Children and Secondhand
 

Smoke Exposure
 

Excerpts from
 

The Health Consequences
 

of Involuntary Exposure
 

to Tobacco Smoke
 

A Report of the Surgeon General
 

Department of Health and Human Services
 
Children and Secondhand 

Smoke Exposure 

Excerpts from 

The Health Consequences 

of Involuntary Exposure 

to Tobacco Smoke 

A Report of the Surgeon General 

2007 

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES 

Public Health Service 

Office of the Surgeon General 

Rockville, MD 
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
 

This publication is available on the World Wide Web at
 

http://www.surgeongeneral.gov/library
 

Suggested Citation 

U.S. Department of Health and Human Services. Chldren and Secondhand Smoke Exposure. 

Excerpts from The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of 

the Surgeon General. Atlanta, GA: 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, 2007. 

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Go to http://www.cdc.gov/tobacco 

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Use of trade names is for identification only and does not constitute endorsement by the 

U.S. Department of Health and Human Services. 
Foreword 

The Health Consequences of Involuntary Exposure to Tobacco Smoke provided a progress 

report on the remarkable reduction in involuntary exposure to secondhand smoke that has 

been achieved over the last 20 years. It also noted the gaps and disparities that remain in 

this regard. This excerpt highlights the serious health risks that secondhand smoke exposure poses to our children and the need to extend the same protections to them that many 

U.S. adults already enjoy. 

Children are more heavily exposed to secondhand smoke than adults. Almost 60 

percent of U.S. children aged 3-11 years, or almost 22 million children, are exposed to 

secondhand smoke. A Healthy People 2010 objective calls for reducing the proportion of 

children aged 6 years and younger who are regularly exposed to secondhand smoke in the 

home from 20 percent in 1998 to 6 percent by 2010. According to the 2005 National Health 

Interview Survey, this proportion may already be as low as 8 percent, suggesting that, 

with sustained and expanded efforts, we may be able to achieve this target. 

However, too many children continue to be exposed. Children who are exposed 

to secondhand smoke are at an increased risk for sudden infant death syndrome, lower 

respiratory infections, middle ear disease, more severe asthma, respiratory symptoms, and 

slowed lung growth. The California Environmental Protection Agency recently estimated 

that 430 infants die from sudden infant death syndrome in the United States every year as 

a result of secondhand smoke exposure. The same agency also estimated that secondhand 

smoke exposure is responsible for 202,300 asthma episodes and 790,000 doctor appointments for U.S. children with ear infections annually. Children whose parents smoke and 

who grow up in homes where smoking is allowed are also more likely to become smokers 

themselves. 

The home is the major setting where children are exposed. Children who live in 

homes where smoking is allowed have higher levels of cotinine, a biological marker for 

secondhand smoke exposure, than children who live in homes where smoking is not 

allowed. One of the strongest predictors of children’s cotinine levels is the number of cigarettes smoked daily in the home. Almost one in four children aged 3 to 11 years lives in a 

household with at least one smoker, compared to only about one in fourteen nonsmoking 

adults. Children are also exposed to secondhand smoke in vehicles. 

Low-income children and African American children are disproportionately exposed 

to secondhand smoke. In fact, cotinine levels suggest that African American children are 

among the most heavily exposed of any population group. These disparities need to be 

better understood and addressed. 

This excerpt moves forward the mission of CDC to promote and protect Americans’ 

health. I applaud those who have had a part in focusing our national attention on accelerating our progress in reducing the burden of disease that smoking and secondhand smoke 

exposure continue to impose on our nation. 

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

Director 

Centers for Disease Control and Prevention 

and 

Administrator 

Agency for Toxic Substances and Disease Registry 

 

Preface 

from the Actng Surgeon General, 

U.S. Department of Health and Human Servces 

The first Surgeon General’s report to conclude that involuntary exposure of nonsmokers to secondhand smoke causes disease was published more than 20 years ago. 

That report concluded that children whose parents smoke are more likely to experience 

respiratory infections and respiratory symptoms. 

Today, massive and conclusive scientific evidence documents the serious health 

risks that secondhand smoke poses to children, and the list of these health conditions has 

lengthened. The 2006 Surgeon General’s report on The Health Consequences of Involuntary 

Exposure to Tobacco Smoke concludes that children who are exposed to secondhand smoke 

are at an increased risk for sudden infant death syndrome, lower respiratory infections, 

middle ear disease, more severe asthma, respiratory symptoms, and slowed lung growth. 

Because their respiratory, immune, and nervous systems are still developing, children are 

especially vulnerable to the health effects of secondhand smoke. In addition, young children typically are exposed to secondhand smoke involuntarily and have limited options 

for avoiding exposure. They depend on their parents and on adults around them for protection. 

On average, children are exposed to more secondhand smoke than nonsmoking adults. Most of these children are exposed to secondhand smoke at home. Children 

continue to be exposed in their homes as a result of the smoking of their parents and 

other adults. Among children younger than 18 years of age, approximately 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. 

We know that making homes smoke-free reduces secondhand smoke exposure 

among children and nonsmoking adults, helps smokers quit, and decreases smoking initiation among youth. What we don’t know, due to a lack of definitive research in this area, 

is what interventions are most effective in convincing parents to take this step. Targeted, 

sustained research in this area is urgently needed, with a special focus on evaluating ongoing initiatives to establish what works. 

The evidence suggests that vehicles can also be a significant source of secondhand 

smoke exposure for children. Children can be regularly exposed to secondhand smoke 

when parents or other adults smoke in these vehicles while they are present. The concentrations of secondhand smoke in vehicles where smoking is occurring can reach very high 

levels. Making vehicles smoke-free would be expected to reduce children’s secondhand 

smoke exposure. Again, the challenge is what approaches are effective and appropriate 

for achieving this objective. To date, it appears that few educational campaigns promoting 

smoke-free home rules have promoted the adoption of similar rules in vehicles. The U.S. 

Environmental Protection Agency has recently begun to address this setting in its educational efforts. 

Parents want nothing but the best for their children. Many parents make great sacrifices for their children’s benefit. If they knew how harmful secondhand smoke was to children, most parents would take steps to protect them. In fact, many parents do attempt to 

protect their children from secondhand smoke, but take measures that are ineffective, such 

as smoking by a window or fan, opening a window, or limiting smoking to certain rooms. 

The 2006 Surgeon General’s report makes clear that establishing a completely smoke-free 

 
home is the only effective way to eliminate secondhand smoke exposure in this setting. It 

is important that parents receive this message. Educational efforts can play a crucial role 

in helping parents understand why they need to protect their children from this health 

hazard and how to do so effectively. 

Pediatricians are especially well-positioned to influence parents on this issue. Because 

of the high levels of secondhand smoke exposure among young children and the health 

problems they experience as a result, their exposure should be considered a significant 

medical issue. Well-child visits provide regular opportunities to screen children for exposure and to educate parents about the importance of protecting children from secondhand smoke. Parents who smoke are likely to see a pediatrician more often than they see 

their own physicians. Pediatrician visits occasioned by an illness related to secondhand 

smoke exposure, such as pneumonia, offer a unique teachable moment. Pediatricians can 

advise parents to quit smoking, and can refer them to the range of evidence-based cessation aids that are available, including cessation assistance through 1-800-QUITNOW and 

FDA-approved cessation medications. In the interim, pediatricians can encourage parents 

to make their homes and cars smoke-free and to always go outside to smoke. The evidence 

indicates that, in addition to protecting their children, this step will also help parents and 

caregivers to quit. 

Exposure to secondhand smoke among children remains a major public health problem. Of the more than 126 million U.S. nonsmokers who are still exposed, almost 40 million are children aged 3 to 18 years. We now have clear evidence that only completely 

smoke-free environments can eliminate secondhand smoke exposure and its related health 

risks. We need to apply this knowledge to educate parents to take action to make the settings where their children spend time smoke-free. The public’s attitudes and social norms 

toward secondhand smoke exposure have changed significantly; it’s high time that we 

build on these changes to protect our children. 

Kenneth P. Moritsugu, M.D., M.P.H. 

Acting Surgeon General 

v 
Introduction
 

These excerpts from the 2006 Surgeon General’s report, The Health Consequences of Involuntary Exposure to Tobacco Smoke, highlight the harmful effects of secondhand smoke exposure on children. The text and tables that follow are drawn directly from the report that was 

released previously by the Surgeon General (USDHHS 2006). 

The report concluded that secondhand smoke causes premature death and disease in 

children. In addition, the report also concluded that children who are exposed to secondhand smoke are at an increased risk for sudden infant death syndrome, lower respiratory 

infections, middle ear disease, more severe asthma, respiratory symptoms, and slowed lung 

growth. The California Environmental Protection Agency (Cal/EPA) has estimated that 430 

infants die from sudden infant death syndrome in the United States every year as a result of 

secondhand smoke exposure (Cal/EPA 2005). The same report also estimated that secondhand smoke exposure is responsible for 202,300 asthma episodes and 790,000 doctor appointments for U.S. children with ear infections annually. 

Children and teens are more heavily exposed to secondhand smoke than adults. Almost 

60 percent of U.S. children aged 3 to 11 years, or almost 22 million children, are exposed to 

secondhand smoke. 

Because their respiratory, immune, and nervous systems are still developing, children 

are especially vulnerable to the health effects of secondhand smoke. In addition, young children typically are exposed to secondhand smoke involuntarily and have limited options for 

avoiding exposure. They depend on their parents and on other adults to protect them. 

The home is the major setting where children are exposed to secondhand smoke. Children who live in homes where smoking is allowed have higher levels of cotinine, a biological 

marker for secondhand smoke exposure, than children who live in homes where smoking is 

not allowed (CDC 2005). Almost one in four children aged 3 to 11 years lives in a household 

with at least one smoker, compared to only about 7 percent of nonsmoking adults. 

The dramatic strides that have been made over the past 20 years in reducing nonsmokers’ secondhand smoke exposure has to some extent left children behind. While increasing 

numbers of homes, including many homes where smokers live, are going smoke-free, the 

pace of progress in this setting has lagged behind the spread of smoke-free environments in 

workplaces and public places. It is ironic that the Americans who are at the greatest risk from 

secondhand smoke and who are least able to defend themselves are also the least protected 

and the most heavily exposed. 

It is high time that we address this disparity. We need to act now to ensure that all parents have the facts they need to make informed decisions to protect their families from this 

completely preventable health hazard. 

References 

California Environmental Protection Agency. Proposed Identficaton of Envronmental Tobacco 

Smoke as a Toxc Ar Contamnant. Part B: Health Effects. Sacramento (CA): California Environmental Protection Agency, Office of Environmental Health Hazard Assessment, 2005. 

Centers for Disease Control and Prevention. Thrd Natonal Report on Human Exposure to Env­

ronmental Chemcals. Atlanta: U.S. Department of Health and Human Services, Centers for 

Disease Control and Prevention, National Center for Environmental Health, 2005. NCEH 

Publication No. 05-0570. 

U.S. Department of Health and Human Services. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General. Atlanta: U.S. Department of Health and 

Human Services, Centers for Disease Control and Prevention, National Center for Chronic 

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

v 

Excerpts from Chapter 1
 

Introduction, Summary, and Conclusions
 

Introduction 3
 

Definitions and Terminology 5
 

Major Conclusions 6
 

References 7
 

1 
 Chapter 1
 
Excerpts: Chldren and Secondhand Smoke Exposure 

Introduction 

The topic of passive or involuntary smoking 

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

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 

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. 

Involuntary smoking was the topic for the entire 

1986 Surgeon General’s report, The Health Consequences of Involuntary Smokng (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; patterns of exposure of nonsmokers to tobacco smoke; 

Introducton, Summary, and Conclusons 3 
Surgeon General’s Report 

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. 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, 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. 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 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. The most recent was the 2005 report of the California Environmental Protection Agency (Cal/EPA 

2005). Over time, research has repeatedly affirmed the 

conclusions of the 1986 Surgeon General’s report 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 result annually 

from exposure to secondhand smoke (Cal/EPA 2005). 

Estimated annual excess deaths for the total U.S. 

 Chapter 1 
Excerpts: Chldren and Secondhand Smoke Exposure 

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 

Definitions and Terminology 

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 

Smokng, 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. 

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 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. 

Introducton, Summary, and Conclusons 5 
Surgeon General’s Report 

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: 

The following conclusions are supported by 

text in the full report that may not be included 

in this excerpt. The full report can be accessed at 

http://www.surgeongeneral.gov/library/secondhandsmoke/report/. 

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, 

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. 

 Chapter 1 
Excerpts: Chldren and Secondhand Smoke Exposure 

References 

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Hazard Assessment Section and Air Toxicology 

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a Toxc Ar Contamnant. Part B: Health Effects. Sacramento (CA): California Environmental Protection 

Agency, Office of Environmental Health Hazard 

Assessment, 2005. 

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of Chemcals to Humans: Tobacco Smokng. Vol. 38. 

Lyon (France): International Agency for Research 

on Cancer, 1986. 

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Smoke: Measurng Exposures and Assessng Health 

Effects. Washington: National Academy Press, 1986. 

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Health Consequences of Smokng: Cancer. A Report of 

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Service, Office on Smoking and Health. 1982. DHHS 

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Health Consequences of Smokng: Chronc Obstructve 

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and Human Services, Centers for Disease Control 

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Smoking and Health, 2004. 

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Health Consequences of Involuntary Exposure to Tobacco 

Smoke: A Report of the Surgeon General. Atlanta: U.S. 

Department of Health and Human Services, Centers for Disease Control and Prevention, National 

Center for Chronic Disease Prevention and Health 

Promotion, Office on Smoking and Health, 2006. 

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

Smokng and Health: Report of the Advsory Commttee to the Surgeon General of the Publc Health Servce. 

Washington: U.S. Department of Health, Education, and Welfare, Public Health Service, Center for 

Disease Control, 1964. PHS Publication No. 1103. 

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

The Health Consequences of Smokng. A Report of the 

Surgeon General: 1972. Washington: U.S. Department of Health, Education, and Welfare, Public 

Health Service, Health Services and Mental Health 

Administration, 1972. DHEW Publication No. 

(HSM) 72-7516. 

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

The Health Consequences of Smokng. A Report of the 

Surgeon General, 1975. Washington: U.S. Department of Health, Education, and Welfare, Public 

Introducton, Summary, and Conclusons 7 
Surgeon General’s Report 

Health Service, Center for Disease Control, 1975. 

DHEW Publication No. (CDC) 77-8704. 

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

Smokng and Health. A Report of the Surgeon General. 

Washington: U.S. Department of Health, Education, and Welfare, Public Health Service, Office of 

the Assistant Secretary for Health, Office of Smoking and Health, 1979. DHEW Publication No. (PHS) 

79-50066. 

U.S. Environmental Protection Agency. 	Respratory 

Health Effects of Passve Smokng: Lung Cancer and 

Other Dsorders. Washington: U.S. Environmental 

Protection Agency, Office of Research and Development, Office of Air Radiation, 1992. Report No. 

EPA/600/6-90/0006F. 

 Chapter 1 
Excerpts from Chapter 4
 

Prevalence of Exposure to Secondhand Smoke
 

Introduction 11
 

Methods 11
 

Estimates of Exposure 12
 

National Trends in Biomarkers of Exposure 12
 

Environmental Sites of Exposure 15
 

Exposure in the Home 1
 

Representative Surveys of Children 17
 

Susceptible Populations 1
 

Measurements of Airborne Tracers in Homes 19
 

Exposure in Public Places 20
 

Restaurants, Cafeterias, and Bars 20
 

Evidence Synthesis 21
 

Conclusions 22
 

Overall Implications 22
 

References 23
 

9 

Excerpts: Chldren and Secondhand Smoke Exposure 

Introduction 

The 1986 U.S. Surgeon General’s report, The 

Health Consequences of Involuntary Smokng, outlined 

the need for valid and reliable methods to more accurately determine and assess the health consequences 

of exposure to secondhand smoke (U.S. Department 

of Health and Human Services [USDHHS] 1986). The 

report concluded that reliable methods were necessary to research the health effects and to characterize 

the public health impact of exposure to secondhand 

tobacco smoke in the home, at work, and in other 

environments. The report noted that without valid 

and reliable evidence, policymakers could not draft 

and implement effective policies to reduce and eliminate exposures: “Validated questionnaires are needed 

for the assessment of recent and remote exposure to 

environmental tobacco smoke in the home, workplace, 

and other environments” (USDHHS 1986, p. 14). 

Since the publication of that report, public health 

investigators have made significant advances in the 

development and application of reliable and valid 

research methods to assess exposure to secondhand 

smoke (Jaakkola and Samet 1999; Samet and Wang 

2000). Several investigators have recently developed 

Methods 

new methods to measure tobacco smoke concentrations 

in indoor environments and have discovered sensitive 

biologic markers of active and involuntary exposures 

(Jaakkola and Samet 1999; Samet and Wang 2000). 

These advances have generated a substantial amount 

of data on exposure of nonsmokers to secondhand 

smoke and have improved the capability of researchers to measure a recent exposure. However, many 

public health investigators agree that more accurate 

tools are still needed to measure temporally remote 

exposures, which, by necessity, are still assessed using 

questionnaires (Jaakkola and Samet 1999). 

The main methods researchers rely on to evaluate secondhand smoke exposure are questionnaires, 

measurements of concentrations of the airborne components of secondhand smoke, and measurements of 

biomarkers (see Chapter 3, Assessment of Exposure 

to Secondhand Smoke in the full report). The discussion that follows on the prevalence of secondhand 

smoke exposure includes current metrics of exposure, 

changes in exposure over time, exposure of special 

populations such as children with asthma and persons 

in prisons, and international differences in exposure. 

To identify research publications on biomarkers of secondhand smoke, the authors of this chapter 

reviewed the published literature for studies on population exposures to and concentrations of secondhand smoke in different environments by conducting 

a Medline search with the following terms: tobacco 

smoke pollution, environmental tobacco smoke, and 

secondhand smoke. These terms were then paired 

with the term population or survey. The authors then 

reviewed abstracts of articles to specifically identify 

studies that used representative surveys of the U.S. 

population for inclusion in this report. 

To specifically identify articles on concentrations of secondhand smoke, the authors used Boolean 

logic to search Medline and Web of Science, pairing 

the selected terms for secondhand smoke (secondhand smoke, environmental tobacco smoke, passive 

smoking, and involuntary smoking) with terms indicative of a location that included home, work, workplace, occupation and restaurants, bars, public places, 

sports, transportation, buses, trains, cars, airplanes, 

casinos, bingo, nightclubs, prisons, correctional institutions, nursing homes, and mental institutions. The 

authors searched for these terms with and without 

other selected terms such as exposure, concentration, 

and level of exposure. The authors also included data 

from a review of studies on the composition and measurement of secondhand smoke (Jenkins et al. 2000). 

Prevalence of Exposure to Secondhand Smoke 11 
Surgeon General’s Report 

This chapter focuses on measured concentrations of airborne nicotine—nicotine is a specific tracer 

for secondhand smoke and has therefore been widely 

used in many studies. This discussion also focuses 

on biomarker levels of cotinine, the metabolite of 

Estimates of Exposure 

nicotine. Thus, the abstracts of articles identified 

through the literature search were further reviewed 

for data that contained measured values of nicotine in 

the air of selected environments. 

National Trends in Biomarkers 

of Exposure 

Beginning in 1988, researchers used serum cotinine measurements to assess exposures to secondhand 

smoke in the United States within the National Health 

and Nutrition Examination Survey (NHANES). The 

NHANES is conducted by the National Center for 

Health Statistics (NCHS), Centers for Disease Control 

and Prevention (CDC), and is designed to examine a 

nationally representative sample of the U.S. civilian 

(noninstitutionalized) population based upon a complex, stratified, multistage probability cluster sampling design (see http://www.cdc.gov/nchs/nhanes. 

htm). The protocols include a home interview followed by a physical examination in a mobile examination center, where blood samples are drawn for serum 

cotinine analysis. NHANES III, conducted from 1988 

to 1994, was the first national survey of secondhand 

smoke exposure of the entire U.S. population aged 

4 through 74 years. There were two phases: Phase 

I from 1988 to 1991, and Phase II from 1991 to 1994. 

There were no further studies between 1995 and 1998. 

In 1999, NCHS resumed NHANES on a continuous 

basis and completed a new nationally representative 

sample every two years. This more recent NHANES 

(1999) also began to draw blood samples for serum 

cotinine analyses from participants aged three years 

and older. 

Researchers have reported serum cotinine levels in nonsmokers from the NHANES for four distinct intervals within the overall time period of 14 

years, from 1988 through 2002: Phase I and Phase II 

of NHANES III, NHANES 1999–2000, and NHANES 

2001–2002 (Pirkle et al. 1996, 2006). Researchers have 

reported additional data on serum cotinine levels in nonsmokers from NHANES 1999–2002 in the 

National Report on Human Exposure to Environmental Chemicals (CDC 2001a, 2003, 2005). To maintain 

comparability among survey intervals, trend data are 

only reported for participants aged four or more years 

in each study interval (Pirkle et al. 2006). Factors that 

affect nicotine metabolism, such as age, race, and the 

level of exposure to secondhand smoke, also influence 

cotinine levels (Caraballo et al. 1998; Mannino et al. 

2001). Because cotinine levels reflect exposures that 

occurred within two to three days, they represent patterns of usual exposure (Jarvis et al. 1987; Benowitz 

1996; Jaakkola and Jaakkola 1997). 

Studies document NHANES serum cotinine levels in both children and adult nonsmokers (Pirkle et 

al. 1996, 2006; CDC 2001a, 2003, 2005). Nonsmoking 

adults were defined in these studies as persons whose 

serum cotinine concentrations were 10 nanograms per 

milliliter (ng/mL) or less, who reported no tobacco or 

nicotine use in the five days before the mobile examination center visit, and who were self-reported former smokers or lifetime nonsmokers. In NHANES 

III, the laboratory limit of detection was 0.050 ng/mL. 

However, the laboratory methods have continued to 

improve, and the detection limit was recently lowered 

to 0.015 ng/mL (CDC 2005; Pirkle et al. 2006). Additionally, researchers have categorized serum cotinine concentrations by age, race, and ethnicity. The 

racial and ethnic categories are non-Hispanic White, 

non-Hispanic Black, Mexican American, or “Other,” 

and are self-reported. The category of “Other” was 

included in these reports in mean and percentile estimates for the total population but not in the geometric 

mean estimates because of small sample sizes (CDC 

2005; Pirkle et al. 2006). 

Figure 4.1 shows the overall proportion of all 

nonsmokers aged four or more years with serum cotinine levels of 0.050 ng/mL or greater for the four survey periods. Pirkle and colleagues (1996) reported 

detectable levels of serum cotinine among nearly all 

nonsmokers (87.9 percent) during Phase I (1988–1991) 

of NHANES III. Exposures among nonsmokers have 

declined significantly since that time (CDC 2005). 

The proportion of U.S. nonsmokers with cotinine 

12 Chapter  
Excerpts: Chldren and Secondhand Smoke Exposure 

concentrations of 0.050 ng/mL or greater fell to 43 

percent in NHANES 2001–2002 (Pirkle et al. 2006). 

Pirkle and colleagues (2006) provided additional 

data on the levels and distribution of serum cotinine 

concentrations in U.S. nonsmokers during 1988–2002. 

Trends in the adjusted geometric mean cotinine concentrations (adjusted for age, race, and gender) are in 

Table 4.1. Since Phase I of NHANES III, secondhand 

smoke exposures measured by serum cotinine concentrations in U.S. nonsmokers aged four or more years 

have declined by about 75 percent (from 0.247 ng/ 

mL to 0.061 ng/mL). While declines among children 

aged 4 through 11 years and young persons aged 12 

through 19 years also have been notable, the declines 

have been smaller than those among adults aged 20 

through 74 years. Trends among racial and ethnic categories were also stratified by age: 4 through 11 years, 

12 through 19 years, and 20 through 74 years. Pirkle 

and colleagues (2006) noted that serum cotinine levels 

in NHANES differed by race and ethnicity. Overall, 

in the order of the adjusted mean cotinine concentrations during each of the four time periods, concentrations among Mexican Americans were less than those 

of non-Hispanic Whites, which were less than those 

of non-Hispanic Blacks; the non-Hispanic Black mean 

cotinine concentrations were significantly higher during each of the four time periods (Pirkle et al. 2006). 

Current patterns of secondhand smoke exposure are reflected in the NHANES 1999–2002 serum 

cotinine concentrations (Table 4.2). As noted in Figure 

4.1, the proportion of U.S. nonsmokers with serum 

cotinine levels of 0.050 ng/mL or greater has declined 

since NHANES III to less than 45 percent. However, 

the proportion of children and nonsmoking adults 

with serum cotinine levels of 0.050 ng/mL or greater 

in NHANES 1999–2002 differs significantly by age, 

from 59.6 percent among children aged 3 through 11 

years to 35.7 percent among nonsmoking adults aged 

60 through 74 years. Additionally, the median cotinine concentration in the serum is significantly higher 

in children aged 3 through 11 years (0.09 ng/mL) than 

in older adults (0.035 ng/mL) (CDC 2005). Children 

aged 3 through 11 years and youth aged 12 through 19 

years are also significantly more likely than adults to 

live in a household with at least one smoker. Estimates 

of the number of secondhand smoke exposures nationwide in 2000 can be extrapolated from national estimates of the proportion of children and nonsmoking 

Prevalence of Exposure to Secondhand Smoke 13 
Surgeon General’s Report 

Table 4.1 	 Trends in serum cotinine levels (nanograms per milliliter) of nonsmokers* stratified by age, 

gender, race, and ethnicity, United States, 1988–2002 

% decline 

NHANES III, NHANES III, from 

Phase I Phase II NHANES NHANES 1988–1991 to 

Population 1988–1991 1991–1994 1999–2000 2001–2002 2001–2002 

Overall 

Aged ≥ 4 years Geometric mean† 0.247 0.182 0.106 0.061 75.3 

95% CI‡ 0.219–0.277 0.165–0.202 0.094–0.119 0.049–0.076 

Aged 4–11 years

 Male Geometric mean 0.283 0.234 0.166 0.098 65.4 

95% CI 0.223–0.360 0.188–0.291 0.105–0.262 0.064–0.151

 Female Geometric mean 0.328 0.285 0.172 0.115 64.9 

95% CI 0.240–0.449 0.235–0.345 0.113–0.262 0.075–0.177

 Race and ethnicity

 Non-Hispanic White Geometric mean 0.295 0.255 0.171 0.100 

95% CI 0.226–0.385 0.214–0.303 0.100–0.293 0.061–0.165

 Non-Hispanic Black Geometric mean 0.534 0.460 0.284 0.261 

95% CI 0.387–0.738 0.393–0.538 0.249–0.324 0.188–0.361

 Mexican American Geometric mean 0.192 0.125 0.080 0.060 

95% CI 0.148–0.250 0.107–0.145 0.066–0.097 0.042–0.086 

Aged 12–19 years

 Male Geometric mean 0.346 0.239 0.189 0.090 74.0 

95% CI 0.255–0.470 0.190–0.300 0.138–0.258 0.061–0.132

 Female Geometric mean 0.280 0.228 0.156 0.078 72.1 

95% CI 0.223–0.353 0.175–0.298 0.124–0.197 0.048–0.126

 Race and ethnicity

 Non-Hispanic White Geometric mean 0.301 0.219 0.170 0.074 

95% CI 0.228–0.396 0.174–0.276 0.139–0.210 0.044–0.123

 Non-Hispanic Black Geometric mean 0.515 0.460 0.263 0.227 

95% CI 0.392–0.677 0.374–0.567 0.229–0.303 0.191–0.270

 Mexican American Geometric mean 0.179 0.143 0.095 0.063 

95% CI 0.139–0.229 0.126–0.162 0.082–0.110 0.045–0.089 

1 Chapter  
Excerpts: Chldren and Secondhand Smoke Exposure 

Table 4.1 Continued 

% decline 

NHANES III, NHANES III, from 

Phase I Phase II NHANES NHANES 1988–1991 to 

Population 1988–1991 1991–1994 1999–2000 2001–2002 2001–2002 

Aged ≥ 20 years

 Male Geometric mean 0.293 0.199 0.106 0.067 77.1 

95% CI 0.259–0.332 0.178–0.222 0.092–0.122 0.054–0.082

 Female Geometric mean 0.188 0.138 0.078 0.042 77.7 

95% CI 0.165–0.215 0.120–0.159 0.072–0.085 0.035–0.050

 Race and ethnicity

 Non-Hispanic White Geometric mean 0.215 0.151 0.085 0.044 

95% CI 0.189–0.244 0.133–0.172 0.077–0.095 0.036–0.055

 Non-Hispanic Black Geometric mean 0.401 0.299 0.135 0.129 

95% CI 0.325–0.494 0.271–0.330 0.116–0.157 0.101–0.163

 Mexican American Geometric mean 0.204 0.138 0.078 0.058 

95% CI 0.165–0.251 0.117–0.162 0.066–0.093 0.040–0.083 

*From four National Health and Nutrition Examination Survey (NHANES) study intervals. 

†

Individuals with serum cotinine levels below the laboratory limit of detection (LOD) were assigned a value of LOD/square 

root of 2. 

‡

CI = Confidence interval.
 

Source: Adapted from Pirkle et al. 2006.
 

adults with measured serum cotinine concentrations 

of 0.05 ng/mL or greater. Overall, based upon serum 

cotinine measures, approximately 22 million children 

aged 3 through 11 years, 18 million nonsmoking youth 

aged 12 through 19 years, and 86 million nonsmoking 

adults aged 20 or more years in the United States were 

exposed to secondhand smoke in 2000 (Table 4.2). 

Although the number of children and nonsmoking adults currently exposed to secondhand smoke 

in the United States remains very large, there have 

been significant declines in the proportion and mean 

concentrations of these exposures since 1988. In order 

to characterize these trends in exposure, data on the 

principal environments where children and nonsmoking adults are typically exposed to secondhand smoke 

are reviewed in the discussion that follows. 

Environmental Sites of Exposure 

The principal places where studies have measured exposures to secondhand smoke represent key 

microenvironments: homes, worksites, and public 

places such as restaurants, malls, and bars. The contributions of these different locations to total personal 

exposures vary across different groups. For example, 

the dominant site of exposure for children is the home, 

whereas worksites are typically important exposure 

locations for nonsmoking adults who may not be 

exposed at home. 

People spend most of their time at home, which 

is potentially the most important location of secondhand smoke exposure for people who live with regular smokers (Klepeis 1999). Because the workplace is 

second only to the home as the location where adults 

spend most of their time, smoking in the workplace has 

been a major contributor to total secondhand smoke 

exposure. The National Human Activity Pattern Survey (NHAPS), conducted from 1992 to 1994, interviewed 9,386 randomly chosen U.S. residents about 

their activities and exposures to secondhand smoke 

(Klepeis 1999; Klepeis et al. 2001). For those persons 

reporting secondhand smoke exposure of at least one 

minute, the average daily duration of the exposure 

Prevalence of Exposure to Secondhand Smoke 15 
Surgeon General’s Report 

Table 4.2 Serum cotinine levels among nonsmokers aged 3 years and older, NHANES* 1999–2002 

% with at least Estimated number of 

Median cotinine % with levels 1 smoker in the persons (in millions) 

level (SE†

) ≥ 0.05 ng/mL§ (SE) home (SE) Total population with serum cotinine 

Age group (95% CI‡

) (95% CI) (95% CI) (2000) levels ≥ 0.05 ng/mL 

≥ 3 years <LOD∆

(<LOD–0.52) 

47.0 (1.9) 

(43.0–50.9) 

11.1 (0.45) 

(10.2–12.0) 

270,005,230 126.9 

3–19 years 0.08 (0.01) 

(0.06–0.11) 

57.7 (2.8) 

(52.0–63.3) 

22.6 (1.4) 

(19.9–25.6) 

69,056,589 39.8

 3–11 years 0.09 (0.02) 

(0.06–0.12) 

59.6 (2.9) 

(53.5–65.4) 

24.9 (1.8) 

(21.5–28.7) 

36,697,776 21.9

 12–19 years 0.07 (0.01) 

(0.05–0.10) 

55.6 (3.1) 

(49.1–61.9) 

19.9 (1.3) 

(17.4–22.7) 

32,358,813 18.0 

≥ 20 years <LOD 

(<LOD–<LOD) 

42.8 (1.9) 

(39.0–46.6) 

6.56 (0.32) 

(5.93–7.25) 

200,948,641 86.0

 20–39 years <LOD 

(<LOD–0.066) 

49.2 (2.9) 

(43.3–55.2) 

6.85 (0.77) 

(5.43–8.61) 

81,562,389 40.1

 40–59 years <LOD 

(<LOD–<LOD) 

41.6 (2.2) 

(37.1–46.2) 

7.3 (0.86) 

(5.73–9.26) 

73,589,052 30.6 

≥ 60 years <LOD 

(<LOD–<LOD) 

35.7 (1.7) 

(32.3–39.4) 

5.12 (0.52) 

(4.15–6.3) 

45,797,200 16.3 

*NHANES = National Health and Nutrition Examination Survey. 

†

SE = Standard error. 

‡

CI = Confidence interval.
 

§

ng/mL = Nanograms per milliliter.
 

LOD = Limit of detection (0.05 ng/mL).
 

Sources: U.S. Bureau of the Census 2005; Centers for Disease Control and Prevention, National Center for Health Statistics, 


unpublished data.
 

and the percentage of respondents who reported an 

exposure in each indoor locale were as follows: 

• 305 minutes in the home (58 percent); 

• 363 minutes in the office or factory (10 percent); 

• 249 minutes in schools or public buildings 


(6 percent); 


• 143 minutes in bars or restaurants (23 percent); 

• 198 minutes in malls or stores (7 percent); 

• 79 minutes in vehicles (33 percent); and 

• 255 minutes in other indoor locations (6 percent)

 (Klepeis 1999). 

Even for adults who live in homes where 

smoking routinely occurs, the workplace can add 

significantly to this exposure. Among NHANES III 

participants who lived in smoke-free homes, a workplace that permitted smoking was typically the major 

contributor to their total secondhand smoke exposure 

(Pirkle et al. 1996). 

Studies have shown that restaurants can be 

important sites of exposures to children as well as 

adults (Maskarinec et al. 2000; McMillen et al. 2003; 

Skeer and Siegel 2003; Siegel et al. 2004), and other 

public places may also contribute substantially to 

exposures of selected segments of the population. 

Finally, persons who cannot move about freely, such 

as those who live in nursing homes, mental institutions, or correctional facilities, may find such exposures unavoidable. 

Exposure in the Home 

Secondhand smoke exposure at home can be 

substantial for both children and adults (Jenkins et al. 

1996a; Pirkle et al. 1996; Klepeis 1999; Klepeis et al. 

2001). This section considers children exposed to secondhand smoke at home separately from adults who 

are exposed at home because the patterns are different 

1 Chapter  
Excerpts: Chldren and Secondhand Smoke Exposure 

for the two groups (Mannino et al. 1996, 1997). The 

definition of “children” varies across the studies cited 

in this report. There are also separate data for special 

populations, including children with asthma, pregnant women, and persons living in the inner city. 

Representative Surveys of Children 

Researchers have conducted a number of local 

(Greenberg et al. 1989), state (King et al. 1998), and 

national (Mannino et al. 1996) surveys of childhood 

exposure to secondhand smoke. One of the best data 

sources available on children’s secondhand smoke 

exposure in the home is the National Health Interview Survey (NHIS). This information can be derived 

from NHIS data by correlating data on smoking in the 

home with data on households with children. NHIS 

data shows that the proportion of children aged 6 

years and younger who are regularly exposed to secondhand smoke in their homes fell from 27 percent 

in 1994 to 20 percent in 1998. Most surveys were primarily based on the indirect indicator of one or more 

smoking adults in a home; estimates of the percentages exposed in the home ranged from 54 to 75 percent of the children (Lebowitz and Burrows 1976; 

Schilling et al. 1977; Ferris et al. 1985). A 1988 survey 

using an indirect indicator estimated that 48.9 percent 

of the children studied had experienced postnatal 

exposures to secondhand smoke (Overpeck and Moss 

1991). Exposure prevalence was higher for children 

in poverty (63.6 percent) or for those whose mothers 

had less than 12 years of education (66.7 percent). An 

analysis of National Health Interview Survey (NHIS) 

data for 1994 showed that 35 percent of U.S. children 

lived in homes where they had contact with a smoker 

at least one day per week (Schuster et al. 2002). 

Use of the indirect approach assumes that the 

presence of a smoking adult in the household results 

in exposure of children to secondhand smoke. Over 

time, as more people recognized the health effects 

from exposure in the home and implemented in-home 

smoking policies, the presence of smoking adults in 

the home has become a less valid indicator of exposure. In a 1991 survey of U.S. adults, 11.8 percent of 

current smokers reported that because no smoking 

had occurred in their homes in the two weeks before 

the survey, their children had not been exposed to 

secondhand smoke in the home (Mannino et al. 1996). 

Using data from the California Tobacco Survey, Gilpin and colleagues (2001) found that the proportion 

of households prohibiting smoking increased from 

50.9 percent in 1993 to 72.8 percent in 1999 (Gilpin 

et al. 2001). The increase was greater in homes with 

smokers, from 20.1 percent in 1993 to 47.2 percent in 

1999 (Pierce et al. 1998; Gilpin et al. 2001). The survey 

did not capture data from nonfamily members who 

may have smoked in the home, nor would it have 

addressed the contamination of one dwelling from 

smokers in another within a multiresidence building. 

Other analyses have used questionnaires 

that ask specifically about the number of cigarettes 

smoked in the home to determine whether children 

were exposed to secondhand smoke. A 1991 nationally representative survey estimated that 31.2 percent 

of U.S. children were exposed daily to secondhand 

smoke in their homes, with an additional 5.8 percent 

exposed at home at least one day in the previous two 

weeks (Mannino et al. 1996). This exposure varied 

significantly by socioeconomic status (SES) (46.5 percent for a lower SES versus 22.5 percent for a higher 

SES) and by region of the country, with the lowest 

exposure (24.3 percent) in the western part of the 

United States (Mannino et al. 1996). In Phase I of the 

NHANES III (collected from 1988 to 1991), 43 percent 

of children aged 2 months through 11 years lived in a 

home with at least one smoker (Pirkle et al. 1996). In 

NHANES 1999–2002, the proportion of children aged 

3 through 11 years living with one or more smokers in 

the household was 24.9 percent (Table 4.2). However, 

59.6 percent of children aged 3 through 11 years had a 

serum cotinine concentration of 0.05 ng/mL or higher. 

State and local surveys have documented higher levels of reported exposure. In a 1985 study from New 

Mexico, 60 to 70 percent of the children had been 

exposed to secondhand smoke (Coultas et al. 1987). In 

a 1986 study of North Carolina infants, 56 percent had 

been exposed (Margolis et al. 1997). On the basis of 

self-reported data on smoking among household residents, CDC estimated in 1996 that 21.9 percent of U.S. 

children had been exposed to secondhand smoke in 

their homes (CDC 1997). The prevalence of exposure 

varied by state, from a low of 11.7 percent in Utah to 

a high of 34.2 percent in Kentucky. However, the data 

on serum cotinine concentrations suggest that these 

estimates are low. 

As noted above, since 1988 the NHANES has 

provided nationally representative measurements 

of serum cotinine levels in both children and adults 

(Pirkle et al. 1996, 2006; CDC 2001a, 2003, 2005). Table 

4.1 shows overall U.S. trends in exposure measured by 

serum cotinine concentrations. Although exposures 

have declined among both children and adults since 

Phase I of NHANES III (1988–1991), the percentage of 

the decline was smaller among children aged 4 through 

11 years. In the NHANES 2001–2002, mean cotinine 

Prevalence of Exposure to Secondhand Smoke 17 
Surgeon General’s Report 

levels were highest among children aged 4 through 

11 years (non-Hispanic Black children in particular) 

(Pirkle et al. 2006). Measured cotinine concentrations 

were more than twice as high among children aged 4 

through 11 years than among nonsmoking adults aged 

20 or more years, and the levels of non-Hispanic Black 

children were two to three times higher than those of 

non-Hispanic White and Mexican American children. 

While metabolic factors can also influence cotinine 

levels (Caraballo et al. 1998; Mannino et al. 2001), the 

racial and ethnic differences in serum cotinine concentrations overall, and particularly among children, 

presumably reflect greater exposures to secondhand 

smoke among non-Hispanic Black populations (Pirkle 

et al. 2006). 

Table 4.2 compares current estimates of national 

exposure by age. In Phases I and II of NHANES III 

(1988–1994), 84.7 percent of children aged 4 through 

11 years had a serum cotinine concentration of 0.05 

ng/mL or greater; 99.1 percent of children with a 

reported exposure in the home and 75.6 percent of 

children without any reported exposure had measurable cotinine levels (Mannino et al. 2001). The strongest predictor of cotinine levels in children was the 

number of cigarettes smoked daily in the home, but 

other factors were also significant predictors, including race, ethnicity, age of the child, size of the home, 

and region of the country (Mannino et al. 2001). In the 

most recent estimates of exposure (Table 4.2), 59.6 percent of children aged 3 through 11 years had a serum 

cotinine concentration of 0.05 ng/mL or greater, and 

24.9 percent reported living with at least one smoker 

in the household. Based upon this estimate of the proportion of children aged 3 through 11 years living with 

a smoker in the household, an estimated nine million 

children or more in this age range may be exposed to 

secondhand smoke. However, serum cotinine measurements indicate an even greater exposed population of almost 22 million children aged 3 through 11 

years in the year 2000. 

Trends in exposure of children to secondhand 

smoke indicate that levels of exposure have declined 

significantly since Phase I of NHANES III (Pirkle et al. 

2006). The multiple factors related to this decline are 

still being studied. Several researchers have suggested 

that a major component of this decline is related to the 

decrease in parental smoking (Shopland et al. 1996) 

and to the increase in household smoking restrictions 

(Gilpin et al. 2001). Data from the 1992 and 2000 NHIS 

(Soliman et al. 2004) indicate that self-reported exposure of nonsmokers to secondhand smoke in homes 

with children declined significantly in the 1990s from 

36 percent in 1992 to 25 percent in 2000. Because 

researchers have identified parental smoking in the 

home as a major source for exposure among younger 

children (Mannino et al. 2001), this decline in reported 

home exposures to secondhand smoke suggests that 

voluntary changes in home policies and smoking 

practices of adults in homes where children reside are 

a major contributing factor to the observed declines in 

serum cotinine concentrations among children since 

Phase I of NHANES III. 

Protecting children from secondhand smoke 

exposure in homes has been the focus of the U.S. Environmental Protection Agency’s parental outreach and 

educational programs to promote smoke-free home 

rules for the last decade. The potential for exposing 

children to secondhand smoke has dropped even 

further as more local and state governments restrict 

smoking in public areas (CDC 1999). Jarvis and colleagues (2000) documented similar findings in data 

from Great Britain. From 1988 to 1996, the proportion 

of homes without smokers increased from 48 to 55 

percent. During this same period, the geometric mean 

salivary cotinine levels decreased from 0.47 to 0.28 

ng/mL among children with nonsmoking parents, 

and from 3.08 to 2.25 ng/mL among children with 

two smoking parents (Jarvis et al. 2000). 

Additional studies that document exposure of 

children in the United States to secondhand smoke in 

the home include three studies that reported the presence of some form of smoking ban at home in many 

households (Norman et al. 1999; Kegler and Malcoe 

2002; McMillen et al. 2003). Norman and colleagues 

(1999) surveyed a representative sample of 6,985 California adults. Kegler and Malcoe (2002) studied 380 

rural, low-income Native American and White parents from northeastern Oklahoma. McMillan and colleagues (2003) conducted a telephone survey of more 

than 4,500 eligible adults across the United States. Two 

other studies also focused on prevalence and patterns 

of childhood household secondhand smoke exposure 

in the United States: CDC (2001b) reported on the 

Behavioral Risk Factor Surveillance System (BRFSS) 

telephone interviews that took place in 20 states, and 

Schuster and colleagues (2002) reported on personal 

interviews with 45,335 respondents from around the 

country in the 1994 NHIS. 

Susceptible Populations 

Some populations may be particularly susceptible to secondhand smoke exposure. Examples 

include persons with asthma or other chronic respiratory diseases, and fetuses exposed to tobacco smoke 

components in utero either by maternal smoking or 

maternal exposure to secondhand smoke. In one 1994 

1 Chapter  
Excerpts: Chldren and Secondhand Smoke Exposure 

community-based study in Seattle, 31 percent of children with asthma reported household exposures 

to secondhand smoke, but only 17 percent of children without asthma reported an exposure (Maier 

et al. 1997). 

Studies have tracked smoking by pregnant 

women using several different data collection systems 

including natality surveys, NHIS, BRFSS, National 

Survey of Family Growth, and since 1989, birth certificates in nearly all states and the District of Columbia (CDC 2001a). The estimates from these different 

sources generally agree that the proportion of women 

who report smoking during pregnancy has decreased 

in recent years, from between 30 and 40 percent in 

the early 1980s to between 10 and 15 percent in the 

late 1990s. By 2003, only an estimated 10.7 percent of 

mothers of a live-born infant reported smoking during pregnancy. However, the prevalence of reported 

smoking was not uniform across all population groups 

or education levels. For example, a CDC report (CDC 

2005) documented that 18 percent of American Indian 

or Alaska Native women reported smoking during 

pregnancy, but only 3 percent of Hispanic women 

reported smoking during pregnancy. And women 

with 9 to 11 years of education were far more likely to 

report smoking (25.5 percent) compared with women 

with 16 or more years of education (1.6 percent) (CDC 

2005). Ebrahim and colleagues (2000) showed that 

the declining trend in smoking during pregnancy in 

recent years is primarily attributable to a decrease 

in smoking prevalence among women of childbearing age, rather than to an increase in smoking cessation during pregnancy. Of the women who reported 

smoking during pregnancy, most (68.6 percent) said 

that they had smoked 10 or fewer cigarettes daily. 

Researchers have also found that pregnant 

women may conceal their smoking from clinicians 

(Windsor et al. 1993; Ford et al. 1997). Thus, smoking 

during pregnancy may be underestimated. Estimates 

of the prevalence of smoking during pregnancy are 

also sensitive to how smoking was defined in a study, 

which may range from any smoking at any time 

during pregnancy to smoking during the final three 

months of pregnancy. 

Complicating the interpretation of findings on 

health effects of secondhand smoke exposure in very 

young children is evidence that a large proportion of 

children are exposed both prenatally and postnatally. 

Overpeck and Moss (1991) used CDC data to show 

that 96 percent of children with prenatal exposures 

also had postnatal exposures. The investigators found 

that 29 percent of the children had been exposed 

prenatally to maternal smoking and that an additional 

21 percent had been exposed to secondhand smoke 

postnatally. A second source of involuntary smoking for a developing fetus is the exposure of a pregnant woman to secondhand smoke. The factors that 

predicted prenatal maternal exposure to secondhand 

smoke were similar to those associated with secondhand smoke exposure in general, such as low SES, low 

levels of education, and living in a small home (Overpeck and Moss 1991). 

Although national surveys have not specifically 

asked about secondhand smoke exposure during 

pregnancy, they have provided estimates of exposure among women of childbearing age. In NHANES 

III, 18 percent of nonsmoking females aged 17 years 

and older reported exposures to secondhand smoke. 

However, the percentages of reported exposures were 

higher among women of childbearing age: 31 percent 

for 17- through 19-year-olds, 30 percent for 20- through 

29-year-olds, and 26 percent for 30- through 39-yearolds (Pirkle et al. 1996). Of the nontobacco users surveyed in 1988–1991, 88 percent had detectable levels of 

serum cotinine (>0.050 ng/mL), a finding that suggests 

an unreported or unknown exposure. These findings 

are consistent with results from a 1985 study of 1,231 

nonsmoking pregnant women in Maine, which found 

that 70 percent of the participants had cotinine levels 

above 0.5 ng/mL (Haddow et al. 1987). 

Measurements of Airborne Tracers in Homes 

Numerous studies have measured second

hand smoke concentrations in homes (Leaderer and 

Hammond 1991; Hammond et al. 1993; Marbury et 

al. 1993; Manning et al. 1994; O’Connor et al. 1995; 

Jenkins et al. 1996a,b; Phillips et al. 1996, 1997a,b, 

1998a–h, 1999a,b). Concentrations of secondhand 

smoke components are higher at the time that the 

cigarettes are smoked compared with a few hours 

later. Measurements taken only during periods 

of smoking document higher concentrations than 

samples measured during both smoking and non

smoking periods. For example, Muramatsu and col

leagues (1984) measured both nicotine and particulate 

matter sequentially for 10 hours in an office. They 

found that the 30-minute nicotine samples ranged 

from 2 to 26 micrograms per cubic meter (μg/m3

) 

during the workday; most values ranged between 5 

and 15 μg/m3. The 10-hour averaged concentration 

was 10 μg/m3, which was based on a shorter time 

period than that used by other studies to obtain stable 

estimates. Most studies have measured concentra

tions averaged over longer periods of time, which 

include periods with and without smoking. 

Prevalence of Exposure to Secondhand Smoke 19 
Surgeon General’s Report 

Studies have demonstrated a high correlation 

(Spearman rho correlation coefficient = 0.74, p <0.001) 

between nicotine concentrations measured in the fam

ily activity rooms and in the kitchens (Emmons et al. 

2001), as well as between concentrations in the activity rooms and in the bedrooms (Spearman correlation 

coefficient = 0.91; 0.90 for homes of smokers only) 

(Marbury et al. 1993). 

The results of several studies that measured nic

otine concentrations in the homes of smokers in the 

United States are presented in the full report (see Fig

ure 4.2 and Table 4.3). Median nicotine concentrations 

were generally between 1 and 3 μg/m3 (averaged over 

14 hours to several weeks), with nicotine concentra

tions ranging from <0.1 to 8 μg/m3 across the span 

from minimum to the 95th percentile. An exception 

was a study of 291 low-income homes in New Eng

land that found 4 homes with concentrations above 

18 μg/m3 (Emmons et al. 2001). Homes where smoking was restricted to the basement or the outdoors 

had lower mean nicotine concentrations of 0.3 μg/m3 

(Marbury et al. 1993). 

Personal sampling of secondhand smoke expo

sure has yielded similar results with measured home 

exposure. In a study of exposure away from work 

(predominantly at home, lasting 16 hours), 306 non

smokers who reported secondhand smoke exposure 

had a mean nicotine exposure of 2.7 μg/m3 (median 

1.2 μg/m3), with a 95th percentile value of 7.9 in 1993 

and 1994 (Jenkins et al. 1996a). Personal sampling of 

100 people in Massachusetts during 1987 and 1988 

found the median of a weekly average of nicotine con

centrations to be 1.0 μg/m3 for nonsmokers married to 

nonsmokers and 3.5 μg/m3 for those married to smok

ers; the respective maximum values were 9.5 and 14 

μg/m3. These values included all exposures throughout the week in homes, workplaces, and public places 

(Coghlin et al. 1989, 1991). To evaluate secondhand 

smoke exposure among pregnant women, partici

pants in two studies wore passive samplers (small 

personal monitors that measure secondhand smoke 

exposure) for one week. Although the two studies 

had similar designs, the investigators reported quite 

different results. Among 36 low-income pregnant 

women in Massachusetts, 80 percent were exposed to 

nicotine at 0.5 μg/m3 or greater, and 25 percent were 

exposed at a concentration above 2.0 μg/m3 (Hammond et al. 1993). The measured exposure was lower 

for 131 pregnant upper-middle-class women in Connecticut who reported secondhand smoke exposure, 

with a median of 0.1 μg/m3 and a 90th percentile of 

0.6 μg/m3 (O’Connor et al. 1995). 

International studies of secondhand smoke expo

sure sponsored by the tobacco industry (Jenkins et al. 

1996a; Phillips et al. 1996, 1997a,b, 1998a–h, 1999a,b) 

followed a similar protocol where participants wore 

a sampling device for 16 to 24 hours. Figure 4.3 in the 

full report illustrates the median nicotine concentra

tions observed “away from work” (predominantly 

at home) in the United States compared with homes 

in Australia and in several European and Asian loca

tions. U.S. homes had the second highest reported 

values after Beijing, which reported a median of 1.3 

μg/m3. Hong Kong homes reported 0.3 μg/m3, which 

was consistent with a study of 300 Chinese homes in 

18 provinces that reported a 0.1 μg/m3 weekly average concentration of nicotine in the homes of smokers 

(Hammond 1999). 

Exposure in Public Places 

Exposures to secondhand smoke in public places 

have been particular public health concerns for more 

than two decades. Although these sites are workplaces 

for some, they may now be the only source of secondhand smoke exposure for most of the U.S. population 

with no home or work exposures. Studies using biomarkers confirm that secondhand smoke exposure in 

public places continues to affect nonsmokers. Using 

NHANES III data, several investigators have shown 

that persons with no home or workplace exposures 

still had detectable levels of cotinine in their serum 

(Pirkle et al. 1996; Mannino et al. 2001). This finding 

suggests that many people are exposed to secondhand 

smoke in other locations. 

Restaurants, Cafeterias, and Bars 

Restaurants, cafeterias, and bars are worksites 

as well as public places where smoking is frequently 

unrestricted or restricted in a manner that does not 

effectively decrease exposure. Servers and bartenders 

working in environments where smoking is permitted 

may be exposed to high levels of secondhand smoke 

(Jarvis et al. 1992; Jenkins and Counts 1999). In a survey of 1,224 residents from Olmsted County, Minnesota, 57 percent of the respondents reported exposures 

to secondhand smoke: 44 percent reported exposures 

in restaurants, 21 percent reported exposures at work, 

and 19 percent reported exposures in bars (Kottke et 

al. 2001). A quarter of the respondents in the NHAPS 

study reported exposures in restaurants or bars on the 

previous day for an average of two and one-half hours 

(Klepeis 1999; Klepeis et al. 2001). Restaurants may be 

the principal point of secondhand smoke exposure for 

children from nonsmoking homes, and an exposure of 

even a short duration may be relevant to acute effects, 

such as inducing or exacerbating an asthma attack. 

20 Chapter  
Excerpts: Chldren and Secondhand Smoke Exposure 

In eating establishments, a wide variability in 

factors determines the concentration of secondhand 

smoke, including the size of the room, ventilation 

rate, number of smokers, and smoking rate. Further

more, these concentrations vary throughout the day 

and evening. Concentrations measured for one to two 

hours during lunch or dinner are likely to be much 

higher than the average concentrations measured 

during a full day or week. The nicotine concentrations 

measured in restaurants have ranged from less than 

detectable to values of 70 μg/m3. 

Tobacco smoke has long been considered a 

nuisance that interferes with the enjoyment of food. 

One approach to reducing exposures of nonsmokers 

has been to establish smoking and nonsmoking sec

tions in restaurants. Nonsmoking sections generally 

do have lower concentrations of secondhand smoke 

(Lambert et al. 1993; Hammond 1999), but they nei

ther eliminate secondhand smoke nor reduce second

hand smoke concentrations to insignificant levels. The 

concentrations of nicotine in nonsmoking sections of 

restaurants persist at high levels. For example, a study 

of seven restaurants in Albuquerque, New Mexico, 

found that half of them had concentrations above 1 

μg/m3 in the nonsmoking sections (Lambert et al. 

1993). Similar results were noted in more than half 

of 71 restaurants surveyed in Indiana where nicotine 

concentrations were above 2 μg/m3 in the nonsmok

ing sections (Hammond and Perrino 2002). In a study 

of waiters exposed to secondhand smoke, the average 

nicotine concentration was as high as 5.8 μg/m3, with 

the upper end of the range at 68 μg/m3 (Maskarinec 

et al. 2000). 

Hammond (1999) reported that nicotine concentrations in cafeterias were somewhat higher than in 

restaurants; average values were between 6 and 14 

μg/m3. Out of the 37 samples from company cafeterias 

in Massachusetts that allowed or restricted workplace 

smoking, two-thirds had nicotine concentrations that 

were above 5 μg/m3

. Secondhand smoke concentra

tions measured during lunchtime at a medical center 

cafeteria revealed large gradients between the smoking and nonsmoking sections. The concentrations 

were generally 25 to 40 μg/m3 in the smoking section, 

2 to 5 μg/m3 in a nonsmoking section that was within 

25 feet of the smoking section, and less than 0.5 μg/ 

m3 in a nonsmoking section that was 30 feet from the 

smoking section (although on one day, the average in 

that section was 1.8 μg/m3). 

Evidence Synthesis 

Since 1986, investigators have reported a substantial amount of new evidence on exposure to 

secondhand smoke. The more recent data provide 

insights into typical patterns of exposure, exposure in 

key microenvironments, and the consequences of various policies intended to reduce exposure. As noted 

in Table 4.1, exposures of nonsmokers to secondhand 

smoke have declined significantly between 1988 and 

2002. These declines have been observed in both children and nonsmoking adults, in both men and women, 

and in all racial and ethnic categories. However, significant levels of exposure persist for the U.S. population in general and for susceptible populations. Table 

4.2 notes estimates for 2000; approximately 127 million children and nonsmoking adults were exposed 

to secondhand smoke. This estimated total includes 

almost 22 million children aged 3 through 11 years, 

and 18 million nonsmoking youth aged 12 through 19 

years. 

The findings consistently show the importance 

of two microenvironments as places for secondhand smoke exposure: the home and the workplace. 

Although microenvironments such as bars and restaurants may also be important for patrons, the home 

and the workplace are particularly significant because 

of the amount of time spent in these two locations. 

For the workplace, restrictions and smoking bans lead 

to much lower concentrations of secondhand smoke 

than in locations where smoking is allowed. 

National surveys indicate that progress in 

reducing secondhand smoke exposure has been variable across the country. Certain states, such as California, Maryland, and Utah, have made significant 

advances in protecting nonsmokers, but others, such 

as Kentucky and Nevada, have not (Gilpin et al. 2001; 

Shopland et al. 2001). Even in locales with smoking 

restrictions in place, significant pockets of exposure 

remain, most notably in homes, some worksites such 

as restaurants and bars, and in automobiles. Exposures in some of these locations can be remedied by 

changing public policy. Exposures in other locations, 

particularly homes and automobiles, can perhaps 

only be addressed through education that alters lifestyle behaviors. 

It is likely that geographic differences in secondhand smoke exposure are related to trends in tobacco 

use and policies that determine where tobacco use 

is permitted (Giovino et al. 1995; Gilpin et al. 2001). 

Wide regional differences exist within the United 

States in secondhand smoke exposure and cotinine 

levels. In the NHANES III data, children with and 

without reported exposures had lower cotinine levels 

if they lived in the western part of the United States 

(Mannino et al. 2001)—a finding that may reflect 

lower community exposures to secondhand smoke. 

Prevalence of Exposure to Secondhand Smoke 21 
Surgeon General’s Report 

Where smoking is allowed, especially at worksites 

and in public places, concentrations are highly variable, so concentrations in individual locations may 

be significantly higher than average. Concentrations 

of secondhand smoke are also typically higher in the 

Conclusions 

workplace and in restaurants than in the home. Policies that restrict smoking to particular areas reduce 

but do not eliminate secondhand smoke exposure. 

Smoke-free polices reduce secondhand smoke concentrations far more effectively. 

The following conclusions are supported by 

text in the full report that may not be included 

in this excerpt. The full report can be accessed at 

http://www.surgeongeneral.gov/library/secondhandsmoke/report/.

 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 Smokng. 

Overall Implications 

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. 

Exposure to secondhand smoke remains a serious public health problem in the United States, with 

exposure of almost 60 percent of children aged 3 

through 11 years and more than 40 percent of nonsmoking adults. Since the publication of the 1986 Surgeon General’s report, measured levels of exposure in 

the United States have declined significantly. However, the proportional decrease has been larger among 

adults than among children, and the most recent data 

suggest that children aged 3 through 11 years have 

serum cotinine concentrations that are more than twice 

as high as those among nonsmoking adults. Data suggest that the home remains the most important target 

for reducing exposures to secondhand smoke, particularly for children but also for middle-aged and older 

adults. Although progress has been made to protect 

nonsmoking workers, continuing efforts are needed 

to protect these workers, and particularly younger 

workers, in all occupational categories. 

Research questions remain regarding exposure 

to secondhand smoke. As noted in the 1986 report, 

no indicator has been developed that can objectively 

estimate long-term exposure or early-life exposure. Secondhand smoke exposure from “shared air 

spaces” within a building is also of concern, as a significant proportion of the population lives in apartment buildings or condominiums where smoking in 

another part of the building might increase tobacco 

smoke exposure for households of nonsmokers. 

22 Chapter  
Excerpts: Chldren and Secondhand Smoke Exposure 

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2 Chapter  
Excerpts from Chapter 5
 

Reproductive and Developmental Effects 


from Exposure to Secondhand Smoke
 

Introduction 29
 

Conclusions of Previous Surgeon General’s Reports and Other Relevant Reports 29
 

Literature Search Methods 29
 

Critical Exposure Periods for Reproductive and Developmental Effects 30
 

Fertility 31
 

Biologic Basis 31
 

Evidence Synthesis 32
 

Conclusion 32
 

Implications 32
 

Pregnancy (Spontaneous Abortion and Perinatal Death) 33
 

Biologic Basis 33
 

Evidence Synthesis 33
 

Conclusion 33
 

Implications 33
 

Infant Deaths 3 

Evidence Synthesis 3 

Conclusion 3 

Implications 3 

Sudden Infant Death Syndrome 3 

Biologic Basis 3
 

Evidence Synthesis 35


Conclusion 36
 

Implications 3
 

Preterm Delivery 3 

Biologic Basis 3
 

Evidence Synthesis 37
 

Conclusion 37
 

Implications 37
 

27 
 

Low Birth Weight 37 

Biologic Basis 37 

Evidence Synthesis 3 

Conclusion 38 

Implications 3 

Congenital Malformations 3 

Biologic Basis 3 

Evidence Synthesis 39 

Conclusion 39 

Implications 39 

Cognitive, Behavioral, and Physical Development 39 

Biologic Basis 39 

Cognitive Development 0 

Evidence Synthesis 0 

Conclusion 0 

Implications 0 

Behavioral Development 0 

Evidence Synthesis 0 

Conclusion 0 

Implications 1 

Height/Growth 1 

Evidence Synthesis 1 

Conclusion 1 

Implications 1 

Childhood Cancer 1 

Biologic Basis 1 

Evidence Synthesis 2 

Conclusions 2 

Implications 3 

Conclusions 3 

Overall Implications 5 

References  

2 
Excerpts: Chldren and Secondhand Smoke Exposure 

Introduction 

This chapter concerns adverse effects on reproduction, infants, and child development from exposure 

to secondhand smoke. Previous Surgeon General’s 

reports have not comprehensively addressed the 

relationship between secondhand smoke exposure 

and reproductive outcomes, infant mortality, or child 

development. The 2001 Surgeon General’s report 

(Women and Smokng) did summarize the literature on 

developmental and reproductive outcomes in relation 

to secondhand smoke exposure, focusing on the specific outcomes of fertility and fecundity, fetal growth 

and birth weight, fetal loss and neonatal mortality, 

and congenital malformations (U.S. Department 

of Health and Human Services [USDHHS] 2001). 

The effects of active smoking by the mother during 

pregnancy were comprehensively reviewed in the 

2004 report (USDHHS 2004). This new report reviews 

the possible effects of secondhand smoke exposure 

on reproductive and developmental outcomes, incorporates the substantial amount of evidence that has 

emerged since the 1986 Surgeon General’s report (The 

Health Consequences of Involuntary Smokng, USDHHS 

1986), and expands upon the 2001 report. 

The epidemiologic evidence is reviewed in 

detail in the full report. Therefore, it is not included 

in this Excerpt. The full report may be accessed at 

http://www.surgeongeneral.gov/library/secondhandsmoke/report. 

Conclusions of Previous Surgeon General’s Reports 

and Other Relevant Reports 

The early literature on secondhand smoke exposure and child health focused on adverse respiratory 

effects. Initial relevant reports were first published in 

the 1960s (Cameron et al. 1969), followed by larger 

studies in the 1970s (Colley 1974; Colley et al. 1974). 

The first summary report to comprehensively address 

reproductive and perinatal effects of secondhand 

smoke exposure was prepared by the California 

Environmental Protection Agency and released in 

Literature Search Methods 

1997 (National Cancer Institute [NCI] 1999). These 

topics were also addressed by a number of other 

agencies and groups, including the United Kingdom 

Department of Health (1998), the World Health Organization (WHO 1999), and the University of Toronto 

(2001). Table 5.1 in the full report summarizes the 

conclusions for reproductive and perinatal outcomes 

from these reports. 

The authors identified most of the literature on 

secondhand smoke exposure and adverse reproductive and perinatal effects through a systematic search 

of the National Library of Medicine’s indexed journals, 

which date back to 1966. The relevant Medical Subject 

Headings (MeSH) terms and text terms were used to 

search PubMed. Text terms were used because many 

of the relevant MeSH terms were not introduced into 

the PubMed key wording scheme until some time 

after 1966. For example, the MeSH term “Tobacco 

Smoke Pollution” was not introduced until 1982. The 

following text terms were also used in the search for 

articles: environmental, tobacco, smoke, secondhand 

smoke, paternal smoking, and passive smoking. By 

combining these text terms and MeSH terms using 

“or” as the Boolean connector, nearly 4,500 citations 

were identified. The authors also used this strategy 

to identify relevant research on outcomes. The results 

of each outcome-relevant search were then combined 

with the secondhand smoke-relevant search using 

“and” as the Boolean connector. These citations were 

imported into a database. Using title and abstract 

information, the authors selected the relevant articles 

for review. Finally, the references in the articles were 

reviewed for additional citations that were not identified through the PubMed searches. 

Reproductve and Developmental Effects from Exposure to Secondhand Smoke 29 
Surgeon General’s Report 

Critical Exposure Periods for Reproductive and Development Effects 

Assessing exposures to secondhand smoke in 

studies of fertility, fetal development, infant development, and child health and development is complex. 

For each of the three biologically relevant periods— 

preconception, pregnancy, and postdelivery—a 

number of potentially different biologic mechanisms 

of injury exist from exposure to secondhand smoke. 

Even within the nine months of pregnancy, vulnerability to the effects of secondhand smoke may change, 

reflecting differing mechanisms of injury as fetal 

organs develop and the fetus grows. Moreover, there 

are multiple environments where the woman or child 

is exposed to secondhand smoke (e.g., workplace, 

home, and day care), as well as multiple sources of 

secondhand smoke exposure for each of these environments (e.g., household members, day care providers, and coworkers). Finally, because of the potential 

impact of active maternal smoking (USDHHS 2004), 

active smoking before and during pregnancy needs 

to be taken into account when assessing the potential 

independent effects of exposure to secondhand smoke. 

Maternal smoking has well-characterized adverse 

effects for several outcomes, such as fertility, sudden 

infant death syndrome (SIDS), and child growth and 

development. Thus, the effects of exposure to secondhand smoke may be confounded by those of maternal 

smoking. 

Secondhand smoke exposure may have adverse 

effects potentially throughout the reproductive 

and developmental processes. During the preconception period, maternal exposure to secondhand 

smoke can potentially affect female fertility by 

altering the balance of hormones that affect oocyte 

production, including growth hormone, cortisol, 

luteinizing hormones, and prolactin (Mattison 1982; 

Daling et al. 1987; Mattison and Thomford 1987), or 

by reducing motility in the female reproductive tract 

(Mattison 1982; Daling et al. 1987). However, separating the potential effect of secondhand smoke 

exposure on the mother’s reproductive process 

and the effect of active paternal smoking on the 

father’s reproductive process is very difficult. 

Although the evidence is mixed, active smoking has been shown to affect sperm morphology, motility, and concentration (Rosenberg 1987; 

USDHHS 2004). Cigarette smoke may also lead to 

infertility through a combined effect of decreased 

sperm motility with active paternal smoking and 

decreased tubal patency with active maternal smoking and secondhand smoke exposure. 

During pregnancy, maternal exposure to 

secondhand smoke could potentially affect the pregnancy by increasing the risk for spontaneous abortion 

or by interfering with the developing fetus through 

growth restrictions or congenital malformations (NCI 

1999; WHO 1999). During gestation, windows of 

susceptibility exist when the developing embryo or 

fetus is vulnerable to various intrauterine conditions 

or exposures. Organogenesis occurs mainly during 

the embryonic period (weeks three through eight of 

gestation), which is also the time when major malformations are most likely to develop. During weeks 

9 through 38 of gestation, susceptibility decreases and 

insults are more likely to lead to minor malformations 

or functional defects (Sadler 1990). 

Finally, secondhand smoke exposure in the 

postpartum period could affect the developing infant 

and child, resulting in a number of adverse health outcomes. Given the developmental processes in progress, infants and children are considered to be more 

vulnerable to the effects of environmental exposures 

than are adults (Goldman 1995; Dempsey et al. 2000). 

Mechanisms that could lead to compromised physical and cognitive development as a result of exposure 

to secondhand smoke may be similar to the processes that affect fetal development, such as hypoxia 

(USDHHS 1990; Lambers and Clark 1996). One review 

of the impact of prenatal exposure to nicotine summarized numerous animal studies that demonstrated 

the effects of nicotine on cognitive processes among 

exposed rats and guinea pigs, such as impeded learning abilities or increased attention or memory deficits (Ernst et al. 2001). In animal and human studies, 

prenatal nicotine exposure affected aspects of neural 

functioning such as the activation of neurotransmitter systems, which may lead to permanent alterations 

in the developing brain through changes in gene 

expression. The proposed consequences of altered 

gene expression included disturbances in neuronal 

pathfinding and in cell regulation and differentiation 

(Ernst et al. 2001). Other animal studies have shown 

that newborn rats exposed to sidestream smoke have 

reduced DNA and protein concentrations in the brain 

(Gospe et al. 1996). Ideally, researchers should have 

information on secondhand smoke exposures for all 

relevant periods that relate to the outcome under 

30 Chapter 5 
Excerpts: Chldren and Secondhand Smoke Exposure 

study, because different physiologic processes may be 

affected across developmental periods. However, this 

information is frequently unavailable in a particular 

study. 

Secondhand smoke exposures most commonly 

occur in the home or workplace, and exposures in public places tend to be more sporadic. Recent exposure 

assessment and monitoring studies have shown that 

the home tends to be a greater source of secondhand 

smoke exposure than the workplace (Emmons et al. 

1994; Pirkle et al. 1996; Hammond 1999), particularly 

since workplace smoking bans have become more 

restrictive (Marcus et al. 1992) (Chapter 3, Assessment of Exposure to Secondhand Smoke, in the full 

report, and Chapter 4, Prevalence of Exposure to 

Secondhand Smoke). In the home, the major sources of 

exposures to secondhand smoke have been smoking 

Fertility 

by the spouse or partner and other household members. Paternal smoking has been the most commonly 

measured source of secondhand smoke in the home 

(USDHHS 1986), and paternal smoking status tends 

to be constant across the three developmental periods: 

preconception, prenatal, and postnatal (USDHHS 

1986). Although many studies have not considered 

smoking in the home by other household members, 

some studies have documented that such smoking could be a significant source of secondhand 

smoke exposure for women (Pattishall et al. 1985; 

Rebagliato et al. 1995; Pirkle et al. 1996; Ownby et 

al. 2000; Kaufman et al. 2002). Studies on workplace 

exposure have focused on whether or not the person 

was exposed, but less attention has been paid to quantifying the exposure (Misra and Nguyen 1999). 

Biologic Basis 

Infertility is commonly defined as a failure to 

conceive after 12 months of unprotected intercourse. 

Infertility should not be confused with fecundability, which is defined as the probability of conception 

during one menstrual cycle and measured by time to 

pregnancy. Thus, low fecundability is delayed conception. The biologic plausibility that secondhand 

smoke exposure affects human fertility and fecundability is supported by both animal and human studies of active smoking, which include exposure to the 

same materials as involuntary smoking. In animal 

studies, numerous investigators have demonstrated 

the biologic effects of nicotine in disrupting oviduct 

function (Neri and Marcus 1972; Ruckebusch 1975) 

and in delaying blastocyst formation and implantation (Yoshinaga et al. 1979). Investigations of assisted 

reproduction among humans who actively smoke 

have also provided information on possible mechanisms of infertility and delayed conception from secondhand smoke exposure. Several studies of assisted 

reproductive techniques have suggested that active 

maternal smoking reduces the estradiol level in follicular fluid (Elenbogen et al. 1991; Van Voorhis et al. 

1992), impedes ovulation induction (Van Voorhis et 

al. 1992; Chung et al. 1997), reduces the fertilization 

rate (Elenbogen et al. 1991; Rosevear et al. 1992), and 

retards the embryo cleavage rate (dose-dependent) 

(Hughes et al. 1992). Metabolites of cigarette smoke 

have been measured in the follicular fluid of active 

smokers at assisted reproduction clinics (Trapp et al. 

1986; Weiss and Eckert 1989; Rosevear et al. 1992) and 

in the cervical mucus of active smokers in a cervical 

cancer study (Sasson et al. 1985). 

Together, the evidence from studies of biologic 

mechanisms and the findings of numerous epidemiologic studies have led to the conclusion that active 

maternal smoking causes reduced fertility. An early 

review by Stillman and colleagues (1986) of studies of 

natural reproduction in addition to the two most recent 

Surgeon General’s reports (USDHHS 2001, 2004) support this conclusion of a causal association, and findings of meta-analyses have provided estimates of the 

magnitude of the effect of maternal smoking on fertility. Hughes and Brennan (1996) combined the results 

of seven studies on in vitro fertilization with gamete 

intrafallopian transfer. Comparing smokers and nonsmokers, the researchers obtained a combined odds 

ratio (OR) for conception of 0.57 (95 percent confidence interval [CI], 0.42–0.78). Similarly, Augood and 

colleagues (1998) pooled nine studies that compared 

smokers with nonsmokers and found a combined OR 

of 0.66 (95 percent CI, 0.49–0.88) for the number of 

Reproductve and Developmental Effects from Exposure to Secondhand Smoke 31 
Surgeon General’s Report 

pregnancies per cycle of in vitro fertilization. In their 

meta-analysis of 12 studies, Augood and colleagues 

(1998) compared smokers with nonsmokers and found 

that the overall OR for infertility was 1.60 (95 percent 

CI, 1.34–1.91). Several investigators found a doseresponse trend between the level of active maternal 

smoking and decreased fertility (Baird and Wilcox 

1985; Suonio et al. 1990; Laurent et al. 1992). 

Although active paternal smoking could also 

play a role in infertility by affecting sperm quality, 

the 2004 Surgeon General’s report found conflicting evidence on active smoking and sperm quality 

(USDHHS 2004). In another review, investigators performed a meta-analysis of 20 study populations (from 

18 published papers) on cigarette smoking and sperm 

density and found a weighted estimated reduction of 

13 percent in sperm density (95 percent CI, 8.0–17.1) 

among smokers compared with nonsmokers (Vine et 

al. 1994). The epidemiologic studies that have examined the effect of active paternal smoking on fertility 

are not as consistent in their findings as the studies 

that have investigated active maternal smoking and 

fertility (Underwood et al. 1967; Tokuhata 1968; Baird 

and Wilcox 1985; de Mouzon et al. 1988; Dunphy et al. 

1991; Pattinson et al. 1991; Hughes et al. 1992; Rowlands et al. 1992; Bolumar et al. 1996; Hull et al. 2000). 

One review concluded that paternal smoking had no 

effect on fertility (Hughes and Brennan 1996). 

Several studies that were conducted in reproductive clinics measured tobacco smoke biomarkers 

in nonsmoking men and women exposed to secondhand smoke. Cotinine was measurable in follicular 

fluid, with measurements related to dose (Zenzes et 

al. 1996), and benzo[a]pyrene adducts were found in 

ovarian cells (Zenzes et al. 1998). Both nicotine and 

cotinine were measured in semen of nonsmoking, 

secondhand smoke-exposed men attending a clinic 

specializing in infertility (Pacifici et al. 1995). 

Evidence Synthesis 

The observational evidence is quite limited. The 

four studies that directly address maternal secondhand smoke exposure and fertility differ substantially 

in study design and methods. For example, Chung 

and colleagues (1997) investigated patients who 

were attending a clinic for fertility-related problems 

and examined the success rate of assisted reproduction. Hull and colleagues (2000), on the other hand, 

included pregnant women and examined delayed 

natural conception. In the former study, the investigators did not account for potential confounders and 

obtained retrospective information about exposure 

to secondhand smoke from telephone interviews 

(Chung et al. 1997). Hull and colleagues (2000) relied 

on a self-administered questionnaire to ascertain 

exposure information during pregnancy, and used 

potential confounders in the analysis such as parental 

age, body mass index, and alcohol consumption. The 

evidence from this larger study on natural conception 

is consistent with the biologic framework established 

by the studies on active maternal smoking and fertility (Hull et al. 2000). 

Conclusion 

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. 

Implications 

As exposure of women of reproductive age 

to secondhand smoke continues, this topic needs 

further rigorous investigation. In particular, the frequency and extent of current exposures should be 

characterized. Further epidemiologic studies also 

merit consideration. 

32 Chapter 5 
Excerpts: Chldren and Secondhand Smoke Exposure 

Pregnancy (Spontaneous Abortion and Perinatal Death) 

Biologic Basis 

Fetal loss or spontaneous abortion is defined 

as the involuntary termination of an intrauterine 

pregnancy before 20 weeks of gestation (Anderson 

et al. 1998). Because most early fetal losses are underreported and unrecognized, spontaneous abortions are 

extremely difficult to study. Twenty to 40 percent of all 

pregnancies may terminate too early to be recognized 

or confirmed (Wilcox et al. 1988; Eskenazi et al. 1995). 

Furthermore, the etiology of spontaneous abortion is 

multifactorial and not fully understood. Some early 

miscarriages result from chromosomal abnormalities 

in the developing embryo; others are related to factors associated with maternal age, with the pregnancy 

itself, or to other types of exposures (e.g., occupational 

exposure, alcohol consumption, or fever). Moreover, 

relatively few animal studies have been conducted to 

gain an understanding of how exposure to sidestream 

smoke may affect the processes of spontaneous abortion (NCI 1999). In one study of sea urchins, investigators noted that exposure to nicotine prevented the 

cortical granule reaction, which typically prevents 

the entry of additional sperm into the egg once fertilization has occurred (Longo and Anderson 1970). 

If this same process occurs in the human fertilized 

ovum as a result of nicotine exposure, this may be a 

mechanism by which abnormalities in the developing embryo result in spontaneous abortions (Longo 

and Anderson 1970; Mattison et al. 1989). Several 

tobacco components and metabolites are potentially 

toxic to the developing fetus, including lead, nicotine, 

cotinine, cyanide, cadmium, carbon monoxide (CO), 

and polycyclic aromatic hydrocarbons (Lambers and 

Clark 1996; Werler 1997). Finally, with regard to active 

smoking and spontaneous abortion, many studies 

have reported a greater increase in risk for smokers 

than for nonsmokers, and some studies have demonstrated dose-response relationships (USDHHS 2004). 

Evidence Synthesis 

The few studies that have examined the relationship between involuntary smoking and spontaneous abortion have inconsistent findings. Although 

some studies reported an increased risk for spontaneous abortion among women exposed to secondhand 

smoke at work or at home, many found no association. 

However, for the studies that showed no associations, 

the study samples may have lacked adequate statistical 

power. 

Three studies examined secondhand smoke exposures among women who were nonsmokers. Koo and 

colleagues (1988) examined rates of miscarriage among 

136 nonsmoking wives who were part of a larger study 

on cancer. These 136 women were the controls in this 

study, which ascertained lifetime smoking histories of 

the husbands and reproductive histories of the wives. 

Social and demographic factors differed between 

families with smoking and nonsmoking husbands. The 

crude OR for more than two miscarriages among wives 

with husbands who smoked was 1.81 (95 percent CI, 

0.85–3.85) (adjusted ORs were not reported). Ahlborg 

and Bodin (1991) reported on nonsmoking women 

who were exposed to secondhand smoke at home. Two 

estimates were provided, one for first trimester losses 

(OR = 0.96 [95 percent CI, 0.50–1.86]) and for one second or third trimester losses (OR = 1.06 [95 percent CI, 

0.55–2.05]). Windham and colleagues (1999b) reported 

adjusted ORs for paternal smoking among women who 

were nonsmokers. When maternal age, prior spontaneous abortion, alcohol and caffeine consumption, and 

gestational age at initial interviews were taken into 

account, the investigators obtained an OR of 1.15 (95 

percent CI, 0.86–1.55) for secondhand smoke exposure 

at home. The pooled estimate from these three studies 

(with the two estimates from Ahlborg and Bodin [1991] 

included separately) for secondhand smoke exposure 

in the home or from fathers who smoked and who were 

married to nonsmoking women was 1.18 (95 percent 

CI, 0.92–1.44). 

Future studies not only need to ensure an adequate sample size, but they should give particular 

attention to the difficult issues of confounding and to 

accurate estimates of secondhand smoke exposures in 

the workplace and in the home. 

Conclusion 

1. 	 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. 

Implications 

As for other outcomes that have very few studies, further research is warranted (see “Overall Implications” later in this chapter). 

Reproductve and Developmental Effects from Exposure to Secondhand Smoke 33 
Surgeon General’s Report 

Infant Deaths 

Infant mortality is defined as the death of a 

live-born infant within 364 days of birth. Many of 

the major causes of infant deaths, such as low birth 

weight (LBW), preterm delivery, and SIDS, are also 

associated with exposure to tobacco smoke during and 

after pregnancy. The biologic mechanisms by which 

secondhand smoke exposure leads to these particular 

outcomes are discussed in other parts of this chapter 

and will not be discussed here. In 2002, the infant mortality rate for infants of smokers (11.1 percent) was 68 

percent higher than the rate for infants of nonsmokers (6.6 percent) (Mathews et al. 2004). For each race 

and Hispanic-origin group, the infant mortality rate 

among infants of smokers was higher compared with 

the rate among infants of nonsmokers. 

Evidence Synthesis 

Only two studies examined the relationship of 

involuntary smoking with neonatal mortality. Both 

studies reported associations of secondhand smoke 

exposure from paternal smoking with neonatal mortality. There is significantly more literature on active 

smoking by the mother during pregnancy and neonatal outcome. Although the strength of the relationship 

in these two studies was strong, causality cannot be 

inferred because of the small number of studies and 

Sudden Infant Death Syndrome 

because of inadequate controls for potential confounders. 

Conclusion 

1. 	 The evidence is inadequate to infer the presence or 

absence of a causal relationship between exposure 

to secondhand smoke and neonatal mortality. 

Implications 

In addition to the consistent relationship demonstrated between exposure to secondhand smoke and 

neonatal mortality, numerous studies have reported 

significant associations between active maternal 

smoking during pregnancy and infant mortality. 

Thus, the association of secondhand smoke exposure 

during pregnancy and infant mortality warrants 

further investigation. Moreover, the data cited were 

from older studies, and smoking patterns and levels 

of secondhand smoke exposure may have changed 

since the time some of the studies were conducted. To 

clarify the association between maternal smoking and 

infant mortality, more evidence is needed. 

The sudden, unexplained, unexpected death 

of an infant before one year of age—referred to as 

SIDS—has been investigated in relation to exposure 

of the fetus and infant to smoking by mothers and 

others during the preconception, prenatal, and postpartum periods. The death rate attributable to SIDS 

has declined by more than half during the past two 

decades (Ponsonby et al. 2002; American Academy 

of Pediatrics [AAP] Task Force on SIDS 2005). SIDS 

has decreased dramatically because of interventions 

such as the “Back to Sleep” campaign implemented in 

the 1990s (Gibson et al. 2000; Malloy 2002; Malloy and 

Freeman 2004). Numerous studies have examined the 

association between active smoking among mothers 

during pregnancy and the subsequent risk of SIDS. 

The evidence for active smoking has demonstrated a 

causal association between maternal smoking during 

pregnancy and SIDS (Anderson and Cook 1997; United 

Kingdom Department of Health 1998; USDHHS 2001). 

The 2004 Surgeon General’s report concluded that the 

evidence is sufficient to infer a causal relationship 

between SIDS and maternal smoking during and after 

pregnancy (USDHHS 2004). This new 2006 Surgeon 

General’s report considers exposure of the infant to 

secondhand smoke from the mother, father, or others 

(USDHHS 2006). 

Biologic Basis 

Although studies have identified social and 

behavioral risk factors for SIDS, the biologic mechanism or mechanisms underlying sudden, unexplained, 

3 Chapter 5 
Excerpts: Chldren and Secondhand Smoke Exposure 

unexpected death before one year of age are still 

unknown (Joad 2000; AAP Task Force on SIDS 2005). 

Chapter 2 (Toxicology of Secondhand Smoke) in the 

full report reviews the animal and human studies 

that provide evidence on how prenatal and postnatal 

exposure to nicotine and to other toxicants in tobacco 

smoke may affect the neuroregulation of breathing, 

apneic spells, and risk for sudden infant death. Experimental data from animal models on the neurotoxicity of prenatal and neonatal exposure to nicotine and 

secondhand smoke can be related to several potential 

causal mechanisms for SIDS, including adverse effects 

on brain cell development, synaptic development and 

function, and neurobehavioral activity (Slotkin 1998; 

Slotkin et al. 2001, 2006; Machaalani et al. 2005). Stick 

and colleagues (1996) observed newborns in the hospital and reported reductions in respiratory function 

among infants of smokers compared with infants 

of nonsmokers. Other proposed mechanisms for 

post-partum reductions in respiratory function have 

included irritation of the airways by tobacco smoke, 

susceptibility to respiratory infections that increases 

the risk of SIDS, and a change in the ventilatory 

responses to hypoxia attributable to nicotine (Anderson and Cook 1997). 

A diagnosis of SIDS requires supporting evidence from an autopsy so as to exclude other causes. 

Thus, SIDS is a difficult outcome to study. Numerous studies have examined the association between 

active smoking among mothers during pregnancy 

and the subsequent risk of SIDS. The evidence for 

active smoking has demonstrated a causal association 

between maternal smoking during pregnancy and 

SIDS (Anderson and Cook 1997; United Kingdom 

Department of Health 1998; USDHHS 2001, 2004). 

Evidence Synthesis 

The biologic evidence, especially from animal 

models, indicates multiple mechanisms by which 

exposure to secondhand smoke could cause SIDS. The 

evidence for secondhand smoke exposure and the 

risk of SIDS consistently demonstrates an association 

between postpartum maternal smoking and SIDS. 

The 1997 meta-analysis of 39 relevant studies produced an adjusted OR for postnatal maternal smoking 

of 1.94 (95 percent CI, 1.55–2.43), a level of risk that 

the authors concluded was almost certainly causal 

(Anderson and Cook 1997). Data from the four studies 

published since the 1997 meta-analysis add additional 

support for this conclusion. Nine of the thirteen studies in Table 5.5 (see page 182 in the full report) more 

fully controlled for the major potential confounders 

(e.g., maternal smoking during pregnancy and routine 

sleeping position), and many controlled for a broad 

range of other relevant factors including maternal 

age, birth weight, and bed sharing. The nine studies 

all observed significant positive associations between 

postpartum maternal smoking and SIDS. Moreover, 

several studies demonstrated a dose-response relationship for secondhand smoke exposure attributable 

to postpartum maternal smoking, with increasing 

ORs for higher levels of postpartum maternal smoking. Finally, among the studies of postnatal maternal 

smoking with better adjustment for confounding, the 

adjusted ORs are sufficiently large, all greater than 1.5 

and three of the five greater than 2.0. These ORs make 

it unlikely that this association is attributable to any 

residual confounding from unmeasured factors. 

The epidemiologic evidence for secondhand 

smoke exposure from postpartum maternal smoking associated with the risk of SIDS is consistent and 

strong, and demonstrates a dose-response relationship. Evidence for secondhand smoke exposures from 

fathers and “other” smokers (as well as higher concentrations of nicotine and cotinine in children who die 

from SIDS compared with children who die of other 

causes) provides additional supporting evidence that 

secondhand smoke exposure increases the risk of SIDS. 

Although measures of paternal and “other” smokers 

in the household are not typically considered to be a 

comprehensive indicator of the infant’s exposure to 

secondhand smoke, designs that can evaluate paternal 

smoking have the potential to more fully control for 

the possible confounding of maternal smoking during 

pregnancy. However, when considering evidence that 

supports an association between SIDS and paternal 

and “other” smokers, researchers also recognize the 

possible misclassification of actual infant exposures 

to tobacco smoke from these sources (Klonoff-Cohen 

et al. 1995; Dwyer et al. 1999). Despite this methodologic challenge, researchers observed an elevated OR 

in all nine studies of paternal smoking, ranging from 

1.4 to 3.5, with many estimates around 2 or higher. 

Of these nine studies, five observed an elevated OR 

for households where the fathers smoked compared 

with households where neither parent smoked, and 

an OR of 8.5 for infants of fathers who smoked in 

the same room as the infant, adjusting for maternal 

smoking during pregnancy, routine sleeping position, 

and other factors. Also, out of the nine studies that 

examined paternal smoking, five found a statistically 

significant association between paternal smoking and 

SIDS after adjusting for maternal smoking during 

pregnancy. Despite the potential for misclassification 

Reproductve and Developmental Effects from Exposure to Secondhand Smoke 35 
Surgeon General’s Report 

bias linking paternal smoking to an actual exposure of 

the infant to secondhand smoke, the pooled risk estimate was 1.9 (95 percent CI, 1.01–2.80) from the five 

studies of paternal smoking with stronger designs that 

used meta-analytic approaches and random effects 

modeling. Finally, all of the studies of “other” smokers in the household observed an elevated OR; however, the results that adjusted for maternal smoking 

during pregnancy and other important confounders 

were more mixed. The one study with the strongest 

assessment of infant exposures from “other” smoking 

residents (i.e., live-in adults smoking in the same room 

as the infant) reported an OR of 4.99 (95 percent CI, 

1.69–14.75), with adjustment for multiple risk factors 

including maternal smoking during pregnancy and 

routine sleeping position (Klonoff-Cohen et al. 1995). 

Researchers have established prenatal maternal 

smoking as a major preventable risk for SIDS (USDHHS 2001, 2004; AAP Task Force on SIDS 2005). 

Evidence indicates that exposure of infants to secondhand smoke from postpartum maternal smoking 

has a significant additive effect on risk if the mother 

smoked during pregnancy. In studies that accounted 

for maternal smoking during pregnancy, evidence 

indicates that postpartum maternal smoking, particularly in proximity to the infant, significantly increases 

the risk of SIDS. In addition, epidemiologic evidence 

indicates that postnatal exposure of infants to secondhand smoke from fathers or other live-in smokers can 

also increase the risk of SIDS. Thus, the full range of 

biologic and epidemiologic data are consistent and 

indicate that exposure of infants to secondhand smoke 

causes SIDS. 

Preterm Delivery 

Conclusion 

1. 	 The evidence is sufficient to infer a causal 

relationship between exposure to secondhand 

smoke and sudden infant death syndrome. 

Implications 

On the basis of the epidemiologic risk data, 

researchers have estimated that the population attributable risk of SIDS associated with postnatal exposure 

to secondhand smoke is about 10 percent (Cal/EPA 

2005). Therefore, the evidence indicates that these 

exposures are one of the major preventable risk factors 

for SIDS, and all measures should be taken to protect 

infants from exposure to secondhand smoke. 

There is a need for additional research to further 

characterize the risk of SIDS associated with prenatal 

and postnatal exposure to secondhand smoke, and to 

evaluate the relationship between maternal smoking 

and infant sleeping positions and bed sharing. Future 

research should also focus on better assessments of 

actual exposures of infants to secondhand smoke 

using biochemical assessments and/or more detailed 

interviews, rather than indirect assessments based 

on the smoking status of household adults. Because 

of the continuing and significant racial disparities 

in infant mortality from SIDS (Malloy and Freeman 

2004), there is a need to study the preventable risks 

factors that could be involved. 

Biologic Basis 

Pregnancy complications, including premature 

labor, placenta previa, abruptio placentae, and premature membrane rupture may lead to preterm delivery (<37 completed weeks of gestation). Although 

the underlying mechanisms are not yet fully characterized, maternal active smoking is associated with 

these pregnancy complications (U.S. Department of 

Health, Education, and Welfare [USDHEW] 1979b; 

USDHHS 1980, 2001; Andres and Day 2000). Preterm 

delivery is also associated with active maternal smoking (USDHEW 1979a; USDHHS 1980, 2001; van den 

Berg and Oechsli 1984; Andres and Day 2000). Smoking cessation during pregnancy appears to reduce the 

risk for preterm delivery (van den Berg and Oechsli 

1984; Li et al. 1993; Mainous and Hueston 1994b; 

USDHHS 2001), placenta previa (Naeye 1980), abruptio placentae (Naeye 1980), and premature membrane 

rupture (Harger et al. 1990; Williams et al. 1992); 

but the risk remains high for those who continue 

to smoke throughout pregnancy. Tobacco-specific 

nitrosamines and cotinine have been measured in 

the cervical mucus of women who were active smokers and women who were nonsmokers (McCann et 

al. 1992; Prokopczyk et al. 1997). Given that active 

3 Chapter 5 
Excerpts: Chldren and Secondhand Smoke Exposure 

maternal smoking is associated with preterm delivery, this finding provided further support for the biologic plausibility that secondhand smoke has a role in 

the injurious processes leading to preterm delivery. 

Although the biologic pathway from active maternal 

smoking to preterm delivery is not clear, the evidence 

for this association is strong enough to infer that 

maternal secondhand smoke exposure may also lead 

to preterm delivery. 

Evidence Synthesis 

The few studies that have evaluated the association between secondhand smoke exposure and 

preterm delivery have shown inconsistent findings. 

Of the four studies that found significant associations, 

two studies documented that the risk was significant 

only for women aged 30 years or older. Jaakkola and 

Low Birth Weight 

colleagues (2001) provided the strongest evidence 

for an association using hair nicotine measurements, 

which reduce the probability of exposure misclassification. There is a biologic basis for considering this 

association to be causal. 

Conclusion 

1. 	 The evidence is suggestive but not sufficient to 

infer a causal relationship between maternal 

exposure to secondhand smoke during pregnancy 

and preterm delivery. 

Implications 

Further research should be carried out, although 

studies of substantial size will be needed. 

Biologic Basis 

Low birth weight (LBW), defined as less than 

2,500 g or less than 5.5 pounds, can result from preterm delivery or intrauterine growth retardation 

(IUGR), which can occur simultaneously in a pregnancy. Reduced fetal physical growth during gestation, or IUGR, can lead to a small for gestational 

age (SGA) infant (
10th percentile of expected birth 

weight for a given gestational age) that is either preterm or full term (
37 weeks of gestation), and may or 

may not be LBW. The established link between active 

maternal smoking and LBW is known to occur mainly 

through IUGR rather than through premature birth 

(Chamberlain 1975; Coleman et al. 1979; Wilcox 1993). 

Fetal growth is greatest during the third trimester, 

and studies of active smoking during pregnancy demonstrate no reduction of infant birth weight if smoking ceases before the third trimester (USDHHS 1990, 

2004). In 2003, 12.4 percent of births among smokers 

were LBW (Martin et al. 2005). 

A number of researchers have postulated that 

the limitation of fetal growth from active maternal 

smoking comes from reduced oxygen to the fetus, 

which is directly attributable to CO exposure and 

nicotine-induced vasoconstriction leading to reduced 

uterine and umbilical blood flow (USDHHS 1990, 

2004; Bruner and Forouzan 1991; Rajini et al. 1994; 

Lambers and Clark 1996; Werler 1997; Andres and 

Day 2000). Studies have shown elevated nucleated 

red blood cell counts, a marker of fetal hypoxia, 

among neonates of women who actively smoked 

during pregnancy (Yeruchimovich et al. 1999) and 

among women who were exposed to secondhand 

smoke (Dollberg et al. 2000). Several investigators have also found elevated erythropoietin, the 

protein that stimulates red blood cell production 

and another indicator of hypoxia, in cord blood 

of newborns whose mothers had smoked during 

pregnancy (Jazayeri et al. 1998; Gruslin et al. 2000). 

Because erythropoietin does not cross the placenta, 

it most likely originated from the fetus. A number 

of researchers have also reported that the concentration of erythropoietin is positively correlated 

with the concentration of cotinine measured in cord 

blood (r = 0.41, p = 0.04) (Gruslin et al. 2000), the 

number of cigarettes smoked per day by the mother 

(r = 0.26, p <0.0001) (Jazayeri et al. 1998), and fetal 

growth retardation (r was not presented, p <0.01) 

(Maier et al. 1993). 

Studies have detected nicotine and its metabolites perinatally in umbilical cord serum in infants 

born to nonsmoking mothers, and in the cervical 

Reproductve and Developmental Effects from Exposure to Secondhand Smoke 37 
Surgeon General’s Report 

mucus of nonsmoking women; consequently, many 

researchers agree that the information on active maternal smoking is directly relevant to understanding the 

possible association of maternal secondhand smoke 

exposure and preterm delivery and LBW (USDHHS 

2001). More direct evidence supports the hypothesis 

that maternal secondhand smoke exposure, specifically to nicotine, may lead to LBW through a pathway 

of fetal hypoxia (Çolak et al. 2002). One would expect 

attenuated physiologic effects from exposures to secondhand smoke than from active smoking based on 

relative dose levels, but the same biologic mechanisms 

of effect may apply. 

Evidence Synthesis 

The risk estimates for secondhand smoke exposure and LBW have generally been small and have 

been consistent with the expectation that exposure 

to secondhand smoke should produce a smaller 

effect than exposure to active smoking. Most studies 

show a reduction in the mean birth weight and an 

increased risk for LBW among infants whose mothers 

were exposed to secondhand smoke. Across the studies, diverse potential confounding factors have been 

considered. Despite the lack of statistical significance 

in many of the studies, the consistencies seen in the 

literature have been summarized in several published 

reviews and have provided the strongest argument 

for an association between secondhand smoke and 

LBW. There are several plausible mechanisms by 

which secondhand smoke exposure could influence 

Congenital Malformations 

birth weight. Three comprehensive reviews of the 

literature on secondhand smoke and LBW that were 

published in the past decade all found a small increase 

in risk for LBW or SGA associated with secondhand 

smoke exposure (Misra and Nguyen 1999; Windham 

et al. 1999a; Lindbohm et al. 2002). Based on all of the 

studies that reported on LBW at term or SGA and secondhand smoke exposure, a meta-analysis provided 

a weighted pooled risk estimate of 1.2 (95 percent CI, 

1.1–1.3) for this association (Windham et al. 1999a). 

Given the published review and meta-analysis by 

Windham and colleagues (1999a), an updated metaanalysis of the relevant studies on maternal secondhand smoke exposure and birth weight currently is 

not warranted. 

Conclusion 

1. 	 The evidence is sufficient to infer a causal 

relationship between maternal exposure to 

secondhand smoke during pregnancy and a small 

reduction in birth weight. 

Implications 

Secondhand smoke exposure represents an 

avoidable contribution to birth weight reductions. 

Women, when pregnant, should not smoke or be 

exposed to secondhand smoke. 

Biologic Basis 

Because of the direct fetal effects observed with 

exposure to tobacco smoke and because of the chemically complex and teratogenic nature of cigarette 

smoke, researchers have addressed the association 

between exposure to tobacco smoke and congenital 

malformations. Most of this literature has focused on 

active smoking during pregnancy by the mother, but 

a few studies have examined secondhand smoke exposure. The etiology of most congenital malformations 

is not fully elaborated (Werler 1997), and no studies 

have been conducted to identify the mechanisms by 

which exposure to secondhand smoke may result in 

congenital malformations in humans. The few studies 

that have assessed the effects of sidestream smoke in 

animals have produced little evidence to support an 

association of secondhand smoke exposure and malformations (NCI 1999). Some recent studies suggest 

that susceptibility to some malformations may depend 

in part on the presence of genes that increase susceptibility to tobacco smoke (Wyszynski et al. 1997). Other 

3 Chapter 5 
Excerpts: Chldren and Secondhand Smoke Exposure 

proposed mechanisms include teratogenic effects of 

high concentrations of carboxyhemoglobin and nicotine, or malformations that are the result of exposure 

to some yet unidentified component of the tobacco 

plant shown to be teratogenic if ingested by animals 

(Seidman and Mashiach 1991). 

The evidence on the relationship between maternal smoking during pregnancy and congenital malformations is inconsistent. Most studies have reported no 

association between maternal smoking and congenital malformations as a whole. However, for selected 

malformations, particularly oral clefts, several studies have reported positive associations with active 

smoking during pregnancy by the mother (Little et 

al. 2004a,b; Meyer et al. 2004). In fact, recent studies 

on gene-environment interactions have furthered the 

etiologic understanding of oral clefts and the role of 

smoking (Hwang et al. 1995; Shaw et al. 1996; van 

Rooij et al. 2001, 2002; Lammer et al. 2004). 

Evidence Synthesis 

The evidence regarding the relationship between 

involuntary smoking and congenital malformations is 

inconsistent. The few studies that have been conducted 

have reported no association between involuntary 

smoking and specific or all congenital malformations. 

Investigating congenital malformations is challenging because of the sample size that is necessary to 

study specific malformations. To date, few clues are 

available regarding the hypothesized biologic mechanisms of tobacco smoke and congenital malformations. 

Although two studies have reported elevated rates of 

neural tube defects in association with involuntary 

smoking, this association should be examined further 

in future studies. 

Conclusion 

1. 	 The evidence is inadequate to infer the presence 

or absence of a causal relationship between 

exposure to secondhand smoke and congenital 

malformations. 

Implications 

The topic of tobacco smoke exposure and congenital malformations merits further investigation, 

particularly in part because of the teratogenic nature 

of tobacco smoke. 

Cognitive, Behavioral, and Physical Development
 

Biologic Basis 

In recent years, studies have suggested that 

exposure to tobacco smoke during pregnancy and 

childhood may affect the physical and cognitive 

development of the growing child. Researchers who 

examine the effects of these exposures on childhood 

outcomes need to account for potential confounding 

factors that reflect the various correlates of secondhand smoke exposure that also affect development. 

For example, factors that may affect physical and 

cognitive development include social class, parental 

education, the home environment as it relates to stimulation and developmentally appropriate exposures, 

and pregnancy-related factors such as voluntary 

and involuntary smoking and alcohol and substance 

use. Birth weight may also be a confounding factor 

because it is associated with both smoking (voluntary 

and involuntary) and physical and cognitive development. However, some researchers argue that adjusting for birth weight may overcontrol because it may 

be in the causal pathway from exposure to tobacco 

before birth to the time when childhood outcomes are 

assessed (Baghurst et al. 1992). 

Another methodologic challenge lies in differentiating the effects of exposure to tobacco during and 

after pregnancy. This differentiation is often not possible because of the high correlation of tobacco smoke 

exposure for these two time periods. Studies with 

sufficient populations and detailed information on 

smoking status during both pregnancy and the postpartum period have been able to stratify participants 

into exposure groups: no prenatal or postpartum exposure, no prenatal but some postpartum exposure, and 

both prenatal and postpartum exposures. Other studies have examined the effects of secondhand smoke 

Reproductve and Developmental Effects from Exposure to Secondhand Smoke 39 
Surgeon General’s Report 

exposure from adults other than the mother among 

those children whose mothers did not smoke during 

pregnancy. These categories have served to partially 

address the timing of the exposures and, in particular, 

to control for exposures during pregnancy. 

The mechanisms by which exposures to secondhand smoke may lead to compromised physical and 

cognitive development have not been fully explained 

and may be complex. Some of the mechanisms may 

be similar to those proposed for maternal smoking 

during pregnancy, such as hypoxia or the potentially 

teratogenic effects of tobacco smoke (USDHHS 1990; 

Bruner and Forouzan 1991; Lambers and Clark 1996; 

Werler 1997). Studies document that components of 

secondhand and mainstream smoke are qualitatively 

similar to those of sidestream smoke, but quantitative 

data for doses of tobacco smoke components that 

reach the fetus across the placenta from active and 

involuntary maternal smoking have not been available (Slotkin 1998). This consideration is particularly 

important for outcomes assessed after one year of age 

because the child’s exposure will have occurred for a 

period of time longer than the exposure of the fetus 

during the nine months of pregnancy. 

For cognitive development, investigators have 

proposed a number of effects on central nervous 

system (CNS) development from smoking in general 

and nicotine in particular. First, the fetus may suffer 

from hypoxia as a result of reduced blood flow or 

reduced oxygen levels (USDHHS 1990; Lambers and 

Clark 1996). Alterations in the peripheral autonomic 

pathways may lead to an increased susceptibility to 

hypoxia-induced, short-term and long-term brain 

damage (Slotkin 1998). In one review of prenatal 

nicotine exposure, Ernst and colleagues (2001) summarized numerous animal studies that document the 

impact of nicotine on cognitive processes of exposed 

rats and guinea pigs, such as slowed learning or 

increased attention or memory deficits. These investigators identified animal as well as human studies 

that have demonstrated adverse effects of nicotine 

exposure on neural functioning. Exposure to nicotine 

alters enzyme activity and thus affects brain development, and alters molecular processes that affect neurotransmitter systems and lead to permanent neural 

abnormalities (Ernst et al. 2001). 

Cognitive Development 

Evidence Synthesis 

The literature cited in this discussion examined 

the effects of involuntary smoking on children’s 

cognitive development. However, it is difficult to synthesize the results of these studies because the ages of 

the children, the assessed exposures, and the outcomes 

vary across and even within studies. Moreover, some 

of the findings across and within studies are inconsistent. Eight of the 12 studies that examined associations between involuntary smoking and children’s 

cognitive development reported associations between 

secondhand smoke exposures and reduced levels of 

cognitive development; these investigators had used 

a variety of assessments, such as performance on standardized tests, grade retention, or a diagnosis of mental retardation. The use of various cognitive measures 

across studies precludes an assessment of consistency 

with specific associations. Yet the finding that secondhand smoke exposure was associated with several different outcomes suggests that exposure may, indeed, 

impact the cognitive development of children. More 

studies are clearly needed; of the studies that have 

been conducted, there is a need for additional efforts 

to replicate findings. 

Conclusion 

1. 	 The evidence is inadequate to infer the presence or 

absence of a causal relationship between exposure 

to secondhand smoke and cognitive functioning 

among children. 

Implications 

Further research is needed but there are complex 

challenges to carrying out such studies, given the need 

for longitudinal design and consideration of the many 

factors affecting cognitive functioning. 

Behavioral Development 

Evidence Synthesis 

The evidence for an association between exposure to secondhand smoke and behavioral problems 

in children is inconsistent. Because so few studies 

have been carried out on this topic, more studies are 

clearly warranted. 

Conclusion 

1. 	 The evidence is inadequate to infer the presence or 

absence of a causal relationship between exposure 

to secondhand smoke and behavioral problems 

among children. 

0 Chapter 5 
Excerpts: Chldren and Secondhand Smoke Exposure 

Implications 

Further research is needed, but the same challenges remain that confront research on other effects 

such as cognitive functioning. 

Height/Growth 

Evidence Synthesis 

The evidence for an association between secondhand smoke exposure and children’s height/growth 

is mixed. Those studies that do report associations 

find relatively consistent deficits associated with secondhand smoke exposure. However, the magnitude 

of the effect is small and could reflect residual confounding. 

Childhood Cancer 

Conclusion 

1. 	 The evidence is inadequate to infer the presence or 

absence of a causal relationship between exposure 

to secondhand smoke and children’s height/ 

growth. 

Implications 

The evidence suggests that any effect of secondhand smoke exposure on height is likely to be small 

and of little significance. Research on secondhand 

smoke exposure and height is complicated by the 

many potential confounding factors. 

Biologic Basis 

Tobacco smoke contains numerous carcinogens 

and is a well-established cause of cancer (USDHEW 

1964, 1974; USDHHS 1980, 1986; Smith et al. 1997, 

2000a,b). Numerous animal studies elucidate evidence 

for, and mechanisms of, transplacental carcinogenesis 

(Rice 1979; Schuller 1984; Napalkov et al. 1989). For 

example, when the oncogenic compound ethylnitrosourea (ENU) was administered intravenously or 

intraperitoneally to pregnant rabbits, the offspring 

developed renal and neural cancers (Stavrou et al. 

1984). Monkeys are also susceptible to transplacental 

carcinogenesis, with offspring developing vascular 

and a variety of other tumors following prenatal 

administration of ENU to the mother (Rice et al. 1989). 

The strongest human evidence that transplacental carcinogenesis is biologically plausible may be the occurrence of vaginal clear-cell adenocarcinoma among 

young women whose mothers were prescribed diethylstilbesterol during pregnancy (Vessey 1989). 

Limited biologic evidence suggests that involuntary exposure to cigarette smoke may also lead to 

transplacental carcinogenesis. Maternal secondhand 

smoke exposure during pregnancy, as with maternal active smoking during pregnancy, can result in 

increased measurable metabolites of cigarette smoke 

in amniotic fluid (Andresen et al. 1982; Smith et al. 

1982) and in fetal blood (Bottoms et al. 1982; Coghlin 

et al. 1991). For example, thiocyanate levels in fetal 

blood were less than 50 micromoles per liter (μmol/ 

L) when the mother was not exposed to secondhand 

smoke during pregnancy (Bottoms et al. 1982). Among 

mothers who were prenatally exposed to secondhand 

smoke, fetal blood levels of thiocyanate were as high 

as 90 μmol/L, and among mothers who actively 

smoked, the measurements were about 170 μmol/L. 

Notably, however, two studies that measured thiocyanate levels in umbilical cord blood found no differences between secondhand smoke-exposed and 

unexposed nonsmoking women (Manchester and 

Jacoby 1981; Hauth et al. 1984). Hauth and colleagues 

(1984) found thiocyanate levels of 23 μmol/L in 

umbilical cord blood from unexposed infants of nonsmoking mothers and levels of 26 μmol/L in secondhand smoke-exposed infants of nonsmoking mothers 

(defined as living and/or working with someone who 

smoked at least 10 cigarettes per day). Manchester 

and Jacoby (1981) also found similar cord blood levels 

of thiocyanate in unexposed (34 ± 3 μmol/L) and secondhand smoke-exposed (35 ± 3 μmol/L) infants of 

nonsmoking mothers (exposure was defined as living 

with someone who smoked). 

Studies of maternal smoking during pregnancy 

found enhanced transplacental enzyme activation 

(Nebert et al. 1969; Manchester and Jacoby 1981) and 

Reproductve and Developmental Effects from Exposure to Secondhand Smoke 1 
Surgeon General’s Report 

placental DNA adducts (Everson et al. 1986, 1988; 

Hansen et al. 1992), and several animal studies suggested that embryonic exposure to tobacco smoke 

components increased tumor rates (Mohr et al. 1975; 

Nicolov and Chernozemsky 1979). For example, 

diethylnitrosamine administered to female hamsters 

in the last days of pregnancy produced offspring that 

developed respiratory tract neoplasms in nearly 95 

percent of the animals. Cigarette smoke condensate in 

olive oil that was used in another study of pregnant 

hamsters was injected intraperitoneally; it produced 

a variety of tumors in the offspring, including tumors 

of the pancreas, adrenal glands, liver, uterus, and lung 

(Nicolov and Chernozemsky 1979). Human studies 

document an increased frequency of genomic deletions in the hypoxanthine-guanine phosphoribosyltransferase gene found in the cord blood of newborns 

whose mothers were exposed to secondhand smoke 

(compared with newborns of unexposed mothers). 

This finding strongly supports a carcinogenic effect 

of prenatal secondhand smoke exposure, particularly 

since these mutations are characteristic of those found 

in childhood leukemia and lymphoma (Finette et al. 

1998). Prenatal exposure to secondhand smoke may 

also play a role by enhancing any effect of postnatal 

exposure on the development of childhood cancer 

(Napalkov 1973), but the potential effects of prenatal 

and postnatal exposures are difficult to separate given 

the high correlation between prenatal and postnatal 

parental smoking. Several studies have assessed postnatal exposures by measuring cotinine and nicotine 

concentrations in the saliva and urine of infants. The 

investigators found that those infants with reported 

secondhand smoke exposures had significantly higher 

concentrations than those infants with no reported 

exposure in the 24 hours before measuring the concentrations (Greenberg et al. 1984; Crawford et al. 1994). 

Evidence Synthesis 

The strongest evidence for any childhood 

cancer risk from maternal secondhand smoke exposure is specific to leukemias, lymphomas, and brain 

tumors, although the causal pathway may actually 

be through DNA damage to the father’s sperm from 

active smoking rather than through maternal secondhand smoke exposure during pregnancy. Some of the 

epidemiologic studies suggest a slightly increased 

risk in childhood cancers from prenatal and postnatal 

secondhand smoke exposures, but most of the studies were small and did not have the power to detect 

statistically significant associations. In addition, 

most of the studies lacked exposure assessments for 

relevant exposure periods (preconception, prenatal, 

and postnatal), which may also have reduced the risk 

estimates because of nondifferential misclassification 

of exposure status. Risk estimates may be inflated by 

recall bias, especially since interviews to assess exposures took place up to 15 years after birth. Parents 

of children with cancer may be more likely to think 

about possible causes for their child’s illness, thereby 

improving their recall of exposure experiences around 

the time of the pregnancy and birth. Parents of healthy 

children, however, have no particular reason to think 

about their exposure experiences and their recall may 

not be as good. Differential recall is a potential problem common to all case-control studies. If differential 

positive recall between cases and controls is present, it 

will inflate the risk estimate for childhood cancer. 

Researchers have observed exposure-response 

trends for overall cancers as well as for leukemia, 

lymphoma, and brain tumors in a number of studies. Most of the studies adjusted for potentially confounding factors such as the child’s date of birth, age 

at diagnosis, parental education level, parental age at 

child’s birth, socioeconomic status, residence, and race 

by multivariate adjustment or case-control matching. 

Only four studies, however, considered other cancer 

risk factors such as maternal x-rays, drug use, and consumption of foods containing sodium nitrite (PrestonMartin et al. 1982; Howe et al. 1989; Kuijten et al. 1990; 

Bunin et al. 1994). Although active maternal smoking 

during pregnancy does not appear to be related to 

childhood cancer, it was not clear in some studies 

whether mothers who actively smoked were excluded 

from the various analyses that estimated risks from 

paternal smoking. Thus, some of the elevated risks for 

cancer in their offspring from paternal smoking may 

have been compounded by the child’s postnatal exposure to active maternal smoking. 

Conclusions 

1. 	 The evidence is suggestive but not sufficient to 

infer a causal relationship between prenatal and 

postnatal exposure to secondhand smoke and 

childhood cancer. 

2. 	 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. 

2 Chapter 5 
Excerpts: Chldren and Secondhand Smoke Exposure 

3. 	 The evidence is inadequate to infer the presence 

or absence of a causal relationship between 

exposure to secondhand smoke during infancy 

and childhood cancer. 

4. 	 The evidence is suggestive but not sufficient to 

infer a causal relationship between prenatal and 

postnatal exposure to secondhand smoke and 

childhood leukemias. 

5. 	 The evidence is suggestive but not sufficient to 

infer a causal relationship between prenatal and 

postnatal exposure to secondhand smoke and 

childhood lymphomas. 

6. 	 The evidence is suggestive but not sufficient to 

infer a causal relationship between prenatal and 

postnatal exposure to secondhand smoke and 

childhood brain tumors. 

Conclusions 

7. 	 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. 

Implications 

Childhood cancers are diverse in their characteristics and etiology. Although the evidence is inadequate for some sources and periods of exposure, there 

is some evidence indicative of associations of childhood cancer risk with secondhand smoke exposure. 

Further research is needed to provide a better understanding of the potential causal relationships between 

types of exposures to secondhand smoke and childhood cancer risks. 

The following conclusions are supported by 

text in the full report that may not be included 

in this excerpt. The full report can be accessed at 

http://www.surgeongeneral.gov/library/secondhandsmoke/report/. 

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. 

Reproductve and Developmental Effects from Exposure to Secondhand Smoke 3 
Surgeon General’s Report 

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. 

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 5 
Excerpts: Chldren and Secondhand Smoke Exposure 

Overall Implications 

Because infant mortality for the United States is 

quite high compared with other industrialized countries, identifying strategies to reduce the number of 

infant deaths should receive high priority. The epidemiologic evidence for the association of secondhand 

smoke exposure and an increased risk of SIDS indicates that eliminating secondhand smoke exposures 

among newborns and young infants should be part of 

an overall strategy to reduce the high infant mortality 

rate in the United States. 

The available evidence for five reproductive and 

childhood outcomes—childhood cancer, cognitive 

development, behaviors, LBW, and spontaneous abortion—calls for further research with improved methodologies. The methodologic challenges and issues 

that were discussed in relation to exposure assessment and reproductive outcomes might act as a guide 

for future research on these topics. There is a need for 

studies that examine exposure to secondhand smoke 

and childhood cancers to further evaluate the risks for 

specific cancer types. The evidence reviewed in this 

chapter points to germ-cell mutations among fathers 

who smoke as a possible pathway. Additional studies may be warranted that focus on childhood cancer 

and active paternal smoking, with improved controls 

for maternal secondhand smoke exposure and active 

smoking during pregnancy and the exposure of 

infants to secondhand smoke. For secondhand smoke 

and spontaneous abortions, studies using samples 

with adequate statistical power are needed. For all 

outcomes, investigations should include biochemical 

measures of exposures, and these measures should be 

used to determine the presence of dose-response relationships—determining dose-response relationships 

will greatly facilitate the assessment of causality. 

Reproductve and Developmental Effects from Exposure to Secondhand Smoke 5 
Surgeon General’s Report 

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52 Chapter 5 
Excerpts from Chapter 6 

Respiratory Effects in Children 

from Exposure to Secondhand Smoke 

Introduction 55 

Mechanisms of Health Effects from Secondhand Tobacco Smoke 5 

Introduction 5 

Lung Development and Growth 5 

Immunologic Effects and Inflammation 57 

Summary 59 

Methods Used to Review the Evidence 0 

Lower Respiratory Illness in Infancy and Early Childhood 1 

Evidence Synthesis 1 

Conclusions 3 

Implications 3 

Middle Ear Disease and Adenotonsillectomy 3 

Evidence Synthesis 3 

Conclusions  

Implications  

Respiratory Symptoms and Prevalent Asthma in School-Age Children  

Evidence Synthesis  

Conclusions 5 

Implications 5 

Childhood Asthma Onset  

Evidence Synthesis  

Conclusions 7 

Implications 7 

Atopy  

Evidence Synthesis  

Conclusion  

Implications  

Lung Growth and Pulmonary Function 9 

Evidence Synthesis 9 

Conclusion 70 

Implications 70 

Conclusions 70 

Overall Implications 71 

References 73 

 53 

Excerpts: Chldren and Secondhand Smoke Exposure 

Introduction 

Adverse effects of parental smoking on the respiratory health of children have been a clinical and public health concern for decades. As early as 1974, two 

articles published in the journal Lancet alerted readers 

to a possible link between parental smoking and the 

risk of a lower respiratory illness (LRI) among infants 

(Colley et al. 1974; Harlap and Davies 1974). Although 

adverse effects on children from exposure to secondhand tobacco smoke had already been suggested 

(Cameron et al. 1969; Norman-Taylor and Dickinson 

1972), the association with early episodes of acute 

chest illnesses was of immediate and continuing interest because of the suspected long-term consequences 

for lung growth, chronic respiratory morbidity in 

childhood, and adult chronic obstructive lung disease 

(Samet et al. 1983). 

Subsequently, many epidemiologic studies 

have associated parental smoking with respiratory 

diseases and other adverse health effects throughout 

childhood. The exposures covered include maternal 

smoking during pregnancy and afterward, paternal 

smoking, parental smoking generally, and smoking 

by others. In 1986, the evidence was sufficient for the 

U.S. Surgeon General to conclude that the children of 

parents who smoked had an increased frequency of 

acute respiratory illnesses and related hospital admissions during infancy (U.S. Department of Health and 

Human Services [USDHHS] 1986). The 1986 Surgeon 

General’s report also noted that in older children, there 

was an increased frequency of cough and phlegm 

and some evidence of an association with middle ear 

disease. The report also commented on an association 

between slowed lung growth in children and parental 

smoking. Several authoritative reviews by various 

agencies followed the 1986 report (U.S. Environmental Protection Agency [USEPA] 1992; National 

Cancer Institute [NCI] 1999). Some researchers have 

systematically reviewed the literature and, where 

appropriate, carried out meta-analyses (DiFranza and 

Lew 1996; Uhari et al. 1996; Li et al. 1999); the most 

comprehensive systematic review was commissioned 

by the Department of Health in England (Scientific 

Committee on Tobacco and Health 1998). Updated versions of these reviews were then published as a series 

of articles in the journal Thorax (Cook and Strachan 

1997, 1998, 1999; Strachan and Cook 1997, 1998a,b,c; 

Cook et al. 1998). These papers later served as a 

foundation for the 1999 World Health Organization 

(WHO) consultation report on environmental tobacco 

smoke and child health (WHO 1999). This chapter of 

the Surgeon General’s report presents a major update 

of those reviews based on literature searches carried 

out through March 2001. The methodology for these 

reviews is described later in this chapter (see “Methods Used to Review the Evidence”). Selected key 

references published subsequent to these reviews are 

included in an appendix of significant additions to the 

literature at the end of this report. 

The section that follows focuses on the biologic 

basis for respiratory health effects; Chapter 2 (Toxicology of Secondhand Smoke) in the full report provides further background. Separate sections in the full 

report review the evidence for different adverse effects 

of secondhand smoke exposure of children: LRIs in 

infancy and early childhood, middle ear disease and 

adenotonsillectomy, frequency of respiratory symptoms and prevalent asthma in school-age children, and 

cohort and case-control studies of the onset of asthma 

in childhood. There is also a review of the evidence 

for the effects of parental smoking on several physiologic measures, lung function, bronchial reactivity, 

and atopic sensitization. Each section concludes with 

a summary and an interpretation of the evidence. 

The epidemiologic evidence is reviewed in 

detail in the full report. Therefore, it is not included 

in this Excerpt. The full report may be accessed at 

http://www.surgeongeneral.gov/library/secondhandsmoke/report. 

Respratory Effects n Chldren from Exposure to Secondhand Smoke 55 
Surgeon General’s Report 

Mechanisms of Health Effects from Secondhand Tobacco Smoke 

This section reviews the biologic impact of 

secondhand smoke on the respiratory system of the 

child. Subsequent sections summarize the evidence 

for adverse health effects on infants and children and 

describe postulated mechanisms for these effects. 

Chapter 2 in the full report provides additional general data on these mechanisms. 

Introduction 

Pregnant women who smoke expose the fetus 

to tobacco smoke components during a critical window of lung development, with consequences that 

may be persistent. In infancy and early childhood, the 

contributions of prenatal versus postnatal exposures 

to secondhand smoke are difficult to separate because 

women who smoke during pregnancy almost invariably continue to smoke after their children are born. 

For children, exposure to secondhand smoke may lead 

to respiratory illnesses as a result of adverse effects on 

the immune system and on lung growth and development. 

Lung Development and Growth 

Active smoking by the mother during pregnancy 

has causal adverse effects on pregnancy outcomes that 

are well documented (USDHHS 2001, 2004). Exposure 

of pregnant women to secondhand tobacco smoke has 

also been associated with prematurity (Hanke et al. 

1999), reduced birth weight (Mainous and Hueston 

1994; Misra and Nguyen 1999), and small for gestational age outcomes in some studies (Dejin-Karlsson 

et al. 1998). However, the developmental effects on 

the respiratory system from maternal smoking during pregnancy extend beyond those that might be 

expected based on prematurity alone—the airways 

are particularly affected. Studies have demonstrated 

that lower measured airflows associated with secondhand smoke exposure are not completely explained 

by the reduction in somatic growth caused by maternal smoking (Young et al. 2000b). Researchers suspect 

that fetal growth limitations are mediated in part by 

the vasoconstrictive effects of nicotine, which may 

limit uterine blood flow and induce fetal hypoxia 

(Philipp et al. 1984). Fetal hypoxia, in turn, may lead 

to slowed fetal growth and may have direct effects 

on the lung, possibly affecting lung mechanics by 

suppressing the fetal respiratory rate. Studies have 

demonstrated a decrease in fetal movement for at least 

one hour after maternal smoking, which is consistent 

with fetal hypoxia (Thaler et al. 1980). Smoking during pregnancy may also negatively affect the control 

of respiration in the fetus (Lewis and Bosque 1995). 

Researchers have proposed several mechanisms 

that explain the effects of maternal smoking during 

pregnancy on infant lung function. Animal and human 

studies suggest that morphologic and metabolic alterations result from in utero exposure to tobacco smoke 

components that cross the placental barrier (Bassi et 

al. 1984; Philipp et al. 1984; Collins et al. 1985; Chen 

et al. 1987). One study with monkeys that involved 

infusion of nicotine into the mother during pregnancy 

showed lung hypoplasia and changes in the developing alveoli (Sekhon et al. 1999). The investigators 

postulated that the effect was mediated by the nicotine cholinergic receptors, which showed an increased 

expansion and binding with nicotine administration. 

Further research with this model indicated altered 

collagen in the developing lung (Sekhon et al. 2002). 

Studies with this and similar models have shown a 

variety of effects from nicotine on the neonatal lung 

(Pierce and Nguyen 2002). The programming of fetal 

growth genes in utero may have a lifelong effect on 

lung development and disease susceptibility, areas of 

ongoing research in other diseases. There is now substantial research in progress on early life events and 

future disease risk that follows the general hypothesis 

proposed by Barker and colleagues (1996). 

Exposure to secondhand smoke may also lead 

to structural changes in the developing lung. In a rat 

model, Collins and colleagues (1985) found that intrauterine exposure of the pregnant rat to secondhand 

smoke was associated with pulmonary hypoplasia 

in the baby rats with decreased lung volumes; in this 

rat model, exposure reduced the number of sacules 

but increased their size. Brown and colleagues (1995) 

assessed respiratory mechanics in 53 healthy infants, 

and interpreted the pattern of findings to suggest that 

prenatal tobacco smoke exposure from smoking by 

the mother may lead to a reduction in airway size and 

changes in lung properties. 

Lung maturation in utero is regulated by the 

endocrine environment, and the timing of secondhand 

smoke exposures with regard to lung development 

may have a lifelong impact on respiratory function. 

Secondhand smoke components may increase in utero 

5 Chapter  
Excerpts: Chldren and Secondhand Smoke Exposure 

stress responses that then speed lung maturation at 

the expense of lung growth. Several studies have 

demonstrated an effect on the fetal endocrine milieu 

secondary to secondhand smoke exposure (Divers et 

al. 1981; Catlin et al. 1990; Lieberman et al. 1992). Studies have also associated maternal smoking with more 

advanced lung maturity measured by lectin/sphingomyelin (L/S) ratios that were out of proportion to 

fetal size in human infants (Mainous and Hueston 

1994). Cotinine levels measured in the amniotic fluid 

were positively correlated with L/S ratios. Studies 

also noted an increase in free, conjugated, and total 

cortisol levels, suggesting a potentially direct or indirect role for hormonal effects of secondhand smoke 

on the fetus (Lieberman et al. 1992). Other researchers 

have demonstrated higher levels of catecholamines in 

amniotic fluid in pregnant smokers compared with 

pregnant nonsmokers, further supporting an endocrine mechanism for the effect of secondhand smoke 

(Divers et al. 1981). 

Multiple studies suggest that the effect of 

secondhand smoke on the development of the respiratory system begins with in utero exposure (Tager et 

al. 1995; Stick et al. 1996; Lodrup Carlsen et al. 1997). 

Stick and colleagues (1996) reported a dose-dependent 

effect of in utero cigarette smoke exposure in decreasing tidal flow patterns that were measured during 

the first three days of life (i.e., before any postnatal 

exposure). This effect was independent of the effect of 

smoking on birth weight. Hoo and colleagues (1998) 

evaluated respiratory function in preterm infants of 

mothers who did and did not smoke during pregnancy, with the goal of investigating whether the 

effect of prenatal tobacco smoke exposure is limited 

to an influence during the last weeks of gestation. 

The researchers observed that respiratory function 

was impaired in infants born preterm (an average of 

seven weeks early), suggesting that the adverse effect 

of prenatal tobacco smoke exposure is not limited to 

the last weeks of in utero development. The ratio of 

time to peak tidal expiratory flow to expiratory time 

(TPTEF:TE) was lower in infants exposed to secondhand smoke in utero compared with unexposed 

infants (mean 0.369 standard deviation [SD] 0.109 versus mean 0.426 SD 0.135, p 
0.02). Because TPTEF:TE is 

associated with airway caliber, these data imply that 

cigarette smoke exposure in utero may affect airway 

development. Lower maximal forced expiratory flow 

at functional residual capacity (VmaxFRC) (Hanrahan 

et al. 1992) and diminished expiratory flows (Brown 

et al. 1995) in infants exposed in utero to secondhand 

smoke provide further support for the contention 

that infants of mothers who smoke during pregnancy 

have smaller airways. Increased airway wall thickness 

and increased smooth muscle, which can both lead to 

a decreased airway diameter, were found in infants 

exposed to tobacco smoke in utero who had died of 

sudden infant death syndrome (SIDS) (Elliot et al. 

1999). In animal models of secondhand smoke exposure, fetuses of rats exposed to mainstream smoke 

(from active smoking) or to secondhand (sidestream) 

smoke had reduced lung volume, decreased elastic 

tissue within the parenchyma, increased density of 

interstitial tissue, and inadequate development of 

elastin and collagen (Collins et al. 1985; Vidic 1991). 

These animal and human data provide clear evidence 

for an adverse effect of in utero exposure to tobacco 

smoke on the developing lung. Studies also document 

structural changes in animal models and in exposed 

children who have died from SIDS. The physiologic 

findings suggest altered lung mechanics and reduced 

airflow consistent with changes in structure. 

Immunologic Effects and Inflammation 

The development of lung immunophenotype 

(i.e., the pattern of immunologic response in the lung) 

is considered to have a key role in determining the 

risk for asthma, particularly in regard to the T-helper 1 

(Th1) pathway (which mediates cellular immunity) and 

the Th2 pathway (which mediates allergic responses). 

Secondhand smoke exposure may promote immunologic development along Th2 pathways, thus contributing to the intermediate phenotypes associated with 

asthma and with a predilection to chronic respiratory 

disease. Gene-environment interactions that begin in 

utero and persist during critical periods of development after birth represent the least understood, but 

potentially the most important, mechanistic route for 

a lasting influence of secondhand smoke. Although 

a meta-analysis of epidemiologic evidence suggests 

that parental smoking before birth (or early childhood 

secondhand smoke exposure) does not increase the 

risk for allergic sensitization, other lines of mechanistic investigation do show a variety of influences from 

secondhand smoke on immune and inflammatory 

responses (Strachan and Cook 1998b). 

Secondhand smoke effects on T cells may influence gene regulation, inflammatory cell function, 

cytokine production, and immunoglobulin E (IgE) 

synthesis. These effects are particularly important 

to consider in regard to immune system ontogeny 

and for the subsequent development of allergies 

in childhood. Researchers have demonstrated that 

mainstream and sidestream smoke condensates 

Respratory Effects n Chldren from Exposure to Secondhand Smoke 57 
Surgeon General’s Report 

selectively suppress the interferon gamma induction 

of several macrophage functions, including phagocytosis of Ig-opsonized sheep red blood cells, class 

II major histocompatibility complex expression, and 

nitric oxide synthesis, which are all representative 

of effects on immunity (Braun et al. 1998; Edwards 

et al. 1999). Alterations in antigen presentation may 

occur not only in the respiratory tract but also in the 

rest of the body where absorbed toxicants are distributed. Macrophages are potent effector cells for 

immune responsiveness; suppression of their ability 

to respond to environmental challenges could have 

lifelong consequences on immune function. 

Immune responses may also be increased as a 

result of secondhand smoke exposure. Animal studies demonstrate increases in IgE, eosinophils, and 

Th2 cytokines (especially interleukin [IL]-4 and IL-10) 

with exposure to secondhand smoke. These increases 

may augment the potential for allergic sensitization 

and the development of an atopy phenotype. In 

mice sensitized to the ovalbumin (OVA) antigen and 

exposed to secondhand smoke for six hours per day, 

five days per week, for six weeks, researchers measured increases in total IgE, OVA-specific immunoglobulin G1, and eosinophils in the blood (Seymour 

et al. 1997). These measures indicate an increase in the 

allergic response to inhaled antigens. On the basis of 

the results from this mouse model, the investigators 

concluded that allergen sensitization with the increase 

in Th2 responses may contribute to the development 

of allergies in individuals exposed to secondhand 

smoke (Seymour et al. 1997). Other studies have demonstrated an increase in IL-5, granulocytemacrophage 

colony-stimulating factor, and IL-2 in bronchoalveolar 

lavage fluid in mice exposed to OVA along with secondhand smoke. In these mouse models, interferon 

gamma levels decreased. Because mice exposed to 

OVA alone did not experience these cytokine changes, 

secondhand smoke appears able to induce a sensitization phenotype to a usually neutral antigen (Rumold 

et al. 2001). Although the animal data are stronger than 

the human epidemiologic data, studies in humans are 

supportive of an effect of tobacco smoke exposure on 

allergic phenotypes. 

Allergies are caused by multiple interacting 

factors in people with underlying susceptibility. 

Secondhand smoke exposure both in utero and after 

birth may promote the development of an allergic 

phenotype. Antigens presented during the neonatal 

period in mice skew the immune development and 

response along a Th2 pathway (i.e., toward an allergic 

phenotype) (Forsthuber et al. 1996). Human fetuses, 

under the influence of the maternal system mediated 

through the placenta, may develop a Th2 preference 

as a response to an antigen (Michie 1998). Magnusson (1986) studied newborn children of nonallergic 

parents and found evidence suggesting that tobacco 

smoke exposure in utero may promote an allergic phenotype. A threefold increase in risk for an 

elevated IgE level was observed in children whose 

mothers smoked compared with the IgE levels in 

children born to nonsmoking mothers. Total cord 

blood IgE concentrations were substantially higher 

in infants of mothers who smoked (60.8 international 

units [IU]) compared with infants of nonsmoking 

mothers (9.8 IU). 

Atopy may be characterized by either a positive 

IgE-mediated skin test or elevated specific IgE serum 

levels. Atopy represents a risk factor for asthma, and 

an increase in bronchial responsiveness has been associated with higher serum IgE levels. Human studies 

provide mixed evidence as to whether secondhand 

smoke exposures are associated with an increase in 

IgE-mediated responses (Weiss et al. 1985; Martinez 

et al. 1988; Ownby and McCullough 1988; Stankus et 

al. 1988). Weiss and colleagues (1985) demonstrated 

that maternal smoking was associated with atopy in 

children aged five through nine years who were evaluated by skin tests to four common allergens. Ronchetti and colleagues (1990) demonstrated an effect 

of exposure on IgE levels and on eosinophil counts. 

Eosinophil counts were at least three times higher in 

boys exposed to secondhand smoke compared with 

unexposed boys. There was a dose-response relationship between the number of cigarettes to which each 

boy had been exposed and the level of eosinophilia 

(Ronchetti et al. 1990). 

Researchers showed decades ago that mainstream cigarette smoke causes airway inflammation 

(Niewoehner et al. 1974) and an increase in airway 

permeability to small and large molecules in young 

smokers (Simani et al. 1974; Jones et al. 1980). Given 

the qualitative similarities between mainstream smoke 

and secondhand smoke, these effects may be relevant 

to involuntary smoking (USDHHS 1986). 

There are many specific components of secondhand smoke that may adversely affect a child’s lung. 

For example, a bacterial endotoxin known as lipopolysaccharide (LPS) can be detected in both mainstream 

and sidestream tobacco smoke. Studies have detected 

biologically active LPS in mainstream and sidestream 

smoke from regular and light experimental reference cigarettes used in the studies (mainstream: 120 

± 64 nanograms [ng] per regular cigarette, 45.3 ± 16 

ng per light cigarette; sidestream: 18 ± 1.5 ng per 

regular cigarette, 75 ± 49 ng per light cigarette). The 

5 Chapter  
Excerpts: Chldren and Secondhand Smoke Exposure 

investigators suggested that chronic LPS exposure 

from cigarette smoke may contribute to the inflammatory effects of secondhand smoke (Hasday et al. 1999). 

Other studies show that LPS exposure may alter 

responses to allergen challenge (Tulić et al. 2000). 

Researchers need to consider this hypothesized 

role of endotoxin because of the known pathologic 

effects of endotoxins on susceptible individuals. As a 

component of the cell wall of gram-negative bacteria, 

endotoxins are ubiquitous in the environment and 

may be found in high concentrations in household 

dust (Michel et al. 1996) and in ambient air pollution 

(Bonner et al. 1998). Macrophage activation may result 

from exposure to low concentrations of an endotoxin, 

leading to a cascade of inflammatory cytokines (such as 

IL-1, IL-6, and IL-8) and arachidonic acid metabolites, 

which are important in the formation of prostaglandin 

molecules (Bayne et al. 1986; Michie et al. 1988; Ingalls 

et al. 1999). Studies have documented increased levels 

of neutrophils in bronchoalveolar lavage fluid after a 

challenge with dust that contained endotoxins (Hunt 

et al. 1994). Reversible airflow obstruction has been 

associated with the inhalation of endotoxins in the 

air. In a cohort study of infants in Boston, Park and 

colleagues (2001) used a univariate model and found 

a significant association of wheeze in the first year 

of life with elevated dust endotoxin levels (relative 

risk [RR] = 1.29 [95 percent confidence interval (CI), 

1.03–1.62]). In a multivariate model, elevated endotoxin levels in dust were associated with an increased 

risk for repeated wheeze illness in the first year of life 

(RR = 1.56 [95 percent CI, 1.03–2.38]) (Park et al. 2001). 

Exposure to endotoxins from secondhand smoke in 

utero, during infancy, and in childhood may increase 

airway inflammation and may interact synergistically 

with additional secondhand smoke exposures. 

Smoking contributes generally to the particulate 

load in indoor air, and research documents that inhaling particles in the respirable size range contributes to 

pulmonary inflammation (National Research Council 

2004). One consequence of particle-induced inflammation may be an intermediate phenotype with cough 

and wheeze in early childhood. Investigators used a 

guinea pig model of secondhand smoke exposure to 

study sensory nerve pathways for cough and airway 

narrowing in an effort to explain the development of 

cough and wheeze symptoms in children of smokers. When guinea pigs were exposed to sidestream 

smoke for six hours per day, five days per week, from 

one through six weeks of age, they demonstrated an 

increase in excitability of pulmonary C fibers (Mutoh 

et al. 1999) and rapidly adapting receptors (Bonham 

et al. 1996), which are believed to be primarily responsible for eliciting the reflex responses in defending the 

lungs against inhaled irritants and toxins (Lee and 

Widdicombe 2001). These studies have led to the conclusion that cough and wheeze may be produced by 

neural pathway stimulation and irritation. 

Summary 

Childhood respiratory disease covers a spectrum 

of diseases and underlying pathogenetic mechanisms 

that include infection, prenatal alterations in lung 

structure, inflammation, and allergic responses. There 

is a potential for secondhand smoke to contribute over 

the long term to the development of respiratory disease through altered organ maturation and immune 

function. Mechanisms underlying the adverse health 

effects of secondhand smoke vary across the phases 

of lung growth and development, extending from the 

in utero period to the completion of lung growth in 

late adolescence. The long-term effects of secondhand 

smoke is a field of ongoing research. These effects may 

vary among individuals because of individual genetic 

susceptibilities and gene-environment interactions. 

The discussions that follow summarize the available 

observational evidence concerning health effects of 

secondhand tobacco smoke on children, which are 

presumed to reflect the mechanisms reviewed above. 

The discussions also interpret the evidence in the context of this mechanistic understanding. 

Respratory Effects n Chldren from Exposure to Secondhand Smoke 59 
Surgeon General’s Report 

Methods Used to Review the Evidence 

The search strategies and statistical methods for 

pooling that were used for this report were identical 

to those applied to the earlier reviews of this topic carried out by Strachan and Cook (1997). The authors conducted an electronic search of the EMBASE Excepta 

Medica and Medline databases using Medical Subject 

Headings (MeSH) to select published papers, letters, 

and review articles relating to secondhand tobacco 

smoke exposure in children. The EMBASE strategy 

was based on text word searches of titles, keywords, 

and related abstracts; non-English language articles 

were not included. The search was carried out through 

2001. 

Information relating to the odds ratio (OR) for 

the outcome of interest among children with and 

without smokers in the family was extracted from 

each study. Data regarding children exposed and 

unexposed to maternal smoking prenatally or postnatally were extracted separately. This review also 

specifically addresses the effects on children of smoking by other household members (usually the father) 

when the mother was not a smoker. Not every study 

provided information on all of these indices. The most 

common measures were smoking by either parent 

versus neither parent, and the effects of smoking by 

the mother versus only by the father or by neither parent. Few studies distinguished in any detail between 

prenatal and postnatal maternal smoking, but those 

that did were included in the discussion. The ORs for 

the effects of smoking by both parents compared with 

neither parent were also extracted from cross-sectional 

surveys of school-age children. 

Because most studies have used self-reported 

parental smoking behaviors as the principal exposure 

indicator, and because the major sources of exposure 

in western countries are overwhelmingly maternal followed by paternal smoking (Cook et al. 1994), the terms 

parental, maternal, and paternal smoking are used 

throughout this chapter to refer to major sources of 

secondhand tobacco smoke exposure for children. The 

OR was chosen as a measure of association because it 

can be derived from all types of studies—case-control, 

cross-sectional, and cohort. In general, ORs and their 

95 percent CIs were calculated from data in published 

tabulations using the actual numbers of participants, 

or numbers estimated from percentages of published 

column or row totals. This approach allowed for flexibility in combining categories of household tobacco 

smoke exposure for comparability across studies. 

If the number of participants was not provided, the 

published OR and its 95 percent CI were used. For 

some studies, it was necessary to derive an approximate standard error (for the log OR) based on the 

marginal values of the relevant multiplication table (2 

× 2). In situations where ORs were given separately 

for different genders, a pooled OR and 95 percent CI 

were calculated by taking a weighted average (on the 

log scale) using weights inversely proportional to the 

variances. The papers that quoted an incidence rate 

ratio rather than an OR are identified in the summary 

tabulations. 

The literature review also identified information on the extent to which the effects of parental 

smoking were altered by adjustment for potential 

confounding variables, and whether there was evidence of an exposure-response relationship with, 

for example, the amount smoked by either parent. 

Where the presented data could be standardized for 

age, gender, or occasionally for another confounder, 

the Mantel-Haenszel method was used to provide an 

adjusted value. Because there may be multiple published reports for a single study, only one paper from 

each study (usually the most recently published) was 

included in the quantitative meta-analyses. In some 

studies, however, information from other papers contributed to the assessment of potential confounding or 

a dose-response relationship. 

Updated meta-analyses of the health effects 

from parental smoking were conducted specifically 

for this chapter. All pooled estimates were calculated 

using both fixed and random effects models (Egger et 

al. 2001). All updated analyses were carried out using 

Stata. For some outcomes, studies were grouped 

according to the timing of the secondhand smoke 

exposure (e.g., maternal smoking during pregnancy, 

parental smoking from infancy to four years of age, 

and parental smoking at five or more years of age). 

The meta-analysis of the cross-sectional evidence 

relating parental smoking to spirometric indices in 

children updates the 1998 meta-analysis (Cook et 

al. 1998). Both the earlier and the more recent metaanalyses used the same effect measure: the average difference in the spirometric index between exposed and 

unexposed children, expressed as a percentage of the 

level in the unexposed group. The updated synthesis 

considered four different spirometric indices: forced 

vital capacity (FVC), forced expiratory volume in one 

second (FEV1), mid-expiratory flow rate (MEFR), and 

0 Chapter  
Excerpts: Chldren and Secondhand Smoke Exposure 

flow rates at end expiration. Pooled estimates of the 

percentage differences were calculated using both 

fixed and random effects models (Egger et al. 2001). 

To determine whether the exposure classification 

influenced the relationship between parental smoking 

and lung function, studies were pooled within the following exposure groups: both parents did versus did 

not smoke, mother did versus did not smoke, either 

parent versus neither parent smoked, the highest 

versus the lowest cotinine category, and high levels 

of household secondhand smoke versus none. To test 

for effects on the relationship between parental smoking and lung function from adjustment for variables 

other than age, gender, and body size, studies were 

pooled separately depending on adjustment for other 

variables. Lastly, this meta-analysis also assessed 

whether adjusting for socioeconomic measures, such 

as parental education and social class, affected the 

pooled results. 

Lower Respiratory Illnesses in Infancy and Early Childhood
 

This section summarizes the evidence relating 

specifically to acute LRIs in the first two or three years 

of life and updates the previous review by Strachan 

and Cook (1997). Separate discussions review studies 

of asthma incidence, prognosis, and severity as well as 

studies (mostly cross-sectional) of school-age children. 

In developed countries, the specific microbial 

etiology and determinants of some common lower 

respiratory tract illnesses in infancy remain a subject 

of uncertainty and research (Silverman 1993; Wilson 

1994; Monto 2002; Klig and Chen 2003). Although 

many LRIs result from viral infections, there is an 

indication of a prenatally determined susceptibility 

related to lung function abnormalities that is already 

detectable at birth (Dezateux and Stocks 1997). As 

reviewed in the introduction to this chapter, lasting 

effects of in utero exposure to tobacco smoke from 

maternal smoking may increase airway resistance 

and the likelihood of a more severe LRI with infection. 

This review covers the full spectrum of LRIs, including categories considered to reflect infection and the 

category of wheeze, which may be a consequence of 

infection but may also indicate an asthma phenotype. 

There is also an emerging consensus that there 

are several phenotypes of childhood wheeze, each 

with a different pattern of incidence, prognosis, and 

risk factors (Wilson 1994; Christie and Helms 1995). 

However, there is much less certainty about how these 

different “asthma phenotypes” should be characterized for either research or clinical purposes. Findings 

from the Tucson (Arizona) birth cohort study suggest 

physiologic and immunologic differences between the 

phenotypic syndromes of early childhood wheeze, 

the onset of asthma symptoms later in childhood, 

and persistent disease (Martinez et al. 1995; Stein et 

al. 1997). These findings have yet to be replicated in a 

comprehensive way in other large population samples, 

and few large cohort studies are in progress that provide the needed longitudinal data. The classification 

of phenotype in the epidemiologic studies is relevant 

to secondhand smoke if the association of secondhand 

smoke with risk varies across the phenotypes. 

Evidence Synthesis 

The finding of an association between parental 

smoking and LRI is consistent across diverse study 

populations and study designs, methods of case ascertainment, and diagnostic groupings. The association 

cannot be attributed to confounding or publication 

bias. Only two studies found an inverse association. 

One small study that reported an inverse association 

for maternal smoking had wide confidence limits and 

a positive association with cotinine levels in meconium 

(Nuesslein et al. 1999). A study from Brazil found an 

inverse association with pneumonia (Victora et al. 

1994). Studies in developing countries generally have 

tended not to find an increased risk associated with 

exposure of infants and children to parental smoking. 

This pattern may reflect the different nature of LRIs 

in developing countries where bacteria are key pathogens and there is a powerful effect from biomass fuel 

combustion (Smith et al. 2000; Black and Michaelsen 

2002), and where levels of secondhand smoke exposure are possibly lower because of housing characteristics and smoking patterns. 

Some variation among studies in the magnitude 

of OR estimates would be anticipated as patterns of 

smoking differed among countries and over time, and 

the methods of the studies were not consistent in all 

respects. This variation is reflected in statistically significant heterogeneity in some of the pooled analyses. 

Respratory Effects n Chldren from Exposure to Secondhand Smoke 1 
Surgeon General’s Report 

For this reason, the summary ORs derived under the 

fixed effects assumption should be interpreted with 

caution. The random effects method may be more 

appropriate in these circumstances because its wider 

confidence limits reflect the heterogeneity between 

studies. This method is, however, more susceptible 

to the effects of any publication bias because the random effects method gives greater weight to smaller 

studies. Thus, considering the largest studies only, the 

fixed effects estimate for maternal smoking was 1.56 

and the random effects estimate was 1.72. Regardless, 

the pooled estimates were statistically significant and 

it is highly unlikely that the association emerged by 

chance. 

The papers that have been cited were selected 

using keywords relevant to passive/involuntary 

smoking and children in the title or abstract. When 

cross-checked against previous reviews of involuntary smoking in children, major omissions were not 

identified (USDHHS 1986; USEPA 1992; DiFranza 

and Lew 1996; Li et al. 1999), whereas the systematic search identified relevant references not cited 

elsewhere. There is a possibility that the selection 

was biased toward studies reporting a positive association; it is more likely that statistically significant 

findings would be mentioned in the abstract in comparison with nonsignificant or null findings. Three of 

the higher ORs were derived from small case-control 

studies in which involuntary smoking was not the 

focus of the original research (Hall et al. 1984; McConnochie and Roghmann 1986; Hayes et al. 1989), and 

for these three studies publication bias may have been 

operative. The slightly higher pooled ORs obtained 

by the random effects compared with the fixed effects 

method reflect the greater weight assigned by the 

random effects approach to these small studies with 

a relatively large OR. However, inclusion of the large 

Chinese studies (Chen et al. 1988a; Jin and Rossignol 

1993; Chen 1994) in the meta-analysis of the effects of 

smoking by either parent would have had a conservative effect (i.e., a smaller pooled estimate), because 

few mothers smoked in these communities. 

The biologic basis for the association of paternal 

smoking with LRI is possibly complex, and may reflect 

mechanisms of injury that are in play before and after 

birth. These mechanisms operate to make respiratory 

infections more severe or to possibly increase the likelihood of infection. Although viral infection is a wellcharacterized etiologic factor (Graham 1990), there is 

evidence that the severity of the illness may be determined in part by lung function abnormalities detectable from birth that result from maternal smoking 

during pregnancy (Dezateux and Stocks 1997). Many 

early childhood episodes of wheeze, including bronchiolitis, probably form part of this spectrum of viral 

illnesses, although other episodes may be the first 

evidence of more persistent childhood asthma with 

associated atopic manifestations (Silverman 1993; 

Martinez et al. 1995). The evidence does not indicate 

that parental smoking increases the rate of infection with respiratory pathogens. Respiratory viruses 

are isolated with equal frequency among infants in 

smoking and nonsmoking households (Gardner et al. 

1984). 

The effect of parental smoking on the incidence 

of wheeze and nonwheeze illnesses appears similar, 

suggesting a general increase in susceptibility to 

clinical illness upon exposure to respiratory infections 

rather than to influences on mechanisms more specifically related to asthma. 

The pooled results from families with nonsmoking mothers suggest that the effects of parental smoking are at least partly attributable to postnatal (i.e., 

environmental) exposure to tobacco smoke in the 

home. The somewhat stronger effects of smoking by 

the mother compared with other household members 

may be related to the role of the mother as the principal caregiver, which would explain a higher degree 

of postnatal exposure of the child from the mother’s 

smoking. However, there is also evidence pointing to 

altered intrauterine lung development as a specific 

adverse effect of maternal smoking during pregnancy 

(Tager et al. 1993). 

The effect of parental smoking is largely independent of potential confounding variables in studies 

that have measured and incorporated such variables 

into the analyses, suggesting that residual confounding by other factors is unlikely. It thus appears that 

smoking by the parents, rather than characteristics of 

the family related to smoking, adversely affect children 

and cause LRIs. The evidence supports the conclusion 

found in other recent reviews that there is a causal 

relationship between parental smoking and acute 

LRIs (USDHHS 1986; USEPA 1992; DiFranza and Lew 

1996; WHO 1997; Li et al. 1999; California EPA 2005). 

The findings are consistent, properly temporal in 

the exposure-outcome relationship, and biologically 

plausible. The evidence is strongest for the first two 

years of life. The studies that were reviewed also suggest a clear reduction in the estimated effect after two 

to three years of age, particularly for pneumonia and 

bronchitis. The failure to find statistically significant 

associations in some studies of older children should 

not be interpreted, however, as indicative of no effect 

of secondhand smoke exposure at older ages. 

2 Chapter  
Excerpts: Chldren and Secondhand Smoke Exposure 

Conclusions 

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. 

Implications 

Respiratory infections remain a leading cause of 

childhood morbidity in the United States and other 

developed countries and are a leading cause of childhood deaths worldwide. The effect of parental smoking, particularly maternal smoking, is of a substantial 

magnitude. Reducing smoking by parents, beginning 

with maternal smoking during pregnancy, should 

reduce the occurrence of LRI. Health care practitioners 

providing care for pregnant women, infants, and children should urge smoking cessation; parents who are 

unable to quit should be encouraged not to smoke in 

the home. 

Middle Ear Disease and Adenotonsillectomy
 

A possible link between parental smoking and 

the risk of otitis media (OM) with effusion (OME) in 

children was first suggested in 1983 (Kraemer et al. 

1983). A number of subsequent epidemiologic studies have investigated the association of secondhand 

tobacco smoke exposure with diseases of the ear, 

nose, and throat (ENT), and the evidence has been 

summarized in narrative reviews (USEPA 1992; Gulya 

1994; Blakley and Blakley 1995; NCI 1999) and quantitative meta-analyses (DiFranza and Lew 1996; Uhari 

et al. 1996). Strachan and Cook (1998a) systematically 

reviewed the evidence relating parental smoking 

to acute otitis media (AOM), recurrent otitis media 

(ROM), OME (glue ear), and ENT surgery in children. 

This section updates that 1998 review following the 

methods described earlier. Full journal publications 

cited in an overview by Thornton and Lee (1999) were 

also considered, but abstracts and conference proceedings were not included. 

Evidence Synthesis 

Evidence from different study designs and 

for different chronic or recurrent disease outcomes 

related to the middle ear in young children is remarkably consistent in showing a modest elevation in 

risk associated with parental smoking. Although the 

outcome measures used are subject to misclassification, the evidence is nonetheless consistent in spite of 

this heterogeneity. 

Subsequent publications over the last four years 

have not substantially affected the findings of the 1997 

meta-analysis (Strachan and Cook 1998a), although 

quantitative summarization can now be extended to 

AOM. No single study addresses all of the potential 

methodologic concerns about selection (referral) bias, 

information (reporting) bias, or confounding. However, multiple studies that have considered these 

potential methodologic problems using objective measurements, matched designs, or multivariate analyses 

have found that the association of secondhand smoke 

exposure with middle ear disease persists with little 

alteration in the magnitude of the effect across studies, or within studies that controlled for potential confounding. There are multiple potential pathogenetic 

mechanisms related to the effects of tobacco smoke 

components on the upper airway (Samet 2004) (see 

also Chapter 2, Toxicology of Secondhand Smoke in 

the full report). A causal association between acute 

and chronic middle ear disease and secondhand 

smoke exposure is thus biologically plausible. 

Respratory Effects n Chldren from Exposure to Secondhand Smoke 3 
Surgeon General’s Report 

Conclusions 

1. 	 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. 

2. 	 The evidence is suggestive but not sufficient 

to infer a causal relationship between parental 

smoking and the natural history of middle ear 

effusion. 

3. 	 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. 

Implications 

The etiology of acute and chronic middle ear 

disease is still a focus of investigation. Nonetheless, 

the finding that parental smoking causes middle ear 

disease offers an opportunity for the prevention of 

this common problem. Health care providers making 

diagnoses of acute and chronic middle ear disease 

need to communicate with parents who smoke concerning the consequences for their children. 

Respiratory Symptoms and Prevalent Asthma in School-Age Children
 

The first reports (based on telephone surveys) 

documenting an adverse effect of parental smoking on 

the health of children were published in the late 1960s 

(Cameron 1967; Cameron et al. 1969). By the early 

1970s, studies with more formal designs addressed 

respiratory symptoms (Norman-Taylor and Dickinson 1972; Colley 1974; Colley et al. 1974). Since then, 

many epidemiologic studies have found an association 

between parental smoking and respiratory symptoms 

and diseases throughout childhood. These outcomes 

were considered in the 1984 and 1986 reports of the 

Surgeon General (USDHHS 1984, 1986). The narrative review of the 1992 EPA risk assessment (USEPA 

1992) concluded that the evidence causally relating 

secondhand smoke exposure at home to respiratory 

symptoms was very strong among preschool-age 

children, but less compelling in school-age children. 

A subsequent quantitative review did not distinguish 

between different types of secondhand smoke exposure and their effects at different ages (DiFranza and 

Lew 1996). 

This section summarizes the evidence on the 

prevalence of respiratory symptoms and asthma 

in children aged 5 through 16 years, assessed from 

surveys carried out in schools or populations. This 

review includes primarily cross-sectional studies 

and cohorts studied at a single point in time, and 

updates an earlier 1997 review by Cook and Strachan (1997). A subsequent section of this chapter 

addresses studies on the onset of asthma and exposure to secondhand smoke. These two sets of outcome measures for asthma—prevalent and incident 

disease—were separated because disease prevalence 

reflects not only factors determining incidence, but 

factors affecting persistence. The studies of asthma 

prevalence, however, receive further consideration 

when assessing the evidence related to asthma onset. 

There are additional complexities in comparisons 

across studies of varied designs that arise from the 

different approaches used to ascertain the presence 

of asthma, and from the heterogeneity of the asthma 

phenotype by age. Additionally, wheeze, cough, 

phlegm, and breathlessness are common symptoms 

for children with asthma. 

Evidence Synthesis 

This report has described multiple mechanisms 

by which secondhand smoke exposure could increase 

the prevalence of respiratory symptoms and asthma 

in childhood. Secondhand smoke exposure might 

increase the prevalence of respiratory symptoms and 

asthma through in utero effects or through inflammation and an altered lung immunophenotype from 

postnatal exposure. Multiple studies from diverse 

countries consistently show that parental smoking is 

positively associated with the prevalence of asthma 

and respiratory symptoms (including wheeze) in 

 Chapter  
Excerpts: Chldren and Secondhand Smoke Exposure 

schoolchildren; the findings of individual studies as 

well as the pooled analyses show that these associations are unlikely to be attributable to chance alone. 

The magnitude of the effects is similar for the different 

outcome measures. The estimated effects, particularly 

for wheeze, were robust to adjustments for a wide 

range of potentially confounding environmental and 

other factors. This robustness supports the conclusion 

that residual confounding is unlikely to be an issue 

and that the associations between parental smoking 

and the prevalence of asthma and respiratory symptoms in schoolchildren are causal. 

The case for a causal interpretation is further 

strengthened by the trend for the OR to increase with 

the number of parents who smoke (i.e., none, one, or 

both). In the meta-analysis, the trends with the number of smoking parents were statistically significant for 

asthma, wheeze, and cough, and trends were evident 

in most of the individual studies as well. The effect 

of maternal smoking is greater than that of paternal 

smoking, but there is nevertheless evidence for a 

small effect of paternal smoking. Maternal smoking 

is associated with higher cotinine levels in school-age 

children, implying that maternal smoking probably 

has a greater impact on the exposure of children to 

secondhand smoke (Cook et al. 1994). These results 

also imply that the increased risk for asthma and 

other symptoms reflects postnatal exposure, although 

prenatal exposure may also be a contributing factor. 

First, there is an effect of paternal smoking; second, 

risk tends to rise with the number of household smokers; third, many women who do not smoke while 

pregnant smoke after the birth of their children; and 

fourth, limited evidence shows no increase in symptoms in children of former smokers. Few studies have 

examined dose-response trends with the number of 

cigarettes smoked in the household per day or doseresponse trends among exposed children alone. 

The prevalence of symptoms ascertained by 

cross-sectional surveys is determined by both disease 

incidence and prognosis, and the pattern of morbidity tends to be dominated by a large number of 

children with mild symptoms. There are indications 

that secondhand smoke exposure is associated with 

more severe wheeze, both in studies where ORs were 

reported for different severity measures and in studies where ORs were highest when the prevalence of 

wheeze was low. 

Conclusions 

1. 	 The evidence is sufficient to infer a causal 

relationship between parental smoking and 

cough, phlegm, wheeze, and breathlessness 

among children of school age. 

2. 	 The evidence is sufficient to infer a causal 

relationship between parental smoking and ever 

having asthma among children of school age. 

Implications 

Respiratory symptoms are common among 

children, even among those without asthma. Secondhand smoke exposure increases the risk for the major 

symptoms; these symptoms should not be dismissed 

as minor because they may impact the activities of 

the affected children. Secondhand smoke exposure is 

causally associated with asthma prevalence, perhaps 

reflecting a greater clinical severity associated with 

exposure. Secondhand smoke exposure, particularly 

at home, should be addressed by clinicians caring for 

any child with a respiratory complaint and particularly children with asthma. 

Respratory Effects n Chldren from Exposure to Secondhand Smoke 5 
Surgeon General’s Report 

Childhood Asthma Onset 

As discussed earlier in this chapter (see “Lower 

Respiratory Illnesses in Infancy and Early Childhood”), parental smoking is causally associated with 

an increased incidence of acute LRIs, including illnesses with wheeze, in the first one or two years of a 

child’s life. Prevalence surveys of schoolchildren show 

that wheeze and diagnosed asthma are more common 

among children of smoking parents, with a greater 

elevation in risk for outcomes based on definitions of 

wheeze that reflect a greater severity. Evidence presented in the prior section supported conclusions that 

parental smoking was causally associated with respiratory symptoms and prevalent asthma; the crosssectional evidence did not address asthma onset. 

This section reviews cohort and case-control studies 

of wheeze illnesses that provide evidence concerning 

the effects of parental smoking on the incidence, prognosis, and severity of childhood asthma. The design 

of these studies addresses the temporal relationship 

between exposure and disease onset. This discussion 

also considers case-control studies of prevalent asthma 

that provide findings complementary to the surveys 

of schoolchildren. This section represents an update 

of the 1998 review by Strachan and Cook (1998c). 

Evidence Synthesis 

The results summarized in this discussion and 

in previous sections present a complex picture of the 

associations of parental smoking with asthma incidence, prognosis, prevalence, and severity. The rates 

of incidence and recurrence of wheeze illnesses in 

early life are greater if there is smoking in the home, 

particularly by the mother, whereas the incidence of 

asthma during the school-age years is less strongly 

affected by parental smoking. A similar age-related 

decline in the strength of the effect of secondhand 

smoke exposure is evident in cross-sectional studies. 

These findings may simply reflect the diminishing 

level of secondhand tobacco smoke exposure from 

household sources as children age (Irvine et al. 1997; 

Chang et al. 2000). Alternatively or additionally, 

parental smoking may have differential effects on the 

incidence of various forms of wheeze illnesses; there 

may be a stronger effect on the viral infection associated with wheeze that is common in early childhood, 

and a weaker effect on the atopic wheeze that occurs 

often as a later onset component of asthma (Wilson 

1989). Five studies comparing the effect of smoking on 

wheeze in atopic and nonatopic children lend support 

to the latter hypothesis (Kershaw 1987; Palmieri et al. 

1990; Chen et al. 1996; Strachan et al. 1996; Rönmark 

et al. 1999), but a sixth does not (Murray and Morrison 

1990). 

The earlier section on LRIs in infancy presented 

evidence of an increased risk from postnatal exposure 

to smoking by the father in households where the 

mother did not smoke, but there was insufficient evidence to distinguish the separate effects of prenatal 

and postnatal smoking by the mother. Several of the 

cohort studies reviewed here have reported findings 

in relation to maternal smoking during pregnancy. 

These data are limited, and the potential role of prenatal exposure as an independent cause of asthma is still 

unclear. The published data are insufficient to assess 

the independent effect of nonmaternal smoking on the 

incidence or natural history of childhood asthma after 

the first few years of life. Most cohort studies show 

a weak association of asthma incidence with paternal 

smoking. In case-control studies, maternal smoking 

has the dominant effect, with little effect from smoking by the father. 

Although wheeze in infancy is more likely to 

recur if both parents smoke, at least maternal smoking alone is associated with seemingly little long-term 

risk. This indication could also reflect a stronger 

association of parental smoking with nonatopic 

wheeze (“wheezy bronchitis” than with “allergic 

asthma”), which is associated with a better prognosis. On the other hand, atopic children tend to have 

more severe and more frequent or persistent wheeze, 

and case-control studies of (“clinic”) children with 

more severe asthma show a positive association with 

maternal smoking that again appears to be of greater 

importance. Indeed, the pooled OR for smoking by 

either parent from these case-control studies (1.39) 

is somewhat greater than the corresponding pooled 

ORs from cross-sectional surveys of wheeze (1.27) and 

asthma (1.22) among schoolchildren. Furthermore, 

most studies have found a greater severity of disease 

among children with asthma if the parents smoke, and 

prevalence surveys among schoolchildren suggest a 

stronger association with more restrictive (presumably more severe) definitions of wheeze than with any 

recent wheeze. 

These findings by age and phenotype are complex to interpret: studies of incidence and prognosis 

suggest an association of parental smoking primarily 

 Chapter  
Excerpts: Chldren and Secondhand Smoke Exposure 

with early, nonatopic wheeze that tends to run a mild 

and transient course, whereas studies of prevalence 

and severity suggest that secondhand tobacco smoke 

exposure increases the risk of more severe symptoms 

and more outpatient clinic visits or emergency hospital admissions. One explanation for this pattern would 

be to consider secondhand tobacco smoke as a cofactor operating with intercurrent infections as a trigger 

of wheeze attacks, rather than as a factor initiating or 

inducing persistent asthma. This distinction between 

induction (initiation) and exacerbation (provocation) 

also emerges when considering the role of outdoor air 

pollution as a cause of asthma (Department of Health 

Committee on the Medical Effects of Air Pollutants 

1995). There is also strong familial aggregation for 

childhood asthma that certainly has genetic determinants, although research on the genetics of asthma is 

still inconclusive. 

The incidence of both wheeze and nonwheeze 

LRIs in infancy increases to a similar extent if both 

parents smoke, and the increase reflects, at least in 

part, postnatal secondhand (environmental) tobacco 

smoke exposure. It is likely that the clinical severity 

of viral respiratory infections in older children is also 

exacerbated by secondhand smoke exposure, which 

leads to an increased risk of respiratory symptoms 

in general, including wheeze. Among children at low 

risk for wheeze, secondhand smoke exposure at the 

time of an intercurrent infection may be sufficient to 

cause occasional episodes of asthmatic symptoms and 

thus increase the risk of a mild, often transient wheeze 

tendency that the child outgrows as the airways 

become larger or less reactive with increasing age. 

In a previous section of this chapter, the conclusion 

was reached that secondhand smoke exposure from 

parental smoking causes LRIs in infants and children. 

The wheezing that accompanies many of these LRIs 

may be clinically classified as asthma, although the 

cohort study findings suggest that this phenotype is 

not generally persistent as the child ages. 

Some previous reviews have concluded that 

exposure to secondhand smoke is causally associated 

with an increase in the incidence of childhood asthma 

(USEPA 1992; Halken et al. 1995). This association has 

been attributed to chronic (but possibly reversible) 

effects of parental smoking on bronchial hyperreactivity rather than to the acute effects of cigarette smoke 

on airway caliber (USEPA 1992). The most relevant 

evidence for secondhand smoke exposure and onset of 

asthma comes from studies of older children at an age 

when there is reasonable diagnostic certainty. This evidence comes from only a small number of studies and 

their statistical power is limited, particularly within 

specific age strata. In addition, all studies are inherently limited by the difficulty of classifying the outcome, and there may be variations in the phenotypes 

that were considered across the studies. Within these 

constraints, the evidence indicating an association of 

secondhand smoke exposure from parental smoking 

with asthma incidence is inconsistent. The evidence 

for asthma prevalence, by contrast, was sufficient to 

support an inference of causality. 

Conclusions 

1. 	 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. 

2. 	 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. 

Implications 

The etiology of childhood asthma includes the 

interplay of genetic and environmental factors. The 

asthma phenotype likely comprises several distinct 

entities. The evidence is clear in showing that secondhand smoke exposure causes wheeze illnesses in early 

life and makes asthma more severe clinically. This 

evidence provides a strong basis for limiting exposure of infants and children to secondhand smoke, 

even though a causal link with asthma onset is not yet 

established for asthma incidence. 

Respratory Effects n Chldren from Exposure to Secondhand Smoke 7 
Surgeon General’s Report 

Atopy 

The hypothesis that secondhand tobacco smoke 

exposure might increase allergic sensitization was 

first proposed more than 20 years ago (Kjellman 1981). 

However, the role of secondhand smoke exposure 

(specifically from maternal smoking) in allergic sensitization remains uncertain despite many investigations since that time. Some studies have documented 

an association between maternal smoking during 

pregnancy and elevated cord blood total IgE, as well 

as an elevated risk for the development of allergic 

disease (Magnusson 1986; Bergmann et al. 1995). 

Other studies, however, have not replicated these 

findings (Halonen et al. 1991; Oryszczyn et al. 1991; 

Ownby et al. 1991). Many studies have investigated 

the relationships of secondhand smoke exposure from 

parental smoking with cord blood IgE concentrations, 

IgE levels later in childhood, skin-test reactivity, and 

allergic manifestations such as rhinitis (Strachan and 

Cook 1998c). The comprehensive, systematic review 

reported by Strachan and Cook (1998c) of the effects of 

secondhand smoke exposure from parental smoking 

covered IgE levels, skin-prick test reactivity, and allergic rhinitis and eczema. The review included 9 studies 

of IgE levels in neonates, 8 studies of IgE levels in older 

children, 12 studies of skin-prick tests, and 10 studies 

of allergic symptoms (Strachan and Cook 1998c). The 

quantitative summary did not show a significant 

association of maternal smoking with total serum 

IgE, allergic rhinitis, or eczema. The meta-analysis 

for skin-prick test positivity and smoking during 

infancy and pregnancy yielded a pooled OR estimate 

of 0.87 (95 percent CI, 0.62–1.24), suggesting no effect 

of secondhand smoke on skin-prick positivity during 

these stages of development. The summary estimate 

supported a conclusion that maternal smoking before 

birth or parental smoking during infancy is unlikely 

to increase the risk of allergic sensitization. 

This conclusion remains consistent with results 

from studies conducted since this systematic review, 

which also found no increase in risk for allergic sensitization from secondhand smoke exposure. The discussion that follows reviews some of the key studies 

published since 1997. 

Evidence Synthesis 

There are multiple mechanisms by which secondhand smoke exposure might alter the risk for 

allergic diseases in infants and children. Exposure to 

tobacco smoke components from maternal smoking 

during pregnancy might have lasting effects on lung 

and systemic immunophenotypes. Exposures after 

birth might also affect immunophenotype or increase 

susceptibility to sensitization by common allergens. 

The observational evidence across a range of 

outcome measures is inconsistent, however. The 

inconsistency may partially reflect the limited number 

of studies for any particular outcome and the methodologic complexities of studies on atopic disorders. 

Conclusion 

1. 	 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. 

Implications 

Studies on secondhand smoke exposure and 

atopy need to be prospective in design and should 

track exposures back to the pregnancy. Further studies on secondhand smoke and atopy in childhood 

are needed, but the studies need to be large enough 

and need to have sufficient and valid measurements 

of allergic phenotype. Future studies also need to 

address potential genetic determinants of susceptibility, particularly as they modify the effect of secondhand smoke. 

 Chapter  
Excerpts: Chldren and Secondhand Smoke Exposure 

Lung Growth and Pulmonary Function 

Beginning with the 1984 report (USDHHS 1984), 

the U.S. Surgeon General’s reports in this series have 

covered the adverse effects of exposure to secondhand smoke, including effects from maternal smoking 

during pregnancy and effects on lung growth from 

exposure during infancy and childhood. Both crosssectional and cohort studies on this topic have used 

lung function level as the primary indicator. The level 

of lung function achieved at any particular age and 

measured cross-sectionally is an indicator of the rate of 

growth of function up to that age; cohort studies with 

repeated measurements of lung function directly estimate the rate of growth. The 1986 Surgeon General’s 

report, The Health Consequences of Involuntary Smok­

ng, reviewed 18 cross-sectional and cohort studies 

and concluded that “available data demonstrate that 

maternal smoking reduced lung function in young 

children” (USDHHS 1986, p. 54). The report further 

suggests that although this reduction is small, with 

an average of 1 to 5 percent, “some children might 

be affected to a greater extent, and even small differences might be important for children who become 

active cigarette smokers as adults” (USDHHS 1986, p. 

54). The EPA issued its risk assessment in 1992 and 

concluded that the decline in lung function associated 

with exposure to secondhand smoke represented a 

causal effect (USEPA 1992). Similar conclusions were 

reached by the California Environmental Protection 

Agency (NCI 1999) and WHO (1999). Thus, for nearly 

two decades the weight of evidence has been sufficient 

to conclude that prenatal and postnatal tobacco smoke 

exposure is associated with a decrease in lung function in childhood. As discussed earlier in this chapter 

(see “Mechanisms of Health Effects from Secondhand 

Tobacco Smoke”), lung maturation and growth decrements secondary to exposure are reflected in changes 

in measured pulmonary function. 

A 1998 meta-analysis by Cook and colleagues 

(1998) concluded that maternal smoking was associated with reduced ventilatory function assessed by 

spirometry. In a quantitative synthesis of 21 crosssectional studies, the effects of parental smoking on 

lung function were reductions of the FVC by 0.2 percent (95 percent CI, -0.4–0.1), the FEV1 by 0.9 percent 

(95 percent CI, -1.2 to -0.7), the MEFR by 4.8 percent 

(95 percent CI, -5.4 to -4.3), and the end-expiratory 

flow rate (EEFR) by 4.3 percent (95 percent CI, -5.3 to 

-3.3). The meta-analysis also considered six prospective cohort studies and found only a small effect of 

current exposure on decreased growth in lung function. The researchers attributed most of the decreased 

growth to a lasting consequence of in utero exposure 

from maternal smoking (Cook et al. 1998). 

This discussion considers some of the studies 

included in this 1998 meta-analysis in addition to 

studies published subsequently. The studies are both 

cross-sectional and cohort in design, include data on 

maternal smoking during pregnancy and after birth, 

and indicate that maternal smoking during pregnancy 

has a substantially greater adverse effect. As discussed 

above, maternal smoking affects lung development in 

utero perhaps by a direct toxic effect, by gene regulation, or by leading to developmental abnormalities. 

The number of airways in the lung is considered fixed 

by the time a child is born, but the number of alveoli 

in the lung increases until four years of age (Dezateux 

and Stocks 1997). The period from gestation to four 

years of age thus represents a vulnerable time for lung 

growth and development, and exposures during this 

time are potentially the most critical for structural and 

functional lung development and performance. This 

section reviews the evidence that associates different 

phases of lung growth and development with corresponding ages. 

Evidence Synthesis 

Smoking during pregnancy exposes the developing lung to a variety of toxins and reduces the delivery 

of oxygen to the fetus (USDHHS 2001). Animal models indicate structural consequences that may underlie the physiologic effects that are well documented 

shortly after birth. Secondhand smoke exposure from 

parents who smoke would be expected to lead to pulmonary inflammation that would be sustained across 

childhood. 

Thus, there is substantial biologic plausibility 

for causation of reduced lung growth by secondhand 

smoke exposure. Multiple studies have measured lung 

function shortly after birth and document the adverse 

effects on lung function from maternal smoking during pregnancy. The pattern of abnormalities is suggestive of a persistent adverse effect on the airways of the 

fetus from maternal smoking during pregnancy. 

There is also substantial evidence from both 

cross-sectional and cohort studies of a sustained effect 

from in utero exposure, as well as an additional adverse 

effect from postnatal exposure. Multiple studies have 

Respratory Effects n Chldren from Exposure to Secondhand Smoke 9 
Surgeon General’s Report 

shown cumulative consequences of both prenatal and 

postnatal exposures. Across the set of studies, potentially important confounding factors have been given 

consideration and the adverse effects of secondhand 

smoke exposure on lung function cannot be attributed 

to other factors. 

In the context of this body of evidence against 

causal criteria, the effects of prenatal and postnatal exposures merit separate consideration because 

they correspond to substantially different phases of 

development and potential susceptibility. For both 

exposures, the evidence is substantial and consistent. 

There are multiple bases for biologic plausibility, and 

the temporal relationships of exposures with the outcome measures are appropriate. 

Conclusions 

1. 	 The evidence is sufficient to infer a causal 

relationship between maternal smoking during 

pregnancy and persistent adverse effects on lung 

function across childhood. 

Conclusions 

2. 	 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. 

Implications 

Lung growth continues throughout childhood 

and adolescence and is completed by young adulthood, 

when lung growth peaks and then begins to decline as 

a result of aging, smoking, and other environmental 

factors. The evidence shows that parental smoking 

reduces the maximum achieved level, although not to 

a degree (on average) that would impair individuals. 

Nonetheless, a reduced peak level increases the risk 

for future chronic lung disease, and there is heterogeneity of the effect so that some exposed children may 

have a much greater reduction than the mean. In addition, children of smokers are more likely to become 

smokers and thus face a future risk for impairment 

from active smoking. 

The following conclusions are supported by 

text in the full report that may not be included 

in this excerpt. The full report can be accessed at 

http://www.surgeongeneral.gov/library/secondhandsmoke/report/. 

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. 

70 Chapter  
Excerpts: Chldren and Secondhand Smoke Exposure 

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. 

Overall Implications 

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 extensive evidence considered in this chapter causally links parental smoking to adverse health 

effects in children. The association between parental 

smoking and childhood respiratory disease is stronger at younger ages, a pattern plausibly explained 

by a higher level of exposure to secondhand smoke 

among infants and preschool-age children for any 

given level of parental smoking. In general, associations with maternal smoking are stronger than with 

paternal smoking, but for several outcomes, associations were found for smoking by the father in homes 

where the mother does not smoke. This finding argues 

strongly for an independent adverse effect of a postnatal involuntary (environmental) exposure to secondhand smoke in the home. There may be an additional 

hazard related to prenatal exposure of the fetus to 

maternal smoking during pregnancy (USDHHS 2001, 

2004). The published evidence does not adequately 

separate the independent effects on childhood respiratory health of prenatal versus postnatal exposure 

to maternal smoking. This unresolved research issue 

should not detract from the public health message 

that smoking by either parent is potentially damaging 

to the health of children. 

Interpretation of the evidence is perhaps most 

complex in relation to childhood asthma, which is a 

term generally applied to a mixed group of clinical 

phenotypes. Recurrent wheeze illnesses are common 

among young children, and there is controversy 

about whether these illnesses should all be classified 

as “asthma.” Cohort studies show that symptoms do 

not persist for many children beyond the first few 

years of life. The balance of evidence strongly supports a causal relationship between parental smoking 

and the incidence of wheeze illnesses in infancy, the 

prevalence of wheeze and related symptoms among 

schoolchildren, and the relative severity of disease 

among children with physician-diagnosed asthma. 

These are all important indicators of a substantial and 

potentially preventable public health burden. 

The evidence related to the wheeze illnesses 

can be separated to an extent from that related to a 

clearer clinical phenotype of asthma, a chronic condition of variable airflow obstruction with a heightened 

susceptibility to environmental triggers of bronchospasm. The evidence is less clear as to whether parental smoking initiates the disease among previously 

Respratory Effects n Chldren from Exposure to Secondhand Smoke 71 
Surgeon General’s Report 

healthy children. Because the clinical diagnosis of 

asthma relies to a large extent upon a history of recurrent wheeze attacks or other chest illnesses, any exposure (including parental smoking) that increases the 

incidence of such episodes will tend to be associated 

with an apparent increase in the incidence of diagnosed “asthma,” even if secondhand smoke exposure 

does not contribute to the incidence directly. Studies 

of nonspecific bronchial responsiveness, a surrogate 

for the asthma phenotype, offer some insights into the 

long-term susceptibility that underlies chronic asthma. 

Secondhand smoke exposure is linked to an increase 

in responsiveness, beginning with in utero exposure. 

However, bronchial responsiveness is also nonspecifically and transiently increased following respiratory 

tract infections. For this reason, the conclusion regarding parental smoking as a cause of childhood asthma 

has been phrased in less definite terms than the conclusions relating to asthma prevalence and severity. 

72 Chapter  
Excerpts: Chldren and Secondhand Smoke Exposure 

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Respratory Effects n Chldren from Exposure to Secondhand Smoke 77 

Excerpts from Chapter 10 

Control of Secondhand Smoke Exposure 

Introduction 1 

Attitudes and Beliefs About Secondhand Smoke 1 

Trends in Beliefs About Health Risks of Secondhand Smoke 1 

Policy Approaches 1 

Household Smoking Rules 2 

Prevalence and Correlates 2 

Effect of Household Smoking Rules on Secondhand Smoke Exposure  

Effect on Smoking Behavior  

Smoking Restrictions in Other Settings 7 

Day Care 7 

Schools  

Conclusions  

Overall Implications 9 

References 91 

 79 

Excerpts: Chldren and Secondhand Smoke Exposure 

Introduction 

This chapter examines measures to control exposure to secondhand smoke in public places, workplaces, and homes, including legislation, education, 

and approaches based on building designs and operations. The discussion reviews progress toward smokefree indoor spaces in the United States during the past 

three decades, including approaches that have been 

employed to reduce exposure, in the context of exten

sive scientific evidence on health effects and control 

measures. Table 10.1 provides a chronology of some 

landmark or exemplary efforts at all levels of government to limit exposure to secondhand smoke. 

Attitudes and Beliefs About Secondhand Smoke 

A number of nationally representative studies that assessed public attitudes toward smoking in 

public places have been published since the 1960s. 

The 1989 report of the Surgeon General considered 

studies from the previous three decades (USDHHS 

1989). The most recent studies are the NCI’s Tobacco 

Use Supplement to the Current Population Survey 

(CPS) (USDOC 1985, 2004) and the National Health 

Interview Survey (NHIS) (National Center for Health 

Statistics [NCHS] 2004). CPS is a monthly survey 

of about 50,000 households. Questions on smoking 

were included in September 1992, January 1993, and 

May 1993 (Gerlach et al. 1997), and the questions 

were repeated during the same months in 1995–1996, 

1998–1999, and 2001–2002 (Shopland et al. 2001; CDC, 

NCHS, NHIS, public use data tapes, 2001–2002). In the 

text that follows, the dates of surveys are referred to 

as 1993, 1996, 1999, and 2002, respectively. The NHIS 

is a multipurpose health survey conducted by CDC. 

Because the CPS and NHIS represent the most recent 

data available using nationally representative samples, this Surgeon General’s report includes extensive 

analyses of these data. 

Policy Approaches 

Trends in Beliefs About Health Risks of 

Secondhand Smoke 

Surveys conducted in recent years consistently 

show that substantial majorities of the U.S. public 

believe that secondhand smoke exposure is a health 

hazard for nonsmokers. In both 1992 and 2000, NHIS 

asked respondents if they agreed with the statement 

that secondhand smoke is harmful. In both years, 

more than 80 percent of respondents agreed. Individuals with more years of education were more likely to 

believe that secondhand smoke is harmful. According 

to data from the 2001 annual Social Climate Survey of 

Tobacco Control, 95 percent of the adults agreed that 

parental secondhand smoke was harmful to children, 

and 96 percent considered tobacco company claims 

that secondhand smoke is not harmful to be untruthful (McMillen et al. 2003). 

During the past 30 years, policies to restrict 

smoking in public places and in workplaces have been 

implemented with increasing success. Over time, the 

number, strength, and coverage of these policies have 

steadily increased. Although not subject to regulation, 

exposure in the home (the main source of exposure 

for most children at present) has also been the focus 

of intervention research designed, to the extent possible, to help smoking parents protect their children 

from secondhand smoke exposure and to help smokers protect nonsmoking spouses and other adult nonsmokers who live with them. 

Control of Secondhand Smoke Exposure 1 
Surgeon General’s Report 

Household Smoking Rules 

Home smoking restrictions are private household rules that are adopted voluntarily by household 

members. They can include comprehensive rules that 

make homes smokefree in all areas at all times and 

less comprehensive rules that restrict smoking to certain places or times (e.g., allowing smoking only in 

specific rooms, designating certain rooms as smokefree, allowing smoking only when no children are 

present, etc.) (Pyle et al. 2005). The only approach that 

effectively protects nonsmokers from secondhand 

smoke exposure is a rule making the home completely 

smoke-free (Levy et al. 2004). 

Smoke-free home rules and other home smoking restrictions may be implemented for a variety of 

reasons, including 

•	 to protect children in the household from 

secondhand smoke exposure; 

•	 to protect pregnant women in the household 

from secondhand smoke exposure; 

•	 to protect nonsmoking spouses or other 

nonsmoking adult household members from 

secondhand smoke exposure; 

•	 to protect children or adults who have health 

conditions that are exacerbated by secondhand 

smoke exposure or who are at risk for health 

conditions that can be triggered by secondhand 

smoke (e.g., a child with asthma, an adult with 

or at special risk for heart disease); 

•	 to help smokers in the household cut down their 

cigarette consumption; 

• to help smokers quit; 

•	 to help smokers who have quit maintain 

abstinence; 

•	 to set a positive example for children and youth 

in the household, to prevent them from becoming 

smokers themselves; 

• aesthetic, hygienic, economic, and safety considerations, including eliminating the odor of 

secondhand smoke, eliminating cigarette burns, 

and eliminating the risk of fires caused by 

discarded cigarettes; and 

• simply because no one in the household smokes 

anymore (Ferrence et al. 2005). 

Prevalence and Correlates 

Reducing secondhand smoke exposure in the 

home is important because the home is a major source 

of exposure for children and for those nonsmoking adults who are not exposed elsewhere. Reducing exposure in this setting is challenging, however, 

because there are no clearly established interventions 

that effectively reduce exposure at home. In addition, because smoke-free home rules are adopted 

voluntarily, rather than imposed by government bodies or employers, the prevalence of these rules is an 

important indicator of changes in norms regarding 

the social acceptability of smoking. In the text that 

follows, the definition of “children” varies across the 

studies cited. 

In the past decade, substantial increases have 

occurred in the number of U.S. households with private rules to limit secondhand smoke exposure within 

the home. Even smokers are increasingly adopting 

such rules. One of the best data sources available on 

children’s secondhand smoke exposure in the home 

is the NHIS. This information can be derived from 

NHIS data by correlating data on smoking in the 

home with data on households with children. NHIS 

data show that the proportion of children aged 6 

years and younger who are regularly exposed to secondhand smoke in their homes fell from 27 percent in 

1994 to 20 percent in 1998. A recent study by Soliman 

and colleagues (2004) examined data from the NHIS 

and found that the prevalence of secondhand smoke 

exposure in homes with children fell from 35.6 percent in 1992 to 25.1 percent in 2000. The prevalence 

of adult smoking fell by a smaller amount during this 

same period, from 26.5 to 23.3 percent, indicating that 

a portion of the reduced exposure can be explained 

by the increase in home smoking rules. Home exposures declined across all racial, ethnic, educational, 

and income groups that were analyzed. Farkas and 

colleagues (2000) analyzed data from adolescents 

aged 15 through 17 years from the 1993 and 1996 CPS. 

Of those respondents, 48 percent lived in smoke-free 

households in 1993 and 55 percent lived in smoke-free 

homes by 1996. 

2 Chapter 10
Excerpts: Chldren and Secondhand Smoke Exposure 

The CPS data show that the percentage of smokefree homes increased by 40 percent between 1993 and 

2002, from 43 to 66 percent. Households with a smoker 

in the home had lower rates of smoke-free home rules 

than did households without a smoker; however, the 

prevalence of smoke-free rules in homes with smokers increased by 110 percent between 1993 and 1999. 

In a 1997 survey in Oregon, Pizacani and colleagues 

(2003) found similar differences in the prevalence of 

smoke-free home rules between nonsmoking households (85 percent) and households with one or more 

smokers (38 percent). These trends of smoke-free 

home rules were observed in all four regions of the 

country in the CPS data. Individuals living in the West 

reported higher rates of smoke-free homes, but the 

largest increases between 1993 and 2002 were in the 

South and the Midwest. Similarly, there were wide 

variations among states in the percentage of individuals reporting household smoking bans. Utah reported 

the highest rate (83 percent), followed by California 

(78 percent), Arizona (76 percent), and Idaho (74 percent). 

The presence of a child younger than 13 years 

of age was associated with only a slight increase in 

the rate of smoke-free homes compared with homes 

where there were no children under 13 years of age. 

However, a survey of 598 adult smokers living in an 

inner-city neighborhood in Kansas City (Missouri) 

found that after adjusting for age, race, gender, and 

education, a rule banning smoking or restricting it to 

designated locations in the home was significantly 

more likely in households with a child (OR = 2.63 [95 

percent CI, 1.70–4.08]) or a nonsmoking adult partner (OR = 2.07 [95 percent CI, 1.19–3.61]) (Okah et al. 

2002). 

Households with lower incomes reported lower 

rates of smoke-free home rules compared with higher 

income households. The amount smoked was higher 

in lower income homes, whether or not a smoker 

resided in the home (Okah et al. 2002). 

EPA conducted a national telephone survey in 

2003 on children’s secondhand smoke exposure and 

childhood asthma among a random digit-dialed sample of U.S. households, involving 14,685 interviews 

(USEPA 2005). The survey yielded the following 

results: 

• Approximately 11 percent of children aged six 

years and under were reported to be exposed to 

secondhand smoke on a regular basis (four or 

more days per week) in their home. 

• Secondhand 	 smoke exposure is significantly 

higher in households at and below the poverty 

level. 

• Parents account for the vast majority of exposure 

in homes (almost 90 percent of the exposure), 

followed by grandparents and other relatives 

living in the home. 

• The presence of a child with asthma in the home 

was not associated with reduced exposure, 

even in homes with younger children. Children 

with asthma were just as likely to be exposed to 

secondhand smoke as children in general. 

• The contribution of visitors to the regular exposure of children to secondhand smoke was negligible. In households with children aged 6 years 

or younger, only 0.3 percent of children were 

exposed to secondhand smoke by visitors alone. 

Similarly, only 0.5 percent of children under 

18 were exposed solely by visitors. 

The prevalence of smoke-free household rules 

has been studied in California, which has undertaken 

a campaign to promote smoke-free homes as part of 

its comprehensive statewide tobacco control program 

(Gilpin et al. 2001). The 1999 California Tobacco Survey found that 73.2 percent of California homes had a 

smoke-free rule in place. This finding represented an 

increase of 30 percent from 1993. In addition, nearly 

half (47.2 percent) of the smokers lived in a smokefree home—an increase of 135 percent from 1993. An 

additional 21.8 percent of smokers lived in homes 

with some smoking restrictions. Consistent with these 

increases, the percentage of children and adolescents 

protected from secondhand smoke exposure at home 

increased by 15 percent during that same time period 

to 88.6 percent (Gilpin et al. 2001). 

Gilpin and colleagues (1999) used data from the 

1996 California Tobacco Survey (n = 8,904) to evalu¬ate 

factors associated with the adoption of smoke-free 

home rules. The data showed that male smokers were 

more likely than female smokers to report smokefree homes, and household smoking bans were less 

likely with the increased age of current smokers in the 

household. Hispanic and Asian smokers were more 

likely to report smoke-free homes (58 percent and 43 

percent, respectively) than were non-Hispanic Whites 

(32 percent); African Americans were the least likely 

to report smoke-free homes (23 percent). Living in a 

household with a child or with nonsmoking adults 

Control of Secondhand Smoke Exposure 3 
Surgeon General’s Report 

predicted a smoke-free household. After adjusting for 

demographics, the investigators noted that smokers 

were nearly six times more likely to report living in 

a smoke-free home if they lived with a nonsmoking 

adult and child compared with smokers who lived in 

homes without children or adult nonsmokers (59 percent versus 15 percent, respectively). 

Effect of Household Smoking Rules on 

Secondhand Smoke Exposure 

During the past two decades, several data sources 

have consistently shown that a large proportion of 

children in the United States were regularly exposed 

to secondhand smoke. For example, 1988 NHIS data 

revealed that 42.4 percent of children aged five years 

and younger lived with at least one smoker (Overpeck and Moss 1991). Data from the 1991 NHIS indicated that 31.2 percent of children aged 10 years and 

younger were exposed daily to secondhand smoke in 

their homes (Mannino et al. 1996). An important finding was that children from lower income families were 

significantly more likely to be exposed to secondhand 

smoke than were children from higher income families. For example, 41 percent of children from lower 

income families were exposed daily compared with 

only 21 percent of children from higher income families. CDC’s 2005 Third National Report on Human 

Exposure to Environmental Chemicals, drawing on 

data from NHANES, reported that median cotinine 

levels measured during 1999–2002 have fallen by 68 

percent among children, by 69 percent among adolescents, and by 75 percent among adults when compared with median levels from 1988–1991. However, 

the data also show that children’s cotinine levels are 

twice as high as those of adults (CDC 2005b). 

In an intervention study of low-income house

holds with at least one child under three years of age, 

the median household nicotine concentration was 3.3 

μg/m3 (Emmons et al. 2001). A recent study that mea

sured cotinine levels in infants and nicotine levels in 

household dust, in the air, and on household surfaces 

found that smoke-free home rules may substantially 

reduce, but may not completely eliminate, household 

contamination from secondhand smoke, including 

secondhand smoke exposure of infants (Matt et al. 

2004). The study found that infants living with smok

ers in homes with smoke-free rules had lower cotinine 

levels compared with infants from homes with smok

ers without such rules, but cotinine levels were higher 

compared with infants from homes without smokers. 

The same was true of nicotine levels in household 

dust, in air, and on household surfaces. One possible 

explanation for this finding is that even with smokefree home rules, secondhand smoke may enter the 

house in the air, on dust, or on the smoker’s breath or 

clothing. And there is always the possibility that some 

smokers may not be consistently complying with the 

rules or may be overstating the rules. Exposure does 

not appear to be lower in homes with children who 

are at particular risk from secondhand smoke, such 

as children with asthma. Kane and colleagues (1999) 

conducted home visits of 828 households in a lower 

income section of Buffalo (New York) to identify 167 

persons of all ages with asthma and 161 persons without asthma. Self-reported household secondhand 

smoke exposure levels were similar in both groups— 

half of the households reported exposure. 

Interventions to Reduce Home-Based Secondhand 

Smoke Exposure of Children 

Because secondhand smoke exposure poses serious health risks to children and because the home is 

the major source of exposure for children, a number 

of public health practitioners, tobacco control programs, and other organizations at the local, state, and 

national levels have carried out activities intended 

to reduce children’s secondhand smoke exposure in 

the home. As the lead federal government agency in 

this area, EPA has played an especially significant 

role at the national level. EPA has collaborated with 

the health care community, state and local tobacco 

control programs, and other organizations to marshal efforts to institutionalize smoke-free home rules 

(USDHHS 2003). The American Legacy Foundation 

also launched a media initiative in 2005 to promote 

smoke-free homes and vehicles (American Legacy 

Foundation 2005). 

However, few interventions to reduce children’s 

secondhand smoke exposure have been systematically evaluated. The Gude to Communty Preventve 

Servces found insufficient evidence for the effectiveness of community educational initiatives designed 

to reduce secondhand smoke exposure in the home 

(Task Force on Community Preventive Services 2005). 

In a systematic review, the Guide was able to identify 

only three relevant studies and only one study that 

met its criteria. 

Table 10.16 summarizes a number of relevant 

studies (see page 622 in the full report). The early 

studies did not show a significant effect on objective 

exposure measures, although some showed reductions of self-reported exposure. 

Two trials in the United States found substantial reductions in secondhand smoke exposure among 

 Chapter 10 
Excerpts: Chldren and Secondhand Smoke Exposure 

healthy children as a result of an intervention (Hovell et al. 2000a; Emmons et al. 2001). In a randomized 

controlled trial of 291 smoking parents of young children, Emmons and colleagues (2001) used a motivational intervention to reduce household secondhand 

smoke exposure. Participants were low-income families, recruited through primary care settings, with 

children younger than three years of age. Participants 

were randomly assigned to either the motivational 

intervention group or a self-help comparison group; 

follow-up assessments were conducted at three months 

and six months. The motivational intervention consisted of one 30- to 45-minute motivational interview 

session at the participant’s home with a trained health 

educator and four follow-up telephone counseling 

calls. The intervention included feedback to participants regarding baseline levels of airborne nicotine 

and CO in their homes. Families in the self-help group 

were mailed a copy of a smoking cessation manual, a 

secondhand smoke reduction tip sheet, and a resource 

guide. Household nicotine levels were measured by 

a passive diffusion monitor. The six-month nicotine 

levels were significantly lower in motivational intervention households than in the self-help households. 

Repeated measures of analysis of variance across 

baseline, three-month, and six-month time points 

showed a significant time-by-treatment interaction— 

indicating that patterns over time differ by treatment 

group—whereby nicotine levels for the motivational 

intervention group decreased significantly, and nicotine levels for the self-help group increased but were 

not significantly different from baseline. 

Hovell and colleagues (2000a) evaluated a 

seven-session, three-month counseling intervention 

with a randomized trial design involving 108 mothers who had a child under four years of age. Reported 

exposure of children declined from 27.3 cigarettes 

per week at baseline to 4.5 cigarettes per week at 3 

months and to 3.7 cigarettes per week at 12 months in 

the counseled group. The investigators also observed 

reductions in exposure among the controls, but the 

reductions among the intervention participants were 

significantly greater. At the 12-month follow-up 

comparison between the intervention group and the 

controls, the level of self-reported exposure in the 

intervention group was 41.2 percent of the exposure 

of the controls from maternal smoking and 46 percent 

of the exposure of the controls from all sources combined (Hovell et al. 2000a). Urinary cotinine concentrations among children decreased by 4 percent in the 

intervention group but increased by 85 percent in the 

control group. 

Other studies have evaluated family interventions designed to reduce secondhand smoke exposure 

among children with asthma. Hovell and colleagues 

(2002) demonstrated a significant impact on selfreported exposure among a general population of 

families with children who have asthma and an impact 

on self-reported exposure and cotinine levels among 

Hispanic families. 

Gehrman and Hovell (2003) reviewed 19 studies 

of interventions to reduce secondhand smoke exposure among children in the home setting that were published between 1987 and 2002. The interventions fell 

into two categories: (1) physician-based interventions, 

which consisted of information and recommendations delivered orally by a physician or nurse during a 

regularly scheduled appointment (e.g., a well-baby or 

immunization visit) in a pediatrician’s office or other 

health care facility, and (2) home-based interventions, 

which consisted of counseling delivered by a nurse or 

a trained research assistant during a home visit. The 

main outcome of interest was children’s secondhand 

smoke exposure, with parental smoking cessation 

as a secondary outcome of interest in some studies. 

Children’s exposure was primarily measured through 

parental self-report, with some studies also measuring 

children’s urinary cotinine levels. Of the 19 studies, 11 

reported significant reductions in secondhand smoke 

exposure. However, only one of the eight studies that 

monitored children’s cotinine levels reported significant differences in cotinine levels between treatment 

and control groups. Effect sizes (measured as Cohen’s 

d) ranged from -0.14 to 1.04, with a mean effect size 

of 0.34. The review suggests that interventions in this 

area can achieve at least small to moderate effects. 

Gehrman and Hovell (2003) concluded that 

home-based interventions, which tended to be more 

intensive in terms of frequency and duration of contact, generally appeared to be more effective than 

physician-based interventions, which tended to be less 

intensive. Seven of the eight exclusively home-based 

interventions assessed yielded significant effects, 

compared with 4 of the 10 physician-based interventions. The review also found that interventions that 

were explicitly based on behavior change theory (e.g., 

behavior modification theory, social learning/cognitive theory) appeared to be more likely to be effective, 

with eight of the nine interventions that fell into this 

category registering significant secondhand smoke 

reductions. 

Gehrman and Hovell (2003) suggest that optimal 

interventions should combine physician- and homebased approaches, combine immediate steps to reduce 

Control of Secondhand Smoke Exposure 5 
Surgeon General’s Report 

children’s secondhand smoke exposure with cessation support for parents who want to quit, be based on 

behavior change theory (especially in terms of providing participants with concrete skills and strategies to 

help them achieve the desired outcomes), foster participants’ self-efficacy and provide them with ongoing reinforcement for positive behavior changes, and 

be sustained over time. The study also suggests that 

future studies should explore approaches to increasing the effectiveness of physician-based interventions, 

for example, equipping mothers with skills to deal 

with spouses or other household members who are 

contributing to children’s secondhand smoke exposure. In addition, studies should examine efficacy of 

other interventions, including group interventions 

(as opposed to one-on-one interventions), the use of 

motivational interviewing, exploring the link between 

reducing children’s secondhand smoke exposure 

and increasing parental cessation, and interventions 

directed at children (as opposed to interventions 

directed at parents). The authors also emphasize the 

importance of evaluating interventions; they note, 

for example, that while “home-based interventions 

may be particularly promising, . . .future research 

should be done in a systematic, replicable manner 

so that investigators can make more direct comparisons” (Gehrman and Hovell 2003, p. 297). Finally, in 

addition to refining interventions directed at individual behavior change, efforts should be continued to 

increase public awareness and smoking restrictions. 

Hovell and colleagues (2000b) examined the 

effectiveness of available approaches to reducing secondhand smoke exposure among children. The study 

identified three trials reporting that repeated counseling reduced quantitative measures of secondhand 

smoke exposure in asthmatic children and one controlled trial reporting that repeated physician counseling directed toward reducing secondhand smoke 

exposure increased parental cessation. Controlled 

trials of clinicians’ one-time counseling yielded null 

results. The study concluded that one-time clinical 

interventions appeared marginally effective or ineffective. Repeated minimal interventions, while not 

consistently yielding changes in secondhand smoke 

exposure, appeared to hold more promise. However, 

the study calls for further evaluations of this approach, 

specifically large-scale controlled trials. 

Hovell and colleagues (2000b) also note that even 

the interventions that appeared to reduce secondhand 

smoke exposure rarely eliminated it completely and 

suggest that these interventions may need to be sustained over long periods of time. The study points to a 

need for further research on approaches that combine 

counseling to reduce children’s secondhand smoke 

exposure with subsequent counseling to help parents 

quit smoking. Such counseling might include interventions to address situations where the mother, who 

typically is the patient receiving the counseling, is not 

the only smoker in the household or is not a smoker 

at all. Other interventions might be directed at children instead of parents. Still others might address the 

social disparities implicit in the increased prevalence 

of smoking and secondhand smoke exposure among 

low-SES populations and some racial/ethnic groups. 

Hovell and colleagues (2000b) also examined a 

number of other strategies for reducing children’s secondhand smoke exposure, including regulatory, policy, legal, and media approaches. The study concludes 

by noting the importance of pursuing interventions 

in this area within the context of a comprehensive 

approach to tobacco control. 

In addition to the role of the health care sector in 

establishing smoke-free policies and changing norms 

related to smoking in health care settings, the role 

that pediatricians can play in reducing exposure of 

children to secondhand smoke has drawn increasing 

attention. The American Academy of Pediatrics has 

recommended that secondhand smoke exposure of 

children should be discussed as part of pediatric care, 

and providers should follow the Agency for Healthcare Research and Quality (formerly the Agency for 

Health Care Policy and Research) guidelines for working with parents to quit or reduce their smoking (Etzel 

and Balk 1999). The American Academy of Pediatrics 

has identified secondhand smoke exposure as a priority area and is collaborating with EPA and others to 

reduce childhood exposures. 

Effect on Smoking Behavior 

National data have confirmed findings from 

California that relate household smoking rules and 

workplace smoking policies to smoking status. Farkas and colleagues (1999) analyzed 1993 CPS data and 

found that, compared with smokers living under no 

household smoking restrictions, smokers living under 

a total household smoking ban were almost four times 

more likely to report an attempt to quit smoking during the previous 12 months compared with smokers 

with no household smoking restrictions (OR = 3.86 [95 

percent CI, 3.57–4.18]). Smokers who lived in a home 

with a partial smoking ban were almost twice as likely 

to report an attempt to quit during the previous 12 

months (OR = 1.83 [95 percent CI, 1.72–1.92]). The 

investigators also noted a weaker relationship between 

workplace smoking bans compared with workplaces 

 Chapter 10 
Excerpts: Chldren and Secondhand Smoke Exposure 

with no restrictions or restrictions less than a ban on 

smoking in work areas, and reporting an attempt to 

quit (OR = 1.14 [95 percent CI, 1.05–1.24]). Among 

smokers who attempted to quit in the previous year, 

smokers who lived under a household smoking ban 

had an OR of 1.65 (95 percent CI, 1.43–1.91) of abstaining for at least six months compared with smokers 

with no household smoking restrictions, while smokers who lived under a partial household smoking ban 

had an OR of 1.20 (95 percent CI, 1.05–1.38). Smokers 

with a workplace smoking ban who tried to quit had 

an OR of 1.21 (95 percent CI, 1.00–1.45) for abstaining 

for at least six months compared with smokers working under no workplace restrictions or some form 

of restriction less than a work area ban (Farkas et al. 

1999). 

In a recent prospective study of a populationbased cohort of smokers identified from a previous 

telephone survey, Pizacani and colleagues (2004) 

found that smokers living under a full household 

smoking ban at baseline were twice as likely as 

smokers living with no ban or with a partial ban to 

attempt to quit and to abstain for at least one day over 

follow-up of about two years. The study also found 

that among smokers who were preparing to quit 

at baseline, a full ban was associated with a lower 

relapse rate and with more than four times the odds of 

abstaining for seven or more days at follow-up. These 

associations were not found among smokers in the 

precontemplation/contemplation stage of quitting. 

The authors concluded that full household smoking 

bans may facilitate cessation among smokers who are 

preparing to quit by increasing cessation attempts and 

may prolong the time to relapse among these smokers 

(Pizacani et al. 2004). 

Important relationships have also been found 

between household and workplace smoking restrictions and smoking trends among adolescents. After 

adjusting for demographics, school enrollment, and 

having other smokers in the home, adolescents from 

smoke-free households were 26 percent less likely to 

be smokers than adolescents who lived in homes without smoking restrictions. Adolescents who worked 

indoors in smoke-free workplaces were 32 percent 

less likely to be smokers than adolescents whose indoor 

workplaces had a partial work area ban. Smoke-free 

home rules also increased the chances of quitting among 

adolescent smokers; respondents were 1.80 times more 

likely to be former smokers if they lived in smoke-free 

homes (Farkas et al. 2000). The findings of the surveys 

need to be interpreted with consideration of the difficulty in inferring causal directions from cross-sectional 

data. The cohort study of Pizacani and colleagues (2004) 

would not be subject to this potential limitation. 

Smoking Restrictions in Other Settings 

Day Care 

Day care settings present a potentially important source of secondhand smoke exposure for young 

children. In 1995, 75 percent of children (14.4 million) 

younger than five years of age were in some form 

of regular child care arrangement (Smith 1995). A 

national survey conducted in 1990 of 2,003 directors 

of licensed day care centers found that 99 percent of 

these facilities were in compliance with their state laws 

on smoking: 55 percent of the centers were smokefree indoors and outdoors, 26 percent were smokefree indoors only, and 18 percent allowed restricted 

indoor smoking. The best predictors of more stringent 

employee smoking policies were locations in the West 

or South, smaller size, and independent ownership 

(Nelson et al. 1993). This survey also found that of 

the 40 states that regulated employee smoking in day 

care facilities, only 3 states banned indoor smoking 

(Nelson et al. 1993). In a 2004 analysis by the American Lung Association (ALA) of state laws restricting 

smoking, researchers identified 44 states that regulated smoking in day care centers, of which 31 prohibited smoking, 5 allowed smoking only in enclosed and 

separately ventilated areas, and 8 had some other type 

of restriction (ALA 2004). These results only apply to 

licensed facilities and not necessarily to family day 

care or more informal arrangements, which may be 

less restrictive. A large proportion of children are in 

nonfederally funded settings; 50 percent of children 

in day care are cared for by a relative in an informal 

setting. The smoking rules in these settings have not 

been studied. 

In 1994, the U.S. Congress passed the ProChldren Act of 199, which prohibits smoking in Head 

Start facilities and in kindergarten, elementary, and 

secondary schools that receive federal funding from 

the U.S. Department of Education, the U.S. Department of Agriculture, or the U.S. DHHS, with the 

exception of funding from Medicare or Medicaid. This 

legislation also applies to facilities that receive federal 

funding to provide children with routine health care, 

day care, or early childhood development services. 

This measure was reauthorized under the No Chld 

Left Behnd Act of 2001. No nationally representative 

survey of day care facilities has been conducted since 

the enactment of the Pro­Chldren Act of 199. 

Control of Secondhand Smoke Exposure 7 
Surgeon General’s Report 

Schools 

During the past decade, schools have increasingly adopted smoke-free policies to minimize prosmoking social norms, to reduce smoking initiation 

rates, and to protect children from secondhand smoke 

exposure in the school setting. 

At the federal level, the Pro­Chldren Act of 199 

prohibits smoking in facilities where federally funded 

educational, health, library, day care, or child development services are provided to children aged younger 

than 18 years (Federal Register 1994). The Pro­Chldren 

Act of 199 was reauthorized under the No Chld Left 

Behnd Act of 2001. 

Expanding upon the Pro­Chldren Act of 199, 

the CDC Guidelines for School Health Programs to 

Prevent Tobacco Use and Addiction recommend a 

tobacco-free school policy that prohibits students, 

staff, and visitors from using tobacco products in 

school buildings, on school grounds, in school vehicles, and at school-sponsored events (including events 

held on and off school property) (CDC 1994). According to the guidelines, this policy should be in effect at 

all times, even when schools are out of session. The 

tobacco-free environment established by this policy 

protects children from secondhand smoke in school 

buildings and other areas that they frequent as part of 

Conclusions 

their daily school experience and in particular eliminates exposure of children with asthma to secondhand 

smoke (CDC 2005a). These policies also reduce children’s opportunities to use tobacco products and to 

witness others doing so, thus reinforcing the messages 

that children receive in school about the importance 

of healthy, tobacco-free lifestyles. Finally, tobacco-free 

school policies create young people who are prepared 

to—and in fact expect to—matriculate to smoke-free 

workplaces and communities (CDC 1994). 

According to CDC’s School Health Policies and 

Programs Study (SHPPS) 2000, 44.6 percent of schools 

reported tobacco-free school policies consistent 

with CDC recommendations, up from 36 percent in 

SHPPS 1994 (Journal of School Health 2001). The study 

also found that 45.5 percent of districts and 13 states 

reported such policies. Since 2000, the numbers of 

schools, districts, and states with tobacco-free school 

policies have continued to increase. Oregon is the 

most recent state to adopt such a policy. A Healthy 

People 2010 objective calls for establishing comprehensive tobacco-free policies in all junior high schools, 

middle schools, and senior high schools (USDHHS 

2000). While substantial progress has been made on 

this objective, the target is not likely to be met by 2010 

unless activity increases. 

The following conclusions are supported by 

text in the full report that may not be included 

in this excerpt. The full report can be accessed at 

http://www.surgeongeneral.gov/library/secondhandsmoke/report/.

 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. 

 Chapter 10 
Excerpts: Chldren and Secondhand Smoke Exposure 

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 

Overall Implications 

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. 

Total bans on indoor smoking in hospitals, restaurants, bars, and offices will substantially reduce 

secondhand smoke exposure, up to several orders of 

magnitude with incomplete compliance, and, with 

full compliance, exposures will be eliminated. Absent 

a ban, attempts to control secondhand smoke exposure of nonsmoking occupants or patrons have mixed 

results. Uncontrolled air currents, mixed return air 

and ventilation air, and the lack of complete physical barriers lead to persistence of some secondhand 

smoke exposure with partial restriction strategies. The 

few studies that claim unrestricted smoking in offices 

meets ASHRAE standards do not provide convincing 

evidence that exposures of nonsmokers to secondhand 

smoke were adequately reduced (ASHRAE 1999). 

Specially designed smoking areas inside a building 

can effectively isolate secondhand smoke, but effectiveness depends on engineering design and on high 

volume exhaust separated from the main AHU to 

maintain a negative pressure within the physically isolated area. Mechanical air cleaning has not been sufficiently effective to permit exhaust air, transported or 

leaked air from a designated smoking area, or air from 

a physically separated smoking room or lounge to be 

remixed with ventilation air. 

Ventilation rates substantially higher than the 

minimums recommended by ASHRAE (1999) might 

dilute some secondhand smoke constituents in some 

indoor settings to levels indistinguishable (statistically) from levels in buildings that restrict smoking. 

Perhaps, under such circumstances, indoor air quality might be perceived as acceptable at the 80 percent threshold criterion set by ASHRAE for persons 

voluntarily electing to be indoors in the presence of 

active smokers. However, this threshold criterion 

does not adequately account for possible health 

effects associated with exposure to secondhand smoke 

constituents even at low levels. Absent being able to 

specify acceptable levels of airborne contaminants 

and risks associated with secondhand smoke, concentration-based guidelines for secondhand smoke 

cannot be developed. Thus, exposure to secondhand 

smoke components cannot be controlled sufficiently 

through dilution ventilation or by typical air cleaning 

strategies if the goal is to achieve no risk or a negligible risk. The only effective controls that eliminate 

exposures of nonsmokers are the complete physical 

isolation of smoking areas with separate air exhausts 

or a total smoking ban within the structure. This conclusion echoes prior conclusions of federal agencies 

(USDHHS 1986; USEPA 1992; NIOSH 1991). 

Despite wider adoption of smoking restrictions, 

exposures to secondhand smoke persist. Among 

adults, data from the 1991 NHIS Health Promotion 

and Disease Prevention Supplement indicate that 20.2 

percent of lifetime nonsmokers and 23.1 percent of 

former smokers reported any exposure to secondhand 

smoke at home or at work (Mannino et al. 1997). Selfreported data from NHANES III (1988–1991) suggest 

that 37 percent of lifetime nonsmokers were exposed 

to secondhand smoke, and men (46 percent) were 

more likely than women (32 percent) to experience 

exposure (Steenland et al. 1998). Most nonsmokers 

were exposed in the workplace (20 percent) compared 

with those exposed at home (11 percent) or at both 

work and home (6 percent). However, Pirkle and colleagues (1996) used high-performance liquid chromatography atomospheric-pressure chemical ionization 

tandem mass spectrometry to analyze serum cotinine 

levels and found that 87 percent of nonsmokers had 

detectable levels. These investigators also noted that 

children, non-Hispanic Blacks, and males had higher 

levels than the rest of the populations that were studied (Pirkle et al. 1996). 

Control of Secondhand Smoke Exposure 9 
Surgeon General’s Report 

Some evidence suggests that exposure among 

certain ethnic and gender groups may be higher. For 

example, Pletsch (1994) examined self-reported secondhand smoke exposure data from 4,256 Hispanic 

females aged 12 through 49 years who participated in 

the Hispanic Health and Nutrition Examination Survey (NCHS 1985). Pletsch (1994) found that 62 percent 

of Mexican American women, 59 percent of Puerto 

Rican women, and 52 percent of Cuban American 

women were regularly exposed to secondhand smoke 

at home, and 35 percent of Mexican American women, 

28 percent of Puerto Rican women, and 49 percent of 

Cuban American women were regularly exposed at 

work. 

According to NHIS data, most of the U.S. working population (76.5 percent) does not smoke (NCHS, 

public use data tape, 2002). In 2002, there were an 

estimated 100.3 million nonsmoking workers in the 

United States. In a study that compared exposure levels with OSHA’s significant risk standards, more than 

95 percent of the office workers exposed to secondhand smoke in the United States exceeded OSHA’s 

significant risk level for heart disease mortality, and 

60 percent exceeded the significant risk level for lung 

cancer mortality (Repace et al. 1998). Repace and colleagues (1998) estimated excesses of 4,000 heart disease 

deaths and 400 lung cancer deaths were attributable 

to workplace exposure. 

On the basis of this review, it is clear that banning smoking from the workplace is the only effective way to ensure that exposures are not occurring. 

Despite reductions in workplace smoking, significant worker safety issues remain that only smoking 

bans can address. The home remains the most serious 

venue for secondhand smoke exposure. 

90 Chapter 10 
Excerpts: Chldren and Secondhand Smoke Exposure 

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Disease Prevention and Health Promotion, Office 

on Smoking and Health, 1989. DHHS Publication 

No. (CDC) 89-8411. 

U.S. Department of Health and Human Services. 

Healthy People 2010: Understandng and Improvng 

Health. Washington: U.S. Government Printing 

Office, 2000. 

U.S. Department of Health and Human Services. Progress Review: Tobacco Use, May 14, 2003; <http:// 

www.healthypeople.gov/Data/2010prog/ 

focus27/default.htm>; accessed: May 15, 2006. 

U.S. Environmental Protection Agency. 	Respratory 

Health Effects of Passve Smokng: Lung Cancer and 

Other Dsorders. Washington: Environmental Protection Agency, Office of Research and Development, Office of Air and Radiation, 1992. Publication 

No. EPA/600/006F. 

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Children’s Exposure to Environmental Tobacco 

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Control of Secondhand Smoke Exposure 93 

Excerpts: Chldren and Secondhand Smoke Exposure 

A Vision for the Future 

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. 

The 2006 Surgeon General’s report, The Health 

Consequences of Involuntary Exposure to Tobacco Smoke 

(U.S. Department of Health and Human Services 

[USDHHS] 2006) 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 

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 

Smokng (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. The 2006 Surgeon General’s 

report (USDHHS 2006) is based on a far larger body 

of evidence than was available in 1986. The evidence 

reviewed in the 665 pages of the full 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, the 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). The 2006 report also reviews the evidence 

on the multiple mechanisms by which secondhand 

smoke injures the respiratory tract and causes sudden 

infant death syndrome (USDHHS 2006). 

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 

A Vson for the Future 95 
Surgeon General’s Report 

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 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 the 2006 

report are accessible in a database that can be found 

at http://www.cdc.gov/tobacco. With an 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 Thrd Natonal 

Report on Human Exposure to Envronmental Chemcals 

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 nonHispanic 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 smokefree 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. 

9 
Excerpts: Chldren and Secondhand Smoke Exposure 

•	 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. 

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 of children, individuals with existing heart and lung problems, and other vulnerable 

populations, requires a higher priority and greater 

protection. 

Together, the 2004 and 2006 reports of the 

Surgeon General (USDHHS 2004, 2006), 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. 

A Vson for the Future 97 
Surgeon General’s Report 

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