Arsenic methylation capability and hypertension risk in subjects living in arseniasis-hyperendemic areas in southwestern Taiwan

Background: Cumulative arsenic exposure (CAE) from drinking water has been shown to be associated with hypertension in a dose-response pattern. This study further explored the association between arsenic methylation capability and hypertension risk among residents of arseniasis-hyperendemic areas in Taiwan considering the effect of CAE and other potential confounders. Method: There were 871 subjects (488 women and 383 men) and among them 372 were diagnosed as having hypertension based on a positive history or measured systolic blood pressure ≥ 140 mm Hg and/or diastolic blood pressure ≥ 90 mm Hg. Urinary arsenic species were determined by high-performance liquid chromatography-hydride generator and atomic absorption spectrometry. Primary arsenic methylation index [PMI, defined as monomethylarsonic acid (MMA^V) divided by (As^III + As^V)] and secondary arsenic methylation index (SMI, defined as dimethylarsinic acid divided by MMA^V) were used as indicators for arsenic methylation capability. Results: The level of urinary arsenic was still significantly correlated with cumulative arsenic exposure (CAE) calculated from a questionnaire interview (p = 0.02) even after the residents stopped drinking the artesian well water for 2-3 decades. Hypertensive subjects had higher percentages of MMA^V and lower SMI than subjects without hypertension. However, subjects having CAE > 0 mg/L-year had higher hypertension risk than those who had CAE = 0 mg/L-year disregard a high or low methylation index. Conclusion: Inefficient arsenic methylation ability may be related with hypertension risk.