Alzheimer’s disease (AD), non-AD dementia, and Parkinson’s disease (PD) are increasingly common in older adults, yet all risk factors for their onset are not fully understood. Consequently, environmental exposures, including air pollution, have been hypothesized to contribute to the etiology of neurodegeneration. Because persistently elevated rates of AD mortality in the southern Piedmont area of North Carolina (NC) have been documented, we studied mortality and hospital admissions for AD, non-AD dementia, and PD in residential populations aged 65+ with long-term exposures to elevated levels of ambient air particulate matter 2.5 (PM_2.5) exceeding the World Health Organization (WHO) air quality standards (≥10μg/m³). Health data were obtained from the State Center for Health Statistics and the Healthcare Cost and Utilization Project. PM_2.5 levels were obtained from the MODIS/MISR and SeaWiFS datafiles. Residents in the Study group of elevated air particulate matter (87 zip codes with PM_2.5≥10μg/m³) were compared to the residents in the Control group with low levels of air particulate matter (81 zip codes with PM_2.5≤7.61μg/m³), and were found to have higher age-adjusted rates of mortality and hospital admissions for AD, non-AD dementia, and PD, including a most pronounced increase in AD mortality (323/100,000 vs. 257/100,000, respectively). After adjustment for multiple co-factors, the risk of death (odds ratio, or OR) from AD in the Study group (OR = 1.35, 95%CI[1.24–1.48]) was significantly higher than ORs of non-AD dementia or PD (OR = 0.97, 95%CI[0.90–1.04] and OR = 1.13, 95%CI[0.92–1.31]). The OR of hospital admissions was significantly increased only for AD as a primary case of hospitalization (OR = 1.54, 95%CI[1.31–1.82]). Conclusion: NC residents aged 65+ with long-term exposures to ambient PM_2.5 levels exceeding the WHO standard had significantly increased risks of death and hospital admissions for AD. The effects for non-AD dementia and PD were less pronounced.

BACKGROUND In North Carolina, coal-burning power plants remain the major source of electrical production. Coal burning generates coal ash that is stored in landfills and slurry ponds that are often located near residential communities, signifying high potential for environmental contamination and increasing health risks. We reviewed the literature on potential health effects of coal-burning plants to summarize current knowledge on health risks.

An increasing number of studies suggest an important role of host immunity as a barrier to tumor formation and progression. Complex mechanisms and multiple pathways are involved in evading innate and adaptive immune responses, with a broad spectrum of chemicals displaying the potential to adversely influence immunosurveillance. The evaluation of the cumulative effects of low-dose exposures from the occupational and natural environment, especially if multiple chemicals target the same gene(s) or pathway(s), is a challenge. We reviewed common environmental chemicals and discussed their potential effects on immunosurveillance. Our overarching objective was to review related signaling pathways influencing immune surveillance such as the pathways involving PI3K/Akt, chemokines, TGF-β, FAK, IGF-1, HIF-1α, IL-6, IL-1α, CTLA-4 and PD-1/PDL-1 could individually or collectively impact immunosurveillance. A number of chemicals that are common in the anthropogenic environment such as fungicides (maneb, fluoxastrobin and pyroclostrobin), herbicides (atrazine), insecticides (pyridaben and azamethiphos), the components of personal care products (triclosan and bisphenol A) and diethylhexylphthalate with pathways critical to tumor immunosurveillance. At this time, these chemicals are not recognized as human carcinogens; however, it is known that they these chemicalscan simultaneously persist in the environment and appear to have some potential interfere with the host immune response, therefore potentially contributing to promotion interacting with of immune evasion mechanisms, and promoting subsequent tumor growth and progression.