Long-term exposure to ambient ozone appears to accelerate arterial conditions that progress into cardiovascular disease and stroke, according to a new University at Buffalo study.
It’s the first epidemiological study to provide evidence that ozone might advance subclinical arterial disease – injuries that occur to the artery walls prior to a heart attack or stroke – and provides insight into the relationship between ozone exposure and cardiovascular disease risk.
“This may indicate that the association between long-term exposure to ozone and cardiovascular mortality that has been observed in some studies is due to arterial injury and acceleration of atherosclerosis,” said study lead author Meng Wang, assistant professor of epidemiology and environmental health in the UB School of Public Health and Health Professions.
The paper was published in May in the journal Environmental Health Perspectives.
The longitudinal study followed nearly 7,000 people aged 45 to 84 from six U.S. regions: Winston-Salem, North Carolina; New York City; Baltimore; St. Paul, Minnesota; Chicago; and Los Angeles.
Participants were enrolled in the Multi-Ethnic Study of Atherosclerosis (MESA) and have been followed for over a decade.
Atherosclerosis refers to the build-up of plaque, or fatty deposits, in the artery walls, which, over time, restricts blood flow through the arteries.
This can cause blood clots, resulting in a heart attack or stroke, depending on which artery – coronary or carotid, respectively – the plaque accumulates in.
The study found that chronic exposure to ozone was associated with a progression of thickening of the main artery that supplies blood to the head and neck.
It also revealed a higher risk of carotid plaque, a later stage of arterial injury that occurs when there’s widespread plaque buildup in the intima and media, the innermost two layers of an artery wall.
“We used statistical models to capture whether there are significant associations between ozone exposure and these outcomes,” said Wang, who is also a faculty member in the UB RENEW (Research and Education in eNergy, Environment and Water) Institute.
“Based on this model, it suggests that there is an association between long-term exposure to ozone and progression of atherosclerosis.”
While the study finds an association between air pollution and atherosclerosis, researchers aren’t clear on why.
“We can show that there is an association between ozone exposure and this outcome, but the biological mechanism for this association is not well understood,” Wang said.
The study is unique in its focus on ozone exposure rather than particulate matter.
Particle pollution comes from a variety of human and natural activities.
Examples include vehicle exhaust, fossil fuel burning and agricultural and industrial operations and processes. Smog is a harmful byproduct of such activities.
That shouldn’t be confused with the ozone layer in Earth’s upper atmosphere, which shields us from much of the sun’s ultraviolet radiation.
Ground-level ozone, however, causes serious health problems.
Long-term ozone (O3) exposure is associated with cardiovascular mortality, but little is known about the associations between O3 and subclinical arterial disease.
Air pollution is composed of particulate matter (PM) and gaseous pollutants, such as nitrogen dioxide and ozone.
PM is classified according to size into coarse particles (PM10), fine particles (PM2.5) and ultrafine particles.
We aim to provide an original review of the scientific evidence from epidemiological and experimental studies examining the cardiovascular effects of outdoor air pollution. Pooled epidemiological studies reported that a 10 μg/m3 increase in long-term exposure to PM2.5 was associated with an 11% increase in cardiovascular mortality.
Increased cardiovascular mortality was also related to long-term and short-term exposure to nitrogen dioxide.
Exposure to air pollution and road traffic was associated with an increased risk of arteriosclerosis, as shown by premature aortic and coronary calcification. Short-term increases in air pollution were associated with an increased risk of myocardial infarction, stroke and acute heart failure.
The risk was increased even when pollutant concentrations were below European standards.
Reinforcing the evidence from epidemiological studies, numerous experimental studies demonstrated that air pollution promotes a systemic vascular oxidative stress reaction. Radical oxygen species induce endothelial dysfunction, monocyte activation and some proatherogenic changes in lipoproteins, which initiate plaque formation.
Furthermore, air pollution favours thrombus formation, because of an increase in coagulation factors and platelet activation.
Experimental studies also indicate that some pollutants have more harmful cardiovascular effects, such as combustion-derived PM2.5 and ultrafine particles. Air pollution is a major contributor to cardiovascular diseases. Promotion of safer air quality appears to be a new challenge in cardiovascular disease prevention.
General definition
Air pollution is composed of particulate matter (PM) and gaseous components. PM is classified as coarse particles (diameter < 10 μm, ≥ 2.5 μm), fine particles (diameter < 2.5 μm, ≥ 0.1 μm) and ultrafine particles (nanoparticles, diameter < 0.1 μm). PM has a different composition depending on its source.
Carbonaceous particles are derived from combustion sources, such as traffic emission or residential heating, while inorganic particles are represented by, for example, desert dust and mineral dust from agriculture.
Carbonaceous particles are carbon based, but carry on their surface an amount of organic chemicals, such as polycyclic aromatic hydrocarbons and reactive metals [2].
Gaseous pollutants are nitrogen oxides including nitrogen dioxide (NO2) and nitric oxide (NO), ozone, sulphur dioxide (SO2), volatile organic compounds and carbon monoxide (CO).
Besides their own toxicity, SO2 and nitrogen oxides also contribute to particle formation through complex atmospheric photochemical reactions involving ammonia from agriculture.
As they result from gaseous transformation, these particles are called secondary particles, and are essentially composed of inorganic compounds, such as ammonia, sulphates and nitrates.
Ozone is a secondary gaseous pollutant, formed through a photochemical reaction involving sunlight and gaseous precursors such as nitrogen oxides or volatile organic compounds.
Outdoor air pollution sources
In Europe, agriculture is a major source of PM2.5. Nevertheless, particles from agriculture are mainly inorganic particles, which are usually considered to be less toxic than carbonaceous particles from combustion sources, such as road traffic.
Assuming this difference in toxicity, road traffic and residential heating have the largest impact on outdoor air pollution-related mortality in Europe [1].
In North America, industry and power generation using fossil fuels are also important sources of PM. In Africa, natural sources, such as desert dust and biomass burning (natural or man-made fires), contribute largely to ambient air pollution concentrations.
In Asia, residential heating and cooking are the main sources of particles in both outdoor and indoor emissions [1].
Besides the differences between countries and continents, strong differences exist between the main sources of pollutants within the same country, depending on local sources. In large cities, road traffic is a major contributor to global pollutant emissions, and is also the main source of NO2, arising mainly from diesel vehicles.
In Paris, for example, road traffic accounts for 30% of PM emissions, as much as the residential sector, and nearly 60% of emissions of nitrogen oxides [3].
SO2 mainly arises from industrial emissions and maritime transport; however, its contribution to air pollution is decreasing over the years.
Indoor air pollution
In 2010, air pollution led to 7 million premature deaths worldwide, with similar contributions made by indoor and outdoor air pollution [1].
However, indoor air pollution is more heterogeneous, with wide variations in pollutants and sources between countries.
Worldwide, second-hand smoke is a major source of indoor air pollution.
In Asia, cooking and heating with solid fuels are the main sources of indoor air pollution, whereas in Europe, several sources contribute to indoor pollution, such as volatile organic compounds from organic solvents, household products and PM from cooking and wood burning. Nevertheless, a recent European study demonstrated that 60% of the global burden of indoor air pollution-related disease comes from outdoor PM2.5 penetrating inside via air exchange [4].
Consequently, decreasing the burden of disease from indoor air pollution requires measures that affect indoor air pollution sources, ventilation and filtration of outdoor air [4].
When breathed in, it aggressively attacks lung tissue by chemically reacting with it, according to the American Lung Association.
Wang’s study – which includes researchers from the University of Washington and the University of Wisconsin-Madison – has policy implications for the U.S., where the Environmental Protection Agency in 2015 lowered the federal health standards for ozone.
“Most attention to air quality in the United States has focused on particulate matter air pollution,” Wang said.
“However, ozone concentrations within metropolitan areas are not positively correlated with particulate matter pollution.
In addition, mean ozone levels – as reported in this paper – are not declining in the United States, probably due to the worsening of climate change.”
The EPA reports that particulate matter concentrations have decreased across the nation as efforts are made to reduce vehicle emissions and use clean energy.
Ozone, however, is much trickier, Wang notes.
“For policy in the U.S., the focus should be on how to effectively control ozone concentration, which may be harder because it’s a secondary pollutant,” he said.
“With climate change getting worse, this issue may become amplified.”
More information: Meng Wang et al. Long-Term Exposure to Ambient Ozone and Progression of Subclinical Arterial Disease: The Multi-Ethnic Study of Atherosclerosis and Air Pollution, Environmental Health Perspectives (2019). DOI: 10.1289/EHP3325
Journal information: Environmental Health Perspectives
Provided by University at Buffalo
