Prenatal exposure to ambient air pollution predicts telomere length and mitochondrial DNA content in 7-year old children

Introduction: In recent years, studies have emphasized the importance of air pollutants in the formation of reactive oxygen species and inflammation, leading to shorter telomere length and lower mtDNA content. We hypothesize that both telomere length and mitochondrial DNA (mtDNA) content at 7 years of age are inversely associated with prenatal air pollution exposure.

Methods: In this preliminary analysis we used subjects of the sub-cohort of the HELIX project (n=928). Prenatal particulate matter with an aerodynamic diameter < 10 µm (PM₁₀) and nitrogen dioxide (NO2) exposure were estimated using the ESCAPE land-use regression models. Relative telomere length and relative mtDNA content were measured by using real time polymerase chain reaction (qPCR). Effect estimates were calculated using multiple linear mixed models with a random cohort effect and adjusting for relevant covariates.

Results: Preliminary analyses show that both telomere length and mtDNA content at 7 years of age (ranging from 6-11 years) were negatively associated with prenatal NO2 and prenatal PM₁₀ exposure. Each 10 µg/m³ increment in average pregnancy NO2 exposure was associated with shorter telomeres of 18.7% (95% Confidence interval (CI): -25.8, -10.8) at age 7 years. Furthermore, each 10 µg/m³ increase in average pregnancy PM₁₀ exposure was associated with a shorter telomere length of 3.2% (95% CI: -5.5, -0.7) and with a lower mtDNA content of 9.9% (95% CI: -13.0, -6.7) at 7 years of age.

Conclusion: These preliminary results show an inverse relationship between telomere length and mtDNA content at 7 years of age, both considered as molecular markers of ageing, and prenatal air pollution exposure.