Infectious Diseases Division, icddr,b, Dhaka 1212, Bangladesh.
Departments of Community Health Sciences and Epidemiology, Fielding School of Public Health, University of California Los Angeles, CA 90095, USA.
Environ Int. 2017 Apr;101:108-116. doi: 10.1016/j.envint.2017.01.014. Epub 2017 Feb 1.
Exposure to arsenic has been associated with increased risk of reduced lung function in adults, but the adverse impacts in early life are unclear. We aim to examine whether prenatal and childhood arsenic exposure is associated with reduced lung function and increased airway inflammation in school-aged children. Children born in the MINIMat cohort in rural Bangladesh were evaluated at 9years of age (n=540). Arsenic exposure was assessed in urine (U-As) that was collected from mothers during early pregnancy and their children aged 4.5 and 9years. In the 9-year-old children, lung function was assessed using spirometry and airway inflammation was assessed by the NIOX MINO system. C-reactive protein (CRP) and Clara cell secretory protein (CC16) concentrations were measured in plasma by immunoassays. The U-As concentrations in 9-year-old children were lower (median 53μg/l) compared to their mothers (median 76μg/l). Maternal U-As (log transformed) was inversely associated with forced vital capacity (FVC) and forced expiratory volume at 1s (FEV1) (β=-12; 95% CI: -22, -1.5; p=0.031 and β=-12; 95% CI: -22, -1.9; p=0.023, respectively) in all children, and the associations were stronger in boys and among children with adequate height and weight, as well as among those whose mothers had higher percentages of methylarsonic acid (MMA) and lower percentages of dimethylarsinic acid (DMA). U-As (log transformed) at 4.5 and 9years was positively associated with fractional exhaled nitric oxide (FE) concentrations in boys (β=0.89; 95% CI: 0.13, 1.66; p=0.022 and β=0.88; 95% CI: 0.16, 1.61; p=0.017, respectively) but not in girls. Increased CC16 concentrations were associated with higher lung function indices. In conclusion, our findings suggest that prenatal arsenic exposure is related to impaired lung function, while childhood exposure may increase airway inflammation, particularly in boys.
砷暴露已与成年人肺功能下降的风险增加相关，但早期生命中的不良影响尚不清楚。我们旨在研究产前和儿童时期的砷暴露是否与学龄儿童的肺功能下降和气道炎症增加有关。在孟加拉国农村的 MINIMat 队列中出生的儿童在 9 岁时进行了评估（n=540）。在母亲怀孕期间和他们的孩子 4.5 岁和 9 岁时，从尿液（U-As）中评估了砷暴露。在 9 岁的儿童中，使用肺活量计评估肺功能，使用 NIOX MINO 系统评估气道炎症。通过免疫测定法测量血浆中的 C 反应蛋白（CRP）和克拉拉细胞分泌蛋白（CC16）浓度。与母亲相比（中位数 76μg/l），9 岁儿童的 U-As 浓度较低（中位数 53μg/l）。母亲 U-As（对数转换）与用力肺活量（FVC）和 1 秒用力呼气量（FEV1）呈负相关（β=-12；95%CI：-22，-1.5；p=0.031 和β=-12；95%CI：-22，-1.9；p=0.023），在男孩中和在身高和体重充足的儿童中，以及在母亲甲基砷酸（MMA）百分比较高和二甲基砷酸（DMA）百分比较低的儿童中，这种关联更强。4.5 岁和 9 岁时 U-As（对数转换）与男孩的呼出气中一氧化氮分数（FE）浓度呈正相关（β=0.89；95%CI：0.13，1.66；p=0.022 和β=0.88；95%CI：0.16，1.61；p=0.017），但在女孩中没有。CC16 浓度升高与更高的肺功能指数相关。总之，我们的研究结果表明，产前砷暴露与肺功能受损有关，而儿童时期的暴露可能会增加气道炎症，尤其是在男孩中。
