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Per- and polyfluoroalkyl substances (PFAS) have emerged as high-priority contaminants due to their ubiquity and pervasiveness in the environment. Numerous PFAS co-occur across sources of drinking water, including areas in North Carolina (NC) where some detected concentrations are above the Environmental Protection Agency's health advisory levels. Although evidence demonstrates that PFAS exposure induces harmful effects in the liver, the involvement of extracellular vesicles (EVs) as potential mediators of these effects has yet to be evaluated. This study set out to evaluate the hypothesis that PFAS mixtures induce dose-dependent release of EVs from liver cells, with exposures causing differential loading of microRNAs (miRNAs) and PFAS chemical signatures. To test this hypothesis, a defined PFAS mixture was prioritized utilizing data collected by the NC PFAS Testing Network. This mixture contained 3 substances, perfluorooctane sulfonic acid (PFOS), perfluorooctanoic acid (PFOA), and perfluorohexanoic acid (PFHxA), selected based upon co-occurrence patterns and the inclusion of both short-chain (PFHxA) and long-chain (PFOA and PFOS) substances. HepG2 liver cells were exposed to equimolar PFAS, and secreted EVs were isolated from conditioned media and characterized for count and molecular content. Exposures induced a dose-dependent release of EVs carrying miRNAs that were differentially loaded upon exposure. These altered miRNA signatures were predicted to target mRNA pathways involved in hepatic fibrosis and cancer. Chemical concentrations of PFOS, PFOA, and PFHxA were also detected in both parent HepG2 cells and their released EVs, specifically within a 15-fold range after normalizing for protein content. This study therefore established EVs as novel biological responders and measurable endpoints for evaluating PFAS-induced toxicity. [ABSTRACT FROM AUTHOR]

Multiple external stressors are known to have adverse impacts on health and development. Certain groups are more vulnerable and/or more likely to be exposed toenvironmental, psychological, and social stressors simultaneously. Yet, few studies have examined combined exposure to environmental toxicants and psychosocial stress. Here, we integrated environmental chemical exposure data collected using silicone wristbands and self-report social stressor data within the Brain and Early Experience (BEE) perinatal cohort to understand co-exposure to environmental chemicals and social stress. Silicone wristbands were worn for one week by mothers throughout central North Carolina who were 6 months postpartum (n = 97). Exposure to 110 environmental chemicals across eight chemical classes was quantified on silicone wristbands using gas chromatography mass spectrometry. Social stress was evaluated using eight established self-report questionnaires (e.g., Brief Symptom Inventory, Perceived Stress Scale), quantifying experiences such as race-related stress, economic strain, and relationship conflict. Hair cortisol levels were measured as an additional metric of stress. The chemical exposure landscape and associations among chemical exposure, demographic characteristics, and social stress were characterized through individual variable analyses, cluster and data reduction, and compiled scoring approaches to comprehensively evaluate chemical and social stress burdens. We found that chemicals contain co-occurring patterns largely based on chemical class, with phthalates representing the chemical class with highest exposure and polychlorinated biphenyls the lowest. Chemicals showed differential exposure across racial groups, with diethyl phthalate, triphenyl phosphate, and tris(3,5-dimethyl phenyl) phosphate at higher levels in Black participants compared with White participants. Integrating social stressor profiling with chemical exposure data identified one particularly vulnerable subset of participants in which high chemical exposure burden coincided with high experiences of racism and economic stress. These findings demonstrate co-occurring chemical and social stress, warranting further investigation to better understand how these combined stressors may contribute to disparities in maternal and child health., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Lead is an established neurotoxicant, and it has known associations with adverse neurodevelopmental and reproductive outcomes. Exposure to lead at any level is unsafe, and the United States (US) has enacted various federal and state legislations to regulate lead levels in drinking water in K-12 schools and childcare facilities; however, no regulations exist for higher education settings. Upon the discovery of lead in drinking water fixtures in the University of North Carolina at Chapel Hill (UNC-CH) campus, a cross-campus water testing network and sampling plan was developed and deployed. The campaign was based on the US Environmental Protection Agency's (EPA) 3Ts (Training, Testing, and Taking Action) guidance. The seven-month campaign involved 5954 tests on 3825 drinking water fixtures across 265 buildings. A total of 502 (8.43%) tests showed lead above the limit of detection (1 part per billion, ppb), which represented 422 (11.03%) fixtures. Fewer than 1.5% of the tests were above the EPA action level for public water systems (15 ppb). In conclusion, systematic testing of all the fixtures across campus was required to identify localized contamination, and each entity in the cross-campus network undertook necessary roles to generate a successful testing campaign. UNC-CH established preventative measures to test drinking water fixtures every three years, which provide a framework for other higher education institutions in responding to lead contamination.

Context: Alcohol is increasingly recognized as a factor in many boating fatalities, but the association between alcohol consumption and mortality among boaters has not been well quantified., Objectives: To determine the association of alcohol use with passengers' and operators' estimated relative risk (RR) of dying while boating., Design, Setting, and Participants: Case-control study of recreational boating deaths among persons aged 18 years or older from 1990-1998 in Maryland and North Carolina (n = 221), compared with control interviews obtained from a multistage probability sample of boaters in each state from 1997-1999 (n = 3943)., Main Outcome Measure: Estimated RR of fatality associated with different levels of blood alcohol concentration (BAC) among boaters., Results: Compared with the referent of a BAC of 0, the estimated RR of death increased even with a BAC of 10 mg/dL (odds ratio [OR], 1.3; 95% confidence interval [CI], 1.2-1.4). The OR was 52.4 (95% CI, 25.9-106.1) at a BAC of 250 mg/dL. The estimated RR associated with alcohol use was similar for passengers and operators and did not vary by boat type or whether the boat was moving or stationary., Conclusions: Drinking increases the RR of dying while boating, which becomes apparent at low levels of BAC and increases as BAC increases. Prevention efforts targeted only at those operating a boat are ignoring many boaters at high risk. Countermeasures that reduce drinking by all boat occupants are therefore more likely to effectively reduce boating fatalities.