Portal de Periódicos da CAPES

Air pollution: the new cardiovascular risk factor

2008; Wiley; Volume: 38; Issue: 12 Linguagem: Inglês

10.1111/j.1445-5994.2008.01850.x

1445-5994

Jeremy P. Langrish, Nicholas L. Mills, David E. Newby,

Vehicle emissions and performance

In August of this year, the XXIXth Olympic Games held in Beijing China brought the hazards of air pollution exposure into the public eye. International headlines stressed the poor air quality and the potential health effects that might have an adverse impact on the performance of athletes, as well as on those with chronic cardiorespiratory diseases. At least one high-profile marathon runner declared that he would not run in Beijing because of the poor air quality and on arrival to Beijing, the US cycling team wore close-fitting face masks designed to reduce personal exposure to airborne particles. So was this international concern justified? Epidemiological studies have confirmed the link between exposure to air pollution and increased cardiorespiratory mortality.1–3 Chronic exposure to traffic-derived fine-particulate air pollution is associated with the degree of coronary atherosclerosis and coronary artery calcium scores assessed using electron-beam computed tomography.4 Consistent with this and animal models of atherosclerosis,5,6 human exposure to PM2.5 (particles with a mean diameter of 2.5 μm or less) correlates to carotid intima-medial thickness, a measure of subclinical atherosclerosis.7 In the largest study to date (n = 65 893), Miller et al. showed that in postmenopausal women without pre-existing vascular disease, each 10 μg/m3 increase in background fine-particulate air pollution concentrations was associated with a 24% increase in the risk of a cardiovascular event and a 76% increase in the risk of death from cardiovascular disease, including myocardial infarction or stroke.8 In addition to the adverse health effects of chronic exposure, traffic-derived air pollution is associated with the triggering of acute myocardial infarction, with people experiencing a myocardial infarction being three times more likely to have been in road traffic in the hour before the onset of symptoms.9 Although well-described mechanisms underlie the development of cardiovascular disease with traditional risk factors, the pathophysiological effects of air pollution are poorly understood. The exact components of air pollution responsible have yet to be specifically identified, but the epidemiological link is strongest for fine-particulate matter associated with combustion sources and particularly that associated with road traffic.10 Recent studies have used controlled exposures to either concentrated ambient particles or dilute diesel exhaust, the latter being the predominant component of airborne fine-particulate matter in the urban environment. Diesel exhaust is of particular relevance, as in addition to all commercial vehicles approximately 40% of all new domestic vehicles are diesel powered. This proportion may well increase, given the current trend for 'green taxation' linking tax paid by the motorist to carbon dioxide emissions. Although diesel engines produce less gaseous pollution, they emit greater than 100-fold more fine-particulate matter than an equivalent-sized petrol engine with a catalytic converter.11 Short-term exposure to concentrated ambient particulate matter and ozone causes acute arterial vasoconstriction.12 In healthy volunteers, we showed that a 1-h exposure to dilute diesel exhaust at a particle concentration of 300 μg/m3 resulted in vascular endothelial dysfunction, with impaired vasomotor tone and endogenous fibrinolysis.13 Furthermore, using a similar exposure, patients with stable coronary heart disease developed more pronounced myocardial ischaemia during exercise.14 This is further compounded by an increase in platelet activation and thrombogenicity in the first 6 h after exposure.15,16 In combination, these findings may explain the excess of acute and chronic cardiovascular events in the epidemiological studies of air pollution. Regarding global and public health, controlled exposure studies have been criticized due to the relatively high concentration of fine-particulate matter used and some have questioned the relevance of these findings to everyday life. The WHO has set air quality targets for particulate air pollution (PM10– particles with a mean diameter less than 10 μm) to remain below 50 μg/m3. In many of the world's important cities (Table 1), levels of fine-particulate air pollution regularly exceed this target. In Beijing, China, this target was exceeded on 241 days out of 365 in 200617 and levels often exceed 300 μg/m3,18 as used in controlled exposure studies. In Christchurch, New Zealand, this air-quality target has been exceeded on average 29 days each year for the last 5 years, with a peak of 184 μg/m3.19 Many epidemiological studies have been carried out in various countries, with differing estimates of the associated economic impact. For example, it is estimated that each year in New Zealand, air pollution leads to 1100 additional deaths, 700 additional hospital admissions for cardiorespiratory diseases and nearly 2 million 'restricted activity days' costing the economy around $1.1 billion each year.20 In fact, the World Health Organization (WHO) estimates that approximately 3 million deaths worldwide (representing 5% of the total) can be attributed to air pollution exposure annually.18 Although average background pollution levels may not exceed the WHO target in many cities around the world, there is a large variation in the individuals' actual exposure to particulate matter. Traffic-derived air pollution is in the fine and ultrafine range and these particles remain airborne for a considerable length of time, given their small size and tiny mass. The particle concentration, when measured kerbside, can therefore actually be far higher than recorded at background monitoring stations, which tend to be located in quieter areas away from the important roads. This can be important, especially for those, such as traffic wardens, who spend a long time in kerbside environments. Their personal exposure can be as much as 5–10 times higher than that measured at the background sites.21 So how does the risk attributable to air pollution compare to traditionally quoted cardiovascular risk factors? The well-defined risk factors of hypertension, hypercholesterolaemia, diabetes mellitus, family history and smoking have been studied in depth in large epidemiological studies. In comparison to these variables, chronic exposure to fine particulate air pollution gives a dose-dependent and similar risk to hypertension or hypercholesterolaemia (Fig. 1). Modern medical practice is very focused on lowering patients' cardiovascular risk. We regularly monitor patients' blood pressure, cholesterol concentrations and blood sugar and often offer primary prevention medication. There are, in most places, smoking cessation services to help patients reduce tobacco consumption and many countries now have laws banning smoking in all public areas. These primary prevention strategies have a significant influence on the incidence of cardiovascular disease and the implementation of a smoking ban in Scotland recently led to a 17% reduction in the incidence of myocardial infarction.24 What then can we do about air pollution exposure to reduce the potential health effects? Percentage increase in population attributable risk with traditional cardiovascular risk factors from the Framingham22 (solid bars) and QRESEARCH (striped bars) cohorts.23 For comparison, risk attributed to each 10 μg/m3 increase in PM2.5 concentrations (hashed bars) is shown.8 All values shown are for women only to allow comparison. Hypertension means incidence of hypertension in Framingham study and per 20 mmHg increase in systolic blood pressure in QRESEARCH. All other parameters refer only to their incidence. Public awareness of the problem of air pollution has led to significant pressures on countries, and local authorities, to try and reduce local emissions from both traffic and industry. Environmental policy interventions have shown that the reduction of air pollution can have substantial health benefits. For example, in Dublin, Ireland, banning the sale of bituminous coal led to a reduction in cardiovascular deaths.25 Traffic emissions are also modifiable. Modern engines are more fuel efficient, meaning more complete combustion and fewer particle emissions. Automotive industries are now producing cars with exhaust particle traps to try and reduce the environmental impact of their products. More recently, during the Beijing Olympic Games, traffic restrictions were implemented to halve the number of vehicles on the roads based on an odd–even number plate control system. Given Beijing has more than 3.3 million registered vehicles, one would expect this to have a significant environmental and health impact, and, indeed when the Chinese government had a trial run, they reported a 40% reduction in airborne particulate matter. Personal protective equipment, such as the masks worn by the US athletes, also have a potential role in this, although their ability to negate the described health effects has yet to be shown. Air pollution exposure, and particularly fine-particulate matter derived from combustion sources, has emerged as a new risk factor for cardiovascular morbidity and mortality and may actually lead to a similar degree of risk to the well-described risk factors, such as hypertension and hypercholesterolaemia. These effects may be mediated by changes in vascular endothelial function, leading both to the acceleration of the development of atherosclerosis and to the triggering of acute cardiovascular events. Public health measures are now needed to reduce these harmful emissions, such as the introduction of particle traps for diesel exhausts or the development of better fuels. Dr Langrish is supported by a British Heart Foundation Clinical PhD Fellowship (FS/07/048). The authors declare no potential conflict of interest.