Editing Passive smoking (section)

== Evidence ==
[[File:Exposure to secondhand smoke by age, race, and poverty level US.png|thumb|Exposure to secondhand smoke by age, race, and poverty level in the US in 2010]]
[[Epidemiology|Epidemiological]] studies show that non-smokers exposed to secondhand smoke are at risk for many of the health problems associated with direct smoking.{{cn|date=December 2024}}

In 1992, a review estimated that secondhand smoke exposure was responsible for 35,000 to 40,000 deaths per year in the [[United States]] in the early 1980s.<ref name="steenland">{{cite journal |last1=Steenland |first1=K. |title=Passive smoking and the risk of heart disease |journal=JAMA |date=1 January 1992 |volume=267 |issue=1 |pages=94–99 |doi=10.1001/jama.267.1.94 |pmid=1727204 }}</ref> The [[absolute risk increase]] of heart disease due to ETS was 2.2%, while the [[attributable risk percent]] was 23%. A 1997 meta-analysis found that secondhand smoke exposure increased the risk of heart disease by a quarter,<ref>{{cite journal |last1=Law |first1=M R |last2=Morris |first2=J K |last3=Wald |first3=N J |title=Environmental tobacco smoke exposure and ischaemic heart disease: an evaluation of the evidence |journal=BMJ |date=18 October 1997 |volume=315 |issue=7114 |pages=973–980 |doi=10.1136/bmj.315.7114.973 |pmid=9365294 |pmc=2127675 }}</ref> and two 1999 meta-analyses reached similar conclusions.<ref>{{cite journal |last1=Thun |first1=M |last2=Henley |first2=J |last3=Apicella |first3=L |title=Epidemiologic studies of fatal and nonfatal cardiovascular disease and ETS exposure from spousal smoking |journal=Environmental Health Perspectives |date=December 1999 |volume=107 |issue=suppl 6 |pages=841–846 |doi=10.1289/ehp.99107s6841 |pmid=10592140 |pmc=1566204 |jstor=3434563 }}</ref><ref>{{cite journal |last1=He |first1=Jiang |last2=Vupputuri |first2=Suma |last3=Allen |first3=Krista |last4=Prerost |first4=Monica R. |last5=Hughes |first5=Janet |last6=Whelton |first6=Paul K. |title=Passive Smoking and the Risk of Coronary Heart Disease — A Meta-Analysis of Epidemiologic Studies |journal=New England Journal of Medicine |date=25 March 1999 |volume=340 |issue=12 |pages=920–926 |doi=10.1056/NEJM199903253401204 |pmid=10089185 |doi-access=free }}</ref>

Evidence shows that inhaled sidestream smoke, the main component of secondhand smoke, is about four times more toxic than mainstream smoke. This fact has been known to the tobacco industry since the 1980s, though it kept its findings secret.<ref name="diethem2005">{{cite journal |vauthors=Diethelm PA, Rielle JC, McKee M |title=The whole truth and nothing but the truth? The research that Philip Morris did not want you to see |journal=Lancet |volume=366 |issue=9479 |pages=86–92 |year=2005 |pmid=15993237 |doi=10.1016/S0140-6736(05)66474-4 |s2cid=10442244 }}</ref><ref name="glantz2005">{{cite journal |vauthors=Schick S, Glantz S |title=Philip Morris toxicological experiments with fresh sidestream smoke: more toxic than mainstream smoke |journal=Tobacco Control |volume=14 |issue=6 |pages=396–404 |year=2005 |pmid=16319363 |doi=10.1136/tc.2005.011288 |pmc=1748121 }}</ref><ref name="schick2006">{{cite journal |vauthors=Schick S, Glantz SA |title=Sidestream cigarette smoke toxicity increases with aging and exposure duration |journal=Tobacco Control |volume=15 |issue=6 |pages=424–9 |year=2006 |pmid=17130369 |doi=10.1136/tc.2006.016162 |pmc=2563675 }}</ref><ref name="schick2007">{{cite journal |last1=Schick |first1=S. F. |last2=Glantz |first2=S. |title=Concentrations of the Carcinogen 4-(Methylnitrosamino)-1-(3-Pyridyl)-1-Butanone in Sidestream Cigarette Smoke Increase after Release into Indoor Air: Results from Unpublished Tobacco Industry Research |journal=Cancer Epidemiology, Biomarkers & Prevention|date=1 August 2007 |volume=16 |issue=8 |pages=1547–1553 |doi=10.1158/1055-9965.EPI-07-0210 |pmid=17684127 |s2cid=690030 |doi-access=free }}</ref> Some scientists believe that the risk of passive smoking, in particular the risk of developing [[coronary artery disease|coronary heart diseases]], may have been substantially underestimated.<ref>{{cite journal |last1=Whincup |first1=Peter H |last2=Gilg |first2=Julie A |last3=Emberson |first3=Jonathan R |last4=Jarvis |first4=Martin J |last5=Feyerabend |first5=Colin |last6=Bryant |first6=Andrew |last7=Walker |first7=Mary |last8=Cook |first8=Derek G |title=Passive smoking and risk of coronary heart disease and stroke: prospective study with cotinine measurement |journal=BMJ |date=24 July 2004 |volume=329 |issue=7459 |pages=200–205 |doi=10.1136/bmj.38146.427188.55 |pmid=15229131 |pmc=487731 }}</ref>

In 1997, a meta-analysis on the relationship between secondhand smoke exposure and lung cancer concluded that such exposure caused lung cancer. The increase in risk was estimated to be 24% among non-smokers who lived with a smoker.<ref>{{cite journal |last1=Hackshaw |first1=A K |last2=Law |first2=M R |last3=Wald |first3=N J |title=The accumulated evidence on lung cancer and environmental tobacco smoke |journal=BMJ |date=18 October 1997 |volume=315 |issue=7114 |pages=980–988 |doi=10.1136/bmj.315.7114.980 |pmid=9365295 |pmc=2127653 }}</ref> In 2000, Copas and Shi reported that there was clear evidence of publication bias in the studies included in this meta-analysis. They further concluded that after correcting for publication bias, and assuming that 40% of all studies are unpublished, this increased risk decreased from 24% to 15%.<ref>{{cite journal |last1=Copas |first1=J B |last2=Shi |first2=JQ |title=Reanalysis of epidemiological evidence on lung cancer and passive smoking |journal=BMJ |date=12 February 2000 |volume=320 |issue=7232 |pages=417–418 |doi=10.1136/bmj.320.7232.417 |pmid=10669446 |pmc=27286 }}</ref> This conclusion has been challenged on the basis that the assumption that 40% of all studies are unpublished was "extreme".<ref name=IARC2004/>{{rp|1269}} In 2006, Takagi et al. reanalyzed the data from this meta-analysis to account for publication bias and estimated that the relative risk of lung cancer among those exposed to secondhand smoke was 1.19, slightly lower than the original estimate.<ref>{{cite journal |last1=Takagi |first1=Hisato |last2=Sekino |first2=Seishiro |last3=Kato |first3=Takayoshi |last4=Matsuno |first4=Yukihiro |last5=Umemoto |first5=Takuya |title=Revisiting evidence on lung cancer and passive smoking: Adjustment for publication bias by means of "trim and fill" algorithm |journal=Lung Cancer |date=February 2006 |volume=51 |issue=2 |pages=245–246 |doi=10.1016/j.lungcan.2005.11.004 |pmid=16386820 }}</ref> A 2000 meta-analysis found a [[relative risk]] of 1.48 for lung cancer among men exposed to secondhand smoke, and a relative risk of 1.16 among those exposed to it at work.<ref>{{cite journal |last1=Zhong |first1=Lijie |last2=Goldberg |first2=Mark S |last3=Parent |first3=Marie-Élise |last4=Hanley |first4=James A |title=Exposure to environmental tobacco smoke and the risk of lung cancer: a meta-analysis |journal=Lung Cancer |date=January 2000 |volume=27 |issue=1 |pages=3–18 |doi=10.1016/s0169-5002(99)00093-8 |pmid=10672779 }}</ref> Another meta-analysis confirmed the finding of an increased risk of lung cancer among women with spousal exposure to secondhand smoke the following year. It found a relative risk of lung cancer of 1.29 for women exposed to secondhand smoke from their spouses.<ref>{{cite journal |last1=Taylor |first1=Richard |last2=Gumming |first2=Robert |last3=Woodward |first3=Alistair |last4=Black |first4=Megan |title=Passive smoking and lung cancer: a cumulative meta-analysis |journal=Australian and New Zealand Journal of Public Health |date=June 2001 |volume=25 |issue=3 |pages=203–211 |doi=10.1111/j.1467-842x.2001.tb00564.x |pmid=11494987 |s2cid=25724906 |doi-access=free }}</ref> A 2014 meta-analysis noted that "the association between exposure to secondhand smoke and lung cancer risk is well established."<ref>{{cite journal |last1=Kim |first1=Claire H. |last2=Lee |first2=Yuan-Chin Amy |last3=Hung |first3=Rayjean J. |last4=McNallan |first4=Sheila R. |last5=Cote |first5=Michele L. |last6=Lim |first6=Wei-Yen |last7=Chang |first7=Shen-Chih |last8=Kim |first8=Jin Hee |last9=Ugolini |first9=Donatella |last10=Chen |first10=Ying |last11=Liloglou |first11=Triantafillos |last12=Andrew |first12=Angeline S. |last13=Onega |first13=Tracy |last14=Duell |first14=Eric J. |last15=Field |first15=John K. |last16=Lazarus |first16=Philip |last17=Le Marchand |first17=Loic |last18=Neri |first18=Monica |last19=Vineis |first19=Paolo |last20=Kiyohara |first20=Chikako |last21=Hong |first21=Yun-Chul |last22=Morgenstern |first22=Hal |last23=Matsuo |first23=Keitaro |last24=Tajima |first24=Kazuo |last25=Christiani |first25=David C. |last26=McLaughlin |first26=John R. |last27=Bencko |first27=Vladimir |last28=Holcatova |first28=Ivana |last29=Boffetta |first29=Paolo |last30=Brennan |first30=Paul |last31=Fabianova |first31=Eleonora |last32=Foretova |first32=Lenka |last33=Janout |first33=Vladimir |last34=Lissowska |first34=Jolanta |last35=Mates |first35=Dana |last36=Rudnai |first36=Peter |last37=Szeszenia-Dabrowska |first37=Neonila |last38=Mukeria |first38=Anush |last39=Zaridze |first39=David |last40=Seow |first40=Adeline |last41=Schwartz |first41=Ann G. |last42=Yang |first42=Ping |last43=Zhang |first43=Zuo-Feng |title=Exposure to secondhand tobacco smoke and lung cancer by histological type: A pooled analysis of the International Lung Cancer Consortium (ILCCO): Secondhand tobacco smoke and lung cancer |journal=International Journal of Cancer |date=15 October 2014 |volume=135 |issue=8 |pages=1918–1930 |doi=10.1002/ijc.28835 |pmid=24615328 |pmc=4126868 }}</ref>

A minority of epidemiologists have found it hard to understand how secondhand smoke, which is more diluted than actively inhaled smoke, could have an effect that is such a large fraction of the added risk of coronary heart disease among active smokers.<ref name="nature">{{cite journal |author=Novak K |title=Passive smoking: out from the haze |journal=Nature |volume=447 |issue=7148 |pages=1049–51 |year=2007 |pmid=17597735 |doi=10.1038/4471049a |bibcode=2007Natur.447.1049N |s2cid=9627500 |doi-access=free }}</ref><ref>{{cite journal |last1=Bailar |first1=John C. |title=Passive Smoking, Coronary Heart Disease, and Meta-Analysis |journal=New England Journal of Medicine |date=25 March 1999 |volume=340 |issue=12 |pages=958–959 |doi=10.1056/NEJM199903253401211 |pmid=10089192 }}</ref> One proposed explanation is that secondhand smoke is not simply a diluted version of "mainstream" smoke, but has a different composition with more toxic substances per gram of total particulate matter.<ref name="nature"/> Passive smoking appears to be capable of precipitating the acute manifestations of cardio-vascular diseases (atherothrombosis) and may also have a negative impact on the outcome of patients who have acute coronary syndromes.<ref>{{cite journal |last1=Raupach |first1=Tobias |last2=Schäfer |first2=Katrin |last3=Konstantinides |first3=Stavros |last4=Andreas |first4=Stefan |title=Secondhand smoke as an acute threat for the cardiovascular system: a change in paradigm |journal=European Heart Journal |date=1 February 2006 |volume=27 |issue=4 |pages=386–392 |doi=10.1093/eurheartj/ehi601 |pmid=16230308 |doi-access=free }}</ref>

In 2004, the [[International Agency for Research on Cancer]] (IARC) of the [[World Health Organization]] (WHO) reviewed all significant published evidence related to tobacco smoking and cancer. It concluded:

{{blockquote|These meta-analyses show that there is a statistically significant and consistent association between lung cancer risk in spouses of smokers and exposure to second-hand tobacco smoke from the spouse who smokes. The excess risk is of the order of 20% for women and 30% for men and remains after controlling for some potential sources of bias and confounding.<ref name=IARC2004/>}}

Subsequent meta-analyses have confirmed these findings.<ref name="pmid17690135">{{cite journal |last1=Taylor |first1=R. |last2=Najafi |first2=F. |last3=Dobson |first3=A. |title=Meta-analysis of studies of passive smoking and lung cancer: effects of study type and continent |journal=International Journal of Epidemiology |date=1 October 2007 |volume=36 |issue=5 |pages=1048–1059 |doi=10.1093/ije/dym158 |pmid=17690135 |doi-access=free }}</ref><ref name="pmid17267733">{{cite journal |last1=Stayner |first1=Leslie |last2=Bena |first2=James |last3=Sasco |first3=Annie J. |last4=Smith |first4=Randall |last5=Steenland |first5=Kyle |last6=Kreuzer |first6=Michaela |last7=Straif |first7=Kurt |title=Lung Cancer Risk and Workplace Exposure to Environmental Tobacco Smoke |journal=American Journal of Public Health |date=March 2007 |volume=97 |issue=3 |pages=545–551 |doi=10.2105/AJPH.2004.061275 |pmid=17267733 |pmc=1805004 }}</ref>

The National Asthma Council of Australia cites studies showing that secondhand smoke is probably the most important [[Indoor air quality|indoor pollutant]], especially around young children:<ref>{{cite web |title=Health effects of indoor air pollution |url=http://www.nationalasthma.org.au/html/management/infopapers/health_professionals/4005.asp |access-date=2006-07-26 |url-status=dead |archive-url=https://web.archive.org/web/20060805200559/http://www.nationalasthma.org.au/HTML/management/infopapers/health_professionals/4005.asp |archive-date=2006-08-05 }}</ref>
* Smoking by either parent, particularly by the mother, increases the risk of asthma in children.
* The outlook for early childhood asthma is less favourable in smoking households.
* Children with asthma who are exposed to smoking in the home generally have more severe disease.
* Many adults with asthma identify ETS as a trigger for their symptoms.
* Doctor-diagnosed asthma is more common among non-smoking adults exposed to ETS than those not exposed. Among people with asthma, higher ETS exposure is associated with a greater risk of severe attacks.

In [[France]], exposure to secondhand smoke has been estimated to cause between 3,000<ref>{{cite journal |last1=Wirth |first1=N. |last2=Abou-Hamdan |first2=K. |last3=Spinosa |first3=A. |last4=Bohadana |first4=A. |last5=Martinet |first5=Y. |title=Le tabagisme passif |trans-title=Passive smoking |language=fr |journal=Revue de Pneumologie Clinique |date=March 2005 |volume=61 |issue=1 |pages=7–15 |doi=10.1016/s0761-8417(05)84776-5 |pmid=15772574 }}</ref> and 5,000 premature deaths per year, with the larger figure cited by Prime Minister [[Dominique de Villepin]] during his announcement of a nationwide smoke-free law: "That makes more than 13 deaths a day. It is an unacceptable reality in our country in terms of public health."<ref name="France to ban smoking">{{cite news |title=France to ban smoking in public |url=http://news.bbc.co.uk/1/hi/world/europe/6032125.stm |access-date=2006-10-09 |publisher = [[BBC]] |date = 2006-10-08}}</ref>

There is good observational evidence that smoke-free legislation reduces the number of hospital admissions for heart disease.<ref>{{cite journal |last1=Meyers |first1=David G. |last2=Neuberger |first2=John S. |last3=He |first3=Jianghua |title=Cardiovascular Effect of Bans on Smoking in Public Places |journal=Journal of the American College of Cardiology |date=September 2009 |volume=54 |issue=14 |pages=1249–1255 |doi=10.1016/j.jacc.2009.07.022 |pmid=19778665 |doi-access=free }}</ref><ref>{{cite journal |last1=Lin |first1=Hualiang |last2=Wang |first2=Hongchun |last3=Wu |first3=Wei |last4=Lang |first4=Lingling |last5=Wang |first5=Qinzhou |last6=Tian |first6=Linwei |title=The effects of smoke-free legislation on acute myocardial infarction: a systematic review and meta-analysis |journal=BMC Public Health |date=December 2013 |volume=13 |issue=1 |pages=529 |doi=10.1186/1471-2458-13-529 |pmid=23721370 |pmc=3671962 |doi-access=free }}</ref>

=== Exposure and risk levels ===
The [[International Agency for Research on Cancer]] of the [[World Health Organization]] concluded in 2004 that there was sufficient evidence that secondhand smoke caused cancer in humans.<ref name=IARC2004/> Those who work in environments where smoke is not regulated are at higher risk.<ref>{{cite journal |last1=Wells |first1=A J |title=Lung cancer from passive smoking at work |journal=American Journal of Public Health |date=July 1998 |volume=88 |issue=7 |pages=1025–1029 |doi=10.2105/ajph.88.7.1025 |pmid=9663148 |pmc=1508269 }}</ref><ref name="pmid17267733"/> Workers particularly at risk of exposure include those in installation repair and maintenance, construction and extraction, and transportation.<ref name=Fitzsimmons/>

Much research has come from studies of nonsmokers who are married to a smoker. The [[Surgeon General of the United States|US Surgeon General]], in his 2006 report, estimated that living or working in a place where smoking is permitted increases the non-smokers' risk of developing heart disease by 25–30% and lung cancer by 20–30%.<ref>{{Cite book|title = The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General|url = https://www.ncbi.nlm.nih.gov/books/NBK44324/|publisher = Centers for Disease Control and Prevention (US)|date = 2006|access-date = 2015-04-24|pmid = 20669524|series = Publications and Reports of the Surgeon General|author1 = Office on Smoking Health (US)}}</ref>

Similarly, children who are exposed to environmental tobacco smoke are shown to experience a range of adverse effects<ref name="PugmireSweeting2017">{{cite journal |last1=Pugmire |first1=Juliana |last2=Sweeting |first2=Helen |last3=Moore |first3=Laurence |title=Environmental tobacco smoke exposure among infants, children and young people: now is no time to relax |journal=Archives of Disease in Childhood |date=February 2017 |volume=102 |issue=2 |pages=117–118 |doi=10.1136/archdischild-2016-311652 |pmid=28100555 |s2cid=41806496 |doi-access=free }}</ref><ref name="StrachanCook1997">{{cite journal |last1=Strachan |first1=D P |last2=Cook |first2=D G |title=Health effects of passive smoking. 1. Parental smoking and lower respiratory illness in infancy and early childhood |journal=Thorax |date=October 1997 |volume=52 |issue=10 |pages=905–914 |doi=10.1136/thx.52.10.905 |pmid=9404380 |pmc=1758431 }}</ref><ref name="StrachanCook1998">{{cite journal |last1=Strachan |first1=D. P. |last2=Cook |first2=D. G. |title=Health effects of passive smoking. 4. Parental smoking, middle ear disease and adenotonsillectomy in children |journal=Thorax |date=1 January 1998 |volume=53 |issue=1 |pages=50–56 |doi=10.1136/thx.53.1.50 |pmid=9577522 |pmc=1758689 }}</ref> and a higher risk of becoming smokers later in life.<ref>{{cite journal |last1=Song |first1=Anna V. |last2=Glantz |first2=Stanton A. |last3=Halpern-Felsher |first3=Bonnie L. |title=Perceptions of Second-hand Smoke Risks Predict Future Adolescent Smoking Initiation |journal=Journal of Adolescent Health |date=December 2009 |volume=45 |issue=6 |pages=618–625 |doi=10.1016/j.jadohealth.2009.04.022 |pmid=19931835 |pmc=2814413 }}</ref> The [[World Health Organization|WHO]] has identified reduction of exposure to environmental tobacco smoke as key element for actions to encourage healthy child development.<ref>{{cite web|access-date=2024-06-12|title=WHO Framework Convention on Tobacco Control (WHO FCTC)|url=https://www.who.int/europe/teams/tobacco/who-framework-convention-on-tobacco-control-(who-fctc)|website=www.who.int}}</ref>

The US [[Centers for Disease Control and Prevention]] monitors the extent of and trends in exposure to environmental tobacco smoke by measuring serum [[cotinine]] in national health [[Survey (human research)|surveys]].<ref>{{cite journal |last1=Tsai |first1=James |last2=Homa |first2=David M. |last3=Gentzke |first3=Andrea S. |last4=Mahoney |first4=Margaret |last5=Sharapova |first5=Saida R. |last6=Sosnoff |first6=Connie S. |last7=Caron |first7=Kevin T. |last8=Wang |first8=Lanqing |last9=Melstrom |first9=Paul C. |last10=Trivers |first10=Katrina F. |title=Exposure to Secondhand Smoke Among Nonsmokers — United States, 1988–2014 |journal=MMWR. Morbidity and Mortality Weekly Report |date=7 December 2018 |volume=67 |issue=48 |pages=1342–1346 |doi=10.15585/mmwr.mm6748a3|pmid=30521502 |pmc=6329485 }}</ref> The [[prevalence]] of secondhand smoke exposure among U.S. nonsmokers declined from 87.5% in 1988 to 25.2% in 2014. However, nearly half of [[Black people|blacks]] and the poor were exposed in 2014.

=== Interventions to reduce environmental tobacco smoke ===
A systematic review compared smoking control programmes and their effects on smoke exposure in children. The review distinguishes between community-based, ill-child and healthy-child settings and the most common types of interventions were counselling or brief advice during clinical visits. The review did not find superior outcomes for any intervention, and the authors caution that evidence from adult settings may not generalise well to children.<ref name="BehbodSharma2018">{{cite journal |last1=Behbod |first1=Behrooz |last2=Sharma |first2=Mohit |last3=Baxi |first3=Ruchi |last4=Roseby |first4=Robert |last5=Webster |first5=Premila |title=Family and carer smoking control programmes for reducing children's exposure to environmental tobacco smoke |journal=Cochrane Database of Systematic Reviews |date=31 January 2018 |volume=1 |issue=1 |pages=CD001746 |doi=10.1002/14651858.CD001746.pub4 |pmid=29383710 |pmc=6491082 }}</ref>

===Biomarkers===
[[File:Breath CO Monitor.jpg|thumb|Breath CO monitor displaying carbon monoxide concentration of an exhaled breath sample (in ppm) with corresponding percent concentration of carboxyhemoglobin displayed below]]
Environmental tobacco smoke can be evaluated either by directly measuring tobacco smoke pollutants found in the air or by using biomarkers, an indirect measure of exposure. [[Carbon monoxide breath monitor|Carbon monoxide]] monitored through breath, [[nicotine]], [[cotinine]], [[thiocyanates]], and proteins are the most specific biological markers of tobacco smoke exposure.<ref name=Metz05>{{cite journal |vauthors=Metz-Favre C, Donnay C, de Blay F |title=[Markers of environmental tobacco smoke (ETS) exposure] |language=fr |journal=Rev Mal Respir |volume=22 |issue=1 Pt 1 |pages=81–92 |date=February 2005 |pmid=15968761 |doi=10.1016/S0761-8425(05)85439-7 }}</ref><ref>{{cite journal |author=McClure JB |title=Are biomarkers useful treatment aids for promoting health behavior change? An empirical review |journal=Am J Prev Med |volume=22 |issue=3 |pages=200–7 |date=April 2002 |pmid=11897465 |doi=10.1016/S0749-3797(01)00425-1 }}</ref> Biochemical tests are a much more reliable biomarker of secondhand smoke exposure than surveys. Certain groups of people are reluctant to disclose their smoking status and exposure to tobacco smoke, especially pregnant women and parents of young children. This is due to their smoking being socially unacceptable. Also, it may be difficult for individuals to recall their exposure to tobacco smoke.<ref>{{cite journal |vauthors=Klesges RC, Debon M, Ray JW |title=Are self-reports of smoking rate biased? Evidence from the Second National Health and Nutrition Examination Survey |journal=J Clin Epidemiol |volume=48 |issue=10 |pages=1225–33 |date=October 1995 |pmid=7561984 |doi=10.1016/0895-4356(95)00020-5 }}</ref>

A 2007 study in the ''[[Addictive Behaviors]]'' journal found a positive correlation between secondhand tobacco smoke exposure and concentrations of nicotine and/or biomarkers of nicotine in the body. Significant biological levels of nicotine from secondhand smoke exposure were equivalent to nicotine levels from active smoking and levels that are associated with behaviour changes due to nicotine consumption.<ref>{{cite journal |vauthors=Okoli CT, Kelly T, Hahn EJ |title=Secondhand smoke and nicotine exposure: a brief review |journal=Addict Behav |volume=32 |issue=10 |pages=1977–88 |date=October 2007 |pmid=17270359 |doi=10.1016/j.addbeh.2006.12.024 }}</ref>

====Cotinine====
[[Cotinine]], the metabolite of nicotine, is a biomarker of secondhand smoke exposure. Typically, cotinine is measured in the blood, saliva, and urine. Hair analysis has recently become a new, noninvasive measurement technique. Cotinine accumulates in hair during hair growth, which results in a measure of long-term, cumulative exposure to tobacco smoke.<ref name=Florescu09>{{cite journal |vauthors=Florescu A, Ferrence R, Einarson T, Selby P, Soldin O, Koren G |title=Methods for quantification of exposure to cigarette smoking and environmental tobacco smoke: focus on developmental toxicology |journal=Ther Drug Monit |volume=31 |issue=1 |pages=14–30 |date=February 2009 |pmid=19125149 |pmc=3644554 |doi=10.1097/FTD.0b013e3181957a3b }}</ref>  Urinary cotinine levels have been a reliable biomarker of tobacco exposure and have been used as a reference in many epidemiological studies.<ref name="BehbodSharma2018"/> However, cotinine levels found in the urine reflect exposure only over the preceding 48 hours. Cotinine levels of the skin, such as the hair and nails, reflect tobacco exposure over the previous three months and are a more reliable biomarker.<ref name=Metz05/>

====Carbon monoxide (CO)====
[[Carbon monoxide breath monitor|Carbon monoxide monitored via breath]] is also a reliable biomarker of secondhand smoke exposure as well as tobacco use.  With high sensitivity and specificity, it not only provides an accurate measure, but the test is also non-invasive, highly reproducible, and low in cost.  Breath CO monitoring measures the concentration of CO in an exhalation in [[parts per million]], and this can be directly correlated to the blood CO concentration ([[carboxyhemoglobin]]).<ref>{{cite journal |vauthors=Irving JM, Clark EC, Crombie IK, Smith WC |title=Evaluation of a portable measure of expired-air carbon monoxide |journal=Prev Med |volume=17 |issue=1 |pages=109–15 |date=January 1988 |pmid=3362796 |doi=10.1016/0091-7435(88)90076-X }}</ref> Breath CO monitors can also be used by emergency services to identify patients who are suspected of having CO poisoning.