4.5 Mechanisms of disease

Unless otherwise noted, the following section is compiled from reviews published by the International Agency for Research on Cancer (2004),1 California Environmental Protection Agency (20052) and the Office of the US Surgeon General (2006).3

The similarities between secondhand smoke and mainstream smoke make it plausible that exposure to secondhand smoke is a cause of disease, by similar pathways of disease causation as in active smokers. Metabolites from nicotine, carbon monoxide and three major classes of carcinogens found in tobacco smoke—polycyclic aromatic hydrocarbons (PAHs), nitrosamines and aromatic amines—are found in the urine or blood of non-smokers exposed to secondhand smoke, just as in active smokers. Secondhand smoke is regarded as a Group 1 carcinogen (known to cause cancer in humans), for which there is no evidence of a safe level of exposure.

However, because secondhand smoke is diluted by ambient air, exposed non-smokers do not receive as high an exposure to the toxic chemicals in tobacco smoke as do active smokers, and their risk of developing tobacco-caused illness is generally lower.

Compared to active smoking, the number of deaths from secondhand smoke appears high and disproportionate to the relative dose of tobacco smoke that non-smokers inhale. The primary factor that explains this observation is that the dose response to tobacco smoke exposure is not linear for some health effects, in particular cardiovascular disease. A linear relationship is one where a small dose has a small effect and larger doses have a proportionally larger effect. A non-linear relationship is evident between secondhand smoke exposure and heart disease events,3,4 with a low dose exposure (i.e. secondhand smoke exposure) having a larger than anticipated effect in relation to larger doses of exposure through active smoking. Depicted as a graph,4,5 i there is an initial rapid increase in risk at low doses, which flattens out to a more gradual increase in risk at higher doses.46

Therefore the effects of secondhand smoke on heart disease cannot be estimated by scaling down the effects of active smoking in a linear dose-dependent way.3

This is made biologically plausible by evidence that for certain cardiovascular mechanisms such as platelet aggregation, exposure to secondhand smoke elicits a response in non-smokers reaching a similar level or magnitude to that seen in active smokers.3 The result is that the increased risk of an acute heart disease event from secondhand smoke exposure approaches that of light active smoking.4,5,7 Deaths from cardiovascular disease represent the major proportion of adult deaths from secondhand smoke, while representing fewer than 20% of deaths from active smoking (see Chapter 3, Section 3.30).8 Studies of active smoking and low birth weight also show that the sharpest declines in birthweight occur at low levels of exposure.912

Other factors that may influence the magnitude of health effects from secondhand include:

  • The concentration of some toxic compounds in sidestream smoke can be many times that found in mainstream smoke. For example, the polycyclic aromatic hydrocarbon (PAH) content in sidestream smoke is about 10-fold that found in mainstream smoke, while ammonia emissions in secondhand smoke can measure 40 to 170 times higher than in mainstream smoke. Also, as noted in Section 4.2, both fresh and stale sidestream smoke are more toxic than mainstream smoke,13 and the average particle size is smaller than that in mainstream smoke, which also has consequences for health.14
  • Individuals with certain genotypes are more susceptible to some tobacco-related diseases. Among active smokers, genetic variations have been identified which are associated with an increased risk for lung cancer, breast cancer, chronic obstructive pulmonary disease and adverse pregnancy outcomes (such as lowered birthweight and reduced gestation).4 Research on genetic susceptibility among non-smokers exposed to secondhand smoke is limited. Some studies suggest an increased risk for lung cancer in genetically susceptible non-smokers.4,15,16
  • Non-smokers may be more sensitive to certain effects of secondhand smoke than active smokers. For example, smokers may be less sensitive to free radical damage from cigarette smoke than non-smokers because chronic exposures to tobacco smoke in active smokers appear to increase the activity of antioxidant enzymes that control free radicals.

As the following sections show, secondhand smoke is now known to cause a number of diseases and poorer health outcomes for non-smokers. A definition of causality of disease is given in Chapter 3, Section 3.0.1: Defining causality. Even where elevation of risk is small, because of the high number of individuals who may be exposed, secondhand smoke represents a substantial preventable public health risk.

i See copy of graph at http://circ.ahajournals.org/cgi/content/full/120/11/941

Recent news and research

For recent news items and research on this topic, click here (Last updated October 2016 


1. International Agency for Research on Cancer Working Group on the Evaluation of Carcinogenic Risks to Humans. Tobacco smoke and involuntary smoking. IARC monographs on the evaluation of carcinogenic risks to humans, Vol. 83. Lyon, France: IARC, 2004. Available from: http://monographs.iarc.fr/ENG/Monographs/PDFs/index.php

2. Office of Environmental Health Hazard Assessment and California Air Resources Board. Health effects of exposure to environmental tobacco smoke: final report, approved at the Panel's June 24, 2005 meeting. Sacramento: California Environmental Protection Agency, 2005. Available from: http://www.oehha.ca.gov/air/environmental_tobacco/2005etsfinal.html

3. US Department of Health and Human Services. The health consequences of involuntary exposure to tobacco smoke: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2006. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/sgr_2006/index.htm

4. US Department of Health and Human Services. How tobacco smoke causes disease: the biology and behavioral basis for smoking-attributable disease. A report of the Surgeon General. Atlanta, Georgia: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Available from: http://www.surgeongeneral.gov/library/tobaccosmoke/report/index.html

5. Pope 3rd C, Burnett R, Krewski D, Jerrett M, Shi Y, Calle E, et al. Cardiovascular mortality and exposure to airborne fine particulate matter and cigarette smoke. Shape of the exposure-response relationship. Circulation 2009;120(11):941–8. Available from: http://circ.ahajournals.org/cgi/content/full/120/11/941

6. Law M and Wald N. Environmental tobacco smoke and ischemic heart disease. Progress in Cardiovascular Diseases 2003;46:31–8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12920699

7. International Agency for Research on Cancer. Reversal of risk after quitting smoking. Handbooks of cancer prevention, tobacco control, Vol. 11. Lyon, France: IARC, 2007. Available from: http://apps.who.int/bookorders/anglais/detart1.jsp?sesslan=1&codlan=1&codcol=76&codcch=22

8. Collins D and Lapsley H. The costs of tobacco, alcohol and illicit drug abuse to Australian society in 2004–05. Canberra: Department of Health and Ageing, 2008. Available from: http://www.nationaldrugstrategy.gov.au/internet/drugstrategy/publishing.nsf/Content/mono64/$File/mono64.pdf

9. US Department of Health and Human Services. Women and smoking : a report of the Surgeon General. Rockville, Maryland: US Department of Health and Human Services Public Health Service, 2001. Available from: http://www.cdc.gov/tobacco/sgr/sgr_forwomen/index.htm

10. England LJ, Kendrick JS, Gargiullo PM, Zahniser SC and Hannon WH. Measures of maternal tobacco exposure and infant birth weight at term. American Journal of Epidemiology 2001;153(10):954–60. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11384951

11. England LJ, Kendrick JS, Wilson HG, Merritt RK, Gargiullo PM and Zahniser SC. Effects of smoking reduction during pregnancy on the birth weight of term infants. American Journal of Epidemiology 2001;154(8):694–701. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11590081

12. Secker-Walker RH and Vacek PM. Infant birth weight as a measure of harm reduction during smoking cessation trials in pregnancy. Health Education Behaviour 2002;29(5):557–69. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12238700

13. Schick S and Glantz SA. Sidestream cigarette smoke toxicity increases with aging and exposure duration. Tobacco Control 2006;15(6):424–9. Available from: http://tc.bmj.com/cgi/content/abstract/15/6/424

14. Valavanidis A, Fiotakis K and Vlachogianni T. Airborne particulate matter and human health: toxicological assessment and importance of size and composition of particles for oxidative damage and carcinogenic mechanisms. Journal of Environmental Science and Health. Part C, Environmental Carcinogenesis & Ecotoxicology Reviews 2008;26(4):339–62. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19034792

15. Lo Y, Hsiao C, Jou Y, Chang G, Tsai Y, Su W, et al. ATM polymorphisms and risk of lung cancer among never smokers. Lung Cancer 2009;69(2):148–54. Available from: http://www.lungcancerjournal.info/article/PIIS0169500209005844/fulltext

16. Olivo-Marston S, Yang P, Mechanic L, Bowman E, Pine S, Loffredo C, et al. Childhood exposure to secondhand smoke and functional mannose binding lectin polymorphisms are associated with increased lung cancer risk. Cancer Epidemiology, Biomarkers & Prevention 2009;18(12):3375–83. Available from: http://cebp.aacrjournals.org/content/18/12/3375.long

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