International audience | Artificial light at night (ALAN) can disrupt adaptive patterns of physiology and behavior that promote high fitness, resulting in physiological stress and elevation of steroid glucocorticoids (corticosterone, CORT in birds). Elevated CORT may have particularly profound effects early in life, with the potential for enduring effects that persist into adulthood. Research on the consequences of early-life exposure to ALAN remains limited, especially outside of the laboratory, and the effects of early-life light exposure on CORT concentrations in wild nestling birds remain to be elucidated. We used an experimental setup to test the hypothesis that ALAN elevates CORT concentrations in developing free-living birds, by exposing nestling great tits (Parus major) to ALAN inside nest boxes. We measured CORT in feathers grown over the timeframe of the experiment (7 nights), such that CORT concentrations represent an integrative metric of hormone release over the period of nocturnal light exposure, and of development. We also assessed the relationships between feather CORT concentrations, body condition, nestling size rank and fledging success. In addition, we evaluated the relationship between feather CORT concentrations and telomere length. Nestlings exposed to ALAN had higher feather CORT concentrations than control nestlings, and nestlings in poorer body condition and smaller brood members also had higher CORT. On the other hand, telomere length, fledging success, and recruitment rate were not significantly associated with light exposure or feather CORT concentrations. Results indicate that exposure to ALAN elevates CORT concentrations in nestlings, which may reflect physiological stress. In addition, the organizational effects of CORT are known to be substantial. Thus, despite the lack of effect on telomere length and survivorship, elevated CORT concentrations in nestlings exposed to ALAN may have subsequent impacts on later-life fitness and stress sensitivity.

Coke oven emissions (COEs), usually composed of polycyclic aromatic hydrocarbons (PAHs) and so on, may alter the relative telomere length of exposed workers and have been linked with adverse health events. However, the relevant biological exposure limits of COEs exposure has not been evaluated from telomere damage. The purpose of this study is to estimate benchmark dose (BMD) of urinary PAHs metabolites from COEs exposure based on telomere damage with RTL as a biomarker. A total of 544 exposed workers and 238 controls were recruited for participation. High-performance liquid chromatography and qPCR were used to detect concentrations of urinary mono-hydroxylated PAHs and relative telomere length in peripheral blood leukocytes for all subjects. The benchmark dose approach was used to estimate benchmark dose (BMD) and its lower 95% confidence limit (BMDL) of urinary OH-PAHs of COEs exposure based on telomere damage. Our results showed that telomere length in the exposure group (0.75 (0.51, 1.08)) was shorter than that in the control group (1.05 (0.76,1.44))(P < 0.05), and a dose-response relationship was shown between telomere damage and both 1-hydroxypyrene and 3-hydroxyphenanthrene in urine. The BMDL of urinary 1-hydroxypyrene from the optimal model for telomere damage was 1.96, 0.40, and 1.01 (μmol/mol creatinine) for the total, males, and females group, respectively. For 3-hydroxyphenanthrene, the BMDL was 0.94, 0.33, and 0.49 (μmol/mol creatinine) for the total, males, and females. These results contribute to our understanding of telomere damage induced by COEs exposure and provide a reference for setting potential biological exposure limits.

Growing evidence suggests that anthropogenic noise has deleterious effects on the behavior and physiology of free-living animals. These effects may be particularly pronounced early in life, when developmental trajectories are sensitive to stressors, yet studies investigating developmental effects of noise exposure in free-living populations remain scarce. To elucidate the effects of noise exposure during development, we examined whether noise exposure is associated with shorter telomeres, duller carotenoid-based coloration and reduced body mass in nestlings of a common urban bird, the great tit (Parus major). We also assessed how the noise environment is related to reproductive success. We obtained long-term measurements of the noise environment, over a ∼24-h period, and characterized both the amplitude (measured by LAₑq, LA₉₀, LA₁₀, LAₘₐₓ) and variance in noise levels, since more stochastic, as well as louder, noise regimes might be more likely to induce stress. In our urban population, noise levels varied substantially, with louder, but less variable, noise characteristic of areas adjacent to a highway. Noise levels were also highly repeatable, suggesting that individuals experience consistent differences in noise exposure. The amplitude of noise near nest boxes was associated with shorter telomeres among smaller, but not larger, brood members. In addition, carotenoid chroma and hue were positively associated with variance in average and maximum noise levels, and average reflectance was negatively associated with variance in background noise. Independent of noise, hue was positively related to telomere length. Nestling mass and reproductive success were unaffected by noise exposure. Results indicate that multiple dimensions of the noise environment, or factors associated with the noise environment, could affect the phenotype of developing organisms, that noise exposure, or correlated variables, might have the strongest effects on sensitive groups of individuals, and that carotenoid hue could serve as a signal of early-life telomere length.

Increasing evidence shows that impaired telomere function is associated with male infertility, and various environmental factors are believed to play a pivotal role in telomerase deficiency and telomere shortening. Benzo[a]pyrene (B[a]P), a ubiquitous pollutant of polycyclic aromatic hydrocarbons (PAHs), can act as a reproductive toxicant; however, the adverse effect of B[a]P on telomeres in male reproductive cells has never been studied, and the related mechanisms remain unclear. In this study, we explored the effects of benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE), the active metabolite of B[a]P, on telomere dysfunction in mouse spermatocyte-derived cells (GC-2) and also the potential role of telomerase in BPDE-induced spermatogenic cell damage. The results showed that BPDE induced cell viability inhibition, senescence, and apoptosis in GC-2 cells in a dose-dependent manner. Shortened telomeres, telomere-associated DNA damage, reduced telomerase activity, and TERT expression were also observed in BPDE-treated cells, accompanied with the activation of DNA damage response pathway (ATM/Chk1/p53/p21). Moreover, by establishing the TERT knockdown and re-expression cell models, we found that TERT regulated telomere length and the expression of DNA damage response-related proteins to influence senescence and apoptosis in GC-2 cells. These in vitro findings were further confirmed in vivo in the testicular cells of rats orally administrated with B[a]P for 7 days. B[a]P treatment resulted in histological lesions, apoptosis, and senescence in the testes of rats, which were accompanied by shortened telomeres, reduced levels of TERT protein, and increased expression of DNA damage response-related proteins. In conclusion, it can be concluded that TERT-mediated telomere dysfunction contributes to B[a]P- and BPDE-induced senescence and apoptosis through DNA damage response in male reproductive cells.

The contribution of diesel exhaust to atmospheric pollution is a major concern for public health, especially in terms of occurrence of lung cancers. The present study aimed at addressing the toxic effects of a repeated exposure to these emissions in an animal study performed under strictly controlled conditions. Rats were repeatedly exposed to the exhaust of diesel engine. Parameters such as the presence of a particle filter or the use of gasoil containing rapeseed methyl ester were investigated. Various biological parameters were monitored in the lungs to assess the toxic and genotoxic effects of the exposure. First, a transcriptomic analysis showed that some pathways related to DNA repair and cell cycle were affected to a limited extent by diesel but even less by biodiesel. In agreement with occurrence of a limited genotoxic stress in the lungs of diesel-exposed animals, small induction of γ-H2AX and acrolein adducts was observed but not of bulky adducts and 8-oxodGuo. Unexpected results were obtained in the study of the effect of the particle filter. Indeed, exhausts collected downstream of the particle filter led to a slightly higher induction of a series of genes than those collected upstream. This result was in agreement with the formation of acrolein adducts and γH2AX. On the contrary, induction of oxidative stress remained very limited since only SOD was found to be induced and only when rats were exposed to biodiesel exhaust collected upstream of the particle filter. Parameters related to telomeres were identical in all groups. In summary, our results point to a limited accumulation of damage in lungs following repeated exposure to diesel exhausts when modern engines and relevant fuels are used. Yet, a few significant effects are still observed, mostly after the particle filter, suggesting a remaining toxicity associated with the gaseous or nano-particular phases.

Air pollution remains the major environmental problem globally. There is extensive evidence showing that the variety of air pollutants from environmental and occupational exposures cause adverse effects to our health. The clinical symptoms of those effects may present at a late stage, so surveillance is difficult to manage. Several biomarkers have been used for the early detection of health issues following exposure to air pollution, including the use of telomere length which indicates cellular senescence in response to oxidative stress. Oxidative stress is one of the most plausible mechanisms associated with exposure to air pollutants. Some specific contexts including age groups, gender, ethnicity, occupations, and health conditions, showed significant alterations in telomere length after exposure to air pollutants. Several reports demonstrated both negative and positive associations between telomere length and air pollution, the studies using different concentrations and exposure times to air pollution on the study of telomere lengths. Surprisingly, some studies reported that low levels of exposure to air pollutants (lower than regulated levels) caused the alterations in telomere length. Those findings suggest that telomere length could be one of most practical biomarkers in air pollution surveillance. Therefore, this review aimed to summarize and discuss the relationship between telomere length and exposure to air pollution. The knowledge from this review will be beneficial for the planning of public health to reduce health problems in the general population, particularly in vulnerable people, who still live in areas with high air pollution.

Comprehensively understanding the factors affecting physiology and fitness in urban wildlife requires concurrently considering multiple stressors. To this end, we simultaneously assessed how metal pollution and proximity to roads affect body condition and telomere shortening between days 8 and 15 of age in nestling great tits (Parus major), a common urban bird. We employed a repeated-measures sampling design to compare telomere shortening and body condition between nestlings from four urban study sites south of Antwerp, Belgium, which are located at different distances from a metal pollution point source. In addition, we explored associations between metal exposure and telomere dynamics on the individual level by measuring blood concentrations of five metals/metalloids, of which lead, copper and zinc were present at concentrations above the limit of detection. To assess whether roadway-associated stressors (e.g. noise and air pollution) might affect nestling condition and telomere shortening, we measured the proximity of nest boxes to roads. Metal exposure was not associated with nestling telomere length or body condition, despite elevated blood lead concentrations close to the metal pollution source (mean ± SE = 0.270 ± 0.095 μg/g wet weight at the most polluted study site), suggesting that nestlings may have some capacity to detoxify metals. However, nestlings from nest boxes near roads exhibited more telomere shortening between days 8 and 15 of age, and shorter telomeres at day 15. Nestlings in poorer condition also had shorter telomeres, but proximity to the road was unrelated to body condition. Thus, nutritional stress is unlikely to mediate the relationship between proximity to roads and telomere length. Rather, proximity to roads could have affected telomere shortening by exposing nestlings to air or noise pollution. Our study highlights that traffic-related pollution, which is implicated in human health problems, might also affect urban wildlife.

Telomere length (TL) has been suggested to be a surrogate for cellular ageing, and a record of cumulative inflammation and oxidative stress over life. An emerging body of evidence has associated exposure to air pollution to changes in TL. To date there is no available systematic review of literature on this association. We aimed to systematically review and conduct meta-analysis of published studies on the relationship between air pollution and TL in adults. Electronic databases were systematically searched for available English language studies on the association between air pollution and TL published up to 1 July 2018. Meta-analyses were conducted following MOOSE guidelines. The heterogeneity in the reported associations was assessed using Cochran's Q test and quantified as I² index. Publication bias was assessed using Egger's regression. Our search identified 19 eligible studies including 11 retrospective and eight prospective studies of which, four had excellent quality, ten had good quality and five had fair quality. Meta-analysis result of two studies on long-term exposure to PM₂.₅ showed an inverse association between these exposures and TL (for 5 μg/m³ PM₂.₅–0.03 95% CI; −0.05, −0.01). Meta-analysis of short-term exposure to PM₂.₅ with three studies and Polychlorinated Biphenyls (PCBs) with two studies revealed a direct association between these exposures and TL (0.03 95% CI; 0.02, 0.04 and 0.10 95% CI; 0.06, 0.15 respectively). No statistically significant relationship between exposure to PM₁₀ and polycyclic aromatic hydrocarbons (PAHs) exposure and TL were observed. We observed suggestive evidence for associations between air pollution and TL with potentially different direction of associations for short- and long-term exposures.

Evidence has shown that leukocyte telomere length (LTL) at birth is related to the susceptibility to various diseases in later life and the setting of newborn LTL is influenced by the intrauterine environment. Perfluoroalkyl and polyfluoroalkyl substances (PFASs), as a kind of persistent organic pollutants, are commonly used in commercial and domestic applications and are capable of crossing the maternal-fetal barrier during pregnancy. We hypothesized that intrauterine exposure to PFASs may affect fetal LTL by increasing oxidative stress. To verify this hypothesis, LTL, concentrations of PFASs and reactive oxygen species (ROS) were measured in umbilical cord blood of 581 newborns from a prospective cohort. Our results showed that there were interactions between PFOS/PFDA and sex on LTL and ROS. The LTL was significantly shorter (0.926 ± 0.053 vs 0.945 ± 0.054, P = .023 for PFOS; 0.919 ± 0.063 vs 0.940 ± 0.059, P = .011 for PFDA) and the ROS levels were extremely higher (252.9 ± 60.5 [M] vs 233.5 ± 53.6 [M], P = .031 for PFOS; 255.2 ± 62.9 [M] vs 232.9 ± 58.3 [M], P = .011 for PFDA) in the female newborns whose PFOS or PFDA concentrations fell in the upmost quartile compared with those in the lowest quartile after adjusting for potential confounders. ROS levels were inversely associated with LTL in female newborns (β = −1.42 × 10⁻⁴, P = .022). 13% of the effect of PFOS on female LTL was mediated through ROS approximately by the mediation analyses. However, in male newborns, no relationships among PFASs, ROS and LTL were observed. Our findings suggest a “programming” role of PFASs on fetal telomere biology system in females in intrauterine stage.

Arsenic, cadmium and lead are toxic environmental contaminants. They were shown to be associated with telomere length (TL) in adults. Although they can cross the placental barrier, the effect of prenatal exposure of these metals on newborn TL is unknown. The aim of this study was to examine whether prenatal exposure to heavy metals has an impact on newborn leucocyte TL. A birth-cohort study was conducted with 409 pregnant women and their newborns in Myanmar. During the first visit, face-to-face interviews were conducted, and maternal spot urine sampling was performed. Cord blood samples were collected during follow-up. Urinary heavy metal concentration was measured by ICP-MS and adjusted for creatinine. Relative TL was measured by quantitative real-time polymerase chain reaction. The extent of prenatal arsenic, cadmium and lead exposure and their associations with newborn leucocyte TL were assessed using multivariate linear regression. The median values of maternal urinary arsenic, cadmium, and lead concentrations were 73.9, 0.9, and 1.8 μg/g creatinine, respectively. Prenatal arsenic and cadmium exposure was significantly associated with newborn TL shortening (lowest vs highest quartile, coefficient = - 0.13, 95% CI: - 0.22, - 0.03, p = 0.002, and coefficient = - 0.17, 95% CI: - 0.27, - 0.07, p = 0.001, respectively), and the associations remained robust after adjusting for confounders. There was no significant association between prenatal lead exposure and newborn TL. The present study identified the effect of arsenic and cadmium exposure on TL shortening, even in utero exposure at a lower concentration.