Environmental Impacts on Cardiovascular Health and Biology: An Overview

Abstract

Environmental stressors associated with human activities (e.g., air and noise pollution, light disturbance at night) and climate change (e.g., heat, wildfires, extreme weather events) are increasingly recognized as contributing to cardiovascular morbidity and mortality. These harmful exposures have been shown to elicit changes in stress responses, circadian rhythms, immune cell activation and oxidative stress, as well as traditional cardiovascular risk factors (e.g., hypertension, diabetes, obesity) that promote cardiovascular diseases. In this overview, we summarize evidence from human and animal studies of the impacts of environmental exposures and climate change on cardiovascular health. In addition, we discuss strategies to reduce the impact of environmental risk factors on current and future cardiovascular disease burden, including urban planning, personal monitoring, and mitigation measures.

Introduction

Despite medical advances in prevention and treatment, cardiovascular disease remains the leading cause of death worldwide. Management efforts in the previous decades have largely focused on traditional risk factors like hypertension, hypercholesterolemia, diabetes, smoking, and genetic predispositions; yet, there is increasing evidence that environmental toxins and stressors contribute to cardiovascular disease risk^{1, 2} (Figure). Environmental contributors to cardiovascular disease represent an enormous opportunity to alter disease course by reducing these modifiable risk factors.

Figure: Environmental Exposures and Cardiovascular Health.

Numerous harmful exposures have adverse effects on cardiovascular risk factors and outcomes via multiple overlapping pathways.

In this review, we discuss the impact of various environmental exposures including chemical and non-chemical pollutants, as well as climate change related stressors, on the cardiovascular system. We summarize how these environmental exposures affect cardiovascular health and highlight associated mechanisms and epidemiological outcomes. The review outlines these broad concepts and serves as an introduction to the other reviews in this Circulation Research Compendium. The authors of the reviews in this compendium have contributed Key Highlights and Research Gaps that can be found with their corresponding sections herein.

Air Pollution

Ambient air pollution is comprised of particulate matter (PM) and gaseous pollutants such as ozone, nitrogen oxides, carbon monoxide, and sulfur dioxide. In addition, air pollution contains hazardous air pollutants such as volatile organic compounds (VOCs), benzene, polycyclic aromatic hydrocarbons, acrolein and others. Exposure to ambient air pollution reduces the global average life expectancy by 2.9 years,³ with more than 50% of excess deaths due to cardiovascular disease (CVD), ischemic heart disease, stroke, diabetes and hypertension.⁴ Of the many components of ambient air pollution, PM is the strongest driver of cardiovascular risk and adverse outcomes. PM is a complex mixture of particles of different sizes originating from many different sources, with source determining composition, and composition determining biological effects. Particles typically contain inorganic matter, heavy metals, water, and numerous organic products of incomplete combustion of petroleum products. Fine PM (PM with diameter ≤2.5 μm, PM_2.5), is particularly well-studied, since this is identified by the Clean Air Act as a “criteria air pollutant” regulated by the Environmental Protection Agency’s National Ambient Air Quality Standards; in contrast, unregulated ultrafine PM (PM <0.1 μm in diameter) shows associations with CVD but has been studied less. PM_2.5 can originate from fossil fuel use, industrial processes, and power generation, with vehicle exhaust accounting for up to 50% of outdoor sources.^{5, 6} PM_2.5 exposure is associated with hypertension, endothelial dysfunction, coagulation and thrombosis, arrhythmias, and atherosclerosis.⁷ Short-term exposures (hours to days) in human epidemiological studies to high concentrations of PM_2.5 are associated with acute outcomes, such as myocardial infarction, likely because they trigger acute plaque rupture.⁸ In contrast, longer-term exposures (weeks to years) are linked with chronic processes like atherosclerosis. At the same time, animal models and in vitro experiments support epidemiological associations suggesting mechanisms of toxicity that include oxidative stress that triggers vascular endothelium dysfunction and inflammation.⁵ For example, experimental PM exposure in animal models causes monocytes to migrate from the bone marrow into peripheral tissues; there, reactive oxygen species generation increases inflammation via activation of the master transcriptional regulator of inflammation NFκB.^{9, 10} In addition, PM_2.5 activates the mouse sympathetic nervous system¹¹ and increases calcium sensitivity via Rho/ROCK signaling,¹² thereby promoting arterial hypertension. Furthermore, PM_2.5 has recently been shown to disrupt circadian rhythms, causing sleep disturbances and altered lipid metabolism, that are associated with atherosclerotic cardiovascular disease.^{13, 14} Together, these results across species and study type suggest that ambient PM_2.5 triggers several pathophysiological pathways that manifest cardiometabolic diseases.

Recently, wildfires have become a large contributor to PM_2.5 exposure and threaten cardiovascular health worldwide.¹⁵ Due to climate change, wildfires have become larger and more frequent around the world. Daily exposure to wildfire smoke has increased in 77% of countries around the globe over the last two decades, with China and India experiencing the largest increases.¹⁶ Wildfire smoke PM_2.5 is associated with 675,000 annual deaths globally,¹⁵ underscoring the danger that wildfire smoke poses to human health worldwide. Wildfire smoke contains entrained soils and gaseous pollutants; PM comprised of products from incomplete combustion of cellulose and lignin found in wood; sugars, resins, waxes, and inorganic salts;¹⁷ differing substantially from the composition of ambient PM. PM_2.5 exposure from wildfires has been associated with elevated blood pressure,^{18, 19} increased emergency department visits for myocardial infarction and stroke,^{20, 21} and out of hospital cardiac arrest.²² PM_2.5 from wildfires is estimated to have effects on cardiovascular events that are comparable to PM_2.5 from other sources²³ making increasingly severe wildfire events an emerging threat to cardiovascular health.

Key Highlights from the article “Impact of Wildfires on Cardiovascular Health” by Williams, et al²⁴ include:

“Epidemiological evidence has revealed positive associations between WFS inhalation and immediate cardiovascular morbidity and mortality, with laboratory studies in animal and cell exposure models providing insight on underlying physiological processes and molecular mechanisms. While the immediate effects of WFS inhalation may be mediated by autonomic nervous system activation, pro-oxidative and inflammatory mediators released from the acute site of injury in the lungs may contribute to adverse cardiovascular tissue remodeling over time.”

Although excess mortality associated with PM_2.5 exposure is 10–20 times higher than other hazardous air pollutants,²⁵ nitrogen oxides, ozone and VOCs also have adverse cardiovascular effect. Increased long-term exposure to nitrogen oxides has been shown by meta-analysis to be associated with significant increases in cardiovascular mortality.²⁶ Ozone is naturally occurring; at ground level, however, is a major secondary pollutant formed through photochemical reactions of nitrogen oxide and VOCs. Short term increases in ozone were shown to be significantly associated with acute coronary events²⁷ and out-of-hospital cardiac arrests.²⁸ VOCs are primarily produced by human activity, particularly the burning of fossil fuels and have been linked with endothelial injury.²⁹ Along with continued increases in VOCs, increasing ambient temperatures lead to increases in ground O₃, and by 2030 the maximum daily O₃ concentrations are expected to spike to 1–5 ppb throughout the USA.² These increases are projected to contribute to an additional tens of thousands of O₃-related morbidity and mortality annually.³⁰

Key highlights from the article “Understanding the Cardiovascular and Metabolic Health Effects of Air Pollution in the Context of Cumulative Exposomic Impacts” by Khraishah, et al³¹ include:

“There is a large body of literature supporting the association of air pollution with cardiovascular disease (CVD), and recent research has taken an exposomic approach, considering the totality of environmental exposures throughout an individual’s life. In this review we focus on studies of vulnerable subpopulations, and we explore the concept of allosteric load and the interaction between various exposures (air pollution, ambient temperature, built environment) to result in a common pathway leading to CVD.”

Climate Change

Climate change is a mounting global crisis that manifests multiple environmental hazards impacting cardiovascular health. In addition to air pollution from wildfires, changing temperatures due to climate change can have direct consequences on health, particularly cardiovascular disease.^{32, 33} Though multiple features of climate change can affect cardiovascular health (worsening air quality from fires, molds and pollens; extremes of heat and cold; increased hurricanes, floods, droughts, and other natural disasters),² extreme temperature appears to be among the most direct.^34–38 In 2023, the world experienced the highest temperatures in over 100,000 years, and heat records were eclipsed on every continent during 2022.³⁸ A recent meta-analysis of studies around the world showed that a 1°C increase in temperature was significantly associated with a 0.5% increase and a 2.1% increase in cardiovascular disease-related morbidity and mortality, respectively.³⁷ A study with data across 567 cities in 27 countries showed that temperatures above the 99^th percentile were associated with increased risk of cardiovascular mortality, specifically from ischemic heart disease, stroke, and heart failure.³⁹ Along with high temperature, other atmospheric conditions such as humidity can increase risk of CVD hospitalization.⁴⁰ Extreme cold weather events are also associated with adverse cardiovascular outcomes. Temperatures below the 1^st percentile were also associated with increased risk of death from ischemic heart disease, stroke, and heart failure;³⁹ cold weather events are linked with increase CVD hospitalizations and mortality.^{39, 41} Studies have also associated temperature extremes, particularly excess heat, with increased burden of cardiovascular disease risk factors, including diabetes/glycemic control,^{42, 43} hypertension,⁴⁴ dyslipidemias⁴⁵ and reduced physical activity.⁴⁶

Physiologically, exposure to high ambient temperature causes increased core body temperature and heart rate, dehydration and volume depletion, sympathetic activation, hypercoagulability, and leukocyte and endothelial cell activation.^{47, 48} Conversely, a drop in core body temperature can lead to decreased heart rate, an increase in sympathetic response and vasoconstriction, catecholamine-driven rise in blood pressure, and electrophysiological disturbances. These physiological changes, then, predispose specific subgroups to adverse effects of extreme temperature exposure. Older adults (variably defined, but often ≥65 years) are particularly vulnerable to shifts in ambient temperatures due to age-related changes in circulatory physiology that reduce the ability to adapt to sudden changes imposed by environmental stresses. There was an 85% increase in heat-related deaths of adults aged ≥65 years compared with 1990–2000.³⁸ Older individuals also have higher rates of pre-existing cardiovascular disease (e.g., coronary artery disease, stroke, heart failure) and underlying risk factors (e.g., obesity, diabetes, hypertension, hypercholesterolemia),^{49, 50} which increases the likelihood of using medications (e.g. beta-blockers, diuretics) that can make intrinsic compensatory mechanisms even less able to compensate for temperature extremes.⁵¹

Psychological stress of climate change-related events has also been associated with cardiovascular outcomes. For example, in addition to myocardial infarction and strokes, there are reported increases in Takatsubo cardiomyopathy following hurricanes.⁵² Furthermore, psychological stress is thought to be one of the mechanisms by which these events can worsen pre-existing health disparities, showing stronger affects among marginalized groups.⁵³ Projecting forward, excess cardiovascular deaths due to climate change are expected to increase,⁵⁴ with greater increases among adults ≥ 65 years of age (3.5-fold greater than adults <65 years) and Non-Hispanic Black adults (4.6-fold greater increase in excess deaths versus Non-Hispanic White adults).⁵⁴ Although slight differences in definitions of extreme weather events can have significant effects on reported associations with outcomes,^55–57 the preponderance of evidence supports that these events confer sizeable health risks. Extreme weather events are increasing in frequency and duration, and are predicted continue to increase with rising mean global temperatures;⁵⁸ thus, this ongoing threat to cardiovascular health is likely to continue to evolve.

Key Highlights from the article “Heat and Cardiovascular Mortality: An Epidemiological Perspective” by Singh, et al⁵⁹ include:

“Increased fine particulate matter concentrations and heat are both associated with an increased risk of cardiovascular mortality. However, the interactive effects between these two environmental factors show that air pollution increases the effect of heat on health. In a warming climate and the world population ageing, making the vulnerable subpopulation larger, an increase in heat-related mortality in the future is very likely.”

Noise and Light Pollution

Noise pollution, particularly from road traffic and other transportation noise, is emerging as an underappreciated cardiovascular and metabolic disease risk factor.^{60, 61} Epidemiological studies have shown that traffic noise is associated with increased cardiovascular morbidity and mortality.⁶² Noise cognition results in activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, leading to the release of stress hormones such as cortisol and catecholamines.⁶³ These stress hormones trigger activation of the renin-angiotensin-aldosterone system, and if chronically stimulated, can promote cardiovascular risk factors like hyperglycemia, hypercholesterolemia, and hypertension. Increases in cortisol have also been linked to central obesity and several studies have reported associations of road noise with obesity and adiposity markers.^{64, 65}

Studies in animal models have provided mechanistic insights into how noise exposure alters cardiovascular risk. Early studies in non-human primates and rodents showed that chronic noise exposure (4 weeks to 9 months) causes persistent increases in blood pressure,^{66, 67} which has been linked to impaired vascular reactivity and endothelium-dependent relaxation.⁶⁸ Studies in mice have also shown that aircraft noise exposure triggers endothelial dysfunction and vascular inflammation due to oxidative stress, and increased activation and adhesion of leukocytes,^69–71 which in turn can promote atherosclerosis. Another key pathway through which noise is thought to impair cardiovascular health is sleep disturbance.⁷² Sleep disturbance is known to increase cardiovascular disease risk, and recent studies in mice subjected to sleep fragmentation identified increases in hematopoiesis and circulating monocytes in the development of larger atherosclerotic lesions.⁷³ Interestingly, the noise-induced cardiovascular side effects are completely prevented in Nox2 deficient mice pointing to a crucial role of inflammatory cells in mediating the pathophysiology.⁷⁴ Together, these studies indicate that noise pollution may increase cardiovascular disease by mechanism involving both traditional (e.g., hypertension, obesity, hypercholesterolemia) and non-traditional (e.g., sleep disturbance) cardiovascular risk factors.

Key Highlights from the article “Transportation Noise Pollution and Cardiovascular Health” by Münzel, et al⁷⁵ include:

“Translational studies involving animals and humans provide evidence that noise is linked to disruptions in sleep, redox balance and vascular function and disturbances in autonomic and metabolic processes. Noise-related effects not only exacerbate the adverse health consequences of traditional cardiovascular risk factors, such as arterial hypertension and diabetes but also accelerate atherosclerotic processes and increase the overall risk of CVD.”

The built environment influences cardiovascular risk factors and health beyond noise pollution. Exposure to excess light, particularly in the nighttime, may disrupt circadian rhythm leading to adverse cardiovascular health. A recent longitudinal study from Hong Kong demonstrated higher risk of cardiovascular events with greater exposure to residential nighttime light measured using satellite imaging.⁷⁶ The effect of nighttime light exposure was independent of other urban pollutants including noise and particulate matter. Risk factors including obesity and hypertension as well as preclinical atherosclerosis have also been associated with light pollution in both the indoor and outdoor settings.^{77, 78} In animal models, continuous light exposure led to increased body fat with a lower proportion of brown adipose tissue.⁷⁹ Further mechanistic studies are warranted to evaluate the intersections of light pollution, circadian disruption and cardiovascular pathophysiology.

Per- and polyfluoroalkyl substances, Metals

Perfluoroalkyl substances (PFAS) are anthropogenic organic compounds widely used in manufacturing^{80, 81} and universally detected in humans.⁸² PFAS are absorbed via oral, inhalation and dermal exposure, with highest concentrations in the liver, kidneys and blood; they are not readily metabolized.⁸¹ Possible exposure pathways include food and water consumption, ingestion of house dust, hand-to-mouth transfer from PFAS-containing materials, and inhalation of indoor and ambient air.⁸¹ While serum concentrations of older “legacy” PFAS are decreasing after being phased out of use due to toxicity, concentrations of newer “emerging” PFAS with less clear health risks are on the rise.⁸³ Analyses of the National Health and Nutrition Examination Survey showed common PFAS in serum were significantly associated with increased odds of prevalent CVD and incident CVD events (congestive heart failure, coronary heart disease, angina pectoris, heart attack, and stroke). Proposed mechanisms linking PFAS and CVD include worsening of CVD risk factors such as hyperlipidemia,⁸¹ increasing activation of platelets and promoting hypercoagulability.⁸⁴ Experiments of PFAS in vitro show increases in reactive oxygen species,⁸¹ and worsening endoplasmic reticulum stress, triggering the unfolded protein response, ultimately resulting in oxidative damage.⁸⁵ Increased endothelial permeability, an early marker for and potential driver of atherosclerosis, has also been shown with increased PFAS.⁸⁶ Both coronary heart disease and stroke have been linked with endothelial dysfunction.⁸⁷ Increased PFAS are associated with endothelium-derived microvesicles, which may lead to vascular inflammation and increased carotid intima-media thickness in adolescents and young adults.⁸⁸ Thus, not only are PFAS associated with worsening of CVD risk factors (hyperlipidemia) and CVD events, they also may have direct vasculotoxic and inflammatory effects. Although connections between emerging PFAS and health risks are less well-established, there is a growing body of research implicating both legacy and emerging PFAS in cardiovascular disease. With this family of compound continuing to be expanded, regulations regarding their use have not kept pace with their development.

Key Highlights from the article “Per/Polyfluoroalkyl Substances: Links to Cardiovascular Disease Risk” by Schlezinger, et al⁸⁹ include:

“Frequently termed ‘forever chemicals’ owing to their long half-lives, PFAS are synthetic chemicals extensively used in industrial and consumer products, exposure to which is ubiquitous worldwide. There is compelling evidence that PFAS are linked to cardiovascular risk factors including dyslipidemia and elevated blood pressure.”

A recent scientific statement from the American Heart Association identified contaminant metals as CVD risk factors.⁹⁰ Metal exposures come primarily in the form of ingestion, though metals are also present in particulate matter air pollution. PM can contain Pb, Zn, Cd, As, Ni, and Fe among others. Many of these participate in redox reactions that generate reactive oxygen species leading to oxidative stress, and metals can also act via replacement of essential elements.⁹¹ Putative mechanisms include: impaired vasodilation resulting from oxidative stress,⁹² increased lipid peroxidation,⁹³ endoplasmic reticulum stress,⁹⁴ increased endothelial permeability,⁹⁵ impaired lipid metabolism, and altered foam cell formation.⁹⁶ Increases in blood concentrations of several of these metals are associated with increases in CVD risk.⁹⁷ Markers of exposures to heavy metals have been linked with traditional cardiovascular risk factors: obesity, hypertension, hyperlipidemia and type 2 diabetes;⁹⁸ and even low concentrations can increase cardiovascular risk among those with risk factors.⁹⁹ For example, blood lead and mercury concentrations have been associated with increases in blood lipids.¹⁰⁰ Cadmium concentrations in serum are positively correlated with serum triglycerides and total cholesterol; white blood cells, and C-reactive protein, which are implicated in the pathogenesis of atherosclerosis.¹⁰¹ Heavy metal exposure has also been linked with increased blood pressure,¹⁰² coronary artery disease, stroke¹⁰³ and peripheral artery disease¹⁰⁴ even at concentrations below safety standards. A recent meta-analysis of 37 cohorts in multiple countries showed increases in lead, cadmium, arsenic and copper were significantly associated with increases in coronary heart disease, overall cardiovascular disease.¹⁰⁵ Globally, deaths from cardiovascular disease related to lead exposure were recently estimated to range from 45–90 per 100,000 adults.¹⁰⁶ In addition, unequal distributions of heavy metals among subpopulations may be a driver of race- and socioeconomic-associated cardiovascular health inequities.^106–108 Overall, this suggests relationships with cardiovascular risk factors as well as cardiovascular disease directly, making heavy metal exposure an important contributor to cardiovascular risk.

Key Highlights from the article “Heavy metal exposure and cardiovascular disease” by Pan, et al¹⁰⁹ include:

“Most heavy metals are harmful environmental pollutants and pose hazards to human health when environmental exposure occurs in daily life. Related specifically to cardiovascular diseases, heavy metal exposure may result in hypertension, atherosclerosis, and/or arrhythmia, whilst chelation therapy may mitigate such adverse effects on the cardiovascular system.”

Neighborhood Factors and Health Equity

There is growing awareness of the impact that the built environment and neighborhood characteristics can have on cardiovascular health.¹¹⁰ Neighborhoods contain particular combinations of physical, psychosocial, cultural, and political features that contribute to community health. Increased cardiovascular risk can be ascribed to the absence of health-promoting factors such as walkability: less walkable neighborhoods are associated with a higher likelihood of coronary artery disease, hypertension, high cholesterol, obesity, and diabetes.¹¹¹ For people with coronary artery disease, living in a neighborhood with lower access to healthy foods (i.e., a “food desert”) is associated with worse cardiovascular outcomes even after accounting for their traditional risk factor burden.¹¹² Lower median neighborhood income is associated with higher 1-year mortality rates after a myocardial infarction.¹¹³ Residents of disadvantaged neighborhoods also have worse healthcare access and are less likely to receive preventive services or access primary care¹¹⁴ likely increasing cardiac admissions.¹¹⁵ Consistent with this, studies have shown that neighborhood disadvantages are associated with poor cardiovascular risk factor control, increased prevalence of cardiovascular disease,¹¹⁶ coronary heart disease¹¹⁷ and increased cardiovascular mortality.^{118, 119}

Cardiovascular risk is also increased with the presence of unhealthy factors: high residential density, poorly designed/older buildings (leading to greater exposure to temperature extremes, poor air quality), increased pollution (air, water, noise),^{114, 120, 121} and socioeconomic and discrimination-related stressors.^{122, 123} Conversely, the presence of some neighborhood features has been shown to be associated with improved cardiovascular health; on meta-analysis, increases in green space significantly reduce mortality from CVD, ischemic heart disease, and cerebrovascular disease, reduce and stroke incidence/prevalence.¹²⁴ There is also a growing literature describing the links between social networks, often strongly driven by neighborhood, and cardiovascular health. Social networks can influence health in both positive (e.g. social support and resilience) and negative ways (e.g. reinforcing harmful behaviors such as smoking).¹²⁵ In addition, social factors and socioeconomic status are shown to interact with environmental exposures since both pollutants and chronic stress can alter metabolic function, oxidative stress, inflammation and other drivers of cardiovascular disease.¹²⁶ These complex and interconnected neighborhood exposures can lead to differing outcomes by neighborhood. Many features of the build environment were constructed decades ago and perpetuate historical racial discrimination (i.e., “redlining”¹²⁷) with ongoing systemic inequities among marginalized communities. Even political gerrymandering has been used to dilute the political power of these marginalized groups in ways that increase exposure to environmental pollutants.^{128, 129} With overlapping risk factors exacerbating existing environmental injustice and health disparities, modern city planning efforts must take a sustainability focus to improve the health of communities faced with these exposures.

Key Highlights from the article “Greenspaces with Cardiovascular Health” by Keith, et al¹³⁰ include:

“Our review will focus on the cardiovascular effects of green spaces. In our article we will highlight evidence linking residential proximity to greenspaces to cardiovascular health and discuss potential mechanisms by which both short and long-term exposure to greenspaces improves cardiovascular health.”

Unique Exposome, Common Pathways

As the various physical and chemical environmental exposures associated with industrialization, unhealthy city designs, and climate change continue to increase, there is an emerging emphasis on understanding the “exposome” of an individual. The exposome concept was introduced in 2005¹³¹ to describe the changes in human physiology and pathophysiology induced by lifelong exposure to environmental stressors. Individual environmental risk factors are rarely present in isolation and the potential additive adverse health effects of multi-exposures to disease burden must be considered. For example, exposures to air pollution, light pollution and noise can activate partially overlapping, and potentially synergistic, pathological mechanisms.^{132, 133} Common mechanisms of cardiovascular disease risk attributed to these exposures include oxidative stress, vascular endothelium dysfunction, and increased supply and activation of immune cells.¹ Epidemiologic and animal model studies investigating multi-hit environmental exposures are becoming more frequent,^{132, 134, 135} but are still far from assessing the totality of different environmental stressors throughout the life course. It is also important to assess environmental exposures over time, as susceptibility to the harmful effects of environmental risk factors can occur during specific periods of life (infancy, childhood, adolescence, adulthood, and old age) and with pre-existing chronic diseases, particularly those of the cardio-pulmonary system.

A major challenge with exposome research is the volume of the data that must be considered to assess the combined effects of complex environmental exposures, presenting statistical and bioinformatics hurdles to making associations with outcomes. A comprehensive analysis of the exposome must include: identifying the totality of environmental exposures, determining the footprints of exposures on biological pathways in the host (e.g., by transcriptomics, proteomics, metabolomics and epigenetics), developing reliable biomarkers of exposure, and understanding intersection with genetic predispositions and host comorbities.¹ Further, socioeconomic and mental health determinants represent additional facets of the exposome that must be considered, as these have important biological influences. While each individual has a unique set of exposures over time, the cumulative effects of these converge on similar pathways toward adverse cardiovascular health outcomes.

Strategies to Reduce Environmental Cardiovascular Risk

Although environmental exposures have demonstrable impacts on human health, there are numerous strategies to reduce exposures and mitigate negative health effects. Such interventions are possible individually, locally, regionally or even globally. It is estimated that a phase out from fossil fuels towards clean renewable energy could save up to 5.1 million lives worldwide each year.⁴ Societal policies to improve air quality by reducing emissions, are projected to have benefits on climate change and health.¹³⁶ The WHO has recommended PM_2.5 limits of 5 μg/m3, yet current standards of the US and EU exceed this limit (>9 μg/m3). Granular activated carbon filters, used in some municipal water treatment facilities, can reduce ingestion of PFAS from aqueous sources;¹³⁷ and other PFAS removal methods are under active research.¹³⁸ Local modifications to the built environment (building design, transport infrastructure, green spaces, residential density, noise barriers) in urban areas can also have significant impacts on environmental exposures and cardiovascular health.¹¹⁰ Transportation-related changes (e.g. the transition from combustion engine cars to electric cars) and noise mitigation maneuvers (e.g. speed reduction, barriers and development of low-noise tires) can also reduce environmental CVD risk factors⁶⁰. Greenness, in particular, has been associated with a decrease in major adverse cardiovascular events, as well as cardiovascular mortality.¹³⁹ Although the mechanisms underlying these cardioprotective effects need further study, they have been linked to the ability of greenness to reduce air pollution and local temperatures, relieve stress, and promote physical activity.¹³⁹ Though modifications to the built environment and infrastructure cannot control climate change-related events and their cascading risks, adaptations to these events, along with emergency planning, can lessen some of the adverse health effects of these exposures.¹⁴⁰ The development of such heart-healthy cities will likely result in major public health benefits, including reducing CVD risk.¹³⁹

While local and regional regulations to decrease emissions and exposures take time to be enacted, individual-level interventions can reduce personal exposure. Portable air cleaners are widely available and are effective in improving air quality in indoor spaces.¹⁴¹ Inbuilt filters in home heating and air conditioning units can also be effective in particulate pollution mitigation in indoor spaces.¹⁴² Further, personal protection devices such as personal air purifying respirators and a wide variety of face masks can also reduce pollution exposure. Home water filtration systems can reduce exposure to PFAS and metals in water sources.

Behavior modifications and lifestyle changes can also be helpful in reducing cardiovascular health effects of pollution. Actions such as closing windows and using air filters during air pollution extremes, moving to a safer environment (such as a cooling center) during extreme heat events, and increasing baseline physical activity/exercise can all have a positive impact. It is well known that physical activity can promote health. Indeed, even in a polluted environment, outdoor physical has beneficial effects on the cardiovascular system, including reducing heart rate and heart rate variability indices.¹⁴³ The protective effect of physical activity holds for older adults who are known to be at increased risk for adverse effects of pollution exposure.¹⁴⁴ There is no single action that will reduce the cardiovascular risk of environmental exposures, however. Just as the exposome is a sum total of exposures across numerous environments over time, the “preventome” will require multifactorial interventions over the lifespan for both individuals and communities.

Key Highlights from the article “Personal Strategies to Reduce the Cardiovascular Impacts of Environmental Exposures” by Bonnani, et al¹⁴⁵ include:

“Evidence suggests portable air cleaners can improve indoor air quality and may lower blood pressure. Smoking cessation markedly reduces exposure to fine particulate matter and contaminant vasculotoxic metals.”

Conclusion

The global population is expected to reach 10 billion people by 2050, with the majority living in urban areas rife with environmental hazards. Societal actions to impose regulatory limits on environmental pollutants and develop strategies to mitigate their effects will require a collaborative approach. Affected and interested parties include: communities; scientific researchers; medical professionals; public health and environmental officials; along with state, local, tribal and federal entities who create laws, ordinances and monitor compliance with environmental law. And, in order to be successful, actions will require cooperation and buy-in from industries and companies whose processes and products generate pollutants. Meaningful progress will require confronting the economic interests of fossil fuel and other environmentally damaging industries, and require scientific advances to further mitigation and phase out fossil fuels. Identifying and quantifying the consequences of environmental hazards on cardiovascular health will require rigorous field studies in humans and the development of appropriate experimental models to study environmental exposures. There is a need to develop new approaches (e.g. in vitro, in silico) that reduce, where possible, the use of animals in research. It will be important to understand the effects of exposure dose and duration of environmental stressors. A significant challenge will be to quantify the additive adverse health effects of multi-pollutant exposures common in urbanized areas (e.g., air and noise and chemical pollution). Progress in this area will require technical advances in quantifying the “exposome” and the biological changes induced by environmental exposures, such as the development of wearable sensors for continuous monitoring of environmental hazards and health outcomes. Current limitations involve privacy concerns surrounding the geographical tracking and collection of personal exposure data required for such comprehensive exposure assessments and calculations of CVD risk, along with challenges involved in the analysis of the large, complex datasets.

Alongside understanding the effects of environmental stressors on cardiovascular health, deeper studies of climate change are needed to understand future hazards and how they may impact the cardiovascular system. The world will have to reckon with differences in global regional exposure to environmental hazards that will have major impacts on countries and populations. In addition, with the growing awareness of the impact that built environments and neighborhood inequalities can have on environmental exposures, greater emphasis should be placed on the development of heart healthy cities and implementation of interventions to address health inequities.

The sixth United Nations Environment Assembly in 2024 emphasized the impact of science to inform policies protective of human health. The sessions opened with the Youth Environment Assembly meeting noting that “their perspectives and solutions are necessary to advance environmental science.”¹⁴⁶ The young generation is acutely attuned to how our world drives our current and future health. Mentoring young scientists in all our research endeavors is key to including the youth voices and a forward-looking approach to ground environmental progress in scientific investigation. Thus, we invited two young scientists to participate in this overarching review manuscript. Jacob Blaustein is a senior at Westfield High school planning to study environmental engineering and Matthew Quisel is a junior at Newton South High School planning to study molecular biology. Both expressed intense interest in contributing to finding solutions to mitigate environmental drivers of cardiovascular health (see inset). Their collaboration with Drs. Hamburg and Wittkopp opens the Circulation Research compendium on “Environmental Impacts on Cardiovascular Health and Biology” that serves as a resource for both cardiovascular and non-cardiovascular scientists on the many environmental exposures that affect the cardiovascular system, and possible solutions for the future.

List of Abbreviations

CVD

cardiovascular disease

PFAS

per- and polyfluoroalkyl substances

PM

particulate matter

PM_2.5

fine particulate matter, <2.5 μm