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.
Highlights
Both short and long-term exposure to traffic-related air pollutants have been associated with asthma and reduced lung function
We focused on vanadium (V) as the trace metal Particulate matter (PM) component because previous studies have shown that ambient levels of V, emitted from the burning of residual oil fuel mainly from residential heating and shipping ports [6] and traffic emissions [7], exhibited marked spatial variability in New York City (NYC) [8]
When the two heating vs nonheating season was replaced with four seasons, the significant associations of PM2.5 and lung function outcomes were replicated. In this nested cohort of African American and Dominican children living in NYC, we found that that 6 day-integrated residential V, but not PM2.5, was associated with lower buccal cell promoter DNA methylation of asthma T helper (Th) gene (i.e. Interleukin 4 (IL4), Interferon gamma (IFNγ)) loci, even after controlling for methylation levels 6 days previously
Summary
Both short and long-term exposure to traffic-related air pollutants have been associated with asthma and reduced lung function. Jung et al Respiratory Research (2017) 18:63 hospitalizations [10], 3) mortality among elderly individuals [11], and 4) wheeze [12] and decreased lung function (i.e., forced vital capacity (FVC)) among children [13]. In the latter case, the V findings persisted after adjusting for co-pollutants (e.g., PM2.5 or elemental carbon (EC)), suggesting that V itself may be an important independent contributor of adverse respiratory effects of PM2.5. Overweight asthmatics exhibited more asthma-like symptoms in association with exposure to PM2.5, nitrogen dioxide (NO2) and polycyclic aromatic hydrocarbons (PAH) [16, 17], and greater declines in lung function in association with exposure to ozone [14]
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