SPONTANEOUS AND INDUCED SISTER-CHROMATID EXCHANGES AND DELAYED CELL-PROLIFERATION IN PERIPHERAL LYMPHOCYTES OF BOWENS-DISEASE PATIENTS AND MATCHED CONTROLS OF ARSENIASIS-HYPERENDEMIC VILLAGES IN TAIWAN

A total of 15 newly-developed Bowen's disease patients and 34 age-sex- residence-matched controls were recruited from three arseniasis-hypere ndemic villages in Taiwan to compare spontaneous and arsenic-induced s ister chromatid exchanges (SCEs), proportion of cells with high freque ncies of SCEs (HFCs), and replication index (RI) in their peripheral l ymphocytes. Arsenic-induced Bowen's disease patients were found to hav e significantly higher spontaneous SCEs and HFCs and a lower spontaneo us RI than in matched controls without or with adjustment for age, gen der, cigarette smoking, alcohol drinking, tea drinking, status of majo r diseases, HBsAg carrier status and arsenic exposure indices through multivariate analysis. Sodium arsenite was found to increase SCEs and HFCs and to decrease RI in a dose-response pattern for both cases and controls. The arsenic-induced decrease in RI was significantly greater in arsenic-induced Bowen's disease patients than in matched controls. The arsenic-induced increases in SCEs and HFCs were also consistently , but not statistically significantly, higher in arsenic-induced Bowen 's disease patients than in matched controls at all arsenite treatment levels of 0.5, 1.0 and 2.0 mu M. The arsenic-induced increase in cyto genetic damages and decrease in cell proliferation among arsenic-induc ed Bowen's disease patients compared with matched controls may result from their long-term exposure to inorganic arsenic through consumption of high-arsenic artesian well water, elevated individual genetic and acquired susceptibility to arsenic-induced damage, or both.