The public health burden of environmental air pollution has been increasingly recognized . Since the evidence of the dramatic effects of unusual acutely increased exposure to air pollution (i.e. Meuse Valley, Belgium, 1930, or the ‘great smog’ in London, 1952) [2,3], a large body of literature has provided epidemiological and pathophysiological data supporting the association between air pollution and general mortality and morbidity from respiratory and cardiovascular diseases [1,4–7]. These effects have been shown to occur not only after acute exposure to markedly elevated concentrations of air pollutants, but even after short-term and long-term relatively low levels of exposure [8,9]. Beyond the exacerbation of individual risk in vulnerable subjects (elderly persons or those with preexisting cardio-respiratory disease), the unavoidable chronic exposure of large populations to these risks makes air pollution a major health problem . The World Health Organization (WHO) estimates that urban air pollution was responsible for 1.3 million annual deaths in the year 2008 (i.e. 2.4% of the total deaths worldwide) and caused about 9% of the lung cancer deaths, 5% of cardiopulmonary deaths and about 1% of respiratory infection deaths .
Sources of air pollution include natural phenomena (biogenic sources, for example volcanoes, wildfires or land dust) and human activities (anthropogenic sources). Natural pollutants may be problematic in some circumstances, but most harmful health effects are related to human-generated sources of air pollution, categorized as mobile and stationary sources. The former include motor vehicle exhausts, the latter consist of non-moving sources, such as household combustion devices, industrial facilities and power plants . In addition to primary pollutants, directly emitted from a source (for example, carbon monoxide from vehicle exhausts or sulphur dioxide from industrial processes), secondary pollutants are produced by chemical reactions of primary emissions in the atmosphere (for example, ozone generated by the reaction of volatile hydrocarbons with the sunlight). The result of these multiple, concurrent sources and processes is a complex mixture (Table 1) of gaseous and particulate matter (PM). Depending on its sources and geographical location, the composition of air pollution may be extremely heterogeneous, and further variations in a single location are related to meteorological conditions and differences in human activities over time, including time of the day, day of the week, or trends (for example the increase of diesel engines, which produce less carbon dioxide but about 100-fold higher particulate emissions than gasoline engines) .
|Gaseous substances||Carbon monoxide (CO), carbon dioxide (CO2), nitrogen dioxide (NO2), nitric oxide (NO3), sulphur dioxide (SO2), ozone (O3), volatile organic compounds (hydrocarbons, quinones)|
|Particulate matter (PM)*||Metals, coarse particles (PM10), fine particles (PM2.5), ultrafine particles (PM0.1), nanoparticles|
All components of air pollution are harmful to health, but the most numerous and severe effects have been attributed to PM, because particles may contain and transport in the respiratory tract a broad range of toxic substances . In this respect, the toxic potential of PM is inversely related to its aerodynamic diameter (AD) [14–16]. On inhalation, coarse PM (PM10, i.e. particles with AD between 2.5 and 10 μm) is arrested in the nasal cavities and upper airways, whereas fine and, particularly, ultrafine PM (PM2.5 and PM0.1, i.e. particles with < 2.5 and 0.1 μm in AD, respectively) may penetrate deeper up to the lung alveoli and even pass to the bloodstream, where some components may exert direct adverse effects [15–17]. However, more convincing evidence of such translocations (directly as naked particles, or via endocytosis by alveolar macrophages or endothelial cells) has been achieved in animal models than in human studies [16–19]. The heterogeneous composition of PM includes combustion products and suspended crustal materials, as well as biological materials such as pollen, endotoxins, bacteria, spores and viruses. In urban areas, traffic of motor vehicles is a major source of PM, with diesel exhaust accounting for up to 40% of airborne PM . On the whole, ambient PM is considered the most important indicator of the adverse effects on health of global air pollution. The monitoring policies and legislations to improve air quality led to significant benefits in developed countries, whereas many middle-income countries are disproportionately experiencing this burden, due to the lack of strategies for environmental health protection. Indeed, WHO statistics presently report the highest PM10 concentrations in the air of cities in China, India, Pakistan and other rapidly developing countries .
If the consequences of air pollutants on respiratory diseases, such as chronic obstructive pulmonary disease and asthma, are easily conceivable, the even stronger impact on cardiovascular disease, more recently assessed, is probably unexpected and pathogenic mechanisms are more difficult to explain [21,22]. The heterogeneity and complexity of air pollution composition is a further challenge to gain insight into these mechanisms . Interestingly, beyond the effects on atherothrombotic (coronary and cerebrovascular) disease, some recent findings suggest an association of air pollution with venous thromboembolism . In the following paragraphs literature data reporting the relationships between air pollution and cardiovascular and thrombotic diseases will be reviewed, together with the experimental studies that provided possible pathophysiological support for these robust and consistent clinical evidence.