Polyfluoroalkyl chemicals (PFCs)—including perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluorooctane sulfonic acid (PFOS), and perfluorohexane sulfonic acid (PFHxS)—are synthetic compounds that bind to proteins in the liver and serum, and are consistently detected in human serum samples. Epidemiologic studies have reported positive associations between serum PFCs and serum cholesterol levels in humans, but many have included highly exposed populations, and few have evaluated potential effects of PFNA and PFHxS. Nelson et al. (analyzed serum concentrations of PFOA, PFOS, PFNA, and PFHxS in association with serum cholesterol levels, body mass index, waist circumference, and a proxy measure of insulin resistance among participants in the 2003–2004 National Health and Nutrition Examination Survey (NHANES). The authors report that serum levels of total cholesterol and non–high-density cholesterol (non-HDL or “bad” cholesterol) were increased in association with PFOS, PFOA, and PFNA among 860 adults (20–80 years of age) who were not using
cholesterol-lowering medications. In contrast, total cholesterol was inversely associated with serum PFHxS concentrations, and body size and insulin resistance were not consistently associated with PFCs in the study population. The authors conclude that their results suggest effects of environmentally relevant PFC exposures on cholesterol metabolism, but they note that additional studies are needed to confirm associations and clarify biologic mechanisms.
Related News Article: PFCs and Cholesterol: A Sticky Connection
Diethylhexyl phthalate (DEHP) is an industrial plasticizer used in cosmetics, medical devices, food packaging, and other applications. Evidence that DEHP metabolites can activate peroxisome proliferator–activated receptors (PPARs) involved in fatty acid oxidation (PPARα and PPARβ) and adiposite function and insulin resistance (PPARγ) has raised concerns about potential effects of DEHP on metabolic homeostasis. In rodents, PPARα activation also induces hepatic peroxisome proliferation, but this response to PPARα activation is not observed in humans. Feige et al. evaluated systemic and metabolic consequences of high-dose oral DEHP in combination with a high-fat diet in wild-type mice and genetically engineered mouse PPAR models. The authors report that mice exposed to DEHP gained less weight than controls, without modifying their feeding behavior; they also exhibited lower triglyceride levels, smaller adipocytes, and improved glucose tolerance compared with controls. These effects, which were observed in mice fed both high-fat and standard diets, appeared to be mediated by PPARα-dependent activation of hepatic fatty acid catabolism without apparent involvement of PPARβ or PPARγ. However, mouse models that expressed human (versus mouse) PPARα tended to gain more weight on a high-fat diet than their DHEP-unexposed counterparts. The authors conclude that findings support species-specific metabolic effects of DEHP mediated by PPARα activation.
Related News Article: To Each His Own: DEHP Yields Species-Specific Metabolic Phenotypes
Biomonitoring data suggest that humans are widely exposed to phthalate plasticizers such as di(2-ethylhexyl) phthalate (DEHP), but major sources and pathways of exposure have not been determined, despite concerns about the potential for adverse health effects in vulnerable or highly exposed populations. Xu et al. developed a three-compartment model to estimate exposure to DEHP emitted from vinyl flooring in a family residence (including exposure via inhalation, dermal absorption, and oral ingestion) and used this model to identify model parameters with the greatest influence on exposure. Predicted exposure levels varied by a factor of 40 depending on model assumptions, with predicted exposures above reference dose guidelines for DEHP under some scenarios; influential model parameters included surface area and initial concentration of DEHP in vinyl flooring, DEHP emission rates, and room air ventilation rates. The authors conclude that the mechanistic modeling approach they have developed for DEHP can be extended to predict phthalate exposures from other sources, as well as exposures to flame retardants and other semivolatile organic compounds found in homes and consumer products.
Related News Article: Running Phthalates to Ground: Pinpointing Exposure Sources in a Virtual Home
Air pollution has been consistently associated with asthma symptoms, but relatively few studies have evaluated early life exposures and asthma onset. Clark et al. conducted a nested population-based case–control study of childhood asthma diagnosed up to 3–4 years of age among children born in southwestern British Columbia in 1999 and 2000, including 3,482 eligible cases (with a history of hospitalization or at least two asthma diagnoses) and 17,410 age- and sex-matched controls. Administrative and health care data were used to identify eligible children and obtain information on residential histories and potential confounders. Air pollution exposures during pregnancy and the first year of life [specifically, to carbon monoxide, nitric oxide, nitrogen dioxide, particulate matter ≤ 10 µm (PM10) and ≤ 2.5 µm (PM2.5) in aerodynamic diameter, ozone, sulfur dioxide, black carbon, woodsmoke, and proximity to major roads and industrial point sources] were estimated using regulatory monitoring data and land use regression models adjusted for temporal variation. Early life exposures to CO, NO, NO2, PM10, SO2, black carbon, and industrial point sources were positively associated with asthma, with the strongest associations noted for traffic-related pollutants. The authors conclude that results support effects of early exposure to air pollutants on the development of childhood asthma.
Related News Article: Traffic Marker? Early Exposure to Air Pollution Associated with Childhood Asthma
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