WEIGHT OF EVIDENCE CHARACTERIZATION: Under the current guidelines (1986), Cr(VI) is classified as Group A - known human carcinogen by the inhalation route of exposure. Carcinogenicity by the oral route of exposure cannot be determined and is classified as Group D. Under the proposed guidelines (1996), Cr(VI) would be characterized as a known human carcinogen by the inhalation route of exposure on the following basis. Hexavalent chromium is known to be carcinogenic in humans by the inhalation route of exposure. Results of occupational epidemiological studies of chromium-exposed workers are consistent across investigators and study populations. Dose-response relationships have been established for chromium exposure and lung cancer. Chromium-exposed workers are exposed to both Cr(III) and Cr(VI) compounds. Because only Cr(VI) has been found to be carcinogenic in animal studies, however, it was concluded that only Cr(VI) should be classified as a human carcinogen. Animal data are consistent with the human carcinogenicity data on hexavalent chromium. Hexavalent chromium compounds are carcinogenic in animal bioassays, producing the following tumor types: intramuscular injection site tumors in rats and mice, intrapleural implant site tumors for various Cr(VI) compounds in rats, intrabronchial implantation site tumors for various Cr(VI) compounds in rats and subcutaneous injection site sarcomas in rats. In vitro data are suggestive of a potential mode of action for hexavalent chromium carcinogenesis. Hexavalent chromium carcinogenesis may result from the formation of mutagenic oxidatitive DNA lesions following intracellular reduction to the trivalent form. Cr(VI) readily passes through cell membranes and is rapidly reduced intracellularly to generate reactive Cr(V) and Cr(IV) intermediates and reactive oxygen species. A number of potentially mutagenic DNA lesions are formed during the reduction of Cr(VI). Hexavalent chromium is mutagenic in bacterial assays, yeasts and V79 cells, and Cr(VI) compounds decrease the fidelity of DNA synthesis in vitro and produce unscheduled DNA synthesis as a consequence of DNA damage. Chromate has been shown to transform both primary cells and cell lines. HUMAN CARCINOGENICITY DATA: Occupational exposure to chromium compounds has been studied in the chromate production, chromeplating and chrome pigment, ferrochromium production, gold mining, leather tanning and chrome alloy production industries. Workers in the chromate industry are exposed to both trivalent and hexavalent compounds of chromium. Epidemiological studies of chromate production plants in Japan, Great Britain, West Germany, and the United States have revealed a correlation between occupational exposure to chromium and lung cancer, but the specific form of chromium responsible for the induction of cancer was not identified ... Studies of chrome pigment workers have consistently demonstrated an association between occupational chromium exposure (primarily Cr(VI)) and lung cancer. Several studies of the chromeplating industry have demonstrated a positive relationship between cancer and exposure to chromium compounds. ANIMAL CARCINOGENICITY DATA: Animal data are consistent with the findings of human epidemiological studies of hexavalent chromium ... /Chromium (VI)/
Evaluation: There is sufficient evidence in humans for the carcinogenicity of chromium(VI) compounds. Chromium(VI) compounds cause cancer of the lung. Also positive associations have been observed between exposure to Chromium(IV) compounds and cancer of the nose and nasal sinuses. There is sufficient evidence in experimental animals for the carcinogenicity of chromium(VI) compounds. Chromium(VI) compounds are carcinogenic to humans (Group 1). /Chromium(VI) compounds/
Rats were exposed to 0, 0.2, and 1 mg/cu m of chromite ore residue dust (mean diameter 3.3 mum) for 105 wk, and concn of chromium in organs and blood were det. The chromium concn in the lung, kidney, and spleen of rats exposed to 0.2 mg/cu m were 3200, 279.2, and 56.9 ng/g, resp, and those of rats exposed to 1.0 mg/cu m were 87700, 1780, and 382 ng/g, resp The concn in the liver, brain, and blood were >40 ng/g.
Incidental ingestion of Chromite ore processing residue (COPR) particles poses a potential health risk. The purpose of this study was to determine the Cr bioaccessibility from COPR using the in vitro gastrointestinal (IVG) procedure. The bioaccessible Cr(VI) was 53.8% and 42.9%, respectively, in the gastric and intestinal phases from a total of 19490 mg kg(-1) Cr(VI) in COPR. Food intake including milk, dough, and ascorbic acid resulted in a significant decrease in Cr(VI) bioaccessibility. Some organic acids such as lactic, malic, and citric acid moderately reduced Cr(VI), while acetic acid exhibited no capacity for Cr(VI) reduction. The integrated area under the concentration-time curve (AUC) of the IVG extraction was used to calculate bioaccessibility. Compared with the bioaccessibility conventionally estimated using concentrations at the end of the extraction (CEP), the AUC technique should be implemented to confirm the accuracy of the IVG method when reduction of Cr(VI) occurs during the extraction. The absence of Cr(VI) phases in extracted residues as evidenced by XANES and XRPD analysis confirmed the Cr(VI) release and Cr(VI) reduction by food and ascorbic acid. With readily bioaccessible Cr(VI) and rapid human uptake, reduction of Cr(VI) might not be as effective a detoxification pathway as initially thought. /Chromite ore processing residue/
Chromite ore processing residue (COPR) containing measurable levels of hexavalent and trivalent chromium. [Cr(VI) and Cr(III), respectively] has been used to fill in low-lying areas in Hudson County, N.J. While it has been demonstrated that direct dermal contact with solutions containing Cr(VI) may elicit allergic contact dermatitis (ACD) in previously sensitized individuals, it is unknown to what degree skin moisture may solubilize Cr(VI) from COPR adhering to skin. An accurate estimate of this extraction potential is necessary to establish COPR concentrations of Cr(VI) and Cr(III) that are protective of eliciting ACD in sensitized individuals. The purpose of this study was to measure the extractable fraction of Cr(VI) and total chromium [Cr(III) and Cr(VI)] in soils impacted by COPR using human sweat as the extractant. Human sweat was collected from seven male volunteers. Samples of COPR material containing the following Cr(VI) and total chromium concentrations were collected: Cr(VI), 16, 136, and 1240 ppm; total chromium, 932 and 6660 ppm. The samples were sieved to obtain a uniform particle size < 500 microns. The samples were then mixed with human sweat at 30 degrees C for 12 hr, after which the sweat was filtered and analyzed to determine the dissolved concentration of Cr(VI) and total chromium. The data from these analyses show that no detectable levels (limit of detection = 0.010 ppm) of Cr(VI) were leached from COPR containing 16 ppm Cr(VI). At Cr(VI) concentrations of 136 and 1240 ppm, less than 0.1% of the Cr(VI) present in the COPR sample was extracted into sweat, and sweat concentrations were 0.133 ppm Cr(VI) or less. Similarly, the amount of Cr total extracted was 0.3% or less at COPR concentrations as high as 6600 ppm Crtotal, and sweat concentrations were 2.3 ppm Crtotal or less. If a minimum concentration of 10 ppm to 54 ppm Cr(VI) in sweat is required to elicit an ACD response in chromium-sensitive individuals, the current study results suggest that a COPR Cr(VI) concentration of at least 10,000-54,000 ppm would be required to elicit ACD. If 500 ppm (or greater) of solubilized Cr(III) is required to elicit an ACD response, then a COPR concentration of 250,000 ppm Cr(III) or greater would be required to elicit an allergic response. These results suggest that ACD is unlikely to occur as a result of environmental exposure to the COPR. /Chromite ore processing residue/
Chemical reactions in electric pulse dispersion of iron in aqueous solutions
摘要：
IR spectroscopy, X-ray phase, chemical, kinetic, and thermodynamic analyses were used to determine the nature of chemical reactions occurring in electric pulse dispersion of a metal (Fe) in aqueous solutions of inorganic substances (MnSO4, NaH2AsO4, H3AsO3, K2Cr2O7).
