[Fine particulate matter - a health hazard for lungs and other organs?]

Epidemiological studies provide evidence that particulate air pollution (PM10) increases pulmonary as well as cardiovascular mortality. This review summarises current hypotheses on the mechanisms of entry of inhaled fine particles into the systemic circulation and the mechanisms of action on the cardiovascular system.

Following particle deposition in the lungs, soluble components like metal salts or soluble organics are taken up into the pulmonary capillary blood. Ultrafine particles can pass the lung-blood barrier by endocytosis, transcytosis, or stochastic transport, depending on their physicochemical properties, and a fraction (0.1 - 1 %) is thus dislocated into the systemic circulation.

Direct actions of translocated particles, soluble compounds and/or inflammatory mediators have been shown to alter cardiovascular homeostasis. Effects associated with high PM10 are arrhythmias, myocardial infarction, and cardiac failure. Cardiovascular regulation may be impaired by autonomic imbalances such as those caused by inflammatory or stress-related processes. Local or systemic inflammatory responses may cause endothelial dysfunction, a procoagulatory state with the risk of enhanced atherosclerosis. Cardiac function may be impaired by alterations in ion channel functions leading to electrophysiological instability.

Systemic actions of inhaled particles are an important issue in environmental health, and there is evidence that they are in no way limited to the cardiovascular system, but also affect other organs like the brain. Details on particle translocation mechanisms and pathophysiological pathways of action remain to be elucidated.