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In botany, tobacco is "a plant genus of the family solanaceae. Members contain nicotine and more than 4000 other chemicals, including many biologically active chemicals;[1] its dried leaves are used for smoking."

Biological effects of smoking

Atherothrombotic effects

A recent review (2013) by Csordas and Bernard[1] states the following in the abstract:

  • Cigarette smoke is an aerosol that contains >4,000 chemicals, including nicotine, carbon monoxide, acrolein, and oxidant compounds.
  • Exposure to cigarette smoke induces multiple pathological effects in the endothelium, several of which are the result of oxidative stress initiated by reactive oxygen species, reactive nitrogen species, and other oxidant constituents of cigarette smoke.
  • Cigarette-smoke exposure interferes adversely with the control of all stages of [arterial] plaque formation and development and pathological thrombus formation.
  • The reactive oxygen species in cigarette smoke contribute to oxidative stress, upregulation of inflammatory cytokines, and endothelial dysfunction, by reducing the bioavailability of nitric oxide.
  • Plaque formation and the development of vulnerable plaques also result from exposure to cigarette smoke via the enhancement of inflammatory processes and the activation of matrix metalloproteases.
  • Moreover, exposure to cigarette smoke results in platelet activation, stimulation of the coagulation cascade, and impairment of anticoagulative fibrinolysis.
  • Many cigarette-smoke-mediated prothrombotic changes are quickly reversible upon smoking cessation.
  • Public health efforts should urgently promote our understanding of current cigarette-smoke-induced cardiovascular pathology to encourage individuals to reduce their exposure to cigarette smoke and, therefore, the detrimental consequences of associated atherothrombotic disease.

Passive smoking

Passive smoking, also called second-hand or secondhand smoking, is associated with lung cancer,[2][3] coronary heart disease,[4][5] and maybe cognitive impairment.[6]

Smoke free legislation is associated with reductions in hospitalizations for acute coronary syndrome.[7][8]


  1. 1.0 1.1 Csordas A, Bernhard D. (2013) The biology behind the atherothrombotic effects of cigarette smoke. Nat Rev Cardiol 10(4):219-230.
  2. Taylor R, Najafi F, Dobson A (October 2007). "Meta-analysis of studies of passive smoking and lung cancer: effects of study type and continent". Int J Epidemiol 36 (5): 1048–59. DOI:10.1093/ije/dym158. PMID 17690135. Research Blogging. ,
  3. Stayner L, Bena J, Sasco AJ, et al (March 2007). "Lung cancer risk and workplace exposure to environmental tobacco smoke". Am J Public Health 97 (3): 545–51. DOI:10.2105/AJPH.2004.061275. PMID 17267733. Research Blogging.
  4. He J, Vupputuri S, Allen K, Prerost MR, Hughes J, Whelton PK (March 1999). "Passive smoking and the risk of coronary heart disease--a meta-analysis of epidemiologic studies". N. Engl. J. Med. 340 (12): 920–6. PMID 10089185[e]
  5. Teo KK, Ounpuu S, Hawken S, et al (August 2006). "Tobacco use and risk of myocardial infarction in 52 countries in the INTERHEART study: a case-control study". Lancet 368 (9536): 647–58. DOI:10.1016/S0140-6736(06)69249-0. PMID 16920470. Research Blogging.
  6. Llewellyn DJ, Lang IA, Langa KM, Naughton F, Matthews FE (2009). "Exposure to secondhand smoke and cognitive impairment in non-smokers: national cross sectional study with cotinine measurement". BMJ 338: b462. PMID 19213767. PMC 2643443[e]
  7. Pell JP, Haw S, Cobbe S, et al (July 2008). "Smoke-free legislation and hospitalizations for acute coronary syndrome". N. Engl. J. Med. 359 (5): 482–91. DOI:10.1056/NEJMsa0706740. PMID 18669427. Research Blogging.
  8. (January 2009) "Reduced hospitalizations for acute myocardial infarction after implementation of a smoke-free ordinance--City of Pueblo, Colorado, 2002-2006". MMWR Morb. Mortal. Wkly. Rep. 57 (51): 1373–7. PMID 19116606[e]