Plastics derived endocrine-disrupting compounds and their effects on early development

Abstract

Despite the fact that the estrogenic effects of bisphenols were first described 80 years ago, recent data about its potential negative impact on birth outcome parameters raises a strong rationale to investigate further. The adverse health effects of plastics recommend to measure the impacts of endocrine-disrupting compounds (EDCs) such as bisphenols (BPA, BPS, BPF), bis(2-ethylhexyl) phthalate, and dibutyl phthalate (DBP) in human health. Exposure to these compounds in utero may program the diseases of the testis, prostate, kidney and abnormalities in the immune system, and cause tumors, uterine hemorrhage during pregnancy and polycystic ovary. These compounds also control the processes of epigenetic transgenerational inheritance of adult-onset diseases by modulating DNA methylation and epimutations in reproductive cells. The early developmental stage is the most susceptible window for developmental and genomic programming. The critical stages of the events for a normal human birth lie between the many transitions occurring between spermatogenesis, egg fertilization and the fully formed fetus. As the cells begin to grow and differentiate, there are critical balances of hormones, and protein synthesis. Data are emerging on how these plastic-derived compounds affect embryogenesis, placentation and feto-placental development since pregnant women and unborn fetuses are often exposed to these factors during preconception and throughout gestation. Impaired early development that ultimately influences fetal outcomes is at the center of many developmental disorders and contributes an independent risk factor for adult chronic diseases. This review will summarize the current status on the impact of exposure to plastic derived EDCs on the growth, gene expression, epigenetic and angiogenic activities of the early fetal development process and their possible effects on birth outcomes.

Keywords: 11β-HSDs; ARs; DNA methylation; EDC; ERs; IGFs; THRs; birth outcome; bisphenol A (BPA); bisphenol F (BPF); bisphenol S (BPS); endocrine disruptor; environmental estrogens; epigenetics; exposure; fetal programming; genome program; miRNA; obesity; phthalate; placenta; plastics; polycystic ovary syndrome; preeclampsia.