长期高砷暴露人群砷甲基化与皮肤损害关系的研究

目的探讨长期高砷暴露人群砷代谢差异与砷致皮肤损害之间的关系。方法随机选取某砷污染村庄常住居民327名,进行问卷调查和体格检查。二乙基二硫代氨基甲酸银比色法检测发总砷含量,离子色谱氢化物发生原子荧光法测定尿中四种砷代谢形态。结果发砷含量总体较高,但不同程度皮肤损害的4组间发砷含量差异无显著性;尿中DMA和MMA浓度随着年龄增加有上升的趋势,且与皮肤损害程度呈显著正相关,而无机砷浓度与皮肤损害未见显著相关;重度组人群尿中MMA相对比例显著高于其它3组,而重度组DMA/MMA比值显著低于对照组和轻度组;MMA比例与皮肤损害程度呈显著正相关,DMA/MMA比值与皮肤损害程度呈显著负相关;男性对砷的蓄积能力高于女性,但对砷的甲基化能力低于女性;40岁以上人群对砷的甲基化能力高于40岁以下成人;吸烟者和饮酒者对砷的甲基化代谢水平分别低于非吸烟者和非饮酒者。结论砷在人体内的甲基化代谢水平受性别、年龄、吸烟和饮酒等多因素影响;砷致皮肤损伤程度与砷在体内的甲基化程度有关。     

饮水型砷暴露对人群甲基化代谢能力的影响

目的探讨饮水型砷暴露对人群甲基化代谢能力的影响。方法以带有砷化物预处理装置的原子吸收分光光度计测定砷暴露人群及无砷暴露对照人群血、尿中无机砷(iAs)、甲基胂(MMA)、二甲基胂(DMA)含量。以iAs、MMA及DMA的总和表示总胂(tAs)水平;以(MMA+DMA)/tAs及DMA/(MMA+DMA)分别计算一甲基化率(PMI)和二甲基化率(SMI)水平。结果砷暴露人群血中iAs、MMA、DMA、tAs及PMI水平均显著高于相应对照人群的水平,而SMI水平显著低于对照人群。尿中MMA水平分别与血中PMI及SMI水平呈显著正相关(r=0.419,P<0.01)及负相关(r=-0.326,P<0.05)。暴露组和对照组血中各种砷化物水平及甲基化率水平在男女间差异无显著性。结论砷暴露人群与无砷暴露人群相比甲基化率有差异,PMI显著增高,SMI显著降低。人群甲基化率无显著性别差异。     

硼在人群中的暴露

人类硼的暴露有以下来源：来自含硼的天然或地方性的饮用水;在富含硼土壤中生长的,用富硼水灌溉或空中硼微粒污染的农作物;硒居在高硼天然水源中的水生动植物;化妆品或医药制剂中的硼经粘膜或员皮肤吸收;含硼的家庭清洁品,杀虫剂或化肥的吸入,皮肤吸收或偶然摄入;最经常的和明显的人九中硼暴露可能源于食物的摄取,其次为服用饮水的。     

土默特地区三个自然村居民饮水砷暴露与恶性肿瘤

目的 对内蒙古呼和浩特土默特地区三个自然村民恶性肿瘤死亡状况进行回顾性分析,了解恶性肿瘤死亡率与饮水砷浓度的关系。方法 采用回顾性队列研究方法,自1975年1月1日至1997年12月31日历时23年,按接触水砷浓度将2140名调查对象分为：＜0．05mg/L组、0．05－0．50mg/L组和≥0.50mg/L组。结果 饮水砷浓度≥0. 50mg/L组的恶性肿瘤死亡位于第一位,死亡率为983．84／10万人年,显著高于0．05－0．50mg/L组（61．25／10万人年）和＜0．05mg／L组（64．23／10万人年）,其相对危险度是0．05－0．50mg/L组的12．92倍,是＜0．05mg/L组的12．17倍,归因危险百分比分别为92．26％、91．78％。≥0.50mg/L组性肿瘤死亡顺位为肺癌（529．76／10万人年）、肝癌（151．36／10万人年）和食管癌（75．68／10万人年）。同时发现水砷摄入总量与恶性肿瘤死亡间有相关关系。结论 饮水砷暴露与恶性肿瘤死亡率之间存在着较强的联系。说明砷的远期危害是不容忽视的。     

亚慢性饮水砷暴露小鼠组织形态砷的蓄积与分布

目的探讨亚慢性饮水砷暴露小鼠各组织中无机砷及其代谢产物的蓄积与分布规律。方法将40只健康8周龄清洁级昆明雌性小鼠按体重随机分为对照(生理盐水)组和50、100、200 mg/L亚砷酸钠染毒组,每组10只。采用亚砷酸钠自由饮水方式染毒,连续染毒3个月。检测小鼠肝脏、肾脏、脾脏、肺脏、膀胱、大脑皮层、小脑和海马组织中五价无机砷(pentavalent inorganic arsenic,iAs~(5+))、三价无机砷(trivalent inorganic arsenic,iAs~(3+))、单甲基胂酸(monomethylated arsenic,MMA)和二甲基胂酸(dimethylated arsenic,DMA)的含量,并计算总砷(total arsenic,TAs)含量。结果各浓度亚砷酸钠暴露组小鼠肝脏中TAs、iAs~(3+)和DMA的含量与对照组比较,差异均无统计学意义(P0.05)。与50 mg/L亚砷酸钠暴露组比较,100、200 mg/L亚砷酸钠暴露小鼠肾脏、肺脏和膀胱中TAs和DMA含量均升高,差异有统计学意义(P0.05);与100 mg/L亚砷酸钠暴露组比较,200 mg/L亚砷酸钠暴露小鼠肾脏TAs和DMA含量均升高,差异有统计学意义(P0.05)。与50 mg/L亚砷酸钠暴露组比较,200 mg/L亚砷酸钠暴露小鼠脾脏TAs和DMA含量以及膀胱iAs~(3+)含量均升高,差异有统计学意义(P0.05)。与100 mg/L亚砷酸钠暴露组比较,200 mg/L亚砷酸钠暴露小鼠膀胱TAs、iAs~(3+)和DMA含量均升高,差异有统计学意义(P0.05)。与50 mg/L亚砷酸钠暴露组比较,100 mg/L亚砷酸钠暴露小鼠大脑皮层和小脑中TAs含量及200 mg/L亚砷酸钠暴露小鼠大脑皮层和小脑中TAs和DMA的含量均升高,差异有统计学意义(P0.05);与100 mg/L亚砷酸钠暴露组比较,200 mg/L亚砷酸钠暴露小鼠小脑TAs和DMA含量均升高,差异有统计学意义(P0.05)。与50 mg/L亚砷酸钠暴露组比较,200 mg/L亚砷酸钠暴露小鼠海马TAs、MMA和DMA含量均升高,差异有统计学意义(P0.05);与100 mg/L亚砷酸钠暴露组比较,200 mg/L亚砷酸钠暴露小鼠海马MMA含量升高,差异有统计学意义(P0.05)。各浓度亚砷酸钠暴露组小鼠组织中iAs~(3+)以及肺脏和膀胱中MMA的含量间比较,差异均无统计学意义(P0.05)。随着亚砷酸钠暴露浓度的升高,小鼠各组织中TAs和DMA含量均呈上升趋势,膀胱和海马中MMA亦呈上升趋势。100、200 mg/L亚砷酸钠暴露组小鼠各组织中TAs和DMA的含量由高到低依次为膀胱肝脏肺脏肾脏脾脏;部分脑区组织中TAs和DMA的含量由高到低依次为大脑皮层海马小脑。200 mg/L亚砷酸钠暴露组小鼠肺脏、100和200 mg/L亚砷酸钠暴露组小鼠膀胱以及50、100和200 mg/L亚砷酸钠暴露组小鼠海马中可检测出MMA,其它各浓度亚砷酸钠暴露组小鼠组织中MMA均未检出所有亚砷酸钠暴露组小鼠组织中均未检出iAs~(5+)。结论亚慢性饮水砷暴露小鼠组织中形态砷的蓄积与分布具有明显的组织特异性,并且无机砷及其代谢产物能够穿越血脑屏障,区域特异性地蓄积在大脑皮层、小脑和海马组织。     

饮水砷暴露对儿童免疫功能的影响

目的 研究高砷饮水对儿童免疫功能的影响.方法 于2006年选择某高砷饮水地区194名9～13岁小学生作为研究对象,采集家庭饮用水样和空腹晨尿,测定水砷和尿砷含量,按照水砷含量分为对照组(P＜0.05mg/L)、暴露组(≥0.1mg/L),进行T淋巴细胞亚群、免疫球蛋白IgG、IgM、IgA和白细胞介素2(IL-2)测定,并对家庭一般情况、饮水水源情况、儿童健康状况、父母健康及职业暴露情况等进行问卷调查.结果 对照组、暴露组儿童尿砷含量中位数分别为0.02和0.12 mg/L,尿砷与水砷含量呈统计学相关.暴露组儿童T淋巴细胞(CD3~+)、CD4~+、CD8~+亚群百分含量均值和CD4~+/CD8~+的均值低于对照组,经t检验,暴露组CD~(4+)亚群百分含量和CD4~+/CD8~+显著低于对照组(P<0.05),而两组间T淋巴细胞(CD3~+)、CD8~+亚群百分含量差异均无统计学意义(P＞0.05).暴露组男生T淋巴细胞CD~(4+)亚群百分含量显著低于对照组(P＜0.05),暴露组女生CD4~+亚群百分含量和CD4~+/CD8~+显著低于对照组(P<0.05).暴露组儿童血清IgG含量高于对照组(P<0.05),血清IgM含量低于对照组(P<0.05),血清IgA含量两组间差异无统计学意义(P>0.05);对照组和暴露组男生血清免疫球蛋白含量分布情况与全体学生近似,女生血清免疫球蛋白含量差异无统计学意义.两组儿童白细胞介素2含量差异无统计学意义(P>0.05).结论 长期饮用砷含量在0.1 mg/L以上的高砷水对儿童的免疫功能可能造成不利影响.儿童外周血T淋巴细胞亚群是水砷暴露非常敏感的健康效应指标之一.     

杭锦后旗饮水氟砷暴露对儿童智力的影响

目的了解饮水氟、砷暴露对儿童智力的影响,为保护饮水型地方性氟砷中毒病区儿童健康提供科学依据。方法选择内蒙古杭锦后旗农村地区268名小学生作为研究对象,采集家庭饮用水样,测定氟、砷含量;采用联合型瑞文测试对研究对象进行智力测验,并针对家庭一般情况、饮水水源情况、儿童健康状况及其他智力影响因素等情况进行问卷调查。结果杭锦后旗儿童家庭饮用水氟含量为(1.24±0.74)mg/L,砷含量为(0.13±0.16)mg/L,均超过国家饮用水卫生标准限值。饮水砷含量≥0.05 mg/L的女生智商(95.9±14.2)显著低于饮水砷含量<0.05 mg/L的女生(101.3±13.2),而不同水砷浓度男生智商差异无统计学意义。饮水砷浓度≥0.05 mg/L对女生智商影响的调整OR值为2.81,而不同水氟浓度儿童智商差异无统计学意义。结论饮水氟、砷暴露不利于儿童的智力发育,对女生智力的影响较明显。     

成人饮水砷暴露与尿砷排泄量的关系

调查确定墨西哥北部雅基河流域成人饮水砷暴露与尿砷排泄量的关系。对该地区4个镇的常住户进行流行病学调查,并采集成人晨尿,分析尿中砷、无机砷(A s5 、A s3 )、甲基砷和二甲基砷,同时采集并分析饮用水的含砷量。经统计学分析日饮用水砷含量与尿砷排泄量呈正相关,检测分析尿中二甲基砷、无机砷和甲基砷分别占总砷的47.7%~67.1%、16.4%~25.4%和7.5%~15%,其中二甲基砷和甲基砷比已报道的文献均低。研究认为,该地区人群砷甲基转移酶的基因多态性导致不同砷代谢水平。     

不同饮水砷暴露人群尿中的砷代谢物水平

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90 μg/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(monomethylarsine,MMA)、二甲基砷(dimethylarsine,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.     

慢性饮水砷暴露小鼠无机砷代谢产物的蓄积与分布

目的探讨慢性饮水砷暴露小鼠各组织及脑部分区组织中无机砷代谢产物的蓄积与分布规律。方法将40只健康8周龄清洁级昆明雌性小鼠按体重随机分为对照(生理盐水)组、50、100和200 mg/L亚砷酸钠染毒组,每组10只。采用亚砷酸钠自由饮水方式染毒,染毒时间为6个月,检测肝脏、肾脏、脾脏、肺脏、膀胱、大脑皮层、小脑和海马组织中五价无机砷(pentavalent inorganic arsenic,iAs~(5+))、三价无机砷(trivalent inorganic arsenic,iAs~(3+))、单甲基胂酸(monomethylated arsenic,MMA)和二甲基胂酸(dimethylated arsenic,DMA)含量,并计算总砷(total arsenic,TAs)含量。结果与50 mg/L亚砷酸钠暴露组比较,200 mg/L亚砷酸钠暴露组小鼠肝脏和脾脏中TAs和iAs~(3+)的含量以及100、200 mg/L亚砷酸钠暴露组小鼠肾脏中TAs和DMA的含量均升高,差异有统计学意义(P0.05);与100 mg/L亚砷酸钠暴露组比较,200 mg/L亚砷酸钠暴露组小鼠肾脏中TAs和DMA的含量均升高,差异有统计学意义(P0.05)。与50 mg/L亚砷酸钠暴露组比较,200 mg/L亚砷酸钠暴露组小鼠肺脏中TAs的含量及100、200 mg/L亚砷酸钠暴露组小鼠肺脏中iAs~(3+)的含量均升高,差异有统计学意义(P0.05);与100 mg/L亚砷酸钠暴露组比较,200 mg/L亚砷酸钠暴露组小鼠肺脏中TAs的含量和膀胱中iAs~(3+)的含量均升高,差异有统计学意义(P0.05)。与50 mg/L亚砷酸钠暴露组比较,100 mg/L亚砷酸钠暴露组小鼠膀胱中TAs和DMA的含量及200 mg/L亚砷酸钠暴露小鼠膀胱中TAs、iAs~(3+)、MMA和DMA的含量均升高,差异有统计学意义(P0.05)。与50、100 mg/L亚砷酸钠暴露组比较,200 mg/L亚砷酸钠暴露组小鼠大脑皮层中TAs和DMA的含量均升高,差异有统计学意义(P0.05)。与50 mg/L亚砷酸钠暴露组比较,100 mg/L亚砷酸钠暴露组小鼠小脑中TAs的含量及200 mg/L亚砷酸钠暴露组小鼠小脑中TAs和DMA的含量均升高,差异有统计学意义(P0.05)。与50 mg/L亚砷酸钠暴露组比较,100 mg/L亚砷酸钠暴露组小鼠海马中MMA的含量及200 mg/L亚砷酸钠暴露组小鼠海马中DMA的含量均升高,差异有统计学意义(P0.05)。各浓度亚砷酸钠暴露组小鼠肝、脾和肺脏中的DMA含量,肾脏、大脑皮层、小脑和海马中的iAs~(3+)含量,肺脏中的MMA含量以及海马中TAs的含量间比较,差异均无统计学意义(P0.05)。随着亚砷酸钠暴露浓度的升高,小鼠各组织中TAs和DMA的含量均呈上升趋势;肝脏、肾脏、脾脏和大脑皮层中iAs~(3+)的含量均呈上升趋势;肺脏、膀胱和海马中MMA的含量亦呈上升趋势。50和100 mg/L亚砷酸钠暴露组小鼠各组织中TAs和DMA的含量由高到低依次为膀胱脑组织肝脏肾脏肺脏脾脏;iAs~(3+)的含量由高到低依次为肝脏肾脏脾脏膀胱脑组织肺脏;MMA的含量由高到低依次为肺脏膀胱脑组织。100和200 mg/L染砷组小鼠脑部分区组织中TAs和DMA的含量由高到低依次为小脑大脑皮层海马。50、100和200 mg/L亚砷酸钠暴露组肺脏、膀胱和海马中可检测出MMA,其它各浓度亚砷酸钠暴露组小鼠组织中MMA均未检出。所有亚砷酸钠暴露组小鼠组织中均未检出iAs~(5+)。结论慢性饮水无机砷暴露小鼠体内无机砷代谢产物的蓄积与分布具有明显的组织和区域特异性。鉴于无机砷代谢产物的不同毒性,推测膀胱和脑组织可能是慢性无机砷暴露发挥毒性最重要的靶器官,但详细机制尚需进一步的探讨。     

Water Hyacinth Removes Arsenic from Arsenic-Contaminated Drinking Water

Water hyacinth (Eichhornia crassipes) removes arsenic from arsenic-contaminated drinking water. This effect depends on several factors, such as the amount of water hyacinth, amount of arsenic present in the water, duration of exposure, and presence of sunlight and air. On the basis of the present study, the authors suggest that water hyacinth is useful for making arsenic-contaminated drinking water totally arsenic free. Water hyacinth provides a natural means of removing arsenic from drinking water at the household level without monetary cost.     

Mortality in Young Adults following in Utero and Childhood Exposure to Arsenic in Drinking Water

Background: Beginning in 1958, the city of Antofagasta in northern Chile was exposed to high arsenic concentrations (870 µg/L) when it switched water sources. The exposure abruptly stopped in 1970 when an arsenic-removal plant commenced operations. A unique exposure scenario like this—with an abrupt start, clear end, and large population (125,000 in 1970), all with essentially the same exposure—is rare in environmental epidemiology. Evidence of increased mortality from lung cancer, bronchiectasis, myocardial infarction, and kidney cancer has been reported among young adults who were in utero or children during the high-exposure period.Objective: We investigated other causes of mortality in Antofagasta among 30- to 49-year-old adults who were in utero or ≤ 18 years of age during the high-exposure period.Methods: We compared mortality data between Antofagasta and the rest of Chile for people 30–49 years of age during 1989–2000. We estimated expected deaths from mortality rates in all of Chile, excluding Region II where Antofagasta is located, and calculated standardized mortality ratios (SMRs).Results: We found evidence of increased mortality from bladder cancer [SMR = 18.1; 95% confidence interval (CI): 11.3, 27.4], laryngeal cancer (SMR = 8.1; 95% CI: 3.5, 16.0), liver cancer (SMR = 2.5; 95% CI: 1.6, 3.7), and chronic renal disease (SMR = 2.0; 95% CI: 1.5, 2.8).Conclusions: Taking together our findings in the present study and previous evidence of increased mortality from other causes of death, we conclude that arsenic in Antofagasta drinking water has resulted in the greatest increases in mortality in adults < 50 years of age ever associated with early-life environmental exposure.     

居民富砷饮水与肺癌发病关系的研究钝顶螺旋藻抗突变作用的研究

为了解居民饮富砷水与肺癌死亡之间的流行病学关系,采用历史性前瞻的研究方法,研究了８８５人２３年来的资料,结果表明：砷暴露组肺癌的死亡率（１３３．７０／１０万人年）显著高于非暴露组（９．９５／１０万人年）,Ｐ＜０．０１,相对危险度为１３．４４。总砷摄入量与肺癌相对危险性之间呈明显的剂量反应关系对钝顶螺旋藻的抗突变作用进行了研究。结果表明：钝顶螺旋藻在２０００ｍｇ／ｋｇ剂量下,对环磷酰胺所致小鼠骨髓细胞微核增加有拮抗作用（Ｐ＜０．０５）,对丝裂霉素所致小鼠睾丸染色体畸变在染色体畸变细胞率指标上具有拮抗作用（Ｐ＜０．０５）,在性染色体单价体,常染色体单价体,具有拮抗趋势,但无统计学意义（Ｐ＞０．０５）。在６７,６７０ｍｇ／ｋｇ两个低剂量下,对环磷酰胺所致小鼠骨髓细胞微核和对丝裂霉素所致小鼠睾丸染色体畸变在染色体畸变细胞率增高的拮抗作用无统计学差异（Ｐ＞０．０５）。     

原子荧光法测定生活饮用水中的砷

目的采用氢化物发生—原子荧光光谱法测定饮用水中的砷含量。方法在5%硝酸介质中,加入硫脲—抗坏血酸混合试剂,以NaBH420 g/L溶液为还原剂,测定砷荧光强度。结果在最佳实验条件下,测定生活饮用水中的砷含量,回收率砷为90.5%～93.1%。结论此方法简便,快速,准确。     

原子荧光光谱法同时测定水样中的砷和硒研究

目的研究AFS-230双道原子荧光光度计同时测定饮用水中的砷和硒的方法,为检测水样中的砷和硒提供依据。方法选择了最佳的仪器条件,进行了样品处理方法及酸度、硼氢化钾浓度、检出限、线性范围、精密度、加标回收率等研究。结果本法线性关系砷为0~40ug/L,硒为0~80ug/L。检出限砷为0.211ug/L,硒为0.486ug/L。相对标准偏差砷为1.41%,硒为1.06%。平均加标回收率砷为101%;硒为91.3%。结论本方法操作简便,灵敏度高,快速,便于推广,适用于水中砷和硒的测定。     

活性氧化铝吸附法饮水除砷研究

活性氧化铝的除砷机理以吸附为主,其除As~(5+)的效率非常显著地高于As~(3+)。水中As~(3+)用氯氧化后的去除率和As~(5+)相同。含砷0.75mg/L左右的原水将pH调至6.0～6.5的条件下,除砷容量为1.4～2.0mg/g Al_2O_3,处理1m3水的化学品费用为0.221元。1m~3 Al_2O_3每个周期可处理水1700m~3以上。     

活性氧化铝吸附法饮水除砷研究

活性氧化铝的除砷机理以吸附为主,其除As~(5+)的效率非常显著地高于As~(3+).水中As~(3+)用氯氧化后的去除率和As~(5+)相同.含砷0.75mg/L左右的原水将pH调至6.0～6.5的条件下,除砷容量为1.4～2.0mg/g Al_2O_3,处理1m~3水的化学品费用为0.221元.1m~3 Al_2O_3每个周期可处理水1700m~3以上.     

分散式饮水除砷研究

目的：研究分散式饮水除砷技术。方法：采用混凝沉淀和涂铁砂粒吸附除砷。若源水中含有三价砷，可在混凝沉淀前将其氧化。结果：在不调pH值、人工搅拌和室温条件，如果混凝后进行砂滤，当源水五价砷含量小于0．5mg/L和为0．5－1．0、1．0－2．0mg/L时。分别投加硫酸铁20、30、60mg/L，均可使处理后出水砷含量小于0．05mg/L。若三价砷含量为1．0mg/L，按有效氯计投加2．5mg/L次氯酸钠预氧化，在相同条件下，可使三价砷的去除率与五价砷相同。用涂铁砂粒吸附三价与五价砷，均可使出水砷含量小于0．01mg/L。结论：硫酸铁、硫酸铝及其混合物是较实用的分散式饮水除砷剂，次氯酸钠为适宜的三价砷氧化剂。涂铁砂粒能有效地吸附三价与五价砷，且性能稳定。     

Speciation of Arsenic in Exfoliated Urinary Bladder Epithelial Cells from Individuals Exposed to Arsenic in Drinking Water

Background

The concentration of arsenic in urine has been used as a marker of exposure to inorganic As (iAs). Relative proportions of urinary metabolites of iAs have been identified as potential biomarkers of susceptibility to iAs toxicity. However, the adverse effects of iAs exposure are ultimately determined by the concentrations of iAs metabolites in target tissues.

Objective

In this study we examined the feasibility of analyzing As species in cells that originate in the urinary bladder, a target organ for As-induced cancer in humans.

Methods

Exfoliated bladder epithelial cells (BECs) were collected from urine of 21 residents of Zimapan, Mexico, who were exposed to iAs in drinking water. We determined concentrations of iAs, methyl-As (MAs), and dimethyl-As (DMAs) in urine using conventional hydride generation-cryotrapping-atomic absorption spectrometry (HG-CT-AAS). We used an optimized HG-CT-AAS technique with detection limits of 12–17 pg As for analysis of As species in BECs.

Results

All urine samples and 20 of 21 BEC samples contained detectable concentrations of iAs, MAs, and DMAs. Sums of concentrations of these As species in BECs ranged from 0.18 to 11.4 ng As/mg protein and in urine from 4.8 to 1,947 ng As/mL. We found no correlations between the concentrations or ratios of As species in BECs and in urine.

Conclusion

These results suggest that urinary levels of iAs metabolites do not necessarily reflect levels of these metabolites in the bladder epithelium. Thus, analysis of As species in BECs may provide a more effective tool for risk assessment of bladder cancer and other urothelial diseases associated with exposures to iAs.     

No Association between Arsenic Exposure from Drinking Water and Diabetes Mellitus: A Cross-Sectional Study in Bangladesh

Background

The long-term effects of arsenic exposure from drinking water at levels < 300 μg/L and the risk of diabetes mellitus remains a controversial topic.

Method

We conducted a population-based cross-sectional study using baseline data from 11,319 participants in the Health Effects of Arsenic Longitudinal Study in Araihazar, Bangladesh, to evaluate the associations of well water arsenic and total urinary arsenic concentration and the prevalence of diabetes mellitus and glucosuria. We also assessed the concentrations of well water arsenic, total urinary arsenic, and urinary arsenic metabolites in relation to blood glycosylated hemoglobin (HbA1c) levels in subsets of the study population.

Results

More than 90% of the cohort members were exposed to drinking water with arsenic concentration < 300 μg/L. We found no association between arsenic exposure and the prevalence of diabetes. The adjusted odds ratios for diabetes were 1.00 (referent), 1.35 [95% confidence interval (CI), 0.90–2.02], 1.24 (0.82–1.87), 0.96 (0.62–1.49), and 1.11 (0.73–1.69) in relation to quintiles of time-weighted water arsenic concentrations of 0.1–8, 8–41, 41–91, 92–176, and ≥ 177 μg/L, respectively, and 1.00 (referent), 1.29 (0.87–1.91), 1.05 (0.69–1.59), 0.94 (0.61–1.44), and 0.93 (0.59–1.45) in relation to quintiles of urinary arsenic concentrations of 1–36, 37–66, 67–114, 115–204, and ≥ 205 μg/L, respectively. We observed no association between arsenic exposure and prevalence of glucosuria and no evidence of an association between well water arsenic, total urinary arsenic, or the composition of urinary arsenic metabolites and HbA1c level.

Conclusions

Our findings do not support an association of arsenic exposure from drinking water and a significantly increased risk of diabetes mellitus in the range of levels observed. Further prospective studies would be valuable in confirming the findings.