Document omm65Gq7q5k7k4rmVNvZnZrb7

CanTox INTERPRETIVE EVALUATION OF THE POTENTIAL HUMAN HEALTH AND ENVIRONMENTAL EFFECTS OF VINYL CHLORIDE (VCM) AND POLYVINYL CHLORIDE (PVC) Prepared for: The Chlorine Institute 2001 L Street N.W. Suite 605 Washington, DC 20036 March 18, 1993 R&S 143065 Table of Contents CanTox V Page i) PREFACE i ii) EXECUTIVE SUMMARY xiv 1.0 INTRODUCTION 1-1 2.1 SOURCES AND ENVIRONMENTAL FATE 2.1.1 Anthropogenic Sources 2.1.2 Natural Sources 2-1 2-1 2-4 2.2 ENVIRONMENTAL FATE 2.2.1 Physical-chemical. Properties 2.2.2 Environmental Fate .. 2-6 2-6 2-7 2.3 VINYL CHLORIDE REGULATIONS 2.3.1 Regulations of VCM in Air 2.3.1.1 Air Concentrations in Emissions 2.3.1.2 Regulations of VCMin Water 2.3.1.3 Soil 2-11 2-11 2-11 2-11 2-12 3.0 INTRODUCTION 3-1 3.1 ENVIRONMENTALCONCENTRATIONS 3-1 3.1.1 VCM Concentrations Associated With Production/Manufacturing Facilities 3-2 3.1.2 VCM Concentrations Remote from Production and Manufacturing Facilities 3-4 3.2 HAZARD ASSESSMENT 3-4 3.2.1 Polyvinyl Chloride 3-4 3.2.1.1 Bioavailability, Metabolic Conversion (Pharmacokinetics), and Bioaccumulation 3-4 3.2.1.2 Mammalian Toxicology (Laboratory Animal . and 3.2.1.3 Biochemical Studies) Epidemiology Studies ''Vi'" 4O 3-5 3_6 3.2.1.4 Exposure Limits 3-7 3.2.2 Vinyl Chloride *f>3-7 3.2.2.1 Bioavailability, Metabolic Conversion (Pharmacokinetics), " and Bioaccumulation 3-7 3.2.2.2 Mammalian Toxicology (Laboratory Animal and 3.2.2.3 Biochemical Studies) Mechanisms of Toxicity 3-9 3-11 3.2.2.4 Epidemiology Studies 3-12 R&S 143066 3.2.2.5 Exposure Limits 3.3 AQUATIC WILDLIFE HAZARD ASSESSMENT 3.3.1 Lab Studies 3.4 TERRESTRIAL WILDLIFE HAZARD ASSESSMENT 3.5 OTHER ENVIRONMENTAL EFFECTS 3.6 SIGNIFICANCE OF ENVIRONMENTAL CONCENTRATIONS 4.0 REFERENCES CanTox 3-17 3-18 3-18 3-19 3-19 3-19 R&S 143067 List of Tables CanTox Page Table 1-1 Table 1-2 Table 2-1 Table 2-2 Table 3-1 Preliminary List of Chemicals of Concern Per Product Category Representative Priority Chemicals Assessed in Stand-Alone Documents Physical/Chemical Properties PhysicaPChemical Properties of Vinyl Chloride Cancer Risk Estimates for Near-Plant Air Concentrations of VCM v xi 2-7 2-10 3-23 ' SS 73 09 CO woS* O') 00 CanTox i) PREFACE 1 Recently, certain environmental agencies (e.g., UC, 1992) and a number of environmental groups (Verdict of the NorthSea Tribunal, May 1989; GreenPeace, 1991a,b) have expressed the view that the banning of uses of chlorinated chemicals is the only way to ensure future "protection" of the environment. Such extreme reactions are not based on sound scientific information and arguments, and do not consider the impact of lost benefits to society from the removal of a large number of chlorinated chemicals, many of which do not have known or proven replacements. 2 3 4 5 6 7 8 Sound scientific information has been the driving force behind the identification of and solution to historical concerns regarding the health effects of chemicals in the workplace and environment. Similarly, future actions governing the production and use of chemicals by society should also be based on the best possible scientific evaluation of their consequences with respect to maintaining environmental quality and serving ;the benefits of society. Such an evaluation requires an understanding of i) the potential for chlorinated organic chemicals to produce adverse effects on the ecosystem, including humans, ii) the contributions of both anthropogenic {i.e., related to human activities) and natural (independent of human activities) sources of chlorinated chemicals to total environmental loading rates, iii) the environmental fate characteristics of the chemicals that determine the distribution and losses from the environment, and iv) the determination of environmental loading rates from anthropogenic activities tha* could be sustained without the occurrence of adverse effects on the ecosystem. 9 10 11 12 13 14 15 16 17 18 19 20 In an effort to assist continued progress in the application of sound scientific principles to the environmental assessment of chlorinated chemicals, the Chlorine Institute commissioned a detailed review and interpretive evaluation of the scientific information available on the historical, current and future status of chlorinated chemicals in the environment. The objective of this interpretive review was to provide an overview perspective on the potential environmental impacts of chlorine and chlorinated organic chemicals for seven categories of products that involve specific chlorinated organic chemicals. The product categories identified included: 21 22 23 24 2. 2i T R&S 143069 i CanTox chlorine, polychlorinated biphenyls, vinyl chloride/poivvinyl chloride, chlorinated organic solvents, chlorine disinfection of drinking water/waste water, incineration of chlorinated materials, and pulp and paper bleaching and the use of chlorine in the development of pesticides, For the first seven product categories an interpretive review of the human health and environmental impact of representative chlorinated chemicals of potential concern has been prepared and is available from the Chlorine Institute. For the eighth product category, pesticides, a slightly different approach was adopted which addressed the issue of risk/benefit analysis as applied to the use of chlorine in the development of pesticides. 28 29 30 31 32 33 34 35 The protocol followed in preparation of the seven product category documents has been outlined below. 36 37 A preliminary list of chlorinated chemicals of the greatest concern and of the most 38 relevance to each of the product categories was developed based on published quantitative 39 analytical and hazard data. A total of 93.chlorinated chemicals were identified and were 40 grouped by chemical class (f.e., chlorinated inorganics, chlorinated alkanes, chlorinated 41 alkenes) (see Table 1-1). 42 It was beyond the scope and intention of this project to conduct a detailed assessment of 43 the environmental and health effects of all 93 chlorinated chemicals. The pertinent 44 mammalian toxicity data for all 93 were reviewed and the chemicals were further 45 classified according to their mechanisms of action (i.e., gbnotoxic carcinogen, non- 46 genotoxic carcinogen, mutagen, systemic toxicity) based on the mostcritical toxicological 47 endpoint for which a positive effect was observed. This hazard iitforination has been 48 summarized in Appendix I. For some chemicals (i.e., bromodichloroethane, 49 pentachloropropene, pentachlorobutadiene, hexachlorohexatriene, ere.,),no toxicity data 50 was identified in the literature. For these chemicals it is also unlikely that therelisitnuch 51 environmental concentration or emissions data, thus precluding any form of human health 52 or environmental assessment. R&S 143070 ii CanTox Based on the hazard classification, two or three representative chemicals, for which there 54 were considerable hazard data in the scientific literature, from each chemical group, were 55 selected for detailed human health assessment with respect to each product category. 56 This approach tended to focus on the most potent compounds (i.e., carcinogens); 57 however, the authors recognize that not all chlorinated chemicals are carcinogenic and 58 therefore to maintain this perspective, a number of those priority compounds acting via 59 mechanisms not involving carcinogenesis have also been included for detailed discussion 60 (/. e.,2,4-dichlorophenol a systemic toxicant w 2,4,6-trichlorophenol, a liver carcinogen). 61 The human health impact of approximately 42 representative priority chlorinated 62 chemicals/ chemical groups from the original 93 chemicals of concern, relevant to each 63 product category, were selected for detailed assessment (see Table 1-2). 64 Due to the wide range in species sensitivity to specific chemicals within a chemical group 65 and the influence of abiotic and biotic environmental factors on toxicity, environmental 66 effects (aquatic, terrestrial and other) were dealt with on a chemical group basis. This 67 involved an interpretive review of the relevant toxicity data for all of the chlorinated 68 chemicals per chemical group included in the preliminary list (see Table 1-1). 69 A discussion of both natural and anthropogenic sources contributing to historical, present 70 and future environmental concentrations, the physical-chemical properties governing their 71 environmental fate and biological behaviour, and the environmental fate of the 72 representative chlorinated chemicals has also been presented. 73* * To provide a balanced perspective of the potential for human and wildlife exposure to 74 these compounds associated with each product category, historical and present ambient 75 environmental concentrations or emission levels were identified for the representative 76 chemicals on a product category basis. From a comparison of the identified 77 environmental concentration data and the critical hazard data (/. e., exposure limit)', the likelihood of adverse human health or environmental effects associated with each product category was identified. Qualitative estimates of future environmental loading rates based R&S 143071 iii CanTox on best-available technologies, industry standards, and government emission policies, were used to draw predictions regarding future environmental concentrations of chlorinated chemicals and their potential impact on human health and the environment. 81 82 83 Furthermore, to maintain a balanced perspective of the impact of chlorinated chemicals on human and environmental health, the health benefits to society associated with the use of chlorine use (i.e., chlorine disinfection) as well as alternatives were examined and considered in the final conclusions regarding the human health and environmental impact of each product category. 84 85 86 87 88 ' 4; 5rV'' u flo CO -P* Co"JO iv ro Table 1-1 Preliminary List of Chemicals of Concern Per Product Category CHEMICAL OROOP Chemical Drinking Water PRODUCT CATEGORY Waste Water Solvents Incineration Chlorinated Inorganics Chlorinated Alkanes ,, '\ szosn ssu HCl Chlorate Chlorite Dichlorom ethane Chloroform Carbon Tetrachloride Ch loro methane B romodichio romelhane Ch1o rod ibromomethane Trichlorodihyd rcxyethane Chloroethane Dichloroethane l, 1 -Dichloroethane 1,2-Dichlorpethane T rich lorbethane J r 1 J-Trichloroethane 1,1,2-Trichloroethane 1 * 1,2,2-Tetrachloroe hane Bromodichloroethane Hexachloroethane Pentachloroethane Dibromochloropropane Pulp & Paper PVOVCM PCDD/ PCDF/ PCB C anTox Table 1-1 Preliminary List of Chemicals of Concern Per Product Category CHEMICAL GROUP Chemical Drinking Water PRODUCT CATEGORY Wade Water Solvents Incineration Chlorinated Alkenes 1,2-Dichloropropane 1,2-Dibromo-3-chi oro-propane Diehl oroethylene 1,1 -Diehloroethylene 1.2- Diehloroethylene (Cis) I -2, Diehloroethylene (Trans) Trichloroethylene Tetrachloroelhylene 1.3- Diehloropropene (Cis) Pentachloropropene Pentachlorobutadiene Hexachlo robu(adi ene HexachIorocyc Iopentad ie Be He x achJorohe xatriene Vinyl Chloride PVC Chlorinated Acids Polyvinyl Chloriue Monochloroacelic Acid Trichloroacetic Acid Pulp & Paper PVC/VCM (monomer) PCDD' PCDF/ PCS C anTox PlOBPl SSd Table 1-1 Preliminary List of Chemicals of Concern Per Product Category CHEMICAL GROUP Chemical Drinking Water PRODUCT CATEGORY Waste Water Solvents incineration Chlorinated Ketones Chlorinated Benzenes ' k\ Trich 1oroacetone Tetrachloroacelone 1,1 -Djchloropropanone 1,1, l-Trichloropropanone Dichtorocyclopentene-1,2-dkme (various isomers) 3-Chloro-4-(dichloromethylJ* 5-hydroxy-2(5H)-furinone Chlorobenzene Dichlorobenzene 1,2'Dichlorobenzene 1,3-Dichlorobenzene ] t4-Dichlorobenzene Trichlorobenzene 1,2,4-Trichiotoben*me Pe ntach1 (Srobenitne Hekachforobenzene Dichlorololuene 2-Ch1 oroethylbe nzene 1 Pulp &. Paper PVC/VCM PCDD/ PCD FI PCB szoen ssa Table 1-1 Preliminary List of Chemicals of Concern Per Product Category CHEMICAL GROUP Chemical Dhnkmg Water PRODUCT CATEGORY Waste Water Solvents Incineration Chlorinated Phenols, Catechols, Guaiacols 2-Chlorophenol 2,4-Dichforophepol 2,6-Di chlo rophenol 2.4.5-Trichlorophenol 2.4.6-Trichlorophenol 2.3.4.5-Tetrachlorophenol 2.3.4.6-TetrachJorophenol Penttchloropheno] Tetrachlorophenol Dichlorocatechol TelrachJorocatechoJ Trichlorocatechol 3.4.5-Trichlorocatechol 4.5-Dichloroguaiacol Dichloroguaiacol (other isomers) Tetrachloipoguat*co I Trichfproguaiacoli TtichIo rodthydroconi feryI Alcohol Chlorovanillin TrichhirovamltylalcohoJ T rich U>roacetosyringo ne 9ioen ssd DichJoro-3,4'dthydroxypropiophenone Pulp & Paper PVC/VCM PCDD/ PCDF/ PCB C anTox Table 1-1 Preliminary List of Chemicals of Concern Per Product Category CHEMICAL GROUP Chemical Drinking Water PRODUCT CATEGORY Waste Water Solvents Incineration Chlorinated Nitrogenous Compounds Dichloroacelonilrile Chlorinated Aldehydes Nitrochloroform Tnchlnroethanal Cliloropropenal ChIurnme1hoxy d i berun!d ehy de Chhiralliyilrult: Chlorinated PCDD, PCDF 2.3.7.8-TjCDD 1.2.3.7.8-P,CDD 1.2.3.4.7.8 HSCDD 1,2,3,4,8,9-HjCDD 1.2.3.6.7.8 HaCDD 1.2.3.4.6.7.8-H,CDD O.CDD 2.3.7.8-t,CDI* , 2,3,4,7,8-P)CDF l^.V.S-P.CDF \ - S' v, 1,2,3,4,7,8-HSCDF I.2.3.7.8.9H.CDF 1.2.3.6.7.8-H4CDF 2.3.4.6.7.8-HjCDF 1.2.3.4.6.7.8-H,CDF ziom svu Pulp * Paper PVC/VCM PCDD/ PCDF/ PCB Table 1-1 Preliminary List of Chemicals of Concern Per Product Category CHEMICAL GROUP Chemical Drinking Water PRODUCT CATEGORY Waste Water Solvents Incineration PCBs Chlorinated Fatty Acids Chlorinated Resin Acids Chlorinated Amines Chlorinated Ethers Chlorinated Sulfones and Thiophenes TOTAL NO. CHEMICALS 1,2,3,4,7,8,9-H,CDF O.CDF PCBs Dichlorostearic Acid Chlorodehydroabietic acid Dichlorodehydroabietic acid 3 f3T-Dichlorobenzidine 4,4'*methylene-bis-(2-chloroamlme) Bis(2-chloroethyl)eiher Chluro-2-lhiophenic Acid Chlorolhiophenedicarboxy lieAcid 1,1 -Dichlorodimethylflilfone 93 22 49 44 37 Pulp & Psper 54 PVC/VCM 20 PCDD/ PCDF/ PCB 18 8Z0SU S9d Table 1-2 Representative Priority Chemicals Assessed in Stand-Alone Documents CHEMICAL GROUP Chemical Chlorinated Inorganics Cl, ClOj HCl Chlorate Chlorite Chlorinated Alkanes4 Chloroform Carbon Tetrachloride Dichloro methane 1, l-Dichloroethane 1,2-Dichloroethane dichloro methane 1,1,1 -Trichloroethane Chlorinated Aikenes1 Trichloroethylene I, l -Dichloroethyiene Tetrachloroethylen* " Vinyl Chloride/t^VC'' Hexachlorqbueadiene Chlorinated Acids4 . Trichloroacetic acid Chlorine Drinking _________________ Water PRODUCT CATEGORY Waste Water advents Incineration m 'm m Pulp & Paper m PVC/VCM PCB 6zom ssa Table 1-2 Representative Priority Chemicals Assessed in Stand-Alone Documents CHEMICAL GROUP ------------------------------------------------------------------ Chemical Chlorine Chlorinated Ketones1 Trichloroacetone Tetrachloroacetone ], 1 -Dichloropropanone 1,1,1 -Trichloropropanone Dichlorocyclopertterifi-J ,2dione 3-Chloro-4-ldichloromethyl]5-hydroxy-2{5H)-furanone Chlorinated Benzenes1 Hexachlorobenzene Dtchlorobenzene 1.4-Dichlorobenzene 1.4-dichlofiL>beiizene 1.2.4-TrichIorobefizcne Chlorinated Phenols, Catechols, Guaiacols1 PentachlorophenoJ 2,4,6-Trichlorophenol 2f4-Dichlt>rophenul Chlorocalechoic ChloroguiUcol^ /\ Chlorinated Nitro^d^ Coin pounds1 V Dichloroacelonitrile Niirochloroform Drinking Water PRODUCT CATEGORY Waste Water Solvents Incineration Pulp * Paper PVC/VCM 080n S9H PCB Table 1-2 Representative Priority Chemicals Assessed in Stand-Alone Documents CHEMICAL CROUP Chemical Chlorinated Aldehydes* Trichloroethanal Chtoralhy drale PCDD/PCDF" PCBs* Chlorinated Patty Acids* Dichloroslearic acid Chlorinated Resin Acids* Chlorodehydroabielic acid Dichlorodehydroabielic acid Chlorinated Sulfonts and Thiophenes 1, l-Dichlorodimethylaulfone Chlorine Drinking Water PRODUCT CATEGORY Waste Water Solvents Incineration Pulp & Paper * Environmental effects to be discussed for the group of chlorinated chemicals in the preliminary list (see Table 1-1). b Human and mammalian toxicity data to be discussed foil the chemical group. 0 2,3,7.8- substituted dioxin and fiiran isomers. PVC/VCM PCB C anTox i8oen s?d ii) EXECUTIVE SUMMARY CanTox This document focuses on the interpretation of the potential adverse effects of vinyl chloride (VCM) and polyvinyl chloride (PVC) on human health and the environment. Potential secondary effects related to pyrolysis products from VCM and PVC are addressed in the Chlorine Institute document on The Potential Adverse Effects on Human Health and the Environment from the Incineration of Chlorinated Chemicals. 2 3 4 5 6 Physical/Chemical Properties and Environmental Fate 7 Polyvinyl chloride is a polymer of VCM, and is highly stable, solid material that is relatively inert chemically, environmentaily^and biologically. PVC does not depolymerize or degrade under natural environmental conditions,' One of the historical concerns of the presence of nonpolymerized VCM in PVC products have been largely addressed by modified manufacturing and production techniques. Under good manufacturing procedures, the residual concentration of VCM in modem PVC products is below analytical detection limits. 8 9 10 11 12 13 Vinyl chloride monomer (VCM) (also referred to as chloroethene, chloroethylene, monochloroethylene) is a molecule of two carbon atoms joined by an unsaturated bond and containing three hydrogen atoms and one chlorine atom. VCM has a high vapor pressure and is slightly soluble in water, consequently volatilization into the atmosphere is the major transport process in the environment. VCM is highly reactive, and readily polymerizes in the presence of oxygen, sunlight or heat to form PVC. Vinyl chloride monomer rapidly degrades in the troposphere via photochemical oxidation. As indicated by the low log Kow f 1.38, vinyl chloride does not adsorb to organic carbon of soils/sediments or accumulate inbiological tissues. Certain strains (e.g., Mycobacterium) can utilizing vinyl chloride as a carbon andenergy source under aerobic conditions. Mineralization of VCM to C02 can occur under .both aerobic and anaerobic conditions. . 14 15 16 17 18 19 20 21 22 23 24 33 9 CO03 0o3 0N0> XIV Hazard Potential of VCM CanTox 25 As with other chemicals, the potential for adverse effects of VCM depends on the concentrations that occur in target tissues within the body where adverse effects develop. These tissue concentrations depend on the bioavailability of the chemical from various environmental media through different routes of exposure. 26 27 28 29 At room temperature, vinyl chloride is a gas. As such, exposure via inhalation is the most significant route of exposure in the environment and occupational setting. Vinyl chloride is rapidly absorbed by the lung and readily metabolized to the reactive epoxide intermediate chloroethylene oxide, which can rearrange spontaneously to chloroacetaldehyde which is further metabolized. VCM does not accumulate in tissues. v'-y Vinyl chloride is not a potent acute toxic agent, and acute lethality is observed at air concentrations as great as 113,000 to 230,000 ppm (294 to 595 g/m3). At these high exposures VCM acts as a narcotic or anaesthetic agent. Iriyiddition, at high acute doses, tissue damage to lung, liver and kidneys has been observed. Following repeated sub-chronic exposures, the principle target organ for VCM is the liver. 30 31 32 33 34 35 36 37 38 39 VCM is not teratogenic in a number of mammalian laboratory studies. Evidence of carcinogenicity in animals is conclusive based positive data from numerous mammalian laboratory studies. Vinyl chloride administered orally or by inhalation to mice, rats and hamsters produced tumours in the mammary gland, lung, Zymbal gland, and skin and angiosarcomas of the liver. The major conclusions supported by the available toxicity data are: vinyl chloride induced tumours in all species and strains of animals tested; it was found to be a multipotential carcinogen at extreme exposures (t, e., tumours of different types were induced at different sites); angiosarcoma of the liver occurred in all species of aninial tested, vinyl chloride was carcinogenic by inhalation and ingestion, and possibly by injection; obvious;doseresponse relationships were observed for both ingestion and inhalation experiments; treatment duration and schedule markedly affected the neoplastic response, as did the species strain, and sex of the animals tested; neonatal animals were highly responsive; vinyl chloride acted as a 40 41 42 43 44 45 46 47 48 R&S 143083 XV CanTox transplacental carcinogen; and it was carcinogenic at low exposure levels (i.e.. 50 ppm and lower). 52 53 Both IARC and the U.S. EPA have concluded that there is sufficient evidence for vinyl chloride carcinogenicity in humans based upon the epidemiological data collected from workers exposed to extreme concentrations between the 1940s and late 1960s. Vinyl chloride exposure has been associated with the development of angiosarcoma of the liver, a very rare tumour type in humans. There is some evidence of a general nonspecific carcinogenic effect, in addition to angiosarcomas, in humans. 54 55 56 57 58 59 The results of in vitro mutagenicity studies and observations of chromosomal aberrations in peripheral blood lymphocytes in occupational workers exposed to VCM indicate a DNA-reactive mechanism for mutagenicity/carcinogenicity. Vinyl chloride has also been shown to be activated, via P450, to a reactive epoxide intermediate, with increased hepatotoxicity following administration of P450 inducers such as phenobarbital, Aroclor 1254 (a PCB mixture), and hexachlorobenzene. V 60 61 62 63 64 65 Sources and Environmental Concentrations 66 The majority of VCM is man-made. The major use of vinyl chloride is in the production of vinyl chloride homopolymer and copolymer resins. Vinyl chlorideia also used to a lesser extent as a component in the synthesis of methyl chloroform and as a comonomer with vinylidene chloride to produce resins. A former use of vinyl chloride was as a propellant in aerosol cans and as a refrigerant. Polyvinyl chloride resins manufactured from VCM are used in the manufacture of a variety of industrial and commercial products ranging from building materials to household and medical items. 67 68 69 70 71 72 73 Undefined quantities of VCM can be produced from bio- and abiotic transformation of chlorinated solvents such as 1,1,1 -trichloroethane and 1,1 -dichloroethane. 1,1,1 -trichloroethane and 1,1-dichloroethane both have a large number of anthropogenic and natural sources. The 74 R&S 143084 xv i CanTox natural sources of these VCM precursors suggest that there may be sources of VCM independent of human activities, although such sources have not been equivocally identified to date. 77 78 The primary source of VCM in the environment is from emissions and effluents from vinyl chloride and polyvinyl chloride production and manufacturing facilities. Such releases rapidly volatilize into the atmosphere. Since 1979, VCM emissions from such production facilities have been regulated in both Canada and the United States. Prior to 1975, it was estimated that American PVC plants released 22.7 million kg of PVC and 110 million kg/year of VCM. Implementation of regulatory standards have substantially reduced total environmental releases of VCM and PVC, and currently the major sources are from accidental releases and spills. 79 80 81 82 83 84 85 The air concentrations of VCM are'greatest near industrial facilities involved in its production and use in various manufacturing processes. Average air concentration of 44 ^g/m3 and 10 to 40 fig/m3 were reported near production facilities for Houston, Texas, and in England in the late 1970s. Air concentrations near production facilities were generally below analytical detection limits (about 13 /xg/m3 or 5 ppb) by the mid 198GsIn the work environment, air concentrations of VCM have decreased over the years with the reduction of emissions through improved operating technologies. Workplace concentrationsin the Netherlands decreased from approximately 1000 ppm in 1945-1955 to 5 ppm after 1975 (Barnes, 1980), and data from the late 1980s to the present indicate workplace air concentrations generally <0.1 ppm with occasional values near 1 ppm in specific production/handling areas. Since production and manufacturing facilities are major sources of VCM, decreases in workplace concentrations would be expected to coincide with decreases in environmental releases. This relationship is supported by the declining environmental concentrations of VCM reported neaf production and manufacturing facilities observed since the early 1980s. 86 87 88 89 90 91 92 93 94 95 96 97 98 99 Potential Significance of Environmental Concentrations of VCM v 100 The available information on the physical/chemical properties, environmental fate characteristics and sources of VCM indicate that the major environmental concerns for VCM are exposures of production and manufacturing workers and possibly populations living near such facilities. R&S 143085 xvii CanTox There would be little opportunity for exposures, and therefore risks of adverse effects, to the general public, or aquatic and terrestrial wildlife from VCM at locations distant from production and manufacturing facilities. As outlined above, the air concentrations near such facilities were historically in the range of 10 - 40 ppb in the mid-1970s. Information from the mid-1980s indicated air concentrations near facilities were generally <5ppb, and based on current air concentrations in the work environment, the concentrations near facilities would be expected to be about 50-fold lower at present. 104 105 106 107 108 109 110 The characterization of the potential health risks that could potentially result from exposures to such air concentrations requires the comparison of resulting levels of exposure against a cancer potency estimate. The U.S. EPA has, over the years, proposed cancer potency slope values for VCM of 0.0174, 0.0295 and 2.3 based on lung and liver tumors, respectively, following inhalation exposure to up to 30,000 ppm VCM and oral exposure to 0-17 mg/kg body weight/day (5 days/week) in laboratory rats. These cancer potency slopes translate into RsD values of 0.575, 0.339 and 0.00435 jig/kg body weight/day at a lifetime risk of one per 100,000, a range of 132-fold. VV\ ill 112 113 114 115 116 117 118 Cancer potency factors estimated from epidemiological studies of workers exposed to VCM in the 1940s, 1950s and 1960s, range from 0.00024 to 0.000024 (mg/kg body weight/day)1. These estimates assume exposures to 100 to 1000 ppm VCM resulted in a mortality incidence due to liver cancer of 2 per 100. The cancer potency estimates from the epidemiological data would translate into RsD values of approximately 42 to 420 ng/kg body Weight/day at a lifetime risk of one per 100,000. These exposure limits differ from those proposed by EPA by some 9500to 95000-fold. 119 120 121 122 123 124 125 Such large differences in cancer potency estimates, using different data and approaches, will 126 result in equivalent differences in the risk estimates, and therefore, the interpretation of the 127 potential significance of the environmental concentrations of VCM#? near 128 production/manufacturing facilities. Risk estimates based on the EPA values range1 from i: approximately 14 to 7800 per 100,000 for the mid-1970s air concentrations, and from 74 to 982 1 per 100,000 for the mid-1980s air concentrations of VCM. Risk estimates based on the 1 R&S 143086 xviii CanTox epidemiological data range from 0.008 to 0.2 per 100,000 for the mid-1970s air concentrations, and from 0.001 to 0.01 for the mid-1980s air concentrations. 132 133 Based on a critical evaluation of the available epidemiological evidence available from workers exposed to VCM between the early 1940s and the 1960s, Doll (1988) concluded that potential risks from VCM to the "general public (if there is any at all) must be negligible". This conclusion is in agreement with the risk assessment summarized above using cancer potency estimates based on epidemiological data. 134 135 136 137 138 139 R&S 143087 xix CanTox Chapter 1 Introduction 1.0 INTRODUCTION CanTox 1 Polyvinyl chloride (PVC) is a rigid "plastic" polymer of vinyl chloride (VCM) and is widely used in the manufacture of a wide range of industrial and commercial products. PVC products are widely used as building materials, furnishings, plumbing materials, appliances and medical items. PVC is a polymer of vinyl chloride (VCM). 2 3 4 5 PVC is physically, chemically and biologically inert; however, VCM is a highly reactive chemical. Although short-term exposures to VCM, even at high ppm concentrations, are without apparent toxic effects, evidence of increased liver cancers in exposed workers raised concerns regarding potential human health effects associated with VCM exposures. This document presents an interpretive evaluation^f potential effects of PVC and VCM through an assessment of i) potential exposures through an analysis of sources, environmental fate characteristics and concentrations in various environmental media through which exposures can occur, ii) an analysis of the potential hazards from PVC and VCM, and iii) the characterization of potential risks to various biological systems by the comparisons between their potential levels of exposure from environmental media and the hazard potential associated with VCM and PVC. The potential concerns regarding pyrolysis products from PVC and VCM are addressed in a separate document from the Chlorine Institute entitled The Potential Adverse Effects on Human Health and the Environment from the Incineration of Chlorinated Chemicals. 6 7 8 9 10 11 12 13 14 15 16 17 18 30 (A 03 OiD TO 1-1 R&S 143093 CanTox Chapter 2 Properties, Sources and Environmental Fate of Vinyl Chloride and Polyvinylchloride 3J U) u w o <tno 2.1 SOURCES AND ENVIRONMENTALFATE CanTox I 2.1.1 Anthropogenic Sources 2 Uses 3 The principal products manufactured from VCM in the USA include PVC homopolymer and copolymer resins. Smaller quantities are used as a component in synthesis of methyl chloroform (1,1,1 -trichloroethane) and as a co-monomer with vinylidene chloride to produce resins (IARC, 1979). The production of methyl chloroform is being phased out in accordance with the Montreal Protocol because of its potential interactions with stratospheric ozone. VCM also was used as a propellant in aerosol calls .and as a refrigerant (Sax, 1986), although these uses have been discontinued and are only of historicalinterest. > 'y Polyvinyl chloride resins produced from VCM are used in the manufacture of a variety of products such as plastic pipes and conduit, floor covering, windows, siding, upholstery, garden hoses, appliances, gramophone records, wire and cable insulation, bottle-cap liners and gaskets, seat covers, plasticized film and automotive floor mats (IARC, 1979). Vinyl chloride-vinyl acetate copolymers are used in the manufacture of vinyl asbestos flooring tiles, gramophone records, coating resins and for sheet extrusion and injection molding. Vinylidene chloride-vinyl chloride copolymers are approved by the U.S. Food and Drug Administration (FDA) for use in food packaging products (e.g., food wrap, shrink film, bottles), tubing used in the dairy industry and various types of tubing and bags used in medical applications (Vinyl Institute, 1993, personal communication). The copolymers also are used as coatings or liners.,for other polymer films, for plastics, paper, paperboard, cassette tapes, ship and railroad tanks, fuel storage tanks, tubes, rods and pipes. In addition, they are used in fibers, cements, laminations, colostomy bags, and as binders for paints and non-woven fabric (Wessling and Edwards, 1971; Roth, 1976; IARC, 1979). 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 33 > (/> 0t3* O <0 2-1 o> VCM Emissions CanTox 25 The major anthropoentic sources of VCM include fugitive emissions during the production of VCM and the manufacture of various products from VCM. Most of the fugitive emissions from these processes are vapors released into the air. As indicated by its environmental fate characteristics, fugitive releases into aqueous media would be rapidly volatilized to the atmosphere. 26 27 28 29 30 Releases of VCM from various facilities have been documented. The estimated releases of VCM to the atmosphere from PVC plants, prior to 1975, was 110 million kg per year in the U.S. (EPA, 1975). An estimated 22.7 million kg of PVC had been released into the environment fromman-made sourcesbefore 1975 (EPA, 1974). 31 32 33 34 In 1981, following the implementation of regulations to control VCM emissions in Canada, a total of 41 emission incidents (e.g., where emission limit of 25 mg/m3 or 10 ppm were exceeded) occurred in Quebec, Ontario and Alberta, resulting in an estimated release of 46 tonnes of VCM. By 1986, the number of incidents of exceedance of the emission limit were reduced to nine and the estimated releases reduced to nine tonnes of VCM (Morcos, 1988). 35 36 37 38 39 Microbial or chemical transformation of chlorinated solvents to VCM, leaching of residual VCM monomer from polyvinyl chloride, and the possibility of degradation or depolymerization of polyvinyl chloride are considered as possible sources of VCM in ground water and landfills. 40 41 42 VCM From TransformationReactions 43 Tetrachloroethene, trichloroethene (Parsons et al., 1984; 1985; Kleopfer et <a/;,;:1985; BarrioLage et al., 1986) and 1,1,1-trichloroethane (Kleopfer et al., 1985; Barrio-Lage e&ah, 1986; fa Molten et al., 1987) can be transformed to VCM, cis- and trans-1,2-dichloroethylene by^fticroorganisms in muck obtained from an aquifer recharge basin. 2-2 44 45 46 33 (A Ck u o C--O4 CanTox In addition, chemical or abiotic transformations of chlorinated solvents, although slower than 48 biotic transformation, may result in VCM production in ground water environments. Abiotic 49 transformations are influenced by the number and type of halogen substitution. As the halogen 50 number increases, oxidation and reduction reactions are more predominant (Vogel et al., 1987). 51 Chemical transformation of 1,1, 1-trichloroethane to 1,1 -dichloroethene then to VCM, has been 52 documented; however, depending on the environment, microbial flora, and organic content, 53 other routes may be favored (e.g., the transformation of 1,1,1-trichloroethane to 1,1- 54 dichloroethane) (Vogel et al, 1987). Abiotic transformations of trichloroethane to VCM are 55 hindered by thermodynamic factors and activation energy barriers (Wolf et al., 1987); therefore, 56 biological, chemical or thermal catalytic effects are required to overcome the barriers. Thus, 57 the contribution of abiotic transformation of chlorinated solvents is small compared to 58 biotransformation (Vinyl Instituted1990). 59 VCM From Residual Monomer in PVC ;d 60 Prior to 1975 polyvinyl chloride contained muchdiigher levels of residual monomer, thus, PVC waste sludges from old material may have contributed to initial VCM levels in landfills. However, the contribution of this source to total VCM releases to the atmosphere, water and soils is probably minor (Molton et al, 1987). 61 62 63 64 The concentrations of VCM observed in landfills are not the result of degradation or 65 depolymerization of polyvinyl chloride. The majority of the sources of VCM observed in 66 landfills is related to the land disposal of PVC production sludges (a.^procedure no longer 67 practised), and the crushing or corrosion of cans where VCM was used as a propellant (such 68 uses were banned in 1974) (Vinyl Institute, 1990). High temperatures are required to produce 69 minor amounts of VCM from PVC, therefore, thermal degradation of PVC in landfills is not 70 a significant source of VCM. Following PVC pyrolysis in air at 350 C, a maximumofi35 ppm 71 of VCM was detected, while a maximum of only 6 ppm was detected following pyrolysis of 72 PVC at 500C in helium (Molton et al., 1987). Photolytic and high energy degradation of PVC are also improbable sources because of the soil cover and the lack of high energy sources in R&S 143098 2-3 CanTox landfills. PVC is also resistant to biological degradation (Vinyl Institute. 1990) and is not known to depolymerize under even severe conditions (Kirk-Othmer, 1983). 75 76 Potential Releases in Remote Locations 77 The environmental fate assessment of VCM concluded it was rapidly eliminated from the atmosphere through various photochemical oxidation processes, and that it would not accumulate in biological systems. The rapid destruction of VCM emitted into the environment would preclude the possibility of significant environmental concentrations occurring at locations remote from its release. Air concentration of VCM near (within a kilometer) production facilities in about 1975 were approximately 10 to 40 ppb (EPA, 1975; Baxter et al., 1977), concentrations about 10,000-fold less than those considered an occupational hazard (Doll, 1988). Therefore, any potential adverse effects from VGM would be confined primarily to occupational settings, and would not be observed in remote locations. 78 79 80 81 82 83 84 85 86 2.1.2 Natural Sources 7 87 At total of at least 1500 halogenated organic chemicals have been identified that are produced by various natural systems, independent of human activities. Many of these are chlorinated organics, and have only been identified in the last decade. The-scientific study of such natural products is a growing field. Most of the research to date has focused on chemical identification, and the total quantities produced by natural systems have no* been determined for most natural sources of chlorinated organics. In the case of chloromethane, total natural sources (primarily from marine and terrestrial biological systems) has been estimated at 5,000*000 tons per year, compared to total man-made chloromethane emissions of about 26,000 tons per year (Gribble, 1992). ' vr y. The evidence for natural sources of vinyl chloride are, at present, indirect. Vinyl chloride derivatives have been identified as natural products of two strains of blue-green algae (Schizothrix calcicola and Oscillatoria nigroviridis) (Gribble, 1992), although these observations to not necessarily mean that these algae produce free VCM. However, tetrachloroethylene, 88 89 90 91 92 93 94 95 96 97 R&S 143099 2A CanTox trichloroethylene (Parsons et al., 1984; 1985; Kleopfer et al., 1985; Barrio-Lage et al., 1986) and 1,1,1-trichloroethane (Kleopfer et al., 1985; Barrio-Lage et al., 1986; Molten et al., 1987) can be transformed to VCM by both biological and abiotic processes, and these sources of VCM have been identified as concerns in landfills that received VCM wastes (EPA, 1975). The production of VCM through these processes may also provide a natural source of this chemical to the environment. 101 102 103 104 105 106 A large number of halogenated chemicals are produced naturally in the environment independent of human activities (Siuda and DeBemardis, 1973; Gschwend et al., 1985; Neidleman and Geigart, 1986; Gribble, 1992); Enzyme systems (e.g., chloroperoxidase and likely others as yet undefined) in biological systems produce a wide array of chlorinated, iodinated, brominated and fluoridated alkanes, alkenes, ketdries, alcohols, carboxylic acids, and simple and complex cyclic/polycyclic organic chemicals (Gschwend et al., 1985; Gribble, 1992). 107 108 109 110 111 112 Naturally formed organohalogens are an integral part of humic soils. Analysis of soil pyrolysates by GC/MS-NCI/SIM indicated thb presence of at least twenty different organochlorine compounds, many of which could not be completely identified by this analysis because of low concentrations and overlapping non-ehlorinated components. The analyses indicated the presence of dichloropropane or chlorobenzene, several chlorinated alkanes or chlorinated alkenes and chlorophenol (de Lijser et al., 1989). 113 114 115 116 117 118 In addition, a number of physical/chemical processes in the environment also produce a wide array of chlorinated chemicals, including: i) the production of chlorine from chlorides vaporized from the earth's oceans, then the participation of the chlorine in a wide range of atmospheric reactions, ii) volcanic eruptions producing chlorine, hydrochloric acid and a variety of organic chlorine chemicals, including PCBs and chlorinated dioxins/furans, produced as products of incomplete combustion of organic materials and chlorides normally present in plants and animals destroyed by combustion processes associated with the eruptions, and iii) natural combustion processes such as forest and grass fires that bum plants high in chlorides and organic materials (Gschwend et al., 1985; Gribble, 1992). 119 120 121 122 123 124 125 1'' 1 30 (/> CO CanTox Many of the halogenated alkanes identified in the natural environment are also produced by a variety of human activities (e.g., chloroform, carbon tetrachloride, tetrachloroethylene. 1,1,2and 1,1,1-trichloroethane, chlorinated phenols, PCBs, chlorinated dioxins/furans). These anthropogenic sources have been considered in the identification of natural sources by the identification of the chlorinated chemicals in concentrations much greater than general ambient concentrations in remote locations, the identification of specific enzyme systems and substrates that produce the chlorinated chemicals (e.g., chloroperoxidase enzyme producing chlorophenols) and the identification of specific isomers of chlorinated chemicals that are not prevalent in anthropogenic sources (e.g., specific pentachlorobiphenyl isomers associated with volcanic ash) (Gribble, 1992). However, the natural sources of some halogenated chemicals have not been identified, yet the quantities identified exceed those known to arise from anthropogenic sources. For example, Gribble (1992) concluded that the estimated 650,000 tons of tetrafluoromethane was too large to due to anthropogenic sources alone, and it is unclear what portions of the 1,1,1 trichloroethylene (methylchloroform), difluorodichloromethane and fluorotrichloromethane identified at high elevations over eastern Washington are of biogenic origin. 128 129 130 131 132 133 134 135 136 137 138 139 140 141 142 Clearly, the evidence for the natural production of trichloroethylene, tetrachloroethylene and 1,1,1-trichloroethane combined with that for the transformation of these chlorinated alkanes and alkenes to VCM indicates that VCM is likely produced independent of human activities by these natural processes. However, no information is available, on the quantities of the various chlorinated alkanes and alkenes produced by natural processes, therefore estimates of the potential natural production rates of VCM cannot be obtained. ^ 143 144 145 146 147 148 2.2 ENVIRONMENTAL FATE v^ 149 2.2.1 Physical-chemical Properties ' ., /v, 150 The physical/chemical properties of VCM are summarized in (Table 2-1) and show that^CM has a high vapor pressure and low value. PVC, on the other hand, is an inert, highly Stable solid under a wide range of environmental conditions; however, because PVC is a polymer of variable numbers of vinyl chloride units, no physical/chemical properties can be determined. 151 R&S 143101 2-6 CanTox Depending on the polymerization process, some residual free vinyl chloride monomer remaining after the polymerization process; however, the use of best-available-technology involving proper temperature and pressure treatment in the final stages of manufacturing reduced the residual monomer concentrations to below analytical detection limits, 155 156 157 158 Table 2-1 Physical/Chemical Properties Chemical Name Vinyl Chloride Molecular Weight (g/mol)1 62.5 Vapor Pressure (Pa) 354637.5b 1 -from Merck, 1989, " -from Verschueren, 1983. Solubility (pg/L) noo" Logic 1.38 159 160 161 162 163 2.2.2 Environmental Fate 164 PVC is a highly stable polymer that remains a solid and does not degrade or migrate under normal environmental conditions. The environmental fate of degradation products formed during pyrolysis of PVC, and products of incomplete combustion are discussed in the Chlorine Institute document on Incineration of Chlorinated Organic Products. 165 166 167 168 Air 169 Hill et al. (1976) reported that the rate of exchange of gaseous VCM between water and air is twice that of oxygen, thus indicating that volatilization is the major process in the environmental disposition of VCM. The vapor density of VCM is higher than the vapbr density of air, 2.2 verses 1.0 (Anon., 1972), thus vapors of VCM tend to remain near the ground (Sax, 19S6). 170 171 172 173 In the environment, polymerization of VCM occurs in the presence of air, oxygen, sunlight or heat (Sax, 1986). In the troposphere, VCM undergoes photochemical oxidation with hf^rpjcyl radicals to form hydrogen chloride or formyl chloride. Formyl chloride undergoes further reactions to form carbon monoxide and hydrogen chloride. Since these reactions are extremely 174 175 1 1 R&S 143102 2-7 CanTox rapid, the degradation half-life of VCM in the troposphere is less than one day (EPA, 1975; EPA, 1979). 178 179 Water/Sediment 180 Sorption of significant amounts of VCM by sediments would occur only upon continuous input 181 of extremely high concentrations of VCM to aquatic systems (Hill et al, 1976). The adsorption 182 of VCM to particulate matter is considered insignificant as indicated by the same rates of loss 183 from distilled water, river water and industrial effluents (EPA, 1974). The reported log 184 octanol/water partition coefficient (K^) of VCM ranged from 0.60 (Radding et al., 1977) to 185 1.78 (Mckay et al., 1992), thus* adsorption to organic carbon and accumulation in lipid tissues 186 of aquatic biota would not occurs187 VCM is slightly soluble in water; however, due to its high vapor pressure, VCM entering aquatic systems would be rapidly lost to the atmosphere through volatilization (Sax, 1986; Vinyl Institute, 1990). The volatilization half-life of VGM from surface waters ranges from several minutes to a few hours depending on water turbulence (Dilling et al, 1975; Hill et al, 1976; EPA, 1979). 188 189 190 191 192 In groundwater, where volatilization cannot occur, VCM may be slowly hydrolyzed with a halflife of less than ten years (Hill et al, 1976; EPA, 1979; Smith and Dragun, 1984). Reaction products may include chlorinated alcohols and/or carboxylic acids^Smith and Dragun, 1984). 193 194 195 Direct phototransformation of VCM in surface waters would not be expected, since VCM absorbs shorter wavelengths of light than are present in the sunlight radiation, spectra at the earth's surface (Hill et al, 1976; EPA, 1979). However, indirect photolysis may be a factor in the transformation of VCM. Hill et al (1976) demonstrated that inadiatioh witlfultraviolet light transforms VCM, via energy transfer, when acetone or hydrogen peroxide are presesot. In Ss' .'jy such reactions, acetone acts as a high energy triplet sensitizer and hydrogen peroxide as a free radical source. However, oxidation of VCM in natural waters was not considered to be a significant reaction because of low temperatures and oxygen concentrations (Hill et al, 1976). 196 197 198 199 200 R&S 143103 2-8 CanTox There are limited data concerning the biotransformation of VCM. Luera/. (1977) reported that the high volatility of VCM prevented significant transformation in a model ecosystem. Mineralization of VCM to carbon dioxide may be possible under anaerobic conditions; however, further study is required for confirmation (Vogel and McCarty, 1985). 204 205 206 207 Early studies concluded that VCM was resistant to microbial transformation (Hill et al., 1976); however, more recent data shows that a strain of Mycobacterium can use VCM as a carbon and energy source in aerobic environments (Hartman et al., 1985). Mycobacterium were able to metabolize 70% of the carbon present as VCM to carbon dioxide and hydrochloric acid. 208 209 210 211 In soil-groundwater systems reductive dechlorination under anaerobic conditions is the predominant mechanism for the degradation of many volatile chlorinated hydrocarbons, and the production of ethylene from VCM has been hypothesized to occur through this mechanism (Smith and Dragun, 1984). The degradation of 90% of VCM by microorganisms in a shallow aquifer, with about 50% mineralization to carbon dioxide over at 106 day period has been demonstrated using 14C-VCM (Davis and Carpenter, Undated). 212 213 214 215 216 217 Soil 218 There is a paucity of information concerning the fate of VCM in soil. However, it is expected that VCM present in superficial soils would rapidly volatilize to the atmosphere. Sorption of VCM to sediment or soil from aqueous environments is not expected to be a very important transport process (EPA, 1979). As described in the previous section, biotransformation of VCM may occur in groundwater; thus, it is probable that under proper conditions biotransformation would also occur in soils. V 219 220 221 222 223 224 Environmental Fate Fugacity Modelling ', 225 R&S 143104 Fugacity modelling of chemicals in the environment provides predictions of the partitioning, movement and behaviour of chemicals within different environmental media based on the specific physical properties of chemicals. Level I fugacity modelling predicts the distribution 2' 2 2 2-9 CanTox of chemicals to air, water, soil, bottom sediment, fish and suspended sediment given a steady- 229 state situation where no removal of the chemical occurs by any chemical or physical processes. 230 Level n fugacity modelling provides predictions of the rates of loss of chemicals from various 231 compartments by reactive or advective means, again, under steady-state conditions. Level m 232 fugacity modelling provides predictions of the rates at which a particular chemical would move 233 between the various environmental compartments. 234 Vinyl Chloride 235 Level I Fugacity modelling was performed for VCM using physical and chemical properties (Table 2-2). The results are delayed graphically (Figure 2-1). 236 237 ^bleJ^2__Ph^sic^Chemicd^^^^esofVm^lCWoride^^_^__^^____^^^ Temperature C Molecular mass g/mol Vapor pressure Pa Solubility g/m3 Solubility mol/m3 Henry's Law constant Pam3/mol Log octanol-water partition coefficient Octanol-water partition coefficient Organic C-water partition coefficient 25 62.5/'; '' 354637.5 1.1 0.0176 2.0149E7 1.38 23.98833 9.835216 Fish-water partition coefficient Air-water partition coefficient Soil-water partition coefficient Sedt-water partition coefficient Susp sedt-water partition coefficient Amount of chemical moles Fugacity Pa Total of VZ products 1.15144 8128.813 0.2950565 0.590113 0.590113 1000 4.131365E-4 2420508 238 239 240 241 242 243 244 245 246 247 The results of the fugacity modelling indicate that virtually all VCM will partition towards the air with very small amounts distributing to the other compartments. This partitioning is consistent with the high vapor pressure of VCM. Figure 2-1 R&S 143105 2-10 2.3 VINYL CHLORIDE REGULATIONS CanTox 254 2.3.1 Regulations of VCM in Air 255 2.3.1.1 Air Concentrations in Emissions Regulation of emissions of VCM from manufacturing plants in the United States, effective as of July 1, 1979, requires that VCM concentrations in air emissions remain less than 25 mg/m3 (10 ppm) by volume or total releases remain less than 2 kg/day, which ever is greater (Gendron, 1981). According to IARC (1979), the EPA (1977) proposed to be reduced the air emission guideline to 13 mg/m3 (5 ppm) ; ; The Federal Republic of Germany has an emission standard of 3 kg VCM/hour/source (150 mg/m3 at the source) (Thomas, 1977). 256 257 258 259 260 261 262 263 In Canada there are regulations regarding ambient air concentrations and emissions. The Ontario Ministry of the Environment (1991) guideline value for annual average VCM concentrations in ambient air is 0.2 jtg/m3 based on the estimated exposure limit for the potential development of cancer at a risk level of one per 100,000. Elsewhere in Canada, the Federal Vinyl Chloride National Emission Standards Regulations (SOR/79-299) and the Vinyl Chloride Release Regulations (SGR/90-25) stipulate that air VCM concentrations in any process vent must not exceed 25 mg/m3 (10 ppm) (by volume, measured dry and undiluted), or two kg/day VCM released into the ambient air. For polyvinyl chloride plants, the air concentrations in any process vent must not exceed ten ppm VCM. Regulations of emissions specific to the manufacture of certain resins are also included. 264 265 266 267 268 269 270 271 272 273 No information concerning the environmental concentrations or emission regulatory guidelines 274 or criteria for polyvinyl chloride was identified. 275 2.3.1.2 Regulations of VCM in Water 276 -''/sVs The U.S. drinking water criteria value proposed by the EPA (1991) for VCM in water for human consumption was 2 /xg/L. This value was based on estimated exposure limits for 2' ^ go 2' w c-co* 2-11 oo> CanTox potential cancer in humans at a risk level of 10-6. This criteria level was unchanged from that developed for water consumption by the EPA in 1980 (EPA, 1986). EPA (1986) also reported a Maximum Contaminant Level (MCL) of 925 ^g/L for VCM in water. The quality standard specification used for VCM in ground water in New York State is 5.0 /xg/L (New York State Department of Environmental Conservation, 1986). 279 280 281 282 283 2.3.1.3 Soil 284 No information was identified on soil or sediment quality guidelines or criteria for VCM. Since the environmental fate characteristics of VCM indicate that air is its major environmental medium, soil would not be expected to be an important environmental compartment for VCM. 285 286 287 R&S 143107 2-12 30 0 (/) cuo o CanTox Chapter 3 Potential Environmental Hazards and Health Significance qf Environmental Concentrations of VCM R&S 143111 3.0 INTRODUCTION CanTox The methods for characterizing the risks due to exposure to chemicals such as VCM are outlined in the Chlorine Institute document entitled General Introduction and Methodology for the Evaluation of the Potential Environmental Effects of Chlorine and Chlorinated Chemicals. Basically, these methods involve estimating potential human exposures to VCM from various environmental sources, and comparing these exposures to exposure limits that are considered protective of human health. Therefore, Chapter 3 summarizes i) the information available on the concentrations of VCM in various environmental media, ii) the toxicological/epidemiological information available on the potential health hazards that could result from exposures to VCM, iii) the procedures used to estimate an exposure limit for VCM, and iv) the comparison between the estimated exposures through/Various environmental media and the exposure limit to characterize potential human health risks^o VCM. In addition, the potential effects of ambient sources of VCM on aquatic and terrestrial wildlife are assessed. 3 4 5 6 7 8 9 10 11 12 13 3.1 ENVIRONMENTAL CONCENTRATIONS 14 The concentrations of VCM in the environment is determined by the types of environmental releases that occur during production and manufacturing processes. In 1988, an estimated total of approximately 2 million pounds of VCM was either releases or transferred from production facilities in the U.S. Of this total, approximately 67% was released into the air, 0.1% into surface waters and 0.1% to land. The remaining approximately 32% ,was transferred off-site (EPA-TRI, 1988). This information indicates that the environmental, concentrations of vinyl chloride would be highest in air near production and manufacturing facilities. Therefore, the following discussion of environmental concentrations of VCM focuses on air, and is divided into the work place and immediate environment near production/manufacturing facilities, and regions distant (remote) from such facilities. 15 16 17 18 19 20 21 22 23 24 R&S 143112 3-1 CanTox 3.1.1 VCM Concentrations Associated With Production/Manufacturing Facilities 25 Concentrations in the Work Environment 26 Standards for the concentrations of VCM in the work environment were presented in Section 2.3.1. Generally, VCM concentrations in the workplace prior to the 1960s were greater than 100 ppm, were less than 100 ppm after 1960 and decreased to a limit of 5 ppm (8 hour, timeweighted average (TWA)) by 1975 (Doll, 1988; ACGIH, 1991). The current OSHA workplace standard in the U.S. is 1 ppm (8 hr TWA) with a 5 ppm short term exposure limit (STEL). 27 28 29 30 31 Recent data from four PVC resinproduction facilities in the U.S. indicate that the concentrations of VCM (8 hour TWA based on-individual personnel monitoring) in the work environment ranged from approximately <0.25 toiO.5 mg/m3 (< 0.1 to 4.11 ppm) in 1988, and decreased to a range of approximately <0.25 to 2 ,mg/m3 (< 0.1 to 0.77 ppm) in 1992 (January to September only). In 1990, one facility reported 8 hr. TWA air concentrations for instrument technicians and process operators of 35 to 26.5'mg/m3 (13.5 and 10.34 ppm), respectively. Reactor operators, loading personnel and laboratory -technicians showed the greatest potential exposures, with 8 hr. TWA air concentrations ranging from 0.5 to 11 mg/m3 (0.2 to 4.11 ppm) in 1988, decreasing to 0.5 to 2 mg/m3 (0.2 to 0.77 ppm) in 1992 (Vinyl Institute, personal communication, 1992). These data represent the greatest air concentrations reported for the four facilities over the 5 year period, 1988 through 1992. 32 33 34 35 36 37 38 39 40 41 42 Concentrations Near Production/Manufacturing Facilities Localized environmental releases of VCM are associated with production and . manufacturing facilities, therefore, their environmental concentrations are highest in and aroundsuch facilities. Due to the implementation of occupational health standards, the concentrations of VCM in the work environment in the Netherlands decreased from approximately 2600 mg/m3 (l(XJ0ppm) in 1945-1955 to approximately 12 mg/m3 (5 ppm) after 1975 (Barnes, 1980). These decreases in concentrations of VCM in the work environment also would also be indicative of decreases 43 44 45 46 47 48 R&S 143113 3-2 CanTox in environmental releases. However, no information on this point was identified since the focus on measuring air concentrations of VCM has been on various "hot spots". 51 52 Vinyl chloride has been measured in air and in both ground and drinking water in areas near production and manufacturing facilities the United States. Prior to the implementation of VCM emission regulations in 1978, the average air concentrations of VCM at production facilities in the United States was 44 /xg/m3 (17 ppb) (IARC, 1979). In Houston. Texas where large quantities of VCM are produced, air concentrations ranged from 8 /xg/m3 (3.1 ppb) to peak values of 3,200 /xg/m3 (1,200 ppb) (Gordon and Meeks, 1977). In Long Beach, California, ambient air concentrations of VCM near two VCM plants ranged from 260 to 8,800 /xg/m3 (100 to 3,400 ppb), and these facilities' were estimated to have released 12.3 kg of VCM/day in waste water effluent (National Field Investigations Center, 1974). However, within approximately one kilometer of VCM production/mamjfacturing facilities, reported air concentrations of VCM ranged from approximately 26 to 100 /xg/m3 (10 to 40 ppb) (EPA, 1975; Baxter et al., 1977). 53 54 55 56 57 58 59 60 61 62 63 More recent information based on sampling near production/manufacturing facilities since standards for the work environment were reduced to about 13,000 /xg/m3 (5 ppm) in 1975, showed that air concentrations of VCM were near the analytical detection limit (about 13 /xg/m3 or 5 ppb) in three of five British plants. For two other facilities, the VCM air concentrations were approximately 50 /xg/m3 (20 ppb) 100 m outside the facility boundary, and 225 /xg/m3 (88 ppb) just inside the boundary fence (Turner et al., 1984). 64 65 66 67 68 69 The highest level of VCM measured in U.S. drinking water was 10 /xg/L near a production facility (IARC, 1979). Vinyl chloride has also been reported in ground water in the U.S. Measurable levels in California wells averaged 20 /xg/L and were as high as 23 /xg/L (Kizer, 1986). In the Los Angeles area, ground water to contain less than 1 /xg/L of VCM (Baird et al. 1983), while in non-specified areas of Nebraska and California ground water concentrations ranged from 0.75 to 23 /xg/L (Goodenkauf and Atkinson, 1986; CSDHS, 1990). "^0 70 71 72 73 74 75 R&S 143114 3-3 CanTox 3.1.2 VCM Concentrations Remote from Production and Manufacturing Facilities 76 No information was identified on the concentrations of VCM in air in locations remote from industrial activities. However, it would be expected that the VCM concentrations in such locations that are derived from human activities would be below analytical detection limits, based on: i) the continuing decline in VCM concentrations in the workplace (Table 2-2), ii) the low concentrations measured near production/manufacturing facilities using VCM (EPA, 1975; Baxter et al., 1977; Turner et al., 1984), and iii) the rapid vaporization of VCM and subsequent destruction in the atmosphere. 77 78 79 80 81 82 83 3.2 HAZARD ASSESSMENT 84 The chemicals addressed in this document are polyvinyl chloride (PVC) and vinyl chloride (VCM). 85 86 3.2.1 Polyvinylchloride 87 In the scientific literature, PVC has also been referred to as chloroethene homopolymer, chloroethylene polymer, vinyl chloride homopolymer, and vinyl chloride polymer. 88 89 There are limited data regarding the toxicology of PVC, with the majority of studies focusing on the pulmonary effects of this polymer. No data on the embryotoxicity, teratogenicity, metabolism, or mutagenicity of this compound were identified by IARC^1979) or subsequent searches of the available literature. # 90 91 92 93 3.2.1.1 Bioavailability, Metabolic Conversion (Pharmacokinetics), and Bioaccumulation ' 94 95 - '* The available data indicate that following a single dose of intratracheally instilled PVC difst (< 0.5 pim) in rats, the particles are cleared through the lymphatic circulation and progressively accumulate in the tracheobronchial lymph nodes (Agarwal et al., 1978; Takenaka et al., 1987; R&S 143115 3-4 CanTox Agarwal et ai, 1991). Ingested or rectally administered PVC particles were observed within the lymph vessels associated with the intestinal wall of rats, guinea pigs, rabbits, chickens, dogs, and pigs (Volkheimer, 1975). Particles were observed in the blood, bile, urine, and cerebrospinal fluid of dogs, and in the blood of other species, but details of the experimental methods and results were not provided (Volkheimer, 1975). There is no information on the potential bioavailability orbiotransformation ofPCV. 99 100 101 102 103 104 3.2.1.2 Mammalian Toxicology (Laboratory Animal and Biochemical Studies) 105 Lethal Effect 106 PVC is relatively inert and nolethality datahavebeen reported. 107 Non-Lethal Effects 108 The weight-of-available-evidence from data generated by inhalation and intratracheal exposure to PVC particles in experimental animals, indicates that PVC itself possesses little or no biological activity, with its physical presence producing benign pneumoconiosis typical of a nuisance dust at elevated dust concentrations (Pigott and Ishmael, 1979; Groth et ai, 1981; Richards etal., 1981; Wagner and Johnson, 1981; Tetley etal., 1981; Agarwal, 1983; Agarwal et ai, 1991). Flaws in experimental design, and concomitant exposures to other chemicals makes the significance of earlier studies where animal exposed to PVC dusts by inhalation studies showed pulmonary fibrosis and significant respiratory toxicity, (Popow, 1969; Frongia etal., 1974). ... 109 110 111 112 113 114 115 116 117 Carcinogenicity 118 ' - Since vinyl chloride has been recognized as a carcinogen (IARC, 1979, 1987), the potential . Sr carcinogenicity of PVC has received particular scrutiny (Montgomery, 1982). IARC (1979, 1987) concluded that the evidence for PVC carcinogenicity was inadequate based on several 119 R&S 143116 3-5 CanTox animal studies, and that the carcinogenicity of PVC was unclassifiable (Oppenheimer et al., 1952, 1955; Kogan and Tugarinova, 1959; Russell et al., 1959; Raikhlin and Kozan, 1961). 122 123 3.2.1.3 Epidemiology Studies 124 Based upon the epidemiological evidence available, exposure to extreme concentrations of PVC dusts in the work environment can lead to a low grade pneumoconiosis, similar to that experienced with inhalation of other unreactive, nuisance dusts. Chest X-rays of workers often have shown abnormalities, yet these changes have not always been associated with decreased lung function (Miller et al, 1975; Gamble et al., 1975; Lilis et al., 1976; Mastrangelo et al., 1979; Soutar et al., 1980; Chivers et al., 1980; Mastrangelo et al., 1981; Wagoner, 1983; Baser et al., 1985; Ernst et al., 1988; -Sifacusa et al., 1988; Nielsen et al., 1989; Lee et al., 1991; Ng et al., 1991). The epidemiological data on the respiratory effects of PVC dusts in humans also indicates that such exposure has not produced neoplastic effects. v" Other studies have investigated the effects of PVC degradation products, particularly following heating or combustion. PVC, under these conditions, can release hydrogen chloride gas or large amounts of carbon monoxide, depending on the oxygen supply (Montgomery, 1982). 125 126 127 128 129 130 131 132 133 134 135 136 Two large epidemiological studies have been carried out that have examined the mortality and cancer incidences of workers in the plastics industry, including PVC fabricators (Baxter and Fox, 1976; Chiazze et al., 1977). IARC (1979) concluded that*,although there were excess incidences of certain cancers, these studies were limited in that not'hll the workers studied were engaged in activities directly involving PVC. In addition, monomeric vinyl chloride, a recognized human carcinogen, was likely present in these work environments. In 1974, it was reported that PVC leaving certain manufacturing plants may have contained as much as 200-400 ppm vinyl chloride (IARC, 1979), although current manufacturing technology. is capable of producing general PVC which contains less than 1 ppm residual monomer, while modern `ssy'' ^ medical grade PVC is believed to contain less than 10 ppb VCM (Van Dooren, 1991; Ttibmas and Ramstad, 1992). # 137 138 139 140 141 142 143 144 145 146 R&S 143117 3-6 3.2.1.4 Exposure Limits CanTox 148 The American Conference of Governmental Industrial Hygienists (ACGIH) considers occupational exposure to PVC dusts under the category Particulates Not Otherwise Classified (PNOC). The threshold limit value (time-weighted average) (TLV-TWA) for this category is 10 mg/m3 (ACGIH, 1992). The United States Occupational Safety and Health Administration (OSHA) has set limits for inert or nuisance dusts of 15 mg/m3 (total) and 5 mg/m3 (respirable), not regulating PVC directly (29 CFR 1910). Germany, Switzerland, and the United Kingdom have set TLV-TWA limits of PVC (respirable dust) of 5 mg/m3 (ILO, 1991), as have Sweden and Norway (Norsk Hydro, 1992). 149 150 151 152 153 154 155 156 3.2.2 Vinyl Chloride 157 In the scientific literature, VCM has also been referred to as chloroethene, chloroethylene, monochloroethylene, and vinyl chloride monomer. 158 159 3.2.2.1 Bioavailability, Metabolic Conversion (Pharmacokinetics), and Bioaccumulation 160 161 Bioavailability 162 Based on measured 14C in the urine and expired air, between 70 and 95% of the dose was absorbed following a single oral administration of [14C]VCM (0.05-100 mg/kg body weight) to male rats (IARC, 1979). >>" . 163 164 165 Absorption of VCM through the skin is considered to be low. Calculations,based on the percutaneous absorption of VCM using Rhesus monkeys indicated that a six-foot, Wkg man ,-sy exposed to 7000 ppm (dermal) for two hours would absorb the equivalent of approximately .0.2 ppm (EPA, 1980). ^ 166 167 168 R&S 143118 3-7 CanTox At room temperature, VCM exists as a gas, therefore, inhalation is the most significant route of exposure. Data obtained from the rat indicated that VCM is rapidly absorbed by the lung and readily metabolized (Hefner et al., 1975). Following exposure of male rats to 10 ppm [14C]VCM in the air for six hours. 68% of the radioactivity was excreted in the urine within 72 hours, with approximately 2% exhaled unchanged. Similar exposure to 1000 ppm resulted in a lower proportion of radioactivity excreted in the urine and that expired as VCM higher, representing 56 and 12%, respectively (Watanabe et al, 1976; Holmberg, 1984). In a similar system, rats exposed to initial concentrations less than 100 ppm [1,2-UC]VCM in the air absorbed approximately 40% of that inhaled. Within 24 hours, 70% of the radioactivity was recovered in the urine. 170 171 172 173 174 175 176 177 178 179 Metabolism 180 Vinyl chloride is metabolized by the cytochrome P450-dependent polysubstrate monooxygenase system (P450) to the reactive epoxide intermediate chloroethylene oxide, which rearranges spontaneously to chloroacetaidehyde (Bolt etak+ 1976; IARC, 1979). As reviewed in IARC (1979), the epoxide has also been shown to be capable of reacting with macromolecules such as DNA, RNA, and protein, forming covalently bound adducts (Kappus et al, 1975; Kappus et al., 1976; Bolt and Filser, 1977). These reactions have been elucidated through results obtained with mouse or rat subcellular fractions or P450 inhibitors and inducers, as there are no data yet available for this pathway in vivo (Gothe et al, 1974). Chloroacetaidehyde has been shown to combine directly or enzymatically (glutathione S-transferse-mediated) with glutathione to form S-formylmethylglutathione, which is excreted as N-acetyl-S^(2-laydroxyethyl)cysteine. Chloroacetaidehyde is also oxidized to chloroacetic acid, which is either-excreted as such or bound to glutathione in the form of S-carboxymethyl glutathione (Green and Hathway, 1977; Plugge and Safe, 1977). 181 182 183 184 185 186 187 188 189 190 191 192 193 R&S 143119 3-8 Bioaccumulation CanTox 194 As indicated in the preceding sections, VCM is rapidly metabolized and excreted, therefore, it does not accumulate in biological systems. Metabolism is so rapid that no VCM per se has been identified in the tissues of animals following exposure to high concentrations, even though the alkylation of DNA and other macromolecules occurred (Watanabe et al. 1976; Bergman, 1982). Following dosing of rats with [14C]VCM via inhalation and oral routes, between 2-15% of the radioactivity was measured in the carcass after 72 hours (IARC, 1979), however, the identity of the compounds containing the radioactivity wasunknown. 195 196 197 198 199 200 201 Excretion 202 In rats, the majority of VCM absorbed by the body is excreted in the form of highly watersoluble metabolites by the kidneys, with up to 70% of the radioactivity associated with a dose of [UC]VCM being recovered in the urine within 24 hours (Watanabe et al., 1976; Bolt et al., 1976). Metabolites that were not excreted in the urine were partly excreted via the feces and partly via expiration of 14C02 (Green and Hathway, 1975; Bolt et al., 1976) 203 204 205 206 207 3.2.2.2 Mammalian Toxicology (Laboratory Animal and Biochemical Studies) 208 Lethal Effects 209 The acute lethality of VCM is low. The two-hour LCJ0 of VCM for rats, .mice, guinea pigs, and 210 rabbits ranges from 113000 to 230000 ppm (294 to 595 g/m3) (IARC, 1979). Vinyl chloride 211 gas produces narcosis or anesthetic effects, with death following extremes exposures being 212 preceded by excitement,contractions and convulsions,accelerated respiration, and respiratory 213 failure. Microscopically, acutely lethal doses are associated with congestion of tfieiintemal 214 organs, with intense damage to the lungs, liver, and kidneys (IARC, 1979). Hepatotoxicity is 215 observed laboratory animals after single, high but nonlethal exposures (Prodan et al., 1975). 2 The induction of cytochrome P450 mixed function oxidase enzyme systems, and the depletion 7 of hepatic glutathione stores prior to exposure enhances the hepatotoxic effects of VCM (IARC, 7 R&S 143120 3-9 CanTox 1979). This effect is of particular interest in interpreting effects from chronic exposures at low doses in both animals and in humans. 219 220 Non-Lethal Effects 221 Teratogenicity 222 The available studies reviewed by EPA (1987a) indicate that VCM is not teratogenic in mice, rats, or rabbits exposed via inhalation to air concentrations of 500 ppm, 6000 ppm, and 2500 ppm during the period of majpr organogenesis In some cases, inconclusive findings of increased fetal deaths or minor skeletal Variations have been reported; however, these findings occurred only at levels producingmatemaktoxicity (EPA, 1984). 223 224 225 226 227 Carcinogenicity 228 A large number of experimental studies on VCM carcinogenicity in a number of species, routes of exposure and dosages have been reviewed by IARC (1979) (Viola et al., 1971; Holmberg et al., 1976; Maltoni et al., 1981). Based on these studies it was concluded that there is sufficient evidence for carcinogenicity to animals (IARC, 1979, 1987). Vinyl chloride administered orally or by inhalation to mice, rats and hamsters produced an. increased tumor incidence in the mammary gland, lung, Zymbal gland, and skin, in addition to hepatocellular carcinomas and angiosarcomas of the liver. In one study, a combination of orally administered ethanol and inhalation of VCM resulted in more liver tumors (including angiosarcomas) than after treatment with VCM alone (Radike et al., 1981). The most comprehensive and in-depth investigation of VCM carcinogenicity (Maltoni et al., 1981) concluded: i) VCM induced tumors in all species and strains of animals tested; ii) tumors of different types were induced at different sites; iii) angiosarcoma of the liver occurred in all species of animal tested; iv) VCM was carcinogenic by inhalation and ingestion, and possibly by injection; v) obvious dose-response relationships were observed for both ingestion and inhalation experiments; vi) treatment duration and schedule markedly affected the neoplastic response, as did the species strain, and sex of the animals tested; vii) neonatal animals were highly responsive; viii) VCM acted as a transplacental 229 230 231 232 233 234 235 236 237 238 239 240 241 R&S 143121 3-10 CanTox carcinogen; and ix) it was carcinogenic at very low exposure levels (i.e.. 50 ppm and lower) (Calabrese and Kenyon. 1991). 245 246 Mutagenicity 247 Vinyl chloride vapor induced reverse mutations in a number of Salmonella typhimurium strains in the presence of an activation system (i.e. 9000 x g supernatant of rat liver). The response was much greater in the presence of activation systems, yet in its absence, VCM was still able to induce mutations. In addition, VCM has been reported to induce reverse mutations in E. coli, forward mutations in Schizosaccaromyces pombe, mitotic gene conversions in S. cerevisiae, and forward mutations in Chinese hiamster ovary cells. The fact that these responses occurred in the presence of a metabolic activation system, indicated that a metabolite(s) was predominantly responsible for the observed mutagenicity. Vinyl chloride has also been found to give positive responses in the Drosophila sex-linked recessive lethal assay, but negative in other Drosophila assays, including those designed to detect translocations, sex chromosome loss, and dominant lethal effects (IARC, 1979; Calabrese and Kenyon;": 1991). Recently, workers exposed to VCM at levels of 5 to 500 ppm developed chromosomal aberrations in peripheral blood lymphocytes (IARC, 1987). 248 249 250 251 252 253 254 255 256 257 258 259 260 The mutagenicity of several possible metabolites of vinyl chloride has also been examined. 261 Chloroethylene oxide was found to be the strongest mutagen; among those tested in S. 262 ryphimurium, E. coli, S. pombe, S. cerevisiae, and V79- Chinese hamster cells. 263 Chloroacetaldehyde was mutagenic in S. typhimurium and V79 Chihese^hamster cells, while 264 chloroethanol was weakly mutagenic in S. typhimurium, and chloroacetic acid was not mutagenic 265 in S. typhimurium (IARC, 1979). v- , 266 3.2.2.3 Mechanisms of Toxicity '^ 267 R&S 143122 Vinyl chloride has been shown to be activated, via P450 mixed function oxidase enzyme systems, to a reactive epoxide intermediate. Hepatotoxicity increases following administration of P450 inducers such as phenobarbital, aroclor 1254 (a PCB mixture), and hexachlorobenzene 3-11 CanTox (IARC, 1979; Anonymous, 1987). In addition, VCM has been shown to alkylate N4-cvtidine. N*-adenosine, and N7-guanosine of liver DNA in mice (Osterman-Golkar et ai, 1977). 271 272 3.2.2.4 Epidemiology Studies 273 Both IARC and the U.S, EPA have concluded, based on evidence from workers following extended periods (e.g., 20 years or more) to extremely high concentrations of VCM (e.g,, > 100 and possibly up to 1000 ppm), that there is sufficient evidence for VCM carcinogenicity in humans based upon the epidemiological data (EPA, 1987a; IARC, 1987). The critical review of the available epidemiological data conducted by Sir Richard Doll (1988) forms the basis of the following assessment of VGM. As pointed out by Doll (1988), a number of studies of workers exposed to VCM have-demonstrated that excessive exposure are associated with a hazard of angiosarcoma of the Uver. ;: However, when a large number of studies are conducted to address pre-defined correlations between events (e.g., VCM exposure and angiosarcoma), findings of significant correlations would be expected in independent studies about once in 20 times. Therefore, it is important to determine whether the correlations observed are causally related to VCM exposures, or due to chance alone) To address this question, Doll (1988) conducted a critical examination of the epidemiological data from comparable studies. The criteria used to ensure the studies were comparable were: i) the exposure levels to not necessarily have to be the same; ii) the observations of the exposed populations occur over a period of time when a clear hazard existed, and iii) the reference, or control populations from which the expected incidence rates are derived should be as similar to the study population as possible, except for the absence of exposure to the agent in question (.g..,, VCM). Doll (1988) concluded that at the time of his review, four studies were available that met the criteria necessary for comparability: the national survey for the United Kingdom (UK) (Jones, 1988), the national survey in the U.S. (Environmental Health Associates, 1986), and the study of a VCM production/manufacturing facility in Quebec, Canada, (Theriault and Allard,T981) and a VCM production/manufacturing facility in Italy (originally quoted as Belli et al. by^Doll, 1988, but finally published as Maltoni and Cotti, 1988). All four studies encompassed 25*years post-first-exposure. All of the facilities in the four studies included the production of VCM and PVC, but not the manufacture of PVC products, thus avoiding confounding of the interpretation 3-12 274 275 276 277 278 279 280 281 282 283 284 285 286 287 288 289 290 291 292 293 294 295 296 33 </> 4>h CO -A. to CO CanTox of the results by marked differences in the levels of exposure to VCM, and the effects of exposures to PVC dusts (see Section 3.2.1.3 on PVC for discussion of such effects). 300 301 The U.S. study (Environmental Health Associates, 1986) included 10,173 workers (97% white races) from 37 facilities. Twenty-two of the facilities were in the southern U.S., 14 in the northeastem-northcentral, and one in the west. Exposures began at least one year before December 31, 1972, and the first exposures started in 1942. Except for one facility (955 employees followed till December 31, 1972), follow-ups of the workers were conducted to death or until December 31, 1982. A large portion of the workers were observed for 25 or more years after first exposure`since approximately 46% first worked in the facility prior to 1955. Doll (1988) considered there were three minor and two major criticisms of this study. The minor criticisms were: i) the list of employees were compiled by the companies without an independent review, ii) it was assumed all employees were white (3% were black), and white race mortality rates were used for comparisons, and iii) 7.3% of the employees would not be traced. The major criticisms were: i) mortality rates of the workers were compared to those for white males for the whole country, whereas a significant number of the facilities were in the south and these comparisons do not enable consideration of the "healthy worker" effect, and ii) no causes were identified for 97 of the 1,536 deaths in. the cohort, and this deficiency was not considered in calculating the disease specific mortality rates. This deficiency could have resulted in underestimation of the standardized mortality ratios by 6.3%. 302 303 304 305 306 307 308 309 310 311 312 313 314 315 316 317 318 The UK study (Jones, 1988) evaluated 5,498 workers who experienced at least one year of exposure to VCM for at lease 25% of each work week over a period between 1940 and 1974. Vital status was evaluated in December, 1984. Follow-ups were completed on 98.9% of the men, and 780 deaths were identified. Minor criticisms of the study included: i) national mortality rates for England and Wales for 5-year age groups over quinquennial periods for 66 causes of death were used as reference comparisons to the incidence rates for diffeir6nt causes of death in the workers. Definitions for the 66 causes of death were added oyer the observational period, and therefore, not all categories could be compared over all time periods of observation; ii) attempts were made to classify exposures as low, medium or high; however, within the groups the exposures were much higher at the beginning than at the end of the 319 320 321 322 323 324 325 R&S 143124 3-13 CanTox observation period, presumably due to up-grading of the work environment. In addition, workers often moved from one exposure category to another with changes in job specifications. These factors would tend to overestimate the numbers of deaths in the first two exposure categories (Doll, 1988). 329 330 331 332 The Canadian study (Theriault and Allard, 1981) reported on 1,611 of a total of 1,659 (97.1 %) 333 employees who worked between January 1, 1948 and December 31, 1972 at a facility that 334 manufactured VCM and PVC between 1943 and the late 1960s, at which time VCM production 335 ceased but PVC production continued. Detailed occupational and tobacco smoking histories 336 were obtained through union lists and interviews with next-of-kin, and 156 individuals employed 337 for less than 5 years were excluded from the assessment. The workers were divided into three 338 groups: i) exposed to VCM (451 workers); ii) unexposed (870 workers); and iii) others where 339 exposures were uncertain (134 worker^,;who were excluded from the assessment. Follow-ups 340 of death certificates was closed on December 31, 1977. A total of 59 exposed (75 % with > 10 341 years exposure) and 233 unexposed were included in the final assessment, with 342 histological/cytological information sought on -all exposed men who died of cancer. 343 Approximately 44% of the workers were observed > 25 years from the first exposure. Mortality 344 and causes of death as specified on death certificates for the exposed and unexposed groups were 345 compared after standardization for 5-year periods and 5-year age groups; and were compared 346 with the mortality expected for similar sex- and age-groups in Quebec in 1971. This procedure 347 may have caused some distortion in the expected numbers of deaths since it did not cover the 348 1948 to 1977 period; however, Doll (1988) considered such distortion was "unlikely to have 349 been large". 350 The histopathological examinations were particularly valuable in the interpretation of the effects of VCM exposures; and showed that all 8 liver cancers diagnosed were angiosarcomas, and one additional cancer was diagnosed as angiosarcoma of the peritoneum. Two cases'of angiosarcoma had also been certified as hepatic cirrhosis. The relative risk of death from all causes was:0.95, showing the "healthy worker" effect. 351 352 353 354 DO & </> 03 to CanTox The Italian study (Maltoni and Cotti, 1988) began in 1983 and focused on workers from nine 356 VCM and PVC production facilities in Italy. The study was incomplete in 1988. therefore, the 357 Doll (1988) review followed workers up to 1983 from two production facilities which began 358 operations in 1953 (457 and 181 men in each plant). The expected mortality rates were 359 estimated by multiplying the person-years at risk by the corresponding national mortality rates 360 for each 5-year age group and 5-year period of the study. The expected deaths amounted to 361 12.4 and 12.8%, respectively, of the workers in the two plants. The final diagnosis indicated 362 a total of four deaths from liver cancer. Doll (1988) excluded from his analysis, the information 363 from a third Italian facility because none of the follow-ups covered more than 24 years, and the 364 expected mortality was only 3.9% of the workers. 365 A follow-up to the Italian study was published by Pirastu et al. (1990), indicating that extreme 366 VCM exposures of workers were/associated with significant increases in both liver 367 angiosarcomas and hepatocellular carcinoqias. Considerable animal data and human studies on 368 the drug Thorotrast are quoted by the authors as supporting evidence for a relationship between 369 VCM exposure and heptaocellular carcinoma, ^.addition to angiosarcomas. However, no 370 reference is made to the marked hyperproliferative effects observed in laboratory animals 371 following extreme exposures to VCM (Feron et al., 1981) and the documented evidence between 372 hepatocellular hyperproliferation and hepatocellular carcinomas in rodents (Popper and Thomas, 373 1977). In addition, the numerous vagaries associated with death certificate diagnosis of 374 particular types of cancers, as pointed out by Doll (1988), raise/.concerns regarding the data 375 presented by Pirastu et al. (1990). It would appear that the weight-ofiayailable-evidence remains 376 in agreement with the conclusions reached by Doll (1988) that the primary carcinogenic effects 377 of VCM are related to liver angiosarcoma. Although hepatocellular/carcinomas may be 378 associated with extreme exposures to VCM, it would appear that their occurrence is more likely 379 secondary to concurrent hepatocellular hyperproliferation. 380 A number of other studies were also available on Norwegian, Swedish, German, Franc and 381 Japanese workers (Doll, 1988) that contributed supporting evidence, but exhibited a variety of 3 factors that confounded the interpretation of the data produced (e.g., inadequate identification 3 of cohort members lost from follow-up, exposures to a variety of other chemicals in addition to 3 R&S 143126 3-15 CanTox VCM and PVC, lack of comparative mortality statistics for the reference populations during the critical period of worker exposures and mortality). 385 386 From the analyses of the four main studies, using the remaining studies as supporting 387 information, Doll (1988) reached two major conclusions: i) Apart from liver cancer, the overall 388 mortality of the VCM/PVC workers exposed between the 1940s/ 1950s and mid-1970s was what 389 would be expected from industries that do not have unusual hazards of accident or disease. The 390 standard mortality ratios (SMR) of approximately 84 were considered typical for diseases other 391 than cancer, considering the "healthy worker" effect. The SMR of 102 for total cancer 392 mortality, other than cancers of the liver, were considered compatible with the absence of 393 hazard; ii) workers exposed toWCM concentrations of "several hundred parts per million or 394 more" clearly showed an increased hazard (risk) of contracting angiosarcoma of the liver, 395 normally an extremely rare disease (annual incidence of 1 to 2 x 10"7 in the general population; 396 Byren and Holmberg, 1975). Since death certificates are considered highly unreliable in 397 identifying specific types of cancers, Doll (1988) assumed that the 7-fold excess in liver cancers 398 were all due to angiosarcomas. In the four major studies examined, approximately 2% of the 399 deaths observed were attributable to angiosarcoma of the liver. 400 Doll (1988) also concluded it was "difficult to decide whether vinyl chloride produces small risks 401 of cancers, compared to those due to nonoccupational causes, at sites other than the liver". In 402 sufficient evidence was available to confirm, or refute, the possible causal relationships between 403 occupational exposures to VCM and melanoma or cancer of the thyroid, brain, and the lymphatic 404 or haematopoietic systems. In addition, the evidence of increased risks ofiung cancer following 405 occupational exposures to VCM were considered weak and unproven. 406 Doll (1988) also concluded that, since VCM is a proven mutagen and carcinogen in laboratory v ; studies, and a carcinogen to humans, the minute exposures that would result from emissions 407 408 escaping from VCM facilities must cause comparably minute risks to the general publipf' The 409 concentrations of VCM measured near VCM/PVC production/manufacturing facilities are in the < order of 10 to 40 ppb (EPA, 1975; Baxter et al., 1977), or some 10,000-fold less than the < several hundred or more ppm exposures that resulted in measurable occupational hazards. < R&S 143127 3-16 CanTox Therefore, cancer risks to the general public could not possibly be detected, with the possible exception of angiosarcoma of the liver, because of its extremely low incidence rate in the general population. The interpretation of causal relationships between VCM and angiosarcoma incidence in the general population is confounded because thorium dioxide and arsenic in pesticides and medicines have also been associated with the occurrence of angiosarcomas (Doll, 1988). 4i3 414 415 416 417 No cases of angiosarcoma were detected in populations living near VCM or PVC production 418 facilities in Yugoslavia and Sweden (Saric et al, 1976; Elinder et al., 1981). In the UK, one 419 cases out of 14 over a 12 year period was found in a man who lived half a kilometre from a 420 PVC manufacturing facility. In New York state, 5 of 19 cases of angiosarcoma were in people 421 living within 1 mile of facilitiesYising or manufacturing VCM (Baxter et al., 1977). However, 422 more detailed examination of the^neighbourhood" cases showed that 2 could not be attributed 423 to VCM because the men only livedfnear the facilities for 6 and 8 years, respectively, a time 424 period too short for the latency period .needed for angiosarcoma. Therefore, Doll (1988) 425 concluded that the discovery of four cases of angiosarcoma in people who lived near facilities 426 that used VCM indicated there may have beenaitiinute hazard to the general public from the 427 VCM concentrations historically observed around inanufacturing facilities. However, the 428 concentrations of VCM around production facilities has decreased substantially since the 1970s. 429 VCM air concentrations within a few hundred meters of VCM areas were below analytical 430 detection limits (approximately 5 ppb) for three of five facilities in the UK, and the 431 concentrations for the other two facilities were about 20 ppb (100 moutside the boundary fence), 432 and 88 ppb (just inside the boundary fence). However, accidents and production start-ups were v associated with higher concentrations (Turner et al., 1984). Based on this evidence, Doll (1988) 433 434 concluded that "according to any reasonable criterion the hazard to the general public (if there 435 is any at all) must be negligible". 436 3.2.2.S Exposure Limits ` 437 , Sy The U.S. EPA has published several estimates of the potential carcinogenic potency (Qi*) of VCM, based on the application of the linearized multistage model for dose-response extrapolation of data from various laboratory animal studies. In 1980, a Q,' value of 0.0174 43 43 T R&S 143128 3-17 CanTox (mg/kg body weight/day)'1 was calculated based on preliminary data from laboratory rats 441 exposed to 10,000 ppm VCM. In 1985. this Q,- value was modified to 0.0295 (mg/kg body 442 weight/day)'1 using the lung and liver cancer incidence from rats exposed to 30,000 ppm VCM 443 for one year. In 1987, the EPA Carcinogen Assessment Group calculated a potency slope of 444 2.3 (mg/kg body weight/day)1 based on the liver cancer incidence of a 143-week study on rats 445 exposed orally to doses of 0-17 mg/kg body weight/day (5 days/week) (ATSDR, 1989). These 446 three cancer potency slope estimates translate into RsD values of 0.575, 0.339 and 0.00435 447 fig/kg body weight/day at a lifetime risk of one per 100,000, a range of 132-fold. 448 With respect to occupational limits, the American Conference of Governmental Industrial Hygienists (ACGIH) has recommended a Threshold Limit Value (TLV) of 5 ppm (12.8 mg/m3) Time-Weighted Average (TWA)-(ACGIH, 1991), while a workplace standard of 1 ppm TWA was set by the Occupational Safety and Health Administration (OSHA) (ATSDR, 1989; Calabrese and Kenyon, 1991). 449 450 451 452 453 3.3 AQUATIC WILDLIFE HAZARD ASSESSMENT 454 3.3.1 Lab Studies 455 Goldfish exposed to vinyl (polyvinyl chloride) automotive upholstery fabric immersed in water 456 exhibited a variety of toxic effects demonstrated hyperactivity, sluggishness, disoriented 457 swimming, aimless drifting and complete mortality in 24 hours (Ahrens et al., 1978) . 458 Histopathological examination demonstrated congestion, degeneration and haemorrhage in the 459 smaller blood vessels, particularly in the gills, as well as swollen edematous lamellae. Gas 460 chromatography/mass spectrometric analysis identified the major component of thte extract of the 461 fabric as triphenyl phosphate. These results suggested that triphenyl phosphate was the 462 compound released from PVC fabric that caused toxic effects in the goldfish. -:: 463 No further information on the toxic effects of PVC was identified. 4 flo CO 4k CO _L to 3.4 TERRESTRIAL WILDLIFE HAZARD ASSESSMENT CanTox 465 No information was identified specifically on the potential effects of VCM or polyvinyl chloride on terrestrial wildlife. However, the responses of other terrestrial species would be expected to be similar to those demonstrated in the large number of studies on various laboratory animals. 466 467 468 3.5 OTHER ENVIRONMENTAL EFFECTS 469 Since the environmental fate characteristics of VCM indicate it is rapidly transformed in the environment, there would be,little opportunity for effects on the physical environment by VCM per se. 470 471 472 3.6 SIGNIFICANCE OF ENVIRONMENTAL CONCENTRATIONS 473 The evidence reviewed demonstrates that the potential carcinogenicity related to occupational exposure is the primary environmental and human health concern related to VCM and PVC. Therefore, the evaluation of the significance of the concentrations of VCM in the environment will focus on the potential risks of cancer based on the premise that exposures that would not result in unacceptable cancer risks would not produce other adverse effects in the environment. 474 475 476 477 478 The assessment of potential environmental effects of chemicals:are based on a large number of assumptions. Since these assumptions are inherently conservative to avoid underestimating risks due to rare circumstances, the compounding of a number of conservative or worst-case assumptions means that the absolute point estimates of the risk are usually over-estimated, although by an unknown degree. Comparative or incremental risks between the two or more different scenarios, on the other hand, can be estimated with much greater confidence since the same methodologies are used in addressing each situation and major uncertainties arise from the accuracies in estimating exposures. The assumptions used in the estimation of exposure Hmits and various exposure modifying factors are common across the scenarios being compared. 479 480 481 482 483 484 485 486 R&S 143130 3-19 CanTox Therefore, the assessment of the potential carcinogenic risks from VCM and PVC in the environment, as outlined below, is based on a comparison of the predicted risks, as characterized by different assessment procedures, associated with exposures to historical, present-day and predicted future concentrations of VCM in the environment. 488 489 490 491 PVC 492 Except for pyrolytic breakdown products (addressed in a separate Chlorine Institute document on the Interpretive Review of the Potential Human Health and Environmental Effects Associated with the Incineration of Chlorinated Chemicals), the potential human health effects of PVC relate to exposures to PVC dusts in"Work environments. Exposures to such dusts would not be expected to occur outside the work environment. Historically, there were concerns about the measurable concentrations of non-polymerized VCM that could diffuse from materials constructed of PVC, or be released during pyrolysis. Changes in production processes have now resulted in a PVC product where VCM residues are below the detection limits of analytical procedures; thus alleviating potential concerns related to exposures to VCM diffusing from PVC. VCM 493 494 495 496 497 498 499 500 501 502 503 Environmental Concentrations 504 Based on the physical/chemical properties and the resulting information on the environmental fate of VCM (e.g., the majority partitioning into air where it is degraded quickly though reactions catalyzed by ultraviolet light), environmental concentrations, and'therefore levels of potential exposures to VCM, would be virtually zero at locations remote (e.g., several kilometres) from facilities involving the production, manufacturing and disposkl df VCM and v PVC. Therefore, the potential environmental and human health concerns related to VCM would be at locations near (within a few kilometres) of its production and use. 505 506 507 508 509 510 511 Since concentrations of VCM in air are greater inside production and manufacturing facilities, the potential levels of exposure of workers would be greater than for the general population. 3-20 J3 99 in CO CO CanTox Primarily because of greater understanding of the potential risks of angiosarcoma of the liver from VCM exposures, the concentrations of VCM in air in the workplace showed marked decreases from values commonly in the range of 260 to 2600 mg/m3 (approximately 100 to 1000 ppm) prior to 1955 to concentrations of approximately 13 mg/m3 (5 ppm) by about 1975. 514 515 516 517 Further decreases in work environment concentrations have occurred since the mid 1970s. Workplace monitoring data demonstrate that air concentrations in non-production areas of facilities that manufacture and use VCM ranged from < 0.25 to 10.5 mg/m3 (< 0.1 to 4.11 ppm) in 1988, and <0.25 to 2 mg/m3 (<0.1 to 0.77 ppm) in 1992. In areas of plants involved in production and handling, VCM air concentrations ranged from 35 to 26.5 mg/m3 (13.5 and 10.34 ppm) in one facility, and.0.5 to 11 mg/m3 (0.2 to 4.11 ppm) in 1988, decreasing to 0.5 to 2 mg/m3 (0.2 to 0.77 ppm) in 1992 in another facility (Vinyl Institute, personal communication, 1992). These data represent the greatest air concentrations reported for the four facilities over the 5 year period, 1988 through 1992. 518 519 520 521 522 523 524 525 526 Near (within a few hundred metres) VCM and'JPVC production and manufacturing facilities, IARC (1979) reported average air concentrations of 44 fig/m3 (17 ppb) prior to 1979. Other researchers reported a range of 26 to 102 pLg/m3 (10 to 40 ppb) during this same time period (EPA, 1975; Baxter et al, 1977). Air monitoring data collected after 1975, subsequent to the implementation of more stringent standards for workplace air concentrations, showed air concentrations within a few hundred meters of VCM production/handling areas were below analytical detection limits (approximately 13 /zg/m3 or 5 ppb) for three of five facilities in the UK, and the concentrations for the other two facilities were about 20 ppb (100 m outside the boundary fence), and 88 ppb (just inside the boundary fence) (Turner et al, 1984). 527 528 529 530 531 532 533 534 535 Potential Consequences Associated with Environmental Concentrations of VCM 536 Based on the weight-of-available-evidence demonstrating the rapid dispersion and degradation of VCM in the atmosphere, and that the air concentrations measured near (within a kilometre) of VCM/PVC production/manufacturing facilities are below analytical detection limits (e.g., < 5 ppb), exposures of the general public to VCM would be virtually zero. A similar conclusion 3-21 537 r ; iW 4k CO ro CanTox was reached by Doll (1988) regarding potential cancer risks to the general public from potential exposures to VCM emissions from production/manufacturing facilities. Very low exposures may be associated with VCM produced from the degradation of other chlorinated organic chemicals from natural and man-made sources (e.g., 1.1,1-trichloroethane and 1,1-dichloroethane); however, no measurable health risks would be expected from such sources. 541 542 543 544 545 The question of potential risks to the general public living very near VCM production/manufacturing facilities remains to be addressed. The various risk estimates from exposures to the VCM concentrations observed near production/manufacturing facilities, based on the application of the- various EPA cancer potency estimates for VCM, and the cancer incidence rates reported in workers exposed to VCM are summarized in Table 3-1. The first point arising from the various risk estimates in Table 3-1 is the large variation in risks estimated by the different methods. The most recent EPA exposure limit (0.00435 /xg/kg body weight/day) (Calabrese and Kenyon, 1991) results in risk estimates at least 98000-fold greater than estimated by simple linear extrapolation of the cancer incidence observed in workers exposed to VCM concentrations of 100 to 1000 ppm to those observed near production/manufacturing facilities (e.g., 10-40 ppb in the mid 1970s and <5 ppb in the mid 1980s). The 1980 EPA cancer potency estimate for VCM results in cancer mortality incidence at least 7400-fold greater than those predicted from observations in workers. 546 547 548 549 550 551 552 553 554 555 556 557 558 33 99 </) W ww 3-22 Table 3-1 CanTox. Cancer Risk Estimates for Near-Plant Air Concentrations of VCM 559 Cancer Potency Estimate'11 (mg/kg/day)'1 0.0174 (EPA, 1980) 0.295 (EPA, 1985) 2.3 (EPA, 1987b) Predicted Risks Near-Plant<2) (per 100,000) Air Concentrations 10 - 40 ppb(3) Air Concentrations <5 ppb'41 14 - 59 74 25 - 100 26 1954 - 7816 982 560 561 562 563 564 565 566 567 568 Epidemiology 0.00024 @ 100 ppm 0.000024 @ 1000 ppm 0.08 - 0.008 0.2 - 0.02 0.01 0.001 569 570 571 EPA (1980) cancer potency estimate = 0.0174; EPA (1985) cancer potency estimate = 0.0295; EPA (1987b) cancer potency estimate = 2.3, all expressed as (mg/kg body weight/day)'1. Epidemiology cancer potency estimates are based on a liver cancer mortality of 2 per 100 (2%) (Doll, 1988) at estimated air concentrations between 100 and 1000 ppm (IARC, 1979), giving a cancer potency estimate range of 0.00024 to 0.000024 (mg/kg body weight/day)'1, respectively, for a 70 kg individual..breathing 23 m3 of air per day and assuming a linear dose-response extrapolation. Near-plant air concentrations (within a few meters) were 26 to 102 ^g/m3:(lO to 40 ppb) in the mid-1970s (Baxter et al., 1977), and <13 /xg/m3 (<5 ppb) in the mid-1980s (Turner era/., 1984). Exposure estimates calculated for a 70 kg individual breathing 23 m3 of air per day. Predicted risk = (estimated exposure) x cancer potency factor. 572 573 574 575 576 577 578 579 580 581 582 R&S 143134 3-23 CanTox Assuming that environmental concentrations near production facilities were roughly proportional to the air concentrations in the work environment, a reduction in work environment air concentrations to <257 /xg/m3 (< 100 ppb) would be expected to result in an approximately 50fold reduction in air concentrations near production facilities (e.g., concentrations in the range of 0.26 /xg/m3, assuming values of 13 /xg/m3 associated with workplace concentrations at the time Turner et al. (1984) conducted their measurements. Therefore, risks from predicted present-day air concentrations near VCM production/manufacturing facilities would be expected to be some 50-fold less than those estimated in Table 3-1. 584 585 586 587 588 589 590 591 The estimates of risks associated with VCM exposures near production facilities as predicted by the EPA cancer potency factors are in stark disagreement with the conclusions of Doll (1988) that the potential risks associated^with VCM exposures to the "general public (if there is any at all) must be negligible". One major reason for this apparent disagreement in potential risks may be related to the large degree of conservatism inherent in the EPA (1987) exposure limit for VCM as estimated using the linearized multistage model. An indication of this conservatism can be obtained through a comparison of the VCM cancer potency estimate derived by extrapolation of liver cancer mortality observed in workers with the various potency estimates of the EPA. This comparison indicates a difference in cancer potency of between approximately 9500 and 95000-fold. The greatest uncertainty in the epidemiological data lies in the estimated air concentrations to which the workers were exposed. However, even if the VCM exposure levels experienced by the workers were in the range of 10 ppm, the EPA^1987) approach would over- estimate the risk by approximately 950-fold. According to the information available, it is highly unlikely that the VCM air concentrations in work environments were < l<Xppm during the 1950s and 1960s when the workers were exposed (LARC, 1979). -/, 592 593 594 595 596 597 598 599 600 601 602 603 604 605 606 If it is assumed that the cancer potency estimates based on the epidemiological data are reasonable, then the potential risks associated with the air concentrations of VCM predicted near production facilities would be in the range of 1 per 10 million and 1 per 100 million (Tabl3-1). - Such levels of risk would be clearly unmeasurable in any practical sense, and in agreement with the conclusions of Doll (1988) regarding potential risks of liver cancers from VCM exposures to the general public. In the future, improved production and manufacturing control 607 608 609 qo w 3-24 CO 01 CanTox technologies will continue to reduce emissions of VCM from production and manufacturing facilities. These expected reductions will reduce environmental loadings of VCM from anthropogenic point sources, thereby continuing to reduce the already negligible risks currently predicted from environmental concentrations of VCM near production and manufacturing facilities. The above assessment focuses primarily on potential exposures of the general public living near (e.g., within a few kilometres) of VCM production and manufacturing facilities. Since VCM emissions remain almost exclusively in air, and it has a half-life in the environment of only a few days, its concentrations in air would decrease rapidly with distance from point sources. Therefore, potential health risks to the general public in regions remote from VCM production and manufacturing facilities would be negligible, and certainly unmeasurable. 613 614 615 616 617 618 619 620 621 622 Based on the above evaluation, theprimary direct concerns regarding the potential impacts of anthropogenic sources of VCM on human health and the environment relate to point source emissions from facilities that productioa VCM or use it to manufacture various products. Therefore, the reduction or elimination of environmental impacts from VCM must be based on controlling air concentrations due to environmental, releases from production and manufacturing facilities. Historically (e.g., 1940s/50s) the concentrations of VCM reported in the workplace environment would have resulted in unacceptably high risks of cancer in workers. In addition, releases of VCM from production/manufacturing facilities were unacceptably high. The implementation of emission controls in such facilities resulted in substantial (e.g., 200-fold or greater) reductions in VCM concentrations in the workplace. Releases to the surrounding environment would also be substantially reduced through these actions. Therefore, the available information does not indicate excessive cancer risks to workers or populations in the vicinity of industrial facilities that use VCM. 623 624 625 626 627 628 629 630 631 632 633 634 635 v R&S 143136 3-25 CaimTox Chapter 4 References />? . B9 U) w** 03 (> CanTox ACGIH. (1991). Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices, 1991-1992. ACGIH, Cincinnati, OH 45211-4438. `I 2 ACGIH. (1992). Threshold Limit Value for Chemical Substances and Physical Agents and Biological Exposure Indices, 1992-1993. ACGIH, Cincinnati, OH. 3 4 AGARWAL, D.K. (1983). 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