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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 2.5 ) 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.    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 2.5 , 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 PM 2.5 , but not V, appeared associated with lower lung function (i.e., reduced  z -scores for forced expiratory volume in one second (FEV 1 , FEV 1 / forced vital capacity [FEV 1 /FVC] and forced expiratory flow at 25–75% of FVC [FEF 25–75 ]).    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 2.5,  but not V, appeared associated with decrements in lung function among urban children.    Electronic supplementary material  The online version of this article (doi:10.1186/s12931-017-0550-9) contains supplementary material, which is available to authorized users.

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