Feinstaub: Gefahr für Lunge und Kreislauf?

Zusammenfassung

Hintergrund: Epidemiologische Studien zeigen, dass durch Feinstaub nicht nur die pulmonale, sondern auch die kardiovaskuläre Mortalität erhöht wird. Die vorliegende Arbeit fasst den derzeitigen Kenntnisstand über den Weg inhalierter Partikel in die systemische Zirkulation und ihre kardiovaskulären Wirkmechanismen zusammen. Partikelaufnahme: Nach Abscheidung in der Lunge können lösliche Bestandteile inhalierter Partikel direkt in die Blutbahn übertreten, jedoch überwinden auch ultrafeine Partikel die Luft-Blut-Schranke und werden zu 0,1 - 1 % systemisch aufgenommen, offenbar spielen hierbei aktive wie auch passive Transportvorgänge eine Rolle. Wirkungsmechanismen: Toxikologische Studien zeigen, dass kardiovaskulären Wirkungen direkt durch Partikel oder deren lösliche Bestandteile, aber auch durch eine pulmonale Entzündungsantwort bzw. eine systemische Akutphase-Reaktion des Körpers über (a) vegetative Störungen, (b) eine endotheliale Dysfunktion (c) eine Blutgerinnungsneigung und (d) möglicherweise Ionenkanalstörungen am Herzen vermittelt werden können. Ausblick: Systemische Wirkungen von Feinstaub stellen einen wichtigen gesundheitspolitischen Aspekt dar, sind in Einzelheiten aber bislang nicht ausreichend geklärt.

Abstract

Background: 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. Particle Entry: 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. Mechanisms of Action: 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. Outlook: 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.

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