Air pollution and telomere length in adults: A systematic review and meta-analysis of observational studies

Miri, Mohammad; Nazarzadeh, Milad; Alahabadi, Ahmad; Ehrampoush, Mohammad Hassan; Rad, Abolfazl; Lotfi, Mohammad Hassan; Sheikhha, Mohammad Hasan; Sakhvidi, Mohammad Javad Zare; Nawrot, Tim S.; Dadvand, Payam

doi:10.1016/j.envpol.2018.09.130

Cited by 91 publications

(44 citation statements)

References 57 publications

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“…The new findings "confirm what we've seen in other studies 7 showing that air pollution induces this particular response," says Michael Brauer, a professor of occupational and environmental health at the University of British Columbia in Vancouver, Canada, who was not involved in the investigation. However, Brauer adds that further research is still needed to assess the clinical significance of telomere shortening on long-term health outcomes.…”

Section: Science Selectionsupporting

confidence: 81%

Telomere Length and Air Pollution: Observations in Women Who Use Biomass Cookstoves

Schmidt¹

2020

Environ Health Perspect

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Section: Science Selectionsupporting

confidence: 81%

Telomere Length and Air Pollution: Observations in Women Who Use Biomass Cookstoves

Schmidt¹

2020

Environ Health Perspect

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“…2010). Leukocyte telomere length has been most commonly measured in urban air pollution studies (Miri et al. 2019).…”

Section: Discussionmentioning

confidence: 99%

“…2015) and urban air pollution (Martens and Nawrot 2016), have been shown to induce cellular oxidative stress and systemic inflammation and may impact the rate of telomere length attrition by accelerating cell division or inducing DNA damage (Monaghan 2010). Long-term exposure to urban and traffic-related air pollution has been associated with shorter telomere length in a number of studies conducted in healthy adults and elderly populations (Miri et al. 2019).…”

Section: Introductionmentioning

confidence: 99%

Exposure–Response Associations of Household Air Pollution and Buccal Cell Telomere Length in Women Using Biomass Stoves

Yang

Carter

et al. 2019

Environ Health Perspect

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Background:Telomere shortening is associated with early mortality and chronic disease. Recent studies indicate that environmental exposures, including urban and traffic-related air pollution, may shorten telomeres. Associations between exposure to household air pollution from solid fuel stoves and telomere length have not been evaluated.Methods:Among 137 rural Chinese women using biomass stoves (mean=55y of age), we measured 48-h personal exposures to fine particulate matter [PM ≤ 2.5μm in aerodynamic diameter (PM2.5)] and black carbon and collected oral DNA on up to three occasions over a period of 2.5 y. Relative telomere length (RTL) was quantified using a modified real-time polymerase chain reaction protocol. Mixed effects regression models were used to investigate the exposure–response associations between household air pollution and RTL, adjusting for key sociodemographic, behavioral, and environmental covariates.Results:Women’s daily exposures to air pollution ranged from 13–1,136 μg/m3 for PM2.5 (mean=154) and 0.1–34 μg/m3 for black carbon (mean=3.6). Natural cubic spline models indicated a mostly linear association between increased exposure to air pollution and shorter RTL, except at very high concentrations where there were few observations. We thus modeled the linear associations with all observations, excluding the highest 3% and 5% of exposures. In covariate-adjusted models, an interquartile range (IQR) increase in exposure to black carbon (3.1 μg/m3) was associated with shorter RTL [all observations: −0.27 (95% CI: −0.48, −0.06); excluding highest 5% exposures: −1.10 (95% CI: −1.63, −0.57)]. Further adjustment for outdoor temperature brought the estimates closer to zero [all observations: −0.15 (95% CI: −0.36, 0.06); excluding highest 5% exposures: −0.68 (95% CI: −1.26, −0.10)]. Models with PM2.5 as the exposure metric followed a similar pattern.Conclusion:Telomere shortening, which is a biomarker of biological aging and chronic disease, may be associated with exposure to air pollution in settings where household biomass stoves are commonly used. https://doi.org/10.1289/EHP4041

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“…Existing evidence suggests a possible negative association between long-term exposure to air pollution (PM2.5) and LTL, and a positive association between short-term exposure and LTL [16]. However, for carcinogenic PAH exposure, the results are not conclusive.…”

Section: Introductionmentioning

confidence: 95%

The Effects of Everyday-Life Exposure to Polycyclic Aromatic Hydrocarbons on Biological Age Indicators

Pavanello

Campisi

Mastrangelo

et al. 2020

Preprint

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BackgroundFurther knowledge on modifiable aging risk factors is required to mitigate the increasing burden of age-related diseases in a rapidly growing global demographic of elderly individuals. We explored the effect of everyday exposure to carcinogenic polycyclic aromatic hydrocarbons (PAHs), which are fundamental constituents of air pollution, on cellular biological aging. This was determined via the analysis of leukocyte telomere length (LTL), mitochondrial DNA copy number (LmtDNAcn), and by the formation of anti- benzo[a]pyrene diolepoxide (B[a]PDE–DNA) adducts.MethodsThe study population consisted of 585 individuals living in North-East Italy. PAH exposure (diet, indoor activities, outdoor activities, traffic, and residential exposure) and smoking behavior were assessed by questionnaire and through measures of target dose [B[a]PDE–DNA]. LTL, LmtDNAcn and genetic polymorphisms [glutathione S-transferase M1 and T1 (GSTM1; GSTT1)] were measured by polymerase chain reaction methods. Structural equation modelling analysis evaluated these complex relationships.ResultsIn two models investigating LTL and LmtDNAcn, we found an ordered relationship between these measurements and PAH exposure (diet, indoor, outdoor, traffic, residential). Acting through anti-B[a]PDE–DNA adduct formation, we detected reduced LTL (p=0.028) and LmtDNAcn (p=0.018) levels, particularly in males (LTL p=0.006; LmtDNAcn p=0.0001). Active smoking only increased LTL (p=0.0001). Besides this, the most significant determinants of PAH exposure causing an increase in anti-B[a]PDE–DNA were indoor and diet (p=0.0001 for each). while the least significant was outdoor. Lastly, the presence of detoxifying GSTM1 decreased adduct levels.Conclusion New findings stemming from our study suggest that LTL and LmtDNAcn erosion depends on certain preventable everyday life exposure to PAHs. In particular, the clear association with indoor activities, diet, and gender opens new perspectives for tailored preventive measures in age-related diseases, including lung cancer.Capsule:Everyday life exposure to polycyclic aromatic hydrocarbons shortens leukocyte telomere length and mitochondrial DNA copy number through anti-B[a]PDE-DNA adduct formation.

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Air pollution and telomere length in adults: A systematic review and meta-analysis of observational studies

Cited by 91 publications

References 57 publications

Telomere Length and Air Pollution: Observations in Women Who Use Biomass Cookstoves

Telomere Length and Air Pollution: Observations in Women Who Use Biomass Cookstoves

Exposure–Response Associations of Household Air Pollution and Buccal Cell Telomere Length in Women Using Biomass Stoves

The Effects of Everyday-Life Exposure to Polycyclic Aromatic Hydrocarbons on Biological Age Indicators

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