OSHA comments from the January 19, 1989 Final Rule on Air Contaminants Project extracted from 54FR2332 et. seq. This rule was remanded by the U.S. Circuit Court of Appeals and the limits are not currently in force.

CAS: 75-35-4; Chemical Formula: CH2 = CCl2

Previously, OSHA’s Z tables did not include a limit for vinylidene chloride (VDC). The ACGIH has established 5 ppm as an 8-hour TWA and 20 ppm as a 15-minute STEL. NIOSH and OSHA, in 1978, jointly recommended that employee exposure to VDC be reduced to the lowest feasible level on the basis of VDC’s carcinogenicity (NIOSH/OSHA 1978/Ex. 1-1119). OSHA proposed a PEL of 5 ppm (8-hour TWA) and a STEL of 20 ppm. However, in response to record comments, the final rule promulgates a 1-ppm limit as an 8-hour TWA. Vinylidene chloride is a colorless liquid that polymerizes readily.

The acute oral LD(50) for male rats is 2500 mg/kg (Jenkins, Trabulus, and Murphy 1972/Ex. 1-960). The LC(50) for rats exposed to a single four-hour exposure of VDC vapor was reported as 6350 ppm in one study (Siegel, Jones, Coon, and Lyon 1971/Ex. 1-371) and 32,000 ppm in an earlier study (Carpenter, Smyth, and Pozzani 1949/Ex. 1-722). Liquid VDC causes transient irritation to the eyes of rats but has little effect on exposed skin if the VDC is allowed to evaporate (Torkelson and Rowe 1981b, as cited in ACGIH 1986/Ex. 1-3, p. 628).

Prendergast and co-workers (1967/Ex. 1-926) exposed rats, rabbits, guinea pigs, and monkeys eight hours/day, five days/week for six weeks to 395 mg/m3 (100 ppm); these authors saw no visible signs of toxicity while the exposure was in process, but rabbits and monkeys lost weight. These same species were exposed continuously to VDC concentrations of 5, 15, 25, or 47 ppm for 90 days; only the animals exposed to 5 ppm showed no increases in mortality (Prendergast, Jones, Jenkins, and Siegel 1967/Ex. 1-926).

Nasal irritation, liver cell degeneration, and retarded weight gain were reported in rats following 20 six-hour exposures to 500 ppm VDC (Gage 1970/Ex. 1-318); at 200 ppm, only nasal irritation occurred. Studies by Torkelson and Rowe (1981b, as cited in ACGIH 1986/Ex. 1-3, p. 628) in which rats, rabbits, guinea pigs, and dogs were exposed to 25, 50, or 100 ppm VDC for eight hours per day, five days per week for six months revealed injury of the kidneys and liver in all animals at all levels of exposure. Maltoni (1977/Ex. 1-985) and Maltoni, Cotti, Mercy, and Chieco (1977/Ex. 1-1090) conducted an evaluation of VCD’s carcinogenicity in which mice, rats and hamsters were exposed to levels from 10 to 150 ppm for four hours per day, five days per week for 52 weeks, with results reported through week 98 of the study. In those mice exposed to 25 ppm VCD, 21 percent of the males and 1.5 percent of the females developed kidney adenocarcinomas; these tumors were not seen in rats exposed to amounts of VDC up to 150 ppm. Exposures of 100 or 150 ppm in rats did produce a significant increase in mammary adenocarcinomas, and this response was dose-related (Maltoni 1977/Ex. 1-985; Maltoni, Cotti, Morisi, and Chieco 1977/Ex. 1-1090). Overt toxicity and mortality occurred early in the studies after four-hour exposures at levels of 50 ppm in mice and 200 ppm in rats; hamsters exposed to 20 ppm VDC showed no increase in tumor incidence (Maltoni 1977/Ex. 1-985; Maltoni, Cotti, Morisi, and Chieco 1977/Ex. 1-1090).

A study by Murray, Nitschke, Rampy, and Schwetz (1979/Ex. 1-920) investigated the embryotoxic, fetotoxic, and teratogenic effects of inhaled and ingested VDC (in rats) and inhaled VDC (in rabbits). In the inhalation studies, rats were exposed to 20, 80, or 160 ppm VDC for seven hours per day. VDC was toxic to both the adults and their embryos at levels of 80 and 160 ppm among the rats, and at 160 ppm in rabbits. At exposure levels of 20 ppm in rats and 80 ppm in rabbits, neither maternal toxicity nor effects on embryonic or fetal development were noted. In the ingestion study with rats, drinking water containing 200 ppm VDC caused no toxic effects in either the rats or their offspring.

Two strains of rats exposed to 75 or 100 ppm VDC for five days/week, six hours/day for 12 months did not show a significant increase in tumors (Viola and Caputo 1977/Ex. 1-937). Other investigators exposed rats to 25 or 75 ppm by inhalation for six hours/day, five days/week for 18 months, or to 60, 100, or 200 ppm VDC in their drinking water for two years, and found no increase in tumor incidence in these animals (Rampy, Quast, Humiston et al. 1977, as cited in ACGIH 1986/Ex. 1-3, p. 628). In mice, VDC was not active either as a whole mouse skin carcinogen or by subcutaneous injection.

In other studies, VDC proved mutagenic in both E. coli and S . typhimurium strains (Greim, Bonse, Radwan et al. 1975/Ex. 1-904; Bartsch, Malaveille, Montesano, and Tomatis 1975/Ex. 1-889). VDC has been implicated as a tumor initiator in a carcinogenesis bioassay by Van Duuren, Goldschmidt, Loewengart et al. (1979/Ex. 1-936). Studies by Reitz, Watanabe, McKenna et al. (1980/Ex. 1-927) suggest that VCD’s tumorigenicity is a result of its ability to initiate cell injury, rather than of its ability to alter the genetic material of an injured cell. However, VDC has been shown to alkylate DNA in situ and increase the rate of DNA repair to a small extent in mice (Norris and Reitz 1984/Ex. 134B). The actual cell injury is caused by VDC metabolites, which are highly reactive and cytotoxic (Maltoni 1977/Ex. 1-985; Hathway 1977/Ex. 1-906; Henschler and Bonse 1977/Ex. 1-908).

A cohort study of 138 VCD-exposed workers did not identify any VCD-related health effects in these workers (Ott, Fishbeck, Townsend, and Schneider 1976/Ex. 1-924). The cohort was too small to provide any evidence that VDC is not likely to be carcinogenic.

The Chemical Manufacturers Association submitted the results of an NTP gavage study of VDC in mice and rats (NTP 1982/Ex. 134B). The only observed significant increase in tumor incidence occurred in low-dose female mice; this increase was not considered to be related to VDC administration because similar effects were not observed in high-dose female mice, male mice, or rats. The NTP (1982/Ex. 134B) concluded that VDC was not carcinogenic in mice or rats exposed by gavage, but cautioned that a maximum tolerated dose had not been demonstrated and that previously reported studies had shown that carcinogenicity is associated with VDC inhalation by animals.

Based on the carcinogenicity evidence described above, NIOSH (Ex. 8-47, Table N6B) indicated that VDC is a suitable candidate for an individual 6(b) rulemaking. However, the CMA (Ex. 165) was of the opposite opinion, stating that the demonstrated lack of tumor response in most studies, coupled with evidence that VDC metabolism is species-specific, “demonstrates that VDC is unlikely to pose an oncogenic risk to humans” (Ex. 165, p. 42). CMA also objected to the statement by NIOSH and OSHA in the joint Current Intelligence Bulletin on VDC (NIOSH/OSHA 1978/Ex. 1-1119) that VDC be considered a potential carcinogen because of its structural similarity to vinyl chloride; the CMA considered this statement inappropriate, given the toxicity data available.

Matthew Gillen and Scott Schneider of the Workers Institute for Safety and Health (WISH) commented that the proposed 5-ppm PEL and 20-ppm STEL for VDC would not provide sufficient protection from systemic effects (Ex. 116). They pointed out that the study by Prendergast et al. (1967/Ex. 1-926) found 15 ppm to be the lowest effect level for increased mortality in animals, and that the Torkelson and Rowe (1981b, as cited in ACGIH 1986/Ex. 1-3, p. 628) study found liver and kidney injury in animals. These commenters stated that the “ACGIH TLV cannot be considered to provide adequate protection for this substance. Given this fact, OSHA should consider the NIOSH REL of 1 ppm as an interim value until further risk assessment studies can be carried out” (Ex. 116).

OSHA has re-examined the health evidence in light of the comment by WISH, and has determined that the proposed 5-ppm TWA PEL for VDC does not afford workers sufficient protection from systemic effects. Although it is questionable, in the Prendergast et al. (1967/Ex. 1-926) study, that the observed deaths at lower exposure levels were compound-related, histopathologic examination of animals exposed to 47 ppm showed treatment-related liver and kidney damage. Using an exposure regimen similar to occupational exposure (i.e., eight hours/day, five days/week), Torkelson and Rowe (1981b, as cited in ACGIH 1986/Ex. 1-3, p. 628) demonstrated kidney and liver toxicity in four species of animals after exposure to VDC levels as low as 25 ppm were administered for only six months.

OSHA believes that these studies clearly demonstrate that VDC can cause adverse liver and kidney damage at airborne concentrations as low as 25 to 50 ppm and suggest that VDC is a potential occupational carcinogen. Liver and kidney damage and cancer clearly constitute material health impairments within the meaning of the Act. Therefore, OSHA concludes that the proposed limits of 5 ppm as an 8-hour TWA and 20 ppm as a STEL will not sufficiently protect workers from the significant risk of organ damage, and that a further reduction in the PEL is warranted. Accordingly, OSHA is establishing a 1-ppm 8-hour TWA limit for vinylidene chloride in the final rule.

Page last reviewed: September 28, 2011