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 is a complex mixture of thousands of chemical compounds, including at least 250 chemicals known to be toxic or carcinogenic. These include substances known to affect the central nervous system, the immune system, the heart and the liver, and cause eye, skin or respiratory problems. More than 50 known or suspected carcinogens have been found in secondhand smoke.
Gaseous (or vapour phase) components of secondhand smoke known to damage health include: the carcinogen benzene; carbon monoxide, which reduces the oxygen-carrying capacity of the blood; and nitrogen oxides, which affect respiratory function. Secondhand smoke contains probable carcinogens, respiratory irritants and agents toxic to the nervous system or other organs. The California Environmental Protection Agency has identified 19 gases in secondhand smoke, including acrolein, formaldehyde, carbonyl sulphide, hydrazine, pyridine, styrene and toluene, which may have one or more of these harmful properties.
Particulate matter in secondhand smoke contains a number of potent carcinogens. The most studied of these include polycyclic aromatic hydrocarbons (PAHs) including benzo(a)pyrene, aromatic amines 2-naphthylamine and 4-aminobiphenyl, and the tobacco-specific nitrosamines N'-nitrosonornicotine (NNN) and 4-(methylnitrosamino-) 1-(3,pyridyl)-1-butone (NNK). The metabolites of NNK are detectable in the urine of non-smokers exposed to secondhand smoke.4 Polycyclic aromatic hydrocarbons and nitrosamines induce tumours in the respiratory tract and the lung, while the aromatic amines are human bladder carcinogens. A number of carcinogenic heavy metals, and weaker carcinogens that induce tumours in various organs, are also present in the particulate matter.
Most particulate matter in secondhand smoke is in the submicron (< 1µm diameter) range, meaning that it is classified as fine particulate matter (also referred to as respirable suspended particles). They are smaller than the particles in mainstream smoke. In general, smaller particles between 0.1µm and 2.5 µm diameter can penetrate deeper into the lungs, resulting in higher toxicity through oxidative stress and inflammation.5 Short and long-term exposure to fine particulate matter contributes to the aggravation of asthma and other respiratory diseases, lung cancer, cardiovascular disease and death.5,6
Secondhand smoke can be detected in the indoor environment well after it has been generated. Research shows that about half the particulate matter from secondhand smoke is still airborne after five to six hours. Over time, secondhand smoke changes in nature. Gaseous components can react with other pollutants and sunlight to form new chemicals. Particles can coagulate, expand, condense, settle on surfaces, or evaporate, depending on concentration, ventilation, humidity, sunlight and other conditions. However, even after undergoing complex physical and chemical reactions, the majority of particulate matter generated by secondhand smoke remains in the submicron range, and is therefore of toxicological concern on this basis alone.
Many compounds, such as nicotine and some PAHs, exist in both the gaseous and the particulate phase of secondhand smoke. Classified as 'semi-volatile', their ability to change form according to environmental conditions means that they remain detectable in the indoor environment for longer periods after active smoking has ceased. Nicotine may react with hydroxyl radicals in ambient air, giving it a half life of approximately one day.
An analysis of experiments funded by a tobacco company during the 1980s has shown that particulate matter in inhaled fresh sidestream smoke is three to four times as toxic per gram compared with mainstream cigarette smoke.7 Further analysis of the same tobacco industry data has shown that toxicity of sidestream smoke increases by a further two to four times as it ages.8 Therefore, the authors of this study conclude, if aged sidestream smoke is about three times more toxic than fresh sidestream smoke, and fresh sidestream smoke is about four times more toxic than mainstream smoke, then aged sidestream smoke is approximately 12 times more toxic than mainstream smoke. Although non-smokers inhale a much lesser mass of smoke than smokers, secondhand smoke appears to be substantially more toxic than mainstream smoke inhaled by smokers. This helps explain the relatively large biological effects of secondhand smoke.8
The constituents of tobacco smoke are discussed further in Chapter 12, and lists of biologically active compounds in secondhand smoke can be found in the references cited at the start of this section.
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. Stark M, Rohde K, Maher J, Pizacani B, Dent C, Bard R, et al. The impact of clean indoor air exemptions and preemption policies on the prevalence of a tobacco-specific lung carcinogen among nonsmoking bar and restaurant workers. American Journal of Public Health 2007;97(8):1457–63. Available from: http://www.ajph.org/cgi/reprint/97/8/1457
5. 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
6. Brook RD, Rajagopalan S, Pope CA, 3rd, Brook JR, Bhatnagar A, Diez-Roux AV, et al. Particulate matter air pollution and cardiovascular disease: an update to the scientific statement from the American Heart Association. Circulation 2010;121(21):2331–78. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=20458016
7. Schick S and Glantz S. Philip Morris toxicological experiments with fresh sidestream smoke: more toxic than mainstream smoke. Tobacco Control 2005;14(6):396–404. Available from: http://tc.bmjjournals.com/cgi/content/abstract/14/6/396
8. 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