Influence of aging in the modulation of epigenetic biomarkers of carcinogenesis after exposure to air pollution

Fougère, Bertrand; Landkocz, Yann; Lepers, Capucine; Martin, Perrine; Armand, Lucie; Grossin, Nicolas; Verdin, Anthony; Boulanger, Éric; Gosset, Pierre; Sichel, François; Shirali, Pirouz; Billet, Sylvain

doi:10.1016/j.exger.2018.05.018

Cited by 11 publications

(5 citation statements)

References 47 publications

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“…The authors' assumption that for chronic obstructive pulmonary disease and lung cancer, the relative risk (RR) for the same exposure concentration of PM 2·5 was the same for all adults might be incorrect. Previous studies 11,12 have shown that the associated with air pollution for chronic obstructive pulmonary disease and lung cancer varies with age, and these results are biologically plausible. Additionally, the difference in risk across age groups is exacerbated by the fact that the population is rapidly ageing in China, and the incidence of chronic obstructive pulmonary disease and lung cancer is likely to be higher in older populations (aged >55 years) than younger populations (aged <55 years).…”

Section: Air Pollution and Disease Burdenmentioning

confidence: 66%

Air pollution and disease burden

Tong

2019

The Lancet Planetary Health

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Section: Air Pollution and Disease Burdenmentioning

confidence: 66%

Air pollution and disease burden

Tong

2019

The Lancet Planetary Health

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“…As T cells were exposed to FP after their activation by anti‐CD3/CD28 beads, we do not expect any additional T‐cell activation by dying cells as described previously (Yatim, Cullen, & Albert, ). Therefore, we chose these conditions of exposure in agreement with another study (Fougère et al, ). We then studied the influence of the T‐cell exposure to FP on the metabolism and oxidative stress of organic compounds as well as on T‐cell differentiation profiles.…”

Section: Discussionmentioning

confidence: 99%

A prospective pilot study of the T‐lymphocyte response to fine particulate matter exposure

Zallouha

Landkocz

Meausoone

et al. 2020

J of Applied Toxicology

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Exposure to air pollution is associated with increased morbidity and mortality. Once the fine atmospheric particulate matter (FP) is inhaled, some of its compounds can pass through the lungs and reach the bloodstream where they can come into contact with immune cells. Exposure to FP particularly affects sensitive populations such as the elderly. Aging affects the immune system, making the elderly more vulnerable.The project aims to determine the effects of FP exposure on human T cells while looking for biomarkers associated with exposure. Blood samples from 95 healthy subjects in three different age groups (20-30, 45-55 and 70-85 years) were collected to determine a potential age effect. T lymphocytes were isolated to be exposed ex vivo for 72 hours to 45 μg/mL of FP collected in Dunkirk and chemically characterized. Overexpression of the CYP1A1, CYP1B1 and CYP2S1 genes was therefore measured after exposure of the T cells to FP. These genes code for enzymes known to be involved in the metabolic activation of organic compounds such as polycyclic aromatic hydrocarbons detected in the FP sample. T-cell profiling allowed us to suggest a mixed T-helper 1/2 profile caused by exposure to FP. With regard to the influence of age, we have observed differences in the expression of certain genes, as well as an increase in interleukin-4 and -13 concentrations in the elderly. These results showed that exposure of T lymphocytes to FP causes effects on both transcriptomic and cytokine secretion levels. K E Y W O R D Sage, air pollution, fine particulate matter, immunological profile, metabolic activation, T lymphocytes

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“…For instance, the tumor suppressor gene P16 INK4A is frequently hyper-methylated in cancers [84]. Interestingly, P16 INK4A promoter methylation was reported to be significantly increased in PBMCs after exposure to PM [40].…”

Section: Adult Agementioning

confidence: 99%

Particulate matter exposure shapes DNA methylation through the lifespan

2019

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Exposure to airborne particulate matter (PM) has been associated with detrimental health effects. DNA methylation represents the most well-studied epigenetic factor among the possible mechanisms underlying this association. Interestingly, changes of DNA methylation in response to environmental stimuli are being considered for their role in the pathogenic mechanism, but also as mediators of the body adaptation to air pollutants. Several studies have evaluated both global and gene-specific methylation in relation to PM exposure in different clinical conditions and life stages. The purpose of the present literature review is to evaluate the most relevant and recent studies in the field in order to analyze the available evidences on long- and short-term PM exposure and DNA methylation changes, with a particular focus on the different life stages when the alteration occurs. PM exposure modulates DNA methylation affecting several biological mechanisms with marked effects on health, especially during susceptible life stages such as pregnancy, childhood, and the older age. Although many cross-sectional investigations have been conducted so far, only a limited number of prospective studies have explored the potential role of DNA methylation. Future studies are needed in order to evaluate whether these changes might be reverted.

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Influence of aging in the modulation of epigenetic biomarkers of carcinogenesis after exposure to air pollution

Cited by 11 publications

References 47 publications

Air pollution and disease burden

Air pollution and disease burden

A prospective pilot study of the T‐lymphocyte response to fine particulate matter exposure

Particulate matter exposure shapes DNA methylation through the lifespan

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