Effects of air pollution on the

cardiovascular system

Air pollution and human health – a tale as old as time

Introduction

 Air pollutants emitted by industrial, traffic, household, and agricultural sources

 200,000 deaths in the United States per year.
 80% deaths CVD, and > 60% from indoor air pollution.
 More than twenty percent of all cardiovascular disease (CVD) deaths are caused
by air pollution — more than three million deaths every year — and these
numbers will continue to rise unless the global community takes action.
 Nine out of ten people worldwide breathe polluted air, which disproportionately
affects those living in low-resource settings.
 In October 2018, World Health Organization (WHO)
Director-General Dr Tedros Adhanom Ghebreyesus made
headlines around the world by declaring that:
“No one, rich or poor, can escape air pollution. It is a silent
public health emergency”.
Sources of Air Pollution

 Stationary Sources:
Factories, power plants, smelters.

 Area Sources (smaller stationary sources):

Dry cleaners, degreasing operations.

 Mobile Sources:
Cars, buses, planes, trucks, trains.

 Natural Sources:
Windblown dust, volcanic eruptions
 Composition of Air Pollution

 Air pollution consists of aerosols containing a mixture of both particles and gases.
 Particulate matter (PM) is easily measured and readily relatable to the adverse health effects.
 PM stands for particulate matter (also called particle pollution) mixture of solid particles and liquid droplets
found in the air.
 PM10 : inhalable particles, with diameters that are generally 10 micrometres and smaller.
 PM2.5 : fine inhalable particles, with diameters that are generally 2.5 micrometres and smaller.
Size Comparison for PM particles
 Gaseous Pollutants

 Carbon monoxide (CO), nonmethane hydrocarbons, nitrogen oxides (NOx), sulfur oxides (SOx), ozone.

• (O3), and volatile organic carbons (VOCs).

 Outdoor and Indoor Air Pollution

 PM generated by both natural and anthropomorphic sources.

 Processes such as volcanic eruptions, spontaneous forest fires, sea sprays, and soil erosion are natural unpaved
roads, traffic, mining, welding, building and other human activities.
 Most coarse PM (PM10) arises from dust and ground materials, endotoxin, pollen grains, fungal spores,
vegetation, and debris, whereas fine PM (PM2.5) is derived mostly from smog, traffic, and combustion.
 In most urban environments, traffic is the major source of PM
 Combustion of any fossil fuel wood, gas, diesel, and gasoline—generates PM, particularly fine and ultrafine
PM.
Indoor pollution
 Developing countries, indoor air pollution from biomass fuels, coal, and kerosene burned.
 Cooking, particularly frying, is an important source of indoor pollution.
 Cooking indoors can lead to a 10-fold increase in the number of ultrafine particles
 Burning of candles or incense can generate high levels of particulate air pollution.
 Air fresheners generate xylene, aldehydes, and esters, which can react with O3 to produce secondary pollutants
 Pollen, dander, toxic molds, and dust, which frequently consists of fungi, endotoxin and bacteria, as well as tobacco
smoke
 There are few indoor sources of PM2.5, which comes mostly from outdoor sources and traffic
 Living next to a major street increases the levels of indoor PM2.5 and increases exposure to
 traffic-generated pollutants such as NOx and VOCs.
Some groups are at greater risk
 People with heart or lung diseases: are more vulnerable to particle
pollution because of their conditions (such as congestive heart disease,
coronary artery disease, asthma, or chronic obstructive pulmonary
disease.)
 Older adults also are considered at risk, because they are more likely to
have heart and lung disease. (Sometimes that disease hasn’t been
diagnosed yet.).
 Children: because they are more likely to be active, they breathe more
air per pound of body weight than adults, and their bodies are still
developing.
 Pathophysiology

 Ambient air particles (<10 μm) results in the deposition of airborne particles in the
lung,
 PM10 is deposited in the bronchial airways, activates the innate immune response
 Production of interleukin (IL)-8.
 Recruitment of neutrophils to the lung leads to airway inflammation.
 Fine particles are deposited in lung, especially in the alveoli, also pass into circulation.
 Impaired surfactant function could lead to chronic lower airway inflammation
 UFP pass from the lung to other peripheral organs, including the heart and the brain
 Production of reactive oxygen species (ROS)
 Decrease in lung capacity and pulmonary inflammation
 Accumulation of neutrophils, protein and fibrinogen in the bronchoalveolar fluid
 Inducing apoptosis in alveolar macrophages
 Inhibiting PMN phagocytosis and respiratory bursts
 Mild pulmonary inflammation, the systemic consequences of which exacerbate CVD risk.
 PM inhalation directly activates sensory receptors
 Imbalance in the autonomic nervous system, which may affect both cardiac rhythm and cardiac conduction,
leading to an increase in the risk of arrhythmias and SCD, particularly in vulnerable individuals
The biological mechanisms by which inhaled pollutants can cause cardiovascular (CV)
morbidity and mortality
 Air Pollution and Cardiovascular Mortality

 80% of deaths attributable to chronic air pollution are CVD

 Particularly IHD, arrhythmias, heart failure, and cardiac arrest
 10μg/m3 increase in PM2.5 levels is associated with 8% -18% excessive risk of CV mortality
 No threshold has been detected below which air pollution does not affect CV health
 The exposure-response relationship between long-term exposure to PM2.5 and the risk of CVD mortality
steep at low levels of exposure and flattening at high exposure levels, such that most of the risk is imparted
at low levels of exposure
 Risk of CVD mortality caused by long-term PM2.5 exposure may be comparable in different cities, even
with widely different levels of air pollution.
 Short-term increases in PM are associated with increased risk of total mortality.
 10μg/m3 increase in PM2.5, 0.7% to 1.7% increase in all-cause mortality on subsequent days
 Relationship between PM exposure and mortality independent of gaseous co-pollutants
 Smokers, elderly persons, and diabetes or heart failure particularly sensitive to PM exposure.
 Indoor exposure to air pollution is also linked to excessive CV mortality.
 In developing countries, indoor air pollution caused by biomass burning is associated
with 2 million deaths per year
 Use of biomass fuels for cooking and heating increases the risk of coronary heart
disease (CHD) twofold to fourfold
Myocardial Infarction

 Both acute and chronic exposures increase risk

 Elevated risk for MI with exposure to elevated PM or traffic exposure (1, 2, or 6 hours
or a few days)
 The acute risk may remain elevated and may increase even 2 days after exposure
 10% to 20% increase in risk per 10μg/m3 increase in PM2.5 levels
 The risk is more strongly associated with PM2.5
 Mostly to elderly individuals or those with CAD or structural heart disease.
 Obese women may be particularly at risk.
 Long-term exposure to traffic-related air pollution is also associated with MI
recurrence.
 Arrhythmogenesis

 Cardiac electrical instability:

Alterations in heart rate
Heart rate variability
Increase arrhythmia risk
Individuals with pre-existing disease are likely to be more sensitive.

Increase the risk of atrial fibrillation (AF) as

 prolongation of the PR duration
 Increase in the P wave complexity
 Increase the risk of sudden cardiac death (SCD) and fatal CHD.
 Risk higher in elderly persons or individuals who have underlying cardiac disease.
 Strongest for PM10, PM2.5, and O3, a well as traffic-generated pollutants.
 Ambient levels of PM2.5 increased risk of out-of-hospital cardiac arrest, particularly in individuals with high CVD
risk burden.
Heart Failure

 Increase in daily hospitalization for HF

 Increase in HF admissions
 Direct effects of chronic exposure to air pollution on cardiac function and remodelling
have been reported in both human and animal studies
 Air pollution are associated with increased right and left ventricular mass
 Hypertension

 Acutely with changes in systemic arterial BP (approximately 1 to 4 mm Hg per 10μg/m3 increase in PM)
 Effects larger in elderly individuals or those with preexisting CVD.
 Chronic exposure to elevated levels of air pollution may lead to the onset of hypertension.
 Individuals who live near major roadways and are therefore exposed recurrently to traffic- generated pollutants have a
higher prevalence of hypertension.
 Comparing those who live less than 100 m of a major roadway with those who live more than 1000 m, a 9% higher
prevalence has been reported.
 Acute exposure to PM or diesel exhaust could lead to a modest (3 to 4 mm Hg), but rapid increase in systolic BP and a
smaller increase in diastolic BP.
 Significantly, antihypertensive drugs appear to mitigate against the effects of air pollution on BP, and therefore
appropriate medical management of hypertension could attenuate the impact of air pollution exposure.
 Indoor air pollution increases systolic, and to a lesser extent, diastolic BP.
 Indoor air pollution due to the use of solid fuels is also associated with increased prevalence of hypertension
 Management and Intervention

 Difficult to control at an individual level.

 Exposure can be reduced by individual choices to diminish the impact of air pollution on CV health.
 Avoidance of areas of high pollution, especially traffic pollution, particularly by individuals with high CVD risk.
 Because residential proximity to major roadways increases exposure to traffic pollutants, avoidance of such exposure may be
particularly beneficial for post-MI patients or those with HF.
 Most indoor pollutants (e.g., molds, endotoxin, bacteria, dust) can be eliminated by maintaining clean living environments
 Avoiding the use of candles, incense, or air fresheners indoors.
 Discontinuing the use of solid biomass for fuel
 using chimney woodstoves that prevent the accumulation of indoor air particulates.
 Exposure to particles generated by cooking and frying can be minimized by proper ventilation or filtration.
 Most airborne particles can be removed by an electrostatic precipitator in a single-pass efficiency of 90% or greater, even for
smaller particles.
 Vehicle air conditioning can reduce exposure to traffic-generated air pollutants
 Eliminating tobacco smoke might have the most robust effect on improving indoor air quality.
Conclusion

 80% deaths CVD, and > 60% from indoor air pollution
 Particularly IHD, arrhythmias, heart failure, and cardiac arrest
 Most indoor pollutants can be eliminated by maintaining clean living environments.
 Residential proximity to major roadways increases exposure to traffic pollutants
 The future of air pollution as an environmental
determinant of health
 In 2019, air pollution was recognized as the fourth-
highest ranking risk factor for mortality, with more
attributable deaths than high LDL cholesterol, high
body-mass index, physical inactivity, or alcohol use.
 Yet at the time of this publication in 2021, many
physicians, scientific societies, advocates, and
policymakers remain unaware of air pollution’s
prominent position as a threat to health and continue to
operate as if its manifold impacts are negligible,
unmodifiable, or perhaps simply too overwhelming to
confront.
 However, the momentum of international climate change
movements and the dramatic impacts of the COVID-19
pandemic on human society are creating an
unprecedented opportunity to revaluate the role of the
global cardiovascular community in tackling this critical
issue.