五氯苯酚(PCP),一种典型的环境内分泌干扰物和一种新的持久性有机污染物,在世界范围内被广泛用作杀虫剂。虽然它的使用已经被限制了几十年,PCP在环境和人体中仍然普遍存在。尽管已知PCP的内分泌干扰和外源性激素作用,很少有流行病学研究检查这种影响,特别是在敏感人群和关键时期。根据前瞻性出生队列,我们从720对母婴中收集了产妇(妊娠早期;13.0±1.02孕周)和婴儿(产后1.16±0.22个月)的尿液样本.我们旨在检查妊娠早期PCP暴露与母婴泌尿性类固醇激素的关系。包括雌激素(雌酮,E1;雌二醇,E2;雌三醇,E3),孕激素(孕酮,P4;孕烯醇酮,P5;17α-OH-孕酮,17OHP4;17α-OH-孕烯醇酮,17OHP5),和雄激素(睾酮,Testo;双氢睾酮,DHT;脱氢表雄酮,DHEA;雄烯二酮,A4).此外,在婴儿尿液中测量促性腺激素[卵泡刺激素(FSH)和黄体生成素(LH)]。产妇尿液样本中所有性激素的检测频率(>99%)高于婴儿[最高≥80%,E1(3.36%)和E2(21.4%)除外]。发现母体尿液PCP浓度与母体性类固醇激素的增加显着相关;PCP浓度的四分位间增加与激素的百分比变化(%Δ)呈正相关,范围为26.6%至48.5%。另一方面,母体PCP暴露与男性婴儿P4升高相关[%Δ(95%置信区间):10.5(0.56,21.4)],但女性婴儿P4降低[-11.9(-21.8,0.68)].此外,母儿PCP暴露与FSH[%Δ(95%CI):-9.90(-17.0,-2.18)]和LH[-8.44(-16.0,-0.19)]降低显著相关,但不是男婴。敏感性分析,不包括不孕症相关治疗,妊娠并发症,早产,或低出生体重,显示出基本一致的结果。我们的发现表明,产前PCP暴露可能会破坏母婴生殖激素的稳态。然而,需要进一步的研究来证实这一发现。
Pentachlorophenol (PCP), a typical environmental endocrine disruptor and a new persistent organic pollutant, has been extensively used as a pesticide worldwide. Although its use has been restricted for decades, PCP remains prevalent in both the environment and human bodies. Despite the known endocrine-disrupting and exogenous hormonal effects of PCP, few epidemiological studies examined such impact, especially among sensitive populations and during critical periods. Based on a prospective birth cohort in Wuhan, China, we collected maternal (first trimester; 13.0 ± 1.02 gestational weeks) and infant urine samples (1.16 ± 0.22 months postpartum) from 720 mother-infant pairs. We aimed to examine the association of PCP exposure during early pregnancy with maternal and infant urinary sex steroid hormones, including estrogens (estrone, E1; estradiol, E2; estriol, E3), progestogens (progesterone, P4; pregnenolone, P5; 17α-OH-Progesterone, 17OHP4; 17α-OH-Pregnenolone, 17OHP5), and androgens (testosterone, Testo; dihydrotestosterone, DHT; dehydroepiandrosterone, DHEA; androstenedione, A4). Additionally, gonadotropins [follicle-stimulating hormone (FSH) and luteinizing hormone (LH)] were measured in infant urine. Detection frequencies of all the sex steroid hormones in the maternal urine samples (>99 %) were higher than those in the infants\' [most ≥80 %, except for E1 (3.36 %) and E2 (21.4 %)]. Maternal urinary PCP concentration was found to be significantly related with increased maternal sex steroid hormone concentrations; each interquartile increase in PCP concentration was positively related with percent change of the hormones (%Δ) ranging from 26.6 % to 48.5 %. On the other hand, maternal PCP exposure was associated with significantly increased P4 in male infants [%Δ (95 % confidence interval): 10.5 (0.56, 21.4)] but slightly decreased P4 in female infants [-11.9 (-21.8, 0.68)]. In addition, maternal PCP exposure was significantly associated with decreased FSH [%Δ (95 % CI): -9.90 (-17.0, -2.18)] and LH [-8.44 (-16.0, -0.19)] in the female infants, but not in the male infants. Sensitivity analyses, excluding infertility related treatment, pregnancy complications, preterm birth, or low birth weight, showed generally consistent results. Our findings implied that maternal/prenatal PCP exposure might disrupt the homeostasis of maternal and infant reproductive hormones. However, further studies are needed to confirm the findings.