Prenatal Exposure to Ambient Air Pollution and Cerebral Palsy

Author:

Zhang Yu1,Hu Yuhong1,Talarico Robert23,Qiu Xinye1,Schwartz Joel14,Fell Deshayne B.3567,Oskoui Maryam89,Lavigne Eric236,Messerlian Carmen1410

Affiliation:

1. Department of Environmental Health, Harvard T.H. Chan School of Public Heath, Boston, Massachusetts

2. Environmental Health Science and Research Bureau, Health Canada, Ottawa, Ontario, Canada

3. School of Epidemiology and Public Health, University of Ottawa, Ontario, Canada

4. Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, Massachusetts

5. Children’s Hospital of Eastern Ontario Research Institute, Ottawa, Ontario, Canada

6. ICES, Ottawa, Ontario, Canada

7. Now with Pfizer, Kirkland, Quebec, Canada

8. Department of Pediatrics, McGill University, Montreal, Quebec, Canada

9. Department of Neurology and Neurosurgery, McGill University, Montreal, Quebec, Canada

10. Massachusetts General Hospital Fertility Center, Department of Obstetrics and Gynecology, Boston

Abstract

ImportanceAir pollution is associated with structural brain changes, disruption of neurogenesis, and neurodevelopmental disorders. The association between prenatal exposure to ambient air pollution and risk of cerebral palsy (CP), which is the most common motor disability in childhood, has not been thoroughly investigated.ObjectiveTo evaluate the associations between prenatal residential exposure to ambient air pollution and risk of CP among children born at term gestation in a population cohort in Ontario, Canada.Design, Setting, and ParticipantsPopulation-based cohort study in Ontario, Canada using linked, province-wide health administrative databases. Participants were singleton full term births (≥37 gestational weeks) born in Ontario hospitals between April 1, 2002, and March 31, 2017. Data were analyzed from January to December 2022.ExposuresWeekly average concentrations of ambient fine particulate matter with a diameter 2.5 μm (PM2.5) or smaller, nitrogen dioxide (NO2), and ozone (O3) during pregnancy assigned by maternal residence reported at delivery from satellite-based estimates and ground-level monitoring data.Main outcome and measuresCP cases were ascertained by a single inpatient hospitalization diagnosis or at least 2 outpatient diagnoses for children from birth to age 18 years.ResultsThe present study included 1 587 935 mother-child pairs who reached term gestation, among whom 3170 (0.2%) children were diagnosed with CP. The study population had a mean (SD) maternal age of 30.1 (5.6) years and 811 745 infants (51.1%) were male. A per IQR increase (2.7 μg/m3) in prenatal ambient PM2.5 concentration was associated with a cumulative hazard ratio (CHR) of 1.12 (95% CI, 1.03-1.21) for CP. The CHR in male infants (1.14; 95% CI, 1.02-1.26) was higher compared with the CHR in female infants (1.08; 95% CI, 0.96-1.22). No specific window of susceptibility was found for prenatal PM2.5 exposure and CP in the study population. No associations or windows of susceptibility were found for prenatal NO2 or O3 exposure and CP risk.Conclusions and relevanceIn this large cohort study of singleton full term births in Canada, prenatal ambient PM2.5 exposure was associated with an increased risk of CP in offspring. Further studies are needed to explore this association and its potential biological pathways, which could advance the identification of environmental risk factors of CP in early life.

Publisher

American Medical Association (AMA)

Reference55 articles.

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