Agency for Toxic Substances and Disease Registry
Case Studies in Environmental Medicine (CSEM)
Arsenic Toxicity
Who is at Risk
The quantity of arsenic released by human activities exceeds amounts released from natural sources by at least threefold. The major sources of arsenic release to the environment are smelters, coal-fired power plants, and pesticides. Air, water, and soil levels of arsenic are highest near smelters. Urban air is far more contaminated than air in remote areas, and water and soil concentrations are far higher in areas where arsenic-mineral deposits are mined. Besides refinery workers and farmers, other workers at increased risk of arsenic exposure include those in the industries listed previously. People living near smelters and other arsenic-emitting facilities also have potential risk of exposure from fugitive airborne emissions and groundwater contamination.
Arsenic is notorious as a poison because white arsenic (arsenic trioxide) has no odor or taste. Most arsenic poisonings are due to unintentional ingestion by children. In 1989, EPA instituted a phase-out of certain arsenic-containing ant poisons in an effort to reduce the incidence of children's arsenic ingestion.
Wood treated with arsenate wood preservatives is an important source of arsenic exposure. Burning plywood treated with an arsenate wood preservative in a poorly ventilated cabin has been blamed for poisoning a family in rural Wisconsin. Green wood or pressed wood treated with copper arsenate to prevent mildew is commonly used in marine applications, patio decks, and recreational structures for children's playgrounds. Cutting this wood or erosion of the veneer may lead to arsenic exposure. Children who play on wood structures treated with copper arsenate are at risk of dermal contact or ingestion of the arsenical through normal mouthing and play activities.
Methyl transferase enzymes play a necessary role in the methylation of arsenic in mammals. The effect of dietary deficiencies and genetic variability on methylating capacity may have important implications for tissue distribution and individual susceptibility to arsenic toxicity, even in humans. Experimental animals fed protein-deficient diets while exposed to high levels of arsenic have shown decreased methylating capacity, which has led to increased deposits of arsenic in liver, lung, and other organ sites, and, presumably, increased susceptibility to arsenic toxicity.
Arsenic can cross the placenta, exposing the fetus. Significant levels of arsenic were found in an infant born 4 days after the mother ingested arsenic in a suicide attempt. Increased incidence of spontaneous abortions, infant congenital malformations, and decreased birth weights have been reported among women and their offspring living near a copper smelter in Sweden. It is not clear that these events can be ascribed solely to arsenic, since other chemicals (including
lead, cadmium, and sulfur dioxide) were also present; however, teratogenic effects have been reported in arsenic-exposed animals, and chromosomal damage has been found in arsenic-exposed human leukocyte cultures.
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