we have employed to identify the potential benefits f controlling VC, DCM, and PCBs, and to determine which benefits categories to subject to quantitative analysis. As the exhibit indicates, we first conducted an extensive literature review to identify potential benefits. We then screened the available data for each benefits category to determine whether it was sufficient to conduct a quantitative benefits assessment; if so, we judged whether the benefits were likely to be great enough to warrant devoting resources to a quantitative analysis. Benefits categories that passed this screen were evaluated quantitatively; all others were qualitatively assessed. 1-4 CMA114640 Exhibit 1-2 BENEFITS SCREENING PROCESS CMA 114641 Exhibits 1*3 through 1-5 give the results of the screening assessment, listing the potential benefits associated with regulation of the three substances of concern and indicating which categories of benefits have been quantitatively or qualitatively evaluated. As the exhibit indicates, the focus of the VC and DCM analyses is on human health benefits, while the PCB analysis addresses a range of environmental benefits, including extractive, non-extractive, and passive uses.1 * ft*** 1-3 | POTENTIAL BENEFITS OF NSNR CONTROLS: VINYL CHLORIDE . | Benefit Category Reduced Mortality Reduced Morbidity Ecological Benefits Inqiacts of Concern Studies link VC exposure to angiosarcoma of the liver and cancer of the brain, lung, and digestive tract VC can cause hepatic, respiratory, cardiovascular, gastrointestinal, hematological, musculoskeletal, renal, dermal, ocular, and other adverse effects. Byproducts of VC production can adhere to plankton and bioaccumulate in the marine environment Form of Analysis Quantitative . Quantitative Qualitative Exhfcit M POTENTIAL BENEFITS OF NSNR CONTROLS: DICHLOROMETHANE Benefit Category Impmi-tr of Concern Form of Analysis Reduced Mortality Chronic exposure to DCM has been linked to liver and lung cancer. Quantitative V Reduced Morbidity Chronic exposure to DCM has been linked to Central Nervous System effects such as headaches, dizziness, nausea, and memory loss; effects on liver and kidney function; and benign mammary gland tumors. Quantitative Ecological Benefits Exposure to DCM may adversely affect some aquatic organisms, such as freshwater nematodes. Qualitative , * At the instruction of HC, the analysis of PCBs excluded consideration of human health risks. HC considers available data on such risks inconclusive, and therefore insufficient for an analysis of this type. ^ 1-6 CMA 114642 Exhibit 1-5 Benefit Category POTENTIAL BENEFITS OF NSNR CONTROLS: PCBs Impacts of Concern | Form of Analysis Extractive Use Recreational Fishing Diminished abundance and diversity of fish species due to reproductive abnormalities lowers quality of the angling experience. Fish consumption advisories (based on human health concerns) reduce the value of angling experience and affea the choice of fishing location. Quantitative Waterfowl Hunting High tissue concentration levels and potential waterfowl consumption advisories rfimmkh enjoyment of the hunting experience and affect the choice of bunting locations. Quantitative Trapping Decline in mink populations due to reproductive abnormalities limits pelt harvest and diminishes trapping experience. Quantitative Commercial Fishing Diminished abundance and diversity of fish species due to reproductive abnormalities deceases catch. Fish consumption advisories reduce volume of saleable fish. Qualitative Non-Extractive Use Bird Viewing Reductions in bird populations due to reproductive abnormalities and tire presence of physical deformities diminishes the enjoyment of birdwatching. Quantitative Other Recreation Concern over health risks diminishes the enjoyment of swimming, boating, or similar activities and affects the choice of location. Qualitative Passive Use Contaminated environment decreases the value individuals derive from a dean natural resource, above and beyond its direct use. Quantitative Human Health Increased risk of botb mortality (cancer) and morbidity (e.g^ adverse reproductive effects). Qualitative Developing Annual Benefits Estimates We develop quantitative estimates of annual benefits for each substance by estimating annual human health and ecological effects resulting from exposures to the substance, and by valuing those effects using a "benefits transfer" approach. Further, we explicitly incorporate uncertainty into our analysis by using a statistical technique known as Monte Carlo simulation. A summary of the methods employed to estimate annual benefits is provided below. 1-7 CMA 114643 Estimating Human Health and Ecological Effects While the partimiarc of eadi analysis vaiy to some extent, we estimate human health and ecological effects by collecting information on: the sources and releases of each substance; the pathways from these sources to human health and ecological receptors; the concentrations of each substance to which human and ecological receptors are exposed; the estimated dose that humans or biota receive; and dose-response relationships. This information is used to quantify likely human health effects and impairment of ecological r natural resource services. For instance, we use health risk assessment methodologies to develop estimates of the number of cancer cases that would be avoided by controlling VC and DCM.3 For PCBs, we assess the effect of the contaminant on the services provided by natural resources, such as the number of recreational fishing trips affected by PCB contamination in fish. Estimating these effects requires careful consideration of the timing ofbarm to human health and the environment, as well as consideration of the effects of other regulatory measures that may mitigate the risks a substance might otherwise pose. For instance, damages that VC emissions cause in Canada today are likely to be quite small, since (1) VC emissions arc currently regulated under CEPA and (2) pre-CEPA emissions do not cause lingering problems due to the transient nature of VC in the environment Thus, to evaluate the benefits of controlling VC as if it were a new substance, we employ 1970s estimates of average atmospheric concentrations of the pollutant in the vicinity of facilities that used or manufactured it; these estimates, developed prior to the regulation of the substance, allow us to estimate the adverse health impacts that would occur in the absense of controls. For PCBs and DCM we use more ament information, as each substance continues to cause harm in Canada.4 3 For those readers unfamiliar with health risk assessment methods and terms, we have included a brief primer on these topics in Appendix 1A, which is attached to this chapter. 4 While PCBs have been banned from new uses in Canada since 1980, previous discharges of PCBs continue to cause present day problems due to the persistence of the substance in the environment. DCM is not currently regulated under CEPA. to ament releases provide a reasonable basis for assessing the benefits associated with regulating this substance. 1-8 CMA 114644 Valuing Human Health and Ecological Fffrcts We value human health and ecological changes using the benefits transfer approach. Benefits transfer involves the application of value estimates, functions, data and/or models developed in one rem-r* to address a similar resource valuation question in another context. Benefits transfer in its simplest form involves the application of existing "per unit* values derived at one site (or in one study) to estimate the benefits attributable to an environmental improvement at another site. Such transfers may include adjustments to account for differences in the characteristics of the activity evaluated in the existing study versus the characteristics of the activity for the "site" (in this case "country") under analysis. Although this technique has been used for many years to evaluate environmental benefits and to natural resource damages, it continues to generate some controversy in the environmental and natural resource economics community. This controversy focuses on the applieability of value estimates developed for a particular site in one context to the same or similar site in another context Determining whether an existing study is appropriate for benefits transfer requires consideration of the overall quality of that study and the degree to which the case examined by the study is similar to the case of interest (typically referred to as the "policy" case). Factors f concern include: (1) rnmmoriitv Characteristic The commodity (environmental goods and services or human health effects) valued in the policy case and study case should be the same or similar. The magnitude of change in the commodity between the policy and study case should be similar. The availability of substitute sources of environmental goods and services should be similar. The assignment of property rights should be the same (e.g., willingness to pay versus willingness to accept). The temporal perspective (Le., when a commodity is provided and when payment is made) should be the same. (2) Population Characteristics The characteristics of the populations of interest in the study and policy cases (e.g., age, income, proximity to the site or source of risk and degree of environmental concern) should be the same or similar. Any valuation function employed should include socioeconomic variables, to allow the transfer to account for differences in population characteristics between the study and policy cases. 1-9 CMA 114645  The population's familiarity with the environmental problem of concern should be similar in the study case and policy case (Boyle 1992; Dcsvouges 1992; Unsworth 1993). Detailed information on the ranadian and U.S. studies relied upon in this report is provided in Chapters 2,3 and 4. To make the values collected from each study comparable, we use the following approach to adjust for inflation and for the difference in value of the U.S. and Canadian dollars: We adjust- dollar values presented' in past Canadian studies by applying the Canadian Consumer Price Index (CPI) to inflate figures to 199S Canadian dollars. We adjust dollar values presented in past U.S. studies by first translating the U.S. dollar figures to Canadian dollars using the Purchasing Power Parity (PPP) index, and by then applying the Canadian CPI to inflate figures to 1995 Canadian dollars. This approach was recommended to us by the Scientific Authority in consultation with Statistics Canada (De Civita 1996). Incorporating Uncertainty In the course of conducting this effort, we were faced with data uncertainties at several stages. For instance, our ability to estimate the cancer cases resulting from human exposures to VC and DCM is limited by a number of factors, including uncertainty regarding the size of the exposed population and uncertainty as to the actual responses of human receptors. Similarly, there is uncertainty associated with the economic unit values identified for particular benefits categories. To generate annual and total benefits estimates deterministically would imply a higher level of certainty than actually exists. As a result, we explicitly recognize uncertainty associated with key independent variables through the use of a statistical procedure commonly known as Monte Carlo simulation. This technique provides information on the variable of ultimate interest (the dollar value of benefits) that is the function of input variables (c.g, unit economic values) that are probability distributions. The output of this process is a probability distribution reflecting the magnitude and likelihood of various benefit figures.5 For instance, in Chapter 2 we provide benefits estimates associated with avoiding VC-induced cancer cases by reporting not only the mean value, but also the 10th and 90th percentile estimates. Although the selection of these figures as our low- and high-end estimates is arbitrary, We use the computer software program @Risk to conduct our uncertainty analysis. The program offers two sampling techniques: Monte Carlo sampling and Latin Hypercube sampling. We employed Monte Carlo sampling for this analysis. 1-10 CMA 114646 their use should provide a more plausible characterization of the likely range of benefits than would use of the simulation's extreme upper and lower bounds. Developing Total Benefits Estimates Since the benefits of the NSNR will be realized over more than one year, we also estimate the total benefits of regulating each substance. The total benefits estimates are the present value of the stream of annual benefits Hicrrmnteri over a thirty year time period. We selected a thirty year time period as a common and reasonable "long* time horizon (e.g* 30'years is commonly used in estimating total operation and maintenance costs at hazardous,waste sites). We-acknowledge that the selection of 30 years in calculating total benefits for this project is somewhat arbitrary; in reality, the benefits from the NSNR could be longer or shorter than 30 years.* The selection of a discount rate for this type of calculation has been the subject of much debate in the economics profession. Treasury Board, Canada recommends the use of five, 10 and 15 percent real discount rates in conducting analyses of this sort. We have selected lower figures (two, four and six percent), however, as the majority of environmental economists view five, 10 and 15 percent as too high for this type of analysis. The range of discount rates we employ is consistent with the findings of A. Myrick Freeman, a noted resource economist who recently reviewed the literature on this topic and recommends using a discount rate of 2 to 3 percent (Freeman 1993). RESULTS The following discussion summarizes the benefits of controlling or prohibiting the manufacture and/or use ofvinyl chloride, dichloromethane and polychlorinated biphenyls in Canada Detailed information supporting these benefits estimates is provided in the body of the report. Vinyl Chloride (VC1 Vinyl chloride is a chemical compound^that has been used in Canada's industrial and commercial sectors for over 50 years. The primary use of VC is in the production of polyvinyl chloride (PVQ, which is used to manufacture plastic and vinyl products such as electrical wire, food packaging materials, pipe, and other construction products. VC can cause significant adverse * Determining the period of time over which the benefits of the NSNR will accrue depends upon how the NSNR are viewed in relation to other public health and environmental regulations. For example, in the absence of the NSNR regulations, releases of hazardous substances into the environment will be regulated, but in all likelihood only after human health and environmental problems are discovered. Therefore, the benefits of the NSNR accrue between the introduction of the harmful (new) substance and when it would be regulated under the Canadian Environmental Protection Act. The extent of the damages caused in the interim is largely dependent on the nature of the substance. For instance, unregulated PCB discharges of only a few yean can cause 50 or more years of damages, as the substance is persistent in the environment. In contrast, VC is transient in the environment, limiting the time period over which damages are likely to occur. 1-11 CMA 114647 human health effects if production and use of the chemical are not regulated. In the early 1970s, unregulated indoor air concentrations at VC and polyvinyl chloride (FVC) production facilities were extremely high, causing a variety of health problems in plant workers. Further, releases to the ambient air posed significant health risks to those living near VC and PVC production facilities. As a result, the economic benefits of regulating the manufacture and use of VC are significant. As shown in Exhibit 1-6, the annual benefits associated with avoiding worker and general population cancer cases and occupational morbidity are estimated to range from SI52 million to $106.2 million, with a mean estimate of SS3.0 million; total benefits over 30 years, using a four percent discount rate and the mean annual benefits figure, are estimated to be S916.4 million. Additional avoided morbidity benefits may also exist, although we have been unable to-quantify these benefits. Dichloromethane i Dichloromethane is a clear, colorless liquid that is primarily used as a solvent in cleaning or stripping operations (e.g., as a metal pans degreaser), as a solvent and propellant in aerosol products, and as a blowing agent in the production of urethane foams. The benefits of controlling or prohibiting DCM use in Canada are significant. As summarized in Exhibit 1*7, the annual benefits associated with avoiding worker and general population mortality are estimated to range from $123 million to $58.2 million, with a mean estimate of $32.6 million; total benefits over 30 years, using a four percent discount rate and the mean annual benefits figure, are estimated to be SS63.7 million. Additional morbidity or ecological benefits may also exist, though we were not able to quantify such benefits in this report. Polychlorinated Biphenyls fPCBsl Polychlorinated biphenyls (PCBs) are a family of synthetic chemical compounds used extensively as a dielectric fluid in electrical equipment from the 1940s to the 1970s. PCBs can cause significant harm to the environment and human health if production, use, and disposal of the substance are not properly regulated. The results of our analysis indicate that there are significant economic benefits related to the regulation of substances like PCBs through the NSNR. We summarize the range of annual benefits and total benefits in Exhibit 1-8. For the extractive use benefit categories that we were able to monetize, we estimate annual benefits of $83 million to SS7.6 million, with a mean estimate of $303 million; the present value of these benefits over 30 years, using a four percent discount rate and the mean annual benefits figure, is $524.0 million. Our estimate of annual non-extractive use benefits ranges from $5.7 million to $37.4 million, with a mean of $19.1 million; the present value of these benefits, using the four percent discount rate and mean annual benefits figure, equals $3303 million. In addition, our estimate of annual passive use benefits ranges from $21.6 million to $86.4 million, with a mean of $54.0 minion; using the four percent discount rate and mean annual benefits figure for this category yields a present value benefits estimate of $9333 million. As illustrated by these totals, the direct (extractive and non extractive) use and passive use categories each account for roughly 50 percent of the total estimated benefits of controlling PCBs. 1-12 CMA 114648  IF exhibit 1-6 SUMMARY OF ANNUAL ANI) TOTAL BENEFITS: VINYL CHLORIDE ($1995, millions) Annual Benefits Present Value of Total Benefits -- 30 years | Category IjOW Mean High Low @ 6% Mean @ 4% High @2% ] Mortality General Population $10.3 $39.1 $80.0 $141.8 $676.1 $1,791.7 Occupational $4.2 $12.1 $22.9 $57.8 $209.2 $512.9 Morbidity General Population Unknown Unknown Unknown Unknown Unknown Unknown Occupational $0.7 $1.8 $3.3 $9.6 $31.1 $73.9 Ecological Total Sntall > $15.2 Small > $53.0 Small > $106.2 Small > $209.2 Small > $916.4 Small ?>$278.S | C M A114649 1-13 sasas9ss55ssssssss2assasss9Hssssssss^^^^=ss=ssssss:^^=ssas3Ssss&ssaKaB Exhibit 1-7 SUMMARY OF ANNUAL AND TOTAL BENEFITS: DICIILOROMETItANB ($1995, millions) i Calcgory Annual Benefits Low Mean High Present Value of Total Benefits -- 30 years Low @ 6% Mean @ 4% High @ 2% Morlatlly Ocncral Population Occupational 1 Morbidity )6.S $6.3 $16.7 $15.9 $30.0 $2B.2 $89.5 $66.7 $288.6 $274.9 $671.9 $631.6 B General Population 1 Occupational | Ecological ITM Unknown Unknown Sma|l > $12.8 Unknown Unknown Smafl > $32.6 Unknown Unknown Small >$582 Unknown Unknown Small > $1762 Unknown Unknown Smafl >$563.7 Unknown Unknown Small > $1,303.5 CMA 114650 o' 1-14 Category Extractive Use Recreational Fishing Waterfowl Hunting Trapping Commercial Fishing Subtotal Non-Extractive Use Bird Viewing Other Recreation Passive Use Homan Health Total Exhibit 1-8 SUMMARY OP ANNUAL AND 1DTAL BENEFITS: 1'CDs ($1995, millions) Ijow , - . Annual Benefits Mean High Present Value of Total Benefits - 30 yean Ijow (fit 6% Mean @ 4% High @2% | [ $7.3 $0.6 $0.4 Unknown $8.3 $5.7 Unknown $21.6 Not Estimated > $35.6 $2(>.9 $1.3 $11 Unknown $30.3 i1 $19.1 Unknown $54.0 Nol Estimated > $103.4 $47.3 $2.4 $7.9 Unknown $57.6 $100.5 $8.2 $5.5 Unknown $114.2 $37.4 Unknown $86.4 Not Estimated > $181.4 $78.5 Unknown $297.3 Nol Estimated > $490.0 . : $465.2 $22.5 $36.3 Unknown $524.0 $330.3 Unknown $933.8 Not Estimated > $1,788.0 $1,059.4 $53.8 $176.9 Unknown $1,290.1 1 $837.6 Unknown $1,935.1 Not Estimated > $4,062.8 1-15 I imitations The analyses described above are subject to certain limitations. A summary of these limitations for each substance follows. Vinyl <Ttinrite (VQ. To estimate the health effects associated with VC, we make a series of assumptions that introduce uncertainty into the analysis. For instance, our analysis of the incidence of VC-induced cancer in the general population is based on standard assumptions regarding the location and mobility of the affected population, whichmay over- or under-state total cancer cases. Further, our assessment of occupational health effects relies heavily on incidence data collected in the U.S.; we do not know the extent to which plant conditions may differ between U.S. and Canadian facilities. Finally, we have been unable to monetize certain health effects .in this assessment (e^, general population health effects other than cancer). Didiloromethane (DCM). Data limitations affect our ability to estimate occupational exposures for DCM, as it is difficult to estimate how many Canadian workers are chronically, exposed to significant levels of dichloromethane. While we extrapolate information from the U.S. to estimate occupational effects, it is difficult to assess how accurately this method approximates the exposed occupational population in Canada. Further, all the quantified benefits for DCM are based on chronic exposures. Since DCM is known to cause serious health problems when individuals receive acute doses, our health benefits are likely to be somewhat underestimated. Polychlorinated Biphenyls (PCBs). The most significant limitation of our analysis of PCBs is the lack of quantitative estimates for all of the possible benefits resulting from a Canadian environment free of PCBs. For instance, we were unable to estimate or monetize the benefits for commercial fishing and certain recreational activities (e.g^ boating and swimming), and at HCs instruction did not attempt to quantify the human health benefits of PCB control. In addition, numerous factors simultaneously affect the quality of. the aquatic environment, including toxic chemicals other than PCBs (e.g^ mercury, dioxins), pesticides, and municipal wastewater discharges. As a result, it is difficult to isolate the environmental impacts attributable to PCBs. Further, the long-lived nature of PCBs, along with nearly 20 years of PCB regulation, make it difficult to establish a base year from which to estimate annual benefits. ORGANIZATION OF REPORT The remainder of this report provides detailed information on the benefits of controlling or prohibiting the use and/or manufacture of vinyl chloride (Chapter 2), didiloromethane (Chapter 3) and polychlorinated biphenyl: (Chapter 4). Each chapter contains: 1-16 CMA 114652 Background information on the substance, including a description of the compound, information on its use and/or manufacture in Canada, and information on the releases of the substance into the environment; A description of human and ecological exposures to the substance; An overview of the benefits of controlling releases of the substance, using the benefits typology presented above; and A detailed description of the annual and tool benefits that result from controlling these substances. garh chapter also presents the specific limitations associated with these analyses, including key data gaps. 1-17 CMA 114653 REFERENCES FOR CHAPTER 1 Boyle 1991 Boyle, Kevin J. and John C Bergstrom. "Benefit Transfer Studies: Myths, Pragmatism and Idealism.* Water Resources Research, VoL 28, No. 3, March 1992, pp. 657-663. Canada Gazette 1994. "New Substances Notification Regulations," Canada Gazette, Part II, VoL 128, No. 7, 4 June 1994, p. 1481. De Gvita 1996. Letter from Paul De Gvita, Environment Canada, to Brian Morrison, Industrial Economics, Incorporated, 4 March 1996. Desvouges 1991 Desvouges, William, Michael Naughton, and George Parsons. "Benefit Transfer Conceptual Problems in Estimating Water Quality Benefits Using Existing Studies." Water Resources Research, VoL 28, No. 3, March 1991 pp. 675-683. Freeman 1993. Freeman, A. Myrick. The Measurement of Environmental and Resource Values: Theory and Methods. Resources for the Future. 1993. Unsworth 1993. Unsworth, Robert Elizabeth W. Snell and Mark Dickie, The Appicabiluy of a Benefits Transfer Approach to Assess the Economic Benefiss of Reduced Air Toxics Emissions Under the Clean Air Act. Industrial Economics, Incorporated, 1993. 1-18 CMA 114654 Appendix 1A SUPPLEMENTAL INFORMATION ON HEALTH RISK ASSESSMENT 1*19 CMA 114655 SUPPLEMENTAL INFORMATION ON HEALTH RISK ASSESSMENT This appendix provides background information on health risk assessment terms and methods that are used in Chapters 2 and 3. This appendix is divided into two sections. The first addresses carcinogenic health effects; the second addresses noncardnogenic health effects. Since the health risk assessment relies on data and techniques developed in large pan by the US. Environmental Protection Agency (EPA), the appendix focuses on US. EPA terms and methods. CARCINOGENIC EFFECTS' Toxicological assessment of potentially carcinogenic substances often indudes a rating of the "weight of evidence" concerning cardnogenidty. For example, the US. EPA assigns evidence from human and animal studies to one of five categories: (1) suffident evidence, (2) limited evidence, (3) inadequate evidence, (4) no data concerning cardnogenidty, and (5) no evidence of carcinogenicity. US. EPA's classification scheme is presented in Exhibit 1A-1. Exhibit 1A-1 US. EPA CLASSIFICATION SCHEME FOR CARCINOGENS Group Description A Human carcinogen; sufficient human evidence. B1 Probable human, carcinogen; limited human evidence. B2 Probable human carcinogen; suffident animal evidence, inadequate or no human evidence, or no human data. C Possible human carcinogen; limited animal evidence, inadequate or no human evidence, or no human data. D Not classifiable as to human cardnogenidty, inadequate human and animal evidence or no data available. E Evidence of noncardnogenidty for humans. Source: US. EPA, Guidelines for Carcinogen Risk Assessment, 51 FR 33992*34054,1986 In addition to the qualitative rating assigned to potentially carcinogenic substances, US. EPA develops substance-specific cancer slope factors (CSFs) for potential carcinogens. A CSF gives the increase in lifetime cancer risk for an individual continuously exposed to a substance, from birth to . 1 For more detailed information on EPA's method for estimating cancer risks, see U.S. EPA, Risk Assessment Guidance for Superfund, Volume l: Human HenJth Evaluation Manual, December 1989. 1-20 CMA 114656 death, per unit increase in the substance's concentration.1 CSFs provide estimates of risks asyyjateri with low-dose exposure to suspected or known carcinogens. They are estimated from data on high dose human exposures and/or high dose laboratory exposure to animals. The CSF for an agent with an "A* rating will be based - at least in part - on human data, while one with a "B2" rating will be based entirely on animal data. Generating a Cancer Sitme Factor In deriving a CSF, UJS. EPA evaluates available toxicological information about a chemical and selects an appropriate data set. In choosing appropriate data sets, human data of high quality are preferred to animal data. If animal data are used, the species'that responds most similarly to humans is preferable. If there is no dear choice among spedes for which data exist, data for the most sensitive spedes is given the greatest emphasis. Occasionally, when no single study is judged to be most appropriate, U.S. EPA may derive a CSF based on tbe geometric mean of slope factors from severai studies that collectively support the estimate. Concept of Nonthreshold Effects Carcinogens are assumed to have no threshold, ix^ there is no level of exposure that does not pose some probability, however small, of generating a carcinogenic response. Therefore, the development of a CSF usually involves extrapolating from tbe high doses administered to experimental animals to the lower exposure levels expected for human exposure in the environment. Because the extrapolation of the dose-response is to a range where data are not available, the actual CSFs are uncertain. Hence a large margin of safety is built into the slope factors. Generally, U.S. EPA takes a conservative approach in estimating a CSF by calculating the slope factor as the highest value that can be justified with 95 percent confidence. Thus, given the data, it is unlikely that the CSF is greater than that reported. Assessing Carcinogenic Risks A substance-specific CSF is multiplied by the substance-spedfic daily dose to estimate the incremental probability of a person developing cancer over a lifetime (70 years) as a result of exposure to the potential carcinogen. A cancer risk of 1 x 104 implies a probability of one in a million of developing cancer. * U.S. EPA, Integrated Risk Information System, 1995. 1-21 CMA 114657 NONCARCXNOGENIC EFFECTS* Unlike carcinogenic effects, noncarcinogcnic effects are assumed to occur only at exposures above a threshold concentration below which protective mechanisms and function reserve capacities prevent reactions to exposure. Therefore, a range of exposures exists from zero to some finite value that can be tolerated by the individual without the manifestation of an adverse effect. The reference dose (RfD) is an estimate of a daily exposure level for humans, including sensitive subgroups, that is not likely to cause adverse effects during a lifetime of exposure. To develop an RfD, it is necessary to identify the upper bound of a tolerance range for the most sensitive populations. Derivation Pf a Reference Dose In developing an RfD for a substance, U.S. EPA examines all available toxicity studies. If adequate human data are available, this information is used as the basis of the RfD. Otherwise, animal study data are used. When choosing the appropriate human or na1 study to use in deriving the RfD, U.S. EPA must make judgements regarding the relevance and quality of the available experimental studies. In addition, U.S. EPA must identify the effect characterized by the lowest observed adverse effect" (LOAEL), which is referred to as the critical toxic effect, and serves as the basis for the RfD. After the study and critical toxic effect have been selected, \JS. EPA identifies the exposure level that represents the highest exposure level tested in the study at which the critical effect was not observed. This highest "no observed adverse effect lever (NOAEL) is to develop the RfD. Applying Uncertainty Factors The RfD is derived from the NOAEL by consistent application of the following uncertainty factors (UF): A factor of 10 is used to account for variation in biological response to exposure among the general population and is intended to protea sensitive subgroups, such as the elderiy, from adverse effects. * A factor of 10 is used when extrapolating from animate to human* to account for interspecies variability. A factor of 10 is used when a NOAEL derived from a subchronic rather than a chronic study is used as the basis for a chronic RfD. * A factor of 10 is used when a LOAEL rather than a NOAEL is used as the basis for an RfD. For more detailed information on EPA's method for estimating noncancer risks, see U.S. HPA, Risk Assessment Guidance for Superfund Volume J: Human Health Evaluation Manual, December 1989. 1*22 CMA114658 In addition to the UFs listed above, a modifying factor (MF) ranging from greater than zero to 10 is used to reflea a qualitative professional assessment of additional uncertainties in the critical study and in the entire toxicity database for the substance not specifically addressed by the preceding UFs. The default value for the MF is 1.0. Calculation of the Reference, Dose To calculate the RID, the appropriate NOAEL (or LOAEL if a suitable NOAEL is not available) is divided by the produa of all of the applicable uncertainty iaaors and the modifying factor. The calculation is as follows: RfD NOAEL or LOAEUfUF, X UF;.. JC MF) RfDs are expressed in units of mg/kg-day. Asscssinr the Potential for Noncananoeenic Effects The Rfd assumes that there is an exposure threshold below which adverse effects will not occur. If the exposure level (dose) exceeds this threshold, adverse effects could potentially occur. This potential for adverse systemic effects is characterized by the hazard quotient (HQ). The HQ is calculated according to the following equation: HQ Dose/Rfd The greater the value of the HQ above one, the greater the potential for adverse effects. However, the HQ is not a statistical probability; a ratio of 0.001 does not mean that there is a one in one thousand chance of the effect occurring. Furthermore, the potential for adverse effects does not increase linearly as the RfD is approached or exceeded. 1-23 CMA 114659 VINYL CHLORIDE CHAPTER 2 OVERVIEW OF CHAPTER Vinyl chloride (VC), a commercially important chemical compound used in the plastics industry, can cause significant adverse human health effects if production and use of the chemical are not regulated. In this chapter, we characterize and value the health effects that could have been avoided if the New Substances Notification Regulations (NSNR) had been promulgated at the time VC was introduced into Canada. As described below, the New Substances Notification Regulations would have produced significant economic benefits by reducing individual and worker exposures to VC. Summary of Benefits In the early 1970s. unregulated indoor air concentrations at VC and polyvinyl chloride (FVC) production facilities were extremely high, causing a variety of health problems in plant workers. Further, releases to the ambient air posed significant health risks to residents living proximate to VC and PVC production facilities. As a result, the economic benefits of regulating the manufacture and use of VC are significant As shown in Exhibit 2-1, the mean annual benefits associated with avoiding worker and general population cancer-cases and occupational morbidity are estimated to be S53.0 million dollars per year, total benefits over 30 years are estimated to be $916.4 million, using a four percent discount rate. Further, additional avoided morbidity benefits may exist although we have been unable to quantify these benefits for purposes of this report. 1 imitations To estimate the health effects associated with VC, we make a series of assumptions that introduce uncertainty into the analysis. For instance, our analysis of the incidence of VC-induced cancer in the general population is based on standard assumptions regarding the location and mobility of the affected population, which may over- or under-state total cancer cases. Further, our assessment of occupational health effects relies heavily on incidence data collected in the U.S.; we 2-1 CMA 114660 do not know the extent to which plant conditions may differ between U.S. and Canadian facilities.1 Finally, we have been unable to monetize certain health effects in this assessment (e^, general population health effects other than cancer). Specific data limitations are discussed in later sections. EihibitM SUMMARY OF ANNUAL AND TOTAL BENEFITS: CONTROLLING VC MANUFACTURE AND USE IN CANADA PfUffitV Hst^DBlcs ($1995, minions) . Category Annual Benefits Present Value of Total Benefits (30 yens, 4%) Mortality General Population Occupational S39.1 '$12.1 $676.1 $209.2 Morbidity General Population Occupational Unknown S1.8 Unknown $31.1 Ecological Small Small Total >$53fi >$916.4 Orwnitinti of Chapter This chapter is organized into six sections. The first section provides a general description of the VC and PVC industries, including information on VC releases into the environment. We then summarize available data on human health and ecological exposures to VC in uncontrolled settings. The third section describes the health effects that commonly result from VC exposures, covering both carcinogenic and non-carrinogenio- effects. The fourth and most lengthy section of this chapter provides a detailed description of the methods and assumptions used to estimate the incidence of cancer and other health effects in workers and the general population. The final two sections present annual and total benefits estimates, respectively, based on the incidence levels developed in the fourth section. 1 As discussed later in this chapter, we have developed a range of benefits estimates to reflect the uncertainties present in the benefits categories we quantify. ^ 2-2 CMA 114661 BACKGROUND INFORMATION ON VINYL CHLORIDE DesermtioB of the Componnd VC is a chemical compound that has been used in Canada's industrial and commercial sectors for over 50 years. It is a synthetic chemical with no known natural sources. A colorless petrochemical gas, VC has a mild, sweet odor, is slightly soluble in water, and is highly soluble in fats and organic solvents. In addition, VC has a low boiling point, a high vapor pressure, and is a known human carcinogen (U.S. EPA 1994b; VC in Drinking Water 1992). ' The primary use of VC is in the production of PVC PVC is used to manufacture plastic and vinyl products such as electrical wire, insulation and cables, industrial and household equipment, medical supplies, food packaging materials, piping, and other building and construction products. PVC is also used as a raw material in the paper, glass, rubber, and automotive industries, and in the production of 1,14 trichloromethane (VS. EPA 1994b; VC in Drinking Water 1992). In addition, VC was once used as a refrigerant in cooling equipment and as an aerosol propellant in some cosmetics, drugs, pesticides, and other consumer products (Doniger 1978); these uses were discontinued when VCs carcinogenic properties became known. Information on Manufacture in Canada Unlike PCBs and dichloromethane, VC and PVC are manufactured in Canada. The nation's major production facilities - including two VC plants and four PVC plants - are located in Alberta, Ontario, and Quebec. The locations of these plants are presented in Exhibit 2-2. Expansion of these facilities over the past 20 years has increased domestic production of both VC and PVC These facilities, however, are highly mechanized, requiring a relatively small number of workers. Fabrication plants, which manufacture end-use consumer products using PVC resins, are more labor intensive (Doniger 1978). Eihjbtt22 LOCATIONS OF VC AND PVC MANUFACTURING PLANTS Type of Plant Region VC and PVC Fort Saskatchewan, Alberta VC and PVC Sarnia. Ontario PVC Niagara Alls, Ontario PVC Shawinigan, Quebec Source: EC 1986 2-3 CMA 114662 Two primary processes are used to produce VC One involves the pyrolysis of ethylene dichloride (EDC): ethylene is chlorinated to EDC which is then thermally' dehydrochlorinated, producing VC and HO (EC 1986). The other process involves the hydrochlorination of acetylene. In the presence of a catalyst, a vapor-phase reaction occurs between acetylene and hydrogen chloride, producing VC (Lowenbeim 1975). To produce PVC, the monomer VC is polymerized. The concentration of VC entrapped in PVC depends upon the production process; it can range from (U to 8,000 ppm (VS. EPA 1975). In Canada, concentrations ofVC monomer in PVC were reduced drastically between 1973 and 1975, and range from 1 to 10 ppm (VC in Drinking Water 1992). tn thf Fnvipntiwnt Emissions and effluents from VC and PVC processing plants are the primary sources of VC in the work place and in the environment. There are, however, other pathways by which VC can enter the environment, including accidental spills and the outgas of VC from plastic products. Other release routes include the disposal of VC wastes in landfills; the biodegradation of trichlorethylene, tetrachloroethylene and 1,1,1-trichloiomethane; the evaporation of chemical wastes; and tobacco smoke (ATSDR 1993). Once VC enters the environment, it can affect a variety of environmental media. Because VC is highly volatile, it vaporizes easily. Therefore, most VC releases end up in the atmosphere. There is potential for the contamination of other environmental media, however, such as water and soiL The following subsections provide a detailed description of atmospheric, water, and soil contamination from VC releases, as well as potential release routes. Atmospheric Contamination The primary sources of VC in the atmosphere are VC and PVC plant emissions. PVC manufacturing facilities account for approximately 85 percent of VC emissions, while VC facilities account for approximately ten percent* Data on total VC emissions to the atmosphere in the early 1970s from uncontrolled plants are limited; it w estimated, however, that a total of 4,500 tons of VC were emitted to the ambient air in 1973. After imposing controls on VC emissions from VC and PVC plants, emissions were reduced by about 95 percent (EC 1986). VC emissions from VC and PVC plants can be categorized by source: regulated point sources, incidental releases, and fugitive emissions. Regulated point sources include equipment such as the reactor, which may release VC when it is opened for cleaning, maintenance and inspection; the VC condenser, which discharges VC to the atmosphere after treatment by air strippers or other pollution control devices; equipment downstream from the stripper; and process vents. Emissions from incidental releases generally come from emergency venting due to the malfunction or breakdown of equipment. Fugitive emissions originate from sources other than the vent, stack, Due,3 3 The remaining five percent comes from the plastics fabrication industry and other minor sources. 2-4 CMA 114663 or other openings that are specifically designed for the purpose of emitting VC Fugitive emissions can be caused by leaking valves, flanges and seals, open-ended lines, drains, vessel opening losses, building ventilators, and open ponds. Individual occurrences of fugitive emissions may be small although total fugitive VC releases can be large when emissions from all possible sources are summed (EC 1986). Transportation accidents are another source of VC releases to the atmosphere, as not all VC is polymerized into PVC at its initial point of production. VC is typically shipped to PVC factories under pressure as a liquefied gas. In the U.S., for example, about 95 percent of VC is shipp d in rail tank cars; the rest is shipped in tank trucks, barges, and tank vessels. An accidental leak, puncture or explosion of these, containers can release the liquefied gas, which is then likely to evaporate into the atmosphere and pose a potential health risk to transportation Workers, nearby residents, travellers, and safety officers (Doniger 1978). Other potential sources of VC in the atmosphere include the outgas of VC from new plastic products and the volatilization of VC products in municipal and hazardous' waste landfills. In addition, VC is released in the indoor air of VC and PVC plants. As a result, VC and PVC workers without proper protection can be exposed to potentially significant concentrations of the compound. Water Contamination VC releases into the environment can also afreet surface water, groundwater, and drinking water. Surface Water. The most likely source of surface water contamination is wastewater from VC and PVC manufacturers. In Canada, the effluent from the production of PVC is discharged into a variety of waterways, including a waterway in Quebec and the Welland River and St Clair River in Ontario (EC 1988). VC reaching surface water via contaminated effluent is likely to migrate rapidly, on the order of hours or days, to the air (ATSDR 1993). The presence of materials such as fumates, surfactants, and particulates, however, may extend the residence time of VC in water (U.S. EPA 1980). Groundwater. VC can leach into groundwater as a result of spills, leachate from landfills and hazardous waste sites, and effluents from the plastics industry (ATSDR 1993). In addition, the biodegradation of trichloroethylene and perchloroethylene in groundwater can form VC For a variety of reasons, including resistance to microbial degradation, VC can remain in groundwater from months to years (VC in Drinking Water 1992). Drinking Water. Small amounts of VC may be present in public water supplies as a result of industrial wastewater discharges (US. EPA 1980) or as a result of groundwater contamination (see above). The occurrence of VC in potable water, however, is primarily associated with the conveyance of water via PVC pipes manufactured with incompletely polymerized VC monomer. These extremely small amounts of entrapped VC monomer can leach from PVC pipes (VC in Drinking Water 1992). Since the level of ^ 2-5 CMA 114664 residual VC that is not moleculariy bound m PVC pipe is extremely low, exposure to VC. via this patinny is considered unlikely (Coiner 1996). Sog runtmjfaariwi The primary sources of VC releases to soil are spills, effluent discharges, and from disposed VC materials. VC is likely to volatilize rapidly from dry soil surfaces, however, due to. its high vapor pressure. VC placed ten centimeters deep in dry soil, for example, is expected to`have an effective half-life of about 12 hours. In addition, VC has' a low soil organic* carbon, adsorption coefficient, and is highty mobile in soil, suggesting a strong potential to migratefrom soil to groundwater (ATSDR 2993). HUMAN AND ECOLOGICAL EXPOSURES TO VINYL CHLORIDE This section describes the concentrations of VC to which hum*TM and biota were likely t be exposed in the early 1970s. The focus of this section (and the remainder of the analysis) is on human health, as ecological impacts are a relatively minor concern for this compound. The following subsections describe the most common pathways for human exposure to VC, and the concentrations at which VC was found in different subpppulations. We also provide a brief summary of potential ecological effects of VC exposure. As discussed in the fust chapter of this report, we focus on emissions from uncontrolled VC sources to estimate human exposures in this analysis. This approach follows logically from the ultimate goal of this project, to evaluate the benefits of controlling or prohibiting new substances. As a result, much of the information we present in this section is based upon data from the 1970s, when VC emissions were largely uncontrolled. Human F-rposures VC and PVC workers and individuals Irving in close proximity to VC and PVC production facilities were exposed to the greatest concentrations of VC Exhibit 2*3 mmnwriyes the typical concentrations to which various subpopularions were exposed in uncontrolled conditions. 2-6 CMA 114665 Exhibit 2-3 TYPICAL EXPOSURE TO VINYL CHLORIDE VIA INHALATION IN THE EARLY 197fe SubpopuhUxm General population Oppb Individuals living in dose proximity to VC and PVC plants ' 0 to 814 ppb Average VC and PVC workers 1 to 100 ppm Maximally | workers VC and PVC 250 to 300 ppm VC concentrations in ambient air were generally fairly low. Background levels of VC are often expressed in pans per billion (ppb), whereas indoor air concentrations of VC in VC and PVC plants are expressed in parts per million (ppm). The average concentration of VC to which populations living in the vicinity of emissions sources were exposed ranged as high as 814 ppb (ATSDR 1993). For individuals not living in the vicinity of point sources, exposure to VC via inhalation was expected to be essentially zero. Inhalation is also the primary route for occupational exposure. Workers responsible for cleaning reactor vessels, which are the chambers in which VC is convened to PVC in polymerization plants, were frequently exposed to airborne concentrations on the order of 250 to 300 ppm (Amdur 1991). In addition to inhalation, humans can be exposed to VC via ingestion. As discussed above, VC can be found in drinking water at very low concentrations due either to the contamination of underground sources of drinking water or to the migration of VC from PVC pipes. In addition, VC can migrate from packaging material containing VC into food, since the monomer is soluble in alcohols and mineral oil The presence of VC in drinking water or food, however, was relatively uncommon, and the average daily intake of VC through diet was essentially zero (ATSDR 1993). The only potentially significant exposure to VC via ingestion was found in PVC production plants, where workers could have been exposed to VC through the ingestion of PVC dust containing entrapped VC monomer (U.S. HPA 1975). Ecological Exposures Data on the ecological effects of VC contamination are limited. It is unlikely, however, that VC releases to the environment posed a threat of significant ecological damage, due to the quick volatilization of VC into the atmosphere. The potential for biomagnification in the food chain does not appear to'be important because of the high volatility of VC and the fact that it is readily metabolized by higher-trophic-level organisms (ATSDR 1993). 2-7 CMA114666 Qpe of the by-producu of VC production may cause ecological damage if discharged into aquatic environments, as this by-product (EDC tar) can adhere to suhstances such as plankton. In addition, ^nimak rapidly accumulate EDC tar from contaminated sea water. Since these tan have a xegj9M|short half-life, ecological effects from exposure were likely to be much less severe than fromlSpure to other types of chlorinated hydrocarbons (US. EPA1975). THE BENEFITS OF CONTROLLING VINYL CHLORIDE RELEASES: OVERVIEW litis section provides an overview of the benefits associated with the prohibition or control of VC in Canada, Theprimary benefits of controlling VC emissions axe reductions in mortality and morbidity due to VC exposures in the general population and among VC and FVC workers. Once VC is inhaled or ingested, h can cause a variety of advene health effects. In this section, we summarize the considerable amount of information available on the health problems related to VC exposure.* ** Mortality from In the early 1970s, the cancer-causing capacity of VC was recognized. The available epidemiological studies tend to focus on the incidence of angiosarcoma of the fiver, a rare form of cancer, because of the ability to draw a causal relationship between exposure to VC and the development of tumors. Exposure to VC fay inhalation is also suspected to increase the risk of cancer of the brain, lung, and digestive tract (US. EPA 1994b). The types of cancer associated with VC are often fataL Studies demonstrate, for example, a significant association between exposure to PVC dust and the risk of lung cancer mortality (Wagoner 1983). The avenge fife expectancy (post-diagnosis) for an individual who has contracted cancer via exposure to VC is estimated to be 0.4 to 8.9 yean (Sax 1981). Due to the nature of these VC related cancels, we value the cancer cases estimated from VC exposures (later in this chapter) as fatalities. Morbidity **toton to cancer, VC can cause a variety of other deleterious health effects. For mStanCe* iSEn*1"16 can c*usc fiepwfc. respiratory, cardiovascular, gastrointestinal, hematoloMK^eusculoskeletal, renal, and dermal/ocular problems. Specific examples of comm n VC-relatqj^Hpms are listed in Exhibit 2-4. A number of studies suggest that eptiiw to VG^tnqr^^Pptextia]f ftmction and lionnonal lm^' fri lniimtnrand animals (ATSDR 1993). In addition, MMAb stwfies sbfgfit-ag6hHricaIly significant increase"in-chromosomal aberrations in humans exposed to VC, and a variety of studies show that members of communities with nearby VC A 2-8 CMA 114667 polymerization facilities have greater incidences f some forms of developmental toxicity/1 For example, some of these studies show an excess of fetal loss when falhcrs.have been .opposed to VC These studies and others, however, fail to demonstrate a statistically significant correlation between developmental toxicity and either parental occupation or proximity to the facility (ATSDR 1993). NONCARONOGENIC HEALTH EFFECTS FROM VINYL CHLORIDE EXPOSURE Type of Exposure Hfhh Acute exposure to high levels of VC Dizziness, headaches, giddiness,- light-beadedness, nausea, poor memory, tingling sensations, weight loss, chronic bronchitis Chronic exposure to lower levels of VC Liver damage, Raynaud's syndrome, circulatory disturbances in extremities, thrombocytopenia, dermatitis, sderodenna-like skin changes, lytic lesions of the terminal phalanges in bands and feet, pseudo clubbing of fingers, thyroid insufficiency, damage to the spleen and lungs, functional disturbances of the central nervous system Source: ATSDR 1993 ESTIMATING HUMAN HEALTH EFFECTS The following discussion provides specific information on the health-related benefits of controlling VC in Canada. In particular, we describe the detailed methodologies used to estimate general population and occupational cancer cases, as well as morbidity effects in workers. The information developed in this section (e.g, wwiwwi annual cancer cases) serves as the basis for the benefits estimates developed in the following section. Cancer_Cases_Resulting from Exposure to Vinyl Chloride General Population In 1973, the U.S. Environmental Protection Agency conducted a health risk assessment for community exposure to VC in support of regulating air emissions around VC and PVC plants (Kuzmack 1975). To estimate potential exposures, EPA divided the area surrounding each plant into four bands ranging up to five miles from the plant Through standard diffusion modeling of over 40 plants, the annual average ambient VC concentrations in each band were calculated. Detailed information for each individual plant was weighted to reflea differences in the type of plant size of plant, and meteorological and topographic conditions at the plant site. The results were then used to estimate average VC exposures for individuals living in the vicinity of a "model* VC or PVC plant ' Developmental toxicity is the occurrence of adverse effects that may result from exposure^ to a chemical prior to conception, during prenatal development, or postnatally to the time of sexual maturation. 2-9 CMA 114668 We me a TM8r approach to estimate potential VC exposure for the population living dose toVCandPV&ptantt. Rug, w animate the m of the affected population. Because the VC and PVC industry ft based in only four Canadian cities, the size of this subpopulation is relatively small. Exhibit 2*5 praams estimates of the population that resides within specified distances of Canada's two VC and four PVC plants. We developed these estimates using information on the total size and density of the population in each of the cities of interest. A detailed description of how these estimates were developed is provided in Appendix 2A. BAB*2-5 ESTIMATED POPULATION LIVING WITHIN A FIVE-MILE RADIUS OF VC OR PVC PLANTS Dittance from Plant VC Hants PVC Hants Band 1 (0-05 mi) 1,444 2376 Band 2 (05-1 mi) 4,331 8329 Band 3 (1-3 mi) 38.142 61313 Band 4 (3-5 mi) 42340 107389 To estimate the concentrations of VC to which individuals within each band might be exposed, we use the ambient air concentrations provided in the US. EPA study, which are presented in Exhibit 2-6. These figures represent average annual VC concentrations in ambient air near an uncontrolled VC and PVC plant under typical meteorological conditions.4 As shown in this exhibit, VC concentrations are higher around PVC than VC plants. Further, as one would expect, concentrations drop substantially with from the facility. Exhibit 2-7 summarizes our high-end estimates of the number of cancer cases associated with each type of facility. As shown by the rows labelled "VC Concentration" and "Dbse", we estimate the annual dose of VC to which the average person in each band could be subjected based on the estimated annual average concentration of VC to which the individual is exposed, adjusted for average aduh inhalation rates and body weight3 We calculate the individual lifetime ruftcer by multiplying the dose by the cancer slope factor for VC exposure via inhalation.* Finally, we *Tbti *ir concentration estimates presented in the US. EPA study are a result of two independent] SS, the results of which differed by less than 25 percent The data presented in the EPA at included variations in meteorological conditions from location to location (Kuzmack 1975). 3 The average adult inhalation rate is assumed to be 20 mVday, and the average adult body weight is 70 kg (U.S. EPA 1989). * The inhalation cancer slope factor for vinyl chloride iSip^mg/kg-day^CUi). EPA 1994a). ^ 2-10 CMA 114669 the number of annual cancer cases by multiplying the population by the cancer risk and dividing by the average lifespan (70 years)- The rows labelled "Annual Cancer Cases" in Exhibit 2-7 provide a summary of our best high-end estimates of the number of cancer cases likely to be prevented under the New Substances Notification Regulations for those individuals living near a VC or PVC plant7 As shown at the bottom of the exhibit we estimate that 1.7 cancer cases would occur around VC facilities and 9.5 cases around PVC facilities, for a total of 11.2 avoided annual cancer cases. Exhibit 2-6 AVERAGE ANNUAL VINYL CHLORIDE CONCENTRATIONS IN AMBIENT AIR Vinyl Qikmde Ccvecnxntkm (ppb) Distance from Plant VC Plant PVC Plant Band 1 ((HX5 mi) . . 113 323 Band 2 (0.5-1 mi) 20 57 Band 3 (1-3 mi) 5 15 Band 4 (3-5 mi) 2 6 Source: Kimnaek 1975 An on-going U.S. EPA review ofVCs cancer slope factor suggests that the number of cancer cases estimated above may be high. Thcnew slope factorwiH-incorporate pharmacokinetics, which wilTreduce the dope factor and thus, the' indmdt^JpeScoelrancer risk (Guth 1996).' To reflect this information, we have calculated low-end estimates by dividing our high-end estimates by a factor ofTO. As a result, we value the general population mortality benefits in the next section by using annual case estimates that range from 1.1 to 112 annual cancer cases.* 1 1 A detailed example of how these estimates are developed is provided in Appendix 2B. 1 Pharmacokinetics represents the movement of a substance within the body, which is affected by the uptake, distribution, elimination and transformation of the compound within the body. Thus, a'pharmacokinetic model develops an estimated internal dose of the contaminant that is a more accurate measure of exposure than the applied dose. ^ 2-11 CMA 114670 T GENERAL POPULATION GANCSR CASES: HIGH-END ESTIMATE VC Plant PVCPhnt Band 1 ((MLS mi) VC Concentration 1,444 0294 mg/mJ 2576 0840 mg/m* Done. 0084 (mg/kg-day) 0240 (mgAg-day) Cancer Ride 25X10* 72X10* Annual Cancer Can 05 30 Band 2 (05-1 mi) VC Concentration 4531 0052 mg/m* 8,629 `0.148 mg/m* Doae 0015 (mg/kg-day) 0.042 (mg/kg-day) CunrRtt 45X10* 12X10* Annual Cinrrr Cases 03 15 Band 3 (1-3 mi) VC Concentration 38.143 0014 mg/m3 61213 0.039 mg/m3 Doae 0004 (mg/kg-day) 0011 (mg/kg-day) Cancer Risk 15X10* 33X10* Anonal Cancer Cases 06 23 Band 4 (3-5 mi) 42540 0005 mg/m3 107589 0015 mg/m3 Doae 0.001 (mg/kg-day) 0.004 (mg/kg-day) Cancer Risk 45X10* 13X10* . Annual Cancer Cases TOTAL ANNUAL CANCER CASES 03 L7 20 95 >s. f- 2-12 CMA 114671 limitations The methodology described above requires a series of assumptions^ that [may introduce uncertainly the results of this analysis.; For instance, we assume that the population is evenly distributed throughout the reglim! and mat*the VC or PVC plant is located in the center of the region. Further, our approach assumes that the potentially affected population breathes the ambient air within their respective band 24 hours a day, seven days a week, 365 days a year. Our methodology does not consider the travel patterns and daily mobility of each population, and thus the variation in levels of VC exposure. These simplifying assumptions may lead to an over* or under-estimate of cancer cases among the subpopulation surrounding VC and PVC plants. Occupational Before much attention was given to the monitoring of VC levels in the work: place, indoor air concentrations exceeded what health authorities now consider to be acceptable exposure levels.' In the absense of regulations and subsequent controls on VC-related activities, it is possible that VC and PVC workers could be subject to potentially significant cancer risks.10 Estimating Annual Cav* To estimate the annual cancer cases expected within the population of VC and PVC workers under unregulated conditions, we must first estimate the size of the affected occupational population. We do so using data from U.S. VC and PVC facilities. In the early 1970s, 940 production workers were engaged in VC production at 17 U-S. plants, for an average of 55 workers per plant. At PVC facilities, approximately 5,600 workers were engaged in production at 40 facilities, for an average of 140 workers per plant (U.S. EPA 1975)- In Exhibit 2-8, we use these average figures, adjusted upward and downward by 50 percent to account for uncertainty, to project the average number of Canadian workers potentially exposed to high concentrations of VCIU3 As shown in this exhibit, we estimate that between 336 and 1,006 Canadian production workers could be exposed, in the absence of occupational and environmental safety standards, to high concentrations of VC * As of 1978, high levels of VC in the workplace were believed to be responsible for angiosarcoma of the liver in at least 68 workers worldwide (Doniger 1978^ * For the purpose of this analysis we..ignore the; potential mitigation of health risks by occupational health:and safety requirements,- which may only be applied after a problem is discovered. 11 For instance, the "low" estimate of VC workers per plant is simply 55*0.5, or 28 workers. ' a The adjustments for uncertainty reflea the faa that we do not have adequate information on labor intensity and plant size across U.S. and ("anariiap facilities. ^ 2-13 CMA 114672 &d**24 ESTIMATED VC AND PVC WORKER POPULATION IN CANADA VC PVC Total Weskers per plant 28-83 70-210 -- Total, all phots . 56-166 280 - 840 336 - 1.006 The remaining data we use to estimate annual cancer cases among VC and PVC workers is derived from published epidemiologic studies of health effects among workers who were exposed to high concentrations of VC before 1974. We take this approach for two reasons. First, although these studies do not include specific estimates of worker exposure levels, they do provide the most direct indication of the health risks associated with working in these pints. Second, the available cancer slope factor for VC is applicable to exposures up to only several hundred jtg/m1 (approximately 0.1 ppm). It has been well documented that in the U.S. before 1974, exposure to VC concentrations of 250 to 300 ppm was common for many job categories in VC and PVC industries (Doniger 1978). In short, the expected ambient concentration of VC in. the air of uncontrolled VC nd PVC pints significantly exceeds the upperbotmd concentration for which the cancer slope factor is appropriate. Based on a review of four different studies, the US. EPA estimated that the incidence rate of liver angiosarcomas among highly exposed VC and PVC workers (Le^ working in areas with VC concentrations of roughly 200 to 500 ppm), adjusted for the average latency period, is approximately 3J x 10 cases per worker-year of exposure (Ktmnack 1975). Assuming an average career length of 20 yean for these workers, their intfividual lifetime cancer risk is estimated to be 62 x 10*. In other words, approximately six percent of all highly exposed VC and PVC workers would be expected to contract liver angiosarcoma during the course of their lifetime. If we assume that all of the VC and PVC workers in Canada were exposed to high levels f VC in the early 1970s and would have continue4,to be subject to these exposures in the absence f the Regulations, theinddence rate of cancer among VC plant workers would range from 3.4 to 10.0 cases and among PVC plant workers would range froth 1&8 to 50.4 cases, for a total ranging from 20-2 to 60.4 cases. An incidence rate of 20.2 to 60.4 cancer cases is equivalent to approximately one to three total cancer cases per work year for a work force of rite size presented in Exhibit 2-8.M T-t uncommon for peak exposures to read) up to 4,000 ppm for short amounts of i other occupations, before the control of VC levels in the work place, are likely to have been exposed to lower and less sustained <iww*ratio3 One to three cancer cases per work year is high for a relatively small work force. Therefore, it^is unlikely that this situation would continue unabated year after year once the problem was dtscovered. The benefits assodated with even a few years of improved control, however, are significant > 2-14 CMA 114673 ^nytations In ftwiipatinnat effects, we use incidence information from U.S. workers. To the extent that and U.S. worker exposures are different, our estimates could be under or over estimates. Further, we do not take into account the incidence of other types of cancer in the above assessment (i r. cancers other than angiosarcoma of the liver), as we only have qualitative information on the tnadg" of other types of cancer. To the extent these cancers would occur, the estimates presented above could be under-estimates. Nonearcinogenic Effects from fanoanc to Vmvl CMoride General Population: Point Source Exposures Because uncontrolled VC and PVC plants emit high concentrations of VC to the ambient air, individuals living within a five mile radius of these plants could experience nonearcinogenic health effects related to VC emissions. We determined the likelihood of risk of nonearcinogenic effects by calculating a hazard quotient for potentially exposed populations. The hazard quotient is the ratio of the expected dose to a reference dose (RfD) or reference concentration (RfC); a hazard quotient greater than one is an indication that some nonearcinogenic effects may occur.1153 * Generally, an RfD or RfC is used to determine the level below which there are no observed adverse impacts in humans due to daily exposure to a particular toxic substance. The U.S. Environmental Protection Agency, however, has not established an RfD or RfC for VC (ATSDR 1993). Instead, a minimal risk level (MRL) for VC of 0.002 ppm has been derived by ATSDR, based on an animal study.14 Exhibit 2*9 presents the hazard quotients for each band surrounding a VC or PVC plant As indicated in this exhibit, the hazard quotients for individuals living within each band equals or exceeds one in all cases. This information suggests that there is a considerable likelihood that some nonearcinogenic effects could occur in the general population due to VC exposures. We note, howeveiythar US.EPA isinthe process of developing an RfC forVC Although this value has not been released as of yet it is likely to be higher than the MRL established by ATSDR (Guth 1996), which would produce lower hazard quotients. As a result we believe that the figures presented in Exhibit 2-9 should be employed with caution. 13 See Appendix 1A for more information on this topic. w The results of a study conducted by Bi, et al (1985) indicate that exposing rats to 10 ppm of VC for six hours a day, six days a week, for six months of the year, results in increased liver weight The lowest bbseived advene effect level (LOAEL) is 10 ppm/ ATSDR used the results of this study to establish the MRL of 0.002 ppm for humans, using a series of adjustment factors. The adjustment factors account for (1) the difference between intermittent and continuous dosing, (2) the uncertainty surrounding the difference between a LOAEL and a NOAEL, (3) the uncertainty surrounding the extrapolation from animal data to humans, and (4) the uncertainty surrounding hUman variability. The MRL is meant to be used for screening purposes only. The MRL is not used for regulatory action. 2-15 CMA 114674 Exfa2>*t2-9 GENERAL POPULATION NONCARONOGENIC EFFECTS - VC Plant Band 1 (0-CL5 mi) Dose is (mg/kg-day) Hazard Quotient 0084 57 Band 2 (0l5-l mi) Dose in (mg/kg-day) Hazard Quotient 0015 10 Band 3 (1-3 mi) Dose in (mg/kg-day) Hazard Quotient 0004 4 Band 4 (3-5 mi) Dose in (mg/kg-day) Hazard Quotient 0001 1 Note: MRL 0.002 ppm 0.001 (mg/kg-day) PVC Plant 0240 162 0.042 29 . 0011 8 0005 3 General Population: Other Exposures The general population as a whole may lace health risks from VC exposure due to sources of release other than emissions from VC or PVC plants, such as transportation accidents, drinking water contamination, or direct use and disposal of VC under unregulated conditions. In the following subsections, we briefly describe these other sources of VC release and discuss their potential contributions to adverse health effects in the general population. The discussion focuses on noncarrinogenic health effects, since the incremental cancer risks associated with these sources of release are likely to be dwarfed by the cancer risks associated with emissions from VC and PVC production facilities. Transportation Accidents VC produced in Canada is shipped fay pipeline to neighboring PVC plants and by railroad to other plants in Canada, the U.S. and Mexico. VC was also once shipped in tank trades; but this practice wascgscantinued in 1975 due to the unacceptable risk of highway accidents (EC 1986). Shipment QfgpCby nil reduces the risk of accidental release, but does not totally eliminate it In 1980, for exsByfc, a train derailment in MacGregor, Manitoba resulted in a spill of 49.7 tons of VQ accidental remises of VC from tank cars have also occurred in the U.S. Nonetheless, the safety record for VC transport in recent years has been good, suggesting that the risk of noncardnogenic health effects in the general population resulting from transportation accidents is likely to be small * 2-16 CMA 114675 Tanking Water In the absence of regulatory controls, the general population might be exposed to elevated concentrations of VC in drinking water,*due primarily;to the leaching of^YC from PVC pipes. The available data, however, are insufficient to allow us to estimate the extent to which such exposures might occur. For example, the leaching of VC from PVC pipes depends on several factors, including dwell time, which is the period of time water stands in the pipes; leaching rate, which is determined by the amount and distribution of VC in the pipe and in the water, the equilibrium partitioning of VC between the pipe and the water, and the diffusion of leachate out of die pipe and into the air. Few data exist on pipeAvater partitioning coefficients or plastic pipe diffusion coefficients, making the prediction of VC concentrations in water difficult (Podoll 1986). Despite these limitations, the available data suggest that the risks associated with VC in drinking water are likely to be several orders of magnitude below the risks associated with inhalation of VC production emissions. For example, a drinking water study conducted by the U.S. Environmental Protection Agency examined VC concentrations in the drinking water of five water distribution systems using PVC pipes. The highest VC concentration was 0.54 ppb, which came from the most recently installed and longest pipe system. Traces of VC (0.012 to 0.023 ppb) were found in two other systems nine years after installation (VC in Drinking Water 1992). These concentrations are so low that the risks of adverse health effects appears minimal. Other VC Uses and Releases In the absence of regulation, VC might be used in a variety of consumer products. The associated adverse health effects would depend on the type and extent of use, manufacturing processes, and subsequent disposal practices. Since the range of potential practices is highly uncertain, we have not attempted to analyze the health risks they might present Occupational As discussed earlier in this chapter, VC-is known to cause a number of noncarcinogenic health effects in workers exposed to high concentrations of the substance. Information on the incidence of various effects, based on research reported by U.S. EPA in the 1970s, is summarized in Exhibit 2*10. As shown in this exhibit the incidence rates for a number of these health effects are quite high, particularly for exposed workers. While they do not present detailed exposure data for these workers, these studies do provide a dear indication of the range of potential noncarcinogenic effects for workers exposed to VC To provide an indication of the quantitative benefits of reducing or eliminating these health effects, we assume that 10 percent of all highly exposed workers would suffer from one or more -noncarcinogenic effects that would impair their daiiv activities. Based on a worker population of between 336 and 1,000 (see Exhibit 2*8), we estimate that between 34 and 101 workers would be thus affected if VC emissions were uncontrolled. 2-17 CMA 114676 Exhibit 2>10 INCIDENCE RATE OF OCCUPATIONAL NONCARQNOGENIC EFFECTS Study Hcrith literature Review of 12,724 FVC Workers Acroostaolysis1 Raynaud's Syndrome Symptoms2 Sirin [mwih 09% 08% 03% Clinical Observations of 50 Highly Eiposrd PVC Workers Liver Disturbances1 Raynaud's Syndrome Symptoms2 Liver Disturbances1 06% 16% 76% Uver Function Screening Programs for 1,183 PVC Workers Liver Function Abnormalities4 4.8% Source: Kuzmack 1975 Notes: 1. Gradual erosion of bone at fingertips 2. Cold hands and feet 3. Changes in liver function suggestive of cellular liver damage 4. Abnormalities considered serious enough by plant physicians to justify moving workers to areas where there is no exposure to hepatic toxins 1 | VALUING HUMAN HEALTH EFFECTS: ANNUAL VALUES In this section, we describe the process of valuing the health effects analyzed above. As indicated in Exhibit 2*11, we estimate the mean annual benefits associated with avoided morbidity and mortality to be S53.0 million. Below we discuss our approach and calculations. Exhfct2-ll SUMMARY OF BENEFITS ESTIMATES Gtiegmy Mortality General Population Occupational Morbidity General Population Occupational Ecological Total Mean Annual w* (1995$, mBSoos) $39.1 $12.1 Unknown $1.8 Small >$53J0 I 1 2-18 CMA 114677 raianogenic Mortality For purposes of this analysis, we assume that all cancers attributable to VC exposure would be fatal. This assumption is based on the particularly lethal nature of angiosarcoma of the liver, the type of cancer most often contracted from VC exposures.17 To value these effects, we utilize recent research into the smrinieal "value of life" conducted by IEc for the U.S. EPA's Office of Air and Radiation. As part of this effort, IEc evaluated three types of value of life estimates: wage-risk studies, which estimate the additional compensation individuals demand in the labor market for taking ridrier jobs; contingent valuation studies, in which individuals are asked to state their willingness-to-pay to avoid additional increments of statistical mortality risk; and consumer behavior studies, which examine situations other than the labor market that involve risk-dollar tradeoffs. Rawi on this research and analysis, we have developed a lognormal distribution of the value of a statistical life, using a mean value of $6.5 million and a standard deviation of S4.4 million ($1995). Appendix 2C presents a list of the studies used to develop this estimate, which draws largely from a survey article authored by one of the field's leading researchers (Viscua 1992)." In Exhibit 2-12, we nunmarizc the benefits associated with avoided cancer cases from VC exposure in the general population surrounding VC and PVC plants. As shown in this exhibit, the majority of the benefits come from reducing VC exposures to the general population living close to PVC plants. This is not surprising, considering that, under uncontrolled conditions, ambient concentrations of VC around these plants are estimated to be more than twice those around VC plants. Note that the values presented in this table are the tenth percentile, mean, and 90th percentile values from a 1,000 iteration Monte Carlo analysis. We generated the distribution using the lognormal distribution described above to characterize the statistical value of life, coupled with a uniform distribution to represent the estimated number of annual cancer cases, which range from 1.1 to 11.2 per year.1* 17 We note that other researchers have valued carcinogenic health effects using a weighted average of estimates of the "value of life" (for mortality) and "cost of illness" (for non-fatal cases) (CCME 1995). While this approach may be appropriate for forms of cancer that are potentially treatable, we believe that using a weighted average that includes "cost of illness" estimates in our analysis would result in an underestimate of the.benefits of avoiding a generally fatal form of cancer. " The studies cited in Appendix 2C include analyses of compensating wage differentials for fatal injury risk in several countries, including <~anarfa- the Values are reported in the source document in American dollars, and have been convened to Canadian dollars using the method outlined in Chapter 1. We note, however, that the list of studies does not include four wage-risk studies for Canadian labor markets (Vodden et aL 1994, Martinello and Meng 1992, Meng and Smith 1990, and Meng 1989). We have not reviewed these four studies in detail, but have reviewed a summary of the studies contained in a report prepared for the Canadian Council of Ministers of the Environment (CCME 1995). The value of statistical life estimates rcponed for these four studies are comparable to those presented in Appendix 2C, with means tanging from $4.7 million to $7.6 million. The mean of the distribution of values upon which we rely ($6.5 million) would be unchanged if these studies were added to those cited in the appendix. * 17 A uniform distribution in this context means that there is an equal chance that any value between 1.1 and 112 is the true number of eases 2-19 > CMA 114678 Exhibit 2-12 ANNUAL BENEFITS ASSOCIATED WITH AVOIDED DEATHS FROM CANCER IN THE GENERAL POPULATION ($1995, xniOion) -- T>pe of Plant Low Estimate (10th Percentile) *m*e- a- n- (90th Peirentfle) VC $LS S6JD $12.0 PVC S&8 $33.1 ' $68.0 Totals $103 S39J $800 In Exhibit 2-13, we summarize the benefits associated with avoided cancer cases from occupational exposures to VC We used the lognormal distribution to represent the statistical value of life, as described above, and a uniform distribution to represent the likely number of annual cancer cases, which we estimate to range from one to three per year. As shown in this exhibit, the majority of the benefits estimated come from avoided cancer cases among the PVC worker population, which is substantially larger than the population of workers in VC plants. Bdribit2-13 ANNUAL BENEFITS ASSOCIATED WITH AVOIDED DEATHS FROM CANCER IN THE OCCUPATIONAL POPULATION _________________ ($1995, millions) Type of Plant Low Estimate (10th Pcrecndk;) Mean Miyh BitBimf (90th Percentile) VC 108 $2.1 $3.9 PVC . Totals S3.4 $4.2 SlOO $12.1 $19.0 S22S | f 8 I I To provide a sense of the uncertainty associated with the values presented in this table, Exhibit 2-l4|^esents a distribution ofpotential benefits associated with occupational exposures from PVC plants^. As shown in this graphic, total benefits estimates could potentially range from $1.4 million to S$i.4 million, based on this particular Monte Carlo run of 1,000 iterations. 2-20 CMA 114679 Exhibit 2-14 DISTRIBUTION OF ANNUAL BENEFITS FROM AVOIDED PVC WORKER CANCER CASES Values In millions of dollars CMA 114680 Noncamnogenic Effects-1 As above, there are a number of noncardnogenic effects that may result from acute and/or chronic exposures to high concentrations of VC The benefits associated with reducing morbidity can include the following. Avoidance of direct medical costs, including the expenditures to combat a particular illness, such as doctor's fees, hospitalization costs, and pharmaceutical purchases. Indirect costs, including lost wages and leisure time due to illness. Pain and suffering, which encompasses the physical and psychological discomfort associated with morbidity effects (Unsworth 1993). Several estimation techniques have been developed to assign economic benefit estimates to reductions in air pollution related morbidity effects, although these techniques generally address only a portion of total morbidity benefits. Much of the morbidity literature associated with air pollutants focuses on respiratory effects (&&, asthma and bronchitis symptoms caused by air pollutants). While VC is known to cause some respiratory problems (e.g^ chronic bronchitis), more commonly cited noncardnogenic effects are of the type cited in the previous section, such as Raynaud's Syndrome and acroostaolysis. As a result, we value morbidity effects using information collected in the CCME (1995) study on restricted activity days (RADs). RADs are a measure of illness defined as a day on which illness prevents an individual from engaging in some or all of bis or her usual activities, including days spent in bed and days with minor activity restrictions due to illness. As pan of valuing morbidity in the CCME study, the authors analyzed a number of studies estimating RADs. Based on this review, they provide a central estimate of S70 (1994$) per RAD, with a low estimate of $35 per RAD and a high estimate of $105 per RAD. For purposes of our analysis, we have adjusted these figures to annual values by multiplying by 365 days, and have adjusted the figures to 1995 dollars.30 As a result, we value morbidity effects assuming the annual benefits of avoiding restrictionson activity range from $13,000 to $39300 per year, with a mean value of $26,100. In Exhibit 2-15, we summarize the benefits of avoided morbidity from occupational eqwsures. To develop these estimates we use a discrete probability distribution to represent the estimated annual RAD values, and a uniform distribution for the number of cases, which are estimated to range from 34 to 101 per year. As shown in this exhibit, we estimate total benefits to Kang6 million to $33 million per year, with a `mean value of $13 million, based on a Monte Cadg|un of 1300 iterations. Implicit in this approach to developing an annual benefits estimate is the assumption that the activity of affected VC and PVC workers is restricted 365 days a year. Many of the health effects of interest (e.g., acroostaolysis) could have such persistent effects; however, to the extent these health effects would not impair activity year-round, the methodology lends an upward bias to the benefits estimate. 2-22 CMA 114681 Eahihit2-15 ANNUAL BENEFITS ASSOCIATED WITH AVOIDED MORBIDITY IN VC AND FVC WORKERS (is minions) Lor Estimate (10th Peieentfle) Mean High Estimate (90th Percentfle) S0.7 S1.8 S33 VALUING HUMAN HEALTH EFFECTS: TOTAL VALUES The results of the previous section indicate that the annual benefits of controlling VC are considerable. In addition, these benefits presumably would continue to accrue for a number of years, since, in the absence of controls, health effects would continue unabated. In Exhibit 2-16, we summarize our estimates of annual benefits and the present value of total benefits attributable to an environment free of VC As illustrated in this exhibit, we estimate that annual benefits (for quantifiable benefits categories) range from $152 million to $1062 million, with a mean annual benefits estimate of $53.0 million. Further, the present value of benefits ranges from $02 billion to S2.4 billion over a 30 year period, depending upon the annual benefits estimate (low, mean, or high) and discount rate employed.9 See the discussion on discounting in Chapter 1. 2-23 CMA 114682 Exhibit 2-16 SUMMARY OF ANNUAL AND TOTAL BENEFITS: VINYL Cl ILOR1DE ($1995, millions) 1 Category Mortality General Population Occupational 1 Morbidity Annual Benefits Low Mean High Present Value of Total Benefits -- 30 yean Low @ 6% Mean @ 4% High @ 2% SHU $4.2 $39.1 $12.1 $80.0 $22.9 $141.8 $57.8 $676.1 $209.2 $1,791.7 $512.9 I General I Population | Occupational | Ecological 1 Total Unknown Unknown Unknown Unknown $<1.7 Small > $15.2 $1.8 Small > $53.0 $3.3 Small > $106.2 $9.6 Small > $209.2 Unknown $31.1 Small > $916.4 Unknown $73.9 Small > $2478.5 CMA 114683 2-24 references for CHAPTER 2 ATSDR 1993. Agency for Toxic Substances and Disease Registry, U.S. Public Health Service. Toxicological Profile for Vinyl Chloride (Dnrft). April 1993. Amdur 1991. Amdur, Mary 0, John Doull, and Curtis D. Klaassen. Casarett and Doull's Toxicology: The Basic Science of Poisons. Fourth Edition. New York; Pergamon Press, 1991. Boettner 1981 Boettner, EjA, GJ. Ball, Z. Hollingsworth, and R. Aquino. "Organic and Organotin Compounds Leached From PVC and CPVC Pipe," Universtty of Michigan, Ann Arbor School of Public Health, 1981 Cash 1991 Cash, CarL "Shattering PVC roof membranes," Progressive Architecture, Vol. 73, No. 1 p. 43, February 1991 CCME 1995. Environmental and Health Benefits of Cleaner Vehicles and Fuels. Summary Report and Supplemental Reports prepared for the Canadian Council of Ministers of the Environment. Prepared by Carolyn Lang, Hagler Bailly Consulting; Greg Yarwood, ENVIRON International, Inc; Francois Lalonde, Environment Canada; and RobertBtoxara, Ontario Ministry of Environment and Energy. October 1995. Coiner 1996. Personal communication with Ron Coiner, National Sanitation Foundation. Committee 1987. Committee on the Evaluation of Carcinogenic Substances, National Health Council of the Netherlands. "A Scientific Basis for the Risk Assessment of Vinyl Chloride," Regul Toxicol Pharmacol. VoL 7, No. 1, pp. 120-127, March 1987. CPI 1991. CPI Profiles, July 1991. Received from Tedd Brien, Use Patterns Section, Commercial Chemicals Evaluation Branch, Environment Canada. DoE 1992. Department of the Environment "Vinyl Chloride Release Regulations, 1992," Extract Canada Gazette, Part II. December 2,1992. Doll 1988. Doll, R. "Effects of Exposure to Vinyl Chloride. An Assessment of the Evidence," Scandinavian Journal of Work and Environmental Health. Vol 14, No. 2, pp. 61-78, April 1988. Doniger 1978. Doniger, David D. The Law and Policy of Toxic Substances Control: A Case Study of Vinyl Chloride. Resources for the Future, 1978. D&B 1996. Dun &. Bradstreet Canadian Duns Market Identification Dialog File, 1996. EC 1986. Environment Canada. Environmental Status Report 1979*1984; Vinyl Chloride Industry. September 1986. Report EPS 1/AP/l. 2-25 CMA 114684 EC 1988. Environment Canada. Environmental Status Report 1985-1986: Vinyl Chloride Industry. July 1988. Report EPS l/AP/2. EC 1992. Environment Canada. Environmental Status Report 1987-1990: Vinyl Chloride Industry. August 1992. Report EPS l/AP/4. Fisheries 1978. Fisheries and Environment Canada, Environmental Protection Service. Air Pollution Emissions and Control Technology: Vinyl Chloride Industry. March 1978. Economic and Technical Review Report EPS 3-AP-77-4. Fisheries 1977. Environment Canada 1977. Environment Canada, Environmental Protection Service. Emissions of Vinyl Chloride to die Ambient Air Around Manufacturing Facilities in Ontario. December 1977. Surveillance Report EPS 5-AP-77-14. Gutb 1996. Persona] communication with Dan Guth, U.S. Environmental Protection Agency Infante 1976. Infante, Peter F,, Joseph K. Wagoner, Anthony J. McMichael, Richard J. Wasweiler, and Henry Falk. "Genetic Risks of Vinyl Chloride," The Lancet, pp. 734-5, April 3,1976. Kuzmack 1975. Kuzraack, Arnold M. and Robert E McGaugby. Quantitative Risk Assessment for Community Exposure to Vinyl Chloride. Prepared for the US. Environmental Protection Agency. December 5,1975. Lowenheim 1975. Lowenheim, Frederick A. and Marguerite K. Moran. Faith, Keyes, < Clark's Industrial Chemicals. Fourth Edition. New York: John Wiley St Sons, 1975. Maninello and Meng 1992. MartineUo, F. and R. Meng. "Workplance Risks and the Value of Hazard Avoidance." Canadian Journal of Economics, Volume 25, pp. 333-345,1992. Meng 1989. Meng, R. "Compensating Differences in the Canadian Labour Market." Canadian Journal of Economics, Volume 22, pp. 413-424,1989. Meng and Smith 1990. Meng, RA. and DA. Smith "The Valuation of Risk of Death -in Public Sector Decision-Making." Canadian Public Polity, Volume 16. pp. 137-144,1990. NPR1 1993. National Pollutant Release Inventory, 1993, r**i*rfa Podoll 1986. PodoQ, T. "Impact of Leaching by Plastic Pipe, Fittings, and Joining Compounds," Plumbing Materials and.Drinking Water Quality. New Jersey. Noyes Publications, pp. 68-76, 1986. Sax 1981. Sax, N. Irving. Cancer Causing Chemicals. New York: Van Nostrand Reinhold. 1981. As cited in memorandum from Jim Neumann and Bob Unsworth, "Addenda to Mortality Valuation Methodology." September 28,1993. 2-26 CMA 114685 Sdleck 1991- Selleck, R_R and BJ. Marinas. "Analyzing the Permeation of Organic Chemicals Through Plastic Pipes," Journal ofthe American Water Works Association, Vol. S3, No. 7, pp. 92-97, July 1991. Theriault 1983. Theriault, G., H. Ituna, and S. Gingras. "Evaluation of the Association Between Birth Defects and Exposure to Ambient Vinyl Chloride," Teratology. 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"Extraction of Organotin Compounds from Polyvinyl Chloride Pipe," Archives of Environmental Contamination and Toxicology, Vol. 18, No. 6, pp. 839-843, November 1989. 2-27 CMA114686 Vodden et al 1994. Vodden, K, D. Smith, R. Meng et aL The Social Cost ofMotor Vehicle Crashes in Ontario. Prepared for the Government of Ontario, Safety Research' Office, Safety Policy Branch. 1994. 2-28 CMA 114687 Appendix 2A GENERAL POPULATION EXPOSED TO VC EMISSIONS FROM POINT SOURCES Overview Applying ambient air concentration estimates developed in the 1975 EPA study requires that we estimate the number of individuals living proximate to VC and PVC facilities. Specifically, we need to estimate the number of individuals living within four bands located around each facility. The bands have the following distances: Band 1: 0 to 0.5 miles. Band 2: 0.5 to 1 miles. Band 3:1 to 3 miles. Band 4:3 to 5 miles. The pmpose of this appendix is to describe the methodology we employ to estimate the size of the affected population within each band. We use 1991 Canadian census data on the total population and size of the four Canadian cities in which VC and PVC plants are located. Method We develop the estimates of the total affected populations (presented in Exhibit 2-5 of the body of the chapter) by summing affected populations across each of the four cities with VC or PVC manufacturing facilities. We employ the following method to estimate the affected population within each city. Step 1. Based on the area of each city, determine if the city has a radius of less than 5 miles (assuming the city is "round"). If so, determine the number of bands covered by the city (see Exhibit 2A-1 for an illustration for Sarnia, Ontario). Step 2. Calculate the area of each band within the border of each city. Step 3. Assuming a uniform distribution of population within each city, apply population density information for each city to estimate the number of individuals within each band. 2-29 CMA 114688 Exhibit 2A-1 EXAMPLE OF GENERAL POPULATION SURROUNDING A VC OR PVC PLANT IN SARNIA, ONTARIO Ontario is 4.5 miles. This dotted line represents the outer boundary of the town. CMA 114689 Implicit in this approach are the following assumptions: (1) the VC or PVC plant is located in the center of city, and (2) the population of the areas immediately outside of each city is zero.= Results Exhibit 2A-2 summarizes our results by city and population band. Exhibit 2A-2 ESTIMATED POPULATION BY C3TY AND BAND Gty Sarnia, Ontario Niagara Falls. Ontario Shawinigan, Quebec Ft. Saskatchewan. Alberts 1 884 246 1486 559 2 739 3459 1478 Band 3 28301 7485 15486 9442 4 42440 65.050 0 0 Total 74478 73420 19,932 12,079 | | ~ While this second assumption is an over-simplification, it does not have a large impact on our results. 2-31 CMA114690 Appendix ZB ESTIMATING GENERAL POPULATION CANCER CASES: DETAILED EXAMPLE Overview Hie purpose of this appendix is to provide a detailed example of the calculations perf rrned to estimate the total annual cancer cases in the general population living near VC and FVG plants in the absence of controls on VC emissions. The foDowing example estimates the annual number of cases for the 1,444 individuals estimated to live in Band 1 around VC plants. Step 1: Calculate the Ambient Air Concentration of Vinyl Chloride. From the U3. EPA study, we apply an ambient air concentration of 113 ppb to Band 1 (0 to 0.5 miles from a VC facility). We convened this concentration from ppb to mg/m3: Step 2: Calculate the Dose. To estimate the dose to which each resident is potentially exposed, we multiplied the ambient air concentration of VC by the inhalation rate and the inverse of the average weight of an adult: (0.294 rag/m1) * (20 m3/day) * (1/70 kg) 0.084 mg/kg-day Step 3: Calculate the Cancer Risk. To estimate the individual lifetime risk of cancer, we multiplied the dose by the cancer slope factor for VC: (0.084 mg/kg-day) * (03 mg/kg-day)'1 25 x 10*1 Step 4: Calculate the Annual Cancer To estimate the annual number of cancer cases in a given population, we multiplied the cancer risk by the population and divided fay the average adult lifespan: (23 x 10-J) (1,444 people) / (70 years) 032 people/year 2-32 CMA 114691 Appcndk 1C Author amt Year Knekner and Leclh (1991) (US) ESTIMATES USED TO OEMERATE PROPOSED DISmiUimON OF VAt.UE OF UFU Value of life Hot Estimate (51995, millions) Full Reference 08 TJ. Knekner nnd J.D. Leclh. 1991. 'Compcmating Wage Differential! for Fatal ln|ury Rkk In Amlralla, Japan. and 1he United State!," Joumnt of fthi and Uncertainty 4(l):75-90. || 1 || 1 Smith nnd Gilbert (1984) | Dillingham (1V85) I Butter (198.1) U Millet am) Ourta (1991) 1 Moore and Vkcusl (1988a) Vltcutf. Magal, and Huber (1991b) in V.K. Smith and C. Gilbert. 1984. The Implicit Risks tn Life: A Comparative Analysis," Economic! Letter], 16: R 393399. | 1.1 A. Dillingham. 1985. The Influence of Rkk Variable Definition on Value of Life Estimate!," Economic Inquiry | 24:217.294. II 1.5 RJ. Duller. 1983. "Wage and Injury Rate Responses to Shifting Levels of Workers' Compensation* In John D. | Worrall, ed. Safety and the IIW Force, Ithaca: Corned University, II.R Press. g 1.6 T. Miller and J. Gurta. 1991. "Tire Value of Statistical Life In New Zealand,* Report to the New Zealand Ministry 1 of Transport, Land Transport Division. || J.4 M.J. Moore and W.K. Vlseusl. 1988. *Doubllng the Estimated Value of Life: Results Using Mew Occupational | FalaHly Data,* Journal of Mey Anatyds and Management 7(3): 476-490. || 3.7 r W.K. Viseusl, W.A, Magal, and 1. Huber. 1991. "Piking Environmental Health Risks: Survey Assessments ol Risk- 8 Risk and RIsk-DoKar Tradeoffs,* Journal of Emirotimtntat Economies and Management 101:32-57. | Oegu et at. (1985) * Marlr. nnd rrttchatopoulo! (1981) 45 No full reference available ]f J.8 A. Marin and 0. Psacharnpoulos. 1982. The Reward for Rkk In the Labor Market: Evidence frnm the Untied | Kingdom and Reconciliation with Other Studies,* Jentenal of Political Economy 90(4): 827-153. | Kneifner and teeth (1991) (Autlralla) Getting, de Haan. and Schulte (1988) Couiineau, Lacrnli, and Girard (1988) 45 T.J. Knekner and J.D. Leclh. 1991. "Compensatlog Wage Differentials for Fatal Injury Rkk In Australia, Japan, U and the United Slates,* Journal of Rlik and Uncertainty 4(l):75-90. | 4.6 S. Getking. M. de tfaan, and W. Schulte. 1988. The Marginal Value of Job Safety: A Contingent Valuation 8 Study,* Journal of Rkk ond Uncertainly 1(1): 185-100. 8 4.9 J. Couiineau, R. Lacrok, and A. Girard. 1988. 'Occupational Haiard and Wage Compeniiting Differential!* I University of Montreal Wotklng Paper. || Jones-Lee (1989) Dillingham 11985) 5.1 M.W. Jones-Lee. 1989. TTie Eronomfcr of Safety and Physical Risk, Orford: Bull Btickwett. | 5.3 A. Dillingham. 1985. The Influence of Risk Variable Definition on Value of Life Estimates,* Economic Inquiry 1 24:117 294 1 CMA 114692 2-J3 Append)! 2C (continued) ESTIMATES USED TO GENERATE PROPOSED DISTRIBUTION OP VALUE OF LIFE | Author amt Year Value erf Life Deal Estimate (11993, millions) I'atl Reference H D Vkeusl (7(, 79) i R.S. Smith (1976) | V.K. Smith (1976)* 3.6 W.K. Vlscusl. 1971. *Labot Market Vahtalfent rrf IJh and l.lmh: Empirical Eillmalet end Policy ImpKcallnna* Public Policy 16(3): 359-3(6. ..--.-- 1971. 'Wealth Effects and Earnings Premiums for Jnh Hamds* Review rtf Economic} and Sletittlcs 60(3): 4IM-4IA. ............ 1979. Employment Hatatdr An fnie.tr/gifririri of Market Performance, Cambridge: Harvard Unhrtiilly Press. ............1919, 'Job Hatards and Wntkcr Oak Rales: An Analysis of Adaptive Worker Behavior * International 1 Economic Review 10(1): 29-5(. i -- 1979. The Impact of Occopathmal Safety and 1 lenlth Regulation.' DAI Journal of Economic* W(t): 117- 1 140. | 6.) R.S. Smith. 1976. The Occu$*aHonatSafety and 1Icaltlt Act: its Ovett and Achletrmentt, Washington: American | Enterprise InstMute. | 6.4 No rod reference available | | Olicm(l9ai) I Vlitml (1911) 1 R.S. Smith (1974) 1 Moore ami Vlscusl (IM(e) | Knchncr and Lccth (1991) (Japan) 7.1 C.A. OHon 1911. 'An Analysis, of Wage Differential Received by Workers on Dangerous Jobs.' Journal of Human 1 Retomrtt 16:167.163. | W.K. Vheusl. 1961. "Occopatlonal Safety and Ifeahh Rcgttlallone Its Impact and Policy Alternatives,' J. Credne, ed., Rexarch in Putdk f\dkyAnafytb and tlanoxement, vol. 1, Greenwich, Corns.: JAI Press, pp. 7(1-199. 9J R.S. Smith. 1974. The FeasRilllly of an 'Infttry Tas' Approach to Occnpatlonal Safety* Law and Contemporary ftoMrmt 31(4): 730.744. 9.9 MJ. Moore and W.K. VbcosL I960. 'DooMfeg the Estimated Vahae el Ute: Results Using New Occupational FalaHly Data,* Jttumal of PoRcy Anaiydt and Management 7(3): 476490. 10.4 TJ. Knebncr and J.D. Leelh, 1991. *C0m|ictiallng Wage Dilferentlah for Fatal Injury Risk In Australia, Japan, and the United Slates.* Journal of idtk and Uncertainly 4(1):73-90. Hereof amt ScMottman (1917) | U1|h and Fdson (7944) I Leigh (19(7) Gnren (19(() ||11.4 II.W. Hereof, Jr. and A.M. Schkrflman. t907. "Vahilng Rhk In tht Workplace: Market Price, WMIngness to Pay, and ihe Optimal PtovWon of Safety* Unfectdly of Tennessee Woskbt| Paper. 111 f.P. Leigh and R.N. Faison. 1964. 'Estimates of ihe Value of Accident Avoidance at Ihe Joh Depend on 1 Concavity of the Equalizing Differences Carve,' The Quarterly Review of Economkt and Butineu 24(1): 36-66. || |14.1 J.P. Leigh. 19(7. 'Gender, Fhm Sire, Industry and Estimates of Ihe Value-of-Life,* Journal of Health Economici 6: 233-273. | I.1S.4 Oaren. IMS. 'Compensating Wage Differentials and Ihe Endogeneity of fob Riskiness,* The Revierv of Economict and Statitda 70(1): 9-16. |1 Source: W.K. VtscosL IWI Fatal Tradeofft: Public and Private ReipontibilMei for Kith, New Yofl: Oftold University Press. * .Added filer consultitIon w):h Vtscuil. CMA 114693 2-34