Ageing at the level of telomeres in association to residential landscape and air pollution at home and work: a review of the current evidence

Martens, Dries S.; Nawrot, Tim S.

doi:10.1016/j.toxlet.2018.06.1213

Cited by 41 publications

(16 citation statements)

References 122 publications

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“…Black carbon exposure averaged over a year was associated with reduced cognitive function, with stronger effects observed in individuals with longer leukocyte telomeres, a characteristic associated with the capacity to mount a stronger systemic inflammatory response [103]. In addition to this potential role as an effect modifier, telomere length may also reflect oxidative and inflammatory stresses linked to exposures, with long-term exposures to a range of occupational and environmental toxicants generally associated with shorter leukocyte telomere length [104]. This emerging literature supports a role for air pollution in contributing to fetal programming and to accelerated aging, at least in part through cumulative effects of oxidative and inflammatory stresses.…”

Section: Converging Pathways: Oxidative Stress Inflammation and Thementioning

confidence: 99%

Air Pollution, Stress, and Allostatic Load: Linking Systemic and Central Nervous System Impacts

Thomson

2019

JAD

192

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Air pollution is a risk factor for cardiovascular and respiratory morbidity and mortality. A growing literature also links exposure to diverse air pollutants (e.g., nanoparticles, particulate matter, ozone, traffic-related air pollution) with brain health, including increased incidence of neurological and psychiatric disorders such as cognitive decline, dementia (including Alzheimer's disease), anxiety, depression, and suicide. A critical gap in our understanding of adverse impacts of pollutants on the central nervous system (CNS) is the early initiating events triggered by pollutant inhalation that contribute to disease progression. Recent experimental evidence has shown that particulate matter and ozone, two common pollutants with differing characteristics and reactivity, can activate the hypothalamic-pituitary-adrenal (HPA) axis and release glucocorticoid stress hormones (cortisol in humans, corticosterone in rodents) as part of a neuroendocrine stress response. The brain is highly sensitive to stress: stress hormones affect cognition and mental health, and chronic stress can produce profound biochemical and structural changes in the brain. Chronic activation and/or dysfunction of the HPA axis also increases the burden on physiological stress response systems, conceptualized as allostatic load, and is a common pathway implicated in many diseases. The present paper provides an overview of how systemic stress-dependent biological responses common to particulate matter and ozone may provide insight into early CNS effects of pollutants, including links with oxidative, inflammatory, and metabolic processes. Evidence of pollutant effect modification by non-chemical stressors (e.g., socioeconomic position, psychosocial, noise), age (prenatal to elderly), and sex will also be reviewed in the context of susceptibility across the lifespan.

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Section: Converging Pathways: Oxidative Stress Inflammation and Thementioning

confidence: 99%

Air Pollution, Stress, and Allostatic Load: Linking Systemic and Central Nervous System Impacts

Thomson

2019

JAD

192

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“…Exposure to residential greenness and green space was positively associated with mental health outcomes [57,58] whereas the opposite was seen for smoking and air pollution [59][60][61]. Also TL and mtDNAc have been associated with these exposures [62][63][64] and with several mental health disorders [65,66]. However, to our knowledge, this is the first research that combines these exposures, biomarkers and health outcomes.…”

Section: Discussionmentioning

confidence: 87%

Environmental exposures and health behavior in association with mental health: a study design

et al. 2020

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Background Air pollution, green space and smoking are known to affect human health. However, less is known about their underlying biological mechanisms. One of these mechanisms could be biological aging. In this study, we explore the mediation of biomarkers of exposure and biological aging to explain the associations between environmental exposures, health behavior and mental health. Methods The study population of this cross-sectional study (n = 1168) is a subsample of the Belgian 2018 Health Interview Survey (BHIS). Mental health indicators including psychological and severe psychological distress, life satisfaction, vitality, eating disorders, suicidal ideation, subjective health and depressive and anxiety disorders, demographics and health behavior such as smoking are derived from the BHIS. Urine and blood samples are collected to measure respectively the biomarkers of exposure (urinary black carbon (BC) and (hydroxy)cotinine) and the biomarkers of biological aging (mitochondrial DNA content (mtDNAc) and telomere length (TL)). Recent and chronic exposure (μg/m3) to nitrogen dioxide (NO2), particulate matter ≤2.5 μm (PM2.5) and ≤ 10 μm (PM10) and BC at the participants’ residence are modelled using a high resolution spatial temporal interpolation model. Residential green space is defined in buffers of different size (50 m – 5000 m) using land cover data in ArcGIS 10 software. For the statistical analysis multivariate linear and logistic regressions as well as mediation analyses are used taking into account a priori selected covariates and confounders. Results As this study combined data of BHIS and laboratory analyses, not all data is available for all participants. Therefore, data analyses will be conducted on different subsets. Data on air pollution and green space exposure is available for all BHIS participants. Questions on smoking and mental health were answered by respectively 7829 and 7213 BHIS participants. For biomarker assessment, (hydroxy) cotinine, urinary BC and the biomarkers of biological aging are measured for respectively 1130, 1120 and 985 participants. Conclusion By use of personal markers of air pollution and smoking, as well as biological aging, we will gain knowledge about the association between environmental exposures, health behavior, and the mental health status. The results of the study can provide insights on the health of the Belgian population, making it a nationwide interesting study.

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“…This is because of the fact that these targets have been widely studied in adult populations and have been associated with age-related diseases. Telomeres shorten throughout the life-span, and this shortening may be influenced by environmental factors, including air pollution [67]. Telomeres play a role in cell senescence and human aging and are indicative of disease risks, and in this regard, short telomeres have independently of chronological age been associated with higher risks for cardiovascular disease [68], type 2 diabetes [69], respiratory diseases [70], and mortality [71].…”

Section: Air Pollution Exposure and The Aging Phenotypementioning

confidence: 99%

Air pollution-induced placental alterations: an interplay of oxidative stress, epigenetics, and the aging phenotype?

et al. 2019

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According to the "Developmental Origins of Health and Disease" (DOHaD) concept, the early-life environment is a critical period for fetal programming. Given the epidemiological evidence that air pollution exposure during pregnancy adversely affects newborn outcomes such as birth weight and preterm birth, there is a need to pay attention to underlying modes of action to better understand not only these air pollution-induced early health effects but also its later-life consequences. In this review, we give an overview of air pollution-induced placental molecular alterations observed in the ENVIRONAGE birth cohort and evaluate the existing evidence. In general, we showed that prenatal exposure to air pollution is associated with nitrosative stress and epigenetic alterations in the placenta. Adversely affected CpG targets were involved in cellular processes including DNA repair, circadian rhythm, and energy metabolism. For miRNA expression, specific air pollution exposure windows were associated with altered miR-20a, miR-21, miR-146a, and miR-222 expression. Early-life aging markers including telomere length and mitochondrial DNA content are associated with air pollution exposure during pregnancy. Previously, we proposed the air pollution-induced telomere-mitochondrial aging hypothesis with a direct link between telomeres and mitochondria. Here, we extend this view with a potential co-interaction of different biological mechanisms on the level of placental oxidative stress, epigenetics, aging, and energy metabolism. Investigating the placenta is an opportunity for future research as it may help to understand the fundamental biology underpinning the DOHaD concept through the interactions between the underlying modes of action, prenatal environment, and disease risk in later life. To prevent lasting consequences from early-life exposures of air pollution, policy makers should get a basic understanding of biomolecular consequences and transgenerational risks.

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Ageing at the level of telomeres in association to residential landscape and air pollution at home and work: a review of the current evidence

Cited by 41 publications

References 122 publications

Air Pollution, Stress, and Allostatic Load: Linking Systemic and Central Nervous System Impacts

Air Pollution, Stress, and Allostatic Load: Linking Systemic and Central Nervous System Impacts

Environmental exposures and health behavior in association with mental health: a study design

Air pollution-induced placental alterations: an interplay of oxidative stress, epigenetics, and the aging phenotype?

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