Effect of long-term air pollution reduction on insulin resistance and fasting glucose in children: A causal analysis

Observational studies have suggested that air pollution is associated with impaired glucose metabolism; yet randomized controlled trials to confirm the causality of this association are ethically and practically unfeasible. We emulated a hypothetical trial to evaluate the effects of sustained reductions in ambient air pollutants on homeostasis model assessment for insulin resistance (HOMA-IR) and fasting glucose (FG) in children and adolescents. Combining target trial emulation with g-computation, we estimated the effects of sustained hypothetical reductions of air pollutants on HOMA-IR and FG compared to no intervention (natural course). Our sample comprised 1417 children aged 2–9 years at baseline (2007/2008) participating in the pan-European IDEFICS/I.Family cohort. Ambient annual average levels of particulate matter<2.5 μm (PM_2.5), black carbon (BC), and NO₂ were estimated at residential addresses using land use regression models. We found a clear dose-response relationship between sustained reductions in PM_2.5 and BC and decreasing levels of HOMA-IR and FG. Hypothetically reducing PM_2.5 to WHO's recommended annual level of 5 μg/m³, the mean HOMA-IR z-score declined by −0.95 (95 % CI: −1.65; −0.44). Similarly, lowering BC to 0.8 × 10⁻⁵/m reduced HOMA-IR by −0.36 (95 % CI: −0.61; −0.12) and FG by −0.28 (95 % CI: −0.50; −0.04). We found no clear evidence of NO₂ reductions on HOMA-IR and FG. Even at relatively low pollution levels in our cohort, further reductions in PM_2.5 and BC can improve HOMA-IR and FG levels in children and adolescents. Our findings provide evidence for the development of BC recommendations for air quality guidelines.