The Risk Assessment Information System

Toxicity Profiles

Condensed 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.


*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). Retrieve Toxicity Profiles Formal Version

Last Updated 8/29/97

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