Passive smoking

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Tobacco smoke in an Irish pub before a smoking ban came into effect on March 29, 2004 Smoke-by-a-window-in-a-pub.jpg
Tobacco smoke in an Irish pub before a smoking ban came into effect on March 29, 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 diseases caused by active smoking, [1] [2] although to a lower prevalence due to the reduced concentration of smoke that enters the airway.

Contents

According to latest WHO report, 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

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.

Effects

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

Risk to children

Evidence

Exposure to secondhand smoke by age, race, and poverty level in the US in 2010 Exposure to secondhand smoke by age, race, and poverty level US.png
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.

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. [84] 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, [85] and two 1999 meta-analyses reached similar conclusions. [86] [87]

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]

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 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. [117] 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 blacks and the poor were exposed in 2014.

Interventions to reduce environmental tobacco smoke

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

Biomarkers

Breath CO monitor displaying carbon monoxide concentration of an exhaled breath sample (in ppm) with corresponding percent concentration of carboxyhemoglobin displayed below Breath CO Monitor.jpg
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. [119] [120] 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. [121]

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)

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

Pathophysiology

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. [125]

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. [126]

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:

Public opinion

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. [150]

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". [151]

Controversy over harm

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. [152] [153] 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. [154] [155]

Industry-funded studies and critiques

Enstrom and Kabat

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. [156] 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." [157] This paper was widely promoted by the tobacco industry as evidence that the harms of passive smoking were unproven. [158] [159] 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. [160] Notably, the study had failed to identify a comparison group of "unexposed" persons. [161]

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." [162] 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." [163] The Court found that the study had been funded and managed by the Center for Indoor Air Research, [164] 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". [165] 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." [166]

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 World Health Organization (WHO) were suppressing information. The reports, appearing in the British Sunday Telegraph [182] and The Economist , [183] among other sources, [184] [185] [186] 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. [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 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. [189] 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. [190]

EPA lawsuit

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]

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. [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. [195] 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. [196] 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. [197] 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. [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:

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 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. [206]

US racketeering lawsuit against tobacco companies

On September 22, 1999, the U.S. Department of Justice filed a racketeering lawsuit against Philip Morris and other major cigarette manufacturers. [207] 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:

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 restaurants, cafés, and nightclubs, as well as some outdoor open areas. [211] 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 [212] ) 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." [213]

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 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. [224] The U.S. Surgeon General and the European Commission Joint Research Centre have reached similar conclusions. [204] [225] 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. [213] 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. [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. [227] 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. [228] 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. [229] 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. [230]

See also

Related Research Articles

<span class="mw-page-title-main">Cigarette</span> Small roll of cut tobacco designed to be smoked

A cigarette is a narrow cylinder containing a combustible material, typically tobacco, that is rolled into thin paper for smoking. The cigarette is ignited at one end, causing it to smolder; the resulting smoke is orally inhaled via the opposite end. Cigarette smoking is the most common method of tobacco consumption. The term cigarette, as commonly used, refers to a tobacco cigarette, but the word is sometimes used to refer to other substances, such as a cannabis cigarette or an herbal cigarette. A cigarette is distinguished from a cigar by its usually smaller size, use of processed leaf, and paper wrapping, which is typically white. Most modern cigarettes are filtered, although this does not make the smoke inhaled from them contain fewer carcinogens and harmful chemicals.

<span class="mw-page-title-main">Tobacco smoking</span> Practice of burning tobacco and breathing the resulting smoke

Tobacco smoking is the practice of burning tobacco and ingesting the resulting smoke. The smoke may be inhaled, as is done with cigarettes, or simply released from the mouth, as is generally done with pipes and cigars. The practice is believed to have begun as early as 5000–3000 BC in Mesoamerica and South America. Tobacco was introduced to Eurasia in the late 17th century by European colonists, where it followed common trade routes. The practice encountered criticism from its first import into the Western world onwards but embedded itself in certain strata of a number of societies before becoming widespread upon the introduction of automated cigarette-rolling apparatus.The World Health Organization states secondhand smoke—that from other people's smoking—causes 1.3 million of the 8 million annual deaths caused by smoking.

<span class="mw-page-title-main">Hookah</span> Type of water pipe

A hookah, shisha, or waterpipe is a single- or multi-stemmed instrument for heating or vaporizing and then smoking either tobacco, flavored tobacco, or sometimes cannabis, hashish and opium. The smoke is passed through a water basin—often glass-based—before inhalation.

<span class="mw-page-title-main">Smoking cessation</span> Process of discontinuing tobacco smoking

Smoking cessation, usually called quitting smoking or stopping smoking, is the process of discontinuing tobacco smoking. Tobacco smoke contains nicotine, which is addictive and can cause dependence. As a result, nicotine withdrawal often makes the process of quitting difficult.

<span class="mw-page-title-main">Smoking ban</span> Law prohibiting tobacco smoking in a given space

Smoking bans, or smoke-free laws, are public policies, including criminal laws and occupational safety and health regulations, that prohibit tobacco smoking in certain spaces. The spaces most commonly affected by smoking bans are indoor workplaces and buildings open to the public such as restaurants, bars, office buildings, schools, retail stores, hospitals, libraries, transport facilities, and government buildings, in addition to public transport vehicles such as aircraft, buses, watercraft, and trains. However, laws may also prohibit smoking in outdoor areas such as parks, beaches, pedestrian plazas, college and hospital campuses, and within a certain distance from the entrance to a building, and in some cases, private vehicles and multi-unit residences.

<span class="mw-page-title-main">Cotinine</span> Alkaloid found in tobacco

Cotinine is an alkaloid found in tobacco and is also the predominant metabolite of nicotine, typically used as a biomarker for exposure to tobacco smoke. Cotinine is currently being studied as a treatment for depression, post-traumatic stress disorder (PTSD), schizophrenia, Alzheimer's disease and Parkinson's disease. Cotinine was developed as an antidepressant as a fumaric acid salt, cotinine fumarate, to be sold under the brand name Scotine, but it was never marketed.

<span class="mw-page-title-main">Health effects of tobacco</span> Circumstances, mechanisms, and factors of tobacco consumption on human health

Tobacco products, especially when smoked or used orally, have negative effects on human health. Researchers have addressed concerns about these effects for a long time. They have focused primarily on cigarette smoking.

<span class="mw-page-title-main">Sidestream smoke</span> Smoke directly released into the air from a burning cigarette, cigar, or smoking pipe

Sidestream smoke is smoke which goes into the air directly from a burning cigarette, cigar, or smoking pipe. Sidestream smoke is the main component of second-hand smoke (SHS), also known as Environmental Tobacco Smoke (ETS) or passive smoking. The relative quantity of chemical constituents of sidestream smoke are different from those of directly inhaled ("mainstream") smoke, although their chemical composition is similar. Sidestream smoke has been classified as a Class A carcinogen by the U.S. Environmental Protection Agency.


Tobacco harm reduction (THR) is a public health strategy to lower the health risks to individuals and wider society associated with using tobacco products. It is an example of the concept of harm reduction, a strategy for dealing with the use of drugs. Tobacco smoking is widely acknowledged as a leading cause of illness and death, and reducing smoking is vital to public health.

Third-hand smoke is contamination by tobacco smoke that lingers following the extinguishing of a cigarette, cigar, or other combustible tobacco product. First-hand smoke refers to what is inhaled into the smoker's own lungs, while second-hand smoke is a mixture of exhaled smoke and other substances leaving the smoldering end of the cigarette that enters the atmosphere and can be inhaled by others. Third-hand smoke or "THS" is a neologism coined by a research team from the Dana–Farber/Harvard Cancer Center, where "third-hand" is a reference to the smoking residue on surfaces after "second-hand smoke" has cleared out.

<span class="mw-page-title-main">Smoking</span> Practice of inhaling a burnt substance for psychoactive effects

Smoking is a practice in which a substance is combusted and the resulting smoke is typically inhaled to be tasted and absorbed into the bloodstream of a person. Most commonly, the substance used is the dried leaves of the tobacco plant, which have been rolled with a small rectangle of paper into an elongated cylinder called a cigarette. Other forms of smoking include the use of a smoking pipe or a bong.

Tobacco smoking during pregnancy causes many detrimental effects on health and reproduction, in addition to the general health effects of tobacco. A number of studies have shown that tobacco use is a significant factor in miscarriages among pregnant smokers, and that it contributes to a number of other threats to the health of the foetus.

<span class="mw-page-title-main">Animals and tobacco smoke</span> Exposure of animals to tobacco smoke

Animals are exposed to tobacco smoke and other cigarette by-products through their use as experimental subjects and through contact with smokers, as in the case of pets in houses where smoking takes place.

The use of electronic cigarettes (vaping) carries health risks. The risk depends on the fluid and varies according to design and user behavior. In the United Kingdom, vaping is considered by some to be around 95% less harmful than tobacco after a controversial landmark review by Public Health England.

Geoffrey C. Kabat is an American epidemiologist, cancer researcher, and author. He has been on the faculty of the Albert Einstein College of Medicine and State University of New York, Stony Brook. He was co-author of a discredited BMJ study funded by the tobacco industry, that erroneously said there was no association between secondhand smoke and health problems.

<span class="mw-page-title-main">Takeshi Hirayama</span> Japanese epidemiologist (1923–1995)

Takeshi Hirayama was a Japanese cancer epidemiologist and anti-tobacco activist who served as the chief of the epidemiology division at the National Cancer Center in Tokyo from 1965 until 1985. He has been credited with publishing the first study linking passive smoking to lung cancer, and also conducted research on the relationship between certain dietary factors and cancer.

The Center for Indoor Air Research was a tobacco industry front group established by three American tobacco companies—Philip Morris, R.J. Reynolds, and Lorillard—in Linthicum, Maryland, in 1988. The organization funded research on indoor air pollution, some of which pertained to passive smoking and some of which did not. It also funded research pertaining to causes of lung cancer other than passive smoking, such as diet. The organization disbanded in 1998 as a result of the Tobacco Master Settlement Agreement.

<span class="mw-page-title-main">Tobacco-free college campuses</span>

Tobacco-free college campuses are colleges and universities that have implemented policies prohibiting the use of tobacco products at all indoor and outdoor campus locations. Tobacco is known to be harmful to the health of smokers, bystanders, and the environment. Since this issue was first recognized, colleges have been creating policies for tobacco use on campus in an effort to improve health standards, provide more enjoyable campus conditions, and to reduce the negative environmental effects of tobacco.

Sally Katharine Hammond is a Professor of Environmental Health Sciences and Associate Dean of Academic Affairs at the UC Berkeley School of Public Health. Her research considers the impact of pollution and passive smoking on public health. It resulted in the Federal Aviation Administration issuing a ban on smoking on aeroplanes. Hammond serves on the World Health Organization study group on Tobacco Product Regulation.

<span class="mw-page-title-main">Smoker's macrophages</span>

Smoker’s macrophages are alveolar macrophages whose characteristics, including appearance, cellularity, phenotypes, immune response, and other functions, have been affected upon the exposure to cigarettes. These altered immune cells are derived from several signaling pathways and are able to induce numerous respiratory diseases. They are involved in asthma, chronic obstructive pulmonary diseases (COPD), pulmonary fibrosis, and lung cancer. Smoker’s macrophages are observed in both firsthand and secondhand smokers, so anyone exposed to cigarette contents, or cigarette smoke extract (CSE), would be susceptible to these macrophages, thus in turns leading to future complications.

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