Short-term exposure to PM2.5 and vanadium and changes in asthma gene DNA methylation and lung function decrements among urban children

Abstract

BackgroundBoth short and long-term exposure to traffic-related air pollutants have been associated with asthma and reduced lung function. We hypothesized that short-term indoor exposure to fine particulate matter <2.5 μm (PM2.5) and vanadium (V) would be associated with altered buccal cell DNA methylation of targeted asthma genes and decreased lung function among urban children in a nested subcohort of African American and Dominican children.MethodsSix day integrated levels of air pollutants were measured from children’s homes (age 9–14; n = 163), repeated 6 months later (n = 98). Buccal samples were collected repeatedly during visits. CpG promoter loci of asthma genes (i.e., interleukin 4 (IL4), interferon gamma (IFNγ), inducible nitric oxide synthase (NOS2A), arginase 2 (ARG2)) were pyrosequenced and lung function was assessed.ResultsExposure to V, but not PM2.5, was associated with lower DNA methylation of IL4 and IFNγ. In exploratory analyses, V levels were associated with lower methylation of the proinflammatory NOS2A-CpG+5099 among asthmatic overweight or obese children but not nonasthmatics. Short-term exposure to PM2.5, but not V, appeared associated with lower lung function (i.e., reduced z-scores for forced expiratory volume in one second (FEV1, FEV1/ forced vital capacity [FEV1/FVC] and forced expiratory flow at 25–75% of FVC [FEF25–75]).ConclusionsExposure to V was associated with altered DNA methylation of allergic and proinflammatory asthma genes implicated in air pollution related asthma. However, short-term exposure to PM2.5, but not V, appeared associated with decrements in lung function among urban children.Electronic supplementary materialThe online version of this article (doi:10.1186/s12931-017-0550-9) contains supplementary material, which is available to authorized users.

Effects of particulate matter on allergic respiratory diseases

“…Exposure to PM 2.5 is associated with oxidative stress and impaired lung function. 54 , 55 , 56 A burst of reactive oxygen species induced by PM 2.5 was found in the neutrophils of asthmatic patients. 57 Deng et al 58 reported that PM 2.5 induces oxidative stress by increasing the expression of glutamate-cysteine ligase catalytic subunit (GCLC), heme oxygenase-1 (HO-1), and NADPH quinone oxidoreductase (NQO-1)in human lung epithelial cells (A549), and thereby activates Nrf2 in the phosphatidylinositol-4,5-bisphosphate 3-kinase (PIK3)/AKT signaling pathway.…”

The Role and Potential Pathogenic Mechanism of Particulate Matter in Childhood Asthma: A Review and Perspective

“…Hypermethylation of CpG islands in Foxp3 associated with chronic exposure to DEP leads to the suppression of Treg function and increased asthma severity as assessed by symptoms and lung function [77]. In addition, vanadium (a component of ROFA) was associated with altered DNA methylation of allergic and proinflammatory asthma genes implicated in air-pollution-related asthma [78]. Recently, authors have demonstrated that health effects of acute particulate exposure on asthma were associated with changes in cysteinyl leukotriene (CysLTR 1 ) expression and methylation of CpG sites on CysLTR 1 and leukotriene C4 synthase genes [79].…”

Particulate matter exposure shapes DNA methylation through the lifespan

“…Another investigation conducted in New York City, NY, USA, showed how exposure to vanadium (considered as a trace metal component of PM), but not to PM 2.5 , was associated with lower DNA methylation of IL-4 (− 0.80, 95% Cl 0.65–0.98, p < 0.05) and IFN-γ (− 0.81, Cl 0.67–0.98); 6-day integrated levels of air pollutants were measured from homes of 163 children (ages 9–14), and repeated 6 months later [26]. The same authors determined also the effects of black carbon (BC) exposure on DNA methylation of pro-inflammatory genes linked to airway inflammation in asthmatic subjects.…”