Although arsenic in high doses has been associated with an increased risk of cancer, there are no human studies capable of determining whether arsenic in drinking water at or below the current MCL results in an increased risk of cancer. Thus, risk assessment must rely on extrapolation from exposure at higher intakes, well over 50 ppb, such as that found in an epidemiological study in Taiwan. The NRDC and EPA apparently have decided to use the Taiwan study to calculate the risk for arsenic-induced cancer although a 1994 report, partially funded by the National Science Council, showed that the Taiwan data were too fraught with uncertainty to be used as a basis for the agency's revision. There are many reasons for the Taiwan data being an unrealistic measuring stick for deriving an MCL for US drinking water. For example, the population supposedly affected by arsenic toxicity in Taiwan had poor socioeconomic status and were generally undernourished.
High arsenic can make selenium deficiency worse.
Because selenium is known to have anticancer properties it is possible that the arsenic toxic effect in Taiwan was more a response to inadequate selenium. We need data that directly show whether low doses of arsenic have any direct effect on the susceptibility to cancer and other diseases, especially since the body has the ability to handle arsenic in low amounts. Until then, data from animal experiments are useful. After two years on these diets, the rats had no increase in tumors. Other studies with laboratory animals have shown that arsenic actually inhibits cancer.