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

TY - JOUR

T1 - Early-Life Exposure to Ambient Air Pollution from Multiple Sources and Asthma Incidence in Children

T2 - A Nationwide Birth Cohort Study from Denmark

AU - Pedersen, Marie

AU - Liu, Shuo

AU - Zhang, Jiawei

AU - Andersen, Zorana Jovanovic

AU - Brandt, Jørgen

AU - Budtz-Jørgensen, Esben

AU - Bønnelykke, Klaus

AU - Frohn, Lise Marie

AU - Andersen, Anne-Marie Nybo

AU - Ketzel, Matthias

AU - Khan, Jibran

AU - Stayner, Leslie T.

AU - Brunekreef, Bert

AU - Loft, Steffen

PY - 2023/5

Y1 - 2023/5

N2 - 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 ≤2:5 lm (PM 2:5) and PM with aerodynamic diameter ≤10 lm (PM 10 ), nitrogen dioxide (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 propor-tional 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 increas-ing 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 addi-tional 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 lg=m 3 in prenatal exposure was 1.06 [95% confidence interval (CI): 1.04, 1.08] for PM 2:5 and 1.04 (95% CI: 1.02, 1.05) for NO 2, respectively. This association with PM 2:5 was stable after adjustment for NO 2, whereas it attenuated for NO 2 to 1.01 (95% CI: 0.99, 1.03) after adjustment for PM 2:5. For a 0:5-lg=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 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.

AB - 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 ≤2:5 lm (PM 2:5) and PM with aerodynamic diameter ≤10 lm (PM 10 ), nitrogen dioxide (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 propor-tional 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 increas-ing 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 addi-tional 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 lg=m 3 in prenatal exposure was 1.06 [95% confidence interval (CI): 1.04, 1.08] for PM 2:5 and 1.04 (95% CI: 1.02, 1.05) for NO 2, respectively. This association with PM 2:5 was stable after adjustment for NO 2, whereas it attenuated for NO 2 to 1.01 (95% CI: 0.99, 1.03) after adjustment for PM 2:5. For a 0:5-lg=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 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.

UR - http://www.scopus.com/inward/record.url?scp=85158866141&partnerID=8YFLogxK

U2 - 10.1289/EHP11539

DO - 10.1289/EHP11539

M3 - Journal article

C2 - 37162236

SN - 0091-6765

VL - 131

JO - Environmental Health Perspectives

JF - Environmental Health Perspectives

IS - 5

M1 - 057003

ER -