Zorana Jovanovic Andersen

Background: Children’s cognitive development is influenced by dynamic interactions with the surrounding environment. Childhood adversity and air pollution have each been associated with poorer cognitive ability and school achievement. It is hypothesised that these exposures interact, such that cognitive ability in children experiencing high adversity is more vulnerable to the adverse effects of air pollution. However, this has not been examined at the population-level.Methods: We used data from the Danish Life Course (DANLIFE) cohort including information on 12 childhood adversities on all children born in Denmark during 1980-2001. The study population comprised 862,906 children with data on grade point average (GPA) from mandatory 9th-grade exit examinations. We used five previously established childhood adversity trajectory groups during ages 0-15: Low adversity, early life material deprivation, persistent material deprivation, loss or threat of loss, and high adversity. Annually modelled residential air pollution levels (PM2.5, PM10, and NO2) at a 1 km2 resolution during ages 0-15 were linked to each child. Using linear mixed-effects models (random intercept: school), we assessed interactions between childhood adversity groups and each air pollutant on GPA.Findings: Higher exposure to PM2.5 was significantly associated with lower GPA across all adversity groups, with the strongest association in the low adversity group (-0·81 [95% CI: -0·87;-0·74] GPA points per 5 µg/m3 increase in PM2.5) and the weakest in the high adversity group (-0·36 [-0·47;-0·24]). A similar but weaker pattern was observed for PM10, while NO2 showed heterogeneous patterns.Interpretation: Exposure to air pollution was associated with poorer school achievement across all childhood adversity groups. Contrary to our hypothesis, air pollution was most strongly associated with poorer school achievement in children experiencing low adversity. These findings suggest that, at the population-level, co-occurring social and environmental risks may not interact synergistically, reinforcing the importance of universal prevention strategies targeting both exposures.

Background: Prenatal exposure to ambient air pollution has been linked to autism spectrum disorder (ASD), but evidence from low-exposure settings such as Denmark remains limited. Objective: We aimed to examine the association between prenatal exposure to particulate matter with a diameter of ≤2.5 µm (PM _2.5 ), black carbon (BC), and nitrogen dioxide (NO ₂ ) and ASD in children, and to identify the most susceptible groups. Methods: We included 850,361 children born in Denmark between 1990 and 2004 and followed them for ASD diagnoses in the Danish Patient Register until age 15 years. We assigned prenatal PM _2.5 , BC, and NO ₂ levels (Danish Eulerian Hemispheric Model/Urban Background Model) at the mother’s residential address at delivery, and examined the association with ASD using logistic regression with a random intercept for municipality, including interaction terms to assess effect modification by sex, maternal age, smoking status, and socioeconomic status (SES). Results: An interquartile range increase in prenatal exposure to PM _2.5 , BC, and NO ₂ was associated with ASD (adjusted odds ratio; 95% confidence interval = 1.04; 1.00–1.07 per 2.8 µg/m ³ , 1.05; 1.03–1.08 per 0.3 µg/m ³ , and 1.15; 1.11–1.19 per 8 µg/m ³ , respectively). The association between BC and ASD persisted even after adjusting for PM _2.5 . Additionally, the associations between prenatal air pollution exposure and ASD were stronger among children born to older mothers. Conclusion: We found that prenatal exposure to air pollution was associated with ASD even at the relatively low exposure levels observed in Denmark, underscoring the importance of air pollution reduction for ASD prevention. The association with BC was independent of that with PM _2.5 , and children born to older mothers appeared to be particularly vulnerable.

Background: Ultrafine particles (≤100 nm diameter) may have a higher toxicity than larger particles but are still not regulated nor part of routine air pollution monitoring. So far, health effects of long-term exposure to ambient ultrafine particles are not well understood, owing to a lack of exposure data and epidemiological studies. Methods: We conducted a systematic review and meta-analysis on the health effects of long-term exposure to ultrafine particles, including studies published until December 2024. A meta-analysis was conducted for outcomes with at least four available effect estimates. Confidence in the body of evidence was evaluated using the Office of Health Assessment and Translation method. Results: We identified 85 studies investigating various mortality, morbidity and subclinical outcomes. In meta-analyses of single-pollutant models, we found positive associations with natural mortality (hazard ratio 1.06, 95% CI 1.04–1.08) and C-reactive protein (10.14% increase (95% CI −0.51–21.99%) per 10 000 pt·cm ⁻³ increase in long-term exposure to ultrafine particles, with low and inadequate levels of evidence, respectively. The remaining studies revealed overall limited evidence for adverse effects on a wide range of outcomes. Less than half of the studies adjusted for co-pollutants. Conclusion: The evidence base on long-term health effects of ultrafine particles has increased substantially in the past decade, while the overall evidence for independent effects of long-term ultrafine particle exposure remains inadequate to low. More studies are needed to draw firm conclusions about the independent adverse effects of long-term ultrafine particles on various health end-points, with a special focus on the influence of co-pollutant adjustment.

Black carbon (BC) is an air pollutant of emerging concern, and further evidence is needed to understand its health effects. This study investigates the association between gestational BC exposure and birth outcomes, and whether these effects are independent of particulate matter with an aerodynamic diameter of ≤ 2.5 μm (PM _2.5 ) exposure. We used data from the population-based birth cohort, Maternal Air Pollution in Southern Sweden (MAPSS) for the years 2000–2009, including 43,676 mother-child pairs. Maternal exposure to air pollution at residential address was estimated using a high-resolution dispersion model. We used logistic and linear regressions to examine association of air pollution with birth outcomes adjusting for maternal age, Body Mass Index, smoking, education, maternal country of birth, sex of the child, parity, household income, and birth year. We found that BC exposure during pregnancy was associated with birth weight (decrease of 69 g per 1 µg/m³ (95% Confidence Interval (CI): -96, -42) and small for gestational age (SGA) (odds ratio (OR) of 1.29 (95% CI: 1.05, 1.59; p = 0.015) per 1 µg/m³ increase in BC). BC exposure during the second trimester (OR of 1.79 (95% CI: 1.03, 3.09) and PM _2.5 during pregnancy (OR of 1.06 (95% CI: 1.01,1.12) were associated with Low Birth Weight (LBW). Associations with BC remained after adjustment for PM _2.5 . Our study contributes to further evidence of birth weight impact from BC exposure to an emerging pollutant of concern, even in a low-exposure environment. Further, we demonstrate effects of PM _2.5 , but also differentiate independent effects of these two correlated pollutants.

Supplementary Figure S5 shows the results for air pollutants and breast cancer of models including confounders violating the assumption of proportional hazards as strata

Supplementary Table S3 shows air pollution exposure extrapolated back to the time of enrolment and time-varying exposure analysis using residential history between enrolment and end-of follow-up based on the Danish Eulerian Hemispheric Model (DEHM). Extrapolation was performed using the absolute difference and the ratio between the baseline and 2010 periods.

Supplementary Figure S4 shows the natural cubic splines for air pollutants and breast cancer incidence

Supplementary Table S2 shows sensitivity analyses including additional confounders in the subset of the pooled cohort with the available information according to age