Maternal Exposure to Trace Elements, Toxic Metals, and Longitudinal Changes in Infancy Anthropometry and Growth Trajectories: A Prospective Cohort Study.

Exploration of stage-specific effects of maternal exposure to trace elements and toxic metals on infancy continuous growth and trajectories is critical for early-life health management. Within a Chinese prospective cohort in 2014-2015, a total of 919 mother-infant pairs were included, and the urinary levels of 17 elements including vanadium (V), chromium (Cr), manganese, iron, cobalt, nickel, copper, zinc, arsenic, molybdenum, palladium, cadmium, tin, gold, mercury, thallium, and lead in early (mean: 11.9 weeks), and late pregnancy (mean: 32.4 weeks) were assessed. Standardized anthropometric assessments of infants were conducted at 1, 3, 6, 8, and 12 months of age. A three-step longitudinal and high-dimensional data analysis procedure was carried out to estimate the impacts of exposome on dynamic growth. Early-pregnancy exposures to V and Cr were positively associated with repeated measurements of length-for-age z-scores (LAZ). Six trajectories were identified based on LAZ. Maternal single exposure to V and Cr as well as mixed exposure to trace elements in early pregnancy were associated with raised odds for the high-stable group. Our results suggested positive associations between maternal trace element exposome and infancy dynamic growth. V and Cr were the key elements and the early pregnancy might be the critical window.

Evaluation of the bisphenol A-induced vascular toxicity on human umbilical artery.

Bisphenol A (BPA) is one of the most widely used synthetic compound in the manufacture of polycarbonate plastics and epoxy resins. Worryingly, BPA is an endocrine disrupting chemical (EDC) with an estrogenic, androgenic, or anti-androgenic activities. However, the vascular implications of BPA exposome in pregnancy is unclear. In this sense, the present work proposed to understand how BPA exposure impair the vasculature of the pregnant women. To elucidate this, ex vivo studies were performed using human umbilical arteries to explore the acute and chronic effects of BPA. The mode of action of BPA was also explored by analysing the activity (by ex vivo studies) and expression (in vitro studies) analysis of Ca2+ and K+-channels and soluble guanyl cyclase. Moreover, in silico docking simulations were performed to unveil the modes of interactions of BPA with the proteins involved in these signalling pathways. Our study showed that the exposure to BPA may modify the vasorelaxant response of HUA, interfering with NO/sGC/cGMP/PKG pathway by modulation of sGC and activation of BKCa channels. Moreover, our findings suggest that BPA can modulate the HUA reactivity, increasing the L-type Ca2+ Channels (LTCC) activity, a common vascular response observed in hypertensive disorders of pregnancy.

Intrinsic Effects of Exposome in Atopic Dermatitis: Genomics, Epigenomics and Regulatory Layers.

Atopic dermatitis (AD) or atopic eczema is an increasingly manifested inflammatory skin disorder of complex etiology which is modulated by both extrinsic and intrinsic factors. The exposome includes a person's lifetime exposures and their effects. We recently reviewed the extrinsic exposome's environmental risk factors that contribute to AD. The periods of pregnancy, infancy, and teenage years are recognized as crucial stages in the formation of AD, where the exposome leads to enduring impacts on the immune system. However, research is now focusing on the interactions between intrinsic pathways that are modulated by the extrinsic exposome, including genetic variation, epigenetic modifications, and signals, such as diet, stress, and microbiome interactions. As a result, immune dysregulation, barrier dysfunction, hormonal fluctuations, and skin microbiome dysbiosis are important factors contributing to AD development, and their in-depth understanding is crucial not only for AD treatment but also for similar inflammatory disorders.