DDE, a degradation product of DDT, and duration of lactation in a highly exposed area of Mexico.
DDE, a degradation product of DDT, and duration of lactation in a highly exposed area of Mexico.
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DDE，DDT的降解产物，以及墨西哥高度暴露区域的哺乳期。
DOI：
10.1289/ehp.10550
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发表时间：
2008-02
影响因子：
10.4
通讯作者：
Longnecker, Matthew P.
中科院分区：
文献类型：
--
作者：
Cupul-Uicab, Lea A.;Gladen, Beth C.;Hernandez-Avila, Mauricio;Weber, Jean-Philippe;Longnecker, Matthew P.
1，1，1-三氯-2，2-双（4-氯苯基）乙烷（DDT）的主要降解产物1，1-二氯-2，2-双（对氯苯基）乙烯（DDE）的含量较高，在以前的研究中，这与母乳喂养时间较短有关。如果DDE确实缩短了哺乳期，这对婴儿死亡率和使用DDT控制疟疾具有公共卫生重要性。我们的目的是评估母体DDE浓度与随后哺乳期长短的关系。我们在墨西哥一个高度暴露的地区进行了一项相对较大的研究。我们跟踪了784对母子，以确定哺乳期的长短。DDE和DDT在分娩后一天内获得的母体血清中进行测量。我们适合比例风险模型与分层和不分层以前的母乳喂养，因为协会的DDE与哺乳期的持续时间之间的母乳喂养以前可以归因于一个非因果机制。与DDE浓度≤ 3.00 μg/g的受试者相比，根据DDE类别调整的脱机风险比为：浓度3.01-6.00 μg/g，1.27 [95%置信区间（CI），1.04-1.55];浓度6.01-9.00 μg/g，1.23（95% CI，0.92-1.63）;浓度> 9.00 μg/g，1.17（95% CI，0.92-1.49）。既往母乳喂养女性的相应比率为1.40（95%CI，1.06-1.87）; 1.91（95%CI，1.24-2.93）;和1.76（95%CI，1.22-2.53）。既往未进行过母乳喂养的女性分别为1.14（95%CI，0.86-1.52）、0.90（95%CI，0.61-1.31）和0.91（95%CI，0.66-1.26）。我们在墨西哥高暴露地区进行的相对较大的研究数据并不支持暴露于DDE缩短哺乳期长度的假设。在以前母乳喂养的妇女中观察到的这种关联可能归因于非因果机制。尽管如此，滴滴涕是否对人类有其他重要的不利影响仍然是一个悬而未决的问题。
Higher levels of 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE), the major degradation product of 1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane (DDT), have been related to shorter duration of breast-feeding in previous studies. If DDE truly shortens lactation, this has public health importance regarding infant mortality and the use of DDT for malaria control. Our aim was to assess the relationship of maternal DDE concentrations with length of subsequent lactation. We conducted a relatively large study in a highly exposed area of Mexico. We followed 784 mother–son pairs to determine length of lactation. DDE and DDT were measured in maternal serum obtained within a day of delivery. We fit proportional hazard models with and without stratifying by previous breast-feeding, because an association of DDE with duration of lactation among those who breast-fed previously could be attributed to a noncausal mechanism. Compared with those with DDE concentrations ≤ 3.00 μg/g, the adjusted hazard ratios of weaning according to DDE category were, for concentrations 3.01–6.00 μg/g, 1.27 [95% confidence interval (CI), 1.04–1.55]; for concentrations 6.01–9.00 μg/g, 1.23 (95% CI, 0.92–1.63); and for concentrations > 9.00 μg/g, 1.17 (95% CI, 0.92–1.49). The corresponding ratios for women who previously breast-fed were 1.40 (95% CI, 1.06–1.87); 1.91 (95% CI, 1.24–2.93); and 1.76 (95% CI, 1.22–2.53). Those for women who had not breast-fed previously were 1.14 (95% CI, 0.86–1.52); 0.90 (95% CI, 0.61–1.31); and 0.91 (95% CI, 0.66–1.26). Data from our relatively large study in a highly exposed area of Mexico did not support the hypothesis that exposure to DDE shortens length of lactation. The association seen in women who previously breast-fed was likely attributed to a noncausal mechanism. Nonetheless, whether DDT has other important adverse effects on humans is still an open question.
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