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

BackgroundCumulative 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.MethodThere 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 (MMAV) divided by (AsIII + AsV)] and secondary arsenic methylation index (SMI, defined as dimethylarsinic acid divided by MMAV) were used as indicators for arsenic methylation capability.ResultsThe 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 MMAV 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.ConclusionInefficient arsenic methylation ability may be related with hypertension risk.