October 2016 Science Bulletin: Systematic review of air pollution and autism diagnosis; phthalates increase hydrocele risk

October 20, 2016 at 9:34 am | Posted in News and Science Bulletins | Leave a comment

October 2016 Science Bulletin

Air pollution, autism | A Systematic Review and Meta-Analysis of Multiple Airborne Pollutants and Autism Spectrum Disorder. After considering strengths and limitations of the body of research, we concluded that there is “limited evidence of toxicity” for the association between early life exposure to air pollution as a whole and diagnosis of ASD. The strongest evidence was between prenatal exposure to particulate matter and ASD. However, the small number of studies in the meta-analysis and unexplained statistical heterogeneity across the individual study estimates means that the effect could be larger or smaller (including not significant) than these studies estimate.

Air pollution, kidney function | Long-Term Exposure to Ambient Fine Particulate Matter and Renal Function in Older Men: The Veterans Administration Normative Aging Study. In this longitudinal sample of older men, the findings supported the hypothesis that long-term PM2.5 exposure negatively affects renal function and increases renal function decline.

Phthalates, genital abnormalities | First trimester phthalate exposure and male newborn genital anomalies. First trimester urinary DEHP metabolite concentrations were associated with increased odds of any newborn genital anomaly, and this association was primarily driven by isolated hydrocele which made up the majority of anomalies in newborn males. The association with hydrocele has not been previously reported and suggests that it may be an endpoint affected by prenatal phthalate exposures in the first trimester of development. Future human studies should include hydrocele assessment in order to confirm findings.

EDCs, obesity | Endocrine Aspects of Environmental “Obesogen” Pollutants. The key concept is the identification of adipose tissue not only as a preferential site of storage of EDCs, but also as an endocrine organ and, as such, susceptible to endocrine disruption.

 

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