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. 2022 Nov 10;118(14):2880-2902.
doi: 10.1093/cvr/cvab316.

Environmental risk factors and cardiovascular diseases: a comprehensive expert review

Thomas Münzel  1 , Omar Hahad  1 , Mette Sørensen  2   3 , Jos Lelieveld  4 , Georg Daniel Duerr  5 , Mark Nieuwenhuijsen  6   7   8 , Andreas Daiber  1
Affiliations

Environmental risk factors and cardiovascular diseases: a comprehensive expert review

Thomas Münzel et al. Cardiovasc Res. .

Abstract

Non-communicable diseases (NCDs) are fatal for more than 38 million people each year and are thus the main contributors to the global burden of disease accounting for 70% of mortality. The majority of these deaths are caused by cardiovascular disease (CVD). The risk of NCDs is strongly associated with exposure to environmental stressors such as pollutants in the air, noise exposure, artificial light at night, and climate change, including heat extremes, desert storms, and wildfires. In addition to the traditional risk factors for CVD such as diabetes, arterial hypertension, smoking, hypercholesterolaemia, and genetic predisposition, there is a growing body of evidence showing that physicochemical factors in the environment contribute significantly to the high NCD numbers. Furthermore, urbanization is associated with accumulation and intensification of these stressors. This comprehensive expert review will summarize the epidemiology and pathophysiology of environmental stressors with a focus on cardiovascular NCDs. We will also discuss solutions and mitigation measures to lower the impact of environmental risk factors with focus on CVD.

Keywords: Air pollution; Cardiovascular disease; Cardiovascular risk factors; Environmental stressors; Heat; Light pollution; Noise; Oxidative stress.

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Conflict of interest statement

Conflict of interest: none declared.

Figures

Graphical Abstract
Graphical Abstract
Figure 1
Figure 1
The exposome concept. Exposure to environmental risk factors (=external exposome) leads to changes of central biochemical pathways with associated health impact. The central biochemical pathways comprise changes in circadian clock genes leading to impaired rhythmicity and phase-shifts, stress hormone release (cortisol and catecholamines), production of reactive oxygen species by mitochondria and NADPH oxidase in activated immune cells, inflammation with tissue infiltration of activated immune cells, and oxidative damage in different organs. Because classical health risk factors share similar pathomechanisms, people with existing classical health risk factors or disease (e.g. diabetes or hypertension) may experience additive adverse health effects upon exposure to environmental risk factors. HPA, hypothalamic–pituitary–adrenal axis; NOX-2, phagocytic NADPH oxidase (isoform 2); ROS, reactive oxygen species; SNS, sympathetic nervous system. Merged and redrawn from previous reports refs, with permission; Copyright © 2020, The authors; Published by Elsevier B.V.
Figure 2
Figure 2
Noise–stress concept and the adverse health consequences in humans. (A) Noise reaction model for the direct (auditory) and indirect (non-auditory) effects of noise exposure. Adapted from ref. with permission; Copyright © 2014, Oxford University Press. (B) Neuronal activation (arousals), e.g. by noise exposure, causes signalling via the hypothalamic–pituitary–adrenocortical (HPA) axis and sympathetic nervous system (SNS) via corticotrophin-releasing factor (CRF) in the pituitary gland and adrenocorticotropic hormone (ACTH) in the adrenal gland leading to activation of other neurohormones (e.g. the renin–angiotensin–aldosterone system), inflammation and oxidative stress. The adverse effects of cortisol (or corticosterone) and catecholamines on cardiovascular function and molecular targets are well characterized. Adapted from ref. with permission; Copyright © 2013, Campos-Rodríguez et al.; Creative Commons Attribution License (CC BY). (C) Neuronal activation (arousals) and subsequent atherosclerosis with a higher cardiovascular risk by noise exposure was proven in subjects by 18F-PET scans indicating an association of amygdala activation, coronary inflammation, and increased incidence of major adverse cardiovascular events (MACE). Adapted from refs, with permission; Copyright © 2019, Oxford University Press. (D) Flow-mediated dilation (FMD) is measured by high-resolution B-mode ultrasound. Schematic presentation of adverse effects of simulated nighttime aircraft or train noise (either 30 or 60 events for one night) vs. unexposed control group (CTR) on FMD of the brachial artery in response to post-ischaemic hyperaemia and the beneficial acute effects of the antioxidant vitamin C. Results of own studies refs.,
Figure 3
Figure 3
Global burden of disease of air pollution. (A) Disease categories that contribute to excess mortality from the long-term exposure to ambient PM2.5 and O3. COPD, chronic obstructive pulmonary disease; IHD, ischaemic heart diseases; LRI, lower respiratory infections. (B) Mean global and country-level loss of life expectancy from air pollution, tobacco smoking (active and passive), parasitic and vector-borne diseases (e.g. malaria), and all forms of violence (interpersonal, collective conflict, and armed intervention). Adapted from ref. with permission; Copyright © 2020, Oxford University Press.
Figure 4
Figure 4
Air pollution thresholds and guidelines as well as health effects. (A) Data for air pollution obtained from WHO air quality guidelines for particulate matter, ozone, nitrogen dioxide, and sulphur dioxide (update 2005 and summary of risk assessment) (http://apps.who.int/iris/bitstream/10665/69477/1/WHO_SDE_PHE_OEH_06.02_eng.pdf). Comparison of particle size with biochemical and biological entities. Reused from ref. with permission; Copyright © 2017, Oxford University Press. (B) PM2.5 exposure acutely triggers plaque rupture. Adopted from ref. (C) Effects of different legal thresholds for ambient particulate matter (PM2.5) concentrations in USA and Europe on cardiovascular health risk by development of high-risk plaques depicted as exponential fit for original data (left) and zoomed exponential fit with legal thresholds (right). Reused from ref. with permission; Copyright © 2019, Oxford University Press; generated from original data in ref.
Figure 5
Figure 5
Proposed pathophysiological mechanisms of cardiovascular disease induced by environmental air, light, and noise pollution. Major pathomechanisms comprise neuronal activation and stress response, disruption of circadian rhythms, all of which initiates cerebral and systemic inflammation as well as oxidative stress leading to endothelial dysfunction, atherothrombotic changes, dysregulated metabolism, and manifest cardiometabolic diseases. Modified from ref. with permission; Copyright © 2016, Oxford University Press.
Figure 6
Figure 6
Personal mitigation manoeuvres and air pollution (significantly modified from ref.)
Figure 7
Figure 7
The present figure depicts the 15-min city, the brain child of Carlos Moreno, where work, school, entertainment, and other activities are reachable within a 15-min walk of the home., The 15-min city involves the creation of a city of villages and a return to more traditional city design. The 15-min city will encourage more physical activity through more active transport, and is likely to reduce urban inequalities and health inequities. Critically, it will also reduce the need for long distance travel and thereby reduce CO2 emissions, and air pollution and noise levels (for review see ref.) Translation of French words: apprendre = to learn; travailler = to work; partager et réemployer = to share and reuse; s’approvisionner = to supply oneself; s’aérer = to get some fresh air; se cultiver, s’engager = to subdue, to be committed; se soigner = to nurse oneself; circuler = to be on the move; se dépenser = to wear oneself out; bien manger = to eat well; chez moi = at home. Reused from ref. with permission of the copyright owner Micael queiroz, www.micaeldessin.com.
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References

    1. Hughes BB, Kuhn R, Peterson CM, Rothman DS, Solorzano JR, Mathers CD, Dickson JR. Projections of global health outcomes from 2005 to 2060 using the International Futures integrated forecasting model. Bull World Health Organ 2011;89:478–486. - PMC - PubMed
    1. GBD 2016 Disease and Injury Incidence and Prevalence Collaborators . Global, regional, and national incidence, prevalence, and years lived with disability for 328 diseases and injuries for 195 countries, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet 2017;390:1211–1259. - PMC - PubMed
    1. World Health Organization . Noncommunicable diseases: Mortality. https://www.who.int/gho/ncd/mortality_morbidity/en/ (13 October 2021, date last accessed).
    1. GBD 2019 Risk Factors Collaborators . Global burden of 87 risk factors in 204 countries and territories, 1990-2019: a systematic analysis for the Global Burden of Disease Study 2019. Lancet 2020;396:1223–1249. - PMC - PubMed
    1. Bygbjerg IC. Double burden of noncommunicable and infectious diseases in developing countries. Science 2012;337:1499–1501. - PubMed

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