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BACKGROUND: Telomere length is a molecular marker of biological aging. OBJECTIVE: Here we investigated whether early-life exposure to residential air pollution was associated with leukocyte telomere length (LTL) at 8 y of age. METHODS: In a multicenter European birth cohort study, HELIX (Human Early Life Exposome) (n=1,396), we estimated prenatal and 1-y childhood exposure to nitrogen dioxide (NO2), particulate matter with aerodynamic diameter ≤2:5 lm (PM2:5), and proximity to major roads. Average relative LTL was measured using quantitative real-time polymerase chain reaction (qPCR). Effect estimates of the association between LTL and prenatal, 1-y childhood air pollution, and proximity to major roads were calculated using multiple linear mixed models with a random cohort effect and adjusted for relevant covariates. RESULTS: LTL was inversely associated with prenatal and 1-y childhood NO2 and PM2:5 exposures levels. Each standard deviation (SD) increase in prenatal NO2 was associated with a −1:5% (95% CI: −2:8, −0:2) change in LTL. Prenatal PM2:5 was nonsignificantly associated with LTL (−0:7% per SD increase; 95% CI: −2:0, 0.6). For each SD increment in 1-y childhood NO2 and PM2:5 exposure, LTL shortened by −1:6% (95% CI: −2:9, −0:4) and −1:4% (95% CI: −2:9, 0.1), respectively. Each doubling in residential distance to nearest major road during childhood was associated with a 1.6% (95% CI: 0.02, 3.1) lengthening in LTL. CONCLUSION: Lower exposures to air pollution during pregnancy and childhood were associated with longer telomeres in European children at 8 y of age. These results suggest that reductions in traffic-related air pollution may promote molecular longevity, as exemplified by telomere length, from early life onward. [ABSTRACT FROM AUTHOR]

Highlights • Telomere lengths are cellular memories of exposures to inflammation and oxidative stress. • Residential green space, low traffic exposure, and long-term lower exposure to particulate air pollution are associated with longer telomeres. • Adverse environmental exposures may have a long lasting molecular footprint on the ageing process, as reflected by shorter telomere length. • Shorter telomeres reflect higher disease susceptibility and a potential shorter life expectancy. • Adequate reductions in, and protections against, pollutants may lead to decreased comorbidities and increased life-expectancy. Abstract Studies suggest that leukocyte telomere length is an index of systemic ageing. Here, we discuss telomere length as a marker of biological ageing in relation to residential landscape (greenness), residential air pollution and work-related exposures. Telomere lengths are memories of cumulative oxidative and inflammatory stress, and show to have inverse associations with the risk of non-communicable diseases. For this reason, telomeres are considered as markers of biological ageing. Studies at birth, in children, young adulthood, and elderly show that residential green space, lower traffic exposure and long-term lower exposure to particulate air pollution are associated with longer telomeres. Work-related exposures including exposure to toxic metals, polycyclic aromatic hydrocarbons and particulate matter are associated with shorter telomeres for a given age. In contrast to chronic exposures, evidence is present of the observation that recent exposure is associated with longer telomeres. Our overview shows that the magnitude of residential and work-related environmental factors on telomere length are often as important as many classical lifestyle factors. [ABSTRACT FROM AUTHOR]

Introduction Cardio-metabolic risk factors including insulin levels are at young age barely perceived as harmful, but over time these risk factors may track and lead to higher risk of metabolic syndrome. Studies showed that exposure to air pollution is associated with an increased risk of insulin resistance in childhood. We determined whether the origin of type 2 diabetes can be found in the early childhood by examining the levels of insulin in the neonatal cord blood and whether this can be considered as a disease marker for later life. Methods In the ENVIR ON AGE (ENVIRonmental influence ON early AGEing) birth cohort, we recruited 620 mother-infant pairs between February 2nd 2010 until August 12th 2014 at the East-Limburg Hospital in Genk, Belgium. We investigated in 590 newborns the association between cord plasma insulin levels and exposure to particulate matter (PM 2.5 and PM 10 ) and nitrogen dioxide (NO 2 ) in various exposure windows during pregnancy. Trimester-specific air pollutant exposure levels were estimated for each mother's home address using a spatiotemporal model. Results Cord plasma insulin levels averaged 33.1 pmol/L (25-75th percentile: 20.1-53.5), while PM 2.5 exposure during pregnancy averaged (SD) 13.7 μg/m 3 (2.4). Independent of maternal age, newborn's sex, birth weight, gestational age, parity, early-pregnancy BMI, ethnicity, smoking status, time of the day, maternal education, time of delivery, and season of delivery, cord plasma insulin levels increased with 15.8% (95% CI 7.8 to 24.4, p < 0.0001) for each SD increment in PM 2.5 levels during the entire pregnancy and was most pronounced in the 2nd trimester (13.1%, 95% CI 3.4 to 23.7, p = 0.007) of pregnancy. The results for PM 10 exposure were similar with those of PM 2.5 exposure but we did not observe an association between cord blood insulin levels and NO 2 exposure. Conclusions Exposure to particulate air pollution during pregnancy is associated with increased levels of cord plasma insulin at birth. The public health relevance of this association is demonstrated by the fact that a 2.4 μg/m 3 (SD) increase in PM 2.5 during pregnancy on cord plasma insulin levels corresponds to the effect-size of a 9 kg/m 2 higher early-pregnancy BMI on cord plasma. Particulate air pollution induced changes in cord plasma insulin levels during early life and might be a risk factor in the development of metabolic disease, such as glucose intolerance or type 2 diabetes, later in life. [ABSTRACT FROM AUTHOR]

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]