. "3 Experimental Studies Relevant to the Pathophysiology of Secondhand Smoke." Secondhand Smoke Exposure and Cardiovascular Effects: Making Sense of the Evidence. Washington, DC: The National Academies Press, 2010.
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Secondhand Smoke Exposure and Cardiovascular Effects: Making Sense of the Evidence
lar disease is caused by exposure to secondhand smoke (Hatsukami et al., 2006). In this section, however, the committee uses those effects to examine whether secondhand-smoke exposure causes pathophysiologic changes that would contribute to the biological plausibility that decreasing secondhand-smoke exposure could lead to a decrease in acute myocardial infarctions (MIs).
EFFECTS OF CIGARETTE SMOKE
As discussed in several review articles (for examples, see Armani et al., 2009; Burke and FitzGerald, 2003), oxidative stress could mediate many of the effects of smoke on the cardiovascular system. Such stress, during which endogenous antioxidants are overwhelmed by oxidants such as reactive oxygen species and free radicals, results in impaired cellular function. The exact mechanisms whereby oxidative stress leads to cardiovascular disease, such as atherosclerosis, are not clear, but it appears that oxidative stress may play a role in cardiovascular pathophysiology (Ballinger et al., 2002), and it could account for many effects of tobacco-smoke exposure, such as endothelial dysfunction, thrombosis, and inflammation (Raupach et al., 2006; Thomas et al., 2008).
Many constituents of mainstream and sidestream smoke are or produce free radicals capable of producing oxidative stress. Those constituents include vapor-phase carbonyl compounds (such as acrolein), oxides of nitrogen, metabolites of polycyclic aromatic hydrocarbons (PAHs), metals, and particulate matter (PM) (NRC, 1986). Mainstream cigarette smoke increases the concentrations of markers of oxidative stress, lipid peroxidation, protein oxidation, and DNA modification. Isoprostanes, indicators of lipid peroxidation and in vivo oxidation injury, are higher in smokers than in nonsmokers, and their concentrations decreased after smoking cessation for 2 weeks (Morrow et al., 1995). Smokers admitted to a cardiac outpatient center who then quit smoking had decreases in isoprostanes a few days after quitting, and the decreases continued until a steady state was reached 4 weeks after quiting (Pilz et al., 2000). Pignatelli et al. (2001) demonstrated that oxidized plasma proteins, another marker of oxidative stress, are higher in smokers than in nonsmokers.
Ahmadzadehfar et al. (2006) reported that exposure to secondhand smoke significantly increased isoprostane 8-epi-PGF2α in nonsmokers. After repeated secondhand-smoke exposure, isoprostane 8-epi-PGF2α in non-smokers reached nearly the same values as in smokers.
Probst-Hensch (2008) investigated whether the effects of secondhand smoke on the cardiovascular system are mediated by oxidative stress in a