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Cardiovascular consequences of air pollution: what are the mechanisms?
  1. Krishnan Bhaskaran1,
  2. Paul Wilkinson2,
  3. Liam Smeeth1
  1. 1Department of Non-communicable Diseases Epidemiology, London School of Hygiene and Tropical Medicine, London, UK
  2. 2Department of Social and Environmental Health Research, London School of Hygiene and Tropical Medicine, London, UK
  1. Correspondence to Dr Krishnan Bhaskaran, Department of Non-communicable Diseases Epidemiology, London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK; krishnan.bhaskaran{at}lshtm.ac.uk

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Concern over the health effects of air pollution has existed for many decades, arguably peaking in the UK with the infamous London smog of 1952, which caused thousands of deaths and led to the passing of the Clean Air Act in 1956 and similar legislation elsewhere. There have been very large reductions in ambient pollution levels in most high income countries in the decades since. However, even at the relatively low pollutant levels seen more recently in these settings, the epidemiological evidence for adverse effects on human health is clear.

Early time-series studies in the 1990s demonstrated an effect of short-term changes in the levels of pollutants, in particular particulate matter, on overall mortality.1 Subsequent studies of cardiovascular mortality and morbidity suggested that both day-to-day changes in pollutant levels and longer term exposure affect risk. Our recent systematic review found compelling evidence for an effect of air pollution on myocardial infarction specifically.2 A major review of the epidemiological evidence on air pollution and cardiovascular disease more generally, conducted for the UK Department of Health, concluded that ‘a large number of time-series studies show very clearly that, with few exceptions, all of the commonly measured pollutants (particles, ozone, sulphur dioxide, nitrogen dioxide and carbon monoxide) are positively associated with increased mortality and hospital admissions for cardiovascular disease’.3

These consistently observed effects clearly require some mechanistic explanation. To date, the main candidate hypotheses have held that pollutant exposure increases the risk of cardiovascular events via disruption of the autonomic nervous system, an inflammatory response, or both.

Out of control?

One of the leading theories postulates that pollution exposure leads to disturbances in the autonomic …

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