Environmental Pollution and Cardiovascular Disease: Mechanisms,

Risk Factors, and Policy Recommendations

Yuncheng Huang

Fudan University, Shanghai, China

Keywords: Environmental Pollution, Cardiovascular Disease, Public Health Policy.

Abstract: Cardiovascular disease (CVD) results from a combination of genetic and environmental factors. Growing

evidence shows that environmental pollution—such as air pollutants (PM2.5, NO2, O3), waterborne toxins

(heavy metals, organic pollutants), and soil contaminants (phthalates, bisphenol A)—contributes significantly

to CVD. These exposures can increase oxidative stress, activate immune cells, disrupt circadian rhythms, and

trigger stress reactions. They also promote traditional cardio-vascular risk factors like obesity, diabetes, and

hypertension. This review summarizes recent findings on the link between environmental contaminants and

CVD. It proposes strategies for mitigation, including stricter emission standards, expanded monitoring, public

health campaigns, and incorporating environmental exposure assessments into cardiovascular risk screening.

These interventions are essential to reduce pollution-related cardiovascular morbidity and mortality.

1 INTRODUCTION

Cardiovascular disease (CVD) is the leading cause of

mortality worldwide, with its prevalence rising most

sharply in low‑ and middle‑income countries. From

1990 to 2019, the number of cardiovascular disease

cases nearly doubled, the prevalence of

cardiovascular disease increased from 271 million to

523 million worldwide, and the number of

cardiovascular deaths increased from 12.1 million to

18.6 million, according to the Global Burden of

Cardiovascular Disease report (Roth et al., 2020).

Heart and vascular diseases, such as hypertension,

coronary heart disease, cerebrovascular disease,

peripheral vascular disease, heart failure, rheumatic

heart disease, congenital heart disease, and

cardiomyopathy, are collectively referred to as

cardiovascular disease (CVD) by the World Health

Organization (WHO). The escalating human and

economic costs of CVD have made its prevention and

management a critical public health priority (Liu et

al., 2024).

Numerous risk factors are involved in the higher

incidence and mortality of cardiovascular disease.

These include individual habits like drinking and

smoking, family dynamics like marital status, and

environmental influences. The development of

cardiovascular disorders, including hypertension,

coronary heart disease, and stroke, has been

demonstrated to be directly linked to environmental

pollution, particularly contamination of the air, water,

and soil. By altering vascular endothelial function and

hastening atherosclerosis, for example, fine

particulate matter (PM

2.5

) in the atmosphere has been

shown to trigger an inflammatory response, increase

oxidative stress, and contribute to the development of

cardiovascular disease. Furthermore, the

cardiovascular system can be negatively impacted by

toxic compounds found in soil and water pollution

through alterations in hormone levels, immunological

reactions, and other mechanisms. Pollutants can

impact the cardiovascular system via a number of

biological mechanisms, such as thrombosis, oxidative

stress, inflammatory response, changed expression of

genes encoding antioxidants, and extracellular vesicle

release. The formation and progression of CVD are

facilitated by the interactions and connections among

these pathways (Thomas et al., 2025; Omar et al.,

2024). As shown in Figure 1, these mechanisms

elevate cardiovascular risk and contribute to adverse

outcomes such as myocardial infarction, stroke, heart

failure, and arrhythmias.

This review synthesizes recent experimental and

epidemiological data on the links between

environmental pollution and CVD, outlines key

mechanistic insights across air, water, and soil

contaminants, and proposes concise, evidence‑based

interventions to reduce exposure and cardiovascular

risk.

420

Huang, Y.

Environmental Pollution and Cardiovascular Disease: Mechanisms, Risk Factors, and Policy Recommendations.

DOI: 10.5220/0014494400004933

Paper published under CC license (CC BY-NC-ND 4.0)

In Proceedings of the 1st International Conference on Biomedical Engineering and Food Science (BEFS 2025), pages 420-425

ISBN: 978-989-758-789-4

Figure 1. Environmental exposures and cardiovascular

health (Jacob et al., 2024). Numerous harmful exposures

have adverse effects on cardiovascular risk factors and

outcomes via multiple overlapping pathways.

2 AIR POLLUTION

Based on their composition, outdoor air pollutants

can be divided into two categories: particle pollutants

and gaseous pollutants. Based on particle size,

particulate matter (PM) can be categorized as fine

particulate matter (PM

2.5

), ultrafine particles (UFPs),

inhalable particulate matter (PM

), and others.

Carbon monoxide (CO), sulfur dioxide (SO

nitrogen dioxide (NO

), ozone (O

), and other gases

are examples of gaseous pollution. Air pollutants can

be produced and enter the human body from a variety

of sources, including car exhaust, industrial

emissions, forest fires, and other sources, due to the

world's fast industrialization and urbanization (Yue et

al., 2024). Hypertension is a significant risk factor for

cardiovascular conditions such coronary heart

disease, stroke, heart failure, atrial fibrillation,

valvular heart disease, and aortic syndrome,

according to large cohort studies. The risk of various

conditions, including ischemic heart disease,

cerebrovascular disorders, heart failure, and

arrhythmias, may rise with either short-term or long-

term exposure to PM

2.5

. The damaging elements of

PM, such as exposure to lead, cadmium, and arsenic,

are particularly dangerous for the heart and vascular

system and are linked to a higher risk of

cardiovascular disorders. An elevated risk of stroke,

atrial fibrillation, and atrial flutter is linked to

prolonged exposure to NO

. An elevated risk of

cardiovascular death, mostly from ischemic heart

disease, can result from prolonged exposure to O

Hospitalization for ischemic stroke can be

considerably increased by short-term exposure to

environmental SO

, which is linked to cardiogenic

embolism.

2.1 PM

Tiny solid or liquid particles that are suspended in the

atmosphere are referred to as particulate matter (PM).

Particles with a diameter of 10 micrometers or less

are referred to as PM

, while particles with a

diameter of 2.5 micrometers or less are referred to as

2.5

. PM

2.5

and UFPs can penetrate deeper into the

respiratory tract and reach the alveoli because of their

smaller size. This can impact gas exchange and

perhaps have harmful effects on distant organs like

the heart, brain, and placenta. According to research,

exposure to PM

2.5

can raise oxidative stress levels and

produce too many reactive oxygen species (ROS),

which can cause cell damage and serious

inflammatory reactions. These factors can then

accelerate the development and progression of

cardiovascular diseases (CVD). In particular, by

increasing oxidative stress, PM

2.5

can activate cardiac

ryanodine receptor 2 (Ryr2), resulting in intracellular

calcium excess and cardiomyocyte death (Meng et al.,

2022). The development of atherosclerotic plaques

can also be accelerated by PM

2.5

exposure, which can

also cause endoplasmic reticulum stress in

macrophages, encourage Ca

accumulation in

atherosclerotic plaques, raise ROS levels in the

plaques, and increase apoptosis (He et al., 2020).

Intercellular adhesion molecule-1 (ICAM-1) and

vascular cell adhesion molecule-1 (VCAM-1) are

endothelial function adhesion factors that are elevated

in response to short-term exposure to PM

2.5

, causing

endothelial dysfunction. Heart disease or other

cardiovascular problems may eventually arise from

the buildup of arterial plaques brought on by

prolonged exposure to PM

2.5

, which can also cause

vascular inflammation and atherosclerosis.

According to epidemiological research, UFP

exposure quickly lowers HRV, which has an impact

on cardiac autonomic function (Zhang et al., 2022).

Overall, oxidative stress, inflammatory reactions,

endothelial dysfunction, and modulation of the

autonomic nervous system are some of the ways that

2.5

and UFPs negatively impact the cardiovascular

system. The development of cardiovascular disorders

is facilitated by the interaction of these pathways.

2.2 Gaseous Pollutants

The cardiovascular system is largely harmed by

gaseous pollutants through a variety of clinical and

physiologic mechanisms. Atrial fibrillation, atrial

Environmental Pollution and Cardiovascular Disease: Mechanisms, Risk Factors, and Policy Recommendations

421

flutter, and stroke are among the cardiovascular

events that are closely linked to prolonged exposure

to nitrogen dioxide (NO

). NO

can cause oxidative

stress and systemic inflammation, which affects

endothelial cell function and accelerates the

development of atherosclerotic plaques. Arrhythmia

risk may also be raised by the activation of

inflammatory reactions, which may disrupt the

regular activity of cardiomyocytes. Another prevalent

gaseous pollutant, ozone (O

), has a more intricate

mechanism of harm. In addition to interfering with

the metabolism of arachidonic acid, which leads to

the production of thromboxane A2 and 20-hydroxy

arachidonic acid, which activates platelets and causes

oxidative damage, exposure to O

also increases the

expression of coagulation biomarkers, including von

Willebrand factor and clotting factors, to exacerbate

blood coagulation tendencies and raise the risk of

cardiovascular events (Taylor-Clark, 2020).

Significantly, the association between exposure to air

pollution and the emergence of cardiopulmonary

disorders is mediated by extracellular vesicles (EVs).

The pathophysiology of cardiovascular illnesses is

significantly influenced by O

exposure, which

modifies the release of EVs and the expression of the

miRNAs they carry. Hemoglobin's ability to deliver

oxygen is diminished by carbon monoxide's (CO)

strong affinity binding to it, which causes tissue

hypoxia and exacerbates cardiac hypoxia. In addition

to hastening the development of atherosclerotic

plaques, prolonged low-level CO exposure can cause

acute cardiovascular events including myocardial

infarction. Short‑term exposure to sulfur dioxide

(SO

) induces oxidative stress and respiratory

inflammation, which indirectly destabilize

cardiovascular function and increase the risk of

hospitalization for ischemic stroke and cardiogenic

embolism.

3 WATER AND SOIL POLLUTION

The term "soil and water pollution" describes

dangerous materials found in groundwater and water

bodies that could have a negative impact on living

things. Waste disposal, industrial emissions, and

agricultural practices are the primary sources of

contaminants. In addition to damaging aquatic life

and lowering crop production, this pollution has a

major negative impact on human health. The 2019

Global Burden of Disease Study estimates that water

pollution from contaminated water sources killed

about 1.23 million people. Pesticides, plastic debris,

heavy metals, and persistent organic pollutants

(POPs) are examples of common contaminants

(Usman et al.,2024).

3.1 Plastics and Their Additives

Plastics are made of synthetic or organic polymers

and are highly sought after worldwide due to their

excellent qualities, which include flexibility,

durability, and low production costs. Environmental

pollution is caused by common plastic additives

including phthalates, bisphenol A (BPA), and heavy

metals. Phthalates may be linked to cardiovascular

diseases (CVD), especially coronary artery disease

(CAD), according to recent research. Increased

carotid intima-media thickness (CIMT),

atherosclerosis, increased risk of hypertension

(HTN), metabolic syndrome (MetS), oxidative stress,

and insulin resistance have all been linked to elevated

phthalate levels. Polycarbonate plastics and epoxy

resins are two common products made with bisphenol

A (BPA). Numerous epidemiological studies have

demonstrated a strong link between BPA exposure

and an elevated risk of cardiovascular illnesses,

primarily based on data from the National Health and

Nutrition Examination Survey.

3.2 Pesticides and Persistent Organic

Pollutants (POPs)

Because pesticides and persistent organic pollutants

(POPs) are difficult for the environment to break

down, they can linger and find their way into human

bodies through soil and water. Furthermore, it has

been discovered that pesticide exposure raises the

incidence of certain cancers and has a negative impact

on cardiovascular health. Increased oxidative stress,

inflammation, and atherosclerosis could be the cause

of these outcomes. Certain pesticides have the ability

to directly harm cells' mitochondria, increasing

reactive oxygen species (ROS), which in turn causes

oxidative stress and inflammation, endothelial cell

malfunction, and the acceleration of atherosclerosis.

Meanwhile, there is a strong correlation between the

incidence and mortality of cardiovascular illnesses,

particularly with elevated risks of coronary artery

disease (CAD), peripheral artery disease, and CIMT,

and exposure to persistent organic pollutants, such as

perfluoroalkyl compounds. The cardiovascular

system is continuously threatened by prolonged

exposure to pesticides and POPs, with possible

pathogenic pathways including oxidative stress,

inflammatory activation, and endocrine disruption.

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3.3 Heavy Metal Pollution

It has been determined that exposure to heavy metal

pollution increases the incidence of cardiovascular

illnesses (Jacob et al., 2024). Although particulate air

pollution also contains metals, ingestion is the main

way that people are exposed to metals. Among the

most extensively researched environmental

hazardous metals linked to cardiovascular disease

(CVD) are arsenic, cadmium, lead, copper, and

mercury. Numerous studies show that exposure to

metals, even at low levels, can raise the risk of

cardiovascular illnesses and the mortality that goes

along with them. The majority of metal contaminants

cause cardiovascular illnesses by causing oxidative

stress and systemic inflammation, which are

prevalent pathophysiological routes. Atherosclerosis

is facilitated by systemic inflammation, which in turn

stimulates vascular inflammation, endothelial

damage, and coagulation mechanism activation.

Lipid peroxidation, an early indicator of

atherosclerosis, has been discovered to be facilitated

by a variety of hazardous metals. Usually, by

competing with vital metals like calcium, iron, and

zinc in the body, these harmful metals raise the risk of

cardiovascular illnesses. For instance, lead's capacity

to mimic the actions of vital elements like calcium

and iron contributes to its cardiotoxicity. Because of

their similar chemical structures, cadmium and lead

can take the role of zinc in biological processes.

Furthermore, by altering other risk factors, especially

by raising the risk of obesity and hypertension (HTN),

heavy metals may also make cardiovascular disorders

worse (Usman et al.,2024; Jacob et al., 2024) (Figure

2).

4 POLICY RECOMMENDATIONS

AND HEALTH INTERVENTION

MEASURES

4.1 Strengthen Environmental

Protection Policies

Stricter environmental protection laws should be

developed and put into effect by the government to

lessen the negative effects of pollution on

cardiovascular health. Setting stronger emission

limits, encouraging the use of clean energy, and

bolstering the control of pollution in the air, water,

and soil are some specific actions. For instance,

lowering airborne concentrations of nitrogen oxides

and

fine

particulate

matter

(PM

2.5

)

might

lessen

the

Figure 2. Distribution of heavy metals and their effects on

the human cardiovascular system (Pan et al., 2024). The

diagram depicts the distribution of arsenic (As), cadmium

(Cd), lead (Pb), mercury (Hg), and chromium (Cr) in the

environment (rivers, oceans, air, and soil) and the exposure

source (food, drinking water, and industrial products).

When exposure to heavy metals, they enter the body

through inhalation, ingestion and dermal contact,

eventually lead to cardiovascular abnormalities such as

arrhythmia, hypertension and atherosclerosis.

direct damage they do to the cardiovascular system.

At the same time, to guarantee the safety of drinking

water and the health of the food supply chain,

stringent management of soil contamination and

water resources is required, preventing dangerous

compounds from entering the human body through

the food chain. The implementation of these measures

requires coordination and cooperation among

government departments, as well as active public

participation, to achieve continuous improvement in

environmental quality.

4.2 Promote Health Education and

Behavioral Interventions

Preventing cardiovascular illnesses requires

increasing public understanding of environmental

protection and health literacy. The government should

encourage the public to adopt healthy lifestyles that

include balanced diets, regular exercise, quitting

smoking, and consuming alcohol in moderation by

using a variety of channels, including the media,

community events, and online platforms, to spread

information about the link between environmental

pollution and cardiovascular diseases. To lessen the

detrimental effects of environmental pollution, high-

risk groups such as the elderly, children, and people

with cardiovascular problems should receive

personalized health management services. To

improve the future generation's environmental

awareness and health behavior abilities, educational

Environmental Pollution and Cardiovascular Disease: Mechanisms, Risk Factors, and Policy Recommendations

423

institutions should also include environmental health

information in their curricula.

4.3 Enhance Monitoring and Data

Collection

It is crucial to improve data collecting and

environmental pollution indicator monitoring in order

to more accurately evaluate the relationship between

environmental pollution and cardiovascular illnesses.

The government should assist the public in avoiding

high-pollution areas, develop and enhance

environmental monitoring networks, and rapidly

disseminate information about pollution.

Additionally, epidemiological research should be

combined by health departments to continuously

monitor and examine the relationship between

environmental pollution and the incidence of

cardiovascular disease, gathering pertinent data to

support the development of policies. This data's

sharing and public availability will also help research

institutions carry out in-depth analyses to find

successful intervention strategies.

4.4 Enhance Healthcare System

Capacity

Hospitals and other community healthcare facilities

should improve early cardiovascular disease

screening, perform routine cardiovascular health

examinations, promptly identify people who may

have cardiovascular disease, and offer early therapies.

In order to improve medical institutions' capacity to

diagnose and cure cardiovascular diseases brought on

by environmental pollution, the government should

also invest more in equipment and technologies for

cardiovascular disease diagnosis and treatment. To

properly advise patients on their health, healthcare

providers should undergo specific training to increase

their knowledge of how environmental pollution

affects cardiovascular health. In order to guarantee

that more people, particularly those residing in highly

polluted areas, have easy access to cardiovascular

health management services, the government can

simultaneously encourage changes to the health

insurance system.

5 CONCLUSION

Numerous studies have demonstrated the strong

correlation between environmental pollution

(particularly air, water, and soil contamination) and

the onset and progression of cardiovascular disorders.

Through mechanisms like altering vascular

endothelial function and speeding up atherosclerosis,

fine particulate matter (PM

2.5

) in the air can cause

inflammatory reactions, raise oxidative stress, and

encourage the development of cardiovascular

illnesses. Furthermore, the cardiovascular system can

be adversely affected by toxic compounds found in

soil and water pollution through alterations in

hormone levels, immunological reactions, and other

routes. There are several biological ways in which

these pollutants impact the cardiovascular system, but

the main ones are oxidative stress, inflammation,

thrombosis, alterations in the expression of genes that

code for antioxidants, and the release of extracellular

vesicles. These pathways are interrelated and interact

with each other, promoting the onset and

development of cardiovascular diseases.

The government should create and execute

stronger environmental protection policies, such as

raising emission standards, encouraging the use of

clean energy, and bolstering the control of air, water,

and soil pollution, in order to address the threat that

environmental pollution poses to cardiovascular

health. At the same time, it is crucial to promote

healthy lifestyles, raise public knowledge of

environmental protection and health literacy, and

offer high-risk populations individualized health

management services. Important steps to lessen the

detrimental effects of environmental pollution on

cardiovascular health include bolstering the

monitoring of environmental pollution indicators,

gathering pertinent data, and improving the capacity

of the healthcare system to respond. In conclusion, it

is important to consider how environmental

contamination affects cardiovascular health. We can

successfully reduce the detrimental effects of

environmental pollution on cardiovascular health and

raise the general level of cardiovascular health in the

population by putting in place efficient policy

measures, bolstering behavioral and health education

initiatives, and improving the response capabilities of

the healthcare system.

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