Prenatal organochlorine pesticide exposure and the disruption of steroids and reproductive hormones in cord blood: The Hokkaido study
Prenatal organochlorine pesticide exposure and the disruption of steroids and reproductive hormones in cord blood: The Hokkaido study
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DOI：
10.1016/j.envint.2017.10.006
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发表时间：
2018-01-01
影响因子：
11.8
通讯作者：
Kishi, Reiko
中科院分区：
文献类型：
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作者：
Araki, Atsuko;Miyashita, Chihiro;Kishi, Reiko
某些有机氯农药（OCPs）被指定为持久性有机污染物，并在许多国家受到管制。OCP对儿科内分泌的影响是一个问题;然而，关于母亲OCP暴露及其对婴儿激素水平影响的人体研究数据有限。本研究作为北海道研究札幌队列（一项日本前瞻性出生队列研究）的一部分进行。参与者包括2002年至2005年期间在妊娠23-35周时登记的514名妇女;在妊娠晚期收集母体血液样本，并测量29种OCP。脐带血中的生殖激素和类固醇激素水平也进行了测定。母亲和他们的婴儿的特点是从自填问卷和医疗记录。最终，分析了232个同时具有OCP和激素数据的样本。在超过80%的样本中检测到了29种被调查的有机氯农药中的15种，其中p，p '-二氯二苯基二氯乙烯的浓度最高（中值：619皮克/克湿）。OCP和性激素水平之间的关联因性别而异。性别分层后的线性回归模型显示，母亲血液中的氯丹、顺式六氯苯、环氧七氯、灭蚁灵和毒杀芬与男孩中的睾酮、皮质醇、可的松、性激素结合球蛋白、催乳素和雄烯二酮-脱氢表雄酮（DHEA）以及睾酮-雄烯二酮比率呈负相关。此外，这些OCP与DHEA、促卵泡激素（FSH）、肾上腺雄激素-糖皮质激素和FSH-β-B B比值呈正相关。在分类四分位数模型中，睾酮和DHEA分别与OCP呈负相关和正相关。雌二醇-睾酮和肾上腺雄激素-糖皮质激素比值在高四分位数中随着OCP浓度的增加而增加，而睾酮-雄烯二酮比值则趋于降低。性激素结合球蛋白和催乳素与OCP呈负相关。在女孩中，线性回归模型显示，只有p，p '-二氯二苯基三氯乙烷与DHEA水平和肾上腺雄激素-糖皮质激素比值呈负相关，但与可的松水平呈正相关。然而，使用四分位数分类模型未观察到相关性。这些结果表明，产前暴露于OCPs会破坏男孩子宫内胎儿的生殖激素，即使是相对较低的水平。
Certain organochlorine pesticides (OCPs) are designated as persistent organic pollutants and are regulated in many countries. The effects of OCPs on pediatric endocrinology are a concern; however, only limited data exist from human studies on maternal OCP exposure and its effects on infants' hormone levels. This study was conducted as part of the Hokkaido Study Sapporo Cohort, a prospective birth cohort study in Japan. Participants included 514 women who enrolled at 23-35 weeks of gestation between 2002 and 2005; maternal blood samples were collected in late pregnancy, and 29 OCPs were measured. Reproductive and steroid hormone levels in cord blood were also determined. Characteristics of mothers and their infants were obtained from self-administered questionnaires and medical records. Ultimately, 232 samples with both OCP and hormone data were analyzed. Fifteen of 29 investigated OCPs were detected in over 80% of the samples, with p, p'-dichlorodiphenyldi-chloroethylene showing the highest concentration (median value: 619 pg/g-wet). The association between OCPs and sex hormone levels varied by sex. Linear regression models after sex stratification showed that chlordanes, cis-hexachlorobenzene, heptachlor epoxide, Mirex, and toxaphenes in maternal blood were inversely associated with testosterone, cortisol, cortisone, sex hormone-binding globin, prolactin, and androstenedione-dehydroepiandrosterone (DHEA) and testosterone-androstenediones ratios among boys. Furthermore, these OCPs were positively correlated with DHEA, follicle stimulating hormone (FSH), and adrenal androgen-glucocorticoid and FSH-inhibin B ratios among boys. In categorical quartile models, testosterone and DHEA were inversely and positively associated with OCPs, respectively. Estradiol-testosterone and adrenal androgen-glucocorticoid ratios tended to increase with increasing OCP concentrations in the higher quartile, while the testosterone-androstenedione ratio tended to decrease. Sex hormone-binding globulin and prolactin showed an inverse association with OCPs. Among girls, the linear regression model showed that only p, p'-dichlorodiphenyltrichloroethane was inversely associated with the level of DHEA and the adrenal androgen-glucocorticoid ratio, but was positively associated with cortisone levels. However, no associations were observed using the quartile categorical model. These results suggest that prenatal exposure to OCPs disrupt reproductive hormones of fetuses in utero among boys, even at relatively low levels.