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Cadmium Mobilization during Pregnancy and Lactation in Highly Exposed Populations

机译:高暴露人群在怀孕和哺乳期间的镉动员

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Exposure to cadmium has been associated with adverse neurobehavioral outcomes and nephrotoxic effects in both animal and human studies. Cadmium has a biological half-life on the order of decades and is stored in the liver, kidneys and bone. Consequently, breast milk may be a source of infant exposure, particularly in mothers with high cumulative lifetime exposures. We conducted a literature review of studies measuring cadmium in breast milk and of physiologically-based pharmacokinetic (PBPK) models describing cadmium mobilization during pregnancy and lactation. Few studies reported breast milk cadmium concentrations, one in a population living near a metallurgic complex, and the remaining in populations exposed through diet and smoking. The median cadmium concentration in breast milk among these studies ranged from 0.06-0.67 μg/l, and in blood it ranged from 0.54-1.54 μg/l. In a separate study, mean urinary cadmium excretion in smelter community residents was twice that of the reference population, indicating that populations with high cumulative lifetime exposures have a comparatively higher cadmium body burden. Published cadmium PBPK models do not include pregnancy or lactation as excretion pathways for mothers, or breast milk as an exposure pathway for infants. Available PBPK models consider diet and smoking as the primary routes of exposure, and do not account for exposures via dust, soil, or ambient air. Our review of the literature showed that 1) breast milk is an understudied cadmium exposure pathway for infants whose mothers have high cadmium body burden, 2) current PBPK models do not consider pregnancy or lactation as cadmium excretion pathways, and only take into account smoking and diet exposures. Studies monitoring cadmium biomarkers during pregnancy and lactation are necessary in order to estimate prenatal and infant cadmium exposure, and to parameterize PBPK models that incorporate cadmium mobilization during pregnancy and lactation.
机译:在动物和人体研究中,接触镉与不良的神经行为结果和肾毒性作用有关。镉的生物半衰期约为数十年,存储在肝脏,肾脏和骨骼中。因此,母乳可能是婴儿暴露的来源,特别是在累积终身暴露量很高的母亲中。我们对测量母乳中镉的研究以及描述怀孕和哺乳期间镉动员的基于生理的药代动力学(PBPK)模型进行了文献综述。很少有研究报告母乳中镉的浓度,其中一个人口居住在冶金厂附近,而饮食和吸烟暴露的人口中其余的人。在这些研究中,母乳中镉的平均浓度范围为0.06-0.67μg/ l,而血液中的镉浓度范围为0.54-1.54μg/ l。在另一项研究中,冶炼厂社区居民的平均尿镉排泄量是参考人群的两倍,这表明累积终生暴露量较高的人群的镉身体负担相对较高。已发布的PBPB镉模型不包括怀孕或哺乳作为母亲的排泄途径,也不包括母乳作为婴儿的暴露途径。可用的PBPK模型将饮食和吸烟视为主要暴露途径,而不考虑通过灰尘,土壤或环境空气引起的暴露。我们对文献的审查表明,1)对于母亲体内镉含量高的婴儿,母乳是一个未被充分研究的镉暴露途径; 2)当前的PBPK模型并未将怀孕或哺乳视为镉排泄途径,而仅考虑了吸烟和饮食接触。为了评估产前和婴儿的镉暴露,并参数化结合了怀孕和哺乳期镉动员的PBPK模型,有必要进行监测怀孕和哺乳期镉生物标志物的研究。

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