The former OSHA standard for ethylene dichloride (EDC) was 50 ppm as an 8-hour TWA, with a 100-ppm STEL (maximum duration of five minutes in any three hours) and a 200-ppm ceiling; these limits were derived from limits recommended by the American National Standards Institute in 1969. In 1980, the ACGIH reduced its TLV for ethylene dichloride to 10 ppm as an 8-hour TWA. NIOSH (1978q/Ex. 1-1120 and Ex. 8-47, Table N6A) has concluded that ethylene dichloride should be considered a potential human carcinogen and has recommended a 1-ppm TWA REL and a 2-ppm 15-minute short-term limit. OSHA proposed an 8-hour TWA of 1 ppm and a STEL of 2 ppm, and the final rule establishes these limits. Ethylene dichloride is a colorless liquid with an odor typical of the chlorinated hydrocarbons.
Several studies indicate that the former OSHA PELs are insufficient to protect workers against the hepatotoxic and carcinogenic effects of exposure to EDC. A paper by Kozik (1957/Ex. 1-182) reported that workers generally exposed to ethylene dichloride at levels of 10 to 15 ppm but occasionally exposed to levels of 40 ppm experienced increased morbidity, diseases of the liver and bile ducts, and nervous system effects. In addition, Brzozowski and associates (1954/ Ex. 1-63) reported abnormal changes in the blood of 50 percent of workers (8 of 16) exposed to EDC levels of 10 ppm and above (Brzozowski, Czajka, Dutkiewicz et al. 1954/Ex. 1-63).
Many commenters submitted information to the docket on ethylene dichloride (Exs. 3-624, 3-677, 3-678, 3-741, 3-874, 3-1174, 8-47, and 150). Most commenters were of the opinion that a permissible exposure limit of 10 ppm, rather than the proposed 1-ppm limit, would provide adequate protection against EDC's hepatoxic, central nervous system, and hematopoietic effects (Exs. 3-624, 3-677, 3-678, 3-741, 3-874, and 3-1174). Several of these participants also expressed concern about the feasibility of the 1-ppm limit (Exs. 3-624, 3-741, and 3-874). The comments of Richard Olson, representing the Dow Chemical Company, were typical of those of this group of commenters. According to Mr. Olson, OSHA's proposed limit was based on two outdated studies (Kozik 1957/Ex. 1-182 and Brzozowski, Czajka, Dutkiewicz et al. 1954/Ex. 1-63) that are incomplete, reflect outdated work practices, and present results that are based on effects caused by dermal as well as airborne exposures (Ex. 3-741, p. 52). The Chemical Manufacturers Association Ex. 3-874) pointed out that the jobs being performed by the workers monitored in the Brzozowski et al. (1954/Ex. 1-63) study are no longer permitted because EPA has prohibited the use of EDC as a fumigant (Ex. 3-874).
In response to these commenters, OSHA notes that there are many studies reporting serious EDC-related effects among workers exposed to airborne concentrations in the 10- to 15-ppm range. For example, the aircraft workers in the Kozik (1957/Ex. 1-182) study (average 8-hour TWA exposures of 10 to 15 ppm) experienced increased morbidity and lost more workdays than did non-EDC-exposed workers at the same factory. These workers experienced high rates of gastrointestinal disease and liver and gallbladder diseases; these symptoms and diseases are typical EDC exposure effects. Another study (Cetnarowicz 1959) examined refinery workers exposed to EDC at levels ranging from 10 to 200 ppm and found that these workers experienced many of the same symptoms as those seen in the aircraft workers. Clinical analyses confirmed that the liver and gastrointestinal tract were the principal target organs affected by EDC exposure. Rosenbaum (1947) also reported that EDC exposures below 25 ppm (not further specified) caused functional nervous system disorders, including headache, insomnia, and fatigue, and also slowed the heartbeat rate in affected workers.
OSHA finds the evidence presented in these studies consistent, biologically plausible, and convincing. Although specific exposure levels and precise industrial hygiene measurements are not available for some of these studies, the weight of the evidence presented demonstrates that occupational exposures to EDC at levels of 10 ppm or somewhat higher (i.e., in the 14- to 15-ppm range) cause severe health effects in specific target organ systems (i.e., the liver and gastrointestinal tract). The symptoms and signs of EDC's effects have been confirmed both clinically (palpitation of enlarged livers, X-ray evidence of pyloric spasms) and by laboratory analysis (elevated urobilinogen levels, positive Takata-Ara liver function tests, negative glucose tolerance tests). Thus, OSHA finds that EDC's hepatotoxic and gastrointestinal effects clearly warrant a reduction in the PEL to levels substantially below the level (10 ppm) shown to cause toxic liver and other effects. In response to the CMA, OSHA agrees that EPA's ban has eliminated the fumigant exposures described in the Brzozowski et al. (1954/Ex. 1-63) study, which involved concomitant dermal exposures. However, OSHA notes that the dermal LD(50) in rabbits is in the range of 2.8 to 4.9 g/kg, indicating that EDC is not readily absorbed through the skin in toxic quantities. OSHA therefore finds that, although dermal exposure undoubtedly contributed somewhat to the toxic effects seen in the workers in the Brzozowski et al. (1954/ Ex. 1-63) study, airborne exposure was the predominant contributor to these effects.
Some commenters also took issue with OSHA's reference in the proposal to EDC's carcinogenicity. According to these commenters (Exs. 3-677, 3-741, and 3-874), because the NCI bioassay (1978d/Ex. 1-947) in mice and rats involved the use of corn oil as a vehicle, carcinogenic responses may have been enhanced. In addition, because EDC gavage produced greater amounts of the potentially genotoxic glutathione conjugate than did equivalent inhalation doses of EDC, these commenters believe that route of administration may play a critical role in the carcinogenicity of EDC, and thus, that occupational exposures, which are predominantly via inhalation, may not be carcinogenic.
OSHA is aware that inhalation bioassays of EDC did not produce a statistically significant increase in tumors in rats or mice. However, the NCI gavage study (1978d/Ex. 1-947) was positive in rats and mice, and intraperitoneal administration of EDC produced an elevated increase in lung adenomas in strain A mice (Health Assessment Document (HAD) for 1,2-Dichloroethane (Ethylene Dichloride), EPA/600/8-84/006F, p. 1-5, EPA 1985a). Dermal application caused a statistically significant increase in benign lung tumors in mice, although this route did not cause a significant increase in skin tumors. EPA (1985a) concludes that the direct and supporting evidence for the carcinogenicity of EDC includes:
(1) Multiple tumor types in oral bioassays in two species;
(2) Suggestive evidence in two other animal bioassays;
(3) Demonstrated evidence of reactive metabolites and formation of a DNA adduct; and
(4) Evidence that EDC is also a mutagen (EPA 1985a, p. 1-5).
In posthearing comments, NIOSH (Ex. 150, Comments on Ethylene Dichloride) emphasized that the NCI bioassay (NCI 1978d/Ex. 1-947) demonstrated EDC-induced lung neoplasms and lymph system cancers in mice of both sexes, liver cancer in males, and mammary and uterine cancers in females. The AFL-CIO also emphasized EDC's carcinogeneity (Ex. 194). In rats, it produced cancers of the forestomach in males, mammary neoplasms in females, and hemangiosarcomas in animals of both sexes. NIOSH (Ex. 150, Comments on Ethylene Dichloride) concluded its comments by quoting the summary of the IARC (1979b, as cited in Ex. 150) monograph on EDC:
In regard to the technological feasibility of achieving a 1-ppm limit for EDC, the Chemical Manufacturers Association (CMA) states that uniform compliance with the proposed PEL will not be achieved. Manufacturing operations appear to be able to meet a 10-ppm, 8-hour TWA PEL for many routine operations. However, maintenance tasks, sampling, and loading operations will have difficulty meeting a 10-ppm PEL (Ex. 3-874, p. 3). Both the Vinyl Institute (Ex. 3-624) and the Dow Chemical Company (Ex. 3-741) share the CMA's view on the feasibility of achieving the 1-ppm limit. However, OSHA notes that ethylene dichloride is manufactured and used in closed systems (Ex. 3-874) and that 90 percent of all EDC produced in this country is used captively by the producers themselves (84 percent of all EDC produced in the United States is used to make vinyl chloride monomer) (EPA 1985a, p. 1-1). Emissions from closed systems, which include fugitive emissions from process equipment such as pumps, seals, and flanges; emissions during process sampling; emissions during loading operations; and emissions during maintenance operations, are all readily amenable to control through the use of engineering methods or improved work practices. For example, implementation of a rigorous schedule of manual leak detection and repair, the use of sampling bombs or ventilated sampling ports, the use of loading arms for closed-hatch loading of EDC into railcars and tank trucks, installation of vapor return lines or vapor recovery systems on loading docks, and installation of improved maintenance procedures are all inexpensive and effective methods of controlling fugitive emissions from process machinery. In addition, because of the intermittent, nonroutine, and varied nature of maintenance operations, OSHA typically permits the use of respirators during the performance of maintenance tasks. OSHA is also cognizant of the potential for feasibility problems in loading and sampling operations. The Agency will consider the use of respirators for these operations on a case-by-case basis or, as appropriate, on a sector-by-sector basis. However, OSHA finds that EDC producers will generally be able to achieve the 1-ppm 8-hour TWA and the 2-ppm short-term limit by using readily available control technologies and implementing additional work practices.
The Agency concludes that an 8-hour TWA of 1 ppm and a 15-minute STEL of 2 ppm are necessary to protect workers against the significant risks of liver damage, gastrointestinal toxicity, and cancer, all material health impairments that are associated with exposure to ethylene dichloride. OSHA further concludes that the revised limits will substantially reduce these significant occupational risks.