PASSIVE SMOKING AND HEART-DISEASE - MECHANISMS AND RISK

Citation
Sa. Glantz et Ww. Parmley, PASSIVE SMOKING AND HEART-DISEASE - MECHANISMS AND RISK, JAMA, the journal of the American Medical Association, 273(13), 1995, pp. 1047-1053
Citations number
97
Categorie Soggetti
Medicine, General & Internal
ISSN journal
00987484
Volume
273
Issue
13
Year of publication
1995
Pages
1047 - 1053
Database
ISI
SICI code
0098-7484(1995)273:13<1047:PSAH-M>2.0.ZU;2-O
Abstract
Objective.-Recent clinical, laboratory, and epidemiological evidence t hat passive smoking causes heart disease was reviewed, with particular emphasis on understanding the underlying physiological and biochemica l mechanisms. Data Sources.-Publications in the peer-reviewed literatu re were located via MEDLINE, citation in other relevant articles, and appropriate reports by scientific agencies, Greatest emphasis was give n to work published since 1990. Conclusions.-Passive smoking reduces t he blood's ability to deliver oxygen to the heart and compromises the myocardium's ability to use oxygen to create adenosine triphosphate. T hese effects are manifest as reduced exercise capability in people bre athing secondhand smoke, Secondhand smoke increases platelet activity, accelerates atherosclerotic lesions, and increases tissue damage foll owing ischemia or myocardial infarction. The effects of secondhand tob acco smoke on the cardiovascular system are not caused by a single com ponent of the smoke, but rather are caused by the effects of many elem ents, including carbon monoxide, nicotine, polycyclic aromatic hydroca rbons, and other, not fully specified elements in the smoke. Nonsmoker s exposed to secondhand smoke in everyday life exhibit an increased ri sk of both fatal and nonfatal cardiac events.