Chromium is absorbed from oral, inhalation, or dermal exposure and distributes to nearly all tissues, with the highest concentrations found in kidney and liver. Bone is also a major storage site and may contribute to long-term retention. Hexavalent chromium's similarity to sulfate and chromate allow it to be transported into cells via sulfate transport mechanisms. Inside the cell, hexavalent chromium is reduced first to pentavalent chromium, then to trivalent chromium by many substances including ascorbate, glutathione, and nicotinamide adenine dinucleotide. Chromium is almost entirely excreted with the urine. (A12, L16)
IDENTIFICATION AND USE: Chromium (III) acetate is a blue-violet crystalline powder. It is not registered for current pesticide use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses. It is used in dyeing; in tanning; in hardening photographic emulsions; as oxidation catalyst; to improve light stability and dye affinity of textiles and polymers; and in catalyst for polymerization of olefins. HUMAN EXPOSURE AND TOXICITY: There is no data. ANIMAL STUDIES: In studies in which chromium (III) acetate was administered by the oral route to mice and rats and by intrapleural and intramuscular administration to rats, the incidence of tumors was not increased. Salmonella typhimurium strain TA102, particularly suited to the detection of oxidative mutagens, was the most sensitive out of 9 strains of S. typhimurium his- in revealing the mutagenicity of Cr(VI) compounds. The rank of sensitivity was the following: TA102, TA100, TA97, TA92, TA1978, TA98, TA1538 and TA1537, TA1535 being the only insensitive strain. Cr(III) compounds (chromic acetate, chromic nitrate and chromic potassium sulfate) were totally inactive with all strains.
Trivalent chromium may also form complexes with peptides, proteins, and DNA, resulting in DNA-protein crosslinks, DNA strand breaks, DNA-DNA interstrand crosslinks, chromium-DNA adducts, chromosomal aberrations and alterations in cellular signaling pathways. It has been shown to induce carcinogenesis by overstimulating cellular regulatory pathways and increasing peroxide levels by activating certain mitogen-activated protein kinases. It can also cause transcriptional repression by cross-linking histone deacetylase 1-DNA methyltransferase 1 complexes to CYP1A1 promoter chromatin, inhibiting histone modification. Chromium may increase its own toxicity by modifying metal regulatory transcription factor 1, causing the inhibition of zinc-induced metallothionein transcription. (A12, L16, A34, A35, A36)
WEIGHT OF EVIDENCE CHARACTERIZATION: Applying the criteria for evaluating the overall weight of evidence for carcinogenicity to humans outlined in EPA's guidelines for risk assessment (1986), trivalent chromium is most appropriately designated a Group D -- Not classified as to its human carcinogenicity. Using the Proposed Guidelines for Carcinogen Risk Assessment (1996), there are inadequate data to determine the potential carcinogenicity of trivalent chromium ... However, the classification of hexavalent chromium as a known human carcinogen raises a concern for the carcinogenic potential of trivalent chromium. HUMAN CARCINOGENICITY DATA: Occupational exposure to trivalent chromium and other chromium compounds by inhalation has been studied in the chromate manufacturing and ferrochromium industries; however, exposures all include mixed exposures to both Cr(III) and Cr(VI). Cr(VI) species is the likely etiological agent in reports of excess cancer risk in chromium workers. Data addressing exposures to Cr(III) alone are not available and data are inadequate for an evaluation of human carcinogenic potential. ... ANIMAL CARCINOGENICITY DATA: The data from oral and inhalation exposures of animals to trivalent chromium do not support documentation of the carcinogenicity of trivalent chromium. IARC concluded that animal data are inadequate for the evaluation of the carcinogenicity of Cr(III) compounds. Furthermore, although there is sufficient evidence of respiratory carcinogenicity associated with exposure to chromium, the relative contribution of Cr(III), Cr(VI), metallic chromium, or soluble versus insoluble chromium to carcinogenicity cannot be elucidated... /Chromium (III), insoluble salts/
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌性证据
A4；不可归类为人类致癌物。/铬和Cr(III)无机化合物/
A4; Not classifiable as a human carcinogen. /Chromium and Cr(III) inorganic compounds/
Evaluation: There is inadequate evidence in humans for the carcinogenicity of metallic chromium and of chromium(III) compounds. There is inadequate evidence in experimental animals for the carcinogenicity of metallic chromium, barium chromate and chromium(III) compounds. Overall evaluation: Metallic chromium and chromium(III) compounds are not classifiable as to their carcinogenicity to humans (Group 3). /Metallic chromium and chromium(III) compounds/
Novel metal-micelle asbestos and treatment of asbestos and other
申请人：Flow General, Inc.
公开号：US04401636A1
公开（公告）日：1983-08-30
Silicate minerals, including asbestos fibres, are rendered less harmful by forming metal-micelle polymer coatings on the silicate. A metal-micelle polymer coating is formed on a silicate by contacting a silicate mineral, such as asbestos, with a metal-weak base-strong acid aqueous ion system, or a metal-strong base-weak acid ion system. In these systems the metal is selected from the group consisting of manganese, chromium, cobalt, iron, copper, aluminum and mixtures of these metals. The product of reacting asbestos fibres with these systems is less irritating to living cells than asbestos fibres and also has substantially the same physical and chemical properties as asbestos fibres and can thus be substituted for asbestos fibres in most technological applications.
