化合物详情

Sodium dichromate is reported to be non-biodegradable based on results of the Japanese MITI test(1); however, BOD values and test protocols were not reported(SRC).

Using carp (Cyprinus carpio) which were exposed over a 4-week period to sodium dichromate dihydrate concentrations of 1 and 0.1 mg/L, the BCF ranged from <3.6 to <36(1). According to a classification scheme(2), this BCF range suggests that bioconcentration in aquatic organisms is low(SRC).

DRINKING WATER: Sodium dichromate dihydrate is one of a number of inorganic compounds containing hexavalent chromium (CrVI) found in drinking water source supplies as a contaminant resulting from various industrial processes including electroplating operations, leather tanning, and textile manufacturing(1).

/PLANTS/ The Allium anaphase-telophase test was evaluated to find out if it could be recommended in the screening of wastewater for genotoxicity. Five mutagenic or carcinogenic chemicals usually found in wastewater were tested in the Allium anaphase-telophase test. Sodium dichromate (25 uM), benzene (100 uM), dichloromethane (175 uM) and 1,1,1-trichloromethane (175 uM) increased the frequency of chromosome aberrations in the root cells, whereas formaldehyde (1 mM) was found to be non-mutagenic in this test system. Other studies where chemicals were tested in the Allium test were reviewed. For 15 chemicals the results were compared with results from the Ames test, the Microscreen assay, and carcinogenicity tests in rodents. The sensitivity of the Allium test was calculated to be 82%. In...

The substance is very toxic to aquatic organisms. The substance may cause long-term effects in the aquatic environment. It is strongly advised not to let the chemical enter into the environment.

NIOSH (NOES Survey 1981-1983) has statistically estimated that 136,313 workers (24,542 of these are female) were potentially exposed to sodium dichromate in the US(1). Occupational exposure to sodium dichromate may occur through inhalation and dermal contact with this compound at workplaces where sodium dichromate is produced or used(2).

Breathing hexavalent chromium can cause irritation to the lining of the nose, nose ulcers, runny nose, and breathing problems, such as asthma, cough, shortness of breath, or wheezing. Ingestion of hexavalent chromium causes irritation and ulcers in the stomach and small intestine, as well as anemia. Skin contact can cause skin ulcers. (L16)

There is no know antidote for chromium poisoning. Exposure is usually handled with symptomatic treatment. (L16)

LD50: 51.10 mg/kg (Oral, Rat) (L16) LD50: 1000 mg/kg (Dermal, Rabbit) (L16) LC50: 124.42 mg/m3 over 4 hours (Inhalation, Rat) (L16)

Hexavalent chromium is a known carcinogen. Chronic inhalation especially has been linked to lung cancer. Hexavalent chromium has also been know to cause reproductive and developmental defects. (A12)

ACGIH Carcinogen - Confirmed Human.

Inhalation (L16); oral (L16); dermal (L16)

Hexavalent chromium's carcinogenic effects are caused by its metabolites, pentavalent and trivalent chromium. The DNA damage may be caused by hydroxyl radicals produced during reoxidation of pentavalent chromium by hydrogen peroxide molecules present in the cell. 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 methylt...

Intermediate Oral: 0.005 mg/kg/day (L134) Chronic Oral: 0.001 mg/kg/day (L134)

Oral Slope Factor Reference: CALEPA

1, carcinogenic to humans. (L135)

LD50 Rat oral 50 mg/kg

Although the genotoxic mechanism(s) of hexavalent chromium (CrVI) carcinogenicity remain to be fully elucidated, intracellular reduction of CrVI and concomitant generation of reactive intermediates including reactive oxygen species and subsequent oxidative damage to DNA is believed to contribute to the process of carcinogenesis. In the current study, substantial interindividual variation (7.19-25.84% and 8.79-34.72% tail DNA as assessed by conventional and FPG-modified comet assay, respectively) in levels of DNA strand breaks after in vitro treatment of WBC with sodium dichromate (100 micromol/L, 1 hour) was shown within a group of healthy adult volunteers (n = 72) as assessed by both comet and formamidopyrimidine glycosylase-modified comet assays. No statistically significant correlati...