Effects of air pollution on telomere length: Evidence from in vitro to clinical studies

Assavanopakun, Pheerasak; Sapbamrer, Ratana; Kumfu, Sirinart; Chattipakorn, Nipon; Chattipakorn, Nipon

doi:10.1016/j.envpol.2022.120096

Cited by 11 publications

(7 citation statements)

References 61 publications

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“…A similar effect on ageing and cellular senescence has been suggested for various air pollutants, including particulate matter (PM2.5, PM10), NO, or cigarette smoke, and oxidative stress seems to be the most plausible mechanism of interaction [ 64 , 89 , 90 , 91 ]. The study by Kang et al verified the influence of TiO 2 -NP, revealing an increase in ROS production, activation of the p53-mediated response to ROS, and DNA damage in peripheral blood lymphocytes (obtained from a healthy donor) [ 29 ].…”

Section: Resultsmentioning

confidence: 65%

Molecular Mechanisms of N-Acetylcysteine in RSV Infections and Air Pollution-Induced Alterations: A Scoping Review

Wrotek,

Badyda,

Jackowska

2024

IJMS

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N-acetylcysteine (NAC) is a mucolytic agent with antioxidant and anti-inflammatory properties. The respiratory syncytial virus (RSV) is one of the most important etiological factors of lower respiratory tract infections, and exposure to air pollution appears to be additionally associated with higher RSV incidence and disease severity. We aimed to systematically review the existing literature to determine which molecular mechanisms mediate the effects of NAC in an RSV infection and air pollution, and to identify the knowledge gaps in this field. A search for original studies was carried out in three databases and a calibrated extraction grid was used to extract data on the NAC treatment (dose, timing), the air pollutant type, and the most significant mechanisms. We identified only 28 studies conducted in human cellular models (n = 18), animal models (n = 7), and mixed models (n = 3). NAC treatment improves the barrier function of the epithelium damaged by RSV and air pollution, and reduces the epithelial permeability, protecting against viral entry. NAC may also block RSV-activated phosphorylation of the epidermal growth factor receptor (EGFR), which promotes endocytosis and facilitates cell entry. EGFR also enhances the release of a mucin gene, MUC5AC, which increases mucus viscosity and causes goblet cell metaplasia; the effects are abrogated by NAC. NAC blocks virus release from the infected cells, attenuates the cigarette smoke-induced shift from necrosis to apoptosis, and reverses the block in IFN-γ-induced antiviral gene expression caused by the inhibited Stat1 phosphorylation. Increased synthesis of pro-inflammatory cytokines and chemokines is induced by both RSV and air pollutants and is mediated by the nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways that are activated in response to oxidative stress. MCP-1 (monocyte chemoattractant protein-1) and RANTES (regulated upon activation, expressed and secreted by normal T cells) partially mediate airway hyperresponsiveness (AHR), and therapeutic (but not preventive) NAC administration reduces the inflammatory response and has been shown to reduce ozone-induced AHR. Oxidative stress-induced DNA damage and cellular senescence, observed during RSV infection and exposure to air pollution, can be partially reversed by NAC administration, while data on the emphysema formation are disputed. The review identified potential common molecular mechanisms of interest that are affected by NAC and may alleviate both the RSV infection and the effects of air pollution. Data are limited and gaps in knowledge include the optimal timing or dosage of NAC administration, therefore future studies should clarify these uncertainties and verify its practical use.

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Section: Resultsmentioning

confidence: 65%

Molecular Mechanisms of N-Acetylcysteine in RSV Infections and Air Pollution-Induced Alterations: A Scoping Review

Wrotek,

Badyda,

Jackowska

2024

IJMS

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“…Fourth, genome-wide DNA methylation analyses suggest that exposure to long-term ambient air pollution can lead to alterations in DNA methylation whose functions are related to mitochondria and immune responses [ 49 ]. Fifth, air pollution has been associated with accelerated biological ageing as assessed using telomere length and DNA methylation ageing clocks [ 3 , 50 ]. And finally, exposure to air pollutants and noise can exacerbate numerous chronic conditions including cardiovascular or metabolic processes, increasing the risk of functional decline.…”

Section: Discussionmentioning

confidence: 99%

Exposure to residential traffic and trajectories of unhealthy ageing: results from a nationally-representative cohort of older adults

del Río,

Plans-Beriso,

Ramis

et al. 2024

Environ Health

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Background Traffic exposure has been associated with biomarkers of increased biological ageing, age-related chronic morbidities, and increased respiratory, cardiovascular, and all-cause mortality. Whether it is associated with functional impairments and unhealthy ageing trajectories is unknown. Methods Nationally representative population-based cohort with 3,126 community-dwelling individuals aged ≥60 years who contributed 8,291 biannual visits over a 10 year period. Unhealthy ageing was estimated with a deficit accumulation index (DAI) based on the number and severity of 52 health deficits, including 22 objectively-measured impairments in physical and cognitive functioning. Differences in DAI at each follow-up across quintiles of residential traffic density (RTD) at 50 and 100 meters, and closest distance to a petrol station, were estimated using flexible marginal structural models with inverse probability of censoring weights. Models were adjusted for sociodemographic and time-varying lifestyle factors, social deprivation index at the census tract and residential exposure to natural spaces. Results At baseline, the mean (SD) age and DAI score of the participants were 69.0 (6.6) years and 17.02 (11.0) %, and 54.0% were women. The median (IQR) RTD at 50 and 100 meters were 77 (31-467) and 509 (182-1802) vehicles/day, and the mean (SD) distance to the nearest petrol station of 962 (1317) meters. The average increase in DAI (95%CI) for participants in quintiles Q2-Q5 (vs Q1) of RTD at 50 meters was of 1.51 (0.50, 2.53), 0.98 (-0.05, 2.01), 2.20 (1.18, 3.21) and 1.98 (0.90, 3.05), respectively. Consistent findings were observed at 100 meters. By domains, most of the deficits accumulated with increased RTD were of a functional nature, although RTD at 50 meters was also associated with worse self-reported health, increased vitality problems and higher incidence of chronic morbidities. Living closer to a petrol station was associated with a higher incidence of functional impairments and chronic morbidities. Conclusions Exposure to nearby residential traffic is associated with accelerated trajectories of unhealthy ageing. Diminishing traffic pollution should become a priority intervention for adding healthy years to life in the old age.

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“…OS may accelerate telomere shortening by inhibiting telomerase activity. Assavanopakun et al [50] found that OS conditions are commonly associated with reduced telomere length. Furthermore, telomerase activity is related to the duration of OS.…”

Section: Os Mediates Telomere Length Reductionmentioning

confidence: 99%

Progress in Understanding Oxidative Stress, Aging, and Aging-Related Diseases

Yang,

Luo,

Tian

et al. 2024

Antioxidants

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Under normal physiological conditions, reactive oxygen species (ROS) are produced through redox reactions as byproducts of respiratory and metabolic activities. However, due to various endogenous and exogenous factors, the body may produce excessive ROS, which leads to oxidative stress (OS). Numerous studies have shown that OS causes a variety of pathological changes in cells, including mitochondrial dysfunction, DNA damage, telomere shortening, lipid peroxidation, and protein oxidative modification, all of which can trigger apoptosis and senescence. OS also induces a variety of aging-related diseases, such as retinal disease, neurodegenerative disease, osteoarthritis, cardiovascular diseases, cancer, ovarian disease, and prostate disease. In this review, we aim to introduce the multiple internal and external triggers that mediate ROS levels in rodents and humans as well as the relationship between OS, aging, and aging-related diseases. Finally, we present a statistical analysis of effective antioxidant measures currently being developed and applied in the field of aging research.

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Effects of air pollution on telomere length: Evidence from in vitro to clinical studies

Cited by 11 publications

References 61 publications

Molecular Mechanisms of N-Acetylcysteine in RSV Infections and Air Pollution-Induced Alterations: A Scoping Review

Molecular Mechanisms of N-Acetylcysteine in RSV Infections and Air Pollution-Induced Alterations: A Scoping Review

Exposure to residential traffic and trajectories of unhealthy ageing: results from a nationally-representative cohort of older adults

Progress in Understanding Oxidative Stress, Aging, and Aging-Related Diseases

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