Early-Life Exposure to Ambient Air Pollution from Multiple Sources and Asthma Incidence in Children: A Nationwide Birth Cohort Study from Denmark

Abstract

Background: Ambient air pollution exposure has been associated with childhood asthma, but previous studies have primarily focused on prevalence of asthma and asthma-related outcomes and urban traffic-related exposures.

Objective: We examined nationwide associations between pre- and postnatal exposure to ambient air pollution components and asthma incidence in children age 0-19 y.

Methods: Asthma incidence was identified from hospital admission, emergency room, and outpatient contacts among all live-born singletons born in Denmark between 1998 and 2016. We linked registry data with monthly mean concentrations of particulate matter (PM) with aerodynamic diameter $\le 2.5\mu m$ (${\mathrm{PM}}_{2.5}$) and PM with aerodynamic diameter $\le 10\mu m$ (${\mathrm{PM}}_{10}$), nitrogen dioxide (${\mathrm{NO}}_2$), nitrogen oxides, elemental carbon, and organic carbon (OC), sulfur dioxide, ozone, sulfate, nitrate, ammonium, secondary organic aerosols, and sea salt. Associations were estimated with Cox proportional hazard models using fixed prenatal exposure means and time-varying postnatal exposures.

Results: Of the 1,060,154 children included, 6.1% had asthma during the mean follow-up period of 8.8 y. The risk of asthma increased with increasing prenatal exposure to all pollutants except for $O_3$ and sea salt. We also observed increased risk after restriction to asthma after age 4 y, after additional adjustment for area-specific socioeconomic status, and for postnatal exposure to most pollutants. The hazard ratio (HR) associated with an interquartile range increase of 2.4 and $8.7{\mu g/m}^3$ in prenatal exposure was 1.06 [95% confidence interval (CI): 1.04, 1.08] for ${\mathrm{PM}}_{2.5}$ and 1.04 (95% CI: 1.02, 1.05) for ${\mathrm{NO}}_2$, respectively. This association with ${\mathrm{PM}}_{2.5}$ was stable after adjustment for ${\mathrm{NO}}_2$, whereas it attenuated for ${\mathrm{NO}}_2$ to 1.01 (95% CI: 0.99, 1.03) after adjustment for ${\mathrm{PM}}_{2.5}$. For a $0.5{-\mu g/m}^3$ increase in prenatal OC exposure, for which biomass is an important source, the HR was 1.08 (95% CI: 1.06, 1.10), irrespective of adjustment for ${\mathrm{PM}}_{2.5}$.

Discussion: These findings suggest that early-life exposure to ambient air pollution from multiple sources contributes to asthma development. https://doi.org/10.1289/EHP11539.

Figure 1.

Maps of estimated annual exposure to ambient air pollution with ${\mathrm{PM}}_{2.5}$ (top) and ${\mathrm{NO}}_2$ (bottom). The maps on the left show annual mean background concentrations (${\mathrm{\mu }\mathrm{g}/\mathrm{m}}^3$) for 2005 for Denmark in a $1\mathrm{km}\times 1\mathrm{km}$ spatial resolution estimated with the DEHM-UBM AirGIS modeling system described in this work without the contribution from local traffic. The maps to the right are annual concentrations at the specific address locations of those included in the cohort, including the local traffic contribution for 2018 for smaller areas of the city center of Copenhagen and Præstø as example of remote nonurban location. The color scale is in quantiles (not equidistant level ranges) with blue colors referring to the lowest concentrations and red colors to the highest concentrations. The maps are produced using R/RStudio/Shiny/Leaflet programming packages and background maps are Esri.WorldGrayCanvas © Esri, DeLorme, NAVTEQ. Note: ${\mathrm{NO}}_2$, nitrogen dioxide; ${\mathrm{PM}}_{2.5}$, particulate matter with an aerodynamic diameter $<2.5\mathrm{\mu }\mathrm{m}$.