Jennifer M. Strang, M.S.

 The adverse health effects of smoking and smokeless tobacco use are well-known. Smoking is causally associated with lung cancer, emphysema, and cardiovascular disease, and contributes to both a decrease in life expectancy and an increase in morbidity. Given the serious health effects caused by smoking, it is highly probable that exposure to environmental tobacco smoke, also known as "passive smoking" and "involuntary smoking," has a negative impact as well. Indeed, the toxic chemicals that are present in tobacco smoke also reside in ETS; however, their effects are often discounted due to the dilute nature of ETS.

Controversy surrounds the study of ETS. The tobacco industry has accused the EPA and other researchers of publication bias against studies that have failed to reveal a significant relationship between ETS and various health problems, such as lung cancer and heart disease (Bero, Glantz, & Rennie, 1994). Publicly, the tobacco industry has also denied that ETS exposure has adverse health effects, even though internal research supports the conclusion that secondhand smoke is potentially hazardous (Barnes, Hanauer, Slade, Bero, & Glantz, 1995). Research on ETS has also been subject to a variety of methodological problems, which will be addressed in the section on Assessment of ETS exposure. Despite these concerns, support for a significant relationship between ETS exposure and adverse health effects remains strong. The US Environmental Protection Agency (1992), the California Environmental Protection Agency (1997), and the Australian National Health and Medical Research Council (1997) have all conducted extensive reviews of the research on ETS which confirm the relationship between ETS exposure and a variety of health problems.

 Environmental Tobacco Smoke, also known as "secondhand smoke," is derived from a mixture of side-stream smoke (SS) and mainstream smoke (MS). SS is comprised of the smoke that diffuses directly from the burning tobacco into the atmosphere, while MS consists of the smoke exhaled by the smoker. Most tobacco smoke in the environment is comprised of SS, which contains higher levels of toxic compounds than MS (EPA, 1992; NHMRC, 1997). Although the ETS inhaled by non-smokers is dilute compared to the mainstream smoke inhaled by active smokers, research has shown that the two types of smoke are chemically similar (EPA, 1992). Approximately 50 known carcinogens are present in tobacco smoke. Some of the toxic chemicals and carcinogens that reside in ETS include hydrogen cyanide, sulfur dioxide, benzene, formaldehyde, nicotine, and carbon monoxide (California EPA, 1997). In 1992, as the result of an extensive review of the literature on ETS, the US Environmental Protection Agency classified ETS as a known (Group A) human carcinogen (EPA, 1992). According to the EPA, approximately 3,000 lung cancer deaths each year in the United States are attributable to the effects of passive smoking (EPA, 1992). Other disorders that are linked to ETS exposure include cardiovascular disease, respiratory tract infection, exacerbation of pre-existing asthma, development of asthma in previously non-asthmatic children, sudden infant death syndrome (SIDS), middle ear disease, and other types of cancer. Two recent meta-analyses lend further support to the link between ETS, lung cancer, and cardiovascular disease (Hackshaw, Law, & Wald, 1997; Law, Morris, & Wald, 1997).

Americans are exposed to a surprising amount of secondhand smoke at home, in the workplace, and in restaurants and bars. How much exposure is considered harmful? Clearly, some individuals are more at risk than others. Casino workers, for example, are exposed to high levels of ETS on a daily basis. Researchers from the National Institute for Occupational Safety and Health (NIOSH) have determined that non-smoking casino employees have substantially higher levels of serum cotinine, a metabolite of nicotine, than the general population (Trout et al., 1998). Serum cotinine level is an important indicator of the absorption of nicotine into the body. Although non-smokers do not directly inhale nicotine into lungs, as active smokers do, nicotine may still enter the body through the inhalation of ETS.

ETS exposure in the home is also alarmingly prevalent. According to the Third National Health and Nutrition Examination Survey (NHANES III), between 1988 and 1991, 43% of children aged 2 months to 11 years lived in a home with at least 1 smoker, and 37% of adult non-smokers lived in a home with at least 1 smoker or reported ETS exposure at work (Pirkle, Flegal, Bernert, Brody, Etzel, & Maurer, 1996). Serum cotinine levels in the survey respondents indicated that 91.7% of the US population aged 4 years and older had perceptible levels of cotinine. Given the fact that approximately 25% of the US adult population define themselves as active smokers, the detectable levels of cotinine in the other 65% presumably result from ETS exposure. The number of smokers in the home and the number of hours exposed to ETS at work (mean = 4.4 hours) were both positively associated with increased serum cotinine levels.

Other carcinogenic chemicals have also been detected in the urine of non-smokers exposed to ETS. A study conducted by researchers at the University of Minnesota Cancer Center found that the urine of passive smokers contained a carcinogen found only in tobacco smoke (Hecht, 1997). The carcinogen, NNK, is formed from nicotine and is the only known lung carcinogen found exclusively in tobacco smoke. The study’s nine subjects were non-smoking hospital workers who cared for inpatients in the smoking area of a veteran’s hospital. Urine samples were collected three times on one day at the end of the work week. The nine subjects had detectable levels of NNAL-Gluc, a metabolite of NNK produced by the human body. Although their levels were 70 times lower than levels found in active smokers, no NNAL-Gluc was found in the urine of the non-smoking control subjects who were not exposed to ETS. This particular carcinogen is linked to the development of adenocarcinoma, a type of lung cancer common in smokers.

ETS exposure is assessed through surveys and questionnaires, through the measurement of indoor air concentrations of ETS, and through the measurement of biological markers, such as cotinine, in the blood, urine, and saliva (California EPA, 1997). A common problem associated with the use of survey and questionnaire data is misclassification of ETS exposure. Any data collection method that relies on self-report is subject to recall bias. This bias may be positive (an overestimate of the true health effects of ETS) or negative (an underestimate of the true health effects of ETS) (NHMRC, 1997). Most ETS studies use spousal smoking as the sole measure of ETS exposure. However, individuals may under- or over-estimate the smoking habits of family members or fellow employees. In addition, many former smokers report that they have never smoked, which makes it very difficult to interpret any results that show a connection between ETS exposure and a variety of health problems—are these health effects due to ETS exposure or to the fact that the individual was an active smoker 15 years ago? Current smokers may also deny the fact that they smoke, which further complicates results. Finally, non-smoking subjects who live with non-smoking spouses may be misclassified as non-exposed, when they are actually exposed to ETS at work or in social settings on a regular basis. Measurement of biological markers is frequently used to clarify questionnaire responses. The obvious disadvantage to this method is its intrusiveness, as it necessitates collection of blood, urine, or saliva samples. However, biomarkers provide a much more precise measurement of ETS exposure than survey data. When the two methods are used in conjunction, findings are strengthened.

ETS exposure is associated with a variety of health effects, ranging from mild physiological symptoms, such as eye, nose, and throat irritation, coughing, chest discomfort, and increased phlegm production, to more severe disorders, including lung cancer and ischaemic heart disease (Hackshaw, Law, & Wald, 1997; Law, Morris, & Wald, 1997). In 1997, the Australian National Health and Medical Research Council (NHMRC) conducted a comprehensive review of the research on the health effects of secondhand smoke. According to this report, there is a positive association between secondhand smoke and the following disorders: childhood asthma, lower respiratory illness, lung cancer, cardiovascular disease, and sudden infant death syndrome (SIDS). The findings, which support conclusions drawn by the U.S. EPA (1992) and the California EPA (1997), are summarized below (NHMRC, 1997).

1. Asthma in children:

• Children exposed to ETS are approximately 1.4 times as likely to suffer from asthma as non-exposed children.
• In Australia, about 8% of childhood asthma cases (46,500 children) are attributable to passive smoking. This effect increases in children of mothers who smoke more than 10 cigarettes per day.

2. Lower respiratory illness:

• Risk of lower respiratory illnesses (croup, bronchitis, bronchiolitis, & pneumonia) is approximately 60% higher in children exposed to ETS during the first 18 months of life.
• About 13% of lower respiratory illness in Australian children younger than 18 months (16,300 children) is due to ETS exposure.

• There is an increased lung cancer risk of 30% in never-smokers who live with a smoker.

4. Cardiovascular Disease:

• The risk of heart attack or death from coronary heart disease is 24% higher in never-smokers who live with a smoker.

5. Other illnesses:

• Passive smoking contributes to the risk of sudden infant death syndrome (SIDS).
• ETS exposure irritates the eyes and upper respiratory tract.
• ETS may increase the risk of death from all causes.

5. Areas where further research is needed:

• There may be an association between ETS exposure and childhood cancers and stroke in adults.

Given the current medical knowledge of the adverse health effects of passive smoking, clean indoor air has become a top priority across the United States. Numerous federal, state, and local laws limit or eliminate smoking in the workplace, schools, child care centers, health care settings, public transportation, and other enclosed public places, such as stores, banks, theaters, museums, sports stadiums, restaurants and bars (Americans for Nonsmokers’ Rights, 1994). In January 1998, the State of California enacted comprehensive clean indoor air legislation that eliminates smoking in all restaurants and bars across the state. Although support for clean indoor air is widespread, this legislation has generated controversy and discontent. Many restaurant and bar owners claim that the law has hurt their businesses, and many smokers feel as though they are being treated as second-class citizens. Nevertheless, current scientific knowledge of the hazards of secondhand smoke supports the need for comprehensive clean indoor air legislation. Although the presence of ETS is disappearing in the public sector, Americans continue to be exposed to an alarming amount of secondhand smoke at home (Pirkle et al., 1996). Therefore, efforts to create a smoke-free indoor environment must continue to focus on smoking inside the home. Additional information on the reduction of secondhand smoke may be obtained from the United States Environmental Protection Agency.

1. Americans for Nonsmokers’ Rights. (1994). Clean indoor air: A guide to developing policy. Berkeley, CA: Author.

 

2. Australian National Health and Medical Research Council. (1997). The health effects of passive smoking. Canberra, Australia: Australian Government Publishing Service.

 

3. Barnes, D.E., Hanauer, P., Slade, J., Bero, L.A., & Glantz, S.A. (1995). Environmental tobacco smoke: The Brown and Williamson Documents. JAMA, 274, 248-253.

 

4. Bero, L.A., Glantz, S.A., & Rennie, D. (1994). Publication bias and public health policy on environmental tobacco smoke. JAMA, 272, 133-136.

 

5. California Environmental Protection Agency, Office of Environmental Health Hazard Assessment. (1997). Health effects of exposure to environmental tobacco smoke. Sacramento, CA: Author.

 

6. Hackshaw, A.K., Law, M.R., Wald, N.J. (1997). The accumulated evidence on lung cancer and environmental tobacco smoke. British Medical Journal, 7114 (315), 980-988.

 

7. Hecht, S. (1997, September). A metabolite of the lung carcinogen 4-(Methylnitrosamino -1-(3-Pyridyl)-1-Butanone in the urine of people exposed occupationally to environmental tobacco smoke. Poster session presented at the national meeting of the American Chemical Society, Las Vegas, NV.

 

8. Law, M.R., Morris, J.K., & Wald, N.J. (1997). Environmental tobacco smoke exposure and ischaemic heart disease: An evaluation of the evidence. British Medical Journal, 7114 (315), 730-800.

 

9. Pirkle, J.L., Flegal, K.M., Bernert, J.T., Brody, D.J., Etzel, R.A., & Maurer, K.R. (1996). Exposure of the US population to environmental tobacco smoke. JAMA, 275, 1233-1240.

 

10. Redhead, C.S., & Rowberg, R.E. (1995). Environmental tobacco smoke and lung cancer risk. Washington, DC: Congressional Research Service/The Library of Congress.

 

11. Trout et al. (1998). Journal of Occupational and Environmental Medicine, 40, 270-276.

 

12. United States Environmental Protection Agency. (1992). Respiratory health effects of passive smoking: Lung cancer and other disorders. Washington, DC: Author.