Lesson 1, Volume 15—Noncancer Respiratory Health Effects of Environmental Tobacco Smoke in Adults

By Mark D. Eisner, MD, MPH

Objectives

1. To describe the prevalence of environmental tobacco smoke (ETS) exposure among adults with and without asthma.
2. To understand the link between ETS exposure and acute upper respiratory tract irritation in adults.
3. To characterize the association between ETS exposure and new-onset adult asthma.
4. To delineate the relationship between ETS exposure and asthma-like respiratory symptoms.
5. To elucidate the association between ETS and exacerbation of adult asthma.

Keywords

asthma; asthma epidemiology; environmental tobacco smoke; tobacco smoke pollution

Abbreviation

ETS = environmental tobacco smoke

Environmental tobacco smoke (ETS) exposure is widespread, affecting the majority of US adults.¹ A complex mixture of more than 4,000 chemical compounds, ETS contains potent respiratory irritants such as sulfur dioxide, ammonia, formaldehyde, and acrolein.² As a result, ETS exposure has been associated with irritant-related respiratory tract disease in adults, including lower respiratory symptoms and exacerbation of asthma.^2-5

Asthma is a common chronic health condition, affecting 5% of the US adult population.⁶ During the past decade, the prevalence of adult asthma has increased > 50%.⁶ The mortality from asthma has approximately doubled. Understanding the factors contributing to asthma morbidity and mortality has important clinical and public health implications. This lesson evaluates the evidence that ETS exposure (1) is a risk factor for new-onset asthma among adults and (2) exacerbates pre-existing adult asthma, resulting in greater respiratory symptoms and health care utilization.

Prevalence of ETS Exposure

A significant proportion of US adults report exposure to ETS, ranging from 37 to 63%.² The third National Health and Nutrition Examination Survey (NHANES), based on a representative sample of the US population, estimated that 37% of nonsmoking adults are regularly exposed to ETS.¹ The population-based National Health Interview Survey from 1991 found a similar prevalence of ETS exposure among adults (39%).⁷ Using measurements of serum cotinine, the major metabolite of nicotine, the NHANES investigators found that 88% of adults had elevated levels consistent with at least some ETS exposure.

Although they might be expected to avoid ETS, many US adults with asthma experience exposure. Among adult health maintenance organization members with asthma, 38% indicated regular exposure.⁵ In a population-based study from Canada, 42% of nonsmoking children and adults with asthma reported ETS exposure during the previous 24 h, compared with 32% of the general population.⁸ In sum, adults with asthma appear to experience significant ETS exposure.

Acute Upper Respiratory Tract and Mucous Membrane Irritation

ETS constituents, especially vapor phase elements, result in acute noxious stimulation of the upper respiratory tract and corneal mucous membranes.² The water-soluble compounds, such as ammonia, are more likely to be deposited in the upper respiratory tract and cause irritation. Sensory irritation symptoms result, which include the subjective experience of stinging, tingling, or burning involving the mucous membranes.²

ETS exposure most frequently results in eye irritation, affecting the richly innervated cornea.² The majority of 77 young, healthy, nonsmoking volunteers (81%) reported a history of eye irritation after ETS exposure.⁹ Tearing, itching, redness, and excessive blinking were commonly reported symptoms. Nasal irritation, including congestion, rhinorrhea, and sneezing, was the next most commonly reported upper respiratory symptom of ETS exposure. In this study by Bascom et al,⁹ the authors experimentally exposed the same subjects to sidestream tobacco smoke in a climate-controlled chamber. Persons with a reported history of ETS-related upper respiratory symptoms experienced significant increases in nasal airway resistance measured by rhinomanometry. On the other hand, persons without any history of ETS sensitivity had no change in nasal resistance. The ETS-induced elevation in nasal resistance and resultant nasal symptoms appear to occur by a direct irritative, nonallergic mechanism.

Consistent with these experimental findings, workplace ETS exposure appears to cause sensory irritation symptoms. Data from the National Health Interview Survey Occupational Health Supplement indicate that the majority (59%) of nonsmoking persons whose workplaces permit smoking experience discomfort from ETS exposure.¹⁰ Moreover, 16% reported great discomfort. In a study of 137 Canadian office workers, a significant proportion reported eye (44%), nose (61%), and throat irritation (34%) after workplace passive smoke exposure.¹¹ Finally, airline passengers and attendants who were exposed to high levels of air nicotine experienced substantial nasal and eye irritation symptoms.¹² Given the high prevalence of sensory irritation symptoms in ETS-exposed individuals, passive smoking likely results in substantial upper respiratory morbidity.

ETS and New-Onset Adult Asthma

Extensive data support a causal association between ETS exposure and induction of asthma in children.² In a recent meta-analysis of 37 epidemiologic studies, ETS exposure was associated with a greater risk of developing childhood asthma (odds ratio, 1.44; 95% confidence interval, 1.27 to 1.64).² The relationship between ETS exposure and adult-onset asthma has received less research attention.¹³

The Swiss Study on Air Pollution and Lung Diseases in Adults (SAPALDIA) focused on a random sample of adult never smokers aged 18 to 60 years residing in Switzerland (Table 1).¹⁴ In a cross-sectional analysis, investigators observed an association between self-reported ETS exposure during the previous 12 months and a 40% greater risk of self-reported physician diagnosis of asthma. Statistically controlling for age, sex, atopy, education, maternal and paternal smoking during childhood, and parental asthma history had no appreciable impact on this relationship. Furthermore, the investigators observed statistically significant exposure-response trends for hours per day of ETS exposure, number of smokers, and years of exposure.

Hu and colleagues¹⁶ evaluated a cohort of 1,469 seventh-grade students 7 years after participating in a school-based smoking prevention program in southern California. Exposure to parental ETS at baseline was associated with an increased risk of reporting asthma at the 7-year follow-up. Compared with no maternal smoking or light smoking at baseline (< 1/2 pack/d), increased maternal smoking was associated with an increased risk of reporting asthma after controlling for sex, race, and educational attainment. Similarly, increased paternal smoking was related to a greater risk of asthma.

A prospective cohort study of 3,914 adult nonsmoking Seventh-Day Adventists living in California evaluated the relationship between ETS exposure and the incidence of self-reported physician-diagnosed asthma during a 15-year period.^17,18 The investigators reported the 10-year¹⁷ and 15-year cohort follow-up.¹⁸ The cumulative incidence of asthma at 10 years was 21/1,000 for men and 22/1,000 for women. At 15 years, the cumulative incidences were 32/1,000 and 43/1,000, respectively. Duration of working with a smoker was associated with a 50% increased risk of developing asthma for every 10 years working with a smoker. At the 15-year follow-up, duration of working with a smoker was associated with an increased risk of incident asthma for women only. In contrast, there was no reported relationship between duration of residence with a smoker and risk of asthma. In sum, these studies support a causal relationship between ETS exposure and new-onset adult asthma.

ETS and "Asthma-Like" Respiratory Symptoms

Currently, there is no widely accepted "gold standard" for defining asthma. Although self-reported physician-diagnosed asthma is commonly used in survey research, this definition may not detect some individuals with asthma.^19,20 Subject-reported respiratory symptoms, such as wheezing, dyspnea, and cough, may have a greater sensitivity for identifying adults with asthma (albeit a lower specificity).²⁰

Several investigators have examined whether ETS exposure is related to developing adult-onset wheezing and other respiratory symptoms that could reflect asthma (Table 2). In the SAPALDIA study, ETS exposure during the previous 12 months was cross-sectionally associated with a greater risk of wheezing, dyspnea on exertion, and chronic bronchitis symptoms of cough or phlegm production.¹⁴ ETS exposure, then, appeared to be related to both asthma and other less specific lower respiratory tract symptoms.

In an analysis of 43,732 adults completing the Health Promotion and Disease Prevention supplement of the 1991 National Health Interview Survey, Mannino and colleagues⁷ examined the cross-sectional association between self-reported ETS exposure at home or work and the risk of "chronic respiratory disease exacerbation." This study outcome was defined as activity limitation or a physician visit because of asthma, chronic bronchitis, emphysema, or chronic sinusitis. Among never smokers, ETS exposure was associated with an increased risk of chronic respiratory disease exacerbation after controlling for age, socioeconomic status, sex, race, and region of the country. In four other population-based cross-sectional studies conducted in the west of Scotland,^21,22 United States,^23,24 France,²³ and Singapore,²⁵ household ETS exposure was also associated with respiratory symptoms.

Using a case-crossover design, we studied the effects of California State Assembly Bill 13, which prohibited tobacco smoking in bars and taverns, on the respiratory health of bartenders.²⁶ Based on a random sample of all bars and taverns in San Francisco, we interviewed and performed spirometry on 53 bartenders before and after the smoking ban (median length of follow-up, 56 days). At baseline, all 53 subjects reported ETS exposure while working in bars or taverns during the 7 days prior to interview. After the prohibition of smoking went into effect, self-reported workplace ETS exposure sharply declined from a median of 28 to 2 h/wk. Thirty-nine of the 53 bartenders (74%) reported at least one respiratory symptom at baseline (including cough, dyspnea, and wheezing), whereas only 17 (32%) were still symptomatic at follow-up. Of the 39 bartenders reporting baseline symptoms, 23 subjects (59%) no longer indicated any respiratory symptoms after the prohibition of smoking. In particular, 70% of the 17 bartenders reporting baseline wheezing noted resolution after workplace smoking prohibition. In stratified analyses by current smoking status, we observed similar symptom reduction in both current smokers and nonsmokers. After prohibition of workplace smoking, we also observed improvement in mean FVC (0.189 L) and mean FEV₁ (0.039 L). Complete cessation of workplace ETS exposure was associated with an even greater pulmonary function improvement.

In a prospective cohort study, investigators studied the relationship between self-reported ETS exposure and the incidence of respiratory symptoms among 117 young adult never smokers (15 to 40 years).²⁷ ETS-exposed subjects had a higher likelihood of developing wheezing, dyspnea, and cough. Moreover, a total ETS exposure index based on duration and intensity of exposure was associated with a greater risk of developing dyspnea or any respiratory symptom. There was no statistical association between ETS exposure index and risk of wheezing, cough, or phlegm.

Another prospective cohort study examined 100 student nurses, who completed daily symptom diaries for 3 years.²⁸ After controlling for personal smoking, living with a roommate who smoked was associated with a 41% increased risk of developing phlegm production. This study was limited by failure to assess nonresidential ETS exposure and other respiratory symptoms.

In a prospective cohort study, 80 never-smoking adult participants in a university-based physical fitness program were followed for 9 months.²⁹ Subjects who reported residential ETS exposure or baseline respiratory conditions were excluded. Compared with unexposed subjects, a greater proportion of persons reporting ongoing workplace ETS exposure (for 12 months) indicated cough (70 vs 25%), phlegm production (68 vs 20%), or dyspnea (68 vs 15%). Unfortunately, the exclusion of 50% of fitness program participants (for a long list of criteria) may have biased these results in an unpredictable fashion.

A population-based UK cohort study followed 18,559 children born during a single week in March 1958 through age 33, with 31% complete follow-up.³⁰ The study examined the relationship between household ETS exposure and the subsequent incidence of wheezing after controlling for demographic, socioeconomic, and personal smoking variables. At both age 7 and 33 years, maternal smoking during pregnancy was associated with an increased risk of developing wheezing illness. At age 33, maternal smoking at subject age 16 was associated with an increased incidence of wheezing. Overall, these studies support a causal relationship between ETS exposure and the development of lower respiratory tract symptoms.

ETS Exposure and Exacerbation of Pre-existing Adult Asthma

Among children, ETS exposure has been strongly linked with exacerbation of pre-existing asthma.^2,31 Although adults with asthma commonly report ETS exposure as a trigger for asthma exacerbation, the effect of exposure on adult asthma status has received less research.^32,33 In a cross-sectional study, investigators examined the impact of self-reported ETS exposure on 200 never-smoking adults with asthma attending a university-based chest clinic in India (Table 3).⁴ Compared with unexposed patients, adult asthmatics reporting ETS exposure indicated greater reliance on daily bronchodilators (66 vs 56%) and intermittent corticosteroid use (56 vs 42%). Although there was no relationship with hospitalization, ETS-exposed subjects had a higher mean number of emergency department visits for asthma during the previous year (0.82 vs 0.6 visits/person) and more work absence (3.6 vs 3.0 weeks/person). ETS exposure was also associated with worse pulmonary function, including lower FEV₁ (68.7 vs 80.8% of predicted), FEV₁/FVC (63.5 vs 78.4%), and the average forced expiratory flow in the mid portion of the FVC (FEF_25-75%; 54.3 vs 75.7%).

Investigators studied the cross-sectional impact of self-reported regular ETS exposure at work among 2,065 adult participants (20 to 44 years) in the Swedish component of the population-based European Community Respiratory Health Survey.³⁴ In multivariate analysis controlling for age, sex, personal smoking, and work characteristics, regular workplace ETS exposure was associated with an 80% greater risk of respiratory-related work disability, defined as self-reported change in job or leaving work due to affected breathing. Moreover, workplace ETS exposure was associated with a greater risk of work-associated symptomatic asthma, defined as self-reported asthma, airway hyperresponsiveness, and work-related chest tightness or wheezing. Because this analysis focused on workplace factors, home and other sources of ETS exposure were not examined.

In a prospective panel study of 164 adult nonsmokers with asthma, Ostro and colleagues³ examined the impact of ETS exposure on asthma status during a 3-month period. Subjects completed daily diaries including ETS exposure (home and work) and respiratory symptoms. During longitudinal follow-up, ETS exposure was associated with subsequent greater risks of cough, dyspnea, nocturnal asthma symptoms, and restricted activity. In this longitudinal panel study, the close temporal link between ETS exposure and outcome supports a causal relationship between exposure and asthma exacerbation.

A cohort study of 619 adult health maintenance organization members with asthma examined the association between ETS exposure and health outcomes.⁵ The prevalence of self-reported regular ETS exposure was 38%, and a small proportion of subjects (11%) indicated current personal cigarette smoking. Regular ETS exposure was associated with worse asthma-specific quality of life and generic health status (physical functioning and general health domains on the SF-36 questionnaire). During longitudinal follow-up, ETS exposure was associated with a greater incidence of hospital-based episodes of asthma care (28 events/100 vs 10 events/100 person-years). After adjusting for age, sex, and asthma severity, ETS exposure remained associated with a two-fold greater risk of hospital-based care. Excluding current smokers from analysis did not appreciably affect these results. Taken together, these studies support a negative impact of ETS exposure on adults with asthma.

ETS Exposure and Pulmonary Function

Because asthma is characterized by reversible airway obstruction, the effect of ETS exposure on pulmonary function in the adult general population has relevance for asthma. In children, more than 30 studies have linked domestic ETS exposure with decreased development of lung function.² Among adults, most cross-sectional analyses support the association between self-reported ETS exposure and a decrement in pulmonary function.^{21,24,25,35-37} In two other cross-sectional studies, there was no apparent relationship.^23,38 The few prospective investigations have provided mixed results, with some studies demonstrating an association between ETS exposure and decreased pulmonary function over time,^39-41 and others finding no association.⁴² Finally, a study of 26 Canadian bar workers found significant acute decrements in lung function after a work shift.⁴³ Although there is significant heterogeneity among study results, the cross-sectional and longitudinal data together support a small deleterious effect of ETS on pulmonary function.

Controlled Human Exposure Studies

Controlled experimental studies support the biological plausibility of ETS-related asthma exacerbation. In chamber exposure experiments, investigators have studied the impact of acute ETS exposure on asthmatic subjects. Dahms and colleagues⁴⁴ demonstrated a significant decrement (approximately 20%) in FEV₁ and FVC after ETS exposure for 1 h. Similarly, 5 of 10 subjects with baseline airway hyperresponsiveness experienced 10% decrement in FEV₁ after exposure.⁴⁵ Another study found that one third of asthmatic subjects experienced a substantial decline in FEV₁ after chamber exposure (> 20%).⁴⁶ The same group demonstrated that pretreatment with bronchodilators prevented the acute decline in FEV₁ in previously reactive subjects.⁴⁷ In 10 adult subjects with asthma, experimental ETS exposure for 3 h resulted in reduced FEV₁ (5.9%) and FVC (9.1%).⁴⁸ Other studies, however, have found no effect of acute chamber ETS exposure on lung function in asthmatic subjects.^49,50 Interpretation of these controlled exposure studies is limited by small sample size, variable subject inclusion criteria, and variation in chamber exposure methodology. Nonetheless, these experimental studies support a modest adverse effect of acute ETS exposure on pulmonary function.

Conclusions

Scientific studies consistently link ETS exposure with adult asthma morbidity. In samples drawn from different populations, ranging from clinical to population-based samples, investigators have observed the association between ETS exposure and new-onset asthma and asthma exacerbation. Similarly, the relationship between ETS exposure and asthma morbidity has been observed in cross-sectional, case-control, and cohort study designs. Exposure in different environments, such as home and work, has also been linked with asthma. ETS exposure has been associated with new-onset asthma, whether defined as self-reported physician-diagnosed asthma or clinical asthma diagnosis. Furthermore, ETS exposure is associated with related health outcomes, including chronic respiratory disease and respiratory symptoms such as dyspnea, cough, and wheezing. In persons with pre-existing asthma, ETS exposure appears to affect a variety of health outcomes, including disease severity, quality of life, and health care utilization. Taken together, the available scientific literature supports a causal association between ETS exposure and adult asthma onset.

During the past decade, the US morbidity and mortality from asthma have increased substantially. The evidence indicates that adults who are exposed to ETS have a greater risk of developing asthma. Among adults with pre-existing asthma, ETS appears causally related to adverse health outcomes. Based on these and other health consequences, public policies should prohibit smoking in the workplace and other public locations. Prohibition of public smoking would be expected to have beneficial effects on adult respiratory health.

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