Environment international · 2026
Ambient air pollution during pregnancy and offspring cerebral palsy.
СтатьяНазвание и аннотация: Перевод в очереди
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Zhuo Haoran, Ritz Beate, Su Jason G, Nianogo Roch A, Warren Joshua, Liew Zeyan
Аннотация
BACKGROUND: Cerebral palsy (CP) is a permanent neuromotor disorder with childhood onset, and the etiology for most cases remains unexplained.
METHODS: We conducted a population-based case-control study in California during 2000-2015, including all identified CP cases (N = 9,343) from the California's Department of Developmental Services and a control group of 20% random sample of live births without CP (N = 1,560,423). We employed a high-resolution (100 m) spatiotemporal model to estimate prenatal exposures to fine particulate matter (PM2.5), nitrogen dioxide (NO2), ozone (O3), and investigated their impacts on CP through single-pollutant, multiple-pollutant, and chemical-mixture models. Further, we examined the unmeasured confounding bias through the negative control exposure (NCE) design and assessed the potential heterogeneity across CP subtypes.
FINDINGS: Prenatal exposures throughout pregnancy to ambient NO2 (per interquartile-range, OR = 1.14, 95% CI, 1.10-1.18) and O3 (OR = 1.08, 95% CI, 1.05-1.11) were associated with higher odds of CP in offspring. A stronger association emerged when three pollutants were modelled as a mixture (OR = 1.23, 95% CI, 1.17-1.29), especially in the first and third trimesters. Potential interactions were noted across pollutants, with associations for NO2 and O3 strengthening in multiple-pollutant adjusted models or within strata of low PM2.5 (i.e., below the median). PM2.5 was positively associated with CP only in strata of low O3 (OR = 1.14, 95% CI, 1.09-1.19). The 36 months post-birth NCE was not associated with CP, suggesting no strong confounding bias. CP involving ataxic and dyskinetic motor dysfunction was more sensitive to O3 exposure.
CONCLUSIONS: Prenatal exposure to major ambient air pollutants was associated with offspring CP. Future studies to elucidate the underlying mechanisms are recommended.
METHODS: We conducted a population-based case-control study in California during 2000-2015, including all identified CP cases (N = 9,343) from the California's Department of Developmental Services and a control group of 20% random sample of live births without CP (N = 1,560,423). We employed a high-resolution (100 m) spatiotemporal model to estimate prenatal exposures to fine particulate matter (PM2.5), nitrogen dioxide (NO2), ozone (O3), and investigated their impacts on CP through single-pollutant, multiple-pollutant, and chemical-mixture models. Further, we examined the unmeasured confounding bias through the negative control exposure (NCE) design and assessed the potential heterogeneity across CP subtypes.
FINDINGS: Prenatal exposures throughout pregnancy to ambient NO2 (per interquartile-range, OR = 1.14, 95% CI, 1.10-1.18) and O3 (OR = 1.08, 95% CI, 1.05-1.11) were associated with higher odds of CP in offspring. A stronger association emerged when three pollutants were modelled as a mixture (OR = 1.23, 95% CI, 1.17-1.29), especially in the first and third trimesters. Potential interactions were noted across pollutants, with associations for NO2 and O3 strengthening in multiple-pollutant adjusted models or within strata of low PM2.5 (i.e., below the median). PM2.5 was positively associated with CP only in strata of low O3 (OR = 1.14, 95% CI, 1.09-1.19). The 36 months post-birth NCE was not associated with CP, suggesting no strong confounding bias. CP involving ataxic and dyskinetic motor dysfunction was more sensitive to O3 exposure.
CONCLUSIONS: Prenatal exposure to major ambient air pollutants was associated with offspring CP. Future studies to elucidate the underlying mechanisms are recommended.