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目的测定内蒙古高砷病区不同浓度饮水砷暴露人群尿中各种形态砷代谢物和总砷(total arsenic,TAs)含量。方法于2004年10月运用横断面调查方法,随机抽取病区(A村:水砷浓度为240μg/L;B村:水砷浓度为160μg/L;C村:水砷浓度为90μg/L,D村即对照组:水砷浓度<5μg/L)人群尿样,采用氢化物发生原子吸收分光光度法检测尿中各形态砷代谢物和TAs含量。结果随着饮水砷暴露浓度的增高,人群尿中无机砷(inorganic arsenic,iAs)、甲基砷(monomethyl arsine,MMA)、二甲基砷(dimethyl arsine,DMA)和TAs含量均增高(P<0.05)。暴露于相同水砷浓度的条件下,尿中iAs、MMA、DMA和TAs含量以及一甲基化率(primary methylation index,PMI)和二甲基化率(secondary methylation index,SMI)在不同性别间未见统计学差异(P>0.05)。各暴露组成人和儿童尿中PMI和SMI水平分别低于对照组成人和儿童(P<0.05);240μg/L组成人尿中PMI和SMI水平显著低于90和160μg/L暴露组(P<0.05);240μg/L组儿童尿中PMI水平低于160μg/L组儿童(P<0.05),各暴露组儿童尿中SMI水平顺序为160μg/L组>90μg/L组>240μg/L组(P<0.05);各暴露组中儿童尿中SMI水平均高于相应的成人(P<0.05)。结论饮水中高砷暴露可能降低人群对砷的甲基化能力。相同饮水砷暴露水平,男女对砷的甲基化能力无差别,儿童二甲基化能力高于成人。低水平砷暴露可能诱导儿童对砷的二甲基化能力。
Objective To determine urinary levels of arsenic metabolites and total arsenic (TAs) in drinking water with different concentrations of drinking water in high arsenic ward of Inner Mongolia. Methods A cross-sectional investigation was conducted in October 2004. A group of patients were randomly selected from the village (A village: arsenic concentration of 240 μg / L; village B: arsenic concentration of 160 μg / L; C village: arsenic concentration of 90 μg / D village that control group: water arsenic concentration <5μg / L) urine samples from people, the use of hydride Atomic Absorption Spectrophotometry urinary various forms of arsenic metabolites and TAs content. Results With the increase of arsenic exposure in drinking water, the urinary contents of arsenic (iAs), monomethyl arsine (MMA), dimethyl arsine (DMA) and TAs in urine increased (P < 0.05). Urine concentrations of iAs, MMA, DMA and TAs, as well as primary methylation index (PMI) and secondary methylation index (SMI) in urine at the same water arsenic concentration varied between genders No statistical difference (P> 0.05). The urinary PMI and SMI levels in adults and children in each exposure group were lower than those in control adults and children respectively (P <0.05). The levels of PMI and SMI in urine of 240 μg / L group were significantly lower than those of 90 and 160 μg / L exposure groups (P < 0.05). The urinary PMI level in 240 μg / L group was lower than that in 160 μg / L group (P <0.05). The urinary SMI level in each exposure group was 160 μg / L group> 90 μg / L group> 240 μg / L group P <0.05). The urinary SMI levels of children in each exposure group were higher than those of the corresponding adults (P <0.05). Conclusion High arsenic exposure in drinking water may reduce the methylation capacity of arsenic in the population. The same drinking water arsenic exposure levels, men and women had no difference in the methylation capacity of arsenic, children with higher than two adults methylation. Low levels of arsenic exposure may induce children’s ability to dimerize arsenic.