The inhalation of toxic particles and gases reduces the innate defences of the lung by increasing epithelial permeability, decreasing mucociliary clearance and depressing macrophage function. There is also substantial experimental evidence that lung epithelial cells and alveolar macrophages generate a rich milieu of inflammatory mediators when exposed to atmospheric particles that can be measured in induced sputum, BAL fluid and blood. Here we review evidence that these mediators produce an integrated local lung and systemic inflammatory immune response. That results in an increase in the release of leucocytes and platelets from the bone marrow, an increased production of acute phase proteins from the liver and activation of the vascular endothelium to favour the formation of new and destabilization and rupture of existing atherosclerotic plaques. We postulate that when this response is generated in elderly persons whose lungs are compromised by COPD, it may account for the acute exacerbations of COPD that destroy the quality of life and increase the need for medical attention and hospital admissions. Moreover, the accelerated spread of the atherosclerotic process, and destabilization of existing atherosclerotic plaques in experimental animals that develop atherosclerosis naturally when exposed to atmospheric particles, may account for the acute coronary syndromes, myocardial infarction, transient cerebral ischaemia and stroke that have been documented in humans exposed to episodes of air pollution.