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 (2005)2 and the Office of the US Surgeon General (2006).3
Secondhand smoke contains similar constituents to mainstream smoke and has similar mechanisms of disease. 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 and 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 safe level of exposure. Secondhand smoke causes DNA damage through reactive oxygen species, which induce oxidative damage, and through reducing the antioxidant capacity of cells and the ability of DNA to repair itself.4 DNA damage is an integral event in initiating cancer and plays a key role in the pathogenesis of a variety of cardiovascular, lung and neurological diseases.
Secondhand smoke is diluted by ambient air and non-smokers are not exposed to the same dose of toxic chemicals and particulate matter as people who smoke. However, secondhand smoke exposure causes a relatively high burden of disease.
This is partially explained by the nonlinear relationship evident between secondhand smoke exposure and some health effects. 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 does not follow this pattern and is illustrated by the relationship between secondhand smoke exposure and cardiovascular disease.3, 4 A relatively low exposure to secondhand smoke has a larger effect on cardiovascular disease events than what would be anticipated based on events from active smoking. Depicted as a graph,4, 5 there is an initial rapid increase in risk at low doses, which flattens out to a more gradual increase in risk at higher doses.4-6 For this reason the effects of secondhand smoke on cardiovascular 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 magnitude to that seen in active smokers.3 The result is an increased risk of an acute cardiovascular disease event from secondhand smoke exposure that approaches the risk of an event from light active smoking, despite a much lower dose of tobacco smoke.4, 5, 7
Other mechanisms of disease, such as DNA damage, demonstrate a linear dose-response relationship, and exposure to secondhand smoke has been demonstrated to induce DNA damage at very low levels.8
Deaths from cardiovascular disease represent the major proportion of adult deaths from secondhand smoke, yet represent fewer than 20% of deaths from active smoking (see Chapter 3, Section 3.30).9 Studies of active smoking and low birth weight also demonstrate a non-linear relationship with the sharpest decline in birthweight occurring at low levels of exposure.10-13
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. Ammonia emissions in secondhand smoke can measure 40 to 170 times higher than in mainstream smoke. As noted in Section 4.2, both fresh and stale sidestream smoke are more toxic than mainstream smoke,14 and the average particle size is smaller than that in mainstream smoke, which also has consequences for health.15
- 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 low birthweight and premature birth).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, 16, 17
- 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 exposure to tobacco smoke among active smokers may increase the activity of antioxidant enzymes that control DNA damaging free radicals.
As the following sections show, secondhand smoke is known to cause a number of diseases and poorer health outcomes for non-smokers. Evidence regarding the range of diseases and various mechanisms of disease continues to emerge. Even where a relative increase in risk is small, the high number of individuals exposed makes secondhand smoke an important and preventable public health risk.
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.(Last updated May 2019)
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, 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/120/11/94
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, 11 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. Ganapathy V, Ramachandran I, Rubenstein DA, and Queimado L. Detection of in vivo DNA damage induced by very low doses of mainstream and sidestream smoke extracts using a novel assay. American Journal of Preventive Medicine, 2015; 48(1S1):s102–10. Available from: https://www.ncbi.nlm.nih.gov/pubmed/25528699
9. 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
10. 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
11. 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
12. England LJ, Kendrick JS, Wilson HG, Merritt RK, Gargiullo PM, et al. 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
13. 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
14. 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
15. 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
16. Lo Y, Hsiao C, Jou Y, Chang G, Tsai Y, 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
17. Olivo-Marston S, Yang P, Mechanic L, Bowman E, Pine S, 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