Environmental tobacco smoke: Medical and Legal Issues

0025-7125/92 $0.00

CIGARETTE SMOKING

+ .20

ENVIRONMENTAL TOBACCO SMOKE Medical and Legal Issues James

C. Byrd, MD, MPH

In 1987, the Surgeon General and the Committee on Passive Smoking of the National Research Council (NRC) reported on the adverse health effects of environmental tobacco smoke (ETS).21, 92 These two lengthy reviews have generated enormous interest and debate. The conflicting opinions are, in part, due to differences in interpretation of the scientific studies analyzing the effects of ETS. This article summarizes the medical effects of passive smoking and reviews the role of litigation, legislation, and private regulation in the area of ETS.

MEDICAL ISSUES AND ENVIRONMENTAL TOBACCO SMOKE Components of Environmental Tobacco Smoke

Over 4000 chemicals have been identified in smoke, and more than 50 substances in tobacco smoke have been identified as carcinogens in animals or humans. 46 ETS consists of mainstream smoke (MSS), sidestream smoke (SSS), and vapor-phase components that diffuse through cigarette paper into the environment. MSS is the smoke inhaled and exhaled by the smoker, and SSS is the smoke that issues from the end of the cigarette between puffs. ETS is primarily made up of SSS. From the Division of General Internal Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin

MEDICAL CLINICS OF NORTH AMERICA VOLUME 76 • NUMBER 2 • MARCH 1992

377

378

BYRD

Approximately 85% of passive smoke exposure is from SSS and 15% from MSS. The concentrations of physiochemical constituents in MSS and SSS are similar qualitatively but vary widely quantitatively (Table 1). For example, the concentration of carbon monoxide is 2.5 times higher in SSS than in MSS.91 The particulate phase of smoke is a concentrated aerosol with over 5 x 1025 particles/cm3. The particles in SSS have a smaller diameter than the particles in MSS and are more likely to deposit in the most distant alveolar portions of the lung. 52 Also, secondary chemical reactions occur before a nonsmoker inhales ETS, including aging, volatilization, and adsorption of radon daughters or particles. 21 The studies analyzing the differences between MSS and SSS have been conducted in special smoke chambers. Further studies are required to determine how these data correlate with actual indoor conditions because numerous factors affect the level of ETS: room size, ventilation, temperature, humidity, the number of people in the room, the amount and type of tobacco smoked, and the volatility of the agents. 21 Despite the difficulties in measuring the physiochemical constituents of ETS under realistic conditions, several studies have shown that acrolein, carbon monoxide, nicotine, and total respirable particulates are elevated compared with control conditions. Additionally, nicotine, its metabolite cotinine, and carcinogens are detected in the urine, blood, and saliva of nonsmokers with passive smoke exposure. 30,58,60 ETS exposure occurs over an individual's entire lifetime. Although biologic marke.rs can Table 1. CONSTITUENTS OF CIGARETTE SMOKE* AND RATIO OF SIDESTREAM SMOKE (SS) TO MAINSTREAM SMOKE (MS)t MS

Gas phase

Carbon monoxide Carbon dioxide Methane Acetylene Ammonia Hydrogen cyanide Dimethylnitrosamine

Particulate phase

Tar Nicotine Toluene Phenol Naphthalene Benzo (a) pyrene Hydrazine

SS/MS

10-20 mg 20-60 mg 1.3 mg 27 j.1g 80 j.1g 430 j.1g 10-65 j.1g

2,5 8.1 3.1 0,8

1-40 mg 1-2.5 mg 108 j.1g 20-150 j.1g 2.8 j.1g 20-40 j.1g 32 j.1g

1.7 2.7

73

0.25 52

5,6 2.6 16

2.8

30

'Nonfilter cigarette tAdapted from Committee on Passive Smoking of the National Research Council: The physiochemical nature of sidestream smoke and environmental tobacco smoke, Measuring exposure and assessing health effects, Washington, DC, National Academy Press, 1986,

ENVIRONMENTAL TOBACCO SMOKE

379

measure recent exposure, data must be obtained by interview to assess past exposure. Early ETS studies were not standardized regarding the ascertainment of passive smoke exposure, and often they did not evaluate the reliability of the data obtained. Recent studies have utilized better methodology, and two recent studies should further improve techniques to quantify lifetime ETS exposure. 24 , 25 Acute Irritating Effects of Environmental Tobacco Smoke

Many people have an intolerance to ambient tobacco smoke. In one study of 191 allergic nonsmokers and 250 nonallergic nonsmokers, 69% of the nonallergic subjects developed eye irritation when exposed to passive smoke, 29% had nasal symptoms, 32% had headaches, and 25% developed a cough.sO The percentage of subjects who experienced each of these symptoms was higher among patients who reported allergies to smoke. Both smokers and nonsmokers are annoyed by ETS. In a field study of 472 employees (235 smokers, 237 nonsmokers), 44% of smokers and 82% of nonsmokers were disturbed by smoke at work; a quarter of smokers and over half of nonsmokers experienced eye irritation on the job related to smoke. 95 In the same study, further experiments were conducted in a climatic chamber, varying the concentration of numerous constituents of smoke. Subjective eye irritation and mean blink scores increased with increasing smoke concentrations. The eye irritation and blink score increases were noted at realistic carbon monoxide levels of 1.3 to 10.0 parts per million (ppm) and began within 15 minutes of exposure. In order to maintain a carbon monoxide level below 2.0 pp m, it is estimated that ventilation in a room with smokers must be two to four times greater than in a room in which nobody smokes. 95 The odor of ETS is distinctive and unpleasant for many individuals. It appears to be principally related to the vapor phase and is resistant to filtration systems but can be removed by ventilation systems. The American Society of Heating, Refrigeration and Air Conditioning Engineers (ASHRAE) has developed a standard for odor quality.12 ASHRAE specifies that 80% of the occupants in a room must be satisfied with air quality for it to be deemed acceptable. Nonsmokers and visitors are more easily dissatisfied with air quality than are smokers. ASHRAE has suggested air exchange should be four to five times higher in rooms specified as smoking occupancy. Environmental Tobacco Smoke and Children

Infants. Infants may be at particular risk for damage from passive smoking because of the potential impairment of their developing organ systems, most notably the respiratory tract. Measurable levels of coti-

380

BYRD

nine have been found in the saliva and urine of infants with household exposure to ETS. 19 , 41, 60 Three large longitudinal studies have demonstrated an increased incidence of respiratory illnesses and hospitalizations among infants whose parents smoke. 20, 29, 42 In an Israeli study of 10,672 infants (birth to 1 year), there were 9.5 hospitalizations for bronchitis and pneumonia per 100 infants with nonsmoking mothers, compared with 13.1 hospitalizations per 100 infants with smoking mothers (P < 0.001).29 As the number of cigarettes smoked by the mothers increased, so did the hospital admission rates. Among infants whose mothers smoked more than one pack per day, there was an admission rate of 31.7 per 100, a threefold increase over the rate for infants with nonsmoking mothers. The relationship between illness and passive smoke exposure was maintained after controlling for birth weight. British researchers followed 2205 children for 5 years, and found the rates of lower respiratory illness were elevated in smokers' children compared with nonsmokers' children; the rates of disease further escalated when both parents smoked, even when family size, socioeconomic status, and birth weight were controlled. There was no increase in respiratory disease in children aged 2 to 5. 20 The third cohort study was conducted in New Zealand and followed 1265 children for 3 years. 29 Maternal smoking was strongly related to bronchitis/pneumonia in the first year of life. Each increase of five cigarettes per day resulted in an increase of 2.5 to 3.5 incidents of bronchitis and pneumonia per 100 children at risk. Children. Children in households with adult smokers have more restricted activity and bed-disability days than children living with nonsmokers. The more cigarettes consumed per household, the greater the number of sick days.14 Several studies have shown a mild impairment in pulmonary function among children whose parents smoke. 13,86,87,93 In a longitudinal study of 7834 children, increased maternal smoking resulted in a lower forced expiratory volume (FEV I ) at age 8 and a measurable growth retardation in FEV I per pack-year of exposure. 13 History of bronchitis and physician-diagnosed respiratory illness before age 2 were associated with significantly lower baseline FEV I levels. This same finding was backed by another study that followed pulmonary tests in 1156 children for 7 years 86 and controlled for previous FEV I , age, sex, height, weight, and change of health and personal smoking history. After 5 years the rate of pulmonary function growth in nonsmoking children with smoking mothers was 93% of the rate of growth in nonsmoking children with nonsmoking mothers. Childhood reduction in lung growth may predispose individuals to obstructive lung disease by reducing peak lung growth or by accelerating the rate of decline in pulmonary function known to occur among smokers.81 This problem is potentially compounded by the fact that children of smokers are more likely to become smokers.63 Cross-sectional surveys have demonstrated an increase in frequent cough l8 and persistent middle ear effusions 56 among children and adolescents with passive smoke exposure. Parental smoking may be a

ENVIRONMENTAL TOBACCO SMOKE

381

risk factor for the development of childhood asthma; because its physiochemical constituents are more likely to reach small airways, SSS generates greater airway activity in asthmatics. 40 ETS has deleterious effects on the health of infants and children. The long-term effects and consequences of physiologic changes remain unexplored. Studies of the effects of passive smoking among infants and children must deal with several confounding issues. Among infants, the effects of maternal and paternal smoking during pregnancy must be evaluated and controlled to determine the postdelivery effects of ETS. A recent study evaluating the effects of parental smoking on airway responsiveness in early infancy showed that airway responsiveness to inhaled histamine was present among infants less than 1 month old who were exposed to parental smoking in utero. 100 The effect of postnatal ETS exposure and histamine responsiveness requires further study. Moreover, childhood experimentation with cigarette smoking may occur as early as age 6. Thus, studies of children must carefully determine the child's personal smoking history, which may be inaccurately reported by the parents. Environmental Tobacco Smoke and Lung Cancer in Adults

There are clear epidemiologic data that active smoking causes lung cancer. Numerous prospective studies and case-control studies have met the criteria for causality, including biologic plausibility, strength of association, coherence of association as evidenced by a dose-response relationship, appropriate temporal relationship, and consistency of results across studiesY Studies of the association between passive smoking and lung cancer have fulfilled some, but not all, of the criteria for causality. It is biologically plausible that passive smoke exposure might cause lung cancer because passive smoke contains carcinogens and there is no established lower threshold level of exposure for the development of lung cancer. A number of studies have linked passive smoking with the development of lung cancer, but others have shown no association.10, 15, 17, 23, 27, 33, 35, 38, 44, 45, 47, 48, 50, 53-55, 57, 62, 66, 69, 99 On the basis of the conclusions from these studies, the Surgeon General concluded that ETS is a cause of lung cancer.1 The Committee on Passive Smoking from the NRC reviewed the existing scientific literature regarding ETS.2 The committee reported that exposure to ETS increases the incidence of lung cancer in nonsmokers: The risk of lung cancer is approximately 30% higher for nonsmoking spouses of smokers than for nonsmoking spouses of nonsmokers. The Surgeon General and the NRC recognized several deficiencies in the observational studies upon which their conclusions were based. Concerns over the consistency of results across studies are best addressed by examining several of the most important studies.

382

BYRD

Hirayama analyzed the results of a prospective study of 91,540 wives whose husbands' smoking habits were known. 44, 45 The study, which had a 14-year follow-up (1966 to 1979), was designed to determine the health outcomes of factors such as smoking, alcohol consumption, occupation, and marital status. A total of 346 deaths were recorded from lung cancer in women. Of these women, 245 were married and 174 were nonsmokers. The overall standardized mortality for nonsmoking wives of smokers was 1.8 times that of nonsmoking women married to nonsmokers. The likelihood of lung cancer deaths among nonsmoking women increased in direct proportion to the number of cigarettes their husbands smoked. The risk ratios were 1.00 when the husbands were nonsmokers, 1.61 when husbands were exsmokers or daily smokers of 1 to 19 cigarettes, and 2.08 when husbands were daily smokers of 20 or more cigarettes. This paper has been carefully scrutinized, and several criticisms have been raised. Although the study was a prospective cohort study, it was not designed to investigate the effects of passive smoking. There is only limited information concerning the histology of the tumors, and the diagnoses were obtained from death certificates. The effect of indoor pollutants other than smoke (e.g., charcoal, kerosene burners) was not considered,83 and there were concerns that the chi square statistic (used to compare wives of nonsmokers, exsmokers or light smokers, and heavy smokers) was incorrectly reported. 59 In response to these criticisms, the author reported more detailed data confirming initial findings. Other investigators recalculated the chi square value by recombining the data and found highly significant results. 43 The author also showed that the increased risk secondary to passive smoking persisted when analyzed by socioeconomic status. A 1981 case-control study performed in Greece measured the development of lung cancer in nonsmoking women in relation to the personal smoking habits of their husbands. 90 The relative risk for the development of lung cancer for those nonsmoking women was 2.4 for those whose husbands smoked less than a pack a day and 3.4 for those whose husbands smoked more than a pack a day. This study was limited because the control group was chosen from a hospital different from the case hospital, the overall number of cases was low, and cytologic or histologic confirmation was missing in 35% of the cases. Patients with adenocarcinoma were excluded from the study, even though adenocarcinoma is more likely to occur in women and has been causally linked to cigarette smoke. The inclusion of the adenocarcinoma would have increased the number of cases by 35% and possibly strengthened the study's statistical associations. Similar relative risk factors were found in an American study, which also showed that male and female nonsmoking spouses had an increased risk of lung cancer if their spouses smoked and if there was a maternal history of smoking. 23 The cases in this study were confirmed by pathologic examination, but the number of cases was small. Garfinkel et al have completed two studies on passive smoking and lung cancer. 33 , 35 The first, which was part of a longitudinal study

ENVIROf\:MENTAL TOBACCO SMOKE

383

undertaken by the American Cancer Society,35 reported data from 153 patients who died of lung cancer from a group of 176,739 nonsmoking women. The mortality ratio was 1.27 for women married to smokers of less than 20 cigarettes per day and 1.10 for women married to smokers of more than 20 cigarettes per day. Neither mortality ratio was statistically significant, nor was a dose-response relationship seen. One problem with this study, like the Japanese study, was that it was not initially intended to look at the effects of passive smoking. 34 Because data on ETS exposure were collected incidentally, of 564 cases of lung cancer in women, the husbands' smoking status was known for only 153 (27%). In a more recent case-control study of 134 nonsmoking women with lung cancer, smoke exposure was carefully quantified into the following categories: (1) total smoke exposure during the past 5 years at home, at work, and in other areas; (2) total smoke exposure during the past 25 years at home, at work, and in other areas; (3) the amount of time the husband smoked at home; and (4) the total number of cigarettes smoked daily by the husband. 33 In univariate analyses the risk of lung cancer for nonsmoking women revealed nonsignificant odds ratios of 1.13 to 1. 31 when classified by the four exposure categories. However, the odds ratio for women whose husbands smoked more than 20 cigarettes per day at home was 2.11 (95% confidence interval, 1.13 to 3.45). Further multivariate analyses showed a higher risk for lung cancer among nonsmoking wives with increasing exposure to a husband's smoking at home, controlling for many other potentially confounding factors. Passive smoke exposure during childhood and adult life was not noted to be a significant factor in a case-control study of 31 women with lung cancer,99 although childhood pneumonia (relative risk 2.3; 95% confidence interval, 1.1 to 6.7) and exposure to coal burning (relative risk 2.3; 95% confidence interval, 2.0 to 5.5) during childhood were significant risk factors. A five-city US study analyzed 2668 patients with lung cancer and found 134 nonsmokers. 50 Among male nonsmokers, 72% (18/25) reported passive smoke exposure at work, compared with 44% (11/25) of controls (P < 0.05). Passive smoke exposure was not significant for female nonsmokers, but occupation in a textile-related job conferred an increased risk for lung cancer. A study of nonsmoking Hong Kong women revealed no overall increase in lung cancer among those exposed to passive smoke, 55 but longstanding chronic cough was a risk factor. The NRC determined that 13 studies evaluating ETS and lung cancer presented adequate information for comparative analysis and pooling.22 The overall risk of lung cancer in association with ETS exposure was 1.34 (95% confidence interval, 1.18 to 1.53); for women the relative risk was 1.32 (1.16 to 1.51), and for men the relative risk was 1.62 (0.99 to 2.64). The broad confidence interval for men was secondary to fewer studies investigating lung cancer in male nonsmok-

384

BYRD

ers (34 male cases, 643 female cases). Although the NRC investigators concluded that increased risk represents a direct and causal effect, confounding factors associated with both lung cancer and living with a spouse who smokes may lower the overall relative risk moderately to 1.25 for nonsmokers exposed to ETS. The most recent article on ETS and lung cancer was a populationbased, individually matched case-control study from New York state. Compared with previous studies, there was increased methodologic rigor to case ascertainment, interviews with patients, controls, surrogate respondents, and statistical analyses. The study showed that household exposure to 25 or more smoker years during childhood and adolescence doubled the risk of lung cancer (1:2.07; 95% confidence interval, 1.16 to 3.68). Lifetime exposure and spousal exposure were not related to the risk of lung cancer in nonsmokers. The study was criticized on several grounds in subsequent letters to the editor. One writer was concerned about the lack of strength of the statistical association and no adjustment for multiple comparisons. 85 A second group believed that an important confounder, ~-carotene, had not been evaluated and controlled. In a recent study, ~-carotene intake and plasma levels were lower in ETS-exposed nonsmokers than in nonsmokers without ETS exposure. 98 Since ~-carotene intake and plasma levels are depressed in patients with lung cancer, this finding is provocative. A final letter raised concerns about potential occupational confounding because parental occupation is related to childhood cancer, and smokers are overrepresented in industrial jobs with chemical exposure. 82 Although the study may have valid conclusions, the questions raised by the letters must be considered in future studies. Environmental Tobacco Smoke and Cardiorespiratory Disease

Information linking ETS to cardiorespiratory illness has emerged more slowly than that concerning lung cancer. This pattern is similar to the evolution of data regarding active smoking. Lung cancer was the first disease proven to be caused by smoking, followed by chronic obstructive pulmonary disease, ischemic heart disease (IHO), and then many other less prevalent conditions. Because IHO is far more prevalent than lung cancer, an association between passive smoking and IHO would have a much broader public impact. At the time of the 1987 Surgeon General's Report and the NRC review, the data linking passive smoking to IHO were inconclusive. A recent article by Glantz and Parmley reviews epidemiologic data linking ETS to heart disease and offers new physiologic and biochemical data to support the association. 39 As in the NRC analysis, Glantz and Parmley pooled the results of 10 epidemiologic studies reporting the relation between ETS and the risk of heart disease death in a nonsmoking spouse and five studies

ENVIRONMENTAL TOBACCO SMOKE

385

examining nonfatal cardiac events. The pooled relative risk for heart disease for both nonsmoking men and nonsmoking women exposed to spousal ETS was 1.3 (95% confidence intervals: men, 1.1 to 1.6; women, 1.2 to 1.4). The concerns about the size, validity, and confounders that have been raised about passive smoking and lung cancer have also been raised regarding the heart disease studies. In addition to the development of IHO, passive smoking has been associated with acute cardiovascular effects and worsening of angina pectoris. The acute effects of active smoke inhalation on the cardiovascular system include a rise in blood pressure, bradycardia, and constriction of peripheral blood vessels. Experimental exposure to the concentration of smoke found in ETS results in peripheral vasoconstriction with diminished digital pulse wave recording. The vasoconstriction from passive smoke is even more pronounced when SSS is compared with MSS.65 Physical parameters were measured in 10 patients with classic stable angina exposed to three conditions: no smoking (control), exposure to smoke in a ventilated room, and exposure to smoke in an unventilated room. 11 Subjects showed a 22% decline in exercise duration (232 sec to 181 sec) from baseline when exercised in a ventilated smokefilled room and a 38% decrease in time (234 sec to 146 sec) to angina when exercised in an unventilated smoke-filled room. Smoke-exposed groups showed an increase in resting pulse rate, systolic and diastolic blood pressure, and carboxyhemoglobin. 11 In their analysis, Glantz and Parmley supported the epidemiologic evidence between ETS and heart disease by reviewing adverse physiologic and biochemical effects of passive smoking. 39 The paper described the adverse effects of ETS on platelet function by increasing platelet aggregation and direct damage to the arterial endothelium. Also, nonsmokers' platelets appear to be more sensitive to ETS exposure than smokers' platelets. In other experiments, ETS depressed mitochondrial cellular respiration. In sum, there is growing biologic plausibility to the relationship between IHO and ETS. If there is a 30% increased risk of IHO for nonsmokers exposed to ETS, it has been estimated that there may be as many as 37,000 premature heart disease deaths from passive smoking, nearly 10 times the estimate for lung cancer. 98 The data on the effects of passive smoking on adult pulmonary function and respiratory symptoms are conflicting. Ten asthmatics and 10 normal subjects were exposed to passive smoke in an environmental chamber. 44 With only minimal increase in carboxyhemoglobin levels, the asthmatic subjects had a significant decrease in their vital capacities, in FEV l , and in maximal mid expiratory flow rate (MMEF). The decrease in function was noted within 15 minutes and persisted for over an hour. No changes were seen in the pulmonary function of normal subjects. Another study revealed no decrease in pulmonary function among asthmatics after passive smoke exposure. 77 In a large study of asymptomatic adults, pulmonary functions were measured on individuals about to enter a physical fitness program. Nonsmokers exposed to

386

BYRD

tobacco smoke at work had a significant decrease in FEV! and MMEF compared with nonexposed individuals. 99 Although the absolute decrease in pulmonary function was small (5.5% and 13.6% for the FEV! and MMEF, respectively), the workers were relatively young and thus had a lower overall smoke exposure than older individuals. A French study analyzing pulmonary function in adult women exposed to their husbands' smoking found a decrease in pulmonary function in those over age 40.5! The clinical significance of these small changes in pulmonary function in adults is uncertain. Environmental Tobacco Smoke: Summary of Medical Effects

Exposure to ETS by nonsmokers occurs frequently in the home, in the workplace, and in other public areas where smoking is allowed. Despite difficulties in evaluating the effects of low-level ETS exposure, a number of conclusions have been reached 2 !, 39, 92: 1. ETS is a cause of disease in nonsmokers. 2. Children exposed to ETS experience an increase in respiratory infections and a decrease in lung function growth. 3. Adults exposed to ETS experience numerous acute irritating effects. 4. Adults exposed to ETS have an elevated risk for the development of lung cancer and perhaps for the development of ischemic heart disease. 5. Separation of smokers and nonsmokers in the same airspace may reduce but not eliminate exposure of nonsmokers to ETS. LEGAL ISSUES AND ENVIRONMENTAL TOBACCO SMOKE

Adequate medical information now exists for physicians to privately counsel their patients not to smoke and to avoid others' smoke. The medical evidence presented here has also been important in decision-making in the public arena. As medical evidence on the harmful effects of ETS has accumulated since the early 1970s, there has been a parallel increase in legal action, which has taken many forms: States have enacted statutes, cities have passed ordinances, federal legislation has been implemented, constitutional arguments have been put forth, claims to a smoke-free workplace have been considered by the courts, and corporations have adopted nonsmoking policies. Legislation and Regulation

Most legislation restricting smoking has been enacted at the state level. In the early part of this century, state legislation had two

ENVIRONMENTAL TOBACCO SMOKE

387

rationales-protecting the public from fire hazards 96 and preventing the social and physical evils of smoking. 79 Although cigarettes were banned in a dozen states at the peak of this early antismoking movement, the movement lost momentum when enforcement of the laws proved controversial. As part of the reaction against alcohol prohibition, all state laws banning smoking were repealed by 1927. In the early 1970s, however, as the health risks of active smoking became widely recognized, a new wave of state smoking legislation emerged to protect the safety and comfort of nonsmokers.84 Between 1970 and 1974, nine laws were enacted in eight states. Between 1975 and 1979, 29 new laws were passed and 15 additional states adopted smoking regulations. In 1975, Minnesota passed its landmark Clean Indoor Air Act "to protect the health, comfort, and environment by prohibiting smoking in public places and at public meetings except in designated smoking areas." This law became the model for other states. The rate of enactment of state legislation increased throughout the 1970s and continued into the 1980s. As of July 1991, 44 states and the District of Columbia had legislation aimed at reducing involuntary smoke inhalation by restricting smoking in various places (Table 2).88 Now 80% of the US population resides in states with some smoking restriction, compared with 8% in 1971. 3 Most of the six states without smoking legislation are concentrated in the southeastern portion of the country and include North Carolina and Tennessee-two of the six major tobacco-producing states. Current state smoking legislation varies in comprehensiveness and language. A few of these statutes specifically recognize the right of a nonsmoker to breathe clean air.70 The trend over time has been for states and municipalities to revisit and strengthen their smoking restrictions. The legislative clearinghouse for Tobacco Free America has a five-point scale summarizing the strength of state smoking restrictions: none, nominal, basic, moderate, and extensive. 89 By mid-1991, 53% (27 of 51) of states had moderate to extensive smoking restrictions, 23% (12 of 51) had basic restrictions, 12% (6 of 51) had nominal restrictions, and 12% (6 of 51) had no restrictions (Table 2). Congress has been reluctant to enact federal legislation restricting smoking in public places. However, smoking may have been reduced by many actions taken by the federal government such as the requirement, effective since 1965, that each package of cigarettes bear a warning labeF and by its ban of cigarette commercials on television and radio since 1971. 3 In addition, various federal agencies have passed antismoking regulations. The Department of Defense issued a regulation in 1979 prohibiting smoking in auditoriums, elevators, shuttle vehicles, medical care facilities, conference rooms and classrooms, and work areas. s The Department of Veterans Affairs 1986 Smoking Policy allows smoking only in designated areas of VA facilities 93 and allows individual facilities to ban smoking in the entire facility. The General Services Administration restricts smoking in GSA-controlled buildings and facilities. 37 Whereas previous GSA guidelines had banned smoking in auditoriums, classrooms, conference rooms, elevators, restrooms, lob-

388

BYRD

Table 2. LIMITATIONS ON SMOKING IN PUBLIC PLACES State

AL AK AZ AR CA CO CT DE DC FL GA HI ID IL IN lA KS KY LA ME MD MA MI MN MS MO MT NE NV NH NJ NM NY NC NO OH OK OR PA RI SC SO TN TX UT VT VA WA WV WI WY

Overall Strength of Law

None Extensive Basic Nominal Moderate Basic Extensive Nominal Moderate Moderate Nominal Moderate Moderate Moderate Basic Extensive Moderate Nominal None Extensive Basic Basic Moderate Extensive Nominal None Extensive Extensive Basic Extensive Moderate Basic Extensive None Moderate Basic Moderate Moderate Basic Extensive Basic Basic None Basic Extensive Extensive Moderate Moderate Nominal Extensive None

Public Transit

X X X X X X X X X X X X X X

X X X X X

Health Care Offices! Facilities

Elevators

Indoor Arenas

X X X X X X

X X

X X

X X X X

X X X X X

X X

X X

X X

X X X

X X X X X

X X

X X

X

Retail Outlets

Restaurants

X X X X X X

X X

X X

X

X

X

X

X X

X X

X X

X X X

X X

X

X X

X

X

X X X X X

X X X X X

X X X X X

Schools

X X X

X X X

X X X X X

X X

X X X X X

X X X X X

X X X X X

X

X

X

X

X

X

X X X X X X

X X X X X

X X X X X X

X

X

X X

X X

X X

X

X X X

X

X

X

X

X

X X X X X X X

X X X X X X X

X X X

X X X X

X X X X

X X X

X X

X

X

X

X

X

X

X

X

X X X X X X

Adapted from Coalition on SmoKing or Health: State smoking restrictions. Washington, DC, 1991 and State legislative actions on clean indoor air and cigarette excise taxes. Washington, DC, 1989; with permission.

ENVIRONMENTAL TOBACCO SMOKE

389

bies, and medical care facilities, new restrictions allow smoking only in designated office areas, restrooms, and lobbies; signs must be posted to indicate a smoking area. On a trial basis in 1988, Congress enacted legislation to prohibit smoking on domestic flights of 2 hours or less. During this ban the Surgeon General sponsored a study to determine ambient air nicotine levels during flights of approximately 4 hours and to determine if exposure measurements correlated with acute symptoms. 61 In-flight ETS produced measurable levels of cotinine in the urine of passengers and attendants. In-flight nicotine exposure was associated with upper respiratory symptoms and passengers' perceptions of annoyance. This study was instrumental in bringing about a permanent law passed in 1990 which prohibited smoking on domestic flights of 6 hours or less. In 1991, the National Institute for Occupational Safety and Health released a report on the effects of ETS exposure in the workplace. The report concluded that ETS meets the Occupational Safety and Health Administration's criteria to be classified as a potential occupational carcinogen. The report recommended that "exposure be reduced to the lowest feasible concentration and ... the best method for controlling worker exposure to ETS is to eliminate tobacco use from the workplace and to implement a smoking cessation program." JUdicial Action

There has been relatively little judicial action to restrict smoking in public places. Most of the cases that have been tried have involved nonsmoking employees' state law claims to a smoke-free workplace. Smith v. Western Electric Co./ for instance, was brought by a nonsmoker who worked in an open office area with other employees, many of whom smoked. The employee began to experience serious respiratory tract discomfort, and a medical evaluation determined that he suffered an adverse reaction to tobacco smoke. When the employee complained to his employer about the tobacco smoke, he was moved to different locations, but no improvement resulted because each location contained significant amounts of ETS. The employer also supplied the employee with a respirator, but that proved ineffective in protecting him from tobacco smoke. Ultimately, the employer informed the employee that his only alternative was to apply for a job in the computer room where smoking was prohibited, but he would earn $500 less per month. The employee sued, and the court found that the employer had breached its duty to provide a reasonably safe workplace and should be enjoined from allowing such a condition to continue. The court explained that it was well settled within the state that an employer has a duty to its employees to use all reasonable care to provide a reasonably safe workplace, and that the employer in Smith knew that tobacco smoke was harmful to the health of the plaintiff-employee. Furthermore, the court continued, the employer had the authority, ability, and reasonable

390

BYRD

means to control smoking, as evidenced by its ability to keep its computer room smoke-free. Thus, the court concluded, the employer had breached its duty to provide a reasonably safe workplace. Similarly, in Shimp v. New Jersey Bell Telephone Co.,! a New Jersey court held that since smoking had been proven to be a health hazard, the right of employees to a safe working environment made it imperative for smoking to be forbidden in work areas. The plaintiff in that case, an employee of New Jersey Bell Telephone Company who worked in an office where 7 of 13 employees smoked,78 suffered a variety of symptoms as a result of her allergy to cigarette smoke. She was offered the chance to move to a different location, but the move would have entailed a demotion. In ruling on her suit for injunctive relief, the Superior Court held that an employee has a right to work in a safe environment and an employer has a duty to provide a safe workplace.! Cigarette smoke was dangerous to the health of the plaintiff, the judge noted; and she had not assumed the risk of that harm because cigarette smoke is not a necessary result of the operation of the telephone business.! The court granted the injunction and ordered New Jersey Bell to provide the plaintiff with a safe workplace by "restricting the smoking of employees to the non-work areas presently used as a lunch room" and prohibiting smoking "in offices or adjacent consumer service areas.//! Court actions to restrict smoking at work have also been brought under federal nondiscrimination law. In Vickers v. Veterans Administration/ for instance, Mr. Vickers, a VA employee who suffered from an unusual sensitivity to tobacco smoke, alleged that his hypersensitivity to tobacco smoke rendered him a handicapped person within the meaning of the Rehabilitation Act of 1973, a federal antidiscrimination statute. 4 The court determined that Mr. Vickers' hypersensitivity did render him a handicapped person within the meaning of the statute because it limited one of his major life activities-his capacity to work in an environment that was not completely smoke-free. However, the court said, Mr. Vickers was not discriminated against by reason of his handicap. His employer had made reasonable accommodation for him by separating the desks of smokers from nonsmokers, securing a voluntary agreement among smokers in the office to refrain from smoking there, installing vents in Vickers' office, purchasing an air purifier, and offering Vickers another job. 6 Constitutional claims have been used unsuccessfully by nonsmoking plaintiffs in an effort to restrict smoking. The Ninth, the Fifth and Fourteenth, and the First Amendments to the US Constitution have been invoked as support for the nonsmoker's right to breathe clean air. In refusing to recognize a fundamental right under the Ninth Amendment to breathe clean air,72 courts have explained that the right to breathe clean air is not on a constitutional par with the right to privacy and other more appropriately defined Ninth Amendment rights. 36 Claims to smoke-free air under the Fifth and Fourteenth Amendment due-process clauses have also been unsuccessful. These claimants

ENVIRONMENTAL TOBACCO SMOKE

391

have argued that the right to life implies a right to be free from the toxins that endanger life. 74 In Federal Employees for Nonsmokers' Rights v. United States/ the court responded to that argument as follows: If this Court were to recognize that the Fifth and Fourteenth Amendments provided the judicial means to prohibit smoking, it would be creating a legal avenue, heretofore unavailable, through which an individual could attempt to regulate the social habits of his neighbor. This court is not prepared to accept the proposition that life-tenured members of the federal judiciary should engage in such basic adjustments of individual behavior and liberties .... For the Constitution to be read to protect nonsmokers from inhaling tobacco smoke would be to broaden the rights of the Constitution to limits heretofore unheard of, and to engage in that type of adjustment of individual liberties better left to the people acting through legislative processes.

The First Amendment, which has been interpreted to protect the right to receive information and ideas freely/3 has also failed to protect nonsmokers from smoking. In Gasper v. Louisiana Stadium and Exposition District, plaintiffs claimed that their right to exposure to events was impaired because smoking was allowed at the stadium. 36 The Federal Employees plaintiffs made a similar claim. 28 Both courts, however, rejected the First Amendment argument. Outside the area of racial discrimination, the US Supreme Court has required that state action be affirmative; state inaction is not sufficient to constitute a constitutional violation.71 Yet nonsmokers have generally sought relief from state or local government's failure to regulate or prohibit smoking/6 and thus the necessary state action has been missing. In addition, the Supreme Court is reluctant to recognize rights alleged to be "fundamental" unless such rights are "explicitly or implicitly guaranteed by the Constitution."9 Nonsmokers' claims under the First, Fifth, Ninth, and Fourteenth Amendments have not been based directly upon the explicit language of those amendments, but rather upon reading the amendments together to construct "penumbral" claims, which the courts have found implausible. The Supreme Court's holding in Rodriquez 68 indicates that a nonsmoker's claim of a constitutional right to clean air is destined to failure unless the Supreme Court's constitutional analysis changes radically. A third and more successful approach taken by nonsmokers in court is the argument that smoking should be restricted because it is a "public nuisance." Several state statutes specifically designate smoking in public as a public nuisance. 71 Others describe smoking as a health hazard, and plaintiffs in those states could use the public nuisance theory if they could show that tobacco smoke is a health hazard sufficiently unreasonable to constitute a public nuisance. In Stockier v. City of Pontiac, for instance, a nonsmoking plaintiff successfully claimed that public smoking at the Detroit Lions football games was a public nuisance. 74 The court heard medical testimony and other evidence and found that smoking in the stadium did constitute a public nuisance. The court ordered the city to abate the nuisance by prohibiting smoking and the sale of cigarettes within the facility. The city obtained a stay of

392

BYRD

the order, and the parties ultimately reached a settlement agreement that bans smoking in the stands but permits smoking in the concourse areas, restrooms, and private boxes. Finally, nonsmokers may be able to use a product liability theory in court actions against smoking. During the late 1950s and early 1960s, when the link between cigarette smoking and cancer was suspected but not proven, several cancer victim smokers brought product liability actions against cigarette companies. 75 All of the suits failed. A second wave of product liability claims was initiated in the 1980s, when, for the first time, a federal jury held a tobacco company partially responsible for the lung cancer death of a smoker in Cippolone v. Liggett Group, Inc. 16 The verdict was based on the company's violation of express warranties contained in its advertisements and the company's failure to adequately warn the public about the dangers of cigarettes. Although the case established that the tobacco companies are no longer immune to product liability suits, the verdict was limited in terms of the financial damages and the contained recognition that the plaintiff partially assumed the risks of her smoking. Unlike smokers, however, innocent bystanders do not "assume the risk." If a nonsmoking plaintiff can convince the court that tobacco products are legally defective and that they were a substantial factor in the cause of his or her injury, it is conceivable that the product liability theory would be successfully invoked by the passive smoking plaintiff. Even the more promising approaches to judicial restriction of smoking (i.e., safe workplace claims, public nuisance claims, and product liability claims) have significant drawbacks. First, any judicial action by a nonsmoker places the burden of challenging smoking on the nonsmoker. In addition, requiring the courts to consider the plight of nonsmokers on a case-by-case basis would result in too many lawsuits. To date, private sector initiatives seem to be a more effective tool for restricting smoking. Private Initiatives

Private-sector initiatives to restrict smoking-especially in the workplace-gained momentum in the 1980s. Surveys suggest that the diffusion of workplace smoking policies throughout the private sector is occurring in a nonuniform fashion. Smoking policies are slightly more prevalent in large companies than in small businesses; they are more common in the West and Northeast than in the North Central Region or the South; and they are more common in nonmanufacturing than in manufacturing industries. Four factors may explain this growth of workplace smoking policies. The first factor is public support. 67 In 1985, 79% of US adults (including 76% of smokers) favored restricting smoking at work to designated areas. 32 In two worksite surveys conducted by the author, more than 75% of the respondents thought that ETS was unhealthy for

ENVIRONMENTAL TOBACCO SMOKE

393

nonsmokers. However, the desire for further smoking restrictions was not based on concerns about major health problems. Instead, people were simply tired of the annoyance and irritation of ambient smoke. Only 50% of the people irritated by ETS were willing to ask smokers to extinguish their cigarettes. Thus, a worksite policy may obviate the need to ask someone to stop smoking, or, when necessary, the policy legitimizes the request. Second, recently enacted state and local workplace smoking legislation may greatly encourage adoption of policies. The prevalence of private-sector smoking policies is higher in regions with legislation in place. A third factor is the cost associated with smokers in the workplace. Lost productivity factors and higher health costs were estimated at $300 to $800 annually in a 1985 Office of Technology study; others place the average cost to employers per smoking worker at $4,611 per year, a figure reflecting work absences, medical costs, increased insurance costs, worker unproductivity, and maintenance fees. 49 A final factor explaining the growth of workplace smoking policies is growing scientific evidence supporting the view that smoking increases the risk of adverse health consequences for all employees. These factors, which have propelled the growth of workplace smoking policies, are not likely to abate, and the possibility that such policies will withstand challenge is high. Although it is conceivable that, in some situations involving collective bargaining, agreements will prevent employers from adopting no-smoking policies, employers in most cases might adopt such policies even without the impetus of state or local legislation or complaints of nonsmoking employees. In addition to growing numbers of workplace smoking restrictions, it is probable that greater numbers of employers will refuse to hire smokers in the first place; and this exclusion, too, will likely withstand challenge. Smokers are not a "protected group" against which employers may not discriminate. In selecting employees, employers always discriminate in some manner; it is unlikely that their decision not to hire a smoker would be illegal discrimination. Smokers' rights laws, however, are slowly emerging. New Jersey has passed a law and other states are considering legislation that protects currently employed smokers from job discrimination. The tobacco industry, with some success, is promoting this strategy to limit work site and public smoking restrictions. Smokers' rights laws might impact employers' duty to provide a safe working environment by protecting their employees from exposure to agents that can cause disease. SUMMARY

Adequate information is available linking ETS to several medical problems, including respiratory illnesses in children and lung cancer in adults; nonetheless, continuing investigation is necessary to clarify

394

BYRD

several issues. Reliable information needs to be gathered on the quantity and fate of ETS chemicals in ordinary indoor environments; improved surveys quantifying passive smoke exposure should be tested along with the use of biologic markers to quantify exposure-dose relationships in nonsmokers. To date, legislation and private initiatives have been the most promising of the various measures to protect nonsmokers from ETS. While nonsmokers' judicial action has had variable success, it places the burden of challenging smoking on the nonsmoker, and it entails piecemeal, case-by-case resolution. On the other hand, legislation and private policies relieve the nonsmokers' burden to initiate the challenge, and they protect greater numbers of nonsmokers. Furthermore, legislation and policies may have a great number of direct and indirect effects. In the short term, legislation and policies that are adequately implemented and enforced alter the behavior of smokers in areas where smoking is prohibited and should result in a reduced concentration of tobacco smoke in those areas. In the long term, policies and legislation that restrict smoking in public places and the workplace help to reinforce nonsmoking as the normative behavior in society. Smoking restrictions increase public awareness and acceptance of health risks of tobacco smoke. The combination of altered social norms and reduced opportunities to smoke may encourage smokers to quit and nonsmokers, especially adolescents, not to start. ACKNOWLEDGMENT I thank David 1. Schiedermayer, MD, and Robyn Shapiro, JD, for their assistance in preparing this article.

References 1. 2. 3. 4.

5. 6. 7. 8. 9. 10. 11. 12. 13.

145 N.J. Super. 516, 368 A 2d 408 (App. Div. 1976) 15 U.S.c., Sec. 1333, 1976 15 U.s.c., Sec. 1335, 1976 29 U.S.c., Sec. 701-796i (1976 and Supp. 1981). This statute prohibits discrimination against handicapped persons by any organization that receives federal funds. A "handicapped individual" is a person who has a physical impairment which substantially limits one or more major life activities. Id., Sec 706(7) (B) 32 C.F.R., Sec. 203, 1979 549 F. Supp. at 87 549 F. Supp. 85-88 (W.D. Wash. 1982) 598 F. 2d 310 (D.C. Cir.) cert. denied 444 U.S. 926 (1979) 643SW 2d 10 (Mo App 1982) Akiba S, Kato H, Brot WJ: Passive smoking and lung cancer among Japanese women. Cancer Res 46:4804, 1986 Aronow W: Effect of passive smoking on angina pectoris. N Engl J Med 299:21, 1978 ASHRAE Standard 62-81: Ventilation for acceptable indoor air quality. Atlanta, ASHRAE, 1981, P 19 Berkey CS, Ware JH, Dockery DW, et al: Indoor air pollution and pulmonary function growth in pre-adolescent children. Am J Epidemiol 123:250, 1986

ENVIRONMENTAL TOBACCO SMOKE

395

14. Bonham GS, Wilson RA: Children's health in families with cigarette smokers. Am J Public Health 7l:290, 1981 15. Buffler PA, Pickle LW, Mason TJ, et al: The causes of lung cancer in Texas. In Mizeu M, Correa P (eds): Lung Cancer: Causes and Prevention. New York, Verlag-Chemie International, 1984 16. Cippolone v. Liggett Group, Inc., 693 F. Supp. 208 (D.N.J., 1988) 17. Chan Wc, Furry se: Lung cancer in nonsmokers in Hong Kong. In Gunderson E (ed): Cancer Campaign, Vo!. 6. Cancer Epidemiology. Stuttgart, Gustav Fischer Verlag, 1982 18. Charlton A: Children's coughs related to parental smoking. Br Med J 288:1647, 1984 19. Chilmoncyk BA, Knight GJ, Pulomaki GE, et al: Environmental tobacco smoke during infancy. Am J Public Health 80:1205, 1990 20. Colley JRT, Holland WW, Corkhill RT: Incidence of passive smoking and parental phlegm on pneumonia and bronchitis in early childhood. Lancet 2:1031, 1974 21. Committee on Passive Smoking of the National Research Council: The physiochemical nature of side stream smoke and environmental tobacco smoke. Measuring exposures and assessing health effects. Washington, DC, National Academy Press, 1986 22. Committee on Passive Smoking of the National Research Council: Exposure to environmental tobacco smoke and lung cancer. In Environmental Tobacco Smoke. Measuring Exposures and Assessing Health Effects. Washington, DC, National Academy Press, 1986, p 223 23. Correa P, Pickle LW, Fontham E, et al: Passive smoking and lung cancer. Lancet 2:595, 1983 24. Coultas DB, Peake GT, Samet JM: Questionnaire assessment of lifetime and recent exposure to environmental tobacco smoke. Am J Epidemiol 130:338, 1989 25. Cummings KM, Markello SJ, Mahoney MC, et al: Measurement of lifetime exposure to passive smoke. Am J Epidemiol 130:122, 1989 26. Dahms TE, Bolin JF, Slavin RG: Passive smoking: Effects on bronchial asthma. Chest 80:530, 1981 27. Dalager NA, Pickle LW, Mason TJ, et al: The relation of passive smoking to lung cancer. Cancer Res 46:4804, 1986 28. Federal Employees for Nonsmokers' Rights v. United States, 598 F.2d 310 (D.e. Cir.), eert. denied, 444 U.S. 926 (1979) 29. Fergusson OM, Horwood LJ, Shannon FT, et al: Parental smoking and lower respiratory illness in the first three years of life. J Epidemiol Commun Health 35:180, 1981 30. Feyerabend C, Higenbottam T, Russell MAH: Nicotine concentrations in urine and saliva of smokers and nonsmokers. Br Med J 284:1002, 1982 31. Fletcher RH, Fletcher SW, Wagner GH: In Clinical Epidemiology. Baltimore, Williams and Wilkens, 1982, p 185 32. Gallop Organization: "Survey of attitudes toward smoking," survey conducted for the American Lung Association. Prince ton, Gallop Organization, July 1985 33. Garfinkel L, Auerbach 0, Joubert L: Involuntary smoking and lung cancer: A casecontrol study. J Natl Cancer Inst 75:463, 1985 34. Garfinkel L: Passive smoking and cancer-American experience. Prev Med 13:691, 1984 35. Garfinkel L: Time trends in lung cancer mortality among nonsmokers and a note on passive smoking. J Natl Cancer Inst 66:1061, 1981 36. Gasper v. Louisiana Stadium and Exposition District, 577 F 2d 897 (5th Cir. 1978), eert. denied, 439 U.S. 1073 (1979). See also In Re Agent Orange Prod. Liab. Litigation, 475 F. Supp. 928 (E.D.N.Y. 1979); Pinkney v. Ohio Environmental Protection Agency, 375 F. Supp. 305 (N.D. Ohio 1974); Tanner v. Armeo Steel Corp., 340 F. Supp. 532 (S.D. Tex. 1972); Rensell v. State of Oklahoma, 716 F. 2d 1350 (10th Cir. 1983) 37. General Services Administration: Federal property management regulations amendment D. Washington, DC, December 4, 1986 38. Gillis CR, Hole DJ, Hawthorne VM, et al: The effect of environmental tobacco smoke in two urban communities in the west of Scotland. Eur J Respir Dis 133(Suppl):121, 1984

396

BYRD

39. Glantz SA, Parmley WW: Passive smoking and heart disease. Circulation 83:1, 1991 40. Gortmaker SL, Walker DK, Jacobs FH, et al: Parental smoking and the risk of childhood asthma. Am J Public Health 72:574, 1982

41. Greenberg RA, Haley NJ, Etzel RA, et al: Measuring the exposure of infants to tobacco smoke. Nicotine and cotinine in urine and saliva. N Engl J Med 310:1075, 1984 42. Harlap S, Davies AM: Infant admissions to hospital and maternal smoking. Lancet 1:529, 1974 43. Harris JE, DuMouchel WH: Letter to the editor. Br Med J 283:915, 1981 44. Hirayama T: Nonsmoking wives of heavy smokers have a higher risk of lung cancer: A study from Japan. Br Med J 282:183, 1981 45. Hirayama T: Cancer mortality in nonsmoking women with smoking husbands in a large-scale cohort study in Japan. Prev Med 13:680, 1984 46. Hoffman D, Haley NJ, Brunneman KD, et al: Cigarette side stream smoke: Formation, analysis and model studies on the uptake by nonsmokers. Presented at the U.S.Japan meeting on new etiology of lung cancer, Honolulu, March 21-23, 1983 47. Humble CG, Sa met JM, Patyhak DR: Marriage to a smoker and lung cancer risk. Am J Public Health 77:598, 1987 48. Janerich DT, Thompson WD, Varela LR, et al: Lung cancer and exposure to tobacco smoke in the household. N Engl J Med 223:632, 1990 49. Journal of Urban and Contemporary Law 211, 231, n. 124 50. Kabat Ge, Wynder EL: Lung cancer in nonsmokers. Cancer 53:1214, 1984 51. Kauffman F, Tessier J-F, Oriol P: Adult passive smoking in the home environment: A risk factor for chronic air flow limitation. Am J Epidemiol 117:269, 1983 52. Klus H, Kuhn H: Distribution of various tobacco smoke components among mainstream smoke and side stream smoke: A survey. Beitr Tabakforsch Int 11:229, 1982 53. Knoth A, Bohn H, Schmidt F: Passive smoking as a causal factor of bronchial carcinoma in female nonsmokers. Med Klin 78:66, 1983 54. Koo Le, Ho JH-e, Fraumeni JF, et al: Measurements of passive smoking and estimates of risk for lung cancer among nonsmoking Chinese females. Fourth World Conference on Lung Cancer, Toronto, Canada, August 25-30, 1985 55. Koo Le, Ho JH-e, Saw D: Active and passive smoking among female lung cancer patients and controls in Hong Kong. J Exp Clin Cancer Res 4:367, 1983 56. Kraemer MJ, Richardson MA, Weiss NS, et al: Risk factors for persistent middle-ear effusions: Otitis media, catarrh, cigarette smoke exposure, and atopy. JAMA 249:1022, 1983 57. Lee DN, Chamberlain J, Alderson MR: Relationship of passive smoking to risk of lung cancer and other smoking associated diseases. Br J Cancer 54:97, 1986 58. MacIure M, Katz RB, Bryant MS, et al: Elevated blood levels of carcinogens in passive smokers. Am J Public Health 79:1381, 1989 59. Mantel N: Letter to the editor. Br Med J 283:914, 1981 60. Matsukura S, Taminato T, Kitano N, et al: Effects of environmental tobacco smoke on urinary cotinine excretion in nonsmokers. Evidence for passive smoking. N Engl J Med 311:828, 1984 61. Mattson ME, Boyd G, Byar D, et al: Passive smoking on commercial airline flights. JAMA 261:867, 1989 62. Miller GH: Cancer, passive smoking and nonemployed and employed wives. West J Med 140:632, 1984 63. National Institutes of Health: Teenage smoking: National patterns of cigarette smoking, ages 12-18. Washington, De, 1979 64. No 75-131 479 (Cir et. Oakland County, Mich, Dec. 17, 1975) 65. Ohkubo C: Some acute cardiopulmonary effects of mainstream and side stream smoke in man. Prev Med 11:173, 1982 66. Pershagen 0, Hrubec Z, Svensson C: Passive smoking and lung "Cancer in Swedish women. Am J Epidemiol 125:17, 1987 67. Roper Organization: HA study of public attitudes toward cigarette smoking and the tobacco industry in 1978." New York, Roper Organization, May 1978 68. San Antonio Independent School Dist. v. Rodriquez, 411 U.5. 33-34 (1973)

ENVIRONMENTAL TOBACCO SMOKE

397

69. Sandler DP, Everson RB, Wilcox RJ: Passive smoking in adulthood and cancer risk. Am J Epidemiol 121:37, 1985 70. See comment, "The Legal Conflict Between Smokers and Nonsmokers: The Majestic Vice Versus the Right to Clean Air," 45 moo L. Rev., 444, 452, n.68 (1980) 71. See Comment, "The Nonsmoker in Public: A Review and Analysis of Nonsmokers' Rights," 7 San Fran. V.L. Rev. 141, 166 (1979) 72. See e.g., Ely V. Velde, 451 F. 2d 1130 (4th Cir. 1971); Gasper V. Louisiana Stadium and Exposition Post, 577 F. 2d 897 (5th Cir. 1978, cert. denied, 439 U.S. 1073 (1979); Federal Employees for Nonsmokers Rights V. United States, 598 F. 2d 310 (D.C Cir.), cert. denied, 100 S. Ct. 265 (1979); In Re Agent Orange Prod. Liab. Litigation, 475 F Supp. 928 (E.D.N.Y. 1979); Pinkney V. Ohio Environmental Protection Agency, 375 F. Supp. 305 (N.D. Ohio 1974); GASP V. Mecklenburg County, 42 N.C App. 220, 256 S.E. 2d 477 (1979) 73. See Stanley V. Georgia, 394 U.S. 557, 564 (1969); Lamont V. Postmaster Gen., 381 U.S. 301, 307-308 (1965) 74. See, e.g., Environmental Defense Fund v. Hoerner Waldorf Corp., lE, R. 1640, 1641, 3 E.L.R. 20, 794 (D. Mont. 1970) 75. See W. Prosser, The Law of Torts 660 nn82 and 83 (4th ed. 1971) 76. See, e.g., GASP V. Mecklenburg County, 42 N.C App. 220, 256 S.E. 2d 477 (1979); Gasper V. Louisiana Stadium and Exposition Post, 577 F. 2d 897 (5th Cir. 1978), cert. denied 439 U.S. 1073 (1979) 77. Shephard RI, Collins R, Silverman F: "Passive" exposure of asthmatic subjects to cigarette smoke. Environ Res 20:392, 1979 78. Shimp D: How to protect your health at work. Salem, NI, Environmental Improvement Associates, 1976, p 61 79. Sobal R: They Satisfy: The Cigarette in American Life. New York, Anchor Press/ Doubleday, 1978 80. Speer F: Tobacco and the nonsmoker. A study of subjective symptoms. Arch Environ Health 16:443, 1986 81. Speizer FE, Tager IB: Epidemiology of chronic mucus hypersecretion and obstructive airways disease. Epidemiol Rev 1:124, 1979 82. Sterling TD, Weinkam JJ: Letter to the editor. N Engl J Med 324:412, 1991 83. Sterling TD: Letter to the editor. Br Med J 282:1156, 1981 84. Surgeon General's Report: The Health Consequences of Involuntary Smoking. Washington, DC, Government Printing Office, No (CDC) 87-8309, 1987 85. Surrey S, Lee PN: Letter to the editor. N Engl J Med 324:412, 1991 86. Tager IB, Weiss ST, Munoz A, et al: Longitudinal study of the effects of maternal smoking on pulmonary function in children. N Engl J Med 309:699, 1983 87. Tashkin DP, Clark VA, Simmons M, et al: The UCLA population studies of chronic obstructive pulmonary disease. VII. Relationship between parental smoking and children's lung function. Am Rev Respir Dis 129:891, 1984 88. Tobacco-Free America: State smoking restrictions. Washington, DC, 1991 89. Tri-Agency Tobacco Free Project: State legislative actions on clean indoor air and cigarette excise taxes. Washington, DC, 1989 90. Trichopoulos D, Kalandidi A, Spanos L, et al: Lung cancer and passive smoking. Int J Cancer 27: 1, 1981 91. US Department of Health and Human Services: The Health Consequences of Smoking: Cancer. A Report of the Surgeon General. Washington, DC, Government Printing Office, No (PHS) 79-SS071, 1982 92. US Department of Health and Human Services: The Health Consequences of Involuntary Smoking. A Report of the Surgeon General. Washington, DC, Government Printing Office, No (CDC) 87-8309, 1987 93. VA, Department of Medicine and Surgery: Smoking policy in all VA health care facilities. Circular #10-86-30, Washington, DC, March 5, 1986 94. Vedal S, Schenker MB, Samet JM, et al: Risk factors for childhood respiratory disease: Analysis of pulmonary function. Am Rev Respir Dis 130:187, 1984 95. Warner KE: State legislation on smoking and health: A comparison of two policies. Policy Sciences 13:139, 1981 96. Weber A: Annoyance and irritation by passive smoking. Prev Med 13:618, 1984 97. Wells A: An estimate of adult mortality in the United States from passive smoking. Environ Int 14:249, 1988

398

BYRD

98. White JR, Froeb HF: Small-airways dysfunction in nonsmokers chronically exposed to tobacco smoke. N Engl J Med 302:720, 1980 99. Willett WC: Vitamin A and lung cancer. Nutr Rev 48:201, 1990 100. Wu AH, Henderson BE, Pike MC, et al: Smoking and other risk factors for lung cancer in women. J Natl Cancer Inst 74:747, 1985 101. Young S, Le Souef PN, Geehhoed GC, et al: The influence of family history on airway responsiveness in early infancy. N Engl J Med 324:1168, 1991

Address reprint requests to James C. Byrd, MD, MPH Associate Chief of Staff Ambulatory Care Zablocki VA Medical Center Milwaukee, WI 53295