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Impact of exposure to air pollution on asthma: A multi-exposure assessment

Principal Investigator: 

University of Copenhagen, Denmark

This New Investigator Award study will evaluate whether air pollution is associated with increased incidence of asthma in 3 cohorts in Denmark.

Funded under
In review

Poster abstract for HEI Annual Conference 2022

Long-term exposure to ambient air pollution and asthma incidence in children

Marie Pedersen1, Shuo Liu,1 Zorana Jovanovic Andersen,1 Anne-Marie Nybo Andersen, 1 Hans Bisgaard,2 Jørgen Brandt,3 Esben Budtz-Jørgensen,1 Klaus Bønnelykke,2 Lise Marie Frohn,3 Leslie Stayner,4 Jibran Khan, 3 Matthias Ketzel,3 Bert Brunekreef5, Steffen Loft1

1University of Copenhagen, Copenhagen, Denmark; 2Gentofte hospital, Copenhagen, Denmark; 3Aarhus University, Roskilde, Denmark; 4University of Illinois at Chicago, USA; 5Utrecht University, Utrecht, the Netherlands

Background. Long-term exposure to ambient air pollution with particulate matter ≤ 2.5 μm (PM2.5) and nitrogen dioxides (NO2) has been associated with asthma onset in childhood, but existing evidence is limited, and most often, effects of air pollutants have been estimated individually without estimation of the effect of multiple pollutants simutaneously. We investigated the effects of early-life exposure to ambient PM2.5 and NO2 on asthma development in children aged 0-18 years.

Methods. We included all live-born singletons born in Denmark during 1998-2016. We used the unique personal identification number for data linkage and extracted information about asthma, personal characteristics and residential address history from national registers. We defined incidence of asthma as the first registered diagnosis according to ICD-10 codes J45* or J46* from the Danish National Patient Register of  inpatient admissions, emergency room and outpatients contacts for all children. Monthly mean concentrations of PM2.5 and NO2 from all sources were modelled using the multiscale DEHM-UBM-AirGIS dispersion model system. Prenatal and postnatal mean exposures were calculated, taking all residential addresses into account, and using gestational age and date of diagnosis. We used Cox proportional hazard models with age as the time dimension and adjustment for calendar year, sex, parity, season, household income, maternal education, municipality and smoking during pregnancy to estimate hazard ratios (HRs) and 95% confidence intervals (95%CIs) fitted with time-weighted average exposures for the prenatal period (fixed exposure means) and time-varying annual average exposure a year before the event for the postnatal follow-up period (running means).   

Results. Out of the 1,060,154 children, 6.1% had asthma during the mean follow-up of 8.8 years. The prenatal mean (IQR) concentrations of PM2.5 and NO2 were 10.5(2.4) and 17.5(8.7) mg/m3. An IQR increase in prenatal exposure was associtated with an adjusted HR of 1.06 (95% CI: 1.04, 1.08) for PM2.5 and 1.04 (95% CI: 1.02, 1.05) for NO2. The corresponding estimates for postnatal exposures were 1.08 (1.05, 1.10) and 1.02 (1.01, 1.04), respectively. For both pollutants, the associations with postnatal exposures were robust to adjustment for prenatal exposures. For prenatal NO2 the association attenuated to 1.01 (95% CI: 0.99, 1.03) after adjustment for prental exposure to PM2.5 while the association with prenatal exposure to PM2.5 in a two-pollutant model adjusted for prenatal exposure to NO2 was 1.05 (95%CI: 1.03, 1.08). The smaller attenuation of the associations for PM2.5 after mutually adjustment for prenatal exposure to NO2 suggests that the effect of PM2.5 was more robust than the effect associated with NO2.  

Conclusions. Our findings strengthen the growing evidence that supports that long-term exposure to ambient PM2.5 and NO2 contribute to asthma development in children.