OSHA formerly had an 8-hour TWA limit of 0.1 mg/m3 for cobalt metal, dust, and fume. The Agency proposed an 8-hour TWA of 0.05 mg/m3 for these substances, and NIOSH (Ex. 8-47, Table N1) concurred with the proposed limit. The final rule establishes an 8-hour TWA PEL of 0.05 mg/m3 for cobalt metal, dust, and fume; this limit is consistent with that of the ACGIH. Cobalt is a gray, hard, magnetic, and somewhat malleable metal.
Animal studies indicate that high intratracheal doses (10, 25, or 50 mg) of cobalt metal dust can cause obliterative bronchiolitis adenomatosis in guinea pigs (Schepers 1955/ Ex. 1-365). Additional studies in animals have shown that exposure to cobalt dust or fume causes hypersensitivity reactions. Increases in serum A-2 globulin and neuraminic acid occurred in dogs and rabbits exposed by inhalation to cobalt metal, metal fume, or carbide blend; injections of cobalt chloride produced similar reactions (Stokinger and Wagner 1958/Ex. 1-381). Studies conducted in miniswine have shown that inhalation of 0.1 mg/m3 cobalt metal dust (50 percent alpha and 50 percent beta variety, with a size range of from 0.4 um to 3.6 um) has caused early (onset within three months) pulmonary disease. Wheezing, which indicates hypersensitivity, occurred in these animals during the fourth week of exposure to 0.1 or 1.0 mg/m3 for six hours/day, five days/week, for three months following a one-week sensitizing dose (Kerfoot, Fredrick, and Domeier 1975/Ex. 1-145). NIOSH (Ex. 150, Comments on Cobalt) submitted comments pointing out that cobalt and cobalt compounds have caused local, injection-site tumors in experimental animals, and the AFL-CIO (Ex. 194, Appendix A) also noted that a "potential carcinogenic effect" has been identified for cobalt.
Pulmonary disease has been reported frequently in workers exposed to cobalt in the manufacture of cemented tungsten carbide (Miller, Davis, Goldman, and Wyatts 1953/Ex. 1-40; Lundgren and Ohman 1954, as cited in ACGIH 1986/Ex. 1-3, p. 144; Lundgren and Swenson 1953/Ex. 1-816). The adverse effect of exposure is generally chronic interstitial pneumonitis. Fatalities have been reported occasionally from exposures to cobalt at concentrations of 1 to 2 mg/m3 or less (Fairhall, Castberg, Carrozzo, and Brinton 1947/Ex. 1-954; Fairhall, Keenan, and Brinton 1949/Ex. 1-479). An increase in serum A-2 globulin fraction was reported in the case of a welder exposed to fumes containing cobalt; the welder had a history of exertional dyspnea and an abnormal chest X-ray (Siegesmund, Funahashi, and Pintar 1974/Ex. 1-372). Schwartz, Tulipan, and Birmingham (1957c, as cited in ACGIH 1986/Ex. 1-3, p. 144) reported that allergic dermatitis has been caused by contact with cobalt and its compounds. Dr. Michael Silverstein, representing the UAW, commented in testimony (Tr. pp. 7-44 to 7-46) that OSHA should develop ancillary provisions, such as those for medical surveillance and personal protective equipment, to protect exposed workers against skin contact with cobalt. However, as discussed earlier in this preamble, OSHA is currently developing generic standards to address these and other protective measures.
In studies undertaken by the Michigan Department of Health (1946-1964, as cited in ACGIH 1986/Ex. 1-3, p. 144), it was demonstrated that, in the period between 1946 and 1964, improved control measures had successfully reduced cobalt metal dust and fume levels from 14.42 mg/m3 to levels below 0.1 mg/m3; no new cases of systemic toxicity or dermatitis have since been associated with cobalt exposure in these facilities. The Pennsylvania Department of Health demonstrated that concentrations could be controlled easily to 0.07 mg/m3; without controls, concentrations were about 0.5 mg/m3 (ACGIH 1986/Ex. 1-3, p. 144).
In posthearing comments, NIOSH (Ex. 150, Comments on Cobalt) reported the findings of two recent epidemiological studies in cobalt-exposed workers. A cohort mortality study by Mur et al. (1987, as cited in Ex. 150) found a statistically significant increase in lung cancer mortality in cobalt and sodium workers in an electrochemical plant. NIOSH noted that this study had several limitations: the small number of lung cancer cases observed; ascertainment problems; no smoking data; and no exposure data. A recent study of hard metal workers in Great Britain (Kusaka et al. 1986, as cited in Ex. 150) found occupationally induced asthma in cobalt-exposed workers, some of whom had average exposure levels below 0.05 mg/m3. NIOSH (Ex. 150, Comments on Cobalt) also noted that this study had several limitations: the small number of workers with asthma; incomplete occupational histories for some cases; and failure to ascertain confounding exposures.
NIOSH also noted that the PEL of 0.05 mg/m3 may not protect all workers against the development of cobalt-induced asthma (Ex. 150, Comments on Cobalt). Both the UAW (Tr. 7-44/7-46) and Dr. James Melinus of the New York State Department of Public Health (Tr. 11-108) commented that pulmonary disease and ischemic heart disease may be associated with exposures to cobalt at levels of 0.06 mg/m3 and, perhaps, to levels somewhat below. OSHA notes that the studies pointed to by these commenters involve confounding exposures to tungsten, cement, and other hazardous alloys and have other methodological limitations as well.
In the final rule, the Agency is revising its 8-hour TWA limit for cobalt metal, dust, and fumes from 0.1 mg/m3 to 0.05 mg/m3. The Agency concludes that this limit will reduce the significant risk of material impairment of health posed by respiratory disease and pulmonary sensitization, which have been demonstrated to occur at higher levels of exposure. OSHA notes that the very recent literature is suggestive of effects even below this level; the Agency intends to continue to monitor the literature on cobalt in the future.