BACKGROUND Early life exposure to triclosan, an antimicrobial chemical and suspected endocrine disruptor, may adversely affect neurodevelopment. No studies have examined gestational and early childhood exposure to triclosan and children's academic achievement. METHODS Using data from 193 mother-child pairs from the HOME Study, we quantified triclosan in maternal and child urine samples up to nine times between the second trimester of gestation (16-weeks) and age 8 years. At age 8 years, we administered the reading and math components of the Wide Range Achievement Test-4 (WRAT-4) to children. Using multiple informants models, we estimated covariate-adjusted associations of triclosan concentrations during each time period with WRAT-4 scores. We also tested whether associations differed by exposure period and child sex. RESULTS There was evidence that timing of exposure modified the associations between triclosan and reading composite scores (triclosan-exposure period interaction p-value = 0.20), but not math scores (interaction p-value = 0.72). Each 10-fold increase in triclosan concentrations at delivery was associated with lower reading composite scores (β-2.6; 95 % CI-5.0, -0.1). Additionally, we observed weaker and less precise inverse association of math scores with triclosan concentrations at delivery (β-1.9; 95 % CI-4.6, 0.8) and at age 1 year (β-2.0; 95 % CI-6.0, 2.1). BMS-986365 There was not strong evidence that child sex modified the pattern of associations between repeated triclosan measures and WRAT-4 reading composite or math scores (sex-triclosan-exposure period interaction p-values>0.20). CONCLUSION Urinary triclosan concentrations at delivery and at age 1 year, but not other times during gestation or childhood, were associated with lower reading composite and to a lesser extent math test scores at age 8 years in this cohort of U.S. children. Cardiovascular diseases (CVDs) have imposed a massive health and financial burden worldwide with high mortality and morbidity. However, the diagnostic value of current biomarkers might be impaired by a wide variety of noncardiac causes. Moreover, cardiovascular outcomes, survival, and prognosis of patients with CVDs remain poor despite advances in treatment. Therefore, novel diagnostic and therapeutic strategies are urgently required for timely identification of possible heart diseases in the early stage, which might effectively contribute to reducing the CVDs-caused morbidity and mortality. Circular RNA (circRNA) was initially identified as aberrant byproducts or abnormally spliced transcripts. However, with advances in bioinformatics and high-throughput sequencing technology, circRNAs has become an essential topic on a wide range of biological functions and emerged as novel players in diagnostic and therapeutic strategies for CVDs. In this article, we briefly introduce the biogenesis and functions of circRNAs. Moreover, we describe the roles of circRNAs in multiple CVDs, including atherosclerosis, coronary artery disease, myocardial infarction, as well as cardiomyopathy. In addition, we provide an overview on the current challenges and directions for further application. During pregnancy, fetal thyroid hormones (THs) are dependent on maternal placental transport and their physiological level is crucial for normal fetal neurodevelopment. Earlier research has shown that Di-(2-ethylhexyl) phthalate (DEHP) disrupts thyroid function and THs homeostasis in pregnant women and fetuses, and affects placental THs transport. However, the underlying mechanisms are poorly understood. The present study, therefore, aimed to systematically investigate the potential mechanisms of DEHP-induced disruption in the placental THs transport using two human placental trophoblastic cells, HTR-8/SVneo cells and JEG-3 cells. While the exposure of DEHP at the doses of 0-400 μM for 24 h did not affect cell viability, we found reduced consumption of T3 and T4 in the culture medium of HTR-8/Svneo cells treated with DEHP at 400 μM. DEHP treatment did not affect T3 uptake and the expression of monocarboxylate transporters 8 (MCT8) and organic anion transporters 1C1 (OATP1C1). However, DEHP significantly inhibited transthyretin (TTR) internalization, down-regulated TTR, deiodinase 2 (DIO2), and thyroid hormone receptors mRNA expression and protein levels, and up-regulated deiodinase 3 (DIO3) protein levels in a dose-dependent manner. These results indicate that DEHP acts on placental trophoblast cells, inhibits its TTR internalization, down-regulates TTR expression and affects the expression of DIO2, DIO3, and thyroid hormone receptor. These may be the mechanisms by which PAEs affects THs transport through placental. Arsenic is a ubiquitous environmental toxicant, found in high concentrations worldwide. Although abundant research has dealt with arsenic-induced cancers, studies on mechanisms of non-malignant lung diseases have not been complete. In addition, decades of research have mostly concentrated on high-dose arsenic exposure, which has very limited use in modeling the biological effects of today's low-dose exposures. Indeed, accumulated evidence has shown that low-dose arsenic exposure (i.e. ≤100 ppb) may also alter lung homeostasis by causing host susceptibility to viral infection. However, the underlying mechanism of this alteration is unknown. In this study, we found that low-dose sodium arsenite (As (III)) repressed major airway mucins-MUC5AC and MUC5B at both mRNA and protein levels. We further demonstrated that this repression was not caused by cellular toxicity or mediated by the reduction of a common mucin-inducing pathway-EGFR. Other established mucin activators- dsRNA, IL1β or IL17 were not able to override As (III)-induced mucin repression. Interestingly, the suppressing effect of As (III) appeared to be partially reversible, and supplementation of all trans retinoic acid (t-RA) doses dependently restored mucin gene expression. Further analyses indicated that As (III) treatment significantly reduced the protein level of retinoic acid receptors (RARα, γ and RXRα) as well as RARE promoter reporter activity. Therefore, our study fills in an important knowledge gap in the field of low-dose arsenic exposure. The interference of RA signaling, and mucin gene expression may be important pathogenic factors in low-dose arsenic induced lung toxicity.