Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-11-19
pubmed:abstractText
Exposure to particulate air pollution is associated with acute and chronic cardiovascular morbidity and mortality. The mechanisms involved in these effects are not fully elucidated. Research has proved that fine particles, principally the ultrafine fraction, which are predominantly derived from combustion of fossil fuel, are the most toxic. Recent clinical and experimental studies have reported mechanistic observations linking fine and ultrafine particles to the coagulation cascade, platelet function, and subsequent development of atherosclerosis and thrombosis. These effects have been explained either by release of soluble mediators by the lungs, which affect blood coagulation parameters, or by the direct translocation of ultrafine particles into the systemic circulation or the alteration of autonomic cardiac control. Despite recent advances, additional studies are needed to investigate the pathophysiologic mechanisms linking particulate air pollution and hemostasis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1526-0046
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
865-81
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Effects of particulate air pollution on hemostasis.
pubmed:affiliation
K.U. Leuven, Laboratory of Pneumology (Unit of Lung Toxicology), Herestraat 49, B-3000, Leuven, Belgium.
pubmed:publicationType
Journal Article, Review