Blood Pressure Associated with Arsenic Methylation and Arsenic Metabolism Caused by Chronic Exposure to Arsenic in Tube Well Water.

OBJECTIVE: The effects of arsenic exposure from drinking water, arsenic metabolism, and arsenic methylation on blood pressure (BP) were observed in this study. METHODS: The BP and arsenic species of 560 participants were determined. Logistic regression analysis was applied to estimate the odds ratios of BP associated with arsenic metabolites and arsenic methylation capability. RESULTS: BP was positively associated with cumulative arsenic exposure (CAE). Subjects with abnormal diastolic blood pressure (DBP), systolic blood pressure (SBP), and pulse pressure (PP) usually had higher urinary iAs (inorganic arsenic), MMA (monomethylated arsenic), DMA (dimethylated arsenic), and TAs (total arsenic) than subjects with normal DBP, SBP, and PP. The iAs%, MMA%, and DMA% differed slightly between subjects with abnormal BP and those with normal BP. The PMI and SMI were slightly higher in subjects with abnormal PP than in those with normal PP. CONCLUSION: Our findings suggest that higher CAE may elevate BP. Males may have a higher risk of abnormal DBP, whereas females have a higher risk of abnormal SBP and PP. Higher urinary iAs may increase the risk of abnormal BP. Lower PMI may elevate the BP. However, higher SMI may increase the DBP and SBP, and lower SMI may elevate the PP.

[Study advance on haloacetic acids in drinking water].

Haloacetic acids (HAAs) in drinking water have attracted more and more attention of researchers due to their higher potential combination of chlorine, their carcinogenic and mutagenic effects and higher carcinogenic. The formation mechanism, analytical methods, the effects of many factors on HAAs formation such as precursor types, chlorine doses, pH, temperature, bromide, reaction time and seasonal change, toxicological character and the minimizing technology of HAAs in resent studies about HAAs are discussed in details in this paper. Further researches are still needed to clarify the formation mechanism of HAAs and find a feasible minimizing technology. New concerns including toxicological characters that correlate with human and other HAAs exposure routes besides oral ingestion (i.e., inhalation and dermal adsorption) should be put forward.