Intrauterine and early postnatal exposures to submicron particulate matter and childhood allergic rhinitis: A multicity cross-sectional study in China.

Airborne particulate matter pollution has been linked to occurrence of childhood allergic rhinitis (AR). However, the relationships between exposure to particulate matter with an aerodynamic diameter ≤1 μm (PM 1) during early life (in utero and first year of life) and the onset of childhood AR remain largely unknown. This study aims to investigate potential associations of in utero and first-year exposures to size-segregated PMs, including PM 1 , PM 1–2.5 , PM 2.5 , PM 2.5–10 , and PM 10 , with childhood AR. We investigated 29286 preschool children aged 3–6 years in 7 Chinese major cities during 2019–2020 as the Phase II of the China Children, Families, Health Study. Machine learning-based space-time models were utilized to estimate early-life residential exposure to PM 1 , PM 2.5 , and PM 10 at 1 × 1-km resolutions. The concentrations of PM 1–2.5 and PM 2.5–10 were calculated by subtracting PM 1 from PM 2.5 and PM 2.5 from PM 10 , respectively. Multiple mixed-effects logistic models were used to assess the odds ratios (ORs) and 95% confidence intervals (CIs) of childhood AR associated with per 10-μg/m3 increase in exposure to particulate air pollution during in utero period and the first year of life. Among the 29286 children surveyed (mean ± standard deviation, 4.9 ± 0.9 years), 3652 (12.5%) were reported to be diagnosed with AR. Average PM 1 concentrations during in utero period and the first year since birth were 36.3 ± 8.6 μg/m3 and 33.1 ± 6.9 μg/m3, respectively. Exposure to PM 1 and PM 2.5 during pregnancy and the first year of life was associated with an increased risk of AR in children, and the OR estimates were higher for each 10-μg/m3 increase in PM 1 than for PM 2.5 (e.g., 1.132 [95% CI: 1.022–1.254] vs. 1.079 [95% CI: 1.014–1.149] in pregnancy; 1.151 [95% CI: 1.014–1.306] vs. 1.095 [95% CI: 1.008–1.189] in the first year of life). No associations were observed between AR and both pre- and post-natal exposure to PM 1–2.5 , indicating that PM 1 rather than PM 1–2.5 contributed to the association between PM 2.5 and childhood AR. In trimester-stratified analysis, childhood AR was only found to be associated with exposure to PM 1 (OR = 1.077, 95% CI: 1.027–1.128), PM 2.5 (OR = 1.048, 95% CI: 1.018–1.078), and PM 10 (OR = 1.032, 95% CI: 1.007–1.058) during the third trimester of pregnancy. Subgroup analysis suggested stronger PM-AR associations among younger (<5 years old) and winter-born children. Prenatal and postnatal exposures to ambient PM 1 and PM 2.5 were associated with an increased risk of childhood AR, and PM 2.5 -related hazards could be predominantly attributed to PM 1. These findings highlighted public health significance of formulating air quality guideline for ambient PM 1 in mitigating children's AR burden caused by particulate air pollution. • The first study evaluated early-life exposure to ambient PM 1 and childhood AR. • Increased childhood AR risk associated with prenatal and postnatal exposures to ambient PM 1 and PM 2.5. • Later trimesters of gestation might be the sensitive window for early-life PM exposure and childhood AR. • Enhanced effect of early-life PM exposure on childhood AR was observed among younger and winter-born children. [ABSTRACT FROM AUTHOR]