Department of Health and Human Services

The Health Consequences

of Involuntary Exposure

to Tobacco Smoke

A Report of the Surgeon General
Centers for Disease Control and Prevention

Coordinating Center for Health Promotion

National Center for Chronic Disease Prevention and Health Promotion

Office on Smoking and Health

Suggested Citation

U.S. Department of Health and Human Services. The Health Consequences of Involuntary 

Exposure to Tobacco Smoke: A Report of the Surgeon General—Executive Summary.

U.S. Department of Health and Human Services, Centers for Disease Control and 

Prevention, Coordinating Center for Health Promotion, National Center for Chronic 

Disease Prevention and Health Promotion, Office on Smoking and Health, 2006

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U.S. Department of Health and Human Services.
The Health Consequences

of Involuntary Exposure 

to Tobacco Smoke

A Report of the Surgeon General

2006

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES

Public Health Service

Office of the Surgeon General

Rockville, MD
Message from Michael O. Leavitt

Secretary of Health and Human Services

This Surgeon General’s report returns to the topic of the health effects of involuntary exposure to tobacco smoke. The last comprehensive review of this evidence by the Department of 

Health and Human Services (DHHS) was in the 1986 Surgeon General’s report, The Health Consequences of Involuntary Smoking, published 20 years ago this year. This new report updates the 

evidence of the harmful effects of involuntary exposure to tobacco smoke. This large body of 

research findings is captured in an accompanying dynamic database that profiles key epidemiologic findings, and allows the evidence on health effects of exposure to tobacco smoke to 

be synthesized and updated (following the format of the 2004 report, The Health Consequences 

of Smoking). The database enables users to explore the data and studies supporting the conclusions in the report. The database is available on the Web site of the Centers for Disease Control 

and Prevention (CDC) at http://www.cdc.gov/tobacco. I am grateful to the leadership of the 

Surgeon General, CDC’s Office on Smoking and Health, and all of the contributors for preparing 

this important report and bringing this topic to the forefront once again.

Secondhand smoke, also known as environmental tobacco smoke, is a mixture of the smoke 

given off by the burning end of tobacco products (sidestream smoke) and the mainstream smoke 

exhaled by smokers. People are exposed to secondhand smoke at home, in the workplace, and in 

other public places such as bars, restaurants, and recreation venues. It is harmful and hazardous 

to the health of the general public and particularly dangerous to children. It increases the risk 

of serious respiratory problems in children, such as a greater number and severity of asthma 

attacks and lower respiratory tract infections, and increases the risk for middle ear infections. 

It is also a known human carcinogen (cancer-causing agent). Inhaling secondhand smoke causes 

lung cancer and coronary heart disease in nonsmoking adults.

We have made great progress since the late 1980s in reducing the involuntary exposure of 

nonsmokers in this country to secondhand smoke. The proportion of nonsmokers aged 4 and 

older with a blood cotinine level (a metabolite of nicotine) indicating exposure has declined 

from 88 percent in 1988–1991 down to 43 percent in 2001–2002, a decline that exceeds the Healthy 

People 2010 objective for this measure. Despite the great progress that has been made, involuntary exposure to secondhand smoke remains a serious public health hazard that can 

be prevented by making homes, workplaces, and public places completely smoke-free. 

As of the year 2000, more than 126 million residents of the United States aged 3 or older 

still are estimated to be exposed to secondhand smoke. Smoke-free environments are 

the most effective method for reducing exposures. Healthy People 2010 objectives address 

this issue and seek optimal protection of nonsmokers through policies, regulations, and laws 

requiring smoke-free environments in all schools, workplaces, and public places.
Foreword

This twenty-ninth report of the Surgeon General documents the serious and 

deadly health effects of involuntary exposure to tobacco smoke. Secondhand smoke is 

a major cause of disease, including lung cancer and coronary heart disease, in healthy 

nonsmokers.

In 2005, it was estimated that exposure to secondhand smoke kills more than 

3,000 adult nonsmokers from lung cancer, approximately 46,000 from coronary heart disease, and an estimated 430 newborns from sudden infant death syndrome. In addition, 

secondhand smoke causes other respiratory problems in nonsmokers such as coughing, 

phlegm, and reduced lung function. According to the CDC’s National Health Interview 

Survey in 2000, more than 80 percent of the respondents aged 18 years or older believe that 

secondhand smoke is harmful and nonsmokers should be protected in their workplaces.

Components of chemical compounds in secondhand smoke, including nicotine, carbon monoxide, and tobacco-specific carcinogens, can be detected in body fluids of exposed 

nonsmokers. These exposures can be controlled. In 2005, CDC released the Third National 

Report on Human Exposure to Environmental Chemicals, which found that the median cotinine level (a metabolite of nicotine) in nonsmokers had decreased across the life stages: by 

68 percent in children, 69 percent in adolescents, and 75 percent in adults, when samples 

collected between 1999 and 2002 were compared with samples collected a decade earlier. 

These dramatic declines are further evidence that smoking restrictions in public places and 

workplaces are helping to ensure a healthier life for all people in the United States. 

However, too many people continue to be exposed, especially children. The recent 

data indicate that median cotinine levels in children are more than twice those of adults, 

and non-Hispanic blacks have levels that are more than twice as high as those of Mexican 

Americans and non-Hispanic whites. These disparities need to be better understood and 

addressed.

Research reviewed in this report indicates that smoke-free policies are the most 

economic and effective approach for providing protection from exposure to secondhand 

smoke. But do they provide the greatest health impact. Separating smokers and nonsmokers in the same airspace is not effective, nor is air cleaning or a greater exchange of indoor 

with outdoor air. Additionally, having separately ventilated areas for smoking may not 

offer a satisfactory solution to reducing workplace exposures. Policies prohibiting smoking in the workplace have multiple benefits. Besides reducing exposure of nonsmokers 

to secondhand smoke, these policies reduce tobacco use by smokers and change public 

attitudes about tobacco use from acceptable to unacceptable. 

Research indicates that the progressive restriction of smoking in the United States to 

protect nonsmokers has had the additional health impact of reducing active smoking. In 

November 2005, CDC’s Tobacco-Free Campus policy took full effect in all facilities owned 

by CDC in the Atlanta area. As the Director of the nation’s leading health promotion and 

disease prevention agency, I am proud to support this effort. With this commitment, CDC 

continues to protect the health and safety of all of its employees and serves as a role model 

for workplaces everywhere.

Julie Louise Gerberding, M.D., M.P.H.

Director

Centers for Disease Control and Prevention

and

Administrator

Agency for Toxic Substances and Disease Registry

i

Preface

from the Surgeon General,

U.S. Department of Health and Human Services

Twenty years ago when Dr. C. Everett Koop released the Surgeon General’s report, 

The Health Consequences of Involuntary Smoking, it was the first Surgeon General’s report to 

conclude that involuntary exposure of nonsmokers to tobacco smoke causes disease. The 

topic of involuntary exposure of nonsmokers to secondhand smoke was first considered 

in Surgeon General Jesse Steinfeld’s 1972 report, and by 1986, the causal linkage between 

inhaling secondhand smoke and the risk for lung cancer was clear. By then, there was also 

abundant evidence of adverse effects of smoking by parents on their children. 

Today, massive and conclusive scientific evidence documents adverse effects of 

involuntary smoking on children and adults, including cancer and cardiovascular diseases 

in adults, and adverse respiratory effects in both children and adults. This 2006 report of 

the Surgeon General updates the 1986 report, The Health Consequences of Involuntary Smoking, and provides a detailed review of the epidemiologic evidence on the health effects of 

involuntary exposure to tobacco smoke. This new report also uses the revised standard 

language of causality that was applied in the 2004 Surgeon General’s report, The Health 

Consequences of Smoking. 

Secondhand smoke is similar to the mainstream smoke inhaled by the smoker in 

that it is a complex mixture containing many chemicals (including formaldehyde, cyanide, 

carbon monoxide, ammonia, and nicotine), many of which are known carcinogens. Exposure to secondhand smoke causes excess deaths in the U.S. population from lung cancer 

and cardiac related illnesses. Fortunately, exposures of adults are declining as smoking 

becomes increasingly restricted in workplaces and public places. Unfortunately, children 

continue to be exposed in their homes by the smoking of their parents and other adults. 

This exposure leads to unnecessary cases of bronchitis, pneumonia and worsened asthma. 

Among children younger than 18 years of age, an estimated 22 percent are exposed to secondhand smoke in their homes, with estimates ranging from 11.7 percent in Utah to 34.2 

percent in Kentucky. 

As this report documents, exposure to secondhand smoke remains an alarming public health hazard. Approximately 60 percent of nonsmokers in the United States have biologic evidence of exposure to secondhand smoke. Yet compared with data reviewed in the 

1986 report, I am encouraged by the progress that has been made in reducing involuntary 

exposure in many workplaces, restaurants, and other public places. These changes are 

most likely the major contributing factors to the more than 75 percent reduction in serum 

cotinine levels that researchers have observed from 1988 to 1991. However, more than 126 

million nonsmokers are still exposed. We now have substantial evidence on the efficacy 

of different approaches to control exposure to secondhand smoke. Restrictions on smoking can control exposures effectively, but technical approaches involving air cleaning or 

a greater exchange of indoor with outdoor air cannot. Consequently, nonsmokers need 

protection through the restriction of smoking in public places and workplaces and by a 

voluntary adherence to policies at home, particularly to eliminate exposures of children. 

Since the release of the 1986 Surgeon General’s report, the public’s attitude and social 

norms toward secondhand smoke exposure have changed significantly—a direct result of 

the growing body of scientific evidence on the health effects of exposure to secondhand 

smoke that is summarized in this report.

iii
Finally, clinicians should routinely ask about secondhand smoke exposure, particularly in susceptible groups or when a child has had an illness caused by secondhand 

smoke, such as pneumonia. Because of the high levels of exposure among young children, 

their exposure should be considered a significant pediatric issue. Additionally, exposure 

to secondhand smoke poses significant risks for people with lung and heart disease. The 

large body of evidence documenting that secondhand smoke exposures produce substantial and immediate effects on the cardiovascular system indicates that even brief exposures 

could pose significant acute risks to older adults or to others at high risk for cardiovascular 

disease. Those caring for relatives with heart disease should be advised not to smoke in the 

presence of the sick relative.

An environment free of involuntary exposure to secondhand smoke should remain 

an important national priority in order to reach the Healthy People 2010 objectives.

Richard Carmona, M.D., M.P.H., F.A.C.S.

Surgeon General

iv
The Health Consequences of Involuntary Exposure to Tobacco Smoke

Executive Summary 1

Executive Summary

such exposure upon the nonsmoker is available” 

(p. 11–35). The chapter concluded with recommendations for research including epidemiologic and 

clinical studies. The 1982 Surgeon General’s 

report specifically addressed smoking and cancer 

(U.S. Department of Health and Human Services 

[USDHHS] 1982). By 1982, there were three published 

epidemiologic studies on involuntary smoking and 

lung cancer, and the 1982 Surgeon General’s report 

included a brief chapter on this topic. That chapter 

commented on the methodologic difficulties inherent 

in such studies, including exposure assessment, the 

lengthy interval during which exposures are likely 

to be relevant, and accounting for exposures to other 

carcinogens. Nonetheless, the report concluded that 

“Although the currently available evidence is not sufficient to conclude that passive or involuntary smoking 

causes lung cancer in nonsmokers, the evidence does 

raise concern about a possible serious public health 

problem” (p. 251).

Involuntary smoking was also reviewed in the 

1984 report, which focused on chronic obstructive 

pulmonary disease and smoking (USDHHS 1984). 

Chapter 7 (Passive Smoking) of that report included 

a comprehensive review of the mounting information 

on smoking by parents and the effects on respiratory 

health of their children, data on irritation of the eye, 

and the more limited evidence on pulmonary effects 

of involuntary smoking on adults. The chapter began 

with a compilation of measurements of tobacco smoke 

components in various indoor environments. The 

extent of the data had increased substantially since 

1972. By 1984, the data included measurements of 

more specific indicators such as acrolein and nicotine, 

and less specific indicators such as particulate matter 

(PM), nitrogen oxides, and CO. The report reviewed 

new evidence on exposures of nonsmokers using biomarkers, with substantial information on levels of 

cotinine, a major nicotine metabolite. The report anticipated future conclusions with regard to respiratory 

effects of parental smoking on child respiratory health 

(Table 1.1).

Involuntary smoking was the topic for the entire 

1986 Surgeon General’s report, The Health Consequences of Involuntary Smoking (USDHHS 1986). In its 

359 pages, the report covered the full breadth of the 

topic, addressing toxicology and dosimetry of tobacco 

smoke; the relevant evidence on active smoking; 

The topic of passive or involuntary smoking 

was first addressed in the 1972 U.S. Surgeon General’s report (The Health Consequences of Smoking, 

U.S. Department of Health, Education, and Welfare 

[USDHEW] 1972), only eight years after the first Surgeon General’s report on the health consequences of 

active smoking (USDHEW 1964). Surgeon General 

Dr. Jesse Steinfeld had raised concerns about this 

topic, leading to its inclusion in that report. According to the 1972 report, nonsmokers inhale the mixture 

of sidestream smoke given off by a smoldering cigarette and mainstream smoke exhaled by a smoker, a 

mixture now referred to as “secondhand smoke” or 

“environmental tobacco smoke.” Cited experimental 

studies showed that smoking in enclosed spaces could 

lead to high levels of cigarette smoke components in 

the air. For carbon monoxide (CO) specifically, levels 

in enclosed spaces could exceed levels then permitted 

in outdoor air. The studies supported a conclusion that 

“an atmosphere contaminated with tobacco smoke 

can contribute to the discomfort of many individuals” 

(USDHEW 1972, p. 7). The possibility that CO emitted 

from cigarettes could harm persons with chronic heart 

or lung disease was also mentioned.

Secondhand tobacco smoke was then addressed 

in greater depth in Chapter 4 (Involuntary Smoking) 

of the 1975 Surgeon General’s report, The Health Consequences of Smoking (USDHEW 1975). The chapter noted 

that involuntary smoking takes place when nonsmokers inhale both sidestream and exhaled mainstream 

smoke and that this “smoking” is “involuntary” when 

“the exposure occurs as an unavoidable consequence 

of breathing in a smoke-filled environment” (p. 87). The 

report covered exposures and potential health consequences of involuntary smoking, and the researchers 

concluded that smoking on buses and airplanes was 

annoying to nonsmokers and that involuntary smoking had potentially adverse consequences for persons 

with heart and lung diseases. Two studies on nicotine 

concentrations in nonsmokers raised concerns about 

nicotine as a contributing factor to atherosclerotic 

cardiovascular disease in nonsmokers.

The 1979 Surgeon General’s report, Smoking 

and Health: A Report of the Surgeon General (USDHEW 

1979), also contained a chapter entitled “Involuntary 

Smoking.” The chapter stressed that “attention to 

involuntary smoking is of recent vintage, and only 

limited information regarding the health effects of 
Surgeon General’s Report

2 Executive Summary

Table 1.1 Conclusions from previous Surgeon General’s reports on the health effects of secondhand 

smoke exposure

Disease and statement

Surgeon General’s 

report

Coronary heart disease: “The presence of such levels” as found in cigarettes “indicates that 

the effect of exposure to carbon monoxide may on occasion, depending upon the length 

of exposure, be sufficient to be harmful to the health of an exposed person. This would be 

particularly significant for people who are already suffering from. . .coronary heart disease.”

(p. 7)

1972

Chronic respiratory symptoms (adults): “The presence of such levels” as found in cigarettes 

“indicates that the effect of exposure to carbon monoxide may on occasion, depending 

upon the length of exposure, be sufficient to be harmful to the health of an exposed person. 

This would be particularly significant for people who are already suffering from chronic 

bronchopulmonary disease. . . .” (p. 7)

1972

Pulmonary function: “Other components of tobacco smoke, such as particulate matter and 

the oxides of nitrogen, have been shown in various concentrations to affect adversely animal 

pulmonary. . .function. The extent of the contributions of these substances to illness in humans 

exposed to the concentrations present in an atmosphere contaminated with tobacco smoke is 

not presently known.” (pp. 7–8)

1972

Asthma: “The limited existing data yield conflicting results concerning the relationship 

between passive smoke exposure and pulmonary function changes in patients with asthma.”

(p. 13)

1984

Bronchitis and pneumonia: “The children of smoking parents have an increased prevalence of 

reported respiratory symptoms, and have an increased frequency of bronchitis and pneumonia 

early in life.” (p. 13)

1984

Pulmonary function (children): “The children of smoking parents appear to have measurable 

but small differences in tests of pulmonary function when compared with children of 

nonsmoking parents. The significance of this finding to the future development of lung disease 

is unknown.” (p. 13)

1984

Pulmonary function (adults): “. . .some studies suggest that high levels of involuntary 

[tobacco] smoke exposure might produce small changes in pulmonary function in normal 

subjects. . . . Two studies have reported differences in measures of lung function in older 

populations between subjects chronically exposed to involuntary smoking and those who were 

not. This difference was not found in a younger and possibly less exposed population.” (p. 13)

1984

Acute respiratory infections: “The children of parents who smoke have an increased 

frequency of a variety of acute respiratory illnesses and infections, including chest illnesses 

before 2 years of age and physician-diagnosed bronchitis, tracheitis, and laryngitis, when 

compared with the children of nonsmokers.” (p. 13)

1986

Bronchitis and pneumonia: “The children of parents who smoke have an increased frequency 

of hospitalization for bronchitis and pneumonia during the first year of life when compared 

with the children of nonsmokers.” (p. 13)

1986

Cancers other than lung: “The associations between cancers, other than cancer of the lung, 

and involuntary smoking require further investigation before a determination can be made 

about the relationship of involuntary smoking to these cancers.” (p. 14)

1986

Cardiovascular disease: “Further studies on the relationship between involuntary smoking 

and cardiovascular disease are needed in order to determine whether involuntary smoking 

increases the risk of cardiovascular disease.” (p. 14)

1986
The Health Consequences of Involuntary Exposure to Tobacco Smoke

Executive Summary 3

Disease and statement

Surgeon General’s 

report

Chronic cough and phlegm (children): “Chronic cough and phlegm are more frequent in 

children whose parents smoke compared with children of nonsmokers.” (p. 13)

1986

Chronic obstructive pulmonary disease (COPD): “Healthy adults exposed to environmental 

tobacco smoke may have small changes on pulmonary function testing, but are unlikely 

to experience clinically significant deficits in pulmonary function as a result of exposure to 

environmental tobacco smoke alone.” (pp. 13–14)

“The implications of chronic respiratory symptoms for respiratory health as an adult are 

unknown and deserve further study.” (p. 13)

1986

Lung cancer: “Involuntary smoking can cause lung cancer in nonsmokers.” (p. 13) 1986

Middle ear effusions: “A number of studies report that chronic middle ear effusions are more 

common in young children whose parents smoke than in children of nonsmoking parents.”

(p. 14)

1986

Pulmonary function (children): “The children of parents who smoke have small differences in 

tests of pulmonary function when compared with the children of nonsmokers. Although this 

decrement is insufficient to cause symptoms, the possibility that it may increase susceptibility 

to chronic obstructive pulmonary disease with exposure to other agents in adult life, e.g., [sic] 

active smoking or occupational exposures, needs investigation.” (p. 13)

1986

Other:

“An atmosphere contaminated with tobacco smoke can contribute to the discomfort of many 

individuals.” (p. 7)

“Cigarette smoke can make a significant, measurable contribution to the level of indoor air 

pollution at levels of smoking and ventilation that are common in the indoor environment.”

(p. 13)

“Cigarette smoke in the air can produce an increase in both subjective and objective measures 

of eye irritation.” (p. 13)

“Nonsmokers who report exposure to environmental tobacco smoke have higher levels of 

urinary cotinine, a metabolite of nicotine, than those who do not report such exposure.” (p. 13)

“The simple separation of smokers and nonsmokers within the same air space may reduce, but 

does not eliminate, the exposure of nonsmokers to environmental tobacco smoke.” (p. 13)

“Validated questionnaires are needed for the assessment of recent and remote exposure to 

environmental tobacco smoke in the home, workplace, and other environments.” (p. 14)

1972

1984

1984

1984

1986

1986

Sources: U.S. Department of Health, Education, and Welfare 1972; U.S. Department of Health and Human Services 1984, 

1986.

Table 1.1 Continued
Surgeon General’s Report

4 Executive Summary

patterns of exposure of nonsmokers to tobacco smoke; 

the epidemiologic evidence on involuntary smoking 

and disease risks for infants, children, and adults; and 

policies to control involuntary exposure to tobacco 

smoke. That report concluded that involuntary smoking caused lung cancer in lifetime nonsmoking adults 

and was associated with adverse effects on respiratory 

health in children. The report also stated that simply 

separating smokers and nonsmokers within the same 

airspace reduced but did not eliminate exposure to 

secondhand smoke. All of these findings are relevant 

to public health and public policy (Table 1.1). The lung 

cancer conclusion was based on extensive information already available on the carcinogenicity of active 

smoking, the qualitative similarities between secondhand and mainstream smoke, the uptake of tobacco 

smoke components by nonsmokers, and the epidemiologic data on involuntary smoking. The three major 

conclusions of the report (Table 1.2), led Dr. C. Everett Koop, Surgeon General at the time, to comment in 

his preface that “the right of smokers to smoke ends 

where their behavior affects the health and well-being 

of others; furthermore, it is the smokers’ responsibility to ensure that they do not expose nonsmokers to 

the potential [sic] harmful effects of tobacco smoke” 

(USDHHS 1986, p. xii).

Two other reports published in 1986 also reached 

the conclusion that involuntary smoking increased 

the risk for lung cancer. The International Agency 

for Research on Cancer (IARC) of the World Health 

Organization concluded that “passive smoking gives 

rise to some risk of cancer” (IARC 1986, p. 314). 

In its monograph on tobacco smoking, the agency 

supported this conclusion on the basis of the characteristics of sidestream and mainstream smoke, the 

absorption of tobacco smoke materials during an 

involuntary exposure, and the nature of dose-response 

relationships for carcinogenesis. In the same year, the 

National Research Council (NRC) also concluded 

that involuntary smoking increases the incidence of 

lung cancer in nonsmokers (NRC 1986). In reaching 

this conclusion, the NRC report cited the biologic 

plausibility of the association between exposure to 

secondhand smoke and lung cancer and the supporting 

epidemiologic evidence. On the basis of a pooled 

analysis of the epidemiologic data adjusted for bias, 

the report concluded that the best estimate for the 

excess risk of lung cancer in nonsmokers married to 

smokers was 25 percent, compared with nonsmokers married to nonsmokers. With regard to the effects 

of involuntary smoking on children, the NRC report 

commented on the literature linking secondhand 

smoke exposures from parental smoking to increased 

risks for respiratory symptoms and infections and to a 

slightly diminished rate of lung growth.

Since 1986, the conclusions with regard to both the 

carcinogenicity of secondhand smoke and the adverse 

effects of parental smoking on the health of children 

have been echoed and expanded (Table 1.3). In 1992, 

the U.S. Environmental Protection Agency (EPA) published its risk assessment of secondhand smoke as a carcinogen (USEPA 1992). The agency’s evaluation drew 

on toxicologic information on secondhand smoke and 

the extensive literature on active smoking. A comprehensive meta-analysis of the 31 epidemiologic studies of secondhand smoke and lung cancer published 

up to that time was central to the decision to classify 

secondhand smoke as a group A carcinogen—namely, 

a known human carcinogen. Estimates of approximately 3,000 U.S. lung cancer deaths per year in nonsmokers were attributed to secondhand smoke. The 

report also covered other respiratory health effects in 

children and adults and concluded that involuntary 

smoking is causally associated with several adverse 

Table 1.2 Major conclusions of the 1986 Surgeon General’s report, The Health Consequences of Involuntary 

Smoking

1. Involuntary smoking is a cause of disease, including lung cancer, in healthy nonsmokers.

2. The children of parents who smoke compared with the children of nonsmoking parents have an increased frequency 

of respiratory infections, increased respiratory symptoms, and slightly smaller rates of increase in lung function as the 

lung matures.

3. The simple separation of smokers and nonsmokers within the same air space may reduce, but does not eliminate, the 

exposure of nonsmokers to environmental tobacco smoke.

Source: U.S. Department of Health and Human Services 1986, p. 7.
The Health Consequences of Involuntary Exposure to Tobacco Smoke

Executive Summary 5

respiratory effects in children. There was also a quantitative risk assessment for the impact of involuntary 

smoking on childhood asthma and lower respiratory 

tract infections in young children.

In the decade since the 1992 EPA report, scientific 

panels continued to evaluate the mounting evidence 

linking involuntary smoking to adverse health effects 

(Table 1.3). The most recent was the 2005 report of the 

California EPA (Cal/EPA 2005). Over time, research 

has repeatedly affirmed the conclusions of the 1986 

Surgeon General’s reports and studies have further 

identified causal associations of involuntary smoking with diseases and other health disorders. The 

epidemiologic evidence on involuntary smoking has 

markedly expanded since 1986, as have the data on 

exposure to tobacco smoke in the many environments 

where people spend time. An understanding of the 

mechanisms by which involuntary smoking causes 

disease has also deepened.

As part of the environmental health hazard 

assessment, Cal/EPA identified specific health effects 

causally associated with exposure to secondhand 

smoke. The agency estimated the annual excess deaths 

in the United States that are attributable to secondhand smoke exposure for specific disorders: sudden 

infant death syndrome (SIDS), cardiac-related illnesses 

(ischemic heart disease), and lung cancer (Cal/EPA 

2005). For the excess incidence of other health outcomes, either new estimates were provided or estimates from the 1997 health hazard assessment were 

used without any revisions (Cal/EPA 1997). Overall, 

Cal/EPA estimated that about 50,000 excess deaths 

Table 1.3 Selected major reports, other than those of the U.S. Surgeon General, addressing adverse effects 

from exposure to tobacco smoke

Agency Publication

Place and date of 

publication

National Research Council Environmental Tobacco Smoke: Measuring Exposures and 

Assessing Health Effects

Washington, D.C.

United States

1986

International Agency for Research on 

Cancer (IARC)

Monographs on the Evaluation of the Carcinogenic 

Risk of Chemicals to Humans: Tobacco Smoking

(IARC Monograph 38)

Lyon, France

1986

U.S. Environmental Protection Agency 

(EPA)

Respiratory Health Effects of Passive Smoking: Lung 

Cancer and Other Disorders

Washington, D.C.

United States

1992

National Health and Medical Research 

Council

The Health Effects of Passive Smoking Canberra, Australia 

1997

California EPA (Cal/EPA), Office 

of Environmental Health Hazard 

Assessment

Health Effects of Exposure to Environmental Tobacco 

Smoke

Sacramento, California 

United States

1997

Scientific Committee on Tobacco and 

Health

Report of the Scientific Committee on Tobacco 

and Health

London, United 

Kingdom 

1998

World Health Organization International Consultation on Environmental Tobacco 

Smoke (ETS) and Child Health. Consultation Report

Geneva, Switzerland 

1999

IARC Tobacco Smoke and Involuntary Smoking

(IARC Monograph 83)

Lyon, France 

2004

Cal/EPA, Office of Environmental 

Health Hazard Assessment

Proposed Identification of Environmental Tobacco Smoke 

as a Toxic Air Contaminant

Sacramento, California 

United States 

2005
Surgeon General’s Report

6 Executive Summary

result annually from exposure to secondhand smoke 

(Cal/EPA 2005). Estimated annual excess deaths for 

the total U.S. population are about 3,400 (a range of 

3,423 to 8,866) from lung cancer, 46,000 (a range of 

22,700 to 69,600) from cardiac-related illnesses, and 

430 from SIDS. The agency also estimated that between 24,300 and 71,900 low birth weight or preterm deliveries, about 202,300 episodes of childhood 

asthma (new cases and exacerbations), between 

150,000 and 300,000 cases of lower respiratory illness 

in children, and about 789,700 cases of middle ear 

infections in children occur each year in the United 

States as a result of exposure to secondhand smoke.

This new 2006 Surgeon General’s report returns 

to the topic of involuntary smoking. The health effects 

of involuntary smoking have not received comprehensive coverage in this series of reports since 1986. 

Reports since then have touched on selected aspects 

of the topic: the 1994 report on tobacco use among 

young people (USDHHS 1994), the 1998 report on 

tobacco use among U.S. racial and ethnic minorities 

(USDHHS 1998), and the 2001 report on women and 

smoking (USDHHS 2001). As involuntary smoking 

remains widespread in the United States and elsewhere, the preparation of this report was motivated 

by the persistence of involuntary smoking as a public 

health problem and the need to evaluate the substantial new evidence reported since 1986. This report substantially expands the list of topics that were included 

in the 1986 report. Additional topics include SIDS, 

developmental effects, and other reproductive effects; 

heart disease in adults; and cancer sites beyond the 

lung. For some associations of involuntary smoking 

with adverse health effects, only a few studies were 

reviewed in 1986 (e.g., ear disease in children); now, 

the relevant literature is substantial. Consequently, this 

report uses meta-analysis to quantitatively summarize 

evidence as appropriate. Following the approach used 

in the 2004 report (The Health Consequences of Smoking, 

USDHHS 2004), this 2006 report also systematically 

evaluates the evidence for causality, judging the 

extent of the evidence available and then making an 

inference as to the nature of the association.

Organization of the Report 

This twenty-ninth report of the Surgeon General examines the topics of toxicology of secondhand 

smoke, assessment and prevalence of exposure to 

secondhand smoke, reproductive and developmental health effects, respiratory effects of exposure to 

secondhand smoke in children and adults, cancer 

among adults, cardiovascular diseases, and the control of secondhand smoke exposure.

This introductory chapter (Chapter 1) includes a 

discussion of the concept of causation and introduces 

concepts of causality that are used throughout this 

report; this chapter also summarizes the major conclusions of the report. Chapter 2 (Toxicology of Secondhand Smoke) sets out a foundation for interpreting 

the observational evidence that is the focus of most 

of the following chapters. The discussion details the 

mechanisms that enable tobacco smoke components 

to injure the respiratory tract and cause nonmalignant 

and malignant diseases and other adverse effects. 

Chapter 3 (Assessment of Exposure to Secondhand 

Smoke) provides a perspective on key factors that 

determine exposures of people to secondhand smoke 

in indoor environments, including building designs 

and operations, atmospheric markers of secondhand 

smoke, exposure models, and biomarkers of exposure 

to secondhand smoke. Chapter 4 (Prevalence of Exposure to Secondhand Smoke) summarizes findings that 

focus on nicotine measurements in the air and cotinine measurements in biologic materials. The chapter 

includes exposures in the home, workplace, public 

places, and special populations. Chapter 5 (Reproductive and Developmental Effects from Exposure 

to Secondhand Smoke) reviews the health effects on 

reproduction, on infants, and on child development. 

Chapter 6 (Respiratory Effects in Children from Exposure to Secondhand Smoke) examines the effects of 

parental smoking on the respiratory health of children. 

Chapter 7 (Cancer Among Adults from Exposure to 

Secondhand Smoke) summarizes the evidence on cancer of the lung, breast, nasal sinuses, and the cervix. 

Chapter 8 (Cardiovascular Diseases from Exposure to 

Secondhand Smoke) discusses coronary heart disease 

(CHD), stroke, and subclinical vascular disease. Chapter 9 (Respiratory Effects in Adults from Exposure to 

Secondhand Smoke) examines odor and irritation, 

respiratory symptoms, lung function, and respiratory 

diseases such as asthma and chronic obstructive pulmonary disease. Chapter 10 (Control of Secondhand 

Smoke Exposure) considers measures used to control exposure to secondhand smoke in public places, 

including legislation, education, and approaches 

based on building designs and operations. The report 

concludes with “A Vision for the Future.” Major conclusions of the report were distilled from the chapter 

conclusions and appear later in this chapter.
The Health Consequences of Involuntary Exposure to Tobacco Smoke

Executive Summary 7

Preparation of the Report 

This report of the Surgeon General was prepared 

by the Office on Smoking and Health, National Center for Chronic Disease Prevention and Health Promotion, Coordinating Center for Health Promotion, 

Centers for Disease Control and Prevention (CDC), 

and U.S. DHHS. Initial chapters were written by 

22 experts who were selected because of their knowledge of a particular topic. The contributions of the 

initial experts were consolidated into 10 major chapters that were then reviewed by more than 40 peer 

reviewers. The entire manuscript was then sent to 

more than 30 scientists and experts who reviewed 

it for its scientific integrity. After each review cycle, 

the drafts were revised by the scientific editors on 

the basis of the experts’ comments. Subsequently, the 

report was reviewed by various institutes and agencies 

distance it has traveled. The smoke particles change 

in size and composition as gaseous components are 

volatilized and moisture content changes; gaseous 

elements of secondhand smoke may be adsorbed onto 

materials, and particle concentrations drop with both 

dilution in the air or environment and impaction on 

surfaces, including the lungs or on the body. Because 

of its dynamic nature, a specific quantitative definition of secondhand smoke cannot be offered.

This report uses the term secondhand smoke 

in preference to environmental tobacco smoke, even 

though the latter may have been used more frequently 

in previous reports. The descriptor “secondhand” captures the involuntary nature of the exposure, while 

“environmental” does not. This report also refers to 

the inhalation of secondhand smoke as involuntary 

smoking, acknowledging that most nonsmokers do 

not want to inhale tobacco smoke. The exposure of the 

fetus to tobacco smoke, whether from active smoking 

by the mother or from her exposure to secondhand 

smoke, also constitutes involuntary smoking.

within U.S. DHHS. Publication lags, even short ones, 

prevent an up-to-the-minute inclusion of all recently 

published articles and data. Therefore, by the time 

the public reads this report, there may be additional 

published studies or data. To provide published information as current as possible, this report includes an 

Appendix of more recent studies that represent major 

additions to the literature.

This report is also accompanied by a companion 

database of key evidence that is accessible through 

the Internet (http://www.cdc.gov/tobacco). The database includes a uniform description of the studies and results on the health effects of exposure to 

secondhand smoke that were presented in a format 

compatible with abstraction into standardized tables. 

Readers of the report may access these data for additional analyses, tables, or figures.

Definitions and Terminology

The inhalation of tobacco smoke by nonsmokers 

has been variably referred to as “passive smoking” 

or “involuntary smoking.” Smokers, of course, also 

inhale secondhand smoke. Cigarette smoke contains 

both particles and gases generated by the combustion 

at high temperatures of tobacco, paper, and additives. 

The smoke inhaled by nonsmokers that contaminates 

indoor spaces and outdoor environments has often 

been referred to as “secondhand smoke” or “environmental tobacco smoke.” This inhaled smoke is the 

mixture of sidestream smoke released by the smoldering cigarette and the mainstream smoke that is 

exhaled by a smoker. Sidestream smoke, generated 

at lower temperatures and under somewhat different 

combustion conditions than mainstream smoke, tends 

to have higher concentrations of many of the toxins 

found in cigarette smoke (USDHHS 1986). However, 

it is rapidly diluted as it travels away from the burning cigarette.

Secondhand smoke is an inherently dynamic 

mixture that changes in characteristics and concentration with the time since it was formed and the 
Surgeon General’s Report

8 Executive Summary

Evidence Evaluation

evidence syntheses and other summary statements 

may use either the term “increased risk” or “cause” 

to describe instances in which there is sufficient evidence to conclude that active or involuntary smoking 

causes a disease or condition. This four-level framework also sharply and completely separates conclusions regarding causality from the implications of 

such conclusions.

That same framework was used in this report 

on involuntary smoking and health. The criteria 

dating back to the 1964 Surgeon General’s report 

remain useful as guidelines for evaluating evidence 

(USDHEW 1964), but they were not intended to be 

applied strictly or as a “checklist” that needed to be met 

before the designation of “causal” could be applied to an 

association. In fact, for involuntary smoking and 

health, several of the criteria will not be met for 

some associations. Specificity, referring to a unique 

exposure-disease relationship (e.g., the association 

between thalidomide use during pregnancy and 

unusual birth defects), can be set aside as not relevant, 

as all of the health effects considered in this report 

have causes other than involuntary smoking. 

Associations are considered more likely to be causal as 

the strength of an association increases because competing explanations become less plausible alternatives. However, based on knowledge of dosimetry and 

mechanisms of injury and disease causation, the risk 

is anticipated to be only slightly or modestly increased 

for some associations of involuntary smoking with 

disease, such as lung cancer, particularly when the 

very strong relative risks found for active smokers are 

compared with those for lifetime nonsmokers. The 

finding of only a small elevation in risk, as in the 

Table 1.4 Four-level hierarchy for classifying the strength of causal inferences based on available 

evidence

Level 1 Evidence is sufficient to infer a causal relationship.

Level 2 Evidence is suggestive but not sufficient to infer a causal relationship.

Level 3 Evidence is inadequate to infer the presence or absence of a causal relationship (which encompasses 

evidence that is sparse, of poor quality, or conflicting).

Level 4 Evidence is suggestive of no causal relationship.

Source: U.S. Department of Health and Human Services 2004.

Following the model of the 1964 report, the 

Surgeon General’s reports on smoking have included 

comprehensive compilations of the evidence on the 

health effects of smoking. The evidence is analyzed 

to identify causal associations between smoking and 

disease according to enunciated principles, sometimes referred to as the “Surgeon General’s criteria” or 

the “Hill” criteria (after Sir Austin Bradford Hill) for 

causality (USDHEW 1964; USDHHS 2004). Application of these criteria involves covering all relevant 

observational and experimental evidence. The criteria, 

offered in a brief chapter of the 1964 report entitled 

“Criteria for Judgment,” included (1) the consistency 

of the association, (2) the strength of the association, 

(3) the specificity of the association, (4) the temporal 

relationship of the association, and (5) the coherence 

of the association. Although these criteria have been 

criticized (e.g., Rothman and Greenland 1998), they 

have proved useful as a framework for interpreting 

evidence on smoking and other postulated causes 

of disease, and for judging whether causality can be 

inferred.

In the 2004 report of the Surgeon General, The 

Health Consequences of Smoking, the framework for 

interpreting evidence on smoking and health was 

revisited in depth for the first time since the 1964 

report (USDHHS 2004). The 2004 report provided 

a four-level hierarchy for interpreting evidence 

(Table 1.4). The categories acknowledge that evidence 

can be “suggestive” but not adequate to infer a causal 

relationship, and also allows for evidence that is “suggestive of no causal relationship.” Since the 2004 

report, the individual chapter conclusions have consistently used this four-level hierarchy (Table 1.4), but 
The Health Consequences of Involuntary Exposure to Tobacco Smoke

Executive Summary 9

example of spousal smoking and lung cancer risk in 

lifetime nonsmokers, does not weigh against a causal 

association; however, alternative explanations for a 

risk of a small magnitude need full exploration and 

cannot be so easily set aside as alternative explanations for a stronger association. Consistency, coherence, and the temporal relationship of involuntary 

smoking with disease are central to the interpretations 

in this report. To address coherence, the report draws 

not only on the evidence for involuntary smoking, but 

on the even more extensive literature on active smoking and disease.

Although the evidence reviewed in this report 

comes largely from investigations of secondhand 

smoke specifically, the larger body of evidence 

on active smoking is also relevant to many of the 

associations that were evaluated. The 1986 report 

found secondhand smoke to be qualitatively similar 

to mainstream smoke inhaled by the smoker and concluded that secondhand smoke would be expected to 

have “a toxic and carcinogenic potential that would 

and more severe asthma. Smoking by parents 

causes respiratory symptoms and slows lung 

growth in their children.

3. Exposure of adults to secondhand smoke has 

immediate adverse effects on the cardiovascular 

system and causes coronary heart disease and 

lung cancer.

4. The scientific evidence indicates that there is no 

risk-free level of exposure to secondhand smoke.

5. Many millions of Americans, both children and 

adults, are still exposed to secondhand smoke in 

their homes and workplaces despite substantial 

progress in tobacco control.

6. Eliminating smoking in indoor spaces fully protects nonsmokers from exposure to secondhand 

smoke. Separating smokers from nonsmokers, 

cleaning the air, and ventilating buildings cannot 

eliminate exposures of nonsmokers to secondhand smoke.

not be expected to be qualitatively different from that 

of MS [mainstream smoke]” (USDHHS 1986, p. 23). 

The 2004 report of the Surgeon General revisited the 

health consequences of active smoking (USDHHS 

2004), and the conclusions substantially expanded 

the list of diseases and conditions caused by smoking. 

Chapters in the present report consider the evidence on 

active smoking that is relevant to biologic plausibility 

for causal associations between involuntary smoking 

and disease. The reviews included in this report cover 

evidence identified through search strategies set out 

in each chapter. Of necessity, the evidence on mechanisms was selectively reviewed. However, an attempt 

was made to cover all health studies through specified target dates. Because of the substantial amount 

of time involved in preparing this report, lists of new 

key references published after these cut-off dates are 

included in an Appendix. Literature reviews were 

extended when new evidence was sufficient to possibly change the level of a causal conclusion.

Major Conclusions

This report returns to involuntary smoking, the 

topic of the 1986 Surgeon General’s report. Since then, 

there have been many advances in the research on 

secondhand smoke, and substantial evidence has been 

reported over the ensuing 20 years. This report uses 

the revised language for causal conclusions that was 

implemented in the 2004 Surgeon General’s report 

(USDHHS 2004). Each chapter provides a comprehensive review of the evidence, a quantitative synthesis of the evidence if appropriate, and a rigorous 

assessment of sources of bias that may affect interpretations of the findings. The reviews in this report 

reaffirm and strengthen the findings of the 1986 report. 

With regard to the involuntary exposure of nonsmokers to tobacco smoke, the scientific evidence now supports the following major conclusions:

1. Secondhand smoke causes premature death and 

disease in children and in adults who do not 

smoke.

2. Children exposed to secondhand smoke are at an 

increased risk for sudden infant death syndrome 

(SIDS), acute respiratory infections, ear problems, 
Surgeon General’s Report

10 Executive Summary

Chapter Conclusions

8. The evidence is sufficient to infer that exposure 

to secondhand smoke causes endothelial cell 

dysfunctions.

9. The evidence is sufficient to infer that exposure 

to secondhand smoke causes atherosclerosis in 

animal models.

Chapter 3. Assessment of Exposure 

to Secondhand Smoke

Building Designs and Operations

1. Current heating, ventilating, and air conditioning 

systems alone cannot control exposure to 

secondhand smoke.

2. The operation of a heating, ventilating, and air 

conditioning system can distribute secondhand 

smoke throughout a building.

Exposure Models

3. Atmospheric concentration of nicotine is a 

sensitive and specific indicator for secondhand 

smoke.

4. Smoking increases indoor particle concentrations.

5. Models can be used to estimate concentrations of 

secondhand smoke.

Biomarkers of Exposure to Secondhand Smoke

6. Biomarkers suitable for assessing recent exposures 

to secondhand smoke are available.

7. At this time, cotinine, the primary proximate 

metabolite of nicotine, remains the biomarker of 

choice for assessing secondhand smoke exposure.

8. Individual biomarkers of exposure to secondhand smoke represent only one component of 

a complex mixture, and measurements of one 

marker may not wholly reflect an exposure to 

other components of concern as a result of 

involuntary smoking.

Chapter 2. Toxicology of Secondhand 

Smoke

Evidence of Carcinogenic Effects 

from Secondhand Smoke Exposure

1. More than 50 carcinogens have been identified in 

sidestream and secondhand smoke.

2. The evidence is sufficient to infer a causal 

relationship between exposure to secondhand 

smoke and its condensates and tumors in 

laboratory animals.

3. The evidence is sufficient to infer that exposure 

of nonsmokers to secondhand smoke causes a 

significant increase in urinary levels of metabolites of the tobacco-specific lung carcinogen 

4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone 

(NNK). The presence of these metabolites links 

exposure to secondhand smoke with an increased 

risk for lung cancer.

4. The mechanisms by which secondhand smoke 

causes lung cancer are probably similar to 

those observed in smokers. The overall risk of 

secondhand smoke exposure, compared with 

active smoking, is diminished by a substantially 

lower carcinogenic dose.

Mechanisms of Respiratory Tract Injury and Disease 

Caused by Secondhand Smoke Exposure

5. The evidence indicates multiple mechanisms by 

which secondhand smoke exposure causes injury 

to the respiratory tract.

6. The evidence indicates mechanisms by which 

secondhand smoke exposure could increase the 

risk for sudden infant death syndrome.

Mechanisms of Secondhand Smoke Exposure 

and Heart Disease

7. The evidence is sufficient to infer that exposure to 

secondhand smoke has a prothrombotic effect.
The Health Consequences of Involuntary Exposure to Tobacco Smoke

Executive Summary 11

Chapter 4. Prevalence of Exposure 

to Secondhand Smoke

1. The evidence is sufficient to infer that large 

numbers of nonsmokers are still exposed to 

secondhand smoke.

2. Exposure of nonsmokers to secondhand smoke 

has declined in the United States since the 1986 

Surgeon General’s report, The Health Consequences 

of Involuntary Smoking.

3. The evidence indicates that the extent of 

secondhand smoke exposure varies across the 

country.

4. Homes and workplaces are the predominant 

locations for exposure to secondhand smoke.

5. Exposure to secondhand smoke tends to be greater 

for persons with lower incomes.

6. Exposure to secondhand smoke continues in 

restaurants, bars, casinos, gaming halls, and 

vehicles.

Chapter 5. Reproductive and 

Developmental Effects from 

Exposure to Secondhand Smoke

Fertility

1. The evidence is inadequate to infer the presence or 

absence of a causal relationship between maternal 

exposure to secondhand smoke and female 

fertility or fecundability. No data were found on 

paternal exposure to secondhand smoke and male 

fertility or fecundability.

Pregnancy (Spontaneous Abortion and Perinatal Death)

2. The evidence is inadequate to infer the presence or 

absence of a causal relationship between maternal 

exposure to secondhand smoke during pregnancy 

and spontaneous abortion.

Infant Deaths

3. The evidence is inadequate to infer the presence 

or absence of a causal relationship between 

exposure to secondhand smoke and neonatal 

mortality.

Sudden Infant Death Syndrome

4. The evidence is sufficient to infer a causal 

relationship between exposure to secondhand 

smoke and sudden infant death syndrome.

Preterm Delivery

5. The evidence is suggestive but not sufficient to 

infer a causal relationship between maternal 

exposure to secondhand smoke during pregnancy 

and preterm delivery.

Low Birth Weight

6. The evidence is sufficient to infer a causal 

relationship between maternal exposure to 

secondhand smoke during pregnancy and a small 

reduction in birth weight. 

Congenital Malformations

7. The evidence is inadequate to infer the presence 

or absence of a causal relationship between 

exposure to secondhand smoke and congenital 

malformations.

Cognitive Development

8. The evidence is inadequate to infer the presence 

or absence of a causal relationship between 

exposure to secondhand smoke and cognitive 

functioning among children.

Behavioral Development

9. The evidence is inadequate to infer the presence 

or absence of a causal relationship between 

exposure to secondhand smoke and behavioral 

problems among children.

Height/Growth

10. The evidence is inadequate to infer the presence 

or absence of a causal relationship between 

exposure to secondhand smoke and children’s 

height/growth.

Childhood Cancer

11. The evidence is suggestive but not sufficient to 

infer a causal relationship between prenatal and 

postnatal exposure to secondhand smoke and 

childhood cancer.
Surgeon General’s Report

12 Executive Summary

12. The evidence is inadequate to infer the presence 

or absence of a causal relationship between 

maternal exposure to secondhand smoke during 

pregnancy and childhood cancer.

13. The evidence is inadequate to infer the presence 

or absence of a causal relationship between 

exposure to secondhand smoke during infancy 

and childhood cancer.

14. The evidence is suggestive but not sufficient to 

infer a causal relationship between prenatal and 

postnatal exposure to secondhand smoke and 

childhood leukemias.

15. The evidence is suggestive but not sufficient to 

infer a causal relationship between prenatal and 

postnatal exposure to secondhand smoke and 

childhood lymphomas.

16. The evidence is suggestive but not sufficient to 

infer a causal relationship between prenatal and 

postnatal exposure to secondhand smoke and 

childhood brain tumors.

17. The evidence is inadequate to infer the presence or 

absence of a causal relationship between prenatal 

and postnatal exposure to secondhand smoke and 

other childhood cancer types.

Chapter 6. Respiratory Effects 

in Children from Exposure 

to Secondhand Smoke

Lower Respiratory Illnesses in Infancy 

and Early Childhood

1. The evidence is sufficient to infer a causal 

relationship between secondhand smoke exposure 

from parental smoking and lower respiratory 

illnesses in infants and children.

2. The increased risk for lower respiratory illnesses 

is greatest from smoking by the mother.

Middle Ear Disease and Adenotonsillectomy

3. The evidence is sufficient to infer a causal 

relationship between parental smoking and 

middle ear disease in children, including acute 

and recurrent otitis media and chronic middle ear 

effusion.

4. The evidence is suggestive but not sufficient 

to infer a causal relationship between parental 

smoking and the natural history of middle ear 

effusion.

5. The evidence is inadequate to infer the presence 

or absence of a causal relationship between 

parental smoking and an increase in the risk of 

adenoidectomy or tonsillectomy among children.

Respiratory Symptoms and Prevalent Asthma 

in School-Age Children

6. The evidence is sufficient to infer a causal relationship between parental smoking and cough, 

phlegm, wheeze, and breathlessness among 

children of school age.

7. The evidence is sufficient to infer a causal 

relationship between parental smoking and ever 

having asthma among children of school age.

Childhood Asthma Onset

8. The evidence is sufficient to infer a causal 

relationship between secondhand smoke exposure 

from parental smoking and the onset of wheeze 

illnesses in early childhood.

9. The evidence is suggestive but not sufficient to 

infer a causal relationship between secondhand 

smoke exposure from parental smoking and the 

onset of childhood asthma.

Atopy

10. The evidence is inadequate to infer the presence 

or absence of a causal relationship between 

parental smoking and the risk of immunoglobulin 

E-mediated allergy in their children.

Lung Growth and Pulmonary Function

11. The evidence is sufficient to infer a causal 

relationship between maternal smoking during 

pregnancy and persistent adverse effects on lung 

function across childhood.

12. The evidence is sufficient to infer a causal 

relationship between exposure to secondhand 

smoke after birth and a lower level of lung 

function during childhood.
The Health Consequences of Involuntary Exposure to Tobacco Smoke

Executive Summary 13

Chapter 7. Cancer Among Adults from 

Exposure to Secondhand Smoke

Lung Cancer

1. The evidence is sufficient to infer a causal 

relationship between secondhand smoke 

exposure and lung cancer among lifetime 

nonsmokers. This conclusion extends to all 

secondhand smoke exposure, regardless of 

location.

2. The pooled evidence indicates a 20 to 30 percent 

increase in the risk of lung cancer from secondhand 

smoke exposure associated with living with a 

smoker.

Breast Cancer

3. The evidence is suggestive but not sufficient to 

infer a causal relationship between secondhand 

smoke and breast cancer.

Nasal Sinus Cavity and Nasopharyngeal Carcinoma

4. The evidence is suggestive but not sufficient to 

infer a causal relationship between secondhand 

smoke exposure and a risk of nasal sinus cancer 

among nonsmokers.

5. The evidence is inadequate to infer the presence 

or absence of a causal relationship between 

secondhand smoke exposure and a risk of 

nasopharyngeal carcinoma among nonsmokers.

Cervical Cancer

6. The evidence is inadequate to infer the presence 

or absence of a causal relationship between 

secondhand smoke exposure and the risk of 

cervical cancer among lifetime nonsmokers.

Chapter 8. Cardiovascular Diseases from 

Exposure to Secondhand Smoke

1. The evidence is sufficient to infer a causal 

relationship between exposure to secondhand 

smoke and increased risks of coronary heart 

disease morbidity and mortality among both men 

and women.

2. Pooled relative risks from meta-analyses indicate 

a 25 to 30 percent increase in the risk of coronary 

heart disease from exposure to secondhand 

smoke.

3. The evidence is suggestive but not sufficient to 

infer a causal relationship between exposure 

to secondhand smoke and an increased risk of 

stroke.

4. Studies of secondhand smoke and subclinical 

vascular disease, particularly carotid arterial wall 

thickening, are suggestive but not sufficient to 

infer a causal relationship between exposure to 

secondhand smoke and atherosclerosis.

Chapter 9. Respiratory Effects in Adults 

from Exposure to Secondhand Smoke

Odor and Irritation

1. The evidence is sufficient to infer a causal 

relationship between secondhand smoke exposure 

and odor annoyance.

2. The evidence is sufficient to infer a causal 

relationship between secondhand smoke exposure 

and nasal irritation.

3. The evidence is suggestive but not sufficient 

to conclude that persons with nasal allergies 

or a history of respiratory illnesses are more 

susceptible to developing nasal irritation from 

secondhand smoke exposure.

Respiratory Symptoms

4. The evidence is suggestive but not sufficient to 

infer a causal relationship between secondhand 

smoke exposure and acute respiratory symptoms 

including cough, wheeze, chest tightness, and 

difficulty breathing among persons with asthma.

5. The evidence is suggestive but not sufficient to 

infer a causal relationship between secondhand 

smoke exposure and acute respiratory symptoms 

including cough, wheeze, chest tightness, and 

difficulty breathing among healthy persons.

6. The evidence is suggestive but not sufficient to 

infer a causal relationship between secondhand 

smoke exposure and chronic respiratory 

symptoms.
Surgeon General’s Report

14 Executive Summary

Lung Function

7. The evidence is suggestive but not sufficient to 

infer a causal relationship between short-term 

secondhand smoke exposure and an acute decline 

in lung function in persons with asthma.

8. The evidence is inadequate to infer the presence 

or absence of a causal relationship between shortterm secondhand smoke exposure and an acute 

decline in lung function in healthy persons.

9. The evidence is suggestive but not sufficient to infer a causal relationship between chronic secondhand smoke exposure and a small decrement in 

lung function in the general population.

10. The evidence is inadequate to infer the presence or 

absence of a causal relationship between chronic 

secondhand smoke exposure and an accelerated 

decline in lung function.

Asthma

11. The evidence is suggestive but not sufficient to 

infer a causal relationship between secondhand 

smoke exposure and adult-onset asthma.

12. The evidence is suggestive but not sufficient to 

infer a causal relationship between secondhand 

smoke exposure and a worsening of asthma 

control.

Chronic Obstructive Pulmonary Disease

13. The evidence is suggestive but not sufficient to 

infer a causal relationship between secondhand 

smoke exposure and risk for chronic obstructive 

pulmonary disease.

14. The evidence is inadequate to infer the presence 

or absence of a causal relationship between 

secondhand smoke exposure and morbidity in 

persons with chronic obstructive pulmonary 

disease.

Chapter 10. Control of Secondhand Smoke 

Exposure

1. Workplace smoking restrictions are effective in 

reducing secondhand smoke exposure.

2. Workplace smoking restrictions lead to less 

smoking among covered workers.

3. Establishing smoke-free workplaces is the only 

effective way to ensure that secondhand smoke 

exposure does not occur in the workplace.

4. The majority of workers in the United States are 

now covered by smoke-free policies.

5. The extent to which workplaces are covered by 

smoke-free policies varies among worker groups, 

across states, and by sociodemographic factors. 

Workplaces related to the entertainment and 

hospitality industries have notably high potential 

for secondhand smoke exposure.

6. Evidence from peer-reviewed studies shows that 

smoke-free policies and regulations do not have 

an adverse economic impact on the hospitality 

industry.

7. Evidence suggests that exposure to secondhand 

smoke varies by ethnicity and gender. 

8. In the United States, the home is now becoming 

the predominant location for exposure of children 

and adults to secondhand smoke.

9. Total bans on indoor smoking in hospitals, 

restaurants, bars, and offices substantially reduce 

secondhand smoke exposure, up to several orders 

of magnitude with incomplete compliance, and 

with full compliance, exposures are eliminated. 

10. Exposures of nonsmokers to secondhand smoke 

cannot be controlled by air cleaning or mechanical 

air exchange.
The Health Consequences of Involuntary Exposure to Tobacco Smoke

Executive Summary 15

Methodologic Issues

span may be of interest for lung cancer, while only 

more recent exposures may be relevant to the exacerbation of asthma. For CHD, both temporally remote 

and current exposures may affect risk. Assessments 

of exposures are further complicated by the multiplicity of environments where exposures take place and 

the difficulty of characterizing the exposure in some 

locations, such as public places or workplaces. Additionally, exposures probably vary qualitatively and 

quantitatively over time and across locations because 

of temporal changes and geographic differences in 

smoking patterns.

Nonetheless, researchers have used a variety of 

approaches for exposure assessments in epidemiologic studies of adverse health effects from involuntary smoking. Several core concepts that are 

fundamental to these approaches are illustrated in 

Figure 1.1 (Samet and Jaakkola 1999). Cigarette smoking is, of course, the source of most secondhand 

smoke in the United States, followed by pipes, cigars, 

and other products. Epidemiologic studies generally 

focus on assessing the exposure, which is the contact with secondhand smoke. The concentrations of 

secondhand smoke components in a space depend on 

the number of smokers and the rate at which they are 

smoking, the volume into which the smoke is distributed, the rate at which the air in the space exchanges 

with uncontaminated air, and the rate at which the 

secondhand smoke is removed from the air. Concentration, exposure, and dose differ in their definitions, 

although the terms are sometimes used without sharp 

distinctions. However, surrogate indicators that generally describe a source of exposure may also be used 

to assess the exposure, such as marriage to a smoker 

or the number of cigarettes smoked in the home. Biomarkers can provide an indication of an exposure or 

possibly the dose, but for secondhand smoke they are 

used for recent exposure only.

People are exposed to secondhand smoke in a 

number of different places, often referred to as “microenvironments” (NRC 1991). A microenvironment is 

a definable location that has a constant concentration of the contaminant of interest, such as secondhand smoke, during the time that a person is there. 

Some key microenvironments for secondhand smoke 

include the home, the workplace, public places, and 

transportation environments (Klepeis 1999). Based 

Much of the evidence on the health effects of 

involuntary smoking comes from observational epidemiologic studies that were carried out to test hypotheses related to secondhand smoke and risk for diseases 

and other adverse health effects. The challenges faced 

in carrying out these studies reflect those of observational research generally: assessment of the relevant 

exposures and outcomes with sufficient validity and 

precision, selection of an appropriate study design, 

identification of an appropriate and sufficiently large 

study population, and collection of information on 

other relevant factors that may confound or modify 

the association being studied. The challenge of accurately classifying secondhand smoke exposures confronts all studies of such exposures, and consequently 

the literature on approaches to and limitations of 

exposure classification is substantial. Sources of bias 

that can affect the findings of epidemiologic studies 

have been widely discussed (Rothman and Greenland 1998), both in general and in relation to studies 

of involuntary smoking. Concerns about bias apply to 

any study of an environmental agent and disease risk: 

misclassification of exposures or outcomes, confounding effect modification, and proper selection of study 

participants. In addition, the generalizability of findings from one population to another (external validity) further determines the value of evidence from 

a study. Another methodologic concern affecting 

secondhand smoke literature comes from the use of 

meta-analysis to combine the findings of epidemiologic studies; general concerns related to the use of 

meta-analysis for observational data and more specific concerns related to involuntary smoking have 

also been raised. This chapter considers these methodologic issues in anticipation of more specific treatment in the following chapters.

Classification of Secondhand 

Smoke Exposure 

For secondhand smoke, as for any environmental factor that may be a cause of disease, the exposure 

assessment might encompass the time and place of 

the exposure, cumulative exposures, exposure during 

a particular time, or a recent exposure (Jaakkola and 

Jaakkola 1997; Jaakkola and Samet 1999). For example, 

exposures to secondhand smoke across the full life 
Surgeon General’s Report

16 Executive Summary

on the microenvironmental model, total exposure 

can be estimated as the weighted average of the concentrations of secondhand smoke or indicator compounds, such as nicotine, in the microenvironments 

where time is spent; the weights are the time spent in 

each microenvironment. Klepeis (1999) illustrates the 

application of the microenvironmental model with 

national data from the National Human Activity Pattern Survey conducted by the EPA. His calculations 

yield an overall estimate of exposure to airborne particles from smoking and of the contributions to this 

exposure from various microenvironments.

Much of the epidemiologic evidence addresses 

the consequences of an exposure in a particular microenvironment, such as the home (spousal smoking and 

lung cancer risk or maternal smoking and risk for 

asthma exacerbation), or the workplace (exacerbation 

of asthma by the presence of smokers). Some studies 

have attempted to cover multiple microenvironments 

and to characterize exposures over time. For example, 

in the multicenter study of secondhand smoke exposure and lung cancer carried out in the United States, 

Fontham and colleagues (1994) assessed exposures 

during childhood, in workplaces, and at home during adulthood. Questionnaires that assess exposures 

have been the primary tool used in epidemiologic 

studies of secondhand smoke and disease. Measurement of biomarkers has been added in some studies, 

either as an additional and complementary exposure 

assessment approach or for validating questionnaire 

responses. Some studies have also measured components of secondhand smoke in the air.

Questionnaires generally address sources of 

exposure in microenvironments and can be tailored 

to address the time period of interest. Questionnaires represent the only approach that can be used 

to assess exposures retrospectively over a life span, 

because available biomarkers only reflect exposures 

Figure 1.1 The determinants of exposure, dose, and biologically effective dose that underlie the 

development of health effects from smoking

Source: Samet and Jaakkola 1999. Reprinted with permission.

▲

▲

▲

Outdoor 

sources

Indoor 

sources

Concentration Exposure

Etot = ∑ cij * tij

=

Dose

Biologically 

effective

dose

Microenvironmental (mj)

concentrations over time (tj)

t

0

 t1 t2 t3

m1 C10 C11 C12 C13

m2 C20 C21 C22 C23

m3 C30 C31 C32 C33

m4 C40 C41 C42 C43

▲

▲▲

Ventilation 

removal

Dispersion Metabolic 

elimination

Type and rate

of breathing

Individual time (tj) 

present in

location (mj)

▲

▲▲

▲

Human body

Susceptible body surface

Environment

▲

▲ ▲
The Health Consequences of Involuntary Exposure to Tobacco Smoke

Executive Summary 17

over recent days or, at most, weeks. Questionnaires 

on secondhand smoke exposure have been assessed 

for their reliability and validity, generally based on 

comparisons with either biomarker or air monitoring data as the “gold” standard (Jaakkola and 

Jaakkola 1997). Two studies evaluated the reliability 

of questionnaires on lifetime exposures (Pron et al. 

1988; Coultas et al. 1989). Both showed a high degree 

of repeatability for questions concerning whether 

a spouse had smoked, but a lower reliability for 

responses concerning the quantitative aspects of an 

exposure. Emerson and colleagues (1995) evaluated 

the repeatability of information from parents of children with asthma. They found a high reliability for 

parent-reported tobacco use and for the number of 

cigarettes to which the child was exposed in the home 

during the past week.

To assess validity, questionnaire reports of current or recent exposures have been compared with 

levels of cotinine and other biomarkers. These studies 

tend to show a moderate correlation between levels 

of cotinine and questionnaire indicators of exposures 

(Kawachi and Colditz 1996; Cal/EPA 1997; Jaakkola 

and Jaakkola 1997). However, cotinine levels reflect 

not only exposure but metabolism and excretion 

(Benowitz 1999). Consequently, exposure is only one 

determinant of variation in cotinine levels among persons; there also are individual variations in metabolism and excretion rates. In spite of these sources of 

variability, mean levels of cotinine vary as anticipated 

across categories of self-reported exposures (Cal/EPA 

1997; Jaakkola and Jaakkola 1997), and self-reported 

exposures are moderately associated with measured 

levels of markers (Cal/EPA 1997; Jaakkola and 

Jaakkola 1997).

Biomarkers are also used for assessing exposures to secondhand smoke. A number of biomarkers are available, but they vary in their specificity 

and in the dynamics of the temporal relationship 

between the exposure and the marker level (Cal/EPA 

1997; Benowitz 1999). These markers include specific 

tobacco smoke components (nicotine) or metabolites 

(cotinine and tobacco-specific nitrosamines), nonspecific biomarkers (thiocyanate and CO), adducts with 

tobacco smoke components or metabolites (4-aminobiphenyl–hemoglobin adducts, benzo[a]pyrene–DNA 

adducts, and polycyclic aromatic hydrocarbon–

albumin adducts), and nonspecific assays (urinary 

mutagenicity). Cotinine has been the most widely 

used biomarker, primarily because of its specificity, 

half-life, and ease of measurement in body fluids (e.g., 

urine, blood, and saliva). Biomarkers are discussed 

in detail in Chapter 3 (Assessment of Exposure to 

Secondhand Smoke).

Some epidemiologic studies have also incorporated air monitoring, either direct personal sampling 

or the indirect approach based on the microenvironmental model. Nicotine, present in the gas phase of 

secondhand smoke, can be monitored passively with 

a special filter or actively using a pump and a sorbent. 

Hammond and Leaderer (1987) first described a diffusion monitor for the passive sampling of nicotine in 

1987; this device has now been widely used to assess 

concentrations in different environments and to study 

health effects. Airborne particles have also been measured using active monitoring devices.

Each of these approaches for assessing exposures has strengths and limitations, and preference for 

one over another will depend on the research question and its context (Jaakkola and Jaakkola 1997; Jaakkola and Samet 1999). Questionnaires can be used to 

characterize sources of exposures, such as smoking by 

parents. With air concentrations of markers and timeactivity information, estimates of secondhand smoke 

exposures can be made with the microenvironmental 

model. Biomarkers provide exposure measures that 

reflect the patterns of exposure and the kinetics of the 

marker; the cotinine level in body fluids, for example, 

reflects an exposure during several days. Air monitoring may be useful for validating measurements of 

exposure. Exposure assessment strategies are matched 

to the research question and often employ a mixture 

of approaches determined by feasibility and cost 

constraints.

Misclassification of Secondhand 

Smoke Exposure

Misclassification may occur when classifying 

exposures, outcomes, confounding factors, or modifying factors. Misclassification may be differential on 

either exposure or outcome, or it may be random (Armstrong et al. 1992). Differential or nonrandom misclassification may either increase or decrease estimates of 

effect, while random misclassification tends to reduce 

the apparent effect and weaken the relationship of 

exposure with disease risk. In studies of secondhand 

smoke and disease risk, exposure misclassification 

has been a major consideration in the interpretation of 

the evidence, although misclassification of health outcome measures has not been a substantial issue in this 

research. The consequences for epidemiologic studies of misclassification in general are well established 

(Rothman and Greenland 1998).
Surgeon General’s Report

18 Executive Summary

An extensive body of literature on the classification of exposures to secondhand smoke is reviewed 

in this and other chapters, as well as in some publications on the consequences of misclassification 

(Wu 1999). Two general patterns of exposure misclassification are of concern to secondhand smoke: 

(1) random misclassification that is not differential 

by the presence or absence of the health outcome and 

(2) systematic misclassification that is differential by 

the health outcome. In studying the health effects of 

secondhand smoke in adults, there is a further concern as to the classification of the active smoking status (never, current, or former smoking); in studies of 

children, the accuracy of secondhand smoke exposure classification is the primary methodologic issue 

around exposure assessment, but unreported active 

smoking by adolescents is also a concern.

With regard to random misclassification of 

secondhand smoke exposures, there is an inherent degree of unavoidable measurement error in the 

exposure measures used in epidemiologic studies. 

Questionnaires generally assess contact with sources 

of an exposure (e.g., smoking in the home or workplace) and cannot capture all exposures nor the intensity of exposures; biomarkers provide an exposure 

index for a particular time window and have intrinsic 

variability. Some building-related factors that determine an exposure cannot be assessed accurately by a 

questionnaire, such as the rate of air exchange and the 

size of the microenvironment where time is spent, nor 

can concentrations be assessed accurately by subjective reports of the perceived level of tobacco smoke. 

In general, random misclassification of exposures 

tends to reduce the likelihood that studies of secondhand smoke exposure will find an effect. This type of 

misclassification lessens the contrast between exposure groups, because some truly exposed persons are 

placed in the unexposed group and some truly unexposed persons are placed in the exposed group. Differential misclassification, also a concern, may increase 

or decrease associations, depending on the pattern of 

misreporting.

One particular form of misclassification has been 

raised with regard to secondhand smoke exposure 

and lung cancer: the classification of some current or 

former smokers as lifetime nonsmokers (USEPA 1992; 

Lee and Forey 1995; Hackshaw et al. 1997; Wu 1999). 

The resulting bias would tend to increase the apparent association of secondhand smoke with lung cancer, if the misclassified active smokers are also more 

likely to be classified as involuntary smokers. Most 

studies of lung cancer and secondhand smoke have 

used spousal smoking as a main exposure variable. As 

smoking tends to aggregate between spouses (smokers are more likely to marry smokers), misclassification of active smoking would tend to be differential 

on the basis of spousal smoking (the exposure under 

investigation). Because active smoking is strongly 

associated with increased disease risk, greater misclassification of an actively smoking spouse as a nonsmoker among spouses of smokers compared with 

spouses of nonsmokers would lead to risk estimates 

for spousal smoking that are biased upward by the 

effect of active smoking. This type of misclassification is also relevant to studies of spousal exposure 

and CHD risk or other diseases also caused by active 

smoking, although the potential for bias is less because 

the association of active smoking with CHD is not as 

strong as with lung cancer.

There have been a number of publications on 

this form of misclassification. Wu (1999) provides a 

review, and Lee and colleagues (2001) offer an assessment of potential consequences. A number of models have been developed to assess the extent of bias 

resulting from the misclassification of active smokers as lifetime nonsmokers (USEPA 1992; Hackshaw 

et al. 1997). These models incorporate estimates of the 

rate of misclassification, the degree of aggregation of 

smokers by marriage, the prevalence of smoking in 

the population, and the risk of lung cancer in misclassified smokers (Wu 1999). Although debate about 

this issue continues, analyses show that estimates of 

upward bias from misclassifying active smokers as 

lifetime nonsmokers cannot fully explain the observed 

increase in risk for lung cancer among lifetime nonsmokers married to smokers (Hackshaw et al. 1997; 

Wu 1999).

There is one additional issue related to exposure 

misclassification. During the time the epidemiologic 

studies of secondhand smoke have been carried out, 

exposure has been widespread and almost unavoidable. Therefore, the risk estimates may be biased 

downward because there are no truly unexposed 

persons. The 1986 Surgeon General’s report recognized this methodologic issue and noted the need for 

further data on population exposures to secondhand 

smoke (USDHHS 1986). This bias was also recognized 

in the 1986 report of the NRC, and an adjustment for 

this misclassification was made to the lung cancer 

estimate (NRC 1986). Similarly, the 1992 report of the 

EPA commented on background exposure and made 

an adjustment (USEPA 1992). Some later studies have 

attempted to address this issue; for example, in a casecontrol study of active and involuntary smoking and 

breast cancer in Switzerland, Morabia and colleagues 

(2000) used a questionnaire to assess exposure and 
The Health Consequences of Involuntary Exposure to Tobacco Smoke

Executive Summary 19

studies, the methods for meta-analysis, and doseresponse associations (Fleiss and Gross 1991; Tweedie 

and Mengersen 1995; Lee 1998, 1999). In a lawsuit 

brought by the tobacco industry against the EPA, 

the 1998 decision handed down by Judge William 

L. Osteen, Sr., in the North Carolina Federal District 

Court criticized the approach EPA had used to select 

studies for its meta-analysis and criticized the use of 90 

percent rather than 95 percent confidence intervals for 

the summary estimates (Flue-Cured Tobacco Cooperative 

Stabilization Corp. v. United States Environmental Protection Agency, 857 F. Supp. 1137 [M.D.N.C. 1993]). In 

December 2002, the 4th U.S. Circuit Court of Appeals 

threw out the lawsuit on the basis that tobacco companies cannot sue the EPA over its secondhand smoke 

report because the report was not a final agency action 

and therefore not subject to court review (Flue-Cured 

Tobacco Cooperative Stabilization Corp. v. The United 

States Environmental Protection Agency, No. 98-2407 

[4th Cir., December 11, 2002], cited in 17.7 TPLR 2.472 

[2003]).

Recognizing that there is still an active discussion around the use of meta-analysis to pool data 

from observational studies (versus clinical trials), 

the authors of this Surgeon General’s report used 

this methodology to summarize the available data 

when deemed appropriate and useful, even while 

recognizing that the uncertainty around the metaanalytic estimates may exceed the uncertainty indicated by conventional statistical indices, because of 

biases either within the observational studies or produced by the manner of their selection. However, a 

decision to not combine estimates might have produced conclusions that are far more uncertain than 

the data warrant because the review would have 

focused on individual study results without considering their overall pattern, and without allowing for 

a full accounting of different sample sizes and effect 

estimates.

The possibility of publication bias has been 

raised as a potential limitation to the interpretation of 

evidence on involuntary smoking and disease in general, and on lung cancer and secondhand smoke exposure specifically. A 1988 paper by Vandenbroucke 

used a descriptive approach, called a “funnel plot,” 

to assess the possibility that publication bias affected 

the 13 studies considered in a review by Wald and colleagues (1986). This type of plot characterizes the relationship between the magnitude of estimates and their 

precision. Vandenbroucke suggested the possibility 

of publication bias only in reference to the studies of 

men. Bero and colleagues (1994) concluded that there 

identified a small group of lifetime nonsmokers who 

also reported no exposure to secondhand smoke. With 

this subgroup of controls as the reference population, 

the risks of secondhand smoke exposure were substantially greater for active smoking than when the 

full control population was used.

This Surgeon General’s report further addresses 

specific issues of exposure misclassification when 

they are relevant to the health outcome under 

consideration.

Use of Meta-Analysis 

Meta-analysis refers to the process of evaluating and combining a body of research literature that 

addresses a common question. Meta-analysis is composed of qualitative and quantitative components. 

The qualitative component involves the systematic 

identification of all relevant investigations, a systematic assessment of their characteristics and quality, and the decision to include or exclude studies 

based on predetermined criteria. Consideration can 

be directed toward sources of bias that might affect 

the findings. The quantitative component involves the 

calculation and display of study results on common 

scales and, if appropriate, the statistical combination 

of these results across studies and an exploration of 

the reasons for any heterogeneity of findings. Viewing the findings of all studies as a single plot provides 

insights into the consistency of results and the precision of the studies considered. Most meta-analyses are 

based on published summary results, although they 

are most powerful when applied to data at the level of 

individual participants. Meta-analysis is most widely 

used to synthesize evidence from randomized clinical trials, sometimes yielding findings that were not 

evident from the results of individual studies. Metaanalysis also has been used extensively to examine 

bodies of observational evidence.

Beginning with the 1986 NRC report, metaanalysis has been used to summarize the evidence on 

involuntary smoking and health. Meta-analysis was 

central to the 1992 EPA risk assessment of secondhand 

smoke, and a series of meta-analyses supported the 

conclusions of the 1998 report of the Scientific Committee on Tobacco and Health in the United Kingdom. 

The central role of meta-analysis in interpreting and 

applying the evidence related to involuntary smoking and disease has led to focused criticisms of the 

use of meta-analysis in this context. Several papers 

that acknowledged support from the tobacco industry have addressed the epidemiologic findings for 

lung cancer, including the selection and quality of the 
Surgeon General’s Report

20 Executive Summary

had not been a publication bias against studies with 

statistically significant findings, nor against the publication of studies with nonsignificant or mixed findings 

in the research literature. The researchers were able to 

identify only five unpublished “negative” studies, of 

which two were dissertations that tend to be delayed 

in publication. A subsequent study by Misakian and 

Bero (1998) did find a delay in the publication of studies with nonsignificant results in comparison with 

studies having significant results; whether this pattern has varied over the several decades of research on 

secondhand smoke was not addressed. More recently, 

Copas and Shi (2000) assessed the 37 studies considered in the meta-analysis by Hackshaw and colleagues 

(1997) for publication bias. Copas and Shi (2000) found 

a significant correlation between the estimated risk of 

exposure and sample size, such that smaller studies 

tended to have higher values. This pattern suggests 

the possibility of publication bias. However, using a 

funnel plot of the same studies, Lubin (1999) found 

little evidence for publication bias.

On this issue of publication bias, it is critical to 

distinguish between indirect statistical arguments and 

arguments based on actual identification of previously 

unidentified research. The strongest case against substantive publication bias has been made by researchers who mounted intensive efforts to find the possibly 

missing studies; these efforts have yielded little—

nothing that would alter published conclusions 

(Bero et al. 1994; Glantz 2000). Presumably because 

this exposure is a great public health concern, the 

findings of studies that do not have statistically significant outcomes continue to be published (Kawachi 

and Colditz 1996).

The quantitative results of the meta-analyses, 

however, were not determinate in making causal 

inferences in this Surgeon General’s report. In particular, the level of statistical significance of estimates 

from the meta-analyses was not a predominant factor in making a causal conclusion. For that purpose, 

this report relied on the approach and criteria set 

out in the 1964 and 2004 reports of the Surgeon General, which involved judgments based on an array 

of quantitative and qualitative considerations that 

included the degree of heterogeneity in the designs of 

the studies that were examined. Sometimes this heterogeneity limits the inference from meta-analysis by 

weakening the rationale for pooling the study results. 

However, the availability of consistent evidence 

from heterogenous designs can strengthen the metaanalytic findings by making it unlikely that a common 

bias could persist across different study designs and 

populations.

Confounding 

Confounding, which refers in this context to 

the mixing of the effect of another factor with that of 

secondhand smoke, has been proposed as an explanation for associations of secondhand smoke with 

adverse health consequences. Confounding occurs 

when the factor of interest (secondhand smoke) is 

associated in the data under consideration with 

another factor (the confounder) that, by itself, increases 

the risk for the disease (Rothman and Greenland 1998). 

Correlates of secondhand smoke exposures are not 

confounding factors unless an exposure to them 

increases the risk of disease. A factor proposed as 

a potential confounder is not necessarily an actual 

confounder unless it fulfills the two elements of the 

definition. Although lengthy lists of potential confounding factors have been offered as alternatives to 

direct associations of secondhand smoke exposures 

with the risk for disease, the factors on these lists generally have not been shown to be confounding in the 

particular data of interest.

The term confounding also conveys an implicit 

conceptualization as to the causal pathways that link 

secondhand smoke and the confounding factor to 

Direct path 

 Risk for adverse effect

Causal path 

 Risk for adverse effect

 

Confounding 

 SHS

 exposure

 Risk for adverse effect

SHS

exposure

Figure 1.2 Model for socioeconomic status 

(SES) and secondhand smoke (SHS) 

exposure

▲

▲ ▲ ▲

▲

▲

▲▲

▲

▲

▲

▲

Lower

SES

Lower

SES

Lower

SES

Smoking

active ▲

Arrows indicate directionality of association.
The Health Consequences of Involuntary Exposure to Tobacco Smoke

Executive Summary 21

disease risk. Confounding implies that the confounding factor has an effect on risk that is independent of 

secondhand smoke exposure. Some factors considered 

as potential confounders may, however, be in the same 

causal pathway as a secondhand smoke exposure. 

Although socioeconomic status (SES) is often cited 

as a potential confounding factor, it may not have an 

independent effect but can affect disease risk through 

its association with secondhand smoke exposure 

(Figure 1.2). This figure shows general alternative relationships among SES, secondhand smoke exposure, 

and risk for an adverse effect. SES may have a direct 

effect, or it may indirectly exert its effect through an 

association with secondhand smoke exposure, or it 

may confound the relationship between secondhand 

smoke exposure and disease risk. To control for SES 

as a potential confounding factor without considering 

underlying relationships may lead to incorrect risk 

estimates. For example, controlling for SES would not 

be appropriate if it is a determinant of secondhand 

smoke exposure but has no direct effect.

Nonetheless, because the health effects of involuntary smoking have other causes, the possibility of 

confounding needs careful exploration when assessing associations of secondhand smoke exposure with 

adverse health effects. In addition, survey data from 

the last several decades show that secondhand smoke 

exposure is associated with correlates of lifestyle that 

may influence the risk for some health effects, thus 

increasing concerns for the possibility of confounding (Kawachi and Colditz 1996). Survey data from the 

United States (Matanoski et al. 1995) and the United 

Kingdom (Thornton et al. 1994) show that adults with 

secondhand smoke exposures generally tend to have 

less healthful lifestyles. However, the extent to which 

these patterns of association can be generalized, either 

to other countries or to the past, is uncertain.

The potential bias from confounding varies with 

the association of the confounder to secondhand smoke 

exposures in a particular study and to the strength of 

the confounder as a risk factor. The importance of confounding to the interpretation of evidence depends 

further on the magnitude of the effect of secondhand 

smoke on disease. As the strength of an association 

lessens, confounding as an alternative explanation 

for an association becomes an increasing concern. In 

prior reviews, confounding has been addressed either 

quantitatively (Hackshaw et al. 1997) or qualitatively 

(Cal/EPA 1997; Thun et al. 1999). In the chapters in 

this report that focus on specific diseases, confounding is specifically addressed in the context of potential 

confounding factors for the particular diseases.

Tobacco Industry Activities

The evidence on secondhand smoke and disease 

risk, given the public health and public policy implications, has been reviewed extensively in the published peer-reviewed literature and in evaluations by 

a number of expert panels. In addition, the evidence 

has been criticized repeatedly by the tobacco industry 

and its consultants in venues that have included the 

peer-reviewed literature, public meetings and hearings, and scientific symposia that included symposia 

sponsored by the industry. Open criticism in the peerreviewed literature can strengthen the credibility of 

scientific evidence by challenging researchers to consider the arguments proposed by critics and to rebut 

them.

Industry documents indicate that the tobacco 

industry has engaged in widespread activities, however, that have gone beyond the bounds of accepted 

scientific practice (Glantz 1996; Ong and Glantz 2000, 

2001; Rampton and Stauber 2000; Yach and Bialous 

2001; Hong and Bero 2002; Diethelm et al. 2004). 

Through a variety of organized tactics, the industry 

has attempted to undermine the credibility of the scientific evidence on secondhand smoke. 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 (Garne et al. 2005). 

These tactics are not a topic of this report, but to the 

extent that the scientific literature has been distorted, 

they are addressed as the evidence is reviewed. This 

report does not specifically identify tobacco industry 

sponsorship of publications unless that information 

is relevant to the interpretation of the findings and 

conclusions.
Surgeon General’s Report

22 Executive Summary

A Vision for the Future 

consideration. As the public policy debate grew and 

expanded in the 1980s, the scientific evidence on the 

risk of adverse effects from exposure to secondhand 

smoke was presented in a comprehensive context for 

the first time by Surgeon General C. Everett Koop in 

the 1986 report, The Health Consequences of Involuntary 

Smoking (U.S. Department of Health and Human Services [USDHHS] 1986).

The ever-increasing momentum for smoke-free 

indoor environments has been driven by scientific 

evidence on the health risks of involuntary exposure 

to secondhand smoke. This new Surgeon General’s 

report is based on a far larger body of evidence than 

was available in 1986. The evidence reviewed in this 

report confirms the findings of the 1986 report and 

adds new causal conclusions. The growing body of 

data increases support for the conclusion that exposure to secondhand smoke causes lung cancer in lifetime nonsmokers. In addition to epidemiologic data, 

this report presents converging evidence that the 

mechanisms by which secondhand smoke causes lung 

cancer are similar to those that cause lung cancer in 

active smokers. In the context of the risks from active 

smoking, the lung cancer risk that secondhand smoke 

exposure poses to nonsmokers is consistent with an 

extension to involuntary smokers of the dose-response 

relationship for active smokers.

Cardiovascular effects of even short exposures 

to secondhand smoke are readily measurable, and 

the risks for cardiovascular disease from involuntary smoking appear to be about 50 percent less than 

the risks for active smokers. Although the risks from 

secondhand smoke exposures are larger than anticipated, research on the mechanisms by which tobacco 

smoke exposure affects the cardiovascular system 

supports the plausibility of the findings of epidemiologic studies (the 1986 report did not address cardiovascular disease). This 2006 report also reviews 

the evidence on the multiple mechanisms by which 

secondhand smoke injures the respiratory tract and 

causes sudden infant death syndrome.

Since 1986, the attitude of the public toward and 

the social norms around secondhand smoke exposure have changed dramatically to reflect a growing 

viewpoint that the involuntary exposure of nonsmokers to secondhand smoke is unacceptable. As a result, 

increasingly strict public policies to control involuntary exposure to secondhand smoke have been put in 

This country has experienced a substantial 

reduction of involuntary exposure to secondhand 

tobacco smoke in recent decades. Significant reductions in the rate of smoking among adults began even 

earlier. Consequently, about 80 percent of adults are 

now nonsmokers, and many adults and children can 

live their daily lives without being exposed to secondhand smoke. Nevertheless, involuntary exposure to 

secondhand smoke remains a serious public health 

hazard.

This report documents the mounting and now 

substantial evidence characterizing the health risks 

caused by exposure to secondhand smoke. Multiple major reviews of the evidence have concluded 

that secondhand smoke is a known human carcinogen, and that exposure to secondhand smoke causes 

adverse effects, particularly on the cardiovascular 

system and the respiratory tract and on the health 

of those exposed, children as well as adults. Unfortunately, reductions in exposure have been slower 

among young children than among adults during the 

last decade, as expanding workplace restrictions now 

protect the majority of adults while homes remain the 

most important source of exposure for children.

Clearly, the social norms regarding secondhand 

smoke have changed dramatically, leading to widespread support over the past 30 years for a society free 

of involuntary exposures to tobacco smoke. In the first 

half of the twentieth century smoking was permitted 

in almost all public places, including elevators and 

all types of public transportation. At the time of the 

1964 Surgeon General’s report on smoking and health 

(U.S. Department of Health, Education, and Welfare 

[USDHEW] 1964), many physicians were still smokers, and the tables in U.S. Public Health Service (PHS) 

meeting rooms had PHS ashtrays on them. A thick, 

smoky haze was an accepted part of presentations at 

large meetings, even at medical conferences and in the 

hospital environment.

As the adverse health consequences of active 

smoking became more widely documented in the 

1960s, many people began to question whether exposure of nonsmokers to secondhand smoke also posed 

a serious health risk. This topic was first addressed 

in this series of reports by Surgeon General Jesse 

Steinfeld in the 1972 report to Congress (USDHEW 

1972). During the 1970s, policy changes to provide 

smoke-free environments received more widespread 
The Health Consequences of Involuntary Exposure to Tobacco Smoke

Executive Summary 23

place. The need for restrictions on smoking in enclosed 

public places is now widely accepted in the United 

States. A growing number of communities, counties, 

and states are requiring smoke-free environments for 

nearly all enclosed public places, including all private 

worksites, restaurants, bars, and casinos.

As knowledge about the health risks of secondhand smoke exposure grows, investigators continue 

to identify additional scientific questions.

 • Because active smoking is firmly established as a 

causal factor of cancer for a large number of sites, 

and because many scientists assert that there may 

be no threshold for carcinogenesis from tobacco 

smoke exposure, researchers hypothesize that 

people who are exposed to secondhand smoke 

are likely to be at some risk for the same types of 

cancers that have been established as smokingrelated among active smokers.

 • The potential risks for stroke and subclinical vascular disease from secondhand smoke exposure 

require additional research.

 • There is a need for additional research on the 

etiologic relationship between secondhand 

smoke exposure and several respiratory health 

outcomes in adults, including respiratory 

symptoms, declines in lung function, and adultonset asthma.

 • There is also a need for research to further evaluate the adverse reproductive outcomes and 

childhood respiratory effects from both prenatal 

and postnatal exposure to secondhand smoke.

 • Further research and improved methodologies 

are also needed to advance an understanding 

of the potential effects on cognitive, behavioral, 

and physical development that might be related 

to early exposures to secondhand smoke.

As these and other research questions are 

addressed, the scientific literature documenting the 

adverse health effects of exposure to secondhand 

smoke will expand. Over the past 40 years since the 

release of the landmark 1964 report of the Surgeon 

General’s Advisory Committee on Smoking and 

Health (USDHEW 1964), researchers have compiled an 

ever-growing list of adverse health effects caused by 

exposure to tobacco smoke, with evidence that active 

smoking causes damage to virtually every organ of 

the body (USDHHS 2004). Similarly, since the 1986 

report (USDHHS 1986), the number of adverse health 

effects caused by exposure to secondhand smoke has 

also expanded. Following the format of the electronic 

database released with the 2004 report, the research 

findings supporting the conclusions in this report 

will be accessible in a database that can be found at 

http://www.cdc.gov/tobacco. With an this expanding 

base of scientific knowledge, the list of adverse health 

effects caused by exposure to secondhand smoke will 

likely increase.

Biomarker data from the 2005 Third National 

Report on Human Exposure to Environmental Chemicals document great progress since the 1986 report in 

reducing the involuntary exposure of nonsmokers to 

secondhand smoke (CDC 2005). Between the late 1980s 

and 2002, the median cotinine level (a metabolite of 

nicotine) among nonsmokers declined by more than 

70 percent. Nevertheless, many challenges remain to 

maintain the momentum toward universal smokefree environments. First, there is a need to continue 

and even improve the surveillance of sources and levels of exposure to secondhand smoke. The data from 

the 2005 exposure report show that median cotinine 

levels among children are more than twice those of 

nonsmoking adults, and non-Hispanic Blacks have 

levels more than twice those of Mexican Americans 

and non-Hispanic Whites (CDC 2005). The multiple 

factors related to these disparities in median cotinine 

levels among nonsmokers need to be identified and 

addressed. Second, the data from the 2005 exposure 

report suggest that the scientific community should 

sustain the current momentum to reduce exposures 

of nonsmokers to secondhand smoke (CDC 2005). 

Research reviewed in this report indicates that policies creating completely smoke-free environments 

are the most economical and efficient approaches to 

providing this protection. Additionally, neither central heating, ventilating, and air conditioning systems 

nor separately ventilated rooms control exposures 

to secondhand smoke. Unfortunately, data from the 

2005 exposure report also emphasized that young 

children remain an exposed population (CDC 2005). 

However, more evidence is needed on the most effective strategies to promote voluntary changes in smoking norms and practices in homes and private automobiles. Finally, data on the health consequences of 

secondhand smoke exposures emphasize the importance of the role of health care professionals in this 

issue. They must assume a greater, more active 

involvement in reducing exposures, particularly for 

susceptible groups.
Surgeon General’s Report

24 Executive Summary

the health of children, individuals with existing heart 

and lung problems, and other vulnerable populations, 

requires a higher priority and greater protection. 

Together, this report and the 2004 report of the 

Surgeon General, The Health Consequences of Smoking (USDHHS 2004), document the extraordinary 

threat to the nation’s health from active and involuntary smoking. The recent reductions in exposures 

of nonsmokers to secondhand smoke represent significant progress, but involuntary exposures persist 

in many settings and environments. More evidence is 

needed to understand why this progress has not been 

equally shared across all populations and in all parts 

of this nation. Some states (California, Connecticut, 

Delaware, Maine, Massachusetts, New York, Rhode 

Island, and Washington) have met the Healthy People 

2010 objectives (USDHHS 2000) that protect against 

involuntary exposures to secondhand smoke through 

recommended policies, regulations, and laws, while 

many other parts of this nation have not (USDHHS 

2000). Evidence presented in this report suggests that 

these disparities in levels of protection can be reduced 

or eliminated. Sustained progress toward a society 

free of involuntary exposures to secondhand smoke 

should remain a national public health priority.

The findings and recommendations of this report 

can be extended to other countries and are supportive 

of international efforts to address the health effects of 

smoking and secondhand smoke exposure. There is 

an international consensus that exposure to secondhand smoke poses significant public health risks. The 

Framework Convention on Tobacco Control recognizes that protecting nonsmokers from involuntary 

exposures to secondhand smoke in public places 

should be an integral part of comprehensive national 

tobacco control policies and programs. Recent changes 

in national policies in countries such as Italy and Ireland reflect this growing international awareness of 

the need for additional protection of nonsmokers from 

involuntary exposures to secondhand smoke.

When this series of reports began in 1964, the 

majority of men and a substantial proportion of 

women were smokers, and most nonsmokers inevitably must have been involuntary smokers. With the 

release of the 1986 report, Surgeon General Koop noted 

that “the right of smokers to smoke ends where their 

behavior affects the health and well-being of others” 

(USDHHS 1986, p. xii). As understanding increases 

regarding health consequences from even brief exposures to secondhand smoke, it becomes even clearer 

that the health of nonsmokers overall, and particularly 
The Health Consequences of Involuntary Exposure to Tobacco Smoke

Executive Summary 25

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