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 (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. 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. Exposure 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]). 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 PM2.5, but not V, appeared associated with decrements in lung function among urban children.

Asthma gene DNA methylation may underlie the effects of air pollution on airway inflammation. However, the temporality and individual susceptibility to environmental epigenetic regulation of asthma has not been fully elucidated. Our objective was to determine the timeline of black carbon (BC) exposure, measured by personal sampling, on DNA methylation of allergic asthma genes 5 days later to capture usual weather variations and differences related to changes in behavior and activities. We also sought to determine how methylation may vary by seroatopy and cockroach sensitization and by elevated fractional exhaled nitric oxide (FeNO). Personal BC levels were measured during two 24-h periods over a 6-day sampling period in 163 New York City children (age 9–14 years), repeated 6 months later. During home visits, buccal cells were collected as noninvasive surrogates for lower airway epithelial cells and FeNO measured as an indicator of airway inflammation. CpG promoter loci of allergic asthma genes (e.g., interleukin 4 (IL4), interferon gamma (IFNγ), inducible nitric oxide synthase (NOS2A)), arginase 2 (ARG2)) were pyrosequenced at the start and end of each sampling period. Higher levels of BC were associated with lower methylation of IL4 promoter CpG−48 5 days later. The magnitude of association between BC exposure and demethylation of IL4 CpG−48 and NOS2A CpG+5099 measured 5 days later appeared to be greater among seroatopic children, especially those sensitized to cockroach allergens (RR [95% CI] 0.55 [0.37–0.82] and 0.67 [0.45–0.98] for IL4 CpG−48 and NOS2A CpG+5099, respectively), compared to non-sensitized children (RR [95% CI] 0.87 [0.65–1.17] and 0.95 [0.69–1.33] for IL4 CpG−48 and NOS2A CpG+5099, respectively); however, the difference was not statistically different. In multivariable linear regression models, lower DNA methylation of IL4 CpG−48 and NOS2A CpG+5099 were associated with increased FeNO. Our results suggest that exposure to BC may exert asthma proinflammatory gene demethylation 5 days later that in turn may link to airway inflammation. Our results further suggest that seroatopic children, especially those sensitized to cockroach allergens, may be more susceptible to the effect of acute BC exposure on epigenetic changes.

In the 1930’s the United States (US) sponsored Home Owners’ Loan Corporation (HOLC) created maps that determined risk for mortgage lending based on the racial and ethnic composition of neighborhoods leading to disinvestment in “redlined” or highest risk neighborhoods. This historical practice has perpetuated racial and economic segregation, and health disparities, that persist today. Interventions near schools where children spend large portions of the day, could impact large groups of children but schools are an often-overlooked environment for exposure. Despite a declining trend of ambient pollution in New York City (NYC) between 1998 and 2012, little is known about differences in air quality improvement near schools by historical redlining neighborhood status. Our objective was to examine if recent temporal trends of air pollution near NYC public schools differed in historically redlined neighborhoods. We examined annual average street-level concentrations of combustion-related air pollutants (black carbon (BC), particulate matter (PM_2.5), nitrogen dioxide (NO₂), and nitric oxide (NO)), within a 250-m radius around schools using NYC Community Air Survey land-use regression models (n = 1,462). Year of monitoring, historical redlining (binary), and summer ozone were included in multivariable linear regression using generalized estimating equation models. Average annual percent change (APC) in pollutant concentration was calculated. Models were further stratified by historical redlining and a multiplicative interaction term (year of monitoring × historical redlining) was used to assess effect modification. Overall, there was a decreasing trend of BC (APC = −4.40%), PM_2.5 (−3.92%), NO₂ (−2.76%), and NO (−6.20%) during the 10-year period. A smaller reduction of BC, PM_2.5 and NO was observed in redlined neighborhoods (n = 722), compared to others (n = 740): BC (APC: −4.11% vs −4.69%; P_interaction < 0.01), PM_2.5 (−3.82% vs −4.11%; P_interaction < 0.01), and NO (−5.73% vs −6.67%; P_interaction < 0.01). Temporal trends of NO₂ did not differ by historical redlining (P_interaction = 0.60). Despite significant reductions in annual average pollution concentrations across NYC, schools in historically redlined neighborhoods, compared to others, experienced smaller decrease in pollution, highlighting a potential ongoing ramification of the discriminatory practice.

Physical activity is associated with improvement in lung function; however, pollution exposure during physical activity can lead to a transient reduction in lung function. This paradoxical relationship may be linked to altered T regulatory (Treg) cell activity, which increases with exercise and suppresses airway inflammation, but decreases in association with exposure to air pollution. To clarify these relationships, we investigated buccal cell DNA methylation of the forkhead box p3 (FOXP3) gene promoter, a proposed biomarker of Treg activity. We hypothesized that active urban children would have lower FOXP3 promoter methylation, associated with better lung function compared to non-active children. We also hypothesized that this relationship would be attenuated by high exposure to the air pollutant black carbon (BC). We performed a cross-sectional study of 135 children ages 9–14 who live in New York City. Activity was measured across 6 days. BC exposure was assessed by personal monitors worn for two 24-h periods, followed by lung function assessment. Buccal swabs were collected for DNA methylation analysis of three regions (six CpG sites) in the FOXP3 promoter. In multivariable regression models, overall, there was no significant relationship between physical activity and FOXP3 promoter methylation (p > 0.05). However, in stratified analyses, among children with higher BC exposure (≥1200 ng/m3), physical activity was associated with 2.37% lower methylation in promoter 2 (CpGs −77, −65, and −58) (β estimate = −2.37%, p < 0.01) but not among those with lower BC exposure (β estimate = 0.54%, p > 0.05). Differences across strata were statistically significant (p interaction = 0.04). Among all children, after controlling for BC concentration, promoter 2 methylation was associated with reduced FEV1/FVC (β estimate = −0.40%, p < 0.01) and reduced FEF25–75% (β estimate = −1.46%, p < 0.01). Physical activity in urban children appeared associated with lower FOXP3 promoter methylation, a possible indicator of greater Treg function, under conditions of high BC exposure. Reduced FOXP3 promoter methylation was associated with higher lung function. These findings suggest that physical activity may induce immunologic benefits, particularly for urban children with greater risk of impaired lung function due to exposure to higher air pollution. FOXP3 promoter buccal cell methylation may function as a useful biomarker of that benefit.

Background: Outdoor ambient polycyclic aromatic hydrocarbon (PAH) concentrations are variable throughout an urban environment. However, little is known about how variation in semivolatile and nonvolatile PAHs related to the built environment (open space vs. semi-closed space) contributes to differences in concentrations. Methods: We simultaneously collected 14, two-week samples of PAHs from the outside of windows facing the front (adjacent to the street) open side of a New York City apartment building and the alley, semi-closed side of the same apartment unit between 2007 and 2012. We also analyzed samples of PAHs measured from 35 homes across Northern Manhattan and the Bronx, 17 from street facing windows with a median floor level of 4 (range 2–26) and 18 from alley-facing windows with a median floor level of 4 (range 1–15). Results: Levels of nonvolatile ambient PAHs were significantly higher when measured from a window adjacent to a street (an open space), compared to a window 30 feet away, adjacent to an alley (a semi-closed space) (street geometric mean (GM) 1.32 ng/m³, arithmetic mean ± standard deviation (AM ± SD) 1.61 ± 1.04 ng/m³; alley GM 1.10 ng/m³, AM ± SD 1.37 ± 0.94 ng/m³). In the neighborhood-wide comparison, nonvolatile PAHs were also significantly higher when measured adjacent to streets compared with adjacent to alley sides of apartment buildings (street GM 1.10 ng/m³, AM ± SD 1.46 ± 1.24 ng/m³; alley GM 0.61 ng/m³, AM ± SD 0.81 ± 0.80 ng/m³), but not semivolatile PAHs. Conclusions: Ambient PAHs, nonvolatile PAHs in particular, are significantly higher when measured from a window adjacent to a street compared to a window adjacent to an alley, despite both locations being relatively close to street traffic. This study highlights small-scale spatial variations in ambient PAH concentrations that may be related to the built environment (open space vs. semi-closed space) from which the samples are measured, as well as the relative distance from street traffic, that could impact accurate personal exposure assessments.