Abstract
There is strong evidence that particulate air pollution increases the risk of cardiovascular diseases. Fig. 4 summarizes some of the hypothesized pathways. In an effort to provide biologic plausibility for this association, several mechanistic studies have been performed, which have improved the understanding on how PM can affect platelets and the coagulation system and be responsible for the development of atherothrombosis complications. The authors still need to address several remaining questions: (1) What is the role of factors modulating particle translocation, such as the way of exposure, dose, size, surface chemistry, time course, and inflammatory mediators? (2) What are the mechanisms behind the cross-talk between lung macrophages, infiltrating granulocytes, mast cells, and the mediators involved in the activation of peripheral platelets and coagulation factors? (3) Which receptors present on blood platelets are responsible for the particle-induced platelet activation? (4) How do acute and chronic exposures and single versus repeated doses compare in healthy animals and animals with pre-existing cardiovascular diseases? (5) What are the critical chemical and biologic constituents of PM (eg, metals, carbon, polycyclic aromatic hydrocarbons, endotoxin) and what is the role of different PM size fractions, including UFPs (<0.1 μm) and the coarse fraction (PM10 to 2.5), in the adverse cardiovascular effects of air pollution?
Original language | English |
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Pages (from-to) | 865-881 |
Number of pages | 17 |
Journal | Clinics in Occupational and Environmental Medicine |
Volume | 5 |
Issue number | 4 |
DOIs | |
Publication status | Published - Nov 2006 |
Externally published | Yes |
ASJC Scopus subject areas
- Public Health, Environmental and Occupational Health