Respir Res 2017 04 19;18(1):63. Epub 2017 Apr 19.
Division of Pulmonary, Allergy and Critical Care of Medicine, Department of Medicine, College of Physicians and Surgeons, Columbia University, PH8E-101, 630 W. 168 St., New York, NY, 10032, USA.
Background: Both 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 (PM) 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.
Methods: Six 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.
Results: Exposure to V, but not PM, 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 among asthmatic overweight or obese children but not nonasthmatics. Short-term exposure to PM, but not V, appeared associated with lower lung function (i.e., reduced z-scores for forced expiratory volume in one second (FEV, FEV/ forced vital capacity [FEV/FVC] and forced expiratory flow at 25-75% of FVC [FEF]).
Conclusions: Exposure 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 PM but not V, appeared associated with decrements in lung function among urban children.