Document n96NEKNqVVZ155ExrQR7xB032

CanTox Inc. Consultants in Toxicology Health and Environmental Sciences 2233 Argentia Road, Suite 308, Mississauga, Ontario, Canada, L5N 2X7, TEL (905) S42-2900, FAX: (905) 542-1011 November 11, 1993 Dr. H. C. Shah Director, CHEMSTAR Chemical Manufacturers Association 2501 M Street, NW Washington, DC 20037 USA Dear Dr. Shah: Please find enclosed the first draft of comments compiled by CanTox to the ATSDR report on vinyl chloride. We welcome your comments and perhaps could arrange a conference call in the near future to discuss the draft. Yours sincerely, CanTox Inc. Jonathan Daniels, Ph.D. Scientist CC: Dr. Robert Hinderer - BF Goodrich Dr. James Knaak - Occidental Chemical Enel. Vancouver Calgary Mississauga Halifax R&S 150505 DRAFT FOR DISCUSSION Comments Regarding the Agency for Toxic Substances and Disease Registry (ATSDR) Document Entitled "Substance-Specific Applied Research Program Priority Data Needs for Vinyl Chloride" (September, 1992) Prepared By The Chemical Manufacturers Association November 2, 1993 R&S 150506 1 SUMMARY DRAFT FOR DISCUSSION 2 Recently, a report was published by the Agency for Toxic Substances and Disease Registry 3 (ATSDR) which outlined a number of areas in which the agency felt that there were gaps in the 4 available scientific database relating to the compound vinyl chloride monomer (VCM) (ATSDR, 5 1992). The Chemical Manufacturers Association does not agree with many points made in the 6 ATSDR report and is providing these comments in response. 7 Vinyl chloride monomer (VCM) is one of the most intensely studied chemicals in use today. 8 The scientific literature contains a wealth of data describing both the short- and the long-term 9 health effects of exposure to this chemical in humans and in a number of species of experimental 10 animals. As such, the potential hazards associated with VCM are well known, yet ATSDR has 11 called for further testing in its report, even though such information would not contribute any 12 significant new information to the toxicological database on VCM. 13 The report prepared by ATSDR does not adequately acknowledge that the potential risk to 14 humans of a chemical is a factor of both its hazard potential and the level of exposure. A 15 chemical, regardless of its toxicological potential to affect the health of individuals in the vicinity 16 of hazardous waste site, cannot pose a health hazard if there is no or negligible exposure. It is 17 the level of potential exposure to VCM in the vicinity of hazardous waste sites that should be 18 the focus of any future data gathering, and not items such as additional nonclinical testing, 19 epidemiological studies, development of methods to mitigate toxicity, or the creation of a 20 registry of exposed persons around such sites. Furthermore, it is not evident from the ATSDR 21 document that there is recognition that VCM that may be present at waste sites is not the result 22 of disposed of VCM itself or even discarded polyvinyl chloride materials, but rather is the result 23 of degradation of commonly used solvents. Any attempts at reducing the' potential risks 24 associated with living near a hazardous waste site should be addressed through better waste 25 disposal practices. R&S150507 1 1 1.0 INTRODUCTION DRAFT FOR DISCUSSION 2 The Agency for Toxic Substances and Disease Registry (ATSDR) recently released a document 3 Entitled "Substance-Specific Applied Research Program Priority Data Needs for Vinyl Chloride" 4 (ATSDR, 1992). The focus of this document was exposure from hazardous waste sites, vinyl 5 chloride monomer (VCM) is one of the most intensely studies chemicals in use today, with the 6 potential risks of this chemical well known, yet the ATSDR document does not accurately reflect 7 this. The Chemical Manufacturers Association herein provides its comments regarding points 8 made in the ATSDR document in order to clarify the issues. 9 2.0 SPECIFIC COMMENTS - DATA NEEDS 10 In order to respond to the ATSDR report regarding data needs, we have used the ATSDR 11 framework for the sake of organization of these comments. 12 2.1 Exposure to VCM 13 2.1.1 Exposure Levels - Environmental Media 14 The purpose of Section m.A.l.c.i in the ATSDR report was to determine if adequate data on 15 the levels of VCM in ambient and contaminated environments are available for the purposes of 16 conducting meaningful follow-up exposure and health studies. The document provides a series 17 of numbers describing concentrations of VCM detected in air and water media. It does not, 18 however, provide the reader with a sense of what these values actually mean with respect to 19 potential risks, and then concludes that there is a need for such data in environmental media at 20 hazardous waste sites. R&S150508 21 There is a considerable amount of data available concerning VCM concentrations in 22 environmental media around PVC production facilities, and also concentrations of VCM in the 23 indoor work environment at these facilities. In the work place, the data that are available are 2 DRAFT FOR DISCUSSION 1 an excellent source of information with respect to determining the effects of VCM on humans 2 where the exposure to VCM has been documented. This, in turn, allows a more controlled way 3 of determining potential risk to humans, as the exposure has been accurately defined. Such a 4 situation does not exist with respect to hazardous waste sites, as there would be no indication 5 of exposure to the multitude of other compounds that would confound any follow-up 6 epidemiological studies or analyses. 7 Given the fact that the potential risk from VCM around hazardous waste sites is dependent upon 8 the level of exposure, it is worth reviewing the available data from industrial exposure for the 9 purpose of putting relevant exposure into perspective. 10 2.1.1.X VCM in Workplace Air 11 Concentrations of VCM in the workplace prior to the 1960s were greater than 100 ppm and 12 decreased to values less than 100 ppm between the 1960s and mid-1970s, then decreased again 13 to an upper limit of 5 ppm [8 hour, time-weighted-average (TWA)] by 1975 (Doll, 1988; 14 ACGIH, 1991). The current OSHA workplace standard in the United States is 1 ppm (8 hour 15 TWA) with a 5 ppm short-term exposure limit (STEL) (29 CFR 1910.1017). 16 In 1988, the concentrations of VCM (8 hour TWA based on individual personnel monitoring) 17 in the work environment ranged from approximately <0.25 to 10.5 mg/m3 (<0.1 to 4.1 ppm) 18 in four PVC resin production facilities in the United States. Reactor operators, loading 19 personnel and laboratory technicians showed the greatest potential exposures for 8 hour 20 exposures. TWA air concentrations ranged from 0.5 to 11 mg/m3 (0.2 to 4.1 ppm); these air 21 concentrations had decreased to 0.5 to 2 mg/m3 (0.2 to 0.77 ppm) in 1992. In 1990, one facility 22 reported 8 hour TWA concentrations in air for instrument technicians and process operators of 23 35 and 26.5 mg/m3 (13.5 and 10.3 ppm), respectively. By 1992 (January to September data 24 only), the work-place concentrations in these facilities had decreased to a range of approximately 25 <0.25 to 2 mg/m3 (<0.1 to 0.8 ppm). These data represent the greatest concentrations of 26 VCM in air reported for these four facilities over the five year period 1988 through 1992 (Vinyl 3 R&S150509 DRAFT FOR DISCUSSION 1 Institute, personal communication). Localized releases of VCM to the natural environment can 2 occur around production and manufacturing facilities; therefore, the concentrations of VCM are 3 highest near such facilities. 4 2.1.1.2 VCM in Environmental Emissions from Production Facilities 5 Decreases in concentrations of VCM in the work environment discussed above would also be 6 indicative of corresponding decreases in environmental releases from production/manufacturing 7 facilities. VCM has been measured in air around suspected "hot spots" (i.e., in areas near 8 production and manufacturing facilities) in the United States. Prior to the implementation of 9 VCM emission regulations in 1978, the average air concentrations of VCM at production 10 facilities in the United States was 0.04 mg/m3 (0.017 ppm) (IARC, 1979). In Houston, Texas, 11 where large quantities of VCM are produced, air concentrations ranged from 0.008 mg/m3 12 (0.003 ppm) to peak values of 3.2 mg/m3 (1.2 ppm) (Gordon and Meeks, 1977). In Long 13 Beach, California, ambient air concentrations of VCM near two VCM plants ranged from 0.3 14 to 8.8 mg/m3 (0.1 to 3.4 ppm) (National Field Investigations Center, 1974). However, within 15 approximately one kilometer of VCM production/manufacturing facilities, reported air 16 concentrations of VCM ranged from approximately 0.03 to 0.1 mg/m3 (0.01 to 0.04 ppm) (EPA, 17 1975b; Baxter et al., 1977). More recent information based on sampling near 18 production/manufacturing facilities since standards for the work environment were reduced to 19 about 13 mg/m3 (5 ppm) in 1975, showed that air concentrations of VCM were near the 20 analytical detection limit (about 0.013 mg/m3 or 0.005 ppm) in three out of five British plants. 21 For two other facilities, the VCM air concentrations were approximately 0.05 mg/m3 (0.02 ppm) 22 at a location 100 m outside the facility boundary, and 0.2 mg/m3 (0.09 ppm) just inside the 23 boundary fence (Turner et al., 1984). 24 2.1.1.3 Risk from VCM in Workplace Air R&S 150510 25 The best available epidemiological data regarding exposure to VCM were critically reviewed by 26 Sir Richard Doll (Doll, 1988). This review clearly illustrated the current understanding that the 4 DRAFT FOR DISCUSSION 1 potential risk associated with VCM is a factor of the level of exposure, with there being no 2 significant risk to humans below certain levels. The review, which incorporated well3 documented levels of exposure of humans to VCM had two major conclusions: (i) Apart from 4 liver cancer, VCM/PVC workers exposed between the 1940s/1950s and mid-1970s did not have 5 unusual hazards of accident or disease, and (ii) workers exposed to VCM concentrations of 6 "several hundred parts per million or more" clearly showed an increased risk of contracting 7 angiosarcoma of the liver, normally an extremely rare disease (annual incidence of 1 to 2 x 10`7 8 in the general population; Byren and Holmberg, 1975). 9 Doll (1988) concluded that it was "difficult to decide whether vinyl chloride produces a risk of 10 developing cancer other than angiosarcoma of the liver which might be small compared to the 11 risks produced by nonoccupational causes, at sites other than the liver" (Doll, 1988). He also 12 concluded that there was no evidence to support the association between exposure to VCM and 13 any other digestive tract cancer. With respect to the association of exposure to VCM and lung 14 cancer, Doll (1988) concluded that a small hazard may have existed when occupational 15 exposures to VCM were extreme, but that the study data did not conclusively demonstrate this 16 risk and that the increased risk would in any case be negligible at the current small exposures 17 to VCM. 18 2.1.1.4 Risk from Environmental Emissions of VCM in Air 19 In his review, Doll concluded that the minute exposures that would result from emissions 20 escaping from VCM facilities must cause comparably minute risks to the general public. The 21 concentrations of VCM measured near VCM/PVC production/manufacturing facilities are in the 22 order of 0.01 to 0.04 ppm (EPA, 1975b; Baxter et al, 1977), or some 10,000-fold less than the 23 "several hundred parts per million or more " exposures that resulted in measurable occupational 24 hazards. Therefore, an increased risk of cancer to the general public could not possibly be 25 detected, with the possible exception of an increased risk of angiosarcoma of the liver. Any 26 inference that angiosarcoma incidence in the general population is related to VCM exposure, R&S150511 5 DRAFT FOR DISCUSSION 1 however, could be misleading because angiosarcoma may also be caused by thorium dioxide and 2 arsenic in pesticides and by certain medicines (Doll, 1988). 3 Doll (1988) also concluded that there may have been a minute hazard to the general public from 4 the VCM concentrations historically observed around manufacturing facilities. However, the 5 concentrations of VCM around production facilities has decreased substantially since the 1970s. 6 VCM air concentrations within a few hundred meters of VCM areas were below analytical 7 detection limits (< 0.005 ppm) for three of five facilities in the United Kingdom, and the 8 concentrations for the other two facilities were about 0.02 ppm (100 m outside the boundary 9 fence), and 0.09 ppm (just inside the boundary fence). However, accidents and production start10 ups were associated with higher concentrations (Turner et al., 1984). Based on this evidence, 11 Doll (1988) concluded that "according to any reasonable criterion, the hazard to the general 12 public (if there is any at all) must be negligible." 13 2.1.1.5 VCM in Water 14 Vinyl chloride also has been measured in both groundwater and drinking water in the United 15 States. The greatest concentration of VCM measured in drinking water was 0.01 mg/L near a 16 production facility (Safe Drinking Water Committee, 1977; IARC, 1979). Vinyl chloride 17 monomer has also been reported in groundwater in the United States. Measurable levels in 18 California wells averaged 0.02 mg/L and were as high as 0.023 mg/L (Kizer, 1986). In the Los 19 Angeles area, groundwater contained less than 0.001 mg/L of VCM (Baird et al., 1983), while 20 in non-specified areas of Nebraska and California groundwater concentrations ranged from 0.75 21 to 0.023 mg/L (Goodenkauf and Atkinson, 1986; CSDHS, 1990). 22 2.1.1.6 Summary R&S150512 23 As described above, there are good data available from which to predict potential risks of 24 individuals from VCM. In addition to not utilizing the available exposure-response data of VCM 25 in humans, it appears that ATSDR has not exhausted all the avenues for obtaining information 6 DRAFT FOR DISCUSSION 1 on the levels of VCM in ambient and contaminated environments. For example, the CMA is 2 aware of on-going monitoring that is taking place in California and on the East Coast of the 3 United States (***** need to include some more detailed information ****). 4 2.1.2 Exposure Levels - Humans 5 Section m.A.l.c.ii of the ATSDR report states that there is a lack of data regarding levels of 6 vinyl chloride in body tissues or fluids. ATSDR considers these data important for conducting 7 meaningful follow-up exposure and health studies with individuals exposed to VCM and points 8 out that there is no validated biomarker of VCM exposure currently available from which to use 9 for the purposes of dosimetry. The development of the database as described is considered by 10 the Chemical Manufacturers Association to be unnecessary and would appear to be a waste of 11 resources. 12 ATSDR is correct in its view that thiodiglycolic acid, a major metabolite of VCM, is of limited 13 value for the monitoring of VCM exposure due to confounding factors such as variable 14 metabolism between individuals, influences of disease states, and the fact that this metabolite is 15 not unique to VCM exposure. There is currently work going on in this field, although it is not 16 at the stage where it is a reliable predictor of quantitative exposure (***** include references 17 if possible *****). Any type of methodology that ATSDR puts forward to monitor human 18 exposure to VCM must be specific and it must be quantitative. There is no mention in the 19 document that ATSDR acknowledges the work that is currently being undertaken in this area. 20 In addition, ATSDR considers that modeling cannot reliably predict levels of VCM in human 21 tissues for the purposes of further studies, yet it does not give an explanation for this statement. 22 As indicated in the report, there is currently an effort underway at ATSDR to examine data from 23 245 National Priorities List (NPL) sites at which VCM has been found. This database, when 24 completed, will include the concentrations in on-site and off-site media, the sizes of the 25 potentially exposed populations, and an indication of relevant exposure routes. From these 26 concentrations determined by ATSDR, it would be possible to predict potential exposure to 7 R&S150513 DRAFT FOR DISCUSSION 1 VCM and assess the risk, if any, to persons nearby without the need to (a) develop and validate 2 methods for quantifying exposure and (b) actually apply these methods to untold numbers of 3 individuals living within predetermined distances from hazardous waste sites, as is alluded to by 4 ATSDR. 5 As discussed above, the current epidemiological information that was critically reviewed by Doll 6 (1988) has indicated clearly that for individuals living around production facilities, where VCM 7 concentrations in ambient air have ranged from approximately 0.005 to 0.09 ppm since the 8 introduction of standards, the hazard is negligible. Such a conclusion is based upon well 9 documented exposure in industrial workers, where concomitant exposure to other 10 agents/chemicals have been addressed in a way not possible in the recommendation of ATSDR. 11 2.2 Registry of Exposed Persons 12 The ATSDR document states that a registry of individuals exposed to VCM in the environment 13 would provide an important reference tool to aid in assessing long-term health consequences of 14 such exposure (Section HI.2.a). In the opinion of the Chemical Manufacturers Association, no 15 meaningful information would be gleaned regarding the human health effects of VCM, from the 16 setting up of such a registry, that is not already available from the numerous epidemiological 17 reports available that have been based upon occupational exposure to this chemical (see review 18 by Doll, 1988). Such data regarding occupational exposure to VCM also has the advantage that 19 concomitant exposure to other chemicals is minimized when compared to exposure via a 20 hazardous waste site, where it may not be possible or economically feasible to analyze the 21 various media for all possible chemicals that could influence the health of humans in areas 22 adjacent to hazardous waste sites. To open a registry, as ATSDR is recommending, would be 23 prohibitively time-consuming and expensive whilst providing no significant information. It 24 would have to take into account and pay considerable attention to case histories, the long-term 25 exposure history, and the confounding factors, such as smoking, etc. Even if this was 26 undertaken, the fact that it would be impossible to quantitatively document the past exposure to R&S150514 8 DRAFT FOR DISCUSSION 1 VCM from hazardous waste sites and to consider all the possible confounding factors would 2 make this information of little practical use. 3 As indicated previously, even in the case of industrial workers exposed, for all practical 4 purposes to pure VCM, there are levels of exposure that have been found to have no significant 5 effects upon the health of the individuals (Doll, 1988). Only angiosarcoma of the liver has been 6 definitively linked to VCM exposure, except possibly for a possible risk of lung cancer when 7 exposure has been large (Doll, 1988). Based upon these data, even if ATSDR were able to 8 solicit the cooperation of all the people potentially exposed to VCM from living near hazardous 9 waste sites, and had unlimited access to funding, no new information would be generated 10 regarding the potential hazards of VCM. Also, it should be noted that when considering the 11 potential risk of VCM, the production, use, and transportation of VCM provide the more critical 12 areas for monitoring of exposure as compared to disposal sites. 13 2.3 Toxicity of VCM 14 2.3.1 Acute Exposure 15 In Section m.B. 1 .a of the ATSDR report, it is stated that acute duration nonclinical studies are 16 a priority data need in order to identify target organs and levels of exposure which present a 17 significant risk to human health following acute exposure. It is unclear what the relevance of 18 conducting such a study(ies) would be, considering that exposure to VCM at or near a waste 19 disposal site would be expected to be long-term at low concentrations. The effects of longer 20 term exposure in laboratory animals has been previously reviewed by ATSDR in its toxicological 21 profiles on VCM (ATSDR, 1989; ATSDR, 1993). 22 It is typical for acute exposure studies to essentially measure lethality in the test animal, while 23 it seems to be the intent of ATSDR to obtain data regarding more subtle endpoints and no-effect 24 doses for effects that are characteristically obtained from longer term investigations. R & S 150515 9 2.3.2 Reproductive and Developmental Toxicity DRAFT FOR DISCUSSION Animal and human studies with VCM do not indicate effects upon reproduction and/or development, effects suggested in the ATSDR report (Sections HLB.l.e and f). This lack of potential effects of VCM on human offspring was the focus of a 1987 report prepared by the Vinyl Institute and included with these comments as Appendix A (Vinyl Institute, 1987). The ATSDR seems to have incorrectly confused the effects of maternal toxicity at high doses of VCM with reproductive and/or developmental effects in its report. This is particularly evident in ATSDR's review of the studies reported by John et al. (1977; 1981), where groups of pregnant rats, mice and rabbits were exposed via inhalation to VCM at concentrations of 0, 50, 500 or 2,500 ppm for seven hours per day during the critical period of organogenesis. Although the high levels of VCM caused maternal toxicity, there was no significant embryonal or fetal toxicity observed nor were there any teratogenic effects produced in the offspring. 2.4 Biomarkers Biomarkers, in effect, relate directly to other areas discussed in the ATSDR report and in these comments; namely the monitoring of exposure to VCM and the creation of a registry of exposed persons. These items would require sensitive and specific methods of quantitatively documenting V exposure to VCM. Such a biomarker would essentially provide dosimetry data for a particular (j- individual, although the use of such data in comparisons to potential risks would have to be . Ci/', , exhaustively validated in order for them to be of any potential use. As already stated, the ^ Chemical Manufacturers Association feels that no new meaningful information would be ^ provided by the implementation of such programs. u- 2.5 Clinical Methods of Mitigating Toxicity S IS 'SH These comments on clinical methods made by ATSDR (Section in.B.2.d) do not provide meaningful guidance as they could be taken to mean everything from the development of early diagnostic methods to finding a cure for angiosarcoma of the liver. Essentially, toxicity due to DRAFT FOR DISCUSSION 1 VCM could be reduced or eliminated altogether through reduction in exposure. Such results 2 have been clearly demonstrated for industrial exposure (see comment 2.1.1). The reduction or 3 elimination of exposure of individuals to VCM near NPL sites is a factor of better waste 4 management practices and monitoring by federal authorities. 5 3.0 REFERENCES 6 29 CFR 1910. United States Code of Federal Regulations. Title 29 Part 1910. 7 ACGIH. 1991. Threshold Limit Values for Chemical Substances and Physical Agents and 8 Biological Exposure Indices, 1991-1992. ACGIH, Cincinnati, OH 45211-4438. 9 ATSDR. 1993. Toxicological profile for vinyl chloride. Agency for Toxic Substances and 10 Disease Registry, In Press. 11 ATSDR. 1989. Toxicological Profile for Vinyl Chloride. Agency for Toxic Substances and 12 Disease Registry, August 1989 (TP-88/25). 13 ATSDR. 1992. Substance-Specific AppliedResearch Program PriorityData Needs for Vinyl 14 Chloride. Agency for Toxic Substances and DiseaseRegistry, September, 1992. 15 Baird, R., Gute, J,, Jacks, C., Jenkins, R., Neisess, L., Scheybeler, B., van Sluis, R. and 16 Yanko, W. 1983. Health Effects of Water Reuse: A combination of Toxicological and 17 Chemical Methods for Assessment. In: Water Chlorination: Environmental Impact and Health 18 Effects. 19 Baxter, P.J., Anthony, P.P., MacSween, N.M. and Scheuer, P.J. 1977. Angiosarcoma of the 20 liver in Great Britain. Br Med J 1:919-921. R&S150517 11 DRAFT FOR DISCUSSION 1 Byren, D. and Holmberg, B. 1975. Two possible cases of angiosarcoma of the liver in a group 2 of Swedish vinyl chloride workers. Ann, NY. Acad Sci 246:249-250. 3 CSDHS. 1990. Organic Chemical Contamination of Small Public Water Systems in California. 4 Small Water System AB 1803 Final Status Report. California State Department of Health 5 Services (CSDHS), Office of Drinking Water. 6 Doll, R. 1988. Effects of exposure to vinyl chloride. Scand J Work Environ Health 14:61-78. 7 Elinder, C.G. and Pershagen, G. 1981. Pilot Study Concerning the Mortality in Njurunda 8 Community. Swedish Nature Conservancy Board, 1978. 9 EPA. 1975. Standard Support Document and Environmental Impact Statement: Emission 10 Standard for Vinyl Chloride. (U.S.) Environmental Protection Agency, Washington, DC. 11 Goodenkauf, O. and Atkinson, J.C. 1986. Occurrence of volatile organic chemicals in 12 Nebraska groundwater. Ground Water 24(2): 231-233. 13 Gordon, S.J. and Meeks, S.A. 1977. A study of gaseous pollutants in the Houston, Texas area. 14 Am Inst Chem Eng Symp Ser 73:84-94. 15 IARC. 1979. Vinyl Chloride, Polyvinyl Chloride and Vinyl Chloride-Vinyl Acetate 16 Copolymers. In: Some Monomers. Plastics and Synthetic Elastomers and Acrolein. IARC 17 Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Volume 19. 18 International Agency for Research on Cancer, World Health Organization, Lyon, France. 19 John, J., Smith, F. and Swetz, B. 1981. Vinyl chloride: Inhalation teratology in mice, rats, 20 and rabbits. Env Health Perspect 41:171-177. 12 R&S 150518 DRAFT FOR DISCUSSION 1 John, J., Smith, F., Leong, F. and Swetz, B. 1977. The effects of maternally inhaled vinyl 2 chloride on embryonal and fetal development in mice, rats, and rabbits. Toxicol Appl 3 Pharmacol 39:497-513. 4 Kizer, K. 1986. Final Report on a Monitoring Program for Organic Chemical Contamination 5 of Large Public Water Systems in California. Summary Version. Department of Health 6 Services, California. 7 National Field Investigations Center. 1974. Evaluation of Vinyl Chloride Emissions in the 8 Long Beach Area, California. EPA/330/2-74/002, Springfield, Va, NTTS. 9 Safe Drinking Water Committee. 1977. Drinking Water and Health. National Academy of 10 Sciences, Washington, DC., p. 794. 11 Saric, M., Kulcar, Z., Zorica, M. and Gelic, J. 1976. Malignant tumors of the liver and lungs 12 in an area with a PVC industry. Environ Health Perspect 17:644-652. 13 Turner, C.A., Payne, A.P. and Bushby, B.R, 1984. Determination of Ambient Levels of Vinyl 14 Chloride Monomer (VCM) (Around Manufacturers in the UK: Part 7. Warren Spring 15 Laboratory, Department of Trade and Industry, Stevenage, UK. 16 Vinyl Institute. 1987. Potential Effects of Vinyl Chloride on Human Offspring. Prepared by 17 the Medical Subcommittee of the Technical Committee, December 1987. 13 R&S150519