Association between childhood cancer and prenatal exposure to ambient PM2.5 and NO2: a population-based cohort study in Canada.
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BACKGROUND: Prenatal exposure to air pollution may be a risk factor for childhood cancer, but epidemiological evidence is scarce. OBJECTIVE: We investigated whether prenatal exposure to ambient fine particulate matter (PM2.5) and nitrogen dioxide (NO2) was associated with childhood cancer incidence. METHODS: We conducted a cohort study of 1,121,996 newborns in Quebec, Canada, from 2006 to 2020, with follow-up through 2023. Prenatal exposure was estimated at maternal residence using biweekly PM2.5 and weekly NO2 concentrations from satellite-based and land-use regression models, respectively. We estimated associations with any cancer, central nervous system (CNS) tumor and leukemia diagnosed before age 14 years using Cox proportional hazard models adjusted for potential confounders. We examined single- and two-pollutant models and assessed effect modification by maternal and child characteristics, including maternal comorbidity. RESULTS: The cohort included 2,187 incident cancer cases. Adjusted hazard ratios (HR) for any cancer were 1.08 (95 % CI: 0.99-1.17) and 1.06 (95 % CI: 0.98-1.15) per interquartile increase in PM2.5 (2.4 μg/m3) and NO2 (4.8 μg/m3). For CNS tumors, we found positive associations but only in children aged ≥7 years; the HR was 1.35 (95 % CI: 0.98-1.88) for PM2.5 and 1.36 (95 % CI: 0.99-1.88) for NO2. Associations with acute lymphoblastic leukemia (ALL) were 1.06 (95 % CI: 0.90-1.25) for PM2.5 and 1.15 (95 % CI: 0.98-1.37) for NO2. For acute myeloid leukemia (AML), a positive association was suggested for PM2.5 (HR = 1.15; 95 % CI: 0.77-1.70), but the number of cases was low (n = 95). Associations appeared greater among children whose mothers had comorbidities. CONCLUSION: Prenatal exposure to ambient PM2.5 and NO2 may be associated with childhood cancer. Particularly, CNS tumors in children ≥7 years were associated with both pollutants, ALL with NO2, and AML showed suggestive associations with PM2.5. Maternal comorbidities may further increase risk, underscoring the need for large studies to confirm these findings and clarify underlying mechanisms.