Heterogeneity of cardiovascular risk among smokers is related to degree of carbon monoxide exposure

Abstract

Methods: Three hundred and sixty-five men without history of cardiovascular disease (CVD) were followed over 27 years. Leg artery disease was defined as a systolic anklearm pressure ratio (ABPI) below 0.9 in either leg. Incidence of myocardial infarction (MI), stroke and deaths is based on linkage with regional and national registers. The distribution of CO in blood and expired air, respectively, was divided into quartiles.Results: There was a significant inverse relation between ABPI and CO in blood and expired air. Incidence of CVD events and deaths increased progressively with degree of CO exposure. Men with CO in the top quartile had significantly increased risks of CVD events (RR: 2.2; 95% CI: 1.00-4.6) and cardiovascular deaths (RR: 3.2, CI: 1.2-8.3), adjusted for daily tobacco consumption and other potential confounders. Conclusions:In smokers, the prevalence of leg atherosclerosis and incidence of cardiovascular disease is related to the amount of carbon monoxide in blood or expired air.

Carbon monoxide: Anticoagulant or procoagulant?

“…Thus, a consideration of environmental CO exposure and cardiovascular events as well as cerebral vascular events will be presented initially [28][29][30][31][32][33].…”

“…Increased environmental presence of CO in areas with significant [29] or low [30] air pollution was associated with increased incidence of stroke, and increased workplace exposure to CO [31] in nonsmokers was associated with a 1.97-fold increase in ischemic cardiac death. Even more interesting, among tobacco smokers, the degree of increase in COHb was associated with increased cardiovascular events, stroke and death [32,33]. While supportive of the concept that CO may facilitate thrombophilia in these settings, it must be stressed that none of these settings [28][29][30][31][32][33] involved exposure to pure CO without exposure to other potential or actual products of combustion (e.g., fine particulate pollution, tobacco smoke).…”

“…Spectrophotometric measures of resistance to fibrinolysis also demonstrated that these CO poisoning victims had increased plasmatic resistance to fibrinolysis [47]. Taken as a whole, these aforementioned investigations potentially link CO exposure to thrombophilia [28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46], with increased systemic thrombin generation and hypofibrinolysis being possible mechanisms by which CO were posited to mediate thrombotic events [47].…”

“…There is evidence that excessive CO exposure may result in decreased in vivo and in vitro hemostasis in humans and rodents [4][5][6][7][8][18][19][20][21][22][23], potentially by inhibition of platelet aggregation [9][10][11][12][13]15,16,[20][21][22][23]. However, there is also evidence that increased CO exposure can enhance platelet activation [14,17] and cause enhanced coagulation/decreased fibrinolysis in humans and other mammalian species [28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46][47][67][68][69][70]…”

On exposure and response relationships for health effects associated with exposure to vehicular traffic

“…Nevertheless, relationships have been shown previously between COHb levels and the degree of urbanization (Radford and Drizd, 1982), and between COHb levels in donated blood and urban average ambient CO levels (Lipfert, unpublished memorandum). Further, Hart et al (2006) showed that COHb was associated with all-cause mortality even after controlling for self-reported smoking, and Hedblad et al (2005Hedblad et al ( , 2006 showed that high levels of COHb are associated with cardiovascular risk factors and mortality. However, Bono et al (2007) found that smoking effects dominated COHb findings in urban traffic policemen.…”