EDCs can interfere with normal hormone function and metabolism and play a role in pubertal onset. We aimed to systematically identify and evaluate the current evidence on the timing of pubertal onset in girls and boys following prenatal or postnatal exposures to xenobiotic EDCs.
Following PRISMA guidelines, we performed a systematic literature search of original peer-reviewed publications in the PubMed database through a block search approach using a combination of index MeSH and free text search terms. Publications were considered if they covered biomarkers of prenatal or postnatal exposures to xenobiotic EDCs (European Commission\'s list of category 1 EDCs) measured in maternal or child biospecimen and pubertal onset defined by the progression of the following milestones (and assessed in terms of the following measures): menarche (age), thelarche (Tanner staging) and pubarche (Tanner staging), in girls, and genital stage (Tanner staging), testicular volume (ml) and pubarche (Tanner staging), in boys.
The literature search resulted in 703 references, of which we identified 52 publications fulfilling the eligibility criteria for the qualitative trend synthesis and 23 publications for the meta-analysis. The qualitative trend synthesis provided data on 103 combinations of associations between prenatal or postnatal exposure to EDC compounds groups and puberty outcomes and the meta-analysis enabled 18 summary risk estimates of meta-associations.
Statistically significant associations in the qualitative trend synthesis suggested that postnatal exposure to phthalates may be associated with earlier thelarche and later pubarche. However, we did not find consistent evidence in the meta-analysis for associations between timing of pubertal onset in girls and boys and exposures to any of the studied xenobiotic EDCs. We were not able to identify specific pre- or postnatal windows of exposure as particularly critical and susceptible for effects of EDCs. Current evidence is subject to several methodological challenges and inconsistencies and evidence on specific exposure-outcome associations remains too scarce to firmly confirm EDC exposure as a risk factor for changes in age of pubertal onset in the general child population. To create a more uniform foundation for future comparison of evidence and to strengthen pooled studies, we recommend the use of more standardized approaches in the choice of statistical analyses, with exposure transformations, and in the definitions and assessments of puberty outcomes. The impact of mixtures of EDC exposures on the association also remains unestablished and would be valuable to elucidate for prenatal and postnatal windows of exposure. Future large, longitudinal epidemiological studies are needed to clarify the overall association.
EDC可以干扰正常的激素功能和代谢,并在青春期发作中起作用。我们旨在系统地确定和评估有关产前或产后暴露于外源性EDC后女孩和男孩青春期发病时间的当前证据。
遵循PRISMA准则,我们通过使用索引MeSH和自由文本搜索词的组合的块搜索方法,对PubMed数据库中的原始同行评审出版物进行了系统的文献检索.如果出版物涵盖了在母体或儿童生物样本中测量的产前或产后暴露于外源性EDC(欧盟委员会第1类EDC列表)的生物标志物,以及由以下里程碑的进展定义的青春期开始(并根据以下措施进行评估):月经初潮(年龄),thelarche(Tanner分期)和pubarche(Tanner分期),在女孩身上,和生殖器阶段(Tanner分期),睾丸体积(毫升)和阴部(Tanner分期),在男孩。
文献检索产生703个参考文献,其中我们确定了52篇符合定性趋势综合合格标准的出版物和23篇meta分析出版物.定性趋势综合提供了有关产前或产后暴露于EDC化合物组和青春期结局之间的103种关联组合的数据,荟萃分析提供了18种汇总的荟萃关联风险估计。
定性趋势合成中的统计学显著关联表明,出生后接触邻苯二甲酸盐可能与早期和后期性早熟有关。然而,在荟萃分析中,我们没有发现一致的证据表明,女孩和男孩青春期发病的时间与所研究的任何外源性EDC暴露之间存在关联.我们无法确定特定的产前或产后暴露窗对EDC的影响特别重要和易感。目前的证据存在一些方法学上的挑战和不一致之处,关于特定暴露-结果关联的证据仍然很少,无法坚定地确认EDC暴露是一般儿童人群青春期发病年龄变化的风险因素。为未来的证据比较创造更统一的基础,并加强汇总研究,我们建议在选择统计分析时使用更标准化的方法,随着曝光转换,以及青春期结局的定义和评估。EDC暴露混合物对关联的影响也尚未确定,对于阐明产前和产后暴露窗口将是有价值的。未来大,需要进行纵向流行病学研究以澄清总体关联.