Carbon monoxide and cardiovascular disease: an analysis of the weight of evidence.
The role, if any, of environmental tobacco smoke (ETS) in the causation and/or exacerbation of cardiovascular disease remains to be proven and defined. Earlier workers suggested that ETS-associated carbon monoxide, nicotine, and/or polyaromatic hydrocarbons may be causative factors. The purpose of this review was to assess the weight of evidence supporting a role for ambient carbon monoxide in the etiology of human ischemic cardiovascular disease. The findings show that there is scant clinical or experimental evidence to support a role for carbon monoxide in the causation of ischemic heart disease. Further, the results of field studies of relative air quality in nonsmoking and smoking homes, offices, and public places show that ETS contributes only minor and toxicologically insignificant increments in ambient carbon monoxide concentrations. These increments are variable and easily masked by other common carbon monoxide sources such as internal combustion engines and the burning of cooking and heating fuels. It is concluded that if ETS plays a role in the etiology of cardiovascular disease, it is most likely not mediated through carbon monoxide.
Mennear
J H
JH
School of Pharmacy, Campbell University, Buies Creek, North Carolina 27506.
D002248:Carbon Monoxide / Q000009:adverse effects* / Q000378:metabolism; D002263:Carboxyhemoglobin / Q000032:analysis*; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000378:metabolism; D006801:Humans; D012307:Risk Factors; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*
D014028:Tobacco Smoke Pollution; D002248:Carbon Monoxide; D002263:Carboxyhemoglobin