HYPERSENSITIVITY TO MITOMYCIN C-INDUCED SISTER-CHROMATID EXCHANGE AS A BIOMARKER OF PAST EXPOSURE TO ARSENIC

The objective of this study was to determine if cytogenetic markers ca n be used as indicators of prior exposure to arsenic compounds, Baseli ne sister chromatid exchange (SCE) and mitomycin C-induced (MMC) SCE w ere measured in four study populations recruited from a blackfoot (BF) disease endemic area, including 22 patients with cancer (CA) only, 8 patients with both BF disease and CA (BF + CA), 10 patients with BF di sease only, and 26 healthy residents (HRs). Another group of 23 health y, nonarsenic-exposed workers were recruited as external healthy contr ols (HCs). Characteristics of study population were collected by quest ionnaire, and 10 ml of venous blood were drawn for lymphocyte culture. The results showed that the frequencies of baseline SCE did not diffe r among the five study groups, The frequencies of Delta SCE (MMC-induc ed SCE minus baseline SCE) in CA only, BF disease only, and HRs, three arsenic-exposed groups, were significantly higher than in HCs. The fr equency of Delta SCE in the BF + CA group was nonsignificantly higher than in HCs, probably due to small sample size, The frequencies of bot h baseline SCE and Delta SCE did not differ among CA only, BF disease only, BF + CA, and HR groups, The observation that baseline SCE did no t increase in the arsenic-exposed populations indicates either that ex posures were insufficiently high to change this marker or that lesions did not persist, The increased SCE response to MMC in arsenic-exposed populations suggests that previous arsenic exposure may result in hyp ersensitivity of human lymphocytes to carcinogens and/or mutagens, Bot h baseline SCE and Delta SCE were not different among patients with ar senic-induced diseases and healthy normal residents, indicating that h ypersensitivity may have been due to previous arsenic exposure but was not associated with disease status.