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Tobacco smoke in an Irish pub before a smoking ban came into effect on 29 March 2004

Passive smoking is the inhalation of tobacco smoke, called passive smoke, secondhand smoke (SHS) or environmental tobacco smoke (ETS), by individuals other than the active smoker. It occurs when tobacco smoke diffuses into the surrounding atmosphere as an aerosol pollutant, which leads to its inhalation by nearby bystanders within the same environment. Exposure to secondhand tobacco smoke causes many of the same health effects caused by active smoking,[1][2] although at a lower prevalence due to the reduced concentration of smoke that enters the airway.

According to a World Health Organization (WHO) report published in 2023, more than 1.3 million deaths are attributed to passive smoking worldwide every year.[3] The health risks of secondhand smoke are a matter of scientific consensus,[4][5][6] and have been a major motivation for smoking bans in workplaces and indoor venues, including restaurants, bars and night clubs, as well as some open public spaces.[7]

Concerns around secondhand smoke have played a central role in the debate over the harms and regulation of tobacco products. Since the early 1970s, the tobacco industry has viewed public concern over secondhand smoke as a serious threat to its business interests.[8] Despite the industry's awareness of the harms of secondhand smoke as early as the 1980s, the tobacco industry coordinated a scientific controversy with the purpose of stopping regulation of their products.[4]: 1242 [6]

Terminology

[edit]

Fritz Lickint created the term "passive smoking" ("Passivrauchen") in a publication in the German language during the 1930s.[9][10][11] Terms used include "environmental tobacco smoke" to refer to the airborne matter, while "involuntary smoking" and "passive smoking" refer to exposure to secondhand smoke.[12][13] The term "environmental tobacco smoke" can be traced back to a 1974 industry-sponsored meeting held in Bermuda, while the term "passive smoking" was first used in the title of a scientific paper in 1970.[13] The Surgeon General of the United States prefers to use the phrase "secondhand smoke" rather than "environmental tobacco smoke", stating that "The descriptor 'secondhand' captures the involuntary nature of the exposure, while 'environmental' does not."[1]: 9  Most researchers consider the term "passive smoking" to be synonymous with "secondhand smoke".[14] In contrast, a 2011 commentary in Environmental Health Perspectives argued that research into "thirdhand smoke" renders it inappropriate to refer to passive smoking with the term "secondhand smoke", which the authors stated constitutes a pars pro toto.[14]

The term "sidestream smoke" is sometimes used to refer to smoke that goes into the air directly from a burning cigarette, cigar, or pipe,[15] while "mainstream smoke" refers to smoke that a smoker exhales.

Health effects

[edit]

Secondhand smoke causes many of the same diseases as direct smoking, including cardiovascular diseases, lung cancer, and respiratory diseases.[1][2][16] These include:

  • Cancer:
    • General: overall increased risk;[17] reviewing the evidence accumulated on a worldwide basis, the International Agency for Research on Cancer concluded in 2004 that "Involuntary smoking (exposure to secondhand or 'environmental' tobacco smoke) is carcinogenic to humans."[2] The Centers for Disease Control and Prevention reports that about 70 chemicals present in secondhand smoke are carcinogenic.[18]
    • Lung cancer: Passive smoking is a risk factor for lung cancer.[19][20] In the United States, secondhand smoke is estimated to cause more than 7,000 deaths from lung cancer a year among non-smokers.[21] A quarter of all cases occur in people who have never smoked.[22]
    • Breast cancer: The California Environmental Protection Agency concluded in 2005 that passive smoking increases the risk of breast cancer in younger, primarily premenopausal females by 70%[16] and the US Surgeon General has concluded that the evidence is "suggestive", but still insufficient to assert such a causal relationship.[1] In contrast, the International Agency for Research on Cancer concluded in 2004 that there was "no support for a causal relation between involuntary exposure to tobacco smoke and breast cancer in never-smokers."[2] A 2015 meta-analysis found that the evidence that passive smoking moderately increased the risk of breast cancer had become "more substantial than a few years ago".[23]
    • Cervical cancer: A 2015 overview of systematic reviews found that exposure to secondhand smoke increased the risk of cervical cancer.[24]
    • Bladder cancer: A 2016 systematic review and meta-analysis found that secondhand smoke exposure was associated with a significant increase in the risk of bladder cancer.[25]
  • Circulatory system: risk of heart disease[26][27] and reduced heart rate variability.[28]
    • Epidemiological studies have shown that both active and passive cigarette smoking increase the risk of atherosclerosis.[29]
    • Passive smoking is strongly associated with an increased risk of stroke, and this increased risk is disproportionately high at low levels of exposure.[30]
  • Lung problems:
  • Cognitive impairment and dementia: Exposure to secondhand smoke may increase the risk of cognitive impairment and dementia in adults 50 and over.[35] Children exposed to secondhand smoke show reduced vocabulary and reasoning skills when compared with non-exposed children as well as more general cognitive and intellectual deficits.[36]
  • Mental health: Exposure to secondhand smoke is associated with an increased risk of depressive symptoms.[37]
  • During pregnancy:
    • Miscarriage: a 2014 meta-analysis found that maternal secondhand smoke exposure increased the risk of miscarriage by 11%.[38]
    • Low birth weight[16], part B, ch. 3.[39]
    • Premature birth[16], part B, ch. 3[40] (Evidence of the causal link is described only as "suggestive" by the US Surgeon General in his 2006 report.[41]) Laws limiting smoking decrease premature births.[42]
    • Stillbirth and congenital malformations in children[43]
    • Recent studies comparing females exposed to secondhand smoke and non-exposed females, demonstrate that females exposed while pregnant have higher risks of delivering a child with congenital abnormalities, longer lengths, smaller head circumferences, and neural tube defects.[44][45]
  • General:
    • Worsening of asthma, allergies, and other conditions.[46] A 2014 systematic review and meta-analysis found that passive smoking was associated with a slightly increased risk of allergic diseases among children and adolescents; the evidence for an association was weaker for adults.[47]
    • Type 2 diabetes.[48][49][50] It remains unclear whether the association between passive smoking and diabetes is causal.[51]
  • Risk of carrying Neisseria meningitidis or Streptococcus pneumoniae.[24]
  • A possible increased risk of periodontitis.[52]
  • Overall increased risk of death in both adults, where it was estimated to kill 53,000 nonsmokers per year in the U.S in 1991,[53][54] and in children.[55] The World Health Organization states that passive smoking causes about 600,000 deaths a year, and about 1% of the global burden of disease.[56] As of 2017, passive smoking causes about 900,000 deaths a year, which is about 1/8 of all deaths caused by smoking.[57]
  • Skin conditions: A 2016 systematic review and meta-analysis found that passive smoking was associated with a higher rate of atopic dermatitis.[58]

Risk to children

[edit]
Old prevention poster from New Zealand. "When a child breathes air filled with cigarette smoke it can be as bad as if he actually smoked the cigarette himself."
  • Sudden infant death syndrome (SIDS).[59] In his 2006 report, the US Surgeon General concludes: "The evidence is sufficient to infer a causal relationship between exposure to secondhand smoke and sudden infant death syndrome."[60] Secondhand smoking has been estimated to be associated with 430 SIDS deaths in the United States annually.[61]
  • Asthma.[62][63][64] Secondhand smoke exposure is also associated with an almost doubled risk of hospitalization for asthma exacerbation among children with asthma.[65]
  • Lung infections,[66][67][68] also including more severe illness with bronchiolitis[69] and bronchitis,[70] and worse outcome,[69] as well as increased risk of developing tuberculosis if exposed to a carrier.[71] In the United States, it is estimated that secondhand smoke has been associated with between 150,000 and 300,000 lower respiratory tract infections in infants and children under 18 months of age, resulting in between 7,500 and 15,000 hospitalizations each year.[61]
  • Impaired respiratory function and slowed lung growth[70]
  • Allergies[72]
  • Maternal passive smoking increases the risk of non-syndromic orofacial clefts by 50% among their children.[73]
  • Learning difficulties, developmental delays, executive function problems,[74] and neurobehavioral effects.[75][76] Animal models suggest a role for nicotine and carbon monoxide in neurocognitive problems.[68]
  • Increased risk of middle ear infections.[68][77][78]
  • Invasive meningococcal disease.[24][79]
  • Anesthesia complications and some negative surgical outcomes.[80]
  • Sleep disordered breathing: Most studies have found a significant association between passive smoking and sleep disordered breathing in children, but further studies are needed to determine whether this association is causal.[81]
  • Adverse effects on the cardiovascular system of children.[82]

Evidence

[edit]
Exposure to secondhand smoke by age, race, and poverty level in the US in 2010

Epidemiological studies show that non-smokers exposed to secondhand smoke are at risk for many of the health problems associated with direct smoking.[citation needed]

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.[83] 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,[84] and two 1999 meta-analyses reached similar conclusions.[85][86]

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.[87][88][89][90] Some scientists believe that the risk of passive smoking, in particular the risk of developing coronary heart diseases, may have been substantially underestimated.[91]

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.[92] 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%.[93] This conclusion has been challenged on the basis that the assumption that 40% of all studies are unpublished was "extreme".[2]: 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.[94] 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.[95] 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.[96] A 2014 meta-analysis noted that "the association between exposure to secondhand smoke and lung cancer risk is well established."[97]

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.[98][99] 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.[98] 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.[100]

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:

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.[2]

Subsequent meta-analyses have confirmed these findings.[101][102]

The National Asthma Council of Australia cites studies showing that secondhand smoke is probably the most important indoor pollutant, especially around young children:[103]

  • 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[104] 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."[105]

There is good observational evidence that smoke-free legislation reduces the number of hospital admissions for heart disease.[106][107]

Exposure and risk levels

[edit]

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.[2] Those who work in environments where smoke is not regulated are at higher risk.[108][102] Workers particularly at risk of exposure include those in installation repair and maintenance, construction and extraction, and transportation.[109]

Much research has come from studies of nonsmokers who are married to a smoker. The 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%.[110]

Similarly, children who are exposed to environmental tobacco smoke are shown to experience a range of adverse effects[111][112][113] and a higher risk of becoming smokers later in life.[114] The WHO has identified reduction of exposure to environmental tobacco smoke as key element for actions to encourage healthy child development.[115]

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 surveys.[116] 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 and poor people were exposed in 2014.

Interventions to reduce environmental tobacco smoke

[edit]

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.[117]

Biomarkers

[edit]
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 monitored through breath, nicotine, cotinine, thiocyanates, and proteins are the most specific biological markers of tobacco smoke exposure.[118][119] 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.[120]

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.[121]

Cotinine

[edit]

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.[122] Urinary cotinine levels have been a reliable biomarker of tobacco exposure and have been used as a reference in many epidemiological studies.[117] 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.[118]

Carbon monoxide (CO)

[edit]

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).[123] Breath CO monitors can also be used by emergency services to identify patients who are suspected of having CO poisoning.

Pathophysiology

[edit]

A 2004 study by the International Agency for Research on Cancer of the World Health Organization concluded that non-smokers are exposed to the same carcinogens as active smokers. Sidestream smoke contains more than 4,000 chemicals, including 69 known carcinogens. Of special concern are polynuclear aromatic hydrocarbons, tobacco-specific N-nitrosamines, and aromatic amines, such as 4-aminobiphenyl, all known to be highly carcinogenic. Mainstream smoke, sidestream smoke, and secondhand smoke contain largely the same components, however the concentration varies depending on type of smoke.[2] Several well-established carcinogens have been shown by the tobacco companies' own research to be present at higher concentrations in sidestream smoke than in mainstream smoke.[124]

Secondhand smoke has been shown to produce more particulate-matter (PM) pollution than an idling low-emission diesel engine. In an experiment conducted by the Italian National Cancer Institute, three cigarettes were left smoldering, one after the other, in a 60 m3 garage with a limited air exchange. The cigarettes produced PM pollution exceeding outdoor limits, as well as PM concentrations up to 10-fold that of the idling engine.[125]

Secondhand tobacco smoke exposure has immediate and substantial effects on blood and blood vessels in a way that increases the risk of a heart attack, particularly in people already at risk.[126] Exposure to tobacco smoke for 30 minutes significantly reduces coronary flow velocity reserve in healthy nonsmokers.[127] Secondhand smoke is also associated with impaired vasodilation among adult nonsmokers.[128] Secondhand smoke exposure also affects platelet function, vascular endothelium, and myocardial exercise tolerance at levels commonly found in the workplace.[129]

Pulmonary emphysema can be induced in rats through acute exposure to sidestream tobacco smoke (30 cigarettes per day) over a period of 45 days.[130] Degranulation of mast cells contributing to lung damage has also been observed.[131]

The term "third-hand smoke" was recently coined to identify the residual tobacco smoke contamination that remains after the cigarette is extinguished and secondhand smoke has cleared from the air.[132][133][134] Preliminary research suggests that by-products of third-hand smoke may pose a health risk,[135] though the magnitude of risk, if any, remains unknown. In October 2011, it was reported that Christus St. Frances Cabrini Hospital in Alexandria, Louisiana, would seek to eliminate third-hand smoke beginning in July 2012, and that employees whose clothing smelled of smoke would not be allowed to work. This prohibition was enacted because third-hand smoke poses a special danger for the developing brains of infants and small children.[136]

In 2008, there were more than 161,000 deaths attributed to lung cancer in the United States. Of these deaths, an estimated 10% to 15% were caused by factors other than first-hand smoking; equivalent to 16,000 to 24,000 deaths annually. Slightly more than half of the lung cancer deaths caused by factors other than first-hand smoking were found in nonsmokers. Lung cancer in non-smokers may well be considered one of the most common cancer mortalities in the United States. Clinical epidemiology of lung cancer has linked the primary factors closely tied to lung cancer in non-smokers as exposure to secondhand tobacco smoke, carcinogens including radon, and other indoor air pollutants.[137]

Opinion of public health authorities

[edit]

There is widespread scientific consensus that exposure to secondhand smoke is harmful.[4] The link between passive smoking and health risks is accepted by every major medical and scientific organisation, including:

Public opinion

[edit]

Recent major surveys conducted by the U.S. National Cancer Institute and Centers for Disease Control have found widespread public awareness that secondhand smoke is harmful. In both 1992 and 2000 surveys, more than 80% of respondents agreed with the statement that secondhand smoke was harmful. A 2001 study found that 95% of adults agreed that secondhand smoke was harmful to children, and 96% considered tobacco-industry claims that secondhand smoke was not harmful to be untruthful.[149]

A 2007 Gallup poll found that 56% of respondents felt that secondhand smoke was "very harmful", a number that has held relatively steady since 1997. Another 29% believe that secondhand smoke is "somewhat harmful"; 10% answered "not too harmful", while 5% said "not at all harmful".[150]

Controversy over harm

[edit]

As part of its attempt to prevent or delay tighter regulation of smoking, the tobacco industry funded a number of scientific studies and, where the results cast doubt on the risks associated with secondhand smoke, sought wide publicity for those results. The industry also funded libertarian and conservative think tanks, such as the Cato Institute in the United States and the Institute of Public Affairs in Australia which criticised both scientific research on passive smoking and policy proposals to restrict smoking.[151][152] New Scientist and the European Journal of Public Health have identified these industry-wide coordinated activities as one of the earliest expressions of corporate denialism. Further, they state that the disinformation spread by the tobacco industry has created a tobacco denialism movement, sharing many characteristics of other forms of denialism, such as HIV-AIDS denialism.[153][154]

Industry-funded studies and critiques

[edit]

Enstrom and Kabat

[edit]

A 2003 study by James Enstrom and Geoffrey Kabat, published in the British Medical Journal, argued that the harms of passive smoking had been overstated.[155] Their analysis reported no statistically significant relationship between passive smoking and lung cancer, coronary heart disease (CHD), or chronic obstructive pulmonary disease, though the accompanying editorial noted that "they may overemphasise the negative nature of their findings."[156] This paper was widely promoted by the tobacco industry as evidence that the harms of passive smoking were unproven.[157][158] The American Cancer Society (ACS), whose database Enstrom and Kabat used to compile their data, criticized the paper as "neither reliable nor independent", stating that scientists at the ACS had repeatedly pointed out serious flaws in Enstrom and Kabat's methodology prior to publication.[159] Notably, the study had failed to identify a comparison group of "unexposed" persons.[160]

Enstrom's ties to the tobacco industry also drew scrutiny; in a 1997 letter to Philip Morris, Enstrom requested a "substantial research commitment... in order for me to effectively compete against the large mountain of epidemiologic data and opinions that already exist regarding the health effects of ETS and active smoking."[161] In a US racketeering lawsuit against tobacco companies, the Enstrom and Kabat paper was cited by the US District Court as "a prime example of how nine tobacco companies engaged in criminal racketeering and fraud to hide the dangers of tobacco smoke."[162] The Court found that the study had been funded and managed by the Center for Indoor Air Research,[163] a tobacco industry front group tasked with "offsetting" damaging studies on passive smoking, as well as by Philip Morris who stated that Enstrom's work was "clearly litigation-oriented".[164] A 2005 paper in Tobacco Control argued that the disclosure section in the Enstrom and Kabat BMJ paper, although it met the journal's requirements, "does not reveal the full extent of the relationship the authors had with the tobacco industry."[165]

In 2006, Enstrom and Kabat published a meta-analysis of studies regarding passive smoking and coronary heart disease in which they reported a very weak association between passive smoking and heart disease mortality.[166] They concluded that exposure to secondhand smoke increased the risk of death from CHD by only 5%, although this analysis has been criticized for including two previous industry-funded studies that suffered from widespread exposure misclassification.[6]

Gori

[edit]

Gio Batta Gori, a tobacco industry spokesman and consultant[167][168][169] and an expert on risk utility and scientific research, wrote in the libertarian Cato Institute's magazine Regulation that "...of the 75 published studies of ETS and lung cancer, some 70% did not report statistically significant differences of risk and are moot. Roughly 17% claim an increased risk and 13% imply a reduction of risk."[170]

Milloy

[edit]

Steven Milloy, the "junk science" commentator for Fox News and a former Philip Morris consultant,[171][172] claimed that "of the 19 studies" on passive smoking "only 8— slightly more than 42%— reported statistically significant increases in heart disease incidence."[173]

Another component of criticism cited by Milloy focused on relative risk and epidemiological practices in studies of passive smoking. Milloy, who has a master's degree from the Johns Hopkins School of Hygiene and Public Health, argued that studies yielding relative risks of less than 2 were meaningless junk science. This approach to epidemiological analysis was criticized in the American Journal of Public Health:

A major component of the industry attack was the mounting of a campaign to establish a "bar" for "sound science" that could not be fully met by most individual investigations, leaving studies that did not meet the criteria to be dismissed as "junk science."[174]

The tobacco industry and affiliated scientists also put forward a set of "Good Epidemiology Practices" which would have the practical effect of obscuring the link between secondhand smoke and lung cancer; the privately stated goal of these standards was to "impede adverse legislation".[175] However, this effort was largely abandoned when it became clear that no independent epidemiological organization would agree to the standards proposed by Philip Morris et al.[176]

Levois and Layard

[edit]

In 1995, Levois and Layard, both tobacco industry consultants, published two analyses in the journal Regulatory Toxicology and Pharmacology regarding the association between spousal exposure to secondhand smoke and heart disease. Both of these papers reported no association between secondhand smoke and heart disease.[177][178] These analyses have been criticized for failing to distinguish between current and former smokers, despite the fact that former smokers, unlike current ones, are not at a significantly increased risk of heart disease.[6][179]

World Health Organization controversy

[edit]

A 1998 study by the International Agency for Research on Cancer (IARC) on environmental tobacco smoke (ETS) found "weak evidence of a dose–response relationship between risk of lung cancer and exposure to spousal and workplace ETS."[180]

In March 1998, before the study was published, reports appeared in the media alleging that the IARC and the World Health Organization (WHO) were suppressing information. The reports, appearing in the British Sunday Telegraph[181] and The Economist,[182] among other sources,[183][184][185] alleged that the WHO withheld from publication of its own report that supposedly failed to prove an association between passive smoking and a number of other diseases (lung cancer in particular).

In response, the WHO issued a press release stating that the results of the study had been "completely misrepresented" in the popular press and were in fact very much in line with similar studies demonstrating the harms of passive smoking.[186] The study was published in the Journal of the National Cancer Institute in October of the same year, and concluded the authors found "no association between childhood exposure to ETS and lung cancer risk" but "did find weak evidence of a dose–response relationship between risk of lung cancer and exposure to spousal and workplace ETS."[180] An accompanying editorial summarized:

When all the evidence, including the important new data reported in this issue of the Journal, is assessed, the inescapable scientific conclusion is that ETS is a low-level lung carcinogen.[187]

With the release of formerly classified tobacco industry documents through the Tobacco Master Settlement Agreement, it was found (by Elisa Ong and Stanton Glantz) that the controversy over the WHO's alleged suppression of data had been engineered by Philip Morris, British American Tobacco, and other tobacco companies in an effort to discredit scientific findings which would harm their business interests.[188] A WHO inquiry, conducted after the release of the tobacco-industry documents, found that this controversy was generated by the tobacco industry as part of its larger campaign to cut the WHO's budget, distort the results of scientific studies on passive smoking, and discredit the WHO as an institution. This campaign was carried out using a network of ostensibly independent front organizations and international and scientific experts with hidden financial ties to the industry.[189]

EPA lawsuit

[edit]

In 1993, the United States Environmental Protection Agency (EPA) issued a report estimating that 3,000 lung cancer related deaths in the United States were caused by passive smoking annually.[190]

Philip Morris, R.J. Reynolds Tobacco Company, and groups representing growers, distributors and marketers of tobacco took legal action, claiming that the EPA had manipulated this study and ignored accepted scientific and statistical practices.

The United States District Court for the Middle District of North Carolina ruled in favor of the tobacco industry in 1998, finding that the EPA had failed to follow proper scientific and epidemiologic practices and had "cherry picked" evidence to support conclusions which they had committed to in advance.[191] The court stated in part, "EPA publicly committed to a conclusion before research had begun...adjusted established procedure and scientific norms to validate the Agency's public conclusion... In conducting the ETS Risk Assessment, disregarded information and made findings on selective information; did not disseminate significant epidemiologic information; deviated from its Risk Assessment Guidelines; failed to disclose important findings and reasoning..."

In 2002, the EPA successfully appealed this decision to the United States Court of Appeals for the Fourth Circuit. The EPA's appeal was upheld on the preliminary grounds that their report had no regulatory weight, and the earlier finding was vacated.[192]

In 1998, the U.S. Department of Health and Human Services, through the publication by its National Toxicology Program of the 9th Report on Carcinogens, listed environmental tobacco smoke among the known carcinogens, observing of the EPA assessment that "The individual studies were carefully summarized and evaluated."[193]

Tobacco-industry funding of research

[edit]

The tobacco industry's role in funding scientific research on secondhand smoke has been controversial.[194] A review of published studies found that tobacco-industry affiliation was strongly correlated with findings exonerating secondhand smoke; researchers affiliated with the tobacco industry were 88 times more likely than independent researchers to conclude that secondhand smoke was not harmful.[195] In a specific example which came to light with the release of tobacco-industry documents, Philip Morris executives successfully encouraged an author to revise his industry-funded review article to downplay the role of secondhand smoke in sudden infant death syndrome.[196] The 2006 U.S. Surgeon General's report criticized the tobacco industry's role in the scientific debate:

The industry has funded or carried out research that has been judged to be biased, supported scientists to generate letters to editors that criticized research publications, attempted to undermine the findings of key studies, assisted in establishing a scientific society with a journal, and attempted to sustain controversy even as the scientific community reached consensus.[197]

This strategy was outlined at an international meeting of tobacco companies in 1988, at which Philip Morris proposed to set up a team of scientists, organized by company lawyers, to "carry out work on ETS to keep the controversy alive."[198] All scientific research was subject to oversight and "filtering" by tobacco-industry lawyers:

Philip Morris then expect the group of scientists to operate within the confines of decisions taken by PM scientists to determine the general direction of research, which apparently would then be 'filtered' by lawyers to eliminate areas of sensitivity.[198]

Philip Morris reported that it was putting "...vast amounts of funding into these projects... in attempting to coordinate and pay so many scientists on an international basis to keep the ETS controversy alive."[198]

Tobacco industry response

[edit]

Measures to tackle secondhand smoke pose a serious economic threat to the tobacco industry, having broadened the definition of smoking beyond a personal habit to something with a social impact. In a confidential 1978 report, the tobacco industry described increasing public concerns about secondhand smoke as "the most dangerous development to the viability of the tobacco industry that has yet occurred."[199] In United States of America v. Philip Morris et al., the District Court for the District of Columbia found that the tobacco industry "... recognized from the mid-1970s forward that the health effects of passive smoking posed a profound threat to industry viability and cigarette profits," and that the industry responded with "efforts to undermine and discredit the scientific consensus that ETS causes disease."[4]

Accordingly, the tobacco industry have developed several strategies to minimise the impact on their business:

  • The industry has sought to position the secondhand smoke debate as essentially concerned with civil liberties and smokers' rights rather than with health, by funding groups such as FOREST.[200]
  • Funding bias in research;[8] in all reviews of the effects of secondhand smoke on health published between 1980 and 1995, the only factor associated with concluding that secondhand smoke is not harmful was whether an author was affiliated with the tobacco industry.[195] However, not all studies that failed to find evidence of harm were by industry-affiliated authors.
  • Delaying and discrediting legitimate research (see[8] for an example of how the industry attempted to discredit Takeshi Hirayama's landmark study, and[201] for an example of how it attempted to delay and discredit a major Australian report on passive smoking)
  • Promoting "good epidemiology" and attacking so-called junk science (a term popularised by industry lobbyist Steven Milloy): attacking the methodology behind research showing health risks as flawed and attempting to promote sound science. Ong & Glantz (2001) cite an internal Phillip Morris memo giving evidence of this as company policy.[176]
  • Creation of outlets for favourable research. In 1989, the tobacco industry established the International Society of the Built Environment, which published the peer-reviewed journal Indoor and Built Environment. This journal did not require conflict-of-interest disclosures from its authors. With documents made available through the Master Settlement, it was found that the executive board of the society and the editorial board of the journal were dominated by paid tobacco-industry consultants. The journal published a large amount of material on passive smoking, much of which was "industry-positive".[202]

Citing the tobacco industry's production of biased research and efforts to undermine scientific findings, the 2006 U.S. Surgeon General's report concluded that the industry had "attempted to sustain controversy even as the scientific community reached consensus... industry documents indicate that the tobacco industry has engaged in widespread activities... that have gone beyond the bounds of accepted scientific practice."[203] The U.S. District Court, in U.S.A. v. Philip Morris et al., found that "...despite their internal acknowledgment of the hazards of secondhand smoke, Defendants have fraudulently denied that ETS causes disease."[204]

Position of major tobacco companies

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The positions of major tobacco companies on the issue of secondhand smoke is somewhat varied. In general, tobacco companies have continued to focus on questioning the methodology of studies showing that secondhand smoke is harmful. Some (such as British American Tobacco and Philip Morris) acknowledge the medical consensus that secondhand smoke carries health risks, while others continue to assert that the evidence is inconclusive. Several tobacco companies advocate the creation of smoke-free areas within public buildings as an alternative to comprehensive smoke-free laws.[205]

US racketeering lawsuit against tobacco companies

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On September 22, 1999, the U.S. Department of Justice filed a racketeering lawsuit against Philip Morris and other major cigarette manufacturers.[206] Almost 7 years later, on August 17, 2006, U.S. District Court Judge Gladys Kessler found that the Government had proven its case and that the tobacco company defendants had violated the Racketeer Influenced Corrupt Organizations Act (RICO).[4] In particular, Judge Kessler found that PM and other tobacco companies had:

  • conspired to minimize, distort and confuse the public about the health hazards of smoking;
  • publicly denied, while internally acknowledging, that secondhand tobacco smoke is harmful to nonsmokers, and
  • destroyed documents relevant to litigation.

The ruling found that tobacco companies undertook joint efforts to undermine and discredit the scientific consensus that secondhand smoke causes disease, notably by controlling research findings via paid consultants. The ruling also concluded that tobacco companies were fraudulently continuing to deny the health effects of ETS exposure.[4]

On May 22, 2009, a three-judge panel of the U.S. Court of Appeals for the District of Columbia Circuit unanimously upheld the lower court's 2006 ruling.[207][208][209]

Smoke-free laws

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See also: Smoking ban, List of smoking bans, and Smoking bans in private vehicles

As a consequence of the health risks associated with secondhand smoke, many national and local governments have outlawed smoking in indoor public places, including restaurants, cafés, and nightclubs, as well as some outdoor open areas.[210] Ireland was the first country in the world to institute a comprehensive national ban on smoking in all indoor workplaces on 29 March 2004. Since then, many others have followed suit. The countries which have ratified the WHO Framework Convention on Tobacco Control (FCTC) have a legal obligation to implement effective legislation "for protection from exposure to tobacco smoke in indoor workplaces, public transport, indoor public places and, as appropriate, other public places." (Article 8 of the FCTC[211]) The parties to the FCTC have further adopted Guidelines on the Protection from Exposure to secondhand Smoke which state that "effective measures to provide protection from exposure to tobacco smoke ... require the total elimination of smoking and tobacco smoke in a particular space or environment in order to create a 100% smoke-free environment."[212]

Opinion polls have shown considerable support for smoke-free laws. In June 2007, a survey of 15 countries found 80% approval for such laws.[213] A survey in France, reputedly a nation of smokers, showed 70% support.[105]

Effects

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Smoking bans by governments result in decreased harm from secondhand smoke, including less admissions for acute coronary syndrome.[214] In the first 18 months after the town of Pueblo, Colorado, enacted a smoke-free law in 2003, hospital admissions for heart attacks dropped 27%. Admissions in neighbouring towns without smoke-free laws showed no change, and the decline in heart attacks in Pueblo was attributed to the resulting reduction in secondhand smoke exposure.[215] A 2004 smoking ban instituted in Massachusetts workplaces decreased workers' secondhand smoke exposure from 8% of workers in 2003 to 5.4% of workers in 2010.[109] A 2016 review also found that bans and policy changes in specific locations such as hospitals or universities can lead to reduced smoking rates. In prison settings bans might lead to reduced mortality and to lower exposure to secondhand smoke.[216]

In 2001, a systematic review for the Guide to Community Preventive Services acknowledged strong evidence of the effectiveness of smoke-free policies and restrictions in reducing expose to secondhand smoke. A follow-up to this review, identified the evidence on which the effectiveness of smoking bans reduced the prevalence of tobacco use. Articles published until 2005, were examined to further support this evidence. The examined studies provided sufficient evidence that smoke-free policies reduce tobacco use among workers when implemented in worksites or by communities.[217]

While a number of studies funded by the tobacco industry have claimed a negative economic impact from smoke-free laws, no independently funded research has shown any such impact. A 2003 review reported that independently funded, methodologically sound research consistently found either no economic impact or a positive impact from smoke-free laws.[218]

Air nicotine levels were measured in Guatemalan bars and restaurants before and after an implemented smoke-free law in 2009. Nicotine concentrations significantly decreased in both the bars and restaurants measured. Also, the employees' support for a smoke-free workplace substantially increased in the post-implementation survey compared to pre-implementation survey.[219]

Public opinion

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Recent surveys taken by the Society for Research on Nicotine and Tobacco demonstrate supportive attitudes of the public towards smoke-free policies in outdoor areas. A vast majority of the public supports restricting smoking in various outdoor settings. The respondents' support for the policies were for varying reasons such as litter control, establishing positive smoke-free role models for youth, reducing youth opportunities to smoke, and avoiding exposure to secondhand smoke.[220]

Alternative forms

[edit]

Alternatives to smoke-free laws have also been proposed as a means of harm reduction, particularly in bars and restaurants. For example, critics of smoke-free laws cite studies suggesting ventilation as a means of reducing tobacco smoke pollutants and improving air quality.[221] Ventilation has also been heavily promoted by the tobacco industry as an alternative to outright bans, via a network of ostensibly independent experts with often undisclosed ties to the industry.[222] However, not all critics have connections to the industry.

The American Society of Heating, Refrigerating and Air-Conditioning Engineers (ASHRAE) officially concluded in 2005 that while completely isolated smoking rooms do eliminate the risk to nearby non-smoking areas, smoking bans are the only means of eliminating health risks associated with indoor exposure. They further concluded that no system of dilution or cleaning was effective at eliminating risk.[223] The U.S. Surgeon General and the European Commission Joint Research Centre have reached similar conclusions.[203][224] The implementation guidelines for the WHO Framework Convention on Tobacco Control states that engineering approaches, such as ventilation, are ineffective and do not protect against secondhand smoke exposure.[212] However, this does not necessarily mean that such measures are useless in reducing harm, only that they fall short of the goal of reducing exposure completely to zero.

Others have suggested a system of tradable smoking pollution permits, similar to the cap-and-trade pollution permits systems used by the United States Environmental Protection Agency in recent decades to curb other types of pollution.[225] This would guarantee that a portion of bars/restaurants in a jurisdiction will be smoke-free, while leaving the decision to the market.

In animals

[edit]
Main article: Animals and tobacco smoke

Multiple studies have been conducted to determine the carcinogenicity of environmental tobacco smoke to animals. These studies typically fall under the categories of simulated environmental tobacco smoke, administering condensates of sidestream smoke, or observational studies of cancer among pets.

To simulate environmental tobacco smoke, scientists expose animals to sidestream smoke, that which emanates from the cigarette's burning cone and through its paper, or a combination of mainstream and sidestream smoke.[2] The IARC monographs conclude that mice with prolonged exposure to simulated environmental tobacco smoke, that is six hours a day, five days a week, for five months with a subsequent four-month interval before dissection, will have significantly higher incidence and multiplicity of lung tumors than with control groups.

The IARC monographs concluded that sidestream smoke condensates had a significantly higher carcinogenic effect on mice than did mainstream smoke condensates.[2]

Observational studies

[edit]

Secondhand smoke is popularly recognised as a risk factor for cancer in pets.[226] A study conducted by the Tufts University School of Veterinary Medicine and the University of Massachusetts Amherst linked the occurrence of feline oral cancer to exposure to environmental tobacco smoke through an overexpression of the p53 gene.[227] Another study conducted at the same universities concluded that cats living with a smoker were more likely to get feline lymphoma; the risk increased with the duration of exposure to secondhand smoke and the number of smokers in the household.[228] A study by Colorado State University researchers, looking at cases of canine lung cancer, was generally inconclusive, though the authors reported a weak relation for lung cancer in dogs exposed to environmental tobacco smoke. The number of smokers within the home, the number of packs smoked in the home per day, and the amount of time that the dog spent within the home had no effect on the dog's risk for lung cancer.[229]

See also

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References

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[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Passive smoking

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from Grokipedia
Passive smoking, also known as (SHS) exposure, refers to the involuntary inhalation by non-smokers of tobacco smoke generated from the combustion of products by others, encompassing sidestream smoke rising from the lit end of a and mainstream smoke exhaled by active smokers. This exposure primarily occurs in enclosed spaces like households and workplaces, where concentrations of over 70 known carcinogens and thousands of chemicals—many identical to those in inhaled smoke by smokers—can accumulate, albeit diluted compared to active smoking doses. Empirical studies, predominantly observational, have reported associations between SHS and adverse outcomes, including a of among never-smokers exposed to spousal smoking of approximately 1.27 (95% CI 1.17-1.37), though North American cohorts show lower estimates around 1.15, reflecting small absolute increments given the low baseline incidence in non-smokers. Similarly, meta-analyses indicate about a 23% increased risk of from SHS exposure. These findings underpin measures like indoor smoking bans, yet controversies persist due to methodological challenges: small effect sizes susceptible to by unmeasured factors, recall and misclassification biases inflating apparent risks, and publication delays for null results, compounded by historical funding of dissenting reviews (74% of those denying harm). Conservative Bayesian analyses suggest even lower attributable risks, such as 1% for , highlighting the need for causal scrutiny beyond correlative amid potential institutional incentives to emphasize harms.

Definitions and Terminology

Core Definitions

Passive smoking refers to the involuntary of tobacco smoke by non-smokers exposed to the ambient mixture of smoke generated by nearby smoking activity. This exposure arises from two primary sources: mainstream smoke, which is the smoke exhaled by active smokers, and sidestream smoke, which emanates from the burning end of a lit product such as a , , or pipe. The term is synonymous with exposure or environmental tobacco smoke (ETS), denoting the of these airborne particulates and gases in enclosed or semi-enclosed spaces where occurs, without the exposed individual directly engaging in the act of . Unlike active , which involves deliberate puffing and through a tobacco device, passive smoking occurs passively through in the surrounding air, potentially affecting bystanders including children, spouses, and coworkers.

Historical and Alternative Terms

The term passive smoking denotes the non-voluntary inhalation of tobacco smoke by individuals not actively and entered the English with its first recorded use in 1971. Tobacco industry documents indicate internal references to "passive smoke exposure" as early as 1962, reflecting awareness of the phenomenon prior to widespread public discourse. Synonymous alternatives include , with attestations in print dating to 1891, though its application to tobacco specifically gained prominence in the mid-20th century amid growing concerns. Environmental tobacco smoke (ETS) emerged in during the 1970s to describe the dispersion of sidestream and exhaled mainstream smoke into ambient air, often framing exposure as a form of indoor . Involuntary smoking underscores the lack of consent in exposure and appears interchangeably in epidemiological reviews. These terms—passive smoking, , ETS, and involuntary smoking—refer to the same exposure mechanism, as affirmed by authorities, though ETS has been critiqued for potentially diluting perceptions of direct harm by invoking broader environmental framing. Usage varies by context: "secondhand smoke" predominates in U.S. regulatory and media discussions since the 1980s, while "passive smoking" remains common in European and earlier studies.

Composition of Environmental Tobacco Smoke

Mainstream versus Sidestream Smoke

Mainstream smoke refers to the drawn through the by the smoker during , passing through the column and any filter present. Sidestream smoke, in contrast, consists of the emissions released directly from the burning tip of the into the surrounding air between puffs. Environmental tobacco smoke, to which passive smokers are exposed, comprises approximately 85% sidestream smoke and 15% exhaled mainstream smoke, with sidestream smoke undergoing less dilution in indoor settings. The production conditions differ markedly: mainstream smoke forms under high-temperature puffing (typically 800–900°C in the tobacco zone), promoting more complete combustion, whereas sidestream smoke arises from smoldering at lower temperatures (400–700°C), resulting in incomplete combustion and distinct chemical profiles. Undiluted sidestream smoke exhibits elevated concentrations of several toxicants compared to mainstream smoke, including , volatile amines, volatile nitrosamines, nicotine degradation products, and . Yield comparisons from machine-smoked cigarettes demonstrate higher outputs in sidestream smoke for key components. A study of 15 brands found average sidestream-to-mainstream ratios of 3.5 for , 6.6 for , and 6.8 for , with sidestream yields exceeding mainstream for all tested products.
ComponentAverage Sidestream-to-Mainstream Ratio
Tar3.5
Nicotine6.6
Carbon Monoxide6.8
Sidestream smoke particles are generally smaller (mean diameter around 0.3–0.5 μm versus 0.5–1.0 μm for mainstream), enhancing their respirability and potential for deeper penetration. assessments indicate sidestream smoke is more cytotoxic per gram than mainstream smoke, with whole sidestream smoke showing greater than the additive effects of its isolated constituents in bioassays. These differences arise from the lower-temperature chemistry, yielding higher proportions of certain polycyclic aromatic hydrocarbons and other irritants, though direct equivalence in human exposure risks requires accounting for dilution in environmental contexts.

Key Chemical Components

Environmental tobacco smoke (ETS), the primary form of exposure in passive smoking, consists predominantly of sidestream smoke (approximately 85%) emitted from the burning tip of a , with the remainder being mainstream smoke exhaled by the smoker. This mixture contains over 7,000 distinct chemical compounds, many of which are generated or concentrated differently in sidestream versus mainstream smoke due to lower temperatures in the former (around 600°C compared to 900°C in the filter). Sidestream smoke yields higher concentrations of many toxins per unit mass, including up to four times more particulate matter and elevated levels of , , and compared to mainstream smoke. Key gaseous components include carbon monoxide (CO), a colorless, odorless gas that binds to hemoglobin more readily than oxygen, reducing blood oxygen-carrying capacity; hydrogen cyanide (HCN), a respiratory irritant; nitrogen oxides (NOx); and ammonia, which enhances nicotine absorption. Volatile organic compounds (VOCs) such as benzene (a known leukemogen), toluene, and 1,3-butadiene predominate in the vapor phase, with sidestream smoke producing 2–10 times higher yields of benzene and butadiene than mainstream smoke under standard smoking conditions. Carbonyl compounds like formaldehyde (a potent irritant and carcinogen) and acetaldehyde are also more abundant in sidestream smoke, contributing to mucous membrane irritation and potential DNA damage. The particulate phase, often termed "tar," encapsulates semi-volatile and solid compounds adsorbed onto fine particles (primarily PM2.5 size fraction), including polycyclic aromatic hydrocarbons (PAHs) such as benzopyrene, tobacco-specific nitrosamines (TSNAs) like 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), and heavy metals including arsenic, cadmium, chromium, nickel, and polonium-210 (a radioactive alpha-emitter). At least 69–70 of the chemicals in ETS are classified as carcinogenic by agencies like the International Agency for Research on Cancer, with sidestream smoke exhibiting 2–6 times greater tumorigenic potential per gram of condensate than mainstream smoke in bioassays. These components persist in indoor air for hours, facilitating involuntary exposure.
Chemical ClassExamplesNotes on ETS Relevance
GasesCarbon monoxide, hydrogen cyanide, nitrogen oxidesHigh yields in sidestream; CO levels up to 3x mainstream.
VOCsBenzene, 1,3-butadiene, tolueneElevated in sidestream; benzene is a Group 1 carcinogen.
CarbonylsFormaldehyde, acetaldehyde, acroleinIrritants; formaldehyde 3–10x higher in sidestream.
PAHs & TSNAsBenzopyrene, NNKParticulate-bound; potent carcinogens unique to tobacco.
Metals & RadionuclidesArsenic, cadmium, polonium-210Trace but bioavailable; contribute to chronic toxicity.

Exposure Measurement and Levels

Biomarkers of Exposure

, the primary metabolite of , serves as the most reliable and specific for exposure to environmental tobacco smoke (ETS), with a half-life of approximately 15-20 hours allowing detection of recent exposure. Measured in serum, , , or , cotinine levels in non-smokers exposed to (SHS) typically range from 0.1 to 10 ng/mL in serum, far below the >10-50 ng/mL seen in active smokers, enabling differentiation of passive from active exposure. cotinine, often normalized to , offers higher sensitivity for low-level SHS exposure due to concentrations 4-6 times those in blood or , with cutoffs such as <1 ng/mg indicating minimal or no exposure. Carboxyhemoglobin (COHb), formed by carbon monoxide binding to hemoglobin, provides a biomarker for acute ETS exposure, reflecting inhalation within hours due to its shorter half-life of 2-4 hours in room air. In non-smokers, background COHb levels are <1-2%, rising to 2-3% with significant SHS exposure, as observed in children of smoking parents where mean levels exceeded those in unexposed controls by 0.5-1%. Breath carbon monoxide (CO) measurement correlates with COHb and offers a non-invasive alternative, though influenced by ambient CO sources beyond tobacco. Other biomarkers include thiocyanate from hydrogen cyanide, less specific due to dietary sources, and tobacco-specific nitrosamine metabolites like NNAL, which indicate longer-term exposure but are more relevant to potential biological effects than pure exposure quantification. Validation studies confirm cotinine's superiority for ETS due to its tobacco specificity, while combining multiple markers enhances accuracy in assessing exposure dose and recency. Limitations include individual variability in metabolism and potential confounding from nicotine replacement therapies or e-cigarettes, necessitating context-specific interpretation.
BiomarkerBiological MatrixTypical SHS Levels in Non-SmokersHalf-LifeSpecificity
CotinineUrine (ng/mg creatinine)0.1-515-20 hoursHigh (tobacco-specific)
CotinineSerum (ng/mL)0.1-1015-20 hoursHigh
COHbBlood (%)1-32-4 hoursModerate (CO sources)
Breath COExhaled air (ppm)2-6~4 hoursModerate

Environmental and Questionnaire-Based Assessment

Environmental assessment of passive smoking, also known as secondhand smoke (SHS) exposure, involves direct measurement of tobacco smoke constituents in ambient air within microenvironments such as homes, workplaces, or public venues. Common markers include vapor-phase nicotine, captured using passive diffusion monitors that adsorb nicotine onto a filter over periods ranging from hours to weeks, providing integrated exposure estimates. Respirable particulate matter (PM), particularly PM2.5, serves as another key indicator, measured via real-time optical monitors or gravimetric samplers, with SHS contributing elevated levels above 10 μg/m³ in smoking-permitted areas. These methods quantify airborne concentrations but may not reflect individual inhalation due to variations in ventilation, occupant movement, and proximity to sources. Questionnaire-based assessment relies on self-reported data to estimate SHS exposure, typically querying frequency, duration, and intensity in settings like homes (e.g., cohabitation with smokers), workplaces, or public spaces. Instruments often include validated scales, such as those assessing hours per day or days per week exposed, with studies showing moderate correlations (Spearman r ≈ 0.4–0.6) to biomarkers like urinary cotinine when validated against objective measures. However, reliability is limited by recall bias, social desirability (underreporting due to stigma), and misclassification, evidenced by low sensitivity (around 50%) in detecting biomarker-verified exposure despite high specificity (>90%). Combining approaches enhances accuracy; for instance, environmental PM2.5 data from hospitality venues has corroborated reports of reduced exposure post-smoke-free laws, with pre-ban levels exceeding 20 μg/m³ dropping to near-background. Yet, questionnaires alone overestimate or underestimate true exposure in low-income or children’s cohorts, where objective validation reveals discrepancies up to 30% due to unmeasured home ventilation or unreported sources. Overall, while cost-effective for large-scale , self-reports require or environmental corroboration for precision, particularly in contexts.

Epidemiological Evidence on Health Risks

Associations with Respiratory Diseases

Numerous epidemiological studies, primarily observational cohort and case-control designs, have identified associations between secondhand smoke (SHS) exposure and increased incidence or exacerbation of respiratory diseases. In children, prenatal and postnatal SHS exposure shows a positive association with childhood development, with meta-analyses of cohort studies reporting pooled odds ratios (OR) of approximately 1.3 (95% CI: 1.2-1.4) for postnatal exposure and higher risks (OR up to 1.5) when combined with prenatal factors. Postnatal SHS exposure in infants is linked to elevated risks of lower infections (LRTI), including and , with relative risks ranging from 1.6 to 2.5 in systematic reviews of prospective studies, particularly in households with maternal smoking. SHS also correlates with asthma morbidity in children, including more frequent symptoms, emergency visits, and hospitalizations; a review of intervention and observational data attributes this to irritant effects on airways, with exposed asthmatic children experiencing 20-30% higher rates compared to unexposed peers. These associations are stronger in younger children under 5 years, where SHS exposure at home or via parental smoking doubles the odds of wheezing and respiratory symptoms in some population-based surveys. In adults, lifelong or workplace SHS exposure is associated with new-onset and , with cohort studies reporting hazard ratios of 1.2-1.4 for respiratory symptoms and asthma incidence after adjusting for active and confounders. For (COPD), meta-analyses of case-control and cohort data indicate an overall of 1.18 (95% CI: 1.09-1.28) for SHS-exposed never-smokers, with risks escalating to 1.3-1.5 for exposures exceeding 20 years or in spousal smoking scenarios. A 2024 systematic evaluation across global datasets confirmed these links for , LRTI, and COPD, estimating SHS-attributable fractions of 5-10% in never-smoker COPD cases in high-exposure regions.
Respiratory ConditionPopulationKey Association MetricSource
Childhood AsthmaChildren <18OR 1.3 (95% CI: 1.2-1.4) postnatal SHS
LRTI/BronchiolitisInfants <1RR 1.6-2.5 maternal smoking
Adult Asthma/Chronic BronchitisAdults never-smokersHR 1.2-1.4 workplace/home exposure
COPDAdults never-smokersRR 1.18 (95% CI: 1.09-1.28) overall

Cancer Risk Claims

Epidemiological studies have reported associations between exposure to secondhand smoke (SHS) and increased relative risk of lung cancer among never-smokers, with meta-analyses estimating odds ratios typically ranging from 1.2 to 1.4. For instance, the U.S. Centers for Disease Control and Prevention (CDC) asserts that non-smoking adults exposed to SHS face a 20-30% higher risk of lung cancer compared to unexposed non-smokers. A 2024 meta-analysis of U.S. nonsmokers found effect sizes between 1.05 and 3.11 for SHS exposure and lung cancer, with spousal exposure linked to a 41% relative risk increase. These associations are often stronger in populations with prolonged domestic exposure, such as never-smokers living with smoking spouses. However, the absolute risk increment remains small due to the low baseline incidence of lung cancer in never-smokers, estimated at approximately 0.5-1% lifetime risk in unexposed populations, translating to an attributable absolute increase of roughly 0.1-0.3% from typical SHS exposure levels. Claims of causation rely heavily on relative risks from case-control and cohort studies, but these are susceptible to residual confounding from factors like dietary habits, occupational exposures, and genetic predispositions not fully adjusted for in many analyses. A prospective cohort study of over 35,000 never-smokers from the California Cancer Prevention Study, tracking spousal smoking from 1960-1998, found no statistically significant elevation in lung cancer mortality (relative risk 0.94, 95% CI 0.85-1.04) after extensive adjustment, challenging the magnitude of risk asserted in public health summaries. Other cancer sites, such as oral cancer, have been linked to SHS in some reviews, with a 2022 meta-analysis supporting a causal association based on pooled data from never-smokers. Yet, evidence for non-lung cancers is sparser and often derived from smaller datasets, with relative risks similarly modest and lacking robust dose-response gradients. Recent analyses, including a 2024 American Cancer Society report, indicate negligible population-level impacts from SHS-attributable lung cancers in low-exposure settings, underscoring that while relative associations persist in aggregated data, individual-level causality remains debated due to exposure misclassification—wherein subtle active smoking or other unmeasured tobacco contacts may inflate apparent SHS effects. Overall, the epidemiological claims hinge on small risk elevations amid high-variance estimates, prompting scrutiny of whether observed patterns reflect true causation or artifacts of study design limitations.

Cardiovascular and Other Effects

Numerous epidemiological studies have reported associations between exposure to environmental tobacco smoke (ETS) and increased risk of coronary heart disease (CHD) among never-smokers. A 2005 review in Circulation synthesized evidence from multiple cohorts, estimating a 25-30% relative risk increase for CHD, potentially attributable to approximately 35,000 annual deaths in the United States. Similarly, a 1999 prospective study of over 65,000 California adults found a 22% higher CHD mortality rate (rate ratio 1.22, 95% CI 1.07-1.40) among never-smoking men exposed to spousal smoking after adjustment for confounders like age, diet, and physical activity. Meta-analyses of case-control studies have reported adjusted relative risks of 1.28 (95% CI 1.09-1.51) for overall cardiovascular disease (CVD) incidence linked to passive smoking. Stroke risk shows comparable patterns, with meta-analyses indicating 20-30% elevated odds in exposed never-smokers. A 2024 burden-of-proof analysis in Nature Medicine conservatively estimated at least an 8% increase in ischemic heart disease risk and 5% for stroke from secondhand smoke (SHS), based on re-evaluated global data while accounting for biases in reporting. These associations persist across diverse populations, including a Peruvian cross-sectional study linking SHS to higher hypertension prevalence and Framingham risk scores for CVD. However, some cohort data, such as a California Mormon study, found no significant ETS link to CHD mortality after extensive controls, highlighting potential variability due to exposure misclassification or residual confounding. Other reported effects include endothelial dysfunction and reduced myocardial oxygen utilization, observed in controlled human exposures simulating passive smoking levels. SHS has also been associated with modestly elevated type 2 diabetes risk (at least 1% per standardized exposure unit) in recent syntheses, though evidence is sparser than for vascular outcomes. Absolute risks remain low given typical exposure doses, which are orders of magnitude below active smoking, raising questions about proportionality in risk attribution despite consistent relative risk elevations across studies.

Specific Risks to Children and Vulnerable Groups

![Exposure to secondhand smoke by age, race, and poverty level US][float-right]
Children, particularly infants, face elevated risks from secondhand smoke (SHS) exposure, including sudden infant death syndrome (SIDS) and respiratory infections. Maternal smoking during pregnancy doubles the risk of SIDS, with evidence suggesting a causal link due to nicotine's effects on arousal pathways and carbon monoxide's hypoxia induction. Postnatal SHS exposure further increases SIDS incidence, as confirmed in cohort studies showing higher nicotine levels in SIDS victims' lungs compared to controls. A meta-analysis of lower respiratory tract infections in children under 18 months found SHS associated with approximately doubled odds (OR ≈ 2.0), attributing 150,000–300,000 annual cases in the US to passive exposure. SHS exacerbates asthma morbidity in children, with systematic reviews indicating increased severity, emergency visits, and hospitalizations among exposed asthmatics versus unexposed controls. Meta-analyses link postnatal SHS to higher odds of pneumonia incidence in young children (pooled OR >1.5), though study varies. Emerging associates SHS with neurodevelopmental issues, such as a 60% increased ADHD (OR 1.6), but remains inconclusive due to potential confounders like . Among other vulnerable groups, the elderly experience amplified cardiovascular risks from SHS, with exposure raising coronary heart disease odds by 25–30%, equivalent to 35,000 annual deaths. This effect stems from and platelet activation, more pronounced in those with preexisting conditions. SHS also correlates with (OR ≈1.2–1.5) and risk elevation (≈5–8%), particularly in older adults without direct smoking history. Individuals with or compromised immunity show heightened respiratory vulnerability, though quantitative risks mirror pediatric patterns adjusted for baseline .

Critiques and Limitations of Epidemiological Data

Confounding Factors and Study Biases

Confounding factors pose significant challenges in epidemiological research on passive smoking, as variables associated with both environmental tobacco smoke (ETS) exposure and health outcomes can distort apparent causal links. Common confounders include (often proxied by education or income), which correlates with higher smoking prevalence in households and independently elevates risks for respiratory diseases, cancer, and cardiovascular conditions through mechanisms like poorer and limited healthcare access. Dietary factors, such as lower intake of fruits, , and antioxidants, cluster in smoking environments and provide protective effects against and , potentially inflating ETS associations if not fully adjusted. Other lifestyle elements, including alcohol consumption, physical inactivity, and , further confound results, as they covary with spousal or household smoking and influence disease . Occupational exposures to dust, fumes, or carcinogens also overlap with ETS in lower-status jobs, complicating isolation of effects. Residual confounding persists despite statistical controls, given measurement imprecision in these variables and the small relative risks (typically 1.1–1.4) reported for outcomes like or heart disease, which fall within the range of plausible . Unknown or unmeasured confounders, such as genetic predispositions or concurrent environmental pollutants, may explain observed associations, particularly in observational designs lacking . For instance, in spousal exposure studies, the smoking partner's overall health behaviors—not ETS itself—may drive outcomes, as smokers often share diets and habits with nonsmoking spouses. Analyses adjusting for multiple such factors, including age, race/ethnicity, education, BMI, exercise, alcohol, and supplementation, have nullified ETS-mortality links in large cohorts. Study biases exacerbate these issues, with exposure assessment via retrospective questionnaires introducing recall inaccuracies; cases may overreport ETS contact due to knowledge of disease-smoking links, while controls underreport, yielding upward bias in case-control designs. Misclassification of active smoking status is prevalent, with 5–20% of self-reported "never smokers" proven as current or occult smokers via biomarkers like cotinine, artifactually elevating disease rates in the ETS-exposed nonsmoker category and mimicking causal effects. Non-differential exposure misclassification usually attenuates true associations toward the null, but combined with smoker misclassification, it can produce spurious positive findings comparable to reported ETS risks. Publication bias systematically overstates effects, as meta-analyses disproportionately include positive studies; nonsignificant passive smoking results face longer delays to publication or outright suppression, skewing pooled estimates upward. For lung cancer-ETS meta-analyses, adjustments for this bias via methods like trim-and-fill reduce risk ratios to near unity. Critiques of influential reports, such as the U.S. EPA assessment deeming ETS a known , highlight selective inclusion of supportive data, dismissal of null studies, and insufficient scrutiny, potentially driven by agendas over rigorous . These methodological limitations, compounded by institutional pressures favoring alarmist interpretations, have historically amplified perceived ETS hazards beyond empirical support.

Null or Minimal Risk Findings

A of 118,094 adults enrolled in 1959, all initially nonsmokers, tracked mortality through 1998 and assessed environmental tobacco smoke (ETS) exposure via spousal habits. Among never smokers married to smokers compared to those married to never smokers, the adjusted (RR) for was 0.75 (95% CI: 0.42-1.35), for coronary heart disease 0.93 (95% CI: 0.79-1.09), and for overall tobacco-related mortality 0.94 (95% CI: 0.85-1.05), indicating no statistically significant elevation in risk. The authors concluded that these results do not support a causal relationship between ETS exposure and tobacco-related mortality, though a small effect could not be ruled out due to potential residual or exposure misclassification. Statistical reanalyses of early ETS-lung cancer meta-analyses have also yielded null findings when accounting for methodological issues such as and heterogeneity. In a critique, biostatisticians applied random-effects models to data from nine case-control studies, finding a summary of 1.01 (95% CI: 0.87-1.18) for spousal ETS exposure and among nonsmokers, which was not significantly elevated and argued against a meaningful association after correcting for overestimation in fixed-effect models. This analysis highlighted that small reported risks (often around 1.2-1.3 in prior metas) likely reflected Type I errors or biases rather than true effects, as individual studies frequently showed risks indistinguishable from unity. Several individual epidemiological investigations have reported relative risks below 1.1 or non-significant for ETS and key outcomes. For instance, a review of 17 studies on household ETS exposure found multiple cohorts with odds ratios or RRs ranging from 0.7 to 1.1 for in nonsmokers, with no consistent dose-response and several null results attributed to low exposure levels insufficient for causation. Similarly, a 2013 analysis of Japanese nonsmokers exposed to ETS showed no statistically significant link to overall (RR ≈1.0), with elevation limited to a subgroup of workplace-exposed women, suggesting minimal population-level impact. These null findings contrast with meta-analyses pooling positive associations but underscore challenges in detecting small or absent effects amid confounding by factors like diet, , and active misclassification, where ETS risks, if any, appear minimal compared to active (RR >10). Critics of predominant risk narratives note that selective emphasis on positive studies may inflate perceived hazards, while null results from large, long-term cohorts provide evidence against strong .

Dose-Response and Causality Challenges

Establishing a dose-response relationship for passive has proven challenging, as epidemiological studies often fail to demonstrate a consistent biological with increasing exposure intensity, duration, or cumulative dose, a key criterion for inferring under frameworks like Bradford Hill's. For instance, meta-analyses of spousal smoking exposure show only a weak and heterogeneous association with risk in nonsmokers, which diminishes or disappears when stratified by exposure source such as or childhood environments. Unlike active , where relative risks escalate markedly with pack-years (e.g., from 10-fold at 10 pack-years to over 20-fold at 40 pack-years), passive exposure metrics—such as hours per day or years of cohabitation—yield inconsistent gradients, with many studies reporting flat or absent trends after adjustments. The low absolute exposure levels in passive smoking further complicate dose-response assessments, as nonsmokers typically inhale environmental tobacco smoke (ETS) equivalent to approximately 0.5% of the dose from active smoking, based on constituent concentrations and models. This disparity raises issues with linear no-threshold extrapolations from high-dose active smoking , which assume proportional increases at low doses without of a threshold—yet smoke's complex mixture of over 7,000 compounds may exhibit non-linear effects, such as or saturation at low levels, unsupported by direct for ETS. Critics argue that claiming relative risks of 20-30% for spousal exposure (equivalent to 0.1-1 per day) implies implausibly steep curves at minimal doses, while adjusted meta-analyses reducing unadjusted estimates from 23% to near 2% (or even negative) after correcting for misclassification and confounders suggest no meaningful gradient. Causality attribution faces additional hurdles due to the inability to isolate ETS effects amid pervasive confounders and the weak fulfillment of causal criteria. Temporality is inferable from prospective designs, but specificity is lacking, as observed associations overlap with risks from diet, socioeconomic status, and residual active smoking misclassification (e.g., self-reported nonsmokers underreporting light use). Experimental verification is limited, with human chamber studies showing physiological changes at high acute doses but not replicating chronic low-level disease endpoints, and animal models requiring unrealistically high exposures. The coherence criterion is undermined by discrepancies between ETS's diluted carcinogen profile and the high risks projected, prompting arguments for alternative explanations like publication bias favoring positive findings or systematic errors in exposure recall. Overall, while biological plausibility exists from shared smoke components, the tenuous dose-response and attenuated associations post-adjustment cast doubt on strict causality, with some analyses concluding risks indistinguishable from unity.

Experimental and Mechanistic Insights

Animal and In Vitro Studies

Animal studies on (SHS), often using sidestream smoke to simulate environmental tobacco smoke, have primarily focused on respiratory and cardiovascular endpoints in and companion animals. Chronic exposure of mice and rats to SHS in whole-body chambers induced COPD-like pathologies, including with alveolar destruction, airway remodeling, and elevated inflammatory cytokines such as IL-6 and TNF-α, at concentrations equivalent to heavy passive exposure over extended periods. These models revealed mechanisms like , activation (e.g., matrix metalloproteinases), and impaired antioxidant defenses contributing to parenchymal damage. However, such studies typically employ higher smoke densities and shorter durations than lifelong low-level exposure, limiting direct translational relevance due to species differences in and structure. Cardiovascular effects in animal models include endothelial dysfunction and accelerated atherosclerosis following SHS exposure. In rabbits and rats, subchronic SHS inhalation increased arterial stiffness, promoted LDL oxidation, and enhanced plaque formation, with evidence of heightened thrombotic risk via platelet activation. Prenatal or early-life exposure in rodents has shown neurodevelopmental impacts, such as altered hippocampal neurogenesis and behavioral deficits in offspring, linked to nicotine and carbon monoxide crossing the placental barrier. Observations in pet dogs and cats exposed to household SHS demonstrate elevated risks of nasal and lung cancers, with odds ratios up to 2-6 times higher in smokers' homes, attributed to fur trapping smoke particulates and higher minute ventilation relative to body size. In vitro studies expose cell cultures to SHS condensates or gas-phase components, revealing cytotoxicity and genotoxic effects. Human bronchial epithelial cells treated with environmental tobacco smoke extracts exhibited reduced viability, impaired ciliary beat frequency, and increased apoptosis at dilute concentrations mimicking indoor air pollution. Sidestream smoke, richer in certain nitrosamines and volatile organics than mainstream smoke, induced DNA strand breaks, micronuclei formation, and mutagenicity in Ames assays and mammalian cell lines, supporting plausible pathways for carcinogenesis via adduct formation. Metabolic disruptions, including shifts in glycolysis and mitochondrial respiration, were observed in exposed esophageal and lung cells, potentially linking SHS to proliferative changes. These findings provide mechanistic support for observed cellular damage but occur under controlled, non-physiological conditions lacking systemic factors like immune modulation or detoxification.

Human Experimental Exposure Studies

Human experimental exposure studies to passive smoking, also known as environmental tobacco smoke (ETS), typically involve healthy nonsmokers or individuals with conditions like asthma exposed to controlled concentrations of sidestream and diluted mainstream smoke in environmental chambers for short durations, ranging from 10 minutes to 2 hours. These studies measure acute physiological responses, biomarkers of inflammation, and vascular function, providing evidence of biological mechanisms but limited insight into chronic disease outcomes due to ethical constraints on prolonged or high-dose exposures in vulnerable populations. Concentrations are often calibrated to real-world scenarios, such as nicotine levels of 1–4 μg/m³ or carbon monoxide (CO) at 2–5 ppm, simulating heavy indoor passive exposure. Cardiovascular effects have been a primary focus, with brief exposures impairing endothelial function and coronary microvascular dilation. In a 2013 study, 30 minutes of (SHS) exposure at CO levels of 3.2 ppm reduced coronary flow reserve by approximately 30% in healthy adults, an effect reversible within 24–48 hours but indicative of acute vascular stress. Similarly, a 2008 trial exposed participants to SHS for 30 minutes, observing depressed endothelial function and increased circulating , persisting up to 24 hours post-exposure. These findings support acute prothrombotic and vasodilatory disruptions, with effect sizes comparable to 80–90% of active smoking impacts in some metrics, though real-world chronic low-dose relevance remains extrapolated. Respiratory outcomes include transient declines in lung function and heightened . A 2009 chamber study exposed nonsmokers to moderate SHS ( 3.3 μg/m³) for 1 hour, resulting in a 5–10% drop in forced expiratory volume in 1 second (FEV1) and elevated airway cytokines like IL-6 and IL-8, effects more pronounced in males and those with . In asthmatics, ETS challenge exacerbates allergen-induced responses, with one 2006 study showing increased nasal symptoms and after 2 hours of exposure combined with allergen provocation. Such studies confirm irritant and inflammatory responses but note variability by individual sensitivity and exposure intensity. Dose-response patterns emerge in vascular studies, where lower SHS concentrations (e.g., <1 μg/m³ for 30 minutes) yield minimal or no detectable changes in , while higher levels (4–11 μg/m³) consistently impair function. Apparatus designs for "aged" smoke, mimicking sidestream dominance, have enabled precise control, revealing particulate matter and gas-phase components as key contributors to . Limitations include small sample sizes (often n=10–20), focus on surrogates rather than clinical endpoints, and potential overestimation of everyday risks since chamber exposures exceed typical ambient levels by factors of 2–10.

Biological Plausibility Assessment

(SHS), also known as environmental tobacco smoke, consists of mainstream smoke exhaled by active smokers and sidestream smoke emitted from the burning end of cigarettes, containing over 7,000 chemicals, including at least 250 that are toxic or carcinogenic according to the National Toxicology Program. Sidestream smoke typically yields higher concentrations of many toxins per unit than mainstream smoke due to lower temperatures, enhancing its potential biological impact despite overall lower exposure levels in passive scenarios. Biological plausibility for SHS-related harm is supported by evidence of systemic absorption and cellular responses in exposed nonsmokers. Biomarkers such as urinary (a ) and 4-(methylnitrosamino)-1-(3-pyridyl)-1- (NNAL, a ) are detectable in passive smokers, confirming uptake of at levels correlating with exposure duration and proximity. experimental studies demonstrate that brief SHS exposure (e.g., minutes in a ventilated chamber) induces , increased platelet aggregation, and elevated biomarkers of and , such as and F2-isoprostanes, mirroring acute effects seen in active smoking. These changes provide mechanistic links to cardiovascular events, where SHS particles and gases promote and via and adhesion molecule upregulation. For carcinogenesis, plausibility rests on SHS delivering polycyclic aromatic hydrocarbons and nitrosamines that form DNA adducts in lung epithelial cells of exposed individuals, as evidenced by elevated levels of hemoglobin and urinary adducts in nonsmokers from smoking households compared to unexposed controls. In vitro and animal models further illustrate genotoxicity, with SHS extracts causing chromosomal aberrations and mutations at concentrations achievable in real-world passive exposure. Respiratory effects are underpinned by mucociliary clearance impairment and airway inflammation from irritants like acrolein and formaldehyde, leading to histological changes in bronchial tissue. However, the dilute nature of SHS—often 1% or less of active doses—challenges full plausibility for chronic diseases requiring cumulative high-level insult, such as initiation, where linear no-threshold assumptions may overestimate risks absent dose-response thresholds observed in . While acute mechanistic effects are demonstrable, long-term causality in humans hinges on whether low-dose exposures sustain pathological cascades, with some analyses noting weaker correlations for cancer versus cardiovascular outcomes. Overall, biological mechanisms affirm plausibility for adverse effects, particularly acute cardiovascular triggers, but quantitative exposure disparities necessitate caution in extrapolating active directly to passive contexts.

Scientific Consensus, Dissent, and Historical Context

Public Health Authorities' Positions

The (WHO) maintains that there is no safe level of exposure to second-hand tobacco smoke, which it estimates causes over 1.2 million deaths annually worldwide through associations with cardiovascular diseases, respiratory illnesses, and cancers such as . WHO's Framework Convention on Tobacco Control, adopted in 2003 and ratified by over 180 countries, emphasizes comprehensive smoke-free policies in indoor public places, workplaces, and public transport to eliminate exposure, positioning second-hand smoke as a preventable hazard equivalent to active smoking in toxicity. In the United States, the Centers for Disease Control and Prevention (CDC) asserts that exposure has no safe threshold and inflicts immediate adverse effects on the cardiovascular system, increasing risks of coronary heart disease, , and among nonsmokers, with an estimated contribution to more than 40,000 annual deaths in nonsmoking adults and 400 infant deaths. The CDC advocates for total bans on smoking in homes, vehicles, and indoor public spaces, particularly to protect children, citing data that even brief exposure elevates biomarkers of harm like platelet aggregation and . The U.S. Environmental Protection Agency (EPA) classified environmental tobacco smoke as a (known human) in its 1992 risk assessment, based on meta-analyses linking passive smoking to an approximately 19% increased risk of in nonsmokers, with heightened vulnerability in children leading to exacerbated , sudden infant death syndrome, and lower respiratory infections. The EPA's position underscores the inseparability of from degradation, recommending ventilation measures as insufficient substitutes for prohibition, a stance reinforced in subsequent reviews. U.S. reports, including the 1986 edition on involuntary smoking and the 2006 update, affirm causal links to , ischemic heart disease, and middle ear infections in children, declaring separation or ventilation inadequate for risk elimination. These positions collectively form a consensus among major authorities that passive smoking poses quantifiable population-level risks warranting regulatory interventions like smoke-free laws.

Dissenting Scientific Views

A cohort study published in the British Medical Journal in 2003 by epidemiologists James E. Enstrom and Geoffrey C. Kabat analyzed data from the American Cancer Society's Cancer Prevention Study II, tracking over 118,000 lifelong nonsmokers from 1959 to 1998. The researchers found no statistically significant association between exposure to spousal smoking and mortality from coronary heart disease (relative risk [RR] 0.94, 95% confidence interval [CI] 0.85-1.05), lung cancer (RR 0.75, 95% CI 0.51-1.10), or other tobacco-related diseases, concluding that environmental tobacco smoke does not significantly increase long-term mortality risk in this large U.S. population. This prospective study, spanning nearly four decades, highlighted the absence of a dose-response relationship and suggested that prior epidemiological associations may stem from residual confounding or misclassification rather than causation. Critics of the U.S. Environmental Protection Agency's (EPA) 1992 report, which classified environmental tobacco smoke as a (known human) , have argued that the agency's methodology violated scientific standards by selectively including only 16 of 88 studies showing positive associations for , excluding those with null findings, and applying a one-sided 90% to achieve rather than the conventional 95%. In 1998, U.S. District Judge William L. Osteen ruled the report "the product of reasoning 'not reasonably explained'" and vacated its conclusions, citing the EPA's failure to perform full , disregard for contrary evidence, and deviation from guidelines, which undermined claims of a 19-fold risk elevation for nonsmokers. Although an appeals court reinstated the report in 2002 on procedural grounds, dissenting analyses maintain that the EPA's risk estimates (e.g., RR 1.19 for ) were inflated by and inadequate adjustment for confounders like diet and . Dissenting researchers, including Kabat in subsequent reviews, contend that the biological plausibility of passive smoking causing diseases like is low, given exposure levels averaging 1% or less of active doses, which fail to produce measurable biomarkers of in controlled studies or animal models at equivalent concentrations. They argue that small relative risks (often RR <1.2) in spousal and exposure studies are indistinguishable from biases such as recall error in self-reported data or unmeasured factors like active experimentation among "nonsmokers," and that no randomized trials or direct causal mechanisms support the claims. These views, echoed in peer-reviewed critiques, posit that policy-driven consensus has marginalized null findings, with meta-analyses like those by the in the 1990s initially reporting no significant risk before revisions aligned with advocacy positions.

Evolution of Research and Key Milestones

Research on the health effects of passive smoking, also known as involuntary or exposure, began in the early , initially emphasizing acute respiratory issues in children exposed to parental smoking. Early investigations documented elevated rates of and among infants under one year whose parents smoked, establishing a foundation for concerns about environmental tobacco smoke (ETS) beyond direct . These findings built on prior recognition of sidestream smoke's differing from mainstream smoke, prompting questions about non-smokers' vulnerability. A pivotal epidemiological milestone occurred in 1981 with Takeshi Hirayama's in , involving over 120,000 subjects, which reported that non-smoking wives of heavy smokers faced a 2.1-fold increased risk of compared to wives of non-smokers, with a dose-response based on spousal consumption. This was the first large-scale evidence linking passive smoking to in never-smokers, though it relied on spousal exposure recall and faced critiques for potential by diet or misclassification. By , three such studies had emerged, prompting the U.S. Surgeon General's report to highlight a "possible serious problem" from spousal exposure increasing nonsmokers' risk. The 1986 Surgeon General's report marked a causal , concluding that involuntary causes in healthy nonsmokers and exacerbates respiratory conditions in children, based on accumulating epidemiological and biological evidence, including showing uptake. It also addressed acute risks, such as on airplanes, influencing early discussions. Subsequent in the expanded to cardiovascular effects, with meta-analyses estimating 25-30% increased coronary heart disease risk from spousal or exposure, though debates persisted over residual from active history. Into the 2000s, the 2006 Surgeon General's report synthesized over 40 years of data, affirming no safe exposure level and causal links to , ear infections, and in children, alongside adult cancers and heart disease, drawing from dozens of cohort and case-control studies. The National Toxicology Program classified ETS as a known in 2000. Recent analyses, such as a 2024 , have refined risk estimates, attributing at least 8% increased ischemic heart disease and 1% risk to typical exposures, while highlighting gaps in low-dose mechanistic data. This evolution reflects a shift from descriptive to integrated assessments, though methodological challenges like exposure misclassification have prompted ongoing refinements in biomarkers such as levels.

Industry-Funded Research and Critiques

The , facing mounting evidence of environmental tobacco smoke (ETS) risks in the , established the Center for Indoor Air Research (CIAR) in as a nonprofit entity funded primarily by Philip Morris, , and Lorillard, with initial annual contributions exceeding $4 million from these firms. CIAR's stated mission was to support "high-quality, objective" investigations into indoor air pollutants, including ETS constituents like particulate matter and volatile organics, but declassified industry documents indicate it functioned as a mechanism to generate counter-evidence, emphasize alternative pollutants (e.g., or cooking fumes), and advocate ventilation solutions over restrictions. Between 1989 and 1999, CIAR disbursed over $18 million to approximately 53 research projects and 20 fellows, many focusing on ETS exposure metrics in workplaces or homes, often concluding that levels were below regulatory thresholds or mitigable through . A key CIAR-backed effort was the 2003 reanalysis by James E. Enstrom and Geoffrey C. Kabat of the American Cancer Society's Cancer Prevention Study I (CPS-I) cohort, involving over 118,000 adults followed from 1959 to 1998, which reported relative risks (RR) of 0.75 for and 0.91 for coronary heart disease mortality among never-smokers exposed to spousal , with confidence intervals including unity and no dose-response trend observed. from CIAR, totaling around $96,000 for access and , was not initially disclosed in the British Medical Journal publication, prompting editorials and inquiries that revealed prior industry ties, including Enstrom's consultations for the Tobacco Institute in the . The study aligned with earlier industry-supported work, such as analyses of sidestream chemistry showing higher toxin yields per but lower overall exposure in passive scenarios. Critiques of these efforts, drawn from public health analyses and litigation-released archives, portray them as part of a deliberate "whitecoat" strategy to manufacture scientific controversy, akin to tactics used against active links decades earlier. For instance, internal memos from the 1980s outline goals to "neutralize" ETS research by funding sympathetic scientists, critiquing opponents' methodologies (e.g., demanding biochemical markers over self-reports), and promoting "sound science" standards that elevated proof burdens for ETS while accepting weaker evidence for benefits like . Enstrom-Kabat specifically faced accusations of cherry-picking endpoints, ignoring cotinine-validated exposure from later cohorts, and under-adjusting for misclassification biases in spousal reports, which independent reanalyses estimated could inflate type II errors. Industry witnesses in U.S. trials echoed these studies to argue ETS risks were confounded by diet, , or active history, though courts often rejected such claims for lacking mechanistic support beyond . These critiques underscore broader concerns over source credibility, as industry-funded ETS research yielded relative risks consistently near or below 1.0—mirroring some independent findings of modest associations (RR 1.1-1.3)—yet prioritized doubt over replication, with CIAR dissolving in 1998 amid lawsuits exposing its role in delaying clean air laws. While defenders, including the study's authors, assert methodological rigor and alignment with causal criteria like from cohort designs, the pervasive financial incentives have led major journals and bodies like the to impose disclosure mandates and skepticism toward such outputs.

WHO and EPA-Specific Controversies

In 1992, the U.S. Environmental Protection Agency (EPA) released a risk assessment report titled Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders, classifying environmental tobacco smoke (ETS) as a Group A (known human) carcinogen based on a meta-analysis of 30 epidemiological studies showing a statistically significant relative risk of lung cancer among nonsmokers exposed to ETS, estimated at 1.19 overall (with a 19% increased risk). The report attributed approximately 3,000 annual lung cancer deaths in the U.S. to ETS exposure and influenced subsequent regulatory actions, but faced immediate criticism for methodological irregularities, including the exclusion of three major U.S.-based studies that did not support a positive association, the use of a one-tailed statistical test (rather than the standard two-tailed), and lowering the significance threshold from p<0.05 to p<0.10 to achieve nominal significance. Independent reviews, such as one by the EPA's own Risk Criteria Office, highlighted these deviations from standard scientific practice, arguing they inflated the perceived risk without robust justification. The EPA report's conclusions were legally challenged by tobacco companies in Flue-Cured Tobacco Cooperative Stabilization Corp. v. EPA (1998), where U.S. District Judge William Osteen ruled that the agency violated the by failing to respond to contrary evidence, altering analytical criteria post hoc, and conducting a flawed that did not meet its own evidentiary standards for carcinogenicity. Osteen vacated the report's sections, noting the 20% risk elevation fell below epidemiological thresholds for establishing causation and could be confounded by factors like diet or misclassification of smokers as nonsmokers. Although a 2002 appeals court decision reinstated the classification by limiting its review to procedural aspects and deferring to agency expertise on the underlying , the ruling did not resolve ongoing debates about selection and statistical manipulation, with critics maintaining the EPA prioritized policy goals over empirical rigor. The World Health Organization's International Agency for Research on Cancer (IARC), in its 2004 Monograph Volume 83 on Tobacco Smoke and Involuntary Smoking, classified involuntary smoking as carcinogenic to humans (), citing sufficient evidence from 12 cohort and 54 case-control studies showing a pooled of 1.23 (23% increase) for among never-smokers exposed to ETS, particularly from spousal smoking. This assessment built on earlier IARC evaluations and dismissed confounding by active smoking or other biases as minimal, but drew criticism for relying on observational data with inherent limitations, such as self-reported exposure and potential favoring positive associations. A prominent dissenting view came from a 2003 British Medical Journal analysis by James Enstrom and Geoffrey Kabat, using the large CPS-I cohort (over 118,000 never-smokers followed for 39 years), which found no statistically significant ETS-related risk ( 0.94 overall) and argued IARC/WHO overlooked null or protective findings in extended follow-ups of prior studies. IARC's response maintained that Enstrom-Kabat's results were consistent with a modest effect diluted by historical exposure declines, but critics, including independent epidemiologists, contended the WHO process exhibited selective emphasis on weaker case-control studies over stronger prospective cohorts and downplayed absolute risks (e.g., attributable fraction under 1% in low-exposure settings), potentially amplifying policy-driven narratives at the expense of causal scrutiny. Tobacco industry documents later revealed coordinated efforts to undermine IARC conclusions through funding alternative research and lobbying, yet this did not negate scientific critiques of the evidence base's fragility, where small relative risks (often near 1.2) are prone to residual and fail first-principles tests for dose-response consistency seen in active . Both agencies' positions have been defended as precautionary amid imperfect data, but the controversies underscore tensions between regulatory imperatives and demands for stringent evidentiary standards in establishing ETS causality.

Litigation and Regulatory Challenges

In 1998, the U.S. Environmental Protection Agency (EPA) classified environmental tobacco smoke (ETS) as a known in its report "Respiratory Health Effects of Passive Smoking: and Other Disorders," estimating it caused 3,000 deaths annually among nonsmokers. This classification faced immediate legal challenge from tobacco grower cooperatives and industry groups in Flue-Cured Tobacco Cooperative Stabilization Corp. v. U.S. EPA, where plaintiffs argued the EPA deviated from standard scientific procedures. The U.S. District Court for the Middle District of North Carolina ruled the risk assessment arbitrary and capricious under the , citing the EPA's selective use of data—analyzing only six of 30 spousal smoking studies with positive associations while excluding negative ones—unjustified shift from a 90% to 95% , lack of for the quantitative assessment, and violation of the Indoor Radon Policy Act's requirement to consider all relevant studies. The court vacated the ETS carcinogen classification specifically for nonsmoker risk. On appeal, the U.S. Court of Appeals for the Fourth Circuit affirmed the district court's identification of procedural errors but reversed the vacatur, holding that plaintiffs lacked standing to demonstrate economic injury or irreparable harm sufficient to invalidate the report's non-regulatory conclusions. As a result, the EPA's ETS findings persisted without formal rescission, influencing subsequent despite the documented methodological flaws, which critics attributed to regulatory overreach amid pressure from anti-tobacco groups. The (OSHA) encountered similar opposition in its 1994 proposed rule to regulate ETS as an hazard in workplaces, which would have mandated ventilation standards or bans based on estimated risks of 16,000 to 77,000 annual ETS-attributable deaths. groups, including the Tobacco Institute, mounted extensive challenges through public comments, economic impact studies questioning dose-response data, and that highlighted inconsistencies in epidemiological and alternative interpretations of ventilation efficacy. Facing over 100,000 comments—many industry-orchestrated—and internal debates over the rule's scientific foundation, OSHA withdrew the proposal in 2001 without finalizing it, citing resource constraints and unresolved evidentiary gaps rather than outright defeat in court. This retreat underscored regulatory hesitancy when faced with litigation threats emphasizing weak causal links in observational data. Tobacco companies and affected businesses frequently litigated against state and local smoking bans enacted from the 1970s onward, arguing violations of property rights, equal protection, or preemption by higher laws, often as a delay tactic to hinder implementation. For instance, in cases like Gallagher v. City of Clayton (Missouri, 2005), courts rejected claims that bans infringed fundamental rights, affirming smoking as a regulable behavior without strict scrutiny. Industry-backed suits against over 1,600 U.S. smokefree ordinances by 2005 achieved limited successes, such as temporary injunctions or preemption-based blocks in states like those with tobacco-influenced legislatures, but most were unsuccessful, with bans upheld under public health police powers. Internationally, similar patterns emerged, as in European challenges to Directive 2001/37/EC on tobacco products, where industry arguments on proportionality failed before the European Court of Justice, reinforcing regulatory momentum despite procedural critiques. These efforts, while rarely overturning laws outright, prolonged debates and elevated costs for proponents, exploiting evidentiary uncertainties in secondhand smoke exposure metrics.

Policy Interventions and Outcomes

Implementation of Smoke-Free Regulations

The implementation of smoke-free regulations has predominantly occurred through national, state, or local legislation establishing bans on tobacco smoking in enclosed indoor workplaces, public places, hospitality venues, and public transport services. These measures aim to eliminate involuntary exposure to secondhand smoke by requiring 100% smoke-free environments, rejecting alternatives such as ventilation systems, air filtration, or segregated smoking areas as inadequate for protection. The World Health Organization's Framework Convention on Tobacco Control (FCTC), adopted on May 21, 2003, and entering into force on February 27, 2005, provided the primary international impetus via Article 8, which obligates parties to enact and enforce protections against tobacco smoke exposure in specified settings. By 2021, over 80% of FCTC parties had implemented some form of smoke-free legislation aligned with these guidelines, though coverage and stringency varied. Pioneering efforts predated widespread FCTC ratification, with local restrictions emerging in the 1970s, such as Berkeley, California's 1970 ordinance limiting smoking in restaurants and public facilities. Comprehensive national implementation began with Ireland's Public Health (Tobacco) Act on March 29, 2004, which prohibited smoking in all enclosed workplaces—including pubs, restaurants, and offices—with initial fines of up to €3,007 for violations and daily penalties for non-compliant businesses. This was followed by Bhutan's total nationwide ban in 2004 and New York City's indoor ban effective March 30, 2003, covering bars, restaurants, and workplaces. In , enacted the first UK-wide law on March 26, 2006, banning smoking in enclosed public places, while Australia's states progressively adopted comprehensive bans by 2007, starting with in 2000 for hospitality venues. By 2012, at least 55 countries had enacted national comprehensive smoke-free laws covering bars and restaurants without exemptions. Enforcement mechanisms typically involve a combination of proactive inspections by or environmental agencies and reactive responses to public complaints, with graduated penalties including warnings, fines, and potential business closures or license suspensions. In Ireland, the Office of coordinated initial enforcement, achieving over 97% compliance within months through education campaigns and fines totaling €11 million by 2006. U.S. states like , which passed the first comprehensive statewide in December 2002 effective December 8, 2002, rely on local health departments for monitoring, with fines starting at $100 and escalating for repeat offenses. Implementation has faced structural challenges, including tobacco industry lobbying against bans, hospitality sector fears of revenue declines, and resource constraints for enforcement, such as underfunded inspectorates and reliance on complaint-based systems that prioritize high-visibility violations. In developing countries, cultural norms and weak institutional capacity have delayed adoption, with partial exemptions persisting despite FCTC guidelines. Comprehensive laws without loopholes, however, facilitate higher compliance—often exceeding 90%—due to clear rules and reduced enforcement ambiguity compared to partial restrictions. Public education and signage requirements have supported voluntary adherence, mitigating initial resistance.

Measured Effects on Exposure and Health

Implementation of comprehensive smoke-free legislation has been associated with measurable reductions in (SHS) exposure, primarily assessed through biomarkers such as urinary or salivary (a of specific to tobacco smoke) and environmental markers like airborne or particulate matter (PM2.5). In hospitality workers exposed to high pre-ban levels, salivary concentrations declined by approximately 80-90% within months of bans in venues like bars and restaurants, as observed in studies from and where geometric mean levels dropped from 16.0 ng/mL to 0.4 ng/mL post-implementation. Airborne levels in indoor public spaces have similarly decreased by 70-95% following bans, with one review of multiple jurisdictions reporting median reductions exceeding 90% in bars and . These exposure metrics confirm effective enforcement reduces SHS infiltration into non-smoking areas, though residual outdoor or home exposure persists, with public bans indirectly lowering home SHS by 20-30% via behavioral spillovers reducing overall smoking prevalence. Health outcomes linked to reduced SHS exposure post-legislation include declines in acute cardiovascular and respiratory events, often measured via hospital admission rates. A study in Pueblo, Colorado, reported a 27% drop in acute myocardial infarction (AMI) admissions within two years of a local ban, compared to no change in a control county without restrictions, attributing the effect to lowered SHS-related endothelial dysfunction. Meta-analyses of over 50 studies across jurisdictions, including comprehensive bans in Europe and the U.S., indicate average reductions of 10-20% in AMI hospitalizations and 5-15% in overall coronary events, with stronger effects (up to 30%) in high-exposure settings like hospitality. Respiratory outcomes show smaller but consistent benefits, such as 10-20% fewer childhood asthma admissions and reduced chronic obstructive pulmonary disease exacerbations, corroborated by interrupted time-series analyses controlling for secular trends like declining active smoking rates. These associations rely on ecological and quasi-experimental designs, with effect sizes varying by ban comprehensiveness and enforcement; partial bans (e.g., allowing ventilated rooms) yield negligible reductions in biomarkers or admissions. Long-term from Scotland's 2006 nationwide ban showed sustained 17% AMI declines persisting over a decade, independent of broader measures. Birth outcomes, including preterm births, decreased by 5-10% in some analyses, though confounding from concurrent policies limits causal attribution. Overall, while SHS reductions are robustly documented, health effect magnitudes are modest (often <20% for acute events), reflecting SHS's contribution to population risk amid dominant factors like active and comorbidities.

Economic, Social, and Alternative Approaches

Economic analyses of smoke-free policies have predominantly examined their effects on sector revenues, with meta-analyses concluding no substantial overall gains or losses for and bars following implementation. A CDC of multiple U.S. states similarly found no adverse impacts, and in some cases, small positive effects post-ban. However, a study of Ohio's 2006 smoking ban identified economic declines specifically in bars, attributing losses to reduced patronage among smokers without corresponding gains from nonsmokers. These divergent findings reflect methodological differences, such as focus on bar versus subsectors, and underscore debates over whether bans impose net costs on businesses reliant on smoking clientele. Social dimensions of passive smoking interventions encompass shifts in norms, disparities in exposure, and tensions over individual liberties. Smoke-free laws have correlated with decreased social acceptability of and reduced secondhand smoke infiltration in multi-unit housing, particularly benefiting lower-income and minority groups disproportionately exposed pre-ban. Yet, enforcement has sparked social friction, including stigma against smokers and conflicts in shared spaces like homes, where voluntary measures often fail to eliminate exposure for children or nonsmokers. Critics, emphasizing property rights, contend that blanket prohibitions overlook nuanced social contexts, such as adult-only venues, potentially exacerbating divisions without addressing root behaviors like home . Alternative strategies to bans prioritize solutions and behavioral incentives over prohibitions. Enhanced ventilation and air systems, including and molecular filters, have demonstrated reductions in particulates in controlled settings, offering a technical means to mitigate exposure without total elimination of . Designated rooms with extraction, when properly engineered, can isolate pollutants, though authorities maintain these yield negligible protection compared to comprehensive bans due to incomplete of fine particles and gases. Advocates for such approaches argue they preserve economic viability in and respect voluntary choice, citing evidence from partial measures that achieve exposure drops via isolation or positive pressure airflow in residences. Empirical data on long-term remains limited, with consensus favoring bans for maximal reduction but alternatives viable in contexts prioritizing flexibility over absolutism.

Public Perception and Broader Impacts

Surveys and Cultural Shifts

Public opinion surveys have shown a consistent increase in the perception of (SHS), or , as a significant risk. A analysis of national data from 2009-2010 indicated that 64.5% of adults viewed SHS exposure as "very harmful," with state-level variations from 73.5% in to 53.7% in , reflecting regional differences in culture and awareness campaigns. Earlier polls, such as a 1976 Roper Organization survey, already captured emerging concerns, with 51% of Americans favoring bans on in public places despite widespread tolerance of the habit at the time. Support for restrictive policies has grown markedly over decades, driven by accumulating evidence of SHS harms. Gallup polls tracked rising endorsement for outright bans on public smoking, from 39% in 2001 to 58% in 2015 and 62% in 2019, indicating broad bipartisan agreement on limiting exposure in shared spaces. A 2023 meta-analysis of global surveys found 73% average support for smoke-free indoor private places, underscoring near-universal recognition of involuntary exposure as untenable in enclosed environments. These attitudes correlate with demographic factors, including higher concern among nonsmokers and women, though disparities persist by education and smoking status. Cultural shifts have paralleled these survey trends, transitioning from normalized acceptance of ambient tobacco smoke in the mid-20th century to widespread by the 21st. Prior to the , smoking was ubiquitous in public venues, with minimal regard for bystanders, but advocacy and reports like the 1964 U.S. Surgeon General's warning catalyzed a reevaluation, framing SHS as an imposed risk rather than incidental. This evolution eroded libertarian views of personal smoking choices as isolated, replacing them with norms prioritizing collective air quality, as evidenced by declining tolerance in social settings and the rise of "no smoking" . Tobacco industry efforts to portray SHS risks as exaggerated faced countervailing stigma, accelerating voluntary restrictions in workplaces and homes before formal bans. By the , surveys reflected this as a entrenched cultural pivot, with SHS avoidance integrated into everyday behaviors like parental protections and venue policies.

Influence on Individual Liberties and Norms

Concerns over passive smoking have driven the enactment of smoke-free laws in public venues and workplaces, prompting debates on their compatibility with individual liberties. Critics, including advocates, argue that such regulations infringe on property rights by overriding owners' decisions on allowable activities in private establishments, such as bars and restaurants. For instance, libertarian perspectives emphasize that no universal right exists to smoke or prohibit it outright, advocating instead for voluntary agreements between property owners, patrons, and employees to balance freedoms without state intervention. Legal challenges to smoking bans have invoked property rights, with some successes; the New Hampshire Supreme Court in JTR Colebrook, Inc. v. Town of Colebrook ruled against a municipal ban extending to private property, affirming owners' authority over their premises. However, U.S. courts have generally upheld public smoking restrictions, finding no constitutional right to smoke that overrides public health measures, though these rulings prioritize collective protections over individual autonomy in shared spaces. Libertarian critiques further contend that even if secondhand smoke poses risks, bans represent coercive paternalism, potentially violating the non-aggression principle by preempting private resolutions like ventilation or segregation. The passive smoking discourse has reshaped social norms, transforming from a widely tolerated practice to one increasingly stigmatized in communal settings. Prevalent in the mid-20th century, public gave way to desocialization following heightened awareness of secondhand exposure risks, evidenced by declining social acceptability and voluntary restrictions in private homes and events. This cultural shift, accelerated by policy interventions citing passive smoke harms, has fostered intolerance toward smokers in shared environments, eroding norms of personal choice in favor of collective health imperatives. Surveys indicate broad public support for bans, reflecting internalized views that passive exposure justifies curtailing individual behaviors previously deemed private.

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