Particulate and vapor phase constituents of cigarette mainstream smoke and risk of myocardial infarction

Atherosclerosis. 2001 Oct;158(2):257-67. doi: 10.1016/s0021-9150(01)00570-6.

Abstract

On pharmacological and compositional grounds, cigarette mainstream smoke (MS) aerosol can be broadly categorized as consisting of the following constituents: carbon monoxide, other vapor phase components, particulate matter ('tar') and nicotine. The relative risk of coronary artery disease for smoking 20 cigarettes per day has been estimated by meta-analysis of five large prospective epidemiology studies to be 1.78. These four major smoke components are simultaneously delivered to the active smoker as a complex aerosol composed of several billion semi-liquid particles per cm(3) within the mixture of combustion gases. Fractional attribution of the 78% increase in reported risk to a given constituent is problematic because of the complex mixture. However, a significant literature exists which suggests that some general statements regarding smoke constituent-associated risks for development or exacerbation of myocardial infarction are supportable. First, the atherogenic potential of MS is associated with the particulate and vapor phases and not with CO. Nicotine might exert an indirect effect on atherosclerotic plaque development by increasing shear forces in main conduction arteries. Similarly, the thrombogenic potential is associated primarily with the particulate and vapor phases and also possibly with nicotine via platelet aggregation. Vasoconstriction probably results from the actions of nicotine and hypoxia from carbon monoxide. Finally, the arrhythmia-inducing potential may result from catecholamine release following nicotine exposure, with a questionable contribution from carbon monoxide.

Publication types

  • Review

MeSH terms

  • Animals
  • Arrhythmias, Cardiac / etiology
  • Arrhythmias, Cardiac / physiopathology
  • Arteriosclerosis / etiology
  • Arteriosclerosis / physiopathology
  • Carbon Monoxide / adverse effects
  • Carbon Monoxide / analysis
  • Humans
  • Hypoxia / etiology
  • Hypoxia / physiopathology
  • Myocardial Infarction / etiology*
  • Myocardial Infarction / physiopathology
  • Nicotine / adverse effects
  • Nicotine / analysis
  • Platelet Aggregation / drug effects
  • Risk Factors
  • Smoke / analysis*
  • Smoking / adverse effects*
  • Tars / adverse effects
  • Tars / analysis
  • Thrombosis / etiology
  • Thrombosis / physiopathology
  • Tobacco*
  • Vasoconstriction / drug effects

Substances

  • Smoke
  • Tars
  • Nicotine
  • Carbon Monoxide