Passive smoking is the inhalation of smoke, called second-hand smoke (SHS), or environmental tobacco smoke (ETS), by persons other than the intended "active" smoker. It occurs when tobacco smoke permeates any environment, causing its inhalation by people within that environment. Exposure to second-hand tobacco smoke causes disease, disability, and death. The health risks of second-hand smoke are a matter of scientific consensus. These risks have been a major motivation for smoke-free laws in workplaces and indoor public places, including restaurants, bars and night clubs, as well as some open public spaces.
Concerns around second-hand 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 second-hand smoke as a serious threat to its business interests. Harm to bystanders was perceived as a motivator for stricter regulation of tobacco products. Despite the industry's awareness of the harms of second-hand smoke as early as the 1980s, the tobacco industry coordinated a scientific controversy with the aim of forestalling regulation of their products.:1242
General: overall increased risk; 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."
Lung cancer: passive smoking is a risk factor for lung cancer. In the United States passive smoke is estimated to cause more than 7,000 deaths from lung cancer a year among non-smokers.
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% and the US Surgeon General has concluded that the evidence is "suggestive," but still insufficient to assert such a causal relationship. 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." 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."
Pancreatic cancer: A 2012 meta-analysis found no evidence that passive smoking was associated with an increased risk of pancreatic cancer.
Cervical cancer: A 2015 overview of systematic reviews found that exposure to second-hand smoke increased the risk of cervical cancer.
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.
Premature birth, part B, ch. 3 (Note that evidence of the causal link is only described as "suggestive" by the US Surgeon General in his 2006 report.) Laws limiting smoking decrease premature births.
Recent studies comparing females exposed to Environmental Tobacco 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 low birth weight.
Worsening of asthma, allergies, and other conditions. 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.
Overall increased risk of death in both adults, where it is estimated to kill 53,000 nonsmokers per year, making it the 3rd leading cause of preventable death in the U.S, and in children. The World Health Organization states that passive smoking causes about 600,000 deaths a year, and about 1% of the global burden of disease.
Skin conditions: A 2016 systematic review and meta-analysis found that passive smoking was associated with a higher rate of atopic dermatitis.
Risk to children
Sudden infant death syndrome (SIDS). 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." Secondhand smoking has been estimated to be associated with 430 SIDS deaths in the United States annually.
Asthma. Secondhand smoke exposure is also associated with an almost doubled risk of hospitalization for asthma exacerbation among children with asthma.
Lung infections, also including more severe illness with bronchiolitis and bronchitis, and worse outcome, as well as increased risk of developing tuberculosis if exposed to a carrier. In the United States, it is estimated that second-hand 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.
Impaired respiratory function and slowed lung growth
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.
Exposure to secondhand smoke by age, race, and poverty level in the US.
Epidemiological studies show that non-smokers exposed to second-hand smoke are at risk for many of the health problems associated with direct smoking. Most of the research has come from studies of nonsmokers who are married to a smoker. Those conclusions are also backed up by further studies of workplace exposure to smoke.
In 1992, a review estimated that second-hand smoke exposure was responsible for 35,000 to 40,000 deaths per year in the United States in the early 1980s. 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 second-hand smoke exposure increased the risk of heart disease by a quarter, and two 1999 meta-analyses reached similar conclusions.
Evidence shows that inhaled sidestream smoke, the main component of second-hand 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. Some scientists believe that the risk of passive smoking, in particular the risk of developing coronary heart diseases, may have been substantially underestimated.
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 percent among non-smokers who lived with a smoker. 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%. This conclusion has been challenged on the basis that the assumption that 40% of all studies are unpublished was "extreme".: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. 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. 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. A 2014 meta-analysis noted that "the association between exposure to secondhand smoke and lung cancer risk is well established."
A minority of epidemiologists have found it hard to understand how second-hand 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. One proposed explanation is that second-hand 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. 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 suffer acute coronary syndromes.
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.
Subsequent meta-analyses have confirmed these findings.
The National Asthma Council of Australia cites studies showing that second-hand smoke is probably the most important indoor pollutant, especially around young children:
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 second-hand smoke has been estimated to cause between 3,000 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."
There is good observational evidence that smoke-free legislation reduces the number of hospital admissions for heart disease.
The International Agency for Research on Cancer of the World Health Organization concluded in 2004 that there was sufficient evidence that second-hand smoke caused cancer in humans. Those who work in environments where smoke is not regulated are at higher risk. Workers particularly at risk of exposure include those in installation repair and maintenance, construction and extraction, and transportation.
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%. Long term firsthand smoking increases the risk more than 1000%.
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. Biochemical tests are a much more reliable biomarker of second-hand 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.
A 2007 study in the Addictive Behaviors journal found a positive correlation between second-hand tobacco smoke exposure and concentrations of nicotine and/or biomarkers of nicotine in the body. Significant biological levels of nicotine from second-hand smoke exposure were equivalent to nicotine levels from active smoking and levels that are associated with behaviour changes due to nicotine consumption.
Cotinine, the metabolite of nicotine, is a biomarker of second-hand 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. Urinary cotinine levels have been a reliable biomarker of tobacco exposure and have been used as a reference in many epidemiological studies. However, cotinine levels found in the urine only reflect exposure 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.
Carbon monoxide (CO)
Carbon monoxide monitored via breath is also a reliable biomarker of second-hand 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). Breath CO monitors can also be used by emergency services to identify patients who are suspected of having CO poisoning.
Second-hand 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.
Second-hand 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. Exposure to tobacco smoke for 30 minutes significantly reduces coronary flow velocity reserve in healthy nonsmokers. Second-hand smoke is also associated with impaired vasodilation among adult nonsmokers. Second-hand smoke exposure also affects platelet function, vascular endothelium, and myocardial exercise tolerance at levels commonly found in the workplace.
Pulmonary emphysema can be induced in rats through acute exposure to sidestream tobacco smoke (30 cigarettes per day) over a period of 45 days. Degranulation of mast cells contributing to lung damage has also been observed.
The term "third-hand smoke" was recently coined to identify the residual tobacco smoke contamination that remains after the cigarette is extinguished and second-hand smoke has cleared from the air. Preliminary research suggests that by-products of third-hand smoke may pose a health risk, 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.
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 second-hand tobacco smoke, carcinogens including radon, and other indoor air pollutants.
Opinion of public health authorities
There is widespread scientific consensus that exposure to second-hand smoke is harmful. The link between passive smoking and health risks is accepted by every major medical and scientific organisation, including:
Recent major surveys conducted by the U.S. National Cancer Institute and Centers for Disease Control have found widespread public awareness that second-hand smoke is harmful. In both 1992 and 2000 surveys, more than 80% of respondents agreed with the statement that second-hand smoke was harmful. A 2001 study found that 95% of adults agreed that second-hand smoke was harmful to children, and 96% considered tobacco-industry claims that second-hand smoke was not harmful to be untruthful.
A 2007 Gallup poll found that 56% of respondents felt that second-hand smoke was "very harmful", a number that has held relatively steady since 1997. Another 29% believe that second-hand smoke is "somewhat harmful"; 10% answered "not too harmful", while 5% said "not at all harmful".
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 second-hand 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.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.
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. 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." This paper was widely promoted by the tobacco industry as evidence that the harms of passive smoking were unproven. 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. Notably, the study had failed to identify a comparison group of "unexposed" persons.
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." 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." The Court found that the study had been funded and managed by the Center for Indoor Air Research, 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." 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."
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. They concluded that exposure to second-hand 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.
Gio Batta Gori, a tobacco industry spokesman and consultant and an expert on risk utility and scientific research, wrote in the libertarianCato Institute's magazine Regulation that "...of the 75 published studies of ETS and lung cancer, some 70 percent did not report statistically significant differences of risk and are moot. Roughly 17 percent claim an increased risk and 13 percent imply a reduction of risk."
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."
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". 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.
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 second-hand smoke and heart disease. Both of these papers reported no association between second-hand smoke and heart disease. 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.
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 and The Economist, among other sources, 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. 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." 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.
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. 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.
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. 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 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."
Tobacco-industry funding of research
The tobacco industry's role in funding scientific research on second-hand smoke has been controversial. A review of published studies found that tobacco-industry affiliation was strongly correlated with findings exonerating second-hand smoke; researchers affiliated with the tobacco industry were 88 times more likely than independent researchers to conclude that second-hand smoke was not harmful. 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 second-hand smoke in sudden infant death syndrome. 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.
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." 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.
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."
Tobacco industry response
Measures to tackle second-hand 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 second-hand smoke as "the most dangerous development to the viability of the tobacco industry that has yet occurred." 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."
Accordingly, the tobacco industry have developed several strategies to minimise the impact on their business:
The industry has sought to position the second-hand smoke debate as essentially concerned with civil liberties and smokers' rights rather than with health, by funding groups such as FOREST.
Funding bias in research; in all reviews of the effects of second-hand smoke on health published between 1980 and 1995, the only factor associated with concluding that second-hand smoke is not harmful was whether an author was affiliated with the tobacco industry. However, not all studies that failed to find evidence of harm were by industry-affiliated authors.
Delaying and discrediting legitimate research (see for an example of how the industry attempted to discredit Takeshi Hirayama's landmark study, and 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.
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".
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." 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."
Position of major tobacco companies
The positions of major tobacco companies on the issue of second-hand smoke is somewhat varied. In general, tobacco companies have continued to focus on questioning the methodology of studies showing that second-hand smoke is harmful. Some (such as British American Tobacco and Philip Morris) acknowledge the medical consensus that second-hand 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.
conspired to minimize, distort and confuse the public about the health hazards of smoking;
publicly denied, while internally acknowledging, that second-hand 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 second-hand 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.
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.
As a consequence of the health risks associated with second-hand smoke, smoke-free regulations in indoor public places, including restaurants, cafés, and nightclubs have been introduced in a number of jurisdictions, at national or local level, as well as some outdoor open areas.Ireland was the first country in the world to institute a comprehensive national smoke-free law 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) The parties to the FCTC have further adopted Guidelines on the Protection from Exposure to Second-hand 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."
Opinion polls have shown considerable support for smoke-free laws. In June 2007, a survey of 15 countries found 80% approval for smoke-free laws. A survey in France, reputedly a nation of smokers, showed 70% support.
Smoking bans by governments result in decreased harm from second hand smoke including decrease cardiovascular disease. 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 second-hand smoke exposure. 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. A 2016 review also found benefits of decrease exposure to smoke from specific location policies.
In 2001, a systematic review for the Guide to Community Preventative Services acknowledged strong evidence of the effectiveness of smoke-free policies and restrictions in reducing expose to second-hand 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.
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.
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. The result of this smoke-free law provides a considerably more healthy work environment for the staff.
Recent surveys taken by the Society for Research on Nicotine and Tobacco demonstrates 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 reasons for supporting the polices 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.
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. 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. However, not all critics have connections to the industry.
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. The IARC monographs conclude that mice with prolonged exposure to simulated environmental tobacco smoke, that is 6hrs a day, 5 days a week, for five months with a subsequent 4 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.
Second-hand smoke is popularly recognised as a risk factor for cancer in pets. 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. 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. 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.
As of 2003, "secondhand smoke" was the term most used to refer to other people's smoke in the English-language media. Other terms used include "environmental tobacco smoke", while "involuntary smoking" and "passive smoking" are used to refer to exposure to secondhand smoke. 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. The Surgeon General 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.":9 Most researchers consider the term "passive smoking" to be synonymous with "secondhand smoke". 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.
^ abcDiethelm P, McKee M (February 2006). "Lifting the smokescreen: Tobacco industry strategy to defeat smoke free policies and legislation"(PDF). European Respiratory Society and Institut National du Cancer. Archived from the original(PDF) on 3 March 2016. Retrieved 2009-01-17. The industry quickly realised that, if it wanted to continue to prosper, it became vital that research did not demonstrate that tobacco smoke was a dangerous community air pollutant. This requirement has been the central pillar of its passive smoking policy from the early 1970s to the present day
^Alberg, Anthony J.; Brock, Malcolm V.; Ford, Jean G.; Samet, Jonathan M.; Spivack, Simon D. (1 May 2013). "Epidemiology of Lung Cancer". CHEST Journal. 143 (5_suppl): e1S. doi:10.1378/chest.12-2345.
^Bhatnagar, A; Whitsel, LP; Ribisl, KM; Bullen, C; Chaloupka, F; Piano, MR; Robertson, RM; McAuley, T; Goff, D; Benowitz, N; American Heart Association Advocacy Coordinating Committee, Council on Cardiovascular and Stroke Nursing, Council on Clinical Cardiology, and Council on Quality of Care and Outcomes, Research (14 October 2014). "Electronic cigarettes: a policy statement from the American Heart Association". Circulation. 130 (16): 1418–36. doi:10.1161/CIR.0000000000000107. PMID25156991.
^Macacu, A; Autier, P; Boniol, M; Boyle, P (November 2015). "Active and passive smoking and risk of breast cancer: a meta-analysis". Breast Cancer Research and Treatment. 154 (2): 213–24. doi:10.1007/s10549-015-3628-4. PMID26546245.
^Zhou, J; Wellenius, GA; Michaud, DS (December 2012). "Environmental tobacco smoke and the risk of pancreatic cancer among non-smokers: a meta-analysis". Occupational and Environmental Medicine. 69 (12): 853–7. doi:10.1136/oemed-2012-100844. PMID22843437.
^Cumberbatch, Marcus G.; Rota, Matteo; Catto, James W.F.; La Vecchia, Carlo (September 2016). "The Role of Tobacco Smoke in Bladder and Kidney Carcinogenesis: A Comparison of Exposures and Meta-analysis of Incidence and Mortality Risks". European Urology. 70 (3): 458–466. doi:10.1016/j.eururo.2015.06.042.
^Lv, X; Sun, J; Bi, Y; Xu, M; Lu, J; Zhao, L; Xu, Y (15 November 2015). "Risk of all-cause mortality and cardiovascular disease associated with secondhand smoke exposure: a systematic review and meta-analysis.". International journal of cardiology. 199: 106–15. doi:10.1016/j.ijcard.2015.07.011. PMID26188829.
^Dinas, PC; Koutedakis, Y; Flouris, AD (20 February 2013). "Effects of active and passive tobacco cigarette smoking on heart rate variability". International Journal of Cardiology. 163 (2): 109–15. doi:10.1016/j.ijcard.2011.10.140. PMID22100604.
^Zou N, Hong J, Dai QY (February 2009). "Passive cigarette smoking induces inflammatory injury in human arterial walls". Chin. Med. J. 122 (4): 444–8. PMID19302752.
^Oono, I. P.; Mackay, D. F.; Pell, J. P. (21 March 2011). "Meta-analysis of the association between secondhand smoke exposure and stroke". Journal of Public Health. 33 (4): 496–502. doi:10.1093/pubmed/fdr025. PMID21422014.
^Bentayeb, M; Simoni, M; Norback, D; Baldacci, S; Maio, S; Viegi, G; Annesi-Maesano, I (2013). "Indoor air pollution and respiratory health in the elderly". Journal of Environmental Science and Health, Part A. 48 (14): 1783–9. doi:10.1080/10934529.2013.826052. PMID24007433.
^Dogar, OF; Pillai, N; Safdar, N; Shah, SK; Zahid, R; Siddiqi, K (November 2015). "Second-hand smoke and the risk of tuberculosis: a systematic review and a meta-analysis". Epidemiology and Infection. 143 (15): 3158–72. doi:10.1017/S0950268815001235. PMID26118887.
^Hur, Kevin; Liang, Jonathan; Lin, Sandra Y. (January 2014). "The role of secondhand smoke in sinusitis: a systematic review". International Forum of Allergy & Rhinology. 4 (1): 22–28. doi:10.1002/alr.21232.
^Chen, R; Hu, Z; Orton, S; Chen, RL; Wei, L (December 2013). "Association of passive smoking with cognitive impairment in nonsmoking older adults: a systematic literature review and a new study of Chinese cohort". Journal of Geriatric Psychiatry and Neurology. 26 (4): 199–208. doi:10.1177/0891988713496165. PMID23877565.
^Zeng, Yan-Ni; Li, Ya-Min (10 December 2015). "Secondhand smoke exposure and mental health in adults: a meta-analysis of cross-sectional studies". Social Psychiatry and Psychiatric Epidemiology. 51 (9): 1339–48. doi:10.1007/s00127-015-1164-5. PMID26661619.
^Cui, H; Gong, TT; Liu, CX; Wu, QJ (25 January 2016). "Associations between Passive Maternal Smoking during Pregnancy and Preterm Birth: Evidence from a Meta-Analysis of Observational Studies.". PLoS One. 11 (1): e0147848. doi:10.1371/journal.pone.0147848. PMID26808045.
^Been, Jasper; Nurmatov, U. B.; Cox, B; Nawrot, T. S.; Van Schayck, C. P.; Sheikh, A (28 March 2014). "Effect of smoke-free legislation on perinatal and child health: a systematic review and meta-analysis". Lancet. 383 (9928): 1549–60. doi:10.1016/S0140-6736(14)60082-9. PMID24680633.
^Leonardi-Bee, J; Britton, J; Venn, A (April 2011). "Secondhand smoke and adverse fetal outcomes in nonsmoking pregnant women: a meta-analysis". Pediatrics. 127 (4): 734–41. doi:10.1542/peds.2010-3041. PMID21382949.
^Salmasi G, Grady R, Jones J, McDonald SD (2010). "Environmental tobacco smoke exposure and perinatal outcomes: a systematic review and meta-analyses". Acta Obstet Gynecol Scand. 89 (4): 423–41. doi:10.3109/00016340903505748. PMID20085532.
^Janson C (2004). "The effect of passive smoking on respiratory health in children and adults". Int J Tuberc Lung Dis. 8 (5): 510–6. PMID15137524.
^Wei, X; E, M; Yu, S (January 2015). "A meta-analysis of passive smoking and risk of developing Type 2 Diabetes Mellitus". Diabetes research and clinical practice. 107 (1): 9–14. doi:10.1016/j.diabres.2014.09.019. PMID25488377.
^Sun, K; Liu, D; Wang, C; Ren, M; Yang, C; Yan, L (November 2014). "Passive smoke exposure and risk of diabetes: a meta-analysis of prospective studies". Endocrine. 47 (2): 421–7. doi:10.1007/s12020-014-0194-1. PMID24532101.
^Pan, An; Wang, Yeli; Talaei, Mohammad; Hu, Frank B; Wu, Tangchun (December 2015). "Relation of active, passive, and quitting smoking with incident type 2 diabetes: a systematic review and meta-analysis". The Lancet Diabetes & Endocrinology. 3 (12): 958–967. doi:10.1016/S2213-8587(15)00316-2. PMID26388413.
^Kantor, R; Kim, A; Thyssen, JP; Silverberg, JI (December 2016). "Association of atopic dermatitis with smoking: A systematic review and meta-analysis.". Journal of the American Academy of Dermatology. 75 (6): 1119–1125.e1. doi:10.1016/j.jaad.2016.07.017. PMID27542586.
^Anderson, HR; Cook, DG (November 1997). "Passive smoking and sudden infant death syndrome: review of the epidemiological evidence". Thorax. 52 (11): 1003–9. doi:10.1136/thx.52.11.1003. PMID9487351.
^Tinuoye, O.; Pell, J. P.; Mackay, D. F. (28 March 2013). "Meta-Analysis of the Association Between Secondhand Smoke Exposure and Physician-Diagnosed Childhood Asthma". Nicotine & Tobacco Research. 15 (9): 1475–1483. doi:10.1093/ntr/ntt033.
^Wang, Zhen; May, Sara M.; Charoenlap, Suvanee; Pyle, Regan; Ott, Nancy L.; Mohammed, Khaled; Joshi, Avni Y. (November 2015). "Effects of secondhand smoke exposure on asthma morbidity and health care utilization in children: a systematic review and meta-analysis". Annals of Allergy, Asthma & Immunology. 115 (5): 396–401.e2. doi:10.1016/j.anai.2015.08.005.
^ abChatzimichael A, Tsalkidis A, Cassimos D, et al. (2007). "The role of breastfeeding and passive smoking on the development of severe bronchiolitis in infants". Minerva Pediatr. 59 (3): 199–206. PMID17519864.
^Jafta, N; Jeena, PM; Barregard, L; Naidoo, RN (May 2015). "Childhood tuberculosis and exposure to indoor air pollution: a systematic review and meta-analysis". The International Journal of Tuberculosis and Lung Disease. 19 (5): 596–602. doi:10.5588/ijtld.14.0686. PMID25868030.
^Feleszko, W; Ruszczyński, M; Jaworska, J; Strzelak, A; Zalewski, BM; Kulus, M (November 2014). "Environmental tobacco smoke exposure and risk of allergic sensitisation in children: a systematic review and meta-analysis". Archives of Disease in Childhood. 99 (11): 985–92. doi:10.1136/archdischild-2013-305444. PMID24958794.
^Jones, DT; Osterman, MT; Bewtra, M; Lewis, JD (September 2008). "Passive smoking and inflammatory bowel disease: a meta-analysis". The American Journal of Gastroenterology. 103 (9): 2382–93. doi:10.1111/j.1572-0241.2008.01999.x. PMID18844625.
^Chen, R; Clifford, A; Lang, L; Anstey, KJ (October 2013). "Is exposure to secondhand smoke associated with cognitive parameters of children and adolescents?—a systematic literature review". Annals of Epidemiology. 23 (10): 652–61. doi:10.1016/j.annepidem.2013.07.001. PMID23969303.
^Wang, Meng; Wang, Zhi-Ping; Zhang, Meng; Zhao, Zhong-Tang (13 August 2013). "Maternal passive smoking during pregnancy and neural tube defects in offspring: a meta-analysis". Archives of Gynecology and Obstetrics. 289 (3): 513–521. doi:10.1007/s00404-013-2997-3.
^Pineles, B. L.; Park, E.; Samet, J. M. (10 February 2014). "Systematic Review and Meta-Analysis of Miscarriage and Maternal Exposure to Tobacco Smoke During Pregnancy". American Journal of Epidemiology. 179 (7): 807–823. doi:10.1093/aje/kwt334.
^Chiswell, C; Akram, Y (February 2017). "Impact of environmental tobacco smoke exposure on anaesthetic and surgical outcomes in children: a systematic review and meta-analysis.". Archives of Disease in Childhood. 102 (2): 123–130. doi:10.1136/archdischild-2016-310687. PMID27417307.
^Jara, SM; Benke, JR; Lin, SY; Ishman, SL (January 2015). "The association between secondhand smoke and sleep-disordered breathing in children: a systematic review.". The Laryngoscope. 125 (1): 241–7. doi:10.1002/lary.24833. PMID25130300.
^He, J; Vupputuri, S; Allen, K; Prerost, MR; Hughes, J; Whelton, PK (25 March 1999). "Passive smoking and the risk of coronary heart disease—a meta-analysis of epidemiologic studies". The New England Journal of Medicine. 340 (12): 920–6. doi:10.1056/nejm199903253401204. PMID10089185.
^Schick SF, Glantz S (2007). "Concentrations of the carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in sidestream cigarette smoke increase after release into indoor air: results from unpublished tobacco industry research". Cancer Epidemiol. Biomarkers Prev. 16 (8): 1547–53. doi:10.1158/1055-9965.EPI-07-0210. PMID17684127.
^Copas, J B (12 February 2000). "Reanalysis of epidemiological evidence on lung cancer and passive smoking". BMJ. 320 (7232): 417–418. doi:10.1136/bmj.320.7232.417.
^Takagi, H; Sekino, S; Kato, T; Matsuno, Y; Umemoto, T (February 2006). "Revisiting evidence on lung cancer and passive smoking: adjustment for publication bias by means of "trim and fill" algorithm". Lung Cancer (Amsterdam, Netherlands). 51 (2): 245–6. doi:10.1016/j.lungcan.2005.11.004. PMID16386820.
^Zhong, L; Goldberg, MS; Parent, ME; Hanley, JA (January 2000). "Exposure to environmental tobacco smoke and the risk of lung cancer: a meta-analysis". Lung Cancer (Amsterdam, Netherlands). 27 (1): 3–18. doi:10.1016/S0169-5002(99)00093-8. PMID10672779.
^Taylor, Richard; Gumming, Robert; Woodward, Alistair; Black, Megan (June 2001). "Passive smoking and lung cancer: a cumulative meta-analysis". Australian and New Zealand Journal of Public Health. 25 (3): 203–211. doi:10.1111/j.1467-842X.2001.tb00564.x. PMID11494987.
^Kim, CH; Lee, YC; Hung, RJ; McNallan, SR; Cote, ML; Lim, WY; Chang, SC; Kim, JH; Ugolini, D; Chen, Y; Liloglou, T; Andrew, AS; Onega, T; Duell, EJ; Field, JK; Lazarus, P; Le Marchand, L; Neri, M; Vineis, P; Kiyohara, C; Hong, YC; Morgenstern, H; Matsuo, K; Tajima, K; Christiani, DC; McLaughlin, JR; Bencko, V; Holcatova, I; Boffetta, P; Brennan, P; Fabianova, E; Foretova, L; Janout, V; Lissowska, J; Mates, D; Rudnai, P; Szeszenia-Dabrowska, N; Mukeria, A; Zaridze, D; Seow, A; Schwartz, AG; Yang, P; Zhang, ZF (15 October 2014). "Exposure to secondhand tobacco smoke and lung cancer by histological type: a pooled analysis of the International Lung Cancer Consortium (ILCCO)". International Journal of Cancer. Journal International Du Cancer. 135 (8): 1918–30. doi:10.1002/ijc.28835. PMID24615328.
^Raupach T, Schäfer K, Konstantinides S, Andreas S (2006). "Secondhand smoke as an acute threat for the cardiovascular system: a change in paradigm". European Heart Journal. 27 (4): 386–392. doi:10.1093/eurheartj/ehi601. PMID16230308.
^Meyers, DG; Neuberger, JS; He, J (29 September 2009). "Cardiovascular effect of bans on smoking in public places: a systematic review and meta-analysis". Journal of the American College of Cardiology. 54 (14): 1249–55. doi:10.1016/j.jacc.2009.07.022. PMID19778665.
^Klesges RC, Debon M, Ray JW (October 1995). "Are self-reports of smoking rate biased? Evidence from the Second National Health and Nutrition Examination Survey". J Clin Epidemiol. 48 (10): 1225–33. doi:10.1016/0895-4356(95)00020-5. PMID7561984.
^Otsuka R, Watanabe H, Hirata K, et al. (2001). "Acute effects of passive smoking on the coronary circulation in healthy young adults". JAMA. 286 (4): 436–41. doi:10.1001/jama.286.4.436. PMID11466122.
^Celermajer, David S.; Adams, Mark R.; Clarkson, Peter; Robinson, Jacqui; McCredie, Robyn; Donald, Ann; Deanfield, John E. (18 January 1996). "Passive Smoking and Impaired Endothelium-Dependent Arterial Dilatation in Healthy Young Adults". New England Journal of Medicine. 334 (3): 150–155. doi:10.1056/NEJM199601183340303.
^ abBoffetta P, Agudo A, Ahrens W, et al. (1998). "Multicenter case-control study of exposure to environmental tobacco smoke and lung cancer in Europe". J. Natl. Cancer Inst. 90 (19): 1440–50. doi:10.1093/jnci/90.19.1440. PMID9776409.
^Tong EK, England L, Glantz SA (2005). "Changing conclusions on secondhand smoke in a sudden infant death syndrome review funded by the tobacco industry". Pediatrics. 115 (3): e356–66. doi:10.1542/peds.2004-1922. PMID15741361.
^Garne D, Watson M, Chapman S, Byrne F (2005). "Environmental tobacco smoke research published in the journal Indoor and Built Environment and associations with the tobacco industry". Lancet. 365 (9461): 804–9. doi:10.1016/S0140-6736(05)17990-2. PMID15733724.
^The most current positions of major tobacco companies on the issue of passive smoking can be found on their websites. As of 13 January 2009, the following websites contain tobacco-industry positions on the topic:
^Frazer, K; McHugh, J; Callinan, JE; Kelleher, C (27 May 2016). "Impact of institutional smoking bans on reducing harms and secondhand smoke exposure". The Cochrane database of systematic reviews (5): CD011856. doi:10.1002/14651858.CD011856.pub2. PMID27230795.
^Hopkins DP, Razi S, Leeks KD, Priya Kalra G, Chattopadhyay SK, Soler RE (2010). "Smokefree policies to reduce tobacco use. A systematic review". Am J Prev Med. 38 (2 Suppl): S275–89. doi:10.1016/j.amepre.2009.10.029. PMID20117612.
^Barnoya J, Arvizu M, Jones MR, Hernandez JC, Breysse PN, Navas-Acien A (November 2010). "Secondhand smoke exposure in bars and restaurants in Guatemala City: before and after smoking ban evaluation". Cancer Causes Control. 22 (1): 151–6. doi:10.1007/s10552-010-9673-8. PMID21046446.
^Snyder LA, Bertone ER, Jakowski RM, Dooner MS, Jennings-Ritchie J, Moore AS (2004). "p53 expression and environmental tobacco smoke exposure in feline oral squamous cell carcinoma". Vet Pathol. 41 (3): 209–14. doi:10.1354/vp.41-3-209. PMID15133168.
^Bertone ER, Snyder LA, Moore AS (2002). "Environmental Tobacco Smoke and Risk of Malignant Lymphoma in Pet Cats". American Journal of Epidemiology. 156 (3): 268–273. doi:10.1093/aje/kwf044. PMID12142262.
^Reif JS, Dunn K, Ogilvie GK, Harris CK (1992). "Passive smoking and canine lung cancer risk". Am J Epidemiol. 135 (3): 234–9. PMID1546698.