Particulate Air Pollution and Fasting Blood Glucose in Nondiabetic Individuals: Associations and Epigenetic Mediation in the Normative Aging Study, 2000–2011

Air pollution may increase cardiovascular and respiratory risk through inflammatory pathways, but evidence for acute effects has been weak and indirect. Between December 2014 and July 2015, we enrolled 36 healthy, nonsmoking college students for a panel study in Shanghai, China, a city with highly variable levels of air pollution. We measured personal exposure to particulate matter with an aerodynamic diameter less than or equal to 2.5 μm (PM 2.5 ) continuously for 72 hours preceding each of 4 clinical visits that included phlebotomy. We measured 4 inflammation proteins and DNA methylation at nearby regulatory cytosine-phosphate-guanine (CpG) loci. We applied linear mixed-effect models to examine associations over various lag times. When results suggested mediation, we evaluated methylation as mediator. Increased PM 2.5 concentration was positively associated with all 4 inflammation proteins and negatively associated with DNA methylation at regulatory loci for tumor necrosis factor alpha (TNF-α) and soluble intercellular adhesion molecule-1. A 10-μg/m 3 increase in average PM 2.5 during the 24 hours preceding blood draw corresponded to a 4.4% increase in TNF-α and a statistically significant decrease in methylation at one of the two studied candidate CpG loci for TNF-α. Epigenetics may play an important role in mediating effects of PM 2.5 on inflammatory pathways. DNA methylation; fine particulate matter; inflammation; mediation analysis; panel study; personal exposure Abbreviations: CI, confidence interval; CpG, cytosine-phosphate-guanine; CVD, cardiovascular disease; PM, particulate matter; PM 2.5 , particulate matter having an aerodynamic diameter less than or equal to 2.5 μm; RD, respiratory disease; sCD40L, soluble cluster of differentiation 40 (CD40) ligand; sICAM-1, soluble intercellular adhesion molecule-1; TNF-α, tumor necrosis factor alpha.

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“…DNA methylation (global and gene-specific) is a plausible biological mediator of CVD/RD-related events (44)(45)(46)(47)(48)(49).…”

Section: Discussionmentioning

confidence: 99%

Possible Mediation by Methylation in Acute Inflammation Following Personal Exposure to Fine Particulate Air Pollution

Wang

Chen

Shi

et al. 2017

American Journal of Epidemiology

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“…Specifically, our previous publication was the first study examining associations of ambient particles and DNAm-age (Nwanaji-Enwerem et al, 2016). There, we used a tiered approach of adding confounders and covariates based on known relationships of ambient particles with DNA methylation and known relationships of ambient particles with older markers of aging (Horvath, 2013; Madrigano et al, 2011; Baccarelli et al, 2009; Bind et al, 2015; Peng et al, 2016). Tier one adjusted for chronological age and blood cell types.…”

Section: Methodsmentioning

confidence: 99%

Associations between long-term exposure to PM2.5 component species and blood DNA methylation age in the elderly: The VA normative aging study

Nwanaji‐Enwerem

Dai

Colicino

et al. 2017

Environment International

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Background Long-term PM2.5 exposure and aging have been implicated in multiple shared diseases; studying their relationship is a promising strategy to further understand the adverse impact of PM2.5 on human health. Objective We assessed the relationship of major PM2.5 component species (ammonium, elemental carbon, organic carbon, nitrate, and sulfate) with Horvath and Hannum DNA methylation (DNAm) age, two DNA methylation-based predictors of chronological age. Methods This analysis included 552 participants from the Normative Aging Study with multiple visits between 2000 and 2011 (n = 940 visits). We estimated 1-year PM2.5 species levels at participants’ addresses using the GEOS-chem transport model. Blood DNAm-age was calculated using CpG sites on the Illumina HumanMethylation450 BeadChip. We fit linear mixed-effects models, controlling for PM2.5 mass and lifestyle/environmental factors as fixed effects, with the adaptive LASSO penalty to identify PM2.5 species associated with DNAm-age. Results Sulfate and ammonium were selected by the LASSO in the Horvath DNAm-age models. In a fully-adjusted multiple-species model, interquartile range increases in both 1-year sulfate (95%CI: 0.28, 0.74, P < 0.0001) and ammonium (95%CI: 0.02, 0.70, P = 0.04) levels were associated with at least a 0.36-year increase in Horvath DNAm-age. No PM2.5 species were selected by the LASSO in the Hannum DNAm-age models. Our findings persisted in sensitivity analyses including only visits with 1-year PM2.5 levels within US EPA national ambient air quality standards. Conclusion Our results demonstrate that sulfate and ammonium were most associated with Horvath DNAm-age and suggest that DNAm-age measures differ in their sensitivity to ambient particle exposures and potentially disease.

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“…Studies suggest that air pollution exposure upregulates ICAM-1 expression due to reduced epigenetic methylation secondary to high FBG. [38] This, in turn, may increase the ability for inflammatory mediators to penetrate the blood-brain barrier, leading to increased CNS inflammation.…”

Section: Air Pollution and Cognitive Dysfunctionmentioning

confidence: 99%

Clinical effects of air pollution on the central nervous system; a review

Babadjouni

Hodis

Radwanski

et al. 2017

Journal of Clinical Neuroscience

138

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The purpose of this review is to describe recent clinical and epidemiological studies examining the adverse effects of urban air pollution on the central nervous system (CNS). Air pollution and particulate matter (PM) are associated with neuroinflammation and reactive oxygen species (ROS). These processes affect multiple CNS pathways. The conceptual framework of this review focuses on adverse effects of air pollution with respect to neurocognition, white matter disease, stroke, and carotid artery disease. Both children and older individuals exposed to air pollution exhibit signs of cognitive dysfunction. However, evidence on middle-aged cohorts is lacking. White matter injury secondary to air pollution exposure is a putative mechanism for neurocognitive decline. Air pollution is associated with exacerbations of neurodegenerative conditions such as Alzheimer’s and Parkinson’s Diseases. Increases in stroke incidences and mortalities are seen in the setting of air pollution exposure and CNS pathology is robust. Large populations living in highly polluted environments are at risk. This review aims to outline current knowledge of air pollution exposure effects on neurological health.

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Particulate Air Pollution and Fasting Blood Glucose in Nondiabetic Individuals: Associations and Epigenetic Mediation in the Normative Aging Study, 2000–2011

Cited by 109 publications

References 54 publications

Possible Mediation by Methylation in Acute Inflammation Following Personal Exposure to Fine Particulate Air Pollution

Possible Mediation by Methylation in Acute Inflammation Following Personal Exposure to Fine Particulate Air Pollution

Associations between long-term exposure to PM2.5 component species and blood DNA methylation age in the elderly: The VA normative aging study

Clinical effects of air pollution on the central nervous system; a review

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