Rothenberg Sarah E, Korrick Susan A, Fayad Raja
Department of Environmental Health Sciences, University of South Carolina, Columbia, SC, USA.
Channing Division of Network Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Environ Res. 2015 Apr;138:173-80. doi: 10.1016/j.envres.2015.01.018. Epub 2015 Feb 24.
In animal studies obesity is associated with higher blood and tissue mercury concentrations; however human studies are lacking. Although the mechanism underlying this association is uncertain, obesity may alter the metabolism and distribution of methylmercury.
We determined whether obesity influenced blood mercury levels, the majority of which was methylmercury, for U.S. non-pregnant adults (≥20 years) and children (2-19 years) after controlling for methylmercury intake through fish and shellfish consumption, and other confounders.
We completed secondary data analysis of the National Health and Nutrition Examination Survey (NHANES) (2007-2010) for participants who consumed fish/shellfish within 24h of blood collection for mercury analysis. Weighted least squares regression models related blood mercury levels (the dependent variable) to methylmercury exposure (μg) from fish consumed in the previous 24h, body mass index (BMI) (for adults), BMI z-scores (for children), and other confounders.
In adjusted models, blood mercury levels were inversely correlated with BMI for adults [β, 95% confidence interval (CI)=-0.54 (-0.90, -0.18)]. For children, blood mercury levels were inversely correlated with BMI z-scores but the trend was not significant [β (95% CI)=-0.016 (-0.066, 0.035)]. When obese adults or children were compared with those who were overweight/normal weight, blood mercury averaged 22% lower for obese adults (95% CI: -33%, -8.2%), while blood mercury did not differ significantly for obese children [β (95% CI)=-1.7% (-31%, +39%)].
After adjusting for the main, if not exclusive, exogenous source of methylmercury exposure (through fish/shellfish intake) and other confounders, our results support potential changes in the metabolism, distribution or excretion of methylmercury with increasing BMI (for adults).
在动物研究中,肥胖与血液和组织中较高的汞浓度相关;然而,缺乏人体研究。尽管这种关联背后的机制尚不确定,但肥胖可能会改变甲基汞的代谢和分布。
在控制了通过食用鱼类和贝类摄入甲基汞以及其他混杂因素后,我们确定肥胖是否会影响美国非孕妇成年人(≥20岁)和儿童(2 - 19岁)的血液汞水平,其中大部分为甲基汞。
我们对国家健康与营养检查调查(NHANES)(2007 - 2010年)进行了二次数据分析,研究对象为在采集血液进行汞分析前24小时内食用过鱼类/贝类的参与者。加权最小二乘回归模型将血液汞水平(因变量)与前24小时食用鱼类摄入的甲基汞暴露量(μg)、体重指数(BMI)(针对成年人)、BMI z评分(针对儿童)以及其他混杂因素相关联。
在调整后的模型中,成年人的血液汞水平与BMI呈负相关[β,95%置信区间(CI)= -0.54(-0.90,-0.18)]。对于儿童,血液汞水平与BMI z评分呈负相关,但趋势不显著[β(95% CI)= -0.016(-0.066,0.035)]。当将肥胖成年人或儿童与超重/正常体重者进行比较时,肥胖成年人的血液汞平均低22%(95% CI:-33%,-8.2%),而肥胖儿童的血液汞水平无显著差异[β(95% CI)= -1.7%(-31%,+39%)]。
在调整了甲基汞暴露的主要(如果不是唯一)外源性来源(通过摄入鱼类/贝类)和其他混杂因素后,我们的结果支持随着BMI升高(针对成年人)甲基汞在代谢、分布或排泄方面可能发生的变化。