The article "Chromium in Drinking Water: Sources, Metabolism, and Cancer Risks" by Anatoly Zhitkovich discusses the presence and health risks associated with chromium in drinking water, particularly hexavalent chromium (Cr(VI)). Cr(VI) is classified as a known human carcinogen due to its inhalation toxicity and environmental mobility. The article highlights that Cr(VI) can originate from both anthropogenic and natural sources, and it is highly mobile in the environment. Acidic environments with high organic content promote the reduction of Cr(VI) to less toxic Cr(III).
The cellular metabolism of Cr(VI) involves its uptake through sulfate channels and subsequent reduction to Cr(III) by ascorbate and small thiols. This reduction process generates mutagenic Cr-DNA adducts, which are the primary cause of DNA damage and chromosomal breaks. Epidemiological and animal studies suggest that ingestion of Cr(VI) may increase the risk of stomach cancers, and exposure to Cr(VI) in drinking water has induced tumors in the alimentary tract of animals.
The article also examines the mutagenic mechanisms of Cr(VI), including the formation of DNA adducts and chromosomal breaks, and the role of DNA repair mechanisms such as mismatch repair (MMR). It discusses the importance of genotoxic and epigenetic mechanisms in the carcinogenic effects of Cr(VI). Additionally, the article addresses the question of whether human gastric detoxification of low doses of Cr(VI) is complete, suggesting that only 10-20% of ingested Cr(VI) escapes gastric inactivation, which argues against a threshold for cancer risk at low doses.
Overall, the article emphasizes the need for comprehensive risk assessments and regulatory measures to protect public health from the carcinogenic effects of Cr(VI) in drinking water.The article "Chromium in Drinking Water: Sources, Metabolism, and Cancer Risks" by Anatoly Zhitkovich discusses the presence and health risks associated with chromium in drinking water, particularly hexavalent chromium (Cr(VI)). Cr(VI) is classified as a known human carcinogen due to its inhalation toxicity and environmental mobility. The article highlights that Cr(VI) can originate from both anthropogenic and natural sources, and it is highly mobile in the environment. Acidic environments with high organic content promote the reduction of Cr(VI) to less toxic Cr(III).
The cellular metabolism of Cr(VI) involves its uptake through sulfate channels and subsequent reduction to Cr(III) by ascorbate and small thiols. This reduction process generates mutagenic Cr-DNA adducts, which are the primary cause of DNA damage and chromosomal breaks. Epidemiological and animal studies suggest that ingestion of Cr(VI) may increase the risk of stomach cancers, and exposure to Cr(VI) in drinking water has induced tumors in the alimentary tract of animals.
The article also examines the mutagenic mechanisms of Cr(VI), including the formation of DNA adducts and chromosomal breaks, and the role of DNA repair mechanisms such as mismatch repair (MMR). It discusses the importance of genotoxic and epigenetic mechanisms in the carcinogenic effects of Cr(VI). Additionally, the article addresses the question of whether human gastric detoxification of low doses of Cr(VI) is complete, suggesting that only 10-20% of ingested Cr(VI) escapes gastric inactivation, which argues against a threshold for cancer risk at low doses.
Overall, the article emphasizes the need for comprehensive risk assessments and regulatory measures to protect public health from the carcinogenic effects of Cr(VI) in drinking water.