Passive smoking

Passive smoking is the inhalation of

According to latest WHO report, more than 1.3 million deaths are attributed to passive smoking worldwide every year.

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

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 "

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]
• 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:
  • Risk of asthma^[31]
  • Risk of chronic obstructive pulmonary disease (COPD)^[32]
  • According to a 2015 review, passive smoking may increase the risk of tuberculosis infection and accelerate the progression of the disease, but the evidence remains weak.^[33]
  • The majority of studies on the association between secondhand smoke exposure and sinusitis have found a significant association between the two.^[34]
• 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]
  • 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

• 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]
• An increase in
  biomarkers) has been associated with passive smoking in children.^[77]
• Increased risk of
  middle ear infections.^[68][78][79]
• Invasive meningococcal disease.^[24][80]
• Anesthesia complications and some negative surgical outcomes.^[81]
• 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.^[82]
• Adverse effects on the cardiovascular system of children.[83]

Evidence

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

In 1992, a review estimated that secondhand smoke exposure was responsible for 35,000 to 40,000 deaths per year in the

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.[88]^[89][90][91] Some scientists believe that the risk of passive smoking, in particular the risk of developing coronary heart diseases, may have been substantially underestimated.^[92]

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.^[93] 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%.^[94] 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.^[95] 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.^[96] 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.^[97] A 2014 meta-analysis noted that "the association between exposure to secondhand smoke and lung cancer risk is well established."^[98]

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.^[99][100] 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.^[99] 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.^[101]

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.^[102][103]

The National Asthma Council of Australia cites studies showing that secondhand smoke is probably the most important indoor pollutant, especially around young children:^[104]

• 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^[105] 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."^[106]

There is good observational evidence that smoke-free legislation reduces the number of hospital admissions for heart disease.^[107][108]

Exposure and risk levels

The International Agency for Research on Cancer of the World Health Organization concluded in 2004 that there was sufficient evidence that secondhand smoke caused cancer in humans.^[2] Those who work in environments where smoke is not regulated are at higher risk.^[109][103] Workers particularly at risk of exposure include those in installation repair and maintenance, construction and extraction, and transportation.^[110]

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%.^[111]

Similarly, children who are exposed to environmental tobacco smoke are shown to experience a range of adverse effects^{[112][113][114]} and a higher risk of becoming smokers later in life.^[115] The WHO has identified reduction of exposure to environmental tobacco smoke as key element for actions to encourage healthy child development.^[116]

The US

Interventions to reduce environmental tobacco smoke

A systematic review compared smoking control programmes and their effects on smoke exposure in children. The review distinguishes between community-based, ill-child and healthy-child settings and the most common types of interventions were counselling or brief advice during clinical visits. The review did not find superior outcomes for any intervention, and the authors caution that evidence from adult settings may not generalise well to children.^[118]

Biomarkers

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.

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.^[122]

Cotinine

Cotinine, the metabolite of nicotine, is a biomarker of secondhand smoke exposure. Typically, cotinine is measured in the blood, saliva, and urine. Hair analysis has recently become a new, noninvasive measurement technique. Cotinine accumulates in hair during hair growth, which results in a measure of long-term, cumulative exposure to tobacco smoke.^[123] Urinary cotinine levels have been a reliable biomarker of tobacco exposure and have been used as a reference in many epidemiological studies.^[118] 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.^[119]

Carbon monoxide (CO)

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.[127] Exposure to tobacco smoke for 30 minutes significantly reduces coronary flow velocity reserve in healthy nonsmokers.^[128] Secondhand smoke is also associated with impaired vasodilation among adult nonsmokers.^[129] Secondhand smoke exposure also affects platelet function, vascular endothelium, and myocardial exercise tolerance at levels commonly found in the workplace.^[130]

Pulmonary emphysema can be induced in rats through acute exposure to sidestream tobacco smoke (30 cigarettes per day) over a period of 45 days.^[131] Degranulation of mast cells contributing to lung damage has also been observed.^[132]

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.^{[133][134][135]} Preliminary research suggests that by-products of third-hand smoke may pose a health risk,^[136] 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.^[137]

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.^[138]

Opinion of public health authorities

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:

• World Health Organization^[2]
• U.S. National Institutes of Health^[139]
• Centers for Disease Control^[140]
• United States Surgeon General^[1]
• U.S. National Cancer Institute^[141]
• United States Environmental Protection Agency^[142]
• California Environmental Protection Agency^[16]
• American Heart Association,^[143] American Lung Association,^[144] and American Cancer Society^[145]
• American Medical Association^[146]
• American Academy of Pediatrics^[147]
• Australian National Health and Medical Research Council^[148]
• United Kingdom Scientific Committee on Tobacco and Health^[149]

Public opinion

Recent major surveys conducted by the U.S.

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.^[167] 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

Gio Batta Gori, a tobacco industry spokesman and consultant^{[168][169][170]} 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."^[171]

Milloy

Steven Milloy, the "junk science" commentator for Fox News and a former Philip Morris consultant,^[172][173] claimed that "of the 19 studies" on passive smoking "only 8— slightly more than 42%— reported statistically significant increases in heart disease incidence."^[174]

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."^[175]

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".^[176] 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.^[177]

Levois and Layard

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.^[178][179] 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][180]

World Health Organization controversy

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."^[181]

In March 1998, before the study was published, reports appeared in the media alleging that the IARC and the

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.[187] 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."^[181] 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.^[188]

With the release of formerly classified tobacco industry documents through the

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.^[191]

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.^[192] 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.^[193]

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."^[194]

Tobacco-industry funding of research

The tobacco industry's role in funding scientific research on secondhand smoke has been controversial.

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.[198]

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."^[199] 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.^[199]

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."^[199]

Tobacco industry response

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."^[200] 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.^[201]
• 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.^[196] 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^[202] 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
  sound science. Ong & Glantz (2001) cite an internal Phillip Morris memo giving evidence of this as company policy.^[177]
• 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".^[203]

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."[204] 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."^[205]

Position of major tobacco companies

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

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.^{[208][209][210]}

Smoke-free laws

As a consequence of the health risks associated with secondhand smoke, many national and local governments have outlawed smoking in indoor public places, including

Opinion polls have shown considerable support for smoke-free laws. In June 2007, a survey of 15 countries found 80% approval for such laws.[214] A survey in France, reputedly a nation of smokers, showed 70% support.^[106]

Effects

Smoking bans by governments result in decreased harm from secondhand smoke, including less admissions for acute coronary syndrome.^[215] 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.^[216] 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.^[110] 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.^[217]

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.^[218]

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.^[219]

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.^[220]

Public opinion

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.^[221]

Alternative forms

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.^[222] 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.^[223] However, not all critics have connections to the industry.

The

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.^[226] 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

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

Secondhand smoke is popularly recognised as a risk factor for cancer in pets.

• Health effects of tobacco
• Third-hand smoke
• Tobacco control
• Philip Morris v. Uruguay

References