Prenatal triclosan exposure and cord blood immune system biomarkers

The ability of epidemiologic evidence to inform regulatory decisions is largely dependent on the coherence and quality of the published literature. This systematic review examines the quality and consistency of studies assessing health outcomes associated with exposure to triclosan (TCS), an antimicrobial chemical with a short physiologic half-life. We used elements of the Biomonitoring, Environmental Epidemiology, and Short-Lived Chemicals instrument to evaluate aspects of study quality. Each methodological domain -overall design, exposure assessment, and data analysis -was categorized according to three tiers where Tier 1 indicated the highest quality. We also examined consistency of methods, results and reporting as considerations for weight of evidence (WOE) assessment. Studies were considered sufficiently comparable if they addressed the same or similar research questions. Forty-two studies met the criteria for inclusion. Only one randomized cross-over clinical trial of TCS was assigned to Tier 1 for all three domains. Most other studies were assigned to Tier 3 for at least one domain. Although the available literature examined more than 100 different health endpoints and reported hundreds of different measures of association, few studies were considered comparable. For reported measures of association, most were not significantly different from the null; the few statistically significant results represented isolated findings without a discernable across-or within-study pattern. We conclude that the current body of epidemiologic literature does not allow a meaningful WOE assessment due to methodological limitations of individual studies and lack of inter-study consistency. On the other hand, methodologically stronger studies may be used to inform future research. ARTICLE HISTORY

Endocrine-disrupting chemicals (EDCs) interfere with endogenous hormones and are present in many consumer products. In addition, they affect the development and functions of the immune system. The prenatal period is critical, because exposure to EDCs can induce irreversible changes in the immune system and increase susceptibility to asthma and allergies later in life. Nonpersistent EDCs are of most concern owing to their high annual production and potential toxicity. In this review, we summarize the literature on the effects of prenatal exposure to nonpersistent EDCs-phthalates and phenols-on asthma and allergic diseases, describe the underlying biological mechanisms, and make recommendations. Between 2011 and 2020, a total of 19 prospective studies were published. Most of these were focused on phthalates and bisphenol A and few on other bisphenols, parabens, triclosan, and benzophenone-3. Evidence remains insufficient owing to differences in chemical use between countries, sociodemographic characteristics of the study populations, misclassification of exposure due to the high within-subject variability, and heterogeneity in the definition of health outcomes. EDCs can alter airway cell differentiation and gut microbiota, shift the immune response towards T H 2, alter expression of T regulatory cells and T H 17, and weaken innate immunity. In order to better understand the burden of EDCs on the respiratory and immune systems, we require thoughtfully designed studies to assess exposure, appropriately characterize asthma and allergic phenotypes, and evaluate biological mechanisms and EDC mixtures. Research will help to implement public health policies that reduce exposure to EDCs in the community, particularly in pregnant women.

This study explored the influence of triclosan (TCS) in the absence and presence of sodium fluoride (NaF) on estrogenic activity and thyroid function of adolescent female rats. The results indicated that the individual exposure to TCS evoked a significant decline in T and T but the levels of estradiol, FSH, and LH were significantly elevated beside marked up regulation of calbindin-D9k and estrogen α mRNA expression. On the other hand, the single exposure to NaF causes insignificant changes in thyroid hormones, but evoked a trend toward an increase in both estradiol and LH levels. No significant differences in the TSH level were recorded among the experimental groups. The joint exposure to TCS and NaF induced a significant improvement in thyroid and reproductive hormone levels. Overall, these findings revealed that exposure to TCS resulted in significant endocrine and reproductive alterations in immature female rats, while TCS + NaF coexposure resulted in lessening most effects.