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TALC								Related Pages
										*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:** 14807-96-6; **Chemical Formula:** H2O3Si • 3/4 Mg
The former OSHA PEL for nonasbestiform talc was 20 million particles per cubic foot of air (mppcf) as an 8-hour TWA; when expressed as mg/m3, this is comparable to 3 mg/m3. The ACGIH has a TLV-TWA of 2 mg/m3 (15 mppcf) for talc, measured as respirable dust, and this is the limit proposed by OSHA and included in the final rule. NIOSH (Ex. 8-47, Table N1) concurred that this limit is appropriate. Talc is a fine powder that is white to gray-white in color; it is found as a mineral, and the main component is a crystalline hydrated silicate of magnesium that is usually in the form of plates but occasionally may be in the form of fibers.
The health-effects evidence for talc is complicated by the fact that talcs contain amphiboles and other minerals, in addition to platiform talc crystals; adverse health effects appear to be related to the nonplatiform content (that is, to the fiber content) of the talc in question (ACGIH 1986/Ex. 1-3, p. 550). There are conflicting views regarding the extent to which the fibrous constituents are asbestos; however, no health effects information is available that is specifically related to fibrous talc (ACGIH 1986/Ex. 1-3, p. 550).
Numerous epidemiological studies have documented the effects on workers of long-term exposures to talc. In 1942, Porro et al. (1942, as cited in Stokinger 1981b/Ex. 1-1127) published a report in which 15 cases of talc pneumoconiosis, including five postmortem examinations, showed that asbestotic bodies were almost always present in fibrotic areas of the lungs of those workers with talcosis. Siegal and colleagues (1943, as cited in Stokinger 1981b/Ex. 1-1127) noted that the incidence of advanced fibrosis in a group of 221 talc miners and millers was 14.5 percent. These workers were primarily exposed to fibrous talc, which was believed to be responsible for the pathology of the asbestos-like lung lesions. A study by McLaughlin et al. (1949, as cited in Stokinger 1981b/Ex. 1-1127) revealed that talc-induced pneumoconiosis was caused by the fibrous varieties of talc; in animal studies by Schepers and Durkan (1955, as cited in Stokinger 1981b/Ex. 1-1127), the degree of fibrosis in the lung tissue was found to be a function of the length of the talc fibers, rather than of the composition of the talc itself. A paper by Kleinfeld, Giel, Majeranowski, and Messite (1963, as cited in Stokinger 1981b/Ex. 1-1127) reported that postmortem examinations on six talc industry workers showed that the asbestotic bodies found in the lung bronchioles or embedded in fibrous tissue were indistinguishable from the asbestos bodies seen in cases of asbestosis.
Kleinfeld, Messite, Kooyman, and Zaki (1967/Ex. 1-704) later conducted a cohort study of 220 workers who had been employed in a mine that produced talc that had a tremolite and anthophyllite content. Of the 91 deaths in this group, 10 resulted from respiratory cancer and 28 were attributed to pneumoconiosis. The proportional mortality rate from respiratory cancer was four times the expected rate. In 1974, when Kleinfeld, Messite, and Zaki (Ex. 1-705) performed a follow-up study of this group (which at that time consisted of 260 workers [108 deaths]), they found significant differences between the expected and observed mortality in the period 1950 to 1954, but not during 1960 to 1969. These investigators attributed this finding to the reduction in talc dust counts (from averages of 25 to 73 mppcf (approximately 4 to 12 mg/m3) in the years 1948 to 1965 to averages of 9 to 43 mppcf (approximately 1.5 to 6.5 mg/m3) in the period 1966 to 1969). This study also showed a decrease of greater than 50 percent in deaths due to pneumoconiosis in the 1965-to-1969 time period.
Studies by NIOSH (Dement and Zumwald 1978, as cited in ACGIH 1986/Ex. 1-3, p. 552) of 398 white male workers employed between 1947 and 1959 in the talc industries found that 74 of these men had died, and that bronchogenic cancer was the cause of death in nine men; only 3.3 deaths from this cause would have been expected. Nonmalignant respiratory disease (NMRD) exclusive of influenza, pneumonia, and tuberculosis accounted for three deaths; 1.5 would have been expected. From these data, NIOSH concluded that a significant increase in mortality due to bronchogenic cancer and NMRD had occurred as a result of occupational exposure to talc dust. NIOSH’s report also included a morbidity study of 12 talc industry workers, currently employed, in which chest X-rays, lung function tests, and questionnaires were used. This study concluded that a higher prevalence of cough, phlegm, dyspnea, and irregular opacities in chest X-rays existed in these workers than in potash miners; instances of pleural thickening and calcification were greater than in coal and potash miners; and the pulmonary function of talc workers overall was reduced in comparison with that of coal and potash miners employed for the same length of time. The reductions in pulmonary function among the talc workers were dose- and duration-related.
The ACGIH (1986/Ex. 1-3, p. 552) concludes that serious health effects have been associated in the past (i.e., prior to 1945) with exposures to amphibole-containing talc. However, the ACGIH believes that the introduction of mining improvements has all but eliminated “the excess of death rates from pneumoconiosis and lung cancer” (ACGIH 1986/Ex. 1-3, p. 552).
Two recent studies of the health effects associated with talc exposures (Rubino, Scansetti, Piolatto, and Romano 1976/Ex. 1-801; Selevan, Dement, Wagoner, and Froines 1979/Ex. 1-989) are available. The Rubino, Scansetti, Piolatto, and Romano (1976/Ex. 1-801) study found that miners and millers exposed to an average of 849 to 8470 mppcf-years (miners) or 76 to 651 mppcf-years (millers) showed no increase in the number of observed (compared to expected) deaths from causes other than silicosis. These authors concluded that the disease-causing factor in these workers was silica rather than talc (Rubino, Scansetti, Piolatto, and Romano 1976/Ex. 1-801).
The Selevan, Dement, Wagoner, and Froines (1979/Ex. 1-989) study of 392 workers exposed to talc in five mines found nonmalignant respiratory deaths for millers to be almost eight times the expected rate, while miners experienced more than three times the expected mortality rate for NMRD. The ACGIH (1986/Ex. 1-3, p. 552) believes that the Selevan et al. (1979/Ex. 1-989) study is incomplete because confounding factors were not adequately identified and controlled for.
With regard to NIOSH’s findings (Dement and Zumwald 1978, as cited in ACGIH 1986/Ex. 1-3, p. 552) of excess cancer deaths among talc workers, OSHA is currently reviewing the scientific and toxicological data describing the effects of exposure to the nonasbestiform varieties of mineral fibers that are found in talc deposits. OSHA is considering a separate rulemaking to address this issue.
OSHA received few comments regarding its proposed revision to the PEL for respirable talc. John W. Kelse, Corporate Industrial Hygienist for R.T. Vanderbilt, Inc. (Ex. 3-108), supported the proposed 2 mg/m3 respirable talc PEL. Mr. Kelse also recommended that OSHA revise its Table Z-3 entry for “Talc (nonasbestiform)” to “Talc (not containing asbestos)” and the entry for “Talc (fibrous)” to “Talc (containing asbestos).” These changes were suggested because of the potentially ambiguous meanings of the term “fibrous” and “asbestiform.” OSHA concurs with this suggestion and has accordingly revised the respective entries in Tables Z-1-A and Z-3 in this rulemaking. In response to a suggestion by Richard Bidstrup, representing the Rubber Manufacturers Association (Ex. 173, p. 9), OSHA has also revised the entry for talc to clarify that the PEL is measured as respirable dust.
On a related issue, Mr. F.A. Renninger, Senior Vice President of the National Stone Association (Ex. 3-528), suggested that OSHA delete or clarify its current Table Z-3 entry for “Tremolite (see talc fibrous)” since it suggests that all forms of tremolite are considered to be asbestos. As Mr. Renninger points out, the applicability of OSHA’s asbestos standard to the nonasbestiform varieties of tremolite, actinolite, and anthophyllite is currently under administrative stay, and OSHA is presently examining the health evidence for these mineral varieties. However, during this period of administrative stay, exposure to the nonasbestiform varieties of these minerals is covered by OSHA’s comprehensive standard, which appears at 29 CFR 1910.1101. OSHA has therefore revised the entry for tremolite in Table Z-3 to refer to the standard at 29 CFR 1910.1101.
OSHA is establishing an 8-hour TWA limit of 2 mg/m3 for the respirable dust of talc containing no asbestos fibers and less than 1 percent silica. The Agency concludes that this limit will protect workers from the significant risk of nonmalignant respiratory effects associated with exposure to talc dust; OSHA considers these effects material impairments of health. According to the ACGIH (1986/Ex. 1-3), talc may, at times, occur in a fibrous form. At this time, OSHA has not made any determinations with regard to the possible health consequences resulting from exposure to talc fibers.
										
							
								Page last reviewed:  September 28, 2011						Content source:  	National Institute for Occupational Safety and Health NIOSH
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