Exposome and unhealthy aging: environmental drivers from air pollution to occupational exposures

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Abstract

The aging population worldwide is facing a significant increase in age-related non-communicable diseases, including cardiovascular and brain pathologies. This comprehensive review paper delves into the impact of the exposome, which encompasses the totality of environmental exposures, on unhealthy aging. It explores how environmental factors contribute to the acceleration of aging processes, increase biological age, and facilitate the development and progression of a wide range of age-associated diseases. The impact of environmental factors on cognitive health and the development of chronic age-related diseases affecting the cardiovascular system and central nervous system is discussed, with a specific focus on Alzheimer’s disease, Parkinson’s disease, stroke, small vessel disease, and vascular cognitive impairment (VCI). Aging is a major risk factor for these diseases. Their pathogenesis involves cellular and molecular mechanisms of aging such as increased oxidative stress, impaired mitochondrial function, DNA damage, and inflammation and is influenced by environmental factors. Environmental toxicants, including ambient particulate matter, pesticides, heavy metals, and organic solvents, have been identified as significant contributors to cardiovascular and brain aging disorders. These toxicants can inflict both macro- and microvascular damage and many of them can also cross the blood–brain barrier, inducing neurotoxic effects, neuroinflammation, and neuronal dysfunction. In conclusion, environmental factors play a critical role in modulating cardiovascular and brain aging. A deeper understanding of how environmental toxicants exacerbate aging processes and contribute to the pathogenesis of neurodegenerative diseases, VCI, and dementia is crucial for the development of preventive strategies and interventions to promote cardiovascular, cerebrovascular, and brain health. By mitigating exposure to harmful environmental factors and promoting healthy aging, we can strive to reduce the burden of age-related cardiovascular and brain pathologies in the aging population.

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The Hallmarks of Aging

Carlos López-Otín, Maria Blasco, Linda Partridge … (2014)

Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death. This deterioration is the primary risk factor for major human pathologies, including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. Aging research has experienced an unprecedented advance over recent years, particularly with the discovery that the rate of aging is controlled, at least to some extent, by genetic pathways and biochemical processes conserved in evolution. This Review enumerates nine tentative hallmarks that represent common denominators of aging in different organisms, with special emphasis on mammalian aging. These hallmarks are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. A major challenge is to dissect the interconnectedness between the candidate hallmarks and their relative contributions to aging, with the final goal of identifying pharmaceutical targets to improve human health during aging, with minimal side effects. Copyright © 2013 Elsevier Inc. All rights reserved.

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Global burden of 87 risk factors in 204 countries and territories, 1990–2019: a systematic analysis for the Global Burden of Disease Study 2019

Christopher J L Murray, Aleksandr Y Aravkin, Peng Zheng … (2021)

Summary Background Rigorous analysis of levels and trends in exposure to leading risk factors and quantification of their effect on human health are important to identify where public health is making progress and in which cases current efforts are inadequate. The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 provides a standardised and comprehensive assessment of the magnitude of risk factor exposure, relative risk, and attributable burden of disease. Methods GBD 2019 estimated attributable mortality, years of life lost (YLLs), years of life lived with disability (YLDs), and disability-adjusted life-years (DALYs) for 87 risk factors and combinations of risk factors, at the global level, regionally, and for 204 countries and territories. GBD uses a hierarchical list of risk factors so that specific risk factors (eg, sodium intake), and related aggregates (eg, diet quality), are both evaluated. This method has six analytical steps. (1) We included 560 risk–outcome pairs that met criteria for convincing or probable evidence on the basis of research studies. 12 risk–outcome pairs included in GBD 2017 no longer met inclusion criteria and 47 risk–outcome pairs for risks already included in GBD 2017 were added based on new evidence. (2) Relative risks were estimated as a function of exposure based on published systematic reviews, 81 systematic reviews done for GBD 2019, and meta-regression. (3) Levels of exposure in each age-sex-location-year included in the study were estimated based on all available data sources using spatiotemporal Gaussian process regression, DisMod-MR 2.1, a Bayesian meta-regression method, or alternative methods. (4) We determined, from published trials or cohort studies, the level of exposure associated with minimum risk, called the theoretical minimum risk exposure level. (5) Attributable deaths, YLLs, YLDs, and DALYs were computed by multiplying population attributable fractions (PAFs) by the relevant outcome quantity for each age-sex-location-year. (6) PAFs and attributable burden for combinations of risk factors were estimated taking into account mediation of different risk factors through other risk factors. Across all six analytical steps, 30 652 distinct data sources were used in the analysis. Uncertainty in each step of the analysis was propagated into the final estimates of attributable burden. Exposure levels for dichotomous, polytomous, and continuous risk factors were summarised with use of the summary exposure value to facilitate comparisons over time, across location, and across risks. Because the entire time series from 1990 to 2019 has been re-estimated with use of consistent data and methods, these results supersede previously published GBD estimates of attributable burden. Findings The largest declines in risk exposure from 2010 to 2019 were among a set of risks that are strongly linked to social and economic development, including household air pollution; unsafe water, sanitation, and handwashing; and child growth failure. Global declines also occurred for tobacco smoking and lead exposure. The largest increases in risk exposure were for ambient particulate matter pollution, drug use, high fasting plasma glucose, and high body-mass index. In 2019, the leading Level 2 risk factor globally for attributable deaths was high systolic blood pressure, which accounted for 10·8 million (95% uncertainty interval [UI] 9·51–12·1) deaths (19·2% [16·9–21·3] of all deaths in 2019), followed by tobacco (smoked, second-hand, and chewing), which accounted for 8·71 million (8·12–9·31) deaths (15·4% [14·6–16·2] of all deaths in 2019). The leading Level 2 risk factor for attributable DALYs globally in 2019 was child and maternal malnutrition, which largely affects health in the youngest age groups and accounted for 295 million (253–350) DALYs (11·6% [10·3–13·1] of all global DALYs that year). The risk factor burden varied considerably in 2019 between age groups and locations. Among children aged 0–9 years, the three leading detailed risk factors for attributable DALYs were all related to malnutrition. Iron deficiency was the leading risk factor for those aged 10–24 years, alcohol use for those aged 25–49 years, and high systolic blood pressure for those aged 50–74 years and 75 years and older. Interpretation Overall, the record for reducing exposure to harmful risks over the past three decades is poor. Success with reducing smoking and lead exposure through regulatory policy might point the way for a stronger role for public policy on other risks in addition to continued efforts to provide information on risk factor harm to the general public. Funding Bill & Melinda Gates Foundation.

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Neuroinflammation in Alzheimer's disease.

Michael T Heneka, Monica Carson, Joseph El Khoury … (2015)

Increasing evidence suggests that Alzheimer's disease pathogenesis is not restricted to the neuronal compartment, but includes strong interactions with immunological mechanisms in the brain. Misfolded and aggregated proteins bind to pattern recognition receptors on microglia and astroglia, and trigger an innate immune response characterised by release of inflammatory mediators, which contribute to disease progression and severity. Genome-wide analysis suggests that several genes that increase the risk for sporadic Alzheimer's disease encode factors that regulate glial clearance of misfolded proteins and the inflammatory reaction. External factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain and further promote disease progression. Modulation of risk factors and targeting of these immune mechanisms could lead to future therapeutic or preventive strategies for Alzheimer's disease. Copyright © 2015 Elsevier Ltd. All rights reserved.

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Author and article information

Contributors

Zoltan Ungvari:

ORCID: http://orcid.org/0000-0002-6035-6039

zoltan-ungvari@ouhsc.edu

Journal

Journal ID (nlm-ta): GeroScience

Journal ID (iso-abbrev): Geroscience

Title: GeroScience

Publisher: Springer International Publishing (Cham )

ISSN (Print): 2509-2715

ISSN (Electronic): 2509-2723

Publication date (Electronic): 9 September 2023

Publication date PMC-release: 9 September 2023

Publication date Collection: December 2023

Volume: 45

Issue: 6

Pages: 3381-3408

Affiliations

[1 ]Department of Public Health, Faculty of Medicine, Semmelweis University, ( https://ror.org/01g9ty582) Budapest, Hungary

[2 ]Department of Public Health Laboratory, National Public Health Centre, Budapest, Hungary

[3 ]Department of Public Health Siences, Faculty of Health Sciences, Semmelweis University, ( https://ror.org/01g9ty582) Budapest, Hungary

[4 ]Vascular Cognitive Impairment, Neurodegeneration and Healthy Brain Aging Program, Department of Neurosurgery, University of Oklahoma Health Sciences Center, ( https://ror.org/0457zbj98) Oklahoma City, OK USA

[5 ]Oklahoma Center for Geroscience and Healthy Brain Aging, University of Oklahoma Health Sciences Center, ( https://ror.org/0457zbj98) Oklahoma City, OK USA

[6 ]Stephenson Cancer Center, University of Oklahoma, ( https://ror.org/02aqsxs83) Oklahoma City, OK USA

[7 ]Department of Health Promotion Sciences, College of Public Health, University of Oklahoma Health Sciences Center, ( https://ror.org/0457zbj98) Oklahoma City, OK USA

[8 ]International Training Program in Geroscience, Doctoral School of Basic and Translational Medicine/Department of Public Health, Semmelweis University, ( https://ror.org/01g9ty582) Budapest, Hungary

[9 ]Department of Cell Biology, University of Oklahoma Health Sciences Center, ( https://ror.org/0457zbj98) Oklahoma City, OK USA

[10 ]UCL Brain Sciences, University College London, ( https://ror.org/02jx3x895) London, UK

[11 ]Department of Internal Medicine and Oncology, Faculty of Medicine, Semmelweis University, ( https://ror.org/01g9ty582) Budapest, Hungary

[12 ]Department of Translational Medicine, Semmelweis University, ( https://ror.org/01g9ty582) Budapest, Hungary

[13 ]GRID grid.11804.3c, ISNI 0000 0001 0942 9821, Eötvös Loránd Research Network and Semmelweis University (ELKH-SE) Cerebrovascular and Neurocognitive Disorders Research Group, ; Budapest, H-1052 Hungary

[14 ]ELKH-DE Public Health Research Group, Department of Public Health and Epidemiology, Faculty of Medicine, University of Debrecen, ( https://ror.org/02xf66n48) 4032 Debrecen, Hungary

[15 ]Epidemiology and Surveillance Centre, Semmelweis University, ( https://ror.org/01g9ty582) 1085 Budapest, Hungary

Author information

Zoltan Ungvari http://orcid.org/0000-0002-6035-6039

Article

Publisher ID: 913

DOI: 10.1007/s11357-023-00913-3

PMC ID: 10643494

PubMed ID: 37688657

SO-VID: 66e9cee4-9234-4879-9e70-92c7cb8131ad

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Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

History

Date received : 22 June 2023

Date accepted : 14 August 2023

Funding

Funded by: Semmelweis University

Open Access :

Open access funding provided by Semmelweis University.

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Keywords: exposome,aging,environmental pollution,toxicology,accelerated aging,biological age

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Keywords: exposome, aging, environmental pollution, toxicology, accelerated aging, biological age

Exposome and unhealthy aging: environmental drivers from air pollution to occupational exposures

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Abstract

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Aging Pathobiology and Therapeutics

Most cited references 361

The Hallmarks of Aging

Global burden of 87 risk factors in 204 countries and territories, 1990–2019: a systematic analysis for the Global Burden of Disease Study 2019

Neuroinflammation in Alzheimer's disease.

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