DANGERS & EFFECTS OF SECOND-HAND SMOKE

Dangers & Effects of Second-hand Smoke

Dangers & Effects of Second-hand Smoke

Second-hand smoking increases the risk of fatal and nonfatal coronary heart disease by 30%. This effect, while consistently appear in many epidemiological studies, more than would be expected based on the dose of smoke that Second-hand smokers are obtained as compared with smokers: effect of about one-third that observed in smokers, while the relative dose smoke much less. Previous researchers have shown that this apparent discrepancy may be because some aspects of the cardiovascular system, including platelet and endothelial function, are very sensitive, even in relatively small doses of smoke (as compared with smoking), that smokers inhale when around a Second-hand smoking. Indeed, some of the effects of Second-hand smoking on the cardiovascular system of nonsmokers is comparable with the effects of smoking among smokers, perhaps because the effects of toxins in the smoke saturation at relatively low risk. In this issue, Panagiotakos et al paper is another effect of Second-hand smoking: an increase in inflammation, which is a precursor of atherosclerotic plaque. In particular, they showed not only that white blood cells, C-reactive protein, homocysteine, fibrinogen, and oxidized low density lipoprotein (LDL) cholesterol levels were increased among those exposed to secondhand smoke, but this increase was similar to that was observed in smokers.

Mechanisms by which Second-hand smoking increases the risk of heart disease are numerous and include an increase in oxidized cholesterol LDL, increased platelet adherence, mitochondrial damage, and oxidative damage. Instead, what is happening in isolation, these mechanisms interact with each other. In addition, Second-hand smoking is harmful to the endothelium, a vital layer of the coronary arteries. Endothelium selects vasodilating substances such as nitric oxide and prevents inflammatory cells from attaching to the vessel wall. Second-hand smoking hinders the production of nitric oxide.

Study of Al Panagiotakos et al has several strengths but also some limitations. The size of a random sample, the ability to control potential confounding factors (eg diet, physical activity), as well as assessment of Second-hand exposure to smoke at home and at work, some of the benefits of this research. The fact that the cross-sectional data, there was no biochemical verification of Second-hand exposure to smoke (eg, cotinine levels), and that exposure levels are classified only as a regular or occasional, some limitations of this study. Percentage of people who report current exposure (38% never smoking men and 33% of women) seems low, given that the prevalence of smoking in this sample (48% men and 38% of women) is high. This fact makes it more likely that the authors underestimate the actual impact. The implications of this underestimation, however, will distort the results to zero. Elevated levels of inflammatory markers found in this study, surrogate markers of inflammation, leading to atherosclerotic disease and ultimately to an increased risk of cardiovascular disease. To check their results, it would be desirable to have the results of a prospective study.

Although Panagiotakos and others studied the effects of prolonged exposure to tobacco ...