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Improving the quality of life and reducing sudden cardiac death by limiting the impact of heart rhythm disturbances.
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A population-based approach is needed to tackle air pollution, which is now ranked ninth among the greatest modifiable risk factors for cardiovascular disease, according to conclusions at a Spotlight of the Congress Symposium yesterday. Air pollution not only exacerbates existing heart conditions but even appears to play a part in their causation.
The WHO estimated in 2012 that one in eight of total global deaths (around seven million each year) could be attributed to air pollution. The principal culprit appears to be fine nanoparticles known as particulate matter (PM) ≤2.5 μm in diameter (PM2.5) which occur in diesel and petrol exhaust. ‘This ultrafine particulate matter is like a gas and can penetrate deeply into the lungs and reach the blood stream,’ explained David Newby from Edinburgh University.
A number of epidemiological studies have demonstrated links between CVD and air pollution, including the Women’s Health Initiative observational study which considered the full range of air pollutants (including sulphur dioxide, nitrogen dioxide, carbon monoxide, and ozone), but found that only PM2.5 was associated with CVD risk (N Engl J Med 2007, 356: 447-58). The study, which involved over 65,000 postmenopausal women, used readings from monitor stations located near the subject’s homes. The results showed an increased relative risk of 1.76 for death from CVD for every increase of 10-μg/m3 in mean concentration of PM2.5.
There have been concerns of confounding factors, such as socioeconomic status, in such studies. However, Raimund Erbel, from the University of Duisberg-Essen, explained how the German Heinz Nixdorf Recall study, was able to tease apart the independent effects of long term fine PM and long term exposure to noise, both of which have been linked to CVD. The investigators found that fine-particle air pollution as associated with an increase in thoracic aortic calcification burden (considered a measure of subclinical atherosclerosis) by 19.9% per 2.4 ng/m3 (EHJ 2014, 35: 853-60).
To assess causality of the CVD effects of air pollutants, Newby undertook controlled exposure studies (N Engl J Med 2007, 357: 1075-82). Men with CAD were exposed to controlled amounts of dilute diesel exhaust (from an idling diesel engine) to achieve concentrations similar to those occurring in urban traffic situations. The team found that diesel exhaust exacerbated exercise-induced myocardial ischaemia and impaired endogenous fibrinolytic capacity in men with CAD. ‘We demonstrated that inhalation of dilute diesel exhaust affects the blood vessels, clotting ability and may even affect perfusion of the heart,’ said Newby.
Less is known about the connection between air pollution and stroke, explained Massimo Stafoggia, largely because stroke represents a rarer event. The ESCAPE study gained statistical power by pulling together multiple cohorts in Europe to analyse the relationship between stroke (and other health outcomes) and air pollution. Altogether 99,466 participants (from 11 different cohorts) were investigated, of whom 3086 went on to develop stroke. For each participant long-term exposure to ambient pollution had been calculated.
Results showed that a 5-μg/m3 increase in annual PM2.5 exposure was associated with 19% increased risk of incident stroke. ‘It was difficult to find a safe threshold below which there was not some pollution effect in the incidence of stroke,’ said Stafoggia, from Lazio Region Health Service Rome. ‘It means that the cleaner the air you breathe the better.’
Earlier this year the ESC published an expert consensus document on the wide-ranging impact that air pollution is having on CVD (EHJ 2015, 36: 83-93). ‘Cardiologists have an important role to play in both educating their patients and lobbying policymakers to introduce changes. There just isn’t enough public awareness of the substantial impact that air pollution is having on CVD,’ Newby told ESC Congress News.
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