It has long been known that air pollution can adversely affect human health. A number of catastrophic events from the last century, such as the Meuse Valley fog of 1930, taught us that extreme levels of air pollution cause a direct increase in deaths.¹ Evidence has mounted in the past 15 years that, besides the well-known respiratory effects, air pollution can damage the cardiovascular (CV) system.

The landmark Harvard Six City Study, following a cohort of over 8,000 adults for up to 16 years, demonstrated that CV deaths were most frequent in the most polluted cities.² More recently, the Women’s Health Initiative established a strong statistical association between fine particulate air pollution and death from coronary heart disease.³ In Coachella Valley, California, a detailed comparison of daily death counts to air pollution levels indicated that an increase in particulate matter concentration of 10 ug/m3 was associated with a 1% increase in total mortality.⁴

Air pollution consists of both particulate and gaseous components. Ambient particles are subdivided on the basis of aerodynamic diameter (AD) into coarse particles (AD between 2.5 and 10 um) that arise from windblown dust and wildfires, fine particles (AD < 2.5 um) mostly deriving from home wood burning, refineries and tailpipe emissions, and ultrafine particles (AD < 0.1 um), which also derive predominately from tailpipe emissions. Environment Canada routinely records levels of fine particulate matter (PM2.5), as well as gas levels including carbon monoxide, nitrogen dioxide, sulphur dioxide and ozone.

Tailpipe emissions account for a large proportion of the pollution that we inhale on a daily basis, particularly ozone, which is beneficial when in the upper atmosphere but harmful at ground level. In both North America and Europe, direct emissions from personal vehicles and freight transport have been steadily rising. Rapid urbanization and increasing time spent in congested traffic means that exposure is increasing even where pollution levels are reported to be falling. In China, where one-fifth of the globe’s population reside, the rapid economic growth has gone hand in hand with a doubling in transportation use between the years 1990 and 2003, and there are predictions that the number of motorized vehicles could increase by 15-fold over the next 30 years.⁵ And since ground-level ozone pollution worsens with rising temperatures, air quality may become an even greater issue as global warming continues.

Heart attack trigger

The mechanisms of air pollution-induced cardiovascular compromise can be considered in two separate groups — those triggering acute vascular injury and those accelerating chronic atherosclerotic disease. Epidemiological studies correlating the day-to-day variations in atmospheric pollution with daily variations in death and disease have shown that elevated levels of ambient aerosols (including ozone, sulphur dioxide, nitrogen dioxide and carbon monoxide) have been associated with increased cardiac admissions to hospital and acute myocardial infarctions (MIs).⁶ The amount of time people spend on motorcycles and in their cars has been consistently linked to an increased risk of acute MI. Case-crossover studies have shown that heavy traffic exposure can trigger a MI within the hour in susceptible persons.⁷ A controlled provocative study involving 20 men with established coronary artery disease demonstrated how diluted diesel exhaust inhalation caused more marked ST depression during exercise testing than when subjects breathed filtered air.⁸ This study illustrated the profound adverse effect tailpipe emissions can have on coronary perfusion in susceptible individuals.

The triggering of acute vascular injury by air pollutants is thought to be mediated by either a prothrombotic effect, by autonomic deregulation, or by a combination of both mechanisms. Experimental data has demonstrated that ultrafine particles may act as prothrombotic factors, increasing the risk of platelet activation and clot formation. Simultaneous analysis of ambient air pollution levels and coagulation parameters in volunteers have indicated that higher air pollution levels are associated with increased plasma viscosity and a shorter prothrombin time.⁹ There’s also evidence suggesting that air pollution can affect the autonomic control of the heart, which may increase the risk of sudden death. Several studies indicate that air pollution decreases heart rate variability, a marker of cardiac risk.¹⁰

Long-term damage

Air pollution is believed to accelerate chronic vascular disease by inciting endothelial dysfunction mediated by oxidative stress and vascular inflammation. Endothelial dysfunction has been shown to occur in healthy volunteers after as little as 2 hours spent inhaling a mixture of concentrated ambient particles plus ozone.¹¹ Studies done in the Los Angeles basin demonstrated that long-term exposure to air pollution was associated with a significant increase in carotid artery intima media thickness, such that for every 10 ug/m3 increase in fine particulate matter exposure (PM2.5), there was a 6% increase in intima-media thickness.¹² It’s been shown that these air pollutants are fine enough to be inhaled deeply into the alveoli, where they can generate reactive oxygen species, and in turn can trigger pulmonary inflammation. The inflammatory cascade initiated in the lungs can result in a release of inflammatory mediators into the systemic circulation, as evidenced by documented increases in C-reactive protein levels. As well, ultra fine particulate matter has been shown to translocate into the bloodstream and can be found in remote organs, including the heart, where it’s ideally positioned to induce direct toxic CV effects via vascular inflammation.¹³

Politics of prevention

Pollution has been shown to cause unfavourable CV effects even when air meets existing air quality standards. High-risk patients should be urged to take precautions and limit exposure on days with high pollution levels to avoid triggering reactions. With our smoking patients we need to emphasize that air pollution may be cumulative if not synergistic with the cigarette’s injury on the blood vessels. More broadly, in addition to ensuring that our patients’ blood pressures, glucose levels and lipids are under control, we need to raise concern about their exposure to air pollution, and include smog on their list of modifiable risk factors.

While the ideal solution to counter the adverse effects of air pollution on the cardiovascular system is to reduce the sources of pollution, realistically, city smog isn’t going to blow away anytime soon. But that’s not to say we can’t endorse some small steps in the right direction. As a profession of influence, we’d do well to demonstrate environmental stewardship by minimizing our own motor vehicle use, wood burning and power consumption. The established strategies to reduce exposure to air pollutants, such as keeping car travel to a minimum, avoiding travel during peak rush hours, refraining from idling, keeping our vehicles well-tuned, car pooling and preferentially making use of public transit, are obvious and should rank highly. And not to be overlooked on the list is opting for active transportation. We’ve allowed oil to displace food as the predominant energy source for moving ourselves about, and this is an error — both for the health of our planet and for our bodies. Switching to walking or cycling instead of passively driving wouldn’t just improve air quality, it would get us on the right road to raising fitness levels and controlling weight.