ABSTRACT
OBJECTIVES: Tris(4-chlorophenyl) methane (TCPM) and tris(4-chlorophenyl)methanol (TCPMOH) are anthropogenic environmental contaminants believed to be manufacturing byproducts of the organochlorine pesticide dichlorodiphenyltrichloroethane (DDT) due to environmental co-occurrence. TCPM and TCPMOH are persistent, bioaccumulate in the environment, and are detected in human breast milk and adipose tissues. DDT exposures have been previously shown to disrupt insulin signaling and glucoregulation, increasing risk for diabetes. We have previously shown that embryonic exposures organochlorines such as polychlorinated biphenyls disrupted pancreatic development and early embryonic glucoregulatory networks. Here, we determined the impacts of the similar compounds TCPM and TCPMOH on zebrafish pancreatic growth and gene expression following developmental exposures. METHODS: Zebrafish embryos were exposed to 50 nM TCPM or TCPMOH beginning at 24 hr postfertilization (hpf) and exposures were refreshed daily. At 96 hpf, pancreatic growth and islet area were directly visualized in Tg(ptf1a::GFP) and Tg(insulin::GFP) embryos, respectively, using microscopy. Gene expression was assessed at 100 hpf with RNA sequencing. RESULTS: Islet and total pancreas area were reduced by 20.8% and 13% in embryos exposed to 50 nM TCPMOH compared to controls. TCPM did not induce significant morphological changes to the developing pancreas, indicating TCPMOH, but not TCPM, impairs pancreatic development despite similarity in molecular responses. Transcriptomic responses to TCPM and TCPMOH were correlated (R2 = .903), and pathway analysis found downregulation of processes including retinol metabolism, circadian rhythm, and steroid biosynthesis. CONCLUSION: Overall, our data suggest that TCPM and TCPMOH may be hazardous to embryonic growth and development.
Subject(s)
DDT , Zebrafish , Female , Animals , Humans , DDT/metabolism , Methanol , Methane , Organogenesis/genetics , Pancreas , Insulin , Gene ExpressionABSTRACT
Air pollution is one of the major risk factors contributing to adverse public health outcomes worldwide. Fine particulate matter (PM2.5) has been repeatedly associated with increased risk of cardiovascular events, including heart attacks. Because PM2.5 is unequally distributed with elevated concentrations near high-traffic and industrial zones, PM2.5 is an environmental justice issue of major public health concern. In this study, we reviewed the relationship between PM2.5, emergency visits due to heart attacks, and environmental justice in San Diego County using data from CalEnviroScreen 3.0. Our results indicate that PM2.5, diesel PM emissions, and emergency visits due to heart attacks are weakly, but positively correlated (r = 0.3, R2 < 0.1). Areas classified as environmental justice communities, communities comprised more dominantly of nonwhite populations, and communities closer to the San Diego-Tijuana border are exposed disproportionately to air pollution in San Diego County. Overall, this work demonstrates that there is an association between elevated local PM concentrations in San Diego County communities with emergency hospital visits due to heart attacks, and that these associations are an environmental justice issue disproportionally affecting disadvantaged communities.Implications: Particulate matter is an adverse contributor to overall health throughout the lifespan, contributing to diseases such as asthma, hypertension, stroke, and increased risk of cardiovascular events. Here, we assess the relationship between particulate matter and heart attacks in San Diego County using CalEnviroScreen3.0. Using these tools, we also examine correlations between this relationship and different sociodemographic indicators such as age, race, income, and proximity to the high-traffic U.S.-Mexico border. Overall, we show that specific communities around San Diego are more highly exposed to particulate matter, and that these relationships may be disproportionately contributing to heart attacks in disadvantaged communities.
