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
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.