• We are sorry, but NCBI web applications do not support your browser and may not function properly. More information
Logo of nihpaAbout Author manuscriptsSubmit a manuscriptNIH Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
Psychosom Med. Author manuscript; available in PMC Jan 1, 2011.
Published in final edited form as:
PMCID: PMC2804907
NIHMSID: NIHMS163092

Secondhand Smoke Exposure and Depressive Symptoms

Abstract

Objective

To evaluate the association between secondhand smoke (SHS) exposure and depression. Tobacco smoking and depression are strongly associated, but the possible effects of SHS have not been evaluated.

Methods

The 2005 to 2006 National Health and Nutrition Examination Survey (NHANES) is a cross-sectional sample of the noninstitutionalized civilian U.S. population. SHS exposure was measured in adults aged ≥20 years by serum cotinine and depressive symptoms by the Patient Health Questionnaire. Zero-inflated Poisson regression analyses were completed with adjustment for survey design and potential confounders.

Results

Serum cotinine-documented SHS exposure was positively associated with depressive symptoms in never-smokers, even after adjustment for age, race/ethnicity, gender, education, alcohol consumption, and medical comorbidities. The association between SHS exposure and depressive symptoms did not vary by gender, nor was there any association between SHS smoke exposure and depressive symptoms in former smokers.

Conclusions

Findings from the present study suggest that SHS exposure is positively associated with depressive symptoms in never-smokers and highlight the need for further research to establish the mechanisms of association.

Keywords: secondhand smoke, depressive symptoms, tobacco policy, mental health policy

INTRODUCTION

The U.S. Surgeon General has concluded that secondhand smoke (SHS) causes premature death and disease in persons who do not smoke and that no scientific evidence establishes a risk-free level of exposure (1). Currently, only 41.2% of the U.S. population is covered by comprehensive clean indoor air legislation, which prohibits smoking in all workplaces, bars, and restaurants (2). In the National Comorbidity Survey-Replication Study (3), the prevalence of lifetime major depressive disorder was 16.2% (32.6–35.1 million U.S. adults), and it was 6.6% within the last 12 months (13.1–14.2 million U.S. adults). Depression has been related to an increased risk of mortality (4,5) and morbidity (6). The burden of depression worldwide is a major public health issue. In countries with high per capita income, depression is the third leading cause of disability adjusted life years (8–41 million years) (7).

Although smokers are clearly at greater risk for depression (812), the nature of the relationship between smoking and depression is uncertain. Smokers may smoke because they are depressed and therefore “self-medicate” (11), or depression could be the result of smoking (13). Alternatively, a third factor, such as a shared genetic predisposition, may explain this relationship (8). A recent study by Nakata and colleagues (14) found that the self-report of SHS exposure was related to depression among a group of Japanese never-smoking workers. Although the study by Nakata et al. (14) was the first to find an association between SHS and depression, it was limited by the self-report measure of SHS exposure. Arheart and colleagues (15) recently found that self-report of SHS exposure can be an imprecise measure of biologically confirmed SHS exposure.

The purpose of the present study was to explore the possible association between SHS exposure and depressive symptoms in a population-based sample of the U.S. adult population, using an objective, biological measure of SHS exposure. Growing evidence suggests that SHS exposure is associated with chronic diseases, such as cardiovascular disease (16), respiratory disease (17), diabetes mellitus (18), hypertension (19), thyroid disease (20), and cancers (21). All of these chronic conditions are also associated with depression (2226). Thus, chronic diseases may explain the association between SHS exposure and depression. Further, other psychological or biological mechanisms may explain the association between SHS exposure and depression. SHS exposure may be a proxy to stressful living and working environments, and stress has been associated with depression (27,28). In addition, perhaps similar neurobiological mechanisms observed in firsthand smokers may be observed in persons who have SHS exposure. That is, chronic exposure to cigarette smoke may lead to lower levels of dopamine and γ-aminobutyric acid (GABA), which are associated with mood disorders (29,30). Women are also at greater risk for depression than men (3), and the association between SHS exposure and depression may be more apparent for women than men. Therefore, we hypothesized that SHS exposure would be positively associated with depressive symptoms even after adjustment for potential confounders and that the strength of this association differs in men versus women.

METHODS

Description of Survey

The National Health and Nutrition Examination Survey (NHANES) (http://www.cdc.gov/nchs/nhanes.htm), a household survey combined with a medical examination, is conducted every year by the National Center for Health Statistics in the Centers for Disease Control and Prevention. The survey is designed to be representative of the noninstitutionalized civilian U.S. population. Complete data from nonsmokers aged ≥20 years were obtained from the 2005 to 2006 NHANES (n = 2965). The response rate for the interview component was 74.4%, and the response rate for the clinical examination component was 71.5%. This study was approved by the University of Miami Institutional Review Board for human subjects research.

Measures

SHS Exposure

For the 2005 to 2006 NHANES, the detectable limit for serum cotinine (a metabolite of nicotine) was 0.011 ng/mL. As described previously (31,32), the value for data below the detectable limits was the limit divided by the square root of 2. SHS exposure was included in the analyses as the natural log transformation of serum cotinine.

Depressive Symptoms Assessment

The Patient Health Questionnaire-9 (33) was used to measure depressive symptoms. Participants responded to nine items measuring depressive symptoms in the last 2 weeks by choosing either: Not at all (0); Several days (1); More than half the days (2); or Nearly every day (3). A summed score from 0 to 27 was used to classify “Depressive Symptoms” (33). Participants were excluded if they were missing data on ≥3 of the nine items (n = 3). If participants were missing one or two items, scores were imputed substituting the mean of an individual’s nonmissing items for the missing items.

Covariates

Covariates were chosen a priori on the basis of literature review. Covariates were defined as potential confounders if they were associated with both the predictor and outcome and could possibly account for the association between SHS and depressive symptoms. Age, race/ethnicity, gender, education, alcohol consumption, and medical comorbidities were measured by participant self-report. The medical comorbidities in this study were cardiovascular disease (i.e., either angina, congestive heart failure, coronary heart disease, heart attack, or stroke), respiratory disease (i.e., either asthma, chronic bronchitis, or emphysema), diabetes mellitus, hypertension, thyroid disease, and history of cancer. Alcohol consumption was measured as the average number of drinks per day in the last year in a subset of our analytic sample aged 20 years to 59 years (n = 1320).

Sample Selection

Participants were asked if they had smoked ≥100 cigarettes in their lifetime. Those responding “yes” were asked if they currently smoked cigarettes. Self-identified current smokers were excluded in the analysis (n = 943). We also considered those with serum cotinine values of >3 ng/mL as current smokers (n = 124) (34). In addition, participants with incomplete covariate information (age, race/ethnicity, gender, education, and comorbidities) were excluded from the analysis (n = 2). Stratified analyses were performed in “never-smokers” (defined as those who reported not smoking ≥100 cigarettes in their lifetime [n = 2026]) and “former smokers” (defined as those who reported smoking ≥100 cigarettes in their lifetime, but did not currently smoke and who had cotinine values of ≤3 ng/mL [n = 938]).

Statistical Analysis

STATA version 10.0 was used to analyze a continuous measure of depressive symptoms with SHS exposure as the main predictor when adjusting for potential confounders. Because the distribution of depressive symptoms was positively skewed and had an excess of zeros (37.7%), linear regression analyses were not appropriate. Furthermore, the summed score of depressive symptoms is similar to count data (35). Other epidemiological studies have used the same measure of depressive symptoms as a count variable (36,37). We applied both zero-inflated Poisson and zero-inflated negative binomial regressions. The likelihood ratio test was used to determine which method best fit the data. In the present study, zero-inflated Poisson regression fit the data better than zero-inflated negative binomial regression. We also took into account sample weights and the effects of the complex sampling design of the NHANES. Model 1 was adjusted for age, gender, race/ethnicity, and education. Model 2 was further adjusted for medical comorbidities. Finally, subgroup analyses among persons aged 20 years to 59 years were conducted, adjusting for age, gender, race/ethnicity, education, and alcohol consumption to evaluate the significance of this latter covariate as a possible confounder in the relationship between SHS and depressive symptoms.

RESULTS

Sample Characteristics

Table 1 presents the sample characteristics. The mean of serum cotinine (log) was −3.15 (standard error [SE] = 0.05), depression was 2.31 (SE = 0.08), and age was 48.60 (SE = 0.95). Most of the sample was non-Hispanic white (72.9%, SE = 3.07), 12.4% was Hispanic (SE = 1.55), 10.1% was non-Hispanic black (SE = 1.97), and 4.6% was non-Hispanic other (SE = 0.60); 43.6% was male (SE = 1.00) and 56.4% was female (SE = 1.00); 63.6% had < high school education (SE = 1.81), 22.2% had the equivalent of high school education (SE = 1.13), and 14.2% had > high school education (SE = .53).

TABLE 1
Demographics Characteristics of Eligible Sample: 2005–2006 National Health and Nutrition Examination Survey

The interaction between gender and SHS exposure was not significant in never-smokers and in former smokers, when adjusting for age, gender, race/ethnicity, and education (t = 1.13, p= .27 and t = −0.21, p = .83). The association between SHS exposure and depressive symptoms among former smokers was not significant when adjusting for age, race/ethnicity, gender, and education (β = −0.01, SE = 0.04, p = .68). Among never-smokers, SHS exposure was positively associated with depression after adjusting for age, gender, race/ethnicity, and education (β = 0.09, SE = 0.03, p = .02) (Table 2). SHS exposure remained positively associated with depression after further adjustment for cardiovascular disease, respiratory disease, diabetes mellitus, hypertension, thyroid disease, and cancers (β = 0.09, SE = 0.03, p = .03). SHS exposure was positively associated with depression in subgroup analyses (persons aged 20–59 years) for age, gender, race/ethnicity, education, and alcohol consumption (β = 0.10, SE = 0.03, p = .01).

TABLE 2
Association Between Secondhand Smoke Exposure and Level of Depressive Symptoms Among Never-Smokers in 2005–2006 NHANES

DISCUSSION

Sixty-five percent of the working U.S. population is potentially exposed to SHS in the workplace (21), and >35 million U.S. adults may suffer at least one lifetime episode of major depression (3). Thus, our finding that SHS exposure is associated with the level of depressive symptoms among never-smokers is of clear public health significance. The association between SHS exposure and depressive symptoms was not explained by demographics, alcohol consumption, or the presence of chronic conditions.

Several possible explanations may account for our finding that SHS exposure is associated with the level of depressive symptoms in never-smokers, even after controlling for comorbidities and socioeconomic status. SHS exposure may be a proxy for stressful home and occupational environments, given that stress has been related to depression (27,28). Similar to smokers, prolonged SHS exposure among never-smokers may lead to lower levels of dopamine and lower levels of GABA, which have been related to an increased risk for depression (29,30). Recent studies have shown that the dopamine system genotype variability may explain a significant proportion of the interindividual variability in smoking-induced dopamine release, and indicate that smoking-induced dopamine release has a genetic predisposition (3840). Former smokers may have been less subject to nicotine dependence when they smoked (relative to those who continue to smoke) and exhibit homeostatic levels of dopamine and GABA. In addition, by virtue of their current status, former smokers were likely more motivated to quit smoking, consistent with a desire to live a healthy lifestyle, and less likely to be depressed by self-selection (41,42). Of interest, one study found a significantly decreased risk of depression among former smokers, who had quit over 10 years prior compared with an increased risk for nonsmokers and for smokers (28). Therefore, it may be possible that the particular characteristics of the individual (such as their nicotine dependence, personality, and genetic make-up) may play a protective role, as observed in the former smokers in our study.

Strengths, Limitations, and Conclusions

Findings from this study must be interpreted with caution. If first and secondhand smokers are more likely to suffer from depression because of their exposure to cigarettes and the same psychological or biological mechanisms are shared, then it is likely that the temporal association between smoking and depression is that smoking precedes the onset of depression. For firsthand smokers, it is still possible for them to “self-medicate” and the association between firsthand smoking and depression may be bidirectional. However, it is highly unlikely that never-smokers exposed to SHS are self-medicating. This is only the second study to find an association between SHS exposure and depression (14) and, thus, future studies are needed to establish consistent results. The mechanisms of association are also important to establish causality, and further research is needed to examine whether first- and secondhand smokers share similar mechanisms of association.

An advantage of the present analysis is that it addressed the hypothesis that SHS exposure among nonsmokers is associated with increased levels of depressive symptoms, using a population-based U.S. sample. Furthermore, SHS exposure was measured, using an objective biological measure, i.e., serum cotinine, and depressive symptoms was measured by the well-validated Patient Health Questionnaire (33). However, this study is cross-sectional, so temporal associations cannot be established. A small number of intermittent or light smokers, who denied tobacco use, were possibly retained in our analysis, despite excluding participants with cotinine values of >3 ng/mL. However, if these intermittent smokers are present, then they would have not unduly biased our results. The exact mechanism by which SHS exposure is associated with depression is not clear. Research employing longitudinal study designs, which include serial assessment of SHS exposure, is needed to examine causality between SHS and depression. Finally, detailed information on the source(s) of exposure (e.g., at home, work, and/or elsewhere) and a past history of depression are also unknown.

Depression is a major cause of morbidity (6,7,12), mortality (4,5), and reduced worker productivity (43). Studies have shown that banning smoking in workplaces and other public settings leads to immediate reductions in hospitalizations and disease-specific symptoms (4447). However, no previous studies have looked specifically at the impact smoking bans might have on depression and levels of depressive symptomatology. In addition, these data suggest that interventions designed to eliminate smoking in the home are also needed. Modest financial incentives to prevent smoking at home already exist, most directly through owner and renter insurance rates, which can be higher for smokers (48). However, public health campaigns and similar interventions that promote greater awareness of the negative consequences associated with both smoking and SHS exposure are also warranted to encourage individuals to stop smoking inside the home. Thus, policy makers and employers have an important role in developing programs to ban and/or prevent SHS that can be applied in a variety of settings including the workplace, the community, and individual homes.

Acknowledgments

This work was funded, in part, by grants from the Flight Attendant Medical Research Institute (Dr. Lee, Principal Investigator) and Grant R01 OH03915 from the National Institute of Occupational Safety and Health (Dr. Fleming, Principal Investigator).

This study was completed while Frank C. Bandiera was a doctoral student in epidemiology at the University of Miami. Mr. Bandiera is a recipient of an individual pre-doctoral grant from the National Institute of Mental Health to study the association between asthma and mental health outcomes and receive advanced training in statistical methods, genetic epidemiology, behavioral medicine, and psychoneuroimmunology (1F31MH084567).

Because the NHANES is a publicly available database, all authors had access to the data.

Glossary

NHANES
National Health and Nutrition Examination Survey
SHS
secondhand smoke
CDC
Centers for Disease Control and Prevention
OR
odds ratio
GABA
γ-aminobutyric acid

Footnotes

Frank C. Bandiera, MPH, conceived the study, conducted preliminary statistical analyses, and drafted an initial version of the manuscript. David J. Lee, PhD, Lora Fleming, MD, PhD, and Noella Dietz, PhD, assisted with the conceptualization of the study and provided expertise on SHS exposure and health outcomes. They also reviewed and added sections to the manuscript. Kristopher Arheart, EdD, and William G. LeBlanc, PhD, served as statisticians for the study, providing statistical expertise, data analysis, and assisted with revision of the manuscript. Evelyn P. Davila, MPH, Alberto J. Caban-Martinez, Kathryn McCollister, PhD, MPH, Berrin Serdar, MD, PhD, and John E. Lewis, PhD, added sections and assisted in reviewing versions of the manuscript.

REFERENCES

1. United States Department of Health and Human Services. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General. Atlanta: U.S. Department of Health and Human Services. Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office of Smoking and Health; 2006. Introductions, and conclusions. pp. 1–26.
2. ANRF. Summary of 100% smokefree state laws and population protected by state and local laws. American Non-Smokers’ Rights Foundation; 2009. Oct 2 [Accessed November 10, 2009]. http://www.no-smoke.org/pdf/SummaryUSPopList.pdf.
3. Kessler RC, Berglund P, Demler O, Jin R, Koretz D, Merikangas KR, Rush AJ, Walters EE, Wang PS. National Comorbidity Survey Replication. The epidemiology of major depressive disorder: results from the National Comorbidity Survey Replication (NCS-R) JAMA. 2003;289:3095–3105. [PubMed]
4. Everson SA, Roberts RE, Goldberg DE, Kaplan GA. Depressive symptoms and increased risk of stroke mortality over a 29-year period. Arch Intern Med. 1998;158:1133–1138. [PubMed]
5. Zheng D, Macera CA, Croft JB, Giles WH, Davis D, Scott WK. Major depression and all-cause mortality among white adults in the United States. Ann Epidemiol. 1997;7:213–218. [PubMed]
6. Merikangas KR, Ames M, Cui L, Stang PE, Ustun TB, Von Korff M, Kessler RC. The impact of comorbidity of mental and physical conditions on role disability in the US adult household population. Arch Gen Psychiatry. 2007;64:1180–1188. [PMC free article] [PubMed]
7. Lopez AD, Mathers CD, Ezzati M, Jamison DT, Murray CJ. Global and regional burden of disease and risk factors, 2001: systematic analysis of population health data. Lancet. 2006;367:1747–1757. [PubMed]
8. Dierker LC, Avenevoli S, Stolar M, Merikangas KR. Smoking and depression: an examination of mechanisms of comorbidity. Am J Psychiatry. 2002;159:947–953. [PubMed]
9. Glassman AH, Helzer JE, Covey LS, Cottler LB, Stetner F, Tipp JE, Johnson J. Smoking, smoking cessation, and major depression. JAMA. 1990;264:1546–1549. [PubMed]
10. Kendler KS, Neale MC, MacLean CJ, Heath AC, Eaves LJ, Kessler RC. Smoking and major depression. A causal analysis. Arch Gen Psychiatry. 1993;50:36–43. [PubMed]
11. Khantzian EJ. The self-medication hypothesis of substance use disorders: a reconsideration and recent applications. Harv Rev Psychiatry. 1997;4:231–244. [PubMed]
12. Mathers CD, Loncar D. Projections of global mortality and burden of disease from 2002 to 2030. PLoS Med. 2006;3:e442. [PMC free article] [PubMed]
13. Klungsoyr O, Nygard JF, Sorensen T, Sandanger I. Cigarette smoking and incidence of first depressive episode: an 11-year, population-based follow-up study. Am J Epidemiol. 2006;163:421–432. [PubMed]
14. Nakata A, Takahashi M, Ikeda T, Hojou M, Nigam JA, Swanson NG. Active and passive smoking and depression among Japanese workers. Prev Med. 2008;46:451–456. [PubMed]
15. Arheart KL, Lee DJ, Fleming LE, LeBlanc WG, Dietz NA, McCollister KE, Wilkinson JD, Lewis JE, Clark JD, 3rd, Davila EP, Bandiera FC, Erard MJ. Accuracy of self-reported smoking and secondhand smoke exposure in the US workforce: the National Health and Nutrition Examination Surveys. J Occup Environ Med. 2008;50:1414–1420. [PubMed]
16. Stranges S, Bonner MR, Fucci F, Cummings KM, Freudenheim JL, Dorn JM, Muti P, Giovino GA, Hyland A, Trevisan M. Lifetime cumulative exposure to secondhand smoke and risk of myocardial infarction in never smokers: results from the Western New York health study, 1995–2001. Arch Intern Med. 2006;166:1961–1967. [PubMed]
17. Eisner MD, Jacob P, 3rd, Benowitz NL, Balmes J, Blanc PD. Longer term exposure to secondhand smoke and health outcomes in COPD: impact of urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol. Nicotine Tob Res. 2009;11:945–953. [PMC free article] [PubMed]
18. Houston TK, Person SD, Pletcher MJ, Liu K, Iribarren C, Kiefe CI. Active and passive smoking and development of glucose intolerance among young adults in a prospective cohort: CARDIA study. BMJ. 2006;332:1064–1069. [PMC free article] [PubMed]
19. Ren X, Hsu PY, Dulbecco FL, Fleischmann KE, Gold WM, Redberg RF, Schiller NB. Remote second-hand tobacco exposure in flight attendants is associated with systemic but not pulmonary hypertension. Cardiol J. 2008;15:338–343. [PubMed]
20. Metsios GS, Flouris AD, Jamurtas AZ, Carrillo AE, Kouretas D, Germenis AE, Gourgoulianis K, Kiropoulos T, Tzatzarakis MN, Tsatsakis AM, Koutedakis Y. A brief exposure to moderate passive smoke increases metabolism and thyroid hormone secretion. J Clin Endocrinol Metab. 2007;92:208–211. [PubMed]
21. Siegel M, Skeer M. Exposure to secondhand smoke and excess lung cancer mortality risk among workers in the “5 B’s”: bars, bowling alleys, billiard halls, betting establishments, and bingo parlours. Tob Control. 2003;12:333–338. [PMC free article] [PubMed]
22. Chochinov HM. Depression in cancer patients. Lancet Oncol. 2001;2:499–505. [PubMed]
23. Goodwin RD, Jacobi F, Thefeld W. Mental disorders and asthma in the community. Arch Gen Psychiatry. 2003;60:1125–1130. [PubMed]
24. Mezuk B, Eaton WW, Albrecht S, Golden SH. Depression and type 2 diabetes over the lifespan: a meta-analysis. Diabetes Care. 2008;31:2383–2390. [PMC free article] [PubMed]
25. Patten SB, Williams JV, Lavorato DH, Modgill G, Jette N, Eliasziw M. Major depression as a risk factor for chronic disease incidence: longitudinal analyses in a general population cohort. Gen Hosp Psychiatry. 2008;30:407–413. [PubMed]
26. Spijkerman T, de Jonge P, van den Brink RH, Jansen JH, May JF, Crijns HJ, Ormel J. Depression following myocardial infarction: first-ever versus ongoing and recurrent episodes. Gen Hosp Psychiatry. 2005;27:411–417. [PubMed]
27. Hammen C. Stress and depression. Annu Rev Clin Psychol. 2005;1:293–319. [PubMed]
28. Monroe SM, Simons AD. Diathesis-stress theories in the context of life stress research: implications for the depressive disorders. Psychol Bull. 1991;110:406–425. [PubMed]
29. Petty F. GABA and mood disorders: a brief review and hypothesis. J Affect Disord. 1995;34:275–281. [PubMed]
30. Petty F, Kramer GL, Fulton M, Moeller FG, Rush AJ. Low plasma GABA is a trait-like marker for bipolar illness. Neuropsychopharmacology. 1993;9:125–132. [PubMed]
31. Aligne CA, Moss ME, Auinger P, Weitzman M. Association of pediatric dental caries with passive smoking. JAMA. 2003;289:1258–1264. [PubMed]
32. Clark JD, 3rd, Wilkinson JD, LeBlanc WG, Dietz NA, Arheart KL, Fleming LE, Lee DJ. Inflammatory markers and secondhand tobacco smoke exposure among U.S. workers. Am J Ind Med. 2008;51:626–632. [PubMed]
33. Kroenke K, Spitzer RL, Williams JB. The PHQ-9: validity of a brief depression severity measure. J Gen Intern Med. 2001;16:606–613. [PMC free article] [PubMed]
34. Benowitz NL, Bernert JT, Caraballo RS, Holiday DB, Wang J. Optimal serum cotinine levels for distinguishing cigarette smokers and nonsmokers within different racial/ethnic groups in the United States between 1999 and 2004. Am J Epidemiol. 2009;169:236–248. [PubMed]
35. Abdelmonem AAKJ, Ettner SL, Cowan M. Methods for improving regression analysis for skewed continuous or counted responses. Annu Rev Public Health. 2007;28:95–111. [PubMed]
36. Sachdev PS, Parslow RA, Lux O, Salonikas C, Wen W, Naidoo D, Christensen H, Jorm AF. Relationship of homocysteine, folic acid and vitamin B12 with depression in a middle-aged community sample. Psychol Med 205. 35:529–538. [PubMed]
37. Tracy M, Hobfoll SE, Canetti-Nisim D, Galea S. Predictors of depressive symptoms among Israeli Jews and Arabs during the Al aqsa intifada: a population-based cohort study. Ann Epidemiol. 2008;18:447–457. [PMC free article] [PubMed]
38. Brody AL, Mandelkern MA, Olmstead RE, Scheibal D, Hahn E, Shiraga S, Zamora-Paja E, Farahi J, Saxena S, London ED, McCracken JT. Gene variants of brain dopamine pathways and smoking-induced dopamine release in the ventral caudate/nucleus accumbens. Arch Gen Psychiatry. 2006;63:808–816. [PMC free article] [PubMed]
39. Caskey NH, Jarvik ME, Wirshing WC. The effects of dopaminergic D2 stimulation and blockade on smoking behavior. Exp Clin Psychopharmacol. 1999;7:72–78. [PubMed]
40. Caskey NH, Jarvik ME, Wirshing WC, Madsen DC, Iwamoto-Schaap PN, Eisenberger NI, Huerta L, Terrace SM, Olmstead RE. Modulating tobacco smoking rates by dopaminergic stimulation and blockade. Nicotine Tob Res. 2002;4:259–266. [PubMed]
41. Husten CG, Shelton DM, Chrismon JH, Lin YC, Mowery P, Powell FA. Cigarette smoking and smoking cessation among older adults: United States, 1965–94. Tob Control. 1997;6:175–180. [PMC free article] [PubMed]
42. Lancaster T, Stead L, Silagy C, Sowden A. Effectiveness of interventions to help people stop smoking: findings from the Cochrane Library. BMJ. 2000;321:355–358. [PMC free article] [PubMed]
43. Kessler R, White LA, Birnbaum H, Qiu Y, Kidolezi Y, Mallett D, Swindle R. Comparative and interactive effects of depression relative to other health problems on work performance in the workforce of a large employer. J Occup Environ Med. 2008;50:809–816. [PubMed]
44. Bartecchi C, Alsever RN, Nevin-Woods C, Thomas WM, Estacio RO, Bartelson BB, Krantz MJ. Reduction in the incidence of acute myocardial infarction associated with a citywide smoking ordinance. Circulation. 2006;114:1490–1496. [PubMed]
45. Goodman P, Agnew M, McCaffrey M, Paul G, Clancy L. Effects of the Irish smoking ban on respiratory health of bar workers and air quality in Dublin pubs. Am J Respir Crit Care Med. 2007;175:840–845. [PubMed]
46. Larsson M, Boethius G, Axelsson S, Montgomery SM. Exposure to environmental tobacco smoke and health effects among hospitality workers in Sweden–before and after the implementation of a smoke-free law. Scand J Work Environ Health. 2008;34:267–277. [PubMed]
47. Sargent RP, Shepard RM, Glantz SA. Reduced incidence of admissions for myocardial infarction associated with public smoking ban: before and after study. BMJ. 2004;328:977–980. [PMC free article] [PubMed]
48. Hilary Smith. The high cost of smoking. [Accessed October 14, 2008]. http://articles.moneycentral.msn.com/Insurance/InsureYourHealth/HighCostOfSmoking.aspx?page=all.
PubReader format: click here to try

Formats:

Related citations in PubMed

See reviews...See all...

Cited by other articles in PMC

See all...

Links

  • Compound
    Compound
    PubChem Compound links
  • MedGen
    MedGen
    Related information in MedGen
  • PubMed
    PubMed
    PubMed citations for these articles
  • Substance
    Substance
    PubChem Substance links

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...