Toxicity Profiles
Toxicity Summary for CHROMIUM
NOTE:
Although the toxicity values presented in these toxicity profiles
were correct at the time they were produced, these values are subject to change.
Users should always refer to the
Toxicity Value Database
for the current toxicity values.
September 1992
Prepared by: Mary Lou Daugherty, M.S., Chemical Hazard Evaluation and Communication Group, Biomedical and Environmental Information Analysis Section, Health and Safety Research Division*, , Oak Ridge, Tennessee.
Prepared for: OAK RIDGE RESERVATION ENVIRONMENTAL RESTORATION PROGRAM.
*Managed by Martin Marietta Energy Systems, Inc., for the U.S. Department of Energy under
Contract No. DE-AC05-84OR21400.
Elemental chromium (Cr) does not occur in nature, but is present in ores, primarily chromite
(FeOCr2O3) (Hamilton and Wetterhahn, 1988). Only two of the several oxidation states of chromium,
Cr(III) and Cr(VI), are reviewed in this report based on their predominance and stability in the ambient
environment and their toxicity in humans and animals.
Chromium plays a role in glucose and cholesterol metabolism
and is thus an essential element to man and animals (Schroeder et al., 1962).
Non-occupational exposure to the metal occurs via the ingestion of chromium-containing
food and water, whereas occupational exposure occurs via inhalation (Langard,
1982; Pedersen, 1982). Workers in the chromate industry have been exposed
to estimated chromium levels of 10-50 µg/m3 for Cr(III)
and 5-1000 µg/m3 for Cr(VI); however, improvements in the
newer chrome-plating plants have reduced the Cr(VI) concentrations 10- to
40-fold (Stern, 1982).
Chromium(III) is poorly absorbed, regardless of the route of exposure, whereas chromium(VI)
is more readily absorbed (Hamilton and Wetterhahn, 1988). Humans and animals localize chromium in
the lung, liver, kidney, spleen, adrenals, plasma, bone marrow, and red blood cells (RBC) (Langard, 1982;
ATSDR, 1989; Bragt and van Dura, 1983; Hamilton and Wetterhahn, 1988). There is no evidence that
chromium is biotransformed, but Cr(VI) does undergo enzymatic reduction, resulting in the formation
of reactive intermediates and Cr(III) (Hamilton and Wetterhahn, 1988). The main routes for the excretion
of chromium are via the kidneys/urine and the bile/feces (Guthrie, 1982; Langard, 1982).
Animal studies show that Cr(VI) is generally more toxic than Cr(III), but neither oxidation state
is very toxic by the oral route. In long-term studies, rats were not adversely affected by ~1.9 g/kg/day
of chromic oxide [Cr(III)] (diet), 2.4 mg/kg/day of Cr(III) as chromic chloride (drinking water), or 2.4
mg/kg/day of Cr(VI) as potassium dichromate (drinking water) (Ivankovic and Preussmann, 1975;
MacKenzie et al., 1958).
The respiratory and dermal toxicity of chromium are well-documented.
Workers exposed to chromium have developed nasal irritation (at <0.01
mg/m3, acute exposure), nasal ulcers, perforation of the nasal
septum (at ~2 µg/m3, subchronic or chronic exposure) (Hamilton
and Wetterhahn, 1988; ATSDR, 1989; Lindberg and Hedenstierna, 1983) and
hypersensitivity reactions and "chrome holes" of the skin (Pedersen, 1982;
Burrows, 1983; U.S Air Force, 1990). Among the general population, contact
dermatitis has been associated with the use of bleaches and detergents (Love,
1983).
Compounds of both Cr(VI) and Cr(III) have induced developmental effects in experimental animals
that include neural tube defects, malformations, and fetal deaths (Iijima et al., 1983; Danielsson et al.,
1982; Matsumoto et al., 1976).
The subchronic and chronic oral RfD value is 1 mg/kg/day for Cr(III). The subchronic and
chronic oral RfD for Cr (VI) are 0.02 and 0.005 mg/kg/day, respectively (U.S. EPA, 1991a,b; 1992). The
subchronic and chronic oral RfD values for Cr(VI) and Cr(III) are derived from no-observed-adverse-effect levels (NOAELs) of 1.47 g/kg Cr(III)/day and 25 ppm of potassium dichromate (Cr[VI]) in drinking
water, respectively (Ivankovic and Preussmann, 1975; MacKenzie et al., 1958). The inhalation RfC values
for both Cr(III) and Cr(VI) are currently under review by an EPA workgroup.
The inhalation of chromium compounds has been associated with the development of cancer in
workers in the chromate industry. The relative risk for developing lung cancer has been calculated to
be as much as 30 times that of controls (Hayes, 1982; Leonard and Lauwerys, 1980; Langard, 1983).
There is also evidence for an increased risk of developing nasal, pharyngeal, and gastrointestinal
carcinomas (Hamilton and Wetterhahn, 1988). Quantitative epidemiological data were obtained by
Mancuso and Hueper (1951), who observed an increase in deaths (18.2%; p<0.01) from respiratory cancer
among chromate workers compared with 1.2% deaths among controls. In a follow-up study, conducted
when more than 50% of the cohort had died, the observed incidence for lung cancer deaths had
increased to approximately 60% (Mancuso, 1975). The workers were exposed to 1-8 mg/m3/year total
chromium. Mancuso (1975) observed a dose response for total chromium exposure and attributed the
lung cancer deaths to exposure to insoluble [Cr(III)], soluble [Cr(VI)], and total chromium. The results
of inhalation studies in animals have been equivocal or negative (Nettesheim et al., 1971; Glaser et al,
1986; Baetjer et al., 1959; Steffee and Baetjer, 1965).
Based on sufficient evidence for humans and animals, Cr(VI)
has been placed in the EPA weight-of-evidence classification A, human carcinogen
(U.S. EPA, 1991a). For inhalation exposure, the unit risk value is 1.2E-2
(µg/m3)-1 and the slope factor is 4.1E+01 (mg/kg/day)-1
(U.S. EPA, 1991a).
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