Cr levels in the food range from <10 to 1,300 ug/kg, with the highest amount in meat, fish, fruits and vegetables. The primary source of oral exposure to Cr for non-occupational human populations comes from food and drinking water. In contrast, Cr(III) compounds can not enter cells by any transport mechanism. Once inside the cell, Cr(VI) undergoes a rapid metabolic reduction and is converted ultimately to Cr(III). Cr(VI) is structurally similar to sulfate and phosphate anions therefore, cells readily take it up via non-specific anion transporters. Īnother difference between Cr(VI) and Cr(III) is their ability to enter cells, which is the basis of the almost one thousand fold difference in their toxicities. While Cr(III) serves as a nutritional supplement, and may play a role in glucose and lipid metabolism, Cr(VI) is very toxic inducing a wide variety of injuries in cells, such as: DNA damage, chromosomal aberrations, alterations in the epigenome and microsatellite instability. Cr(VI) and Cr(III) differ not only in their oxidation states, but also in their chemical properties and toxicity. This form occurs rarely in nature and is mainly produced from industrial activities. The next most stable form is hexavalent chromium. Cr(III) occurs naturally in chromite ore and is normally used for manufacturing chromium metal and mono- or di-chromates. The most common as well as stable form of chromium is the trivalent form, Cr(III). Chromium has multiple oxidation states, ranging from Cr(0) (elemental chromium) to Cr(VI) (hexavalent chromium). In this review we will focus on the recent progress regarding the toxicity and carcinogenicity of oral exposure to Cr(VI).Ĭhromium is one of the most abundant elements in the Earth’s crust, with an average concentration of 125 mg/kg. Since then, a series of studies have been conducted to investigate the association between oral exposure to Cr(VI) and gastrointestinal cancer, as well as to establish the modes of action (MOA) for small intestinal tumors that occurred in mice in the NTP study. In 2008, The National Toxicology Program (NTP) released a 2-year rodent study on oral exposure of Cr(VI) in drinking water, indicating that Cr(VI) was a carcinogen when ingested. A meta-analysis of data on chromate workers did not support the association between occupational Cr(VI) exposure by inhalation and tumors in the digestive system. A study in China reported an increase of stomach cancer mortality in the area with elevated Cr(VI) concentrations in drinking water but in this study there were some limitations with its statistical power. Individuals with wells are subject to Chromate contamination in their wells via aquafers. In the past, there was extensive discharge to the environment and uptake via aquafers of chrome plating baths and water containing chromate as an antirust agent. Chromate is a very common contaminant in drinking water. However, there are limited human studies on the health effects of Cr(VI) when ingested. The International Agency for Research on Cancer (IARC) has classified Cr(VI) as a human carcinogen through the inhalation route of exposure. Numerous epidemiological studies have reported a high incidence of lung cancer among workers exposed occupationally to Cr(VI) by inhalation. Hexavalent chromium, Cr(VI), is widely used in numerous industrial processes including chrome pigment production, chrome plating, stainless steel manufacturing, and leather tanning. This review will discuss the potential adverse effects of oral exposure to Cr(VI) by presenting up-to-date human and animal studies, examining the underlying mechanisms that mediate Cr(VI) toxicity, as well as highlighting opportunities for future research. Cr(III) can form adducts with DNA that may lead to mutations. Once Cr(VI) enters the cell, it ultimately gets reduced to Cr(III), which mediates its toxicity via induction of oxidative stress during the reduction while Cr intermediates react with protein and DNA. The effects of Cr(VI) oral exposure is mitigated by reduction in the gut, however a portion evades the reductive detoxification and reaches target tissues. In 2008, the National Toxicology Program (NTP) released a 2-year study demonstrating that ingested Cr(VI) was carcinogenic in rats and mice. In contrast, oral exposure to Cr(VI) is widespread and affects many people throughout the globe. However, inhalational exposure to Cr(VI) affects only a small portion of the population, mainly by occupational exposures. Hexavalent chromium is a known carcinogen when inhaled.
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