The study, published in the April issue the International Journal of Cancer, is the first to report diminished expression of DNA repair genes in cells taken directly from humans exposed to arsenic through their environment, according to lead author, Dr. Angeline Andrew, research assistant professor of community and family medicine. She and colleagues Dr. Margaret Karagas, professor of community and family medicine, and Dr. Joshua Hamilton, associate professor of pharmacology and toxicology, compared the arsenic exposure of individuals to expression of DNA repair genes isolated from samples of the same person's blood.
"We were primarily interested in uncovering the mechanism to explain how arsenic causes cancer," said Andrew, noting that arsenic is a well established carcinogen. "This study supports the hypothesis that arsenic may act as a co-carcinogen --not directly causing cancer, but allowing other substances, such as cigarette smoke or ultraviolet light, to cause mutations in DNA more effectively."
The study sheds light on the environmental factors that can increase cancer risk among Americans. The researchers, all faculty in Dartmouth's Center for Environmental Health Sciences and the Norris Cotton Cancer Center, used molecular tools to expand an ongoing study analyzing cancer risk in people exposed to arsenic through their well water.
Previous studies by Karagas and colleagues had established that toenails provide a good biomarker for arsenic exposure -- that is, the arsenic levels in an individual's toenails are well correlated to that person's internal dose of arsenic. When the
Contact: Nancy Serrell
Dartmouth Medical School