by Sean Henahan, Access Excellence

SAN FRANCISCO- Recent studies provide a better understanding of the mechanisms by which second hand tobacco smoke contributes to the development of heart disease, report researchers from UC San Francisco.

Two noted cardiology researchers, Dr. Stanton Glantz and Dr. William Parmley, have done a considerable amount of research on the effects of secondhand tobacco smoke on the heart. The two collaborated on a research project combining their own data with that from other researchers around the world, in an effort to consolidate what is known about the pathogenic mechanisms of tobacco smoke.

The current data demonstrate that the ill effects of secondhand smoke result from many components of tobacco smoke. These include carbon monoxide, nicotine, polycyclic aromatic hydrocarbons and others.

The carbon monoxide produced by passive smoking competes with oxygen for binding sites on red blood cells. This reduces the blood's ability to deliver oxygen to the heart and compromises the heart muscle's ability to use oxygen to create adenosine triphosphate. The carbon monoxide also increases the amount of lactate in venous blood.

As a result of these effects, people exposed to second hand smoke show a reduced exercise capability. For example, studies show that people with existing heart disease cannot exercise as hard or as long when exposed to secondhand smoke. These people are also more likely to develop arrhythmias (irregular heart beats) when exposed to secondhand smoke. Related studies have shown that people with no signs of heart disease take as long as those with heart disease to return to their resting heart rate following exercise when exposed to secondhand smoke.

Several studies have shown that children of smoking parents have increased levels of 2,3-diphosphoglycerate. This enzyme increases the disassociation of oxygen from hemoglobin in red blood cells in an attempt to counterbalance chronic oxygen deprivation.

Second hand smoke, also called sidestream smoke or environmental tobacco smoke, also increases platelet activity, accelerates atherosclerotic lesions, and increases tissue damage following ischemia (insufficient oxygen delivery to the heart or brain) or myocardial infarction (heart attack). Increases in platelet activity are associated with formation of blood clots and atherosclerosis (hardening of the arteries), both of which are factors predisposing for a heart attack.

There is now a considerable amount of data indicating that second hand smoke has different effects on smokers and non-smokers, the researchers note. The hearts of chronic smokers make certain adaptations to compensate for the negative effects of smoking, whereas nonsmokers do not show this 'advantage'.

"The practice-- often advocated by the tobacco industry and its scientific consultants when considering second hand smoke-- of thinking about cigarette equivalents of simple dose-based extrapolations from smokers to non-smokers will lead to gross underestimations of the risks of passive smoking to the cardiovascular system... Leaving aside the philosophical considerations of whether anyone ought to be required to breathe even one cigarette per day under any circumstances, the environmental tobacco smoke experienceed by many people in their daily lives is enough to produce substantial adverse effects on the cardiovascular system," note Parmley and Glantz.

The researchers conclude that second hand smoke is the third leading cause of preventable death, after active smoking and alcohol. They estimate that passive smoking causes as many as 60,000 fatal heart attacks per year and three times as many non-fatal heart attacks.

Passive smoking should be considered on a par with public health problems such as AIDS and illegal drug use, with major efforts expended to protect workers, children and the general public, they note, adding that the simplest and least expensive way to accomplish this is to mandate smoke-free workplaces, schools and public places.