吸烟与饮酒对不同浓度饮水型砷暴露人群尿砷代谢模式的影响

摘要

目的 探讨吸烟、饮酒对砷暴露人群尿砷代谢的影响.方法 2008年选择山西省高砷地区不同饮水砷浓度暴露的年龄≥18岁的成年人作为调查对象,根据饮水砷浓度将调查对象分为3组:高砷暴露组(饮水砷浓度≥0.05 mg/L),低砷暴露组(0.01 mg/L≤饮水砷浓度＜0.05 mg/L),对照组(饮水砷浓度＜0.01mg/L).排除近期食用过海产品以及有慢性饮水型砷中毒症状的人群,通过问卷调查方式确定吸烟、饮酒的情况,同时采集居民家水样,以及调查对象的即时尿样.采用氢化物发生原子吸收分光光度法检测尿中无机砷(iAs)、一甲基砷(MMA)和二甲基砷(DMA)含量.以iAs、MMA及DMA的总和表示总砷(tAs)水平；以iAs/tAs、MMA/tAs和DMA/tAs分别计算iAs％、MMA％、DMA％;以(MMA+ DMA)/tAs及DMA/(MMA+ DMA)分别计算一甲基化率(FMR)和二甲基化率(SMR)水平.结果 共调查395人,高砷暴露组中烟酒嗜好者MMA％(16.24％)高于无烟酒嗜好者(12.16％),烟酒嗜好者的SMR水平(82.19％)低于无烟酒嗜好者(86.13％),差异有统计学意义(P均＜ 0.05),吸烟者、饮酒者与无烟酒嗜好者相比,各评价指标差异无统计学意义(P＞0.05)；在低砷暴露组中吸烟者、烟酒嗜好者的MMA％( 13.86％、13.99％)均高于无烟酒嗜好者(11.83％),吸烟者、烟酒嗜好者的DMA％(72.87％、77.76％)和SMR水平(83.48％、83.90％)均低于无烟酒嗜好者(80.35％、86.54％),差异有统计学意义(P均＜0.05),饮酒者与无烟酒嗜好者相比,各评价指标差异无统计学意义(P＞0.05).对照组人群中吸烟者、烟酒嗜好者的MMA％( 17.27％、17.06％)均高于无烟酒嗜好者(11.52％),吸烟者、烟酒嗜好者的DMA％(73.89％、72.29％)和SMR水平(81.48％、82.58％)均低于无烟酒嗜好者(79.68％、87.19％),差异有统计学意义(P均＜ 0.05),饮酒者与无烟酒嗜好者相比,各评价指标差异无统计学意义(P＞0.05).结论 在不同浓度砷暴露的情况下,吸烟饮酒人群对砷的甲基化能力低于非吸烟饮酒人群.%Objective To explore the effects of smoking and alcohol drinking on arsenic metabolism of people exposed to different concentrations of arsenic in drinking water.Methods Residents in Shanxi exposed to different concentrations of arsenic in drinking water and age ≥ 18 years old adults were chosen as the subjects for this study in 2008,the subjects were divided into three groups according to the concentrations of arsenic in drinking water: high-arsenic exposure group (more than 0.05 mg/L),low-arsenic exposure group (between 0.01 and 0.05 mg/L) and control group(less than 0.01 mg/L),excluded recently had eaten seafood and had poisoning symptoms of chronic arsenic in drinking water in the crowd.Smoking and alcohol drinking habits were investigated by questionnaire.Arsenic species in the urine samples were detected with hydride generation atomic absorption spectroscopy.Total arsenic(tAs) was the sum of iAs％,MMA％ and DMA％.iAs％,MMA％ and DMA％ were calculated as iAs/tAs,MMA/tAs and DMA/tAs,respectively.The first methylation ratio(FMR) and the secondary methylation ratio(SMR) were calculated as (MMA + DMA)/tAs and DMA/(MMA + DMA),respectively.Results Three hundred and ninety-five adults were chosen in this study.In the high exposure group the alcohol drinking and smoking subjects had higher MMA％(16.24％) but lower SMR(82.19％ ) than the non-drinking and non-smoking subjects (12.16％ and 86.13％,respectively).The differences of both MMA％ and SMR were significant(P ＜ 0.05 ).No significant difference was observed between the non-smokingon-drinking subjects and the smoking or the drinking subjects(all P ＞ 0.05 ).In the low exposure group there were higher MMA％( 13.86％,13.99％) lower DMA％(72.87％,77.76％)and lower SMR (83.48％,83.90％ ) in those with smoking or drinking/smoking compared with the non-drinking and non-smoking subjects (11.83％,80.35％ and 86.54％,respectively,all P ＜0.05 ).No significant difference was observed between drinkers and non-drinkingon-smoking subjects(P ＞ 0.05).In the control group there were a higher MMA％( 17.27％,17.06％) lower DMA％ (73.89％,72.29％) and lower SMR (81.48％,82.58％ ) in those with smoking or drinking/smoking compared with the non-drinking and nonsmoking subjects( 11.52％,79.68％ and 87.19％,respectively,all P ＜ 0.05).No significant difference was observed between drinkers and the non-drinkingon-smoking subjects (all P ＞ 0.05).Conclusion The arsenic methylation capacity of people with drinking and smoking is poorer than that of non-drinking and non-smoking subjects after arsenic exposure.