Prenatal bisphenol a and S exposure and atopic disease phenotypes at age 6.

Prenatal bisphenol a and S exposure and atopic disease phenotypes at age 6.
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DOI:
10.1016/j.envres.2023.115630
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发表时间:
2023-03
影响因子:
8.3
通讯作者:
Abigail Gaylord;E. Barrett;S. Sathyanarayana;S. Swan;R. Nguyen;N. Bush;K. Carroll;Drew B. Day;K. Kannan;L. Trasande
Abigail Gaylord;E. Barrett;S. Sathyanarayana;S. Swan;R. Nguyen;N. Bush;K. Carroll;Drew B. Day;K. Kannan;L. Trasande
中科院分区:
环境科学与生态学2区
文献类型:
--
作者:
Abigail Gaylord;E. Barrett;S. Sathyanarayana;S. Swan;R. Nguyen;N. Bush;K. Carroll;Drew B. Day;K. Kannan;L. Trasande

文献摘要

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背景特应性疾病可能受到产前和生命早期暴露于内分泌干扰物(包括双酚)的影响,但流行病学研究的结果好坏参半。本研究的目的是延长流行病学文献,假设儿童具有较高的产前双酚暴露更有可能有儿童特应性diseases.MethodsUrinary双酚A(BPA)和S(BPS)的浓度进行了测量,在每个三个月从501名孕妇在一个多中心,前瞻性妊娠队列。在6岁时,通过标准化ISAAC问卷对曾经的哮喘、当前的哮喘、喘息和食物过敏进行评估。我们构建了广义估计方程,以检查BPA和BPS暴露联合在每个三个月的每一个特应性表型。BPA被建模为对数转换的连续变量,而BPS被建模为检出与未检出。我们还在logistic回归模型中对妊娠平均BPA值和妊娠期间可检测BPS值(0-3)数量的分类指标进行了建模。(OR = 0.78,95%CI = 0.64-0.95,p = 0.01)和仅女性(OR = 0.69,95%CI = 0.52-0.90,p = 0.006)。在雌性BPA的妊娠平均模型中,这种反比关系持续存在(OR = 0.56,95% CI = 0.35-0.90,p = 0.006)。在整个样本中(OR = 1.27,95% CI = 1.02-1.58,p = 0.03)和仅在男性中(OR = 1.48,95% CI = 1.02-2.14,p = 0.04),妊娠中期BPA与更大的食物过敏几率相关。在妊娠平均BPS模型中,男性当前哮喘的几率增加(OR = 1.65,95%CI = 1.01-2.69,p = 0.045)。这些不同的关联值得进一步研究。有一些证据表明,产前BPS与男性哮喘相关,但需要进一步研究,在队列中有更大比例的产前尿液样本可检测到BPS,以验证这些结果。
BackgroundAtopic disease may be influenced by prenatal and early life exposure to endocrine disrupting chemicals, including bisphenols, but results from epidemiological studies have been mixed. This study aimed to extend the epidemiological literature, hypothesizing that children with higher prenatal bisphenol exposure are more likely to have childhood atopic disease.MethodsUrinary bisphenol A (BPA) and S (BPS) concentrations were measured in each trimester from 501 pregnant women in a multi-center, prospective pregnancy cohort. Ever asthma, current asthma, wheeze, and food allergy) were assessed at age six via standardized ISAAC questionnaire. We constructed generalized estimating equations to examine BPA and BPS exposure jointly at each trimester for each atopy phenotype. BPA was modeled as a log-transformed continuous variable, whereas BPS was modeled as detected versus not detected. We also modeled pregnancy-averaged BPA values and a categorical indicator for number of detectable BPS values over pregnancy (0–3) in logistic regression models.ResultsFirst trimester BPA was associated with inverse odds of food allergy among the entire study sample (OR = 0.78, 95% CI = 0.64–0.95, p = 0.01) and females only (OR = 0.69, 95% CI = 0.52–0.90, p = 0.006). The inverse relationship persisted in pregnancy-averaged models of BPA among females (OR = 0.56, 95% CI = 0.35–0.90, p = 0.006). Second trimester BPA was associated with greater odds of food allergy in the entire sample (OR = 1.27, 95% CI = 1.02–1.58, p = 0.03) and among males only (OR = 1.48, 95% CI = 1.02–2.14, p = 0.04). Odds of current asthma increased among males in the pregnancy-averaged BPS models (OR = 1.65, 95% CI = 1.01–2.69, p = 0.045).ConclusionWe saw opposite effects of BPA on food allergy that were trimester- and sex-specific. These divergent associations warrant further investigation. There is some evidence to suggest that prenatal BPS is associated with asthma among males, but further research is required in cohorts with a greater proportion of prenatal urine samples with detectable BPS to validate these results.