Commentary: inflamed about ultrafine particles?

Ambient air pollution has been linked to exacerbation of cardiovascular disease morbidity and mortality. 1 These associations have been strikingly robust and range from the observation of coronary heart disease exacerbation within hours of exposure to an increased risk of ischaemic heart disease mortality for subjects chronically exposed to elevated concentrations of ambient particles. Two main pathological processes, atherosclerosis and thrombosis, lead to acute coronary syndromes such as unstable angina and myocardial infarction. The typical atherosclerotic lesion is a fibro-lipid plaque composed of a pool of lipids covered with a connective tissue cap. Although the plaque narrows the coronary arteries, acute coronary syndromes only occur when a plaque erodes, fissures, or ruptures and a thrombus is formed, which occludes the arteries, partially or totally, and impedes blood flow. There is a strong link between inflammation and coronary heart disease, since factors involved in inflammation and infection seem to play a pro-atherogenic role and inflammation has been identified as a potent risk factor for the acute coronary syndromes. 2 Other risk factors such as cigarette smoking, diabetes, or high body mass index have also been found to be associated with low-grade systemic inflammation, providing a further link between inflammation and acute coronary syndromes. On the other hand, factors alleviating systemic inflammation, for example moderate exercise or weight loss, reduce the risk of acute coronary events. Acute phase proteins, like C-reactive protein (CRP) or fibrinogen, have been identified as biomarkers for inflammatory processes and are important determinants of plaque rupture. 3