Cigarette smoking and the use of other tobacco products constitutes the single most devastating
preventable cause of death in many market economies (Quick et al., 1997). A large body of epidemiological, clinical and pathological studies relates cigarette smoking to the development of cardiovascular heart disease and other chronic diseases, including emphysema, chronic bronchitis and non-fatal strokes. Moreover, a considerable body of research has demonstrated the adverse health consequences of passive smoking, the involuntary exposure of non-smokers to tobacco smoke from smokers in confined environments. This research has led many countries to regulate smoking in public places (Quick et al., 1997). As is the case with the other behavioral outcomes considered here, smoking behavior is multifactorial in its etiology, and there is zvidence pointing to its genetic origins. Twin studies have demonstrated that genetic factors contribute to the initiation of smoking and influence the intensity of smoking cigarettes (number of cigarettes smoked per day; see Pomerleau & Kordia, 1999). A meta-analysis of the data from five studies, each involving more that 1000 twin pairs, found an estimated 60% of the propensity to smoke may be explained by genetic factors (Heath&Madden, 1995). Cigarette smokers are over-represented in many disadvantaged groups, including those with psychiatric and behavioral disorders (Parrott, 2000). Still, there is evidence that environmental and job-related stress may account for a significant proportion of the variance of smoking behavior. Consequently, interest in the pathway leading from stress, and stress at work, to smoking behavior is growing.
Stress and associated emotional responses, including anxiety and irritability, are attenuated by smoking. These effects have been shown to be short-lived (Parrott, 1995). Mood and affective state impairments tend to occur between cigarettes in a repetitive cycle. This cycle provides a clear rationale for the addictive use of cigarettes (Parrott, 1995). Smokers, therefore, obtain only short relief from adverse states of anxiety and irritability that follow the experience of stress. There is evidence from smoking abstaining studies that nicotinewithdrawal symptoms are worse under high environmental stress than under low environmental stress, while post-cigarette relief was also correspondingly greater (Parrott, 2000).
In empirical research, stress is often found to predict smoking behavior while interacting with other predictors, like lack of social support. In a review of the research on smoking behavior among nurses, Adriaanse et al. (1991) found that excessive smoking among both female and male nurses was explained by work stress, lack of social support, and unmet expectations that characterize nurses’ professional socialization. Nurses’ smoking is considered a public health problem since they often act as role models to patients and their families. In several studies, smokers who express high motivation to smoke have reported above-average stress that they had experienced before the smoking, rather than belowaverage stress after smoking (Parrott, 1995). Consequently, stress management and anxiety reduction programs at the workplace have the potential to influence motivation to smoke. Workplace-based smoking cessation programs do bring to the fore, however, the conflict between health and performance. Among aviators, as an example, smoking is a health hazard in the cockpit. Pilots who are required to abstain from smoking during and before flights may suffer cockpit performance decrements (Sommese & Patterson, 1995).
Yet another facet of the complex relationship between stress and cigarette smoking was described by Parrott (1999), who proposed that the evidence on this relationship might be reinterpreted to suggest that smoking actually causes stress. Parrott (1999) pointed out that regular smokers are more stressed than their non-smoking counterparts and that smokers experience an overall reduction in stress when they quit smoking. Another theory holds that
smoking may redistribute stress by modulating moods (Piasecki & Baker, 2000).
Work organizations contribute to and may inhibit (or induce) smoking behavior by three basic processes documented in the research literature. First, work organizations may develop organizational norms with respect to smoking on the job, including the local official definition of permissible smoking and the mechanisms of its control established by management. Second, stressful working conditions, like sustained overload or machine-paced jobs characterized by lack of control, may induce heavy smoking as a coping strategy to alleviate the stressful job conditions. Third, work organizations may explicitly or implicitly encourage the development of occupationally based smoking subcultures. In a survey of 12 000 professional people in 14 occupational categories, Russek (1965) found significant differences in the prevalence of smoking in high-stress occupations as compared with low-stress occupations.
preventable cause of death in many market economies (Quick et al., 1997). A large body of epidemiological, clinical and pathological studies relates cigarette smoking to the development of cardiovascular heart disease and other chronic diseases, including emphysema, chronic bronchitis and non-fatal strokes. Moreover, a considerable body of research has demonstrated the adverse health consequences of passive smoking, the involuntary exposure of non-smokers to tobacco smoke from smokers in confined environments. This research has led many countries to regulate smoking in public places (Quick et al., 1997). As is the case with the other behavioral outcomes considered here, smoking behavior is multifactorial in its etiology, and there is zvidence pointing to its genetic origins. Twin studies have demonstrated that genetic factors contribute to the initiation of smoking and influence the intensity of smoking cigarettes (number of cigarettes smoked per day; see Pomerleau & Kordia, 1999). A meta-analysis of the data from five studies, each involving more that 1000 twin pairs, found an estimated 60% of the propensity to smoke may be explained by genetic factors (Heath&Madden, 1995). Cigarette smokers are over-represented in many disadvantaged groups, including those with psychiatric and behavioral disorders (Parrott, 2000). Still, there is evidence that environmental and job-related stress may account for a significant proportion of the variance of smoking behavior. Consequently, interest in the pathway leading from stress, and stress at work, to smoking behavior is growing.
Stress and associated emotional responses, including anxiety and irritability, are attenuated by smoking. These effects have been shown to be short-lived (Parrott, 1995). Mood and affective state impairments tend to occur between cigarettes in a repetitive cycle. This cycle provides a clear rationale for the addictive use of cigarettes (Parrott, 1995). Smokers, therefore, obtain only short relief from adverse states of anxiety and irritability that follow the experience of stress. There is evidence from smoking abstaining studies that nicotinewithdrawal symptoms are worse under high environmental stress than under low environmental stress, while post-cigarette relief was also correspondingly greater (Parrott, 2000).
In empirical research, stress is often found to predict smoking behavior while interacting with other predictors, like lack of social support. In a review of the research on smoking behavior among nurses, Adriaanse et al. (1991) found that excessive smoking among both female and male nurses was explained by work stress, lack of social support, and unmet expectations that characterize nurses’ professional socialization. Nurses’ smoking is considered a public health problem since they often act as role models to patients and their families. In several studies, smokers who express high motivation to smoke have reported above-average stress that they had experienced before the smoking, rather than belowaverage stress after smoking (Parrott, 1995). Consequently, stress management and anxiety reduction programs at the workplace have the potential to influence motivation to smoke. Workplace-based smoking cessation programs do bring to the fore, however, the conflict between health and performance. Among aviators, as an example, smoking is a health hazard in the cockpit. Pilots who are required to abstain from smoking during and before flights may suffer cockpit performance decrements (Sommese & Patterson, 1995).
Yet another facet of the complex relationship between stress and cigarette smoking was described by Parrott (1999), who proposed that the evidence on this relationship might be reinterpreted to suggest that smoking actually causes stress. Parrott (1999) pointed out that regular smokers are more stressed than their non-smoking counterparts and that smokers experience an overall reduction in stress when they quit smoking. Another theory holds that
smoking may redistribute stress by modulating moods (Piasecki & Baker, 2000).
Work organizations contribute to and may inhibit (or induce) smoking behavior by three basic processes documented in the research literature. First, work organizations may develop organizational norms with respect to smoking on the job, including the local official definition of permissible smoking and the mechanisms of its control established by management. Second, stressful working conditions, like sustained overload or machine-paced jobs characterized by lack of control, may induce heavy smoking as a coping strategy to alleviate the stressful job conditions. Third, work organizations may explicitly or implicitly encourage the development of occupationally based smoking subcultures. In a survey of 12 000 professional people in 14 occupational categories, Russek (1965) found significant differences in the prevalence of smoking in high-stress occupations as compared with low-stress occupations.
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