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Telomere length (TL) and mitochondrial DNA (mtDNA) are central markers of vital biological mechanisms, including cellular aging. Prenatal air pollution exposure may impact molecular markers of aging leading to adverse health effects. To perform a systematic review on human population-based studies investigating the association between prenatal air pollution exposure and TL or mtDNA content at birth. Searches were undertaken on PubMed and Web of Science until July 2023. The framework of the review was based on the PRISMA-P guidelines. Nineteen studies studied prenatal air pollution and TL or mtDNA content at birth. Studies investigating TL or mtDNA content measured at any other time or did not evaluate prenatal air pollution were excluded. Twelve studies (including 4381 participants with study sample range: 97 to 743 participants) investigated newborn TL and eight studies (including 3081 participants with study sample range: 120 to 743 participants) investigated mtDNA content at birth. Seven studies focused on particulate matter (PM 2.5) exposure and newborn TL of which all, except two, showed an inverse association in at least one of the gestational trimesters. Of the eight studies on mtDNA content, four focused on PM 2.5 air pollution with two of them reporting an inverse association. For PM 2.5 exposure, observations on trimester-specific effects were inconsistent. Current literature showing associations with other prenatal air pollutants (including nitrogen oxides, sulfur dioxide, carbon monoxide and ozone) is inconsistent. This review provides initial evidence that prenatal PM 2.5 exposure impacts the telomere-mitochondrial axis of aging at birth. The current evidence did not reveal harmonious observations for trimester-specific associations nor showed consistent effects of other air pollutants. Future studies should elucidate the specific contribution of prenatal exposure to pollutants other than PM in relation to TL and mtDNA content at birth, and the potential later life health consequences. [ABSTRACT FROM AUTHOR]

• Chronic exposure to PM 2.5 is associated with lower child buccal telomere length. • Chronic exposure to PM 2.5 is associated with lower child mitochondrial DNA content. • Recent traffic related air pollution is associated with lower child telomere length. Pro-inflammatory conditions such as air pollution might induce biological ageing. However, the available evidence on such an impact in children is still very scarce. We studied in primary schoolchildren the association of ambient residential air pollution exposure with telomere length (TL) and mitochondrial DNA content (mtDNAc), two important targets of the core axis of ageing. Between 2012 and 2014, buccal TL and mtDNAc were repeatedly assessed using qPCR in 197 Belgian primary schoolchildren (mean age 10.3 years) as part of the COGNAC study. At the child's residence, recent (week), sub-chronic (month) and chronic (year) exposure to nitrogen dioxide (NO 2), particulate matter ≤ 2.5 µm (PM 2.5) and black carbon (BC) were estimated using a high resolution spatiotemporal model. A mixed-effects model with school and subject as random effect was used while adjusting for a priori chosen covariates. An interquartile range (IQR) increment (1.9 µg/m3) in chronic PM 2.5 exposure was associated with a 8.9% (95% CI: −15.4 to −1.9%) shorter TL. In contrast to PM 2.5 , chronic exposure to BC and NO 2 was not associated with TL but recent exposure to BC and NO 2 showed significant inverse associations with TL: an IQR increment in recent exposure to BC (0.9 µg/m3) and NO 2 (10.2 µg/m3) was associated with a 6.2% (95% CI: −10.6 to −1.6%) and 6.4% (95% CI: −11.8 to −0.7%) shorter TL, respectively. Finally, an IQR increment in chronic PM 2.5 exposure was associated with a 12.7% (95% CI: −21.7 to −2.6%) lower mtDNAc. However, no significant associations were seen for NO 2 and BC or for other exposure windows. Chronic exposure to PM 2.5 below the EU threshold was associated with child's shorter buccal TL and lower mtDNAc, while traffic-related pollutants (BC and NO 2) showed recent effects on telomere biology. Our data add to the literature on air pollution-induced effects of TL and mtDNAc, two measures part of the core axis of cellular ageing, from early life onwards. [ABSTRACT FROM AUTHOR]