home edit2 whole TSD November 2002 PDF format - OEHHA

expected rate may be inflated because the age-corrected lung cancer rate in the population of the
county in which the plant is located is only 58% of the incidence in the whole country. Applying 58% to
the expected rate results in a significant increase in the incidence ratio (p < 0.01). Furthermore, using
non-ferrochromium workers as an internal referent population resulted in an 8.5-fold increase in lung
cancer incidence (p = 0.026). Exposure data were based on a 1975 industrial hygiene survey of the
plant. The total chromium content of dust was "with few exceptions" below 1 mg/m 3 . This level
probably underestimates past exposures. Water-soluble chromium (assumed to be hexavalent) ranged
from 11-33% of the total. The presence of high levels of Cr(VI) in previous years was also confirmed
by the finding of' 2 workers with nasal septum perforations. Exposure to asbestos and low levels of
polycyclic aromatic hydrocarbons also occurred, but concentrations were not reported. However,
since the 243 ferrosilicon workers studied were similarly exposed yet experienced no lung cancers, the
effect of these exposures may be minimal.
Animal Studies
There have been at least eighty reported attempts to induce cancer in rodents by administration of
chromium compounds by various routes. These have been reviewed by IARC (1980, 1982) and US
EPA (1984). US EPA (1998) has stated that hexavalent chromium compounds were carcinogenic in
animal assays producing the following tumor types: intramuscular injection site tumors in Fischer 344
and Bethesda Black rats and in C57BL mice; intraplural implant site tumors for various chromium VI
compounds in Sprague-Dawley and Bethesda Black rats; intrabronchial implantation site tumors for
various Cr VI compounds in Wistar rats; and subcutaneous injection site sarcomas in Sprague-Dawley
rats.
It was noted in the chromium TAC document that at the time of document preparation, no chromium
compound had been unequivocally shown to cause a significantly increased number of neoplasms in
experimental animals after exposure by inhalation. At least 7 experiments involving dusts containing
Cr(VI) and/or Cr(III) compounds had been conducted. Although Nettesheim et al. (1971) reported a
significantly increased incidence of alveologenic (not bronchogenic) adenomas and adenocarcinomas in
mice exposed to calcium chromate dust (13 mg/m3 ) over their lifetimes for 5 hr/day, 5 days/wk, this
conclusion could not be confirmed on the basis of the data reported. The authors' statistical
methodology was not reported. Fourteen treated animals (6 males and 8 females) developed tumors,
whereas only 5 control animals (3 males and 2 females) did. However, the numbers of exposed and
control animals were not reported, nor was the distribution of tumor types, so that the claim of a
significant increase of treatment-related tumor incidence could not be validated. CDHS (1990) found
that a later study (Glaser et al., 1986) reported increases in tumors of the lung, pharynx, pituitary,
pancreas, and liver of male rats exposed for 18 months to aerosols of Na 2 Cr 2 O 7 at chromium
concentrations of 100 mg/m 3 . Statistical criteria used for the evaluation of tumor increases were not
discussed by the authors. When analyzed by staff of CDHS, the incidence of respiratory tumors in the
high-dose group, 4/19, was found to be significantly increased above the incidence, 0/37, in controls.
CDHS (1990) also described a oral chromium carcinogenicity bioassay done by Borneff et al. (1968).
Male and female NMRI mice were exposed to 1 mg K 2 CrO 4 per day (added to the regular diet); a
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