How cigarette smoking may increase the risk of anxiety symptoms and anxiety disorders : a critical review of biological pathways

Multiple studies have demonstrated an association between cigarette smoking and increased anxiety symptoms or disorders, with early life exposures potentially predisposing to enhanced anxiety responses in later life. Explanatory models support a potential role for neurotransmitter systems, inflammation, oxidative and nitrosative stress, mitochondrial dysfunction, neurotrophins and neurogenesis, and epigenetic effects, in anxiety pathogenesis. All of these pathways are affected by exposure to cigarette smoke components, including nicotine and free radicals. This review critically examines and summarizes the literature exploring the role of these systems in increased anxiety and how exposure to cigarette smoke may contribute to this pathology at a biological level. Further, this review explores the effects of cigarette smoke on normal neurodevelopment and anxiety control, suggesting how exposure in early life (prenatal, infancy, and adolescence) may predispose to higher anxiety in later life. A large heterogenous literature was reviewed that detailed the association between cigarette smoking and anxiety symptoms and disorders with structural brain changes, inflammation, and cell-mediated immune markers, markers of oxidative and nitrosative stress, mitochondrial function, neurotransmitter systems, neurotrophins and neurogenesis. Some preliminary data were found for potential epigenetic effects. The literature provides some support for a potential interaction between cigarette smoking, anxiety symptoms and disorders, and the above pathways; however, limitations exist particularly in delineating causative effects. The literature also provides insight into potential effects of cigarette smoke, in particular nicotine, on neurodevelopment. The potential treatment implications of these findings are discussed in regards to future therapeutic targets for anxiety. The aforementioned pathways may help mediate increased anxiety seen in people who smoke. Further research into the specific actions of nicotine and other cigarette components on these pathways, and how these pathways interact, may provide insights that lead to new treatment for anxiety and a greater understanding of anxiety pathogenesis.

Does workplace social capital buffer the effects of job stress? A cross-sectional, multilevel analysis of cigarette smoking among U.S. manufacturing workers

Objective: To investigate whether workplace social capital buffers the association between job stress and smoking status. Methods: As part of the Harvard Cancer Prevention Project's Healthy Directions—Small Business Study, interviewer-administered questionnaires were completed by 1740 workers and 288 managers in 26 manufacturing firms (84% and 85% response). Social capital was assessed by multiple items measured at the individual level among workers and contextual level among managers. Job stress was operationalized by the demand-control model. Multilevel logistic regression was used to estimate associations between job stressors and smoking and test for effect modification by social capital measures. Results: Workplace social capital (both summary measures) buffered associations between high job demands and smoking. One compositional item—worker trust in managers—buffered associations between job strain and smoking. Conclusion: Workplace social capital may modify the effects of psychosocial working conditions on health behaviors.

Cigarette smoking and increased anxiety symptoms and disorders

 This research project demonstrated that exposure to cigarette smoke in adolescence, childhood and in utero is prospectively associated with increased levels of anxiety later in life. The results suggest smoking is a plausible risk factor for developing higher levels of anxiety, informing multiple areas for future research into anxiety pathogenesis.

Association between Discoid Lupus erythematosus and Cigarette Smoking - A case-control study

Background. Discoid lupus erythernatosus (DLE) is a chronic cutaneous disease affecting photoexposed areas and has also been associated with cigarette smoking. Objective: To evaluate the association between smoking and DLE. Methods: A case-control study was performed involving 57 cases diagnosed with DLE and 215 healthy controls. Results:A higher smoking prevalence was noted in DLE cases (84.2%) than controls (33.5%), and the odds ratio adjusted for gender, age and ultraviolet index in the city of origin was 14.4 (95% confidence interval 6.2-33.8; multiple logistic regression, p < 0.01). The cumulative smoking exposure was not related to premature DLE development. At the beginning of the disease, smokers had more extensive involvement than nonsmokers; compromise of the upper arms was statistically related to smoking. Conclusion: Cigarette smoking was statistically associated with DLE development. Other studies are needed in order to evaluate the effects of smoking cessation on the course of disease. Copyright (c) 2005 S. Karger AG, Basel.

Association between palmoplantar pustulosis and cigarette smoking in Brazil: a case-control study

BackgroundPalmoplantar pustulosis (PPP) discloses some differences compared to vulgar psoriasis (PV) in terms of age of onset, female predominance and low occurrence of psoriasis lesions elsewhere. Cigarette smoking has been associated to PPP in international studies; nevertheless, these studies were never performed among Brazilian.ObjectivesTo compare prevalence of smoking among PPP, PV and other dermatologic patients (NPD).MethodsCase-control study involving 25 PPP patients from a reference psoriasis centre. Two control groups were matched according to gender and age: 50 patients with PV and 50 NPD. Confounders were adjusted by conditional multiple logistic regression.ResultsAmong cases, 84.0% were female and PPP age of disease onset (41.4 years) was greater than PV (34.5 years). Prevalence of ever smoking was higher among cases (92.0%) than PV (52.0%) and NPD (30.0%). Adjusted odds ratio of PPP ever smoking compared to PV and NPD was 9.5 and 36.2, respectively. All smokers reported the onset of their habit before the development of PPP.ConclusionsThere was significant association between PPP and smoking. However, the impact of giving it up in the clinical course of the disease remains to be established.

Genotoxicity of cigarette smoking in maternal and newborn lymphocytes

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Cigarette smoking and high-risk HPV DNA as predisposing factors for high-grade cervical intraepithelial neoplasia (CIN) in young Brazilian women

Background. This cross-sectional study was designed to evaluate the role of cigarette smoking and high-risk HPV types as risk factors of CIN 2 and 3 in young, sexually active Brazilian women. Materials and method. A series of 100 consecutive women with abnormal Pap smears were recruited, subjected to colposcopy, punch biopsy, and questionnaire for their social, sexual and reproductive factors. Of these, 77 women between 20 and 35 years of age (median 26.5 years) with biopsy-confirmed CIN 1 or CIN 2 and 3, were enrolled in this study. Representative samples from the exocervix and endocervix were obtained for HPV testing with the Hybrid Capture HPV-DNA assay, including the probes for the oncogenic HPV types (16, 18, 31, 33, 35, 45, 51, 52 and 56). Results. The overall rate of CIN 2 and 3 was 23/77 (29.8%). The women with CIN 1, 2 and 3 did not differ from each other with regard to their age, race, schooling, marital status, life-time number of sexual partners, age at first intercourse, use of oral contraceptives, or parity. However, current cigarette smoking was strongly associated with CIN 2 and 3 (p < 0,001), and among smokers, the risk of high-grade CIN increased in parallel with the time of exposure (years of smoking) p = 0.07), HPV-DNA of the oncogenic types was detected in 43 (56%) women, the risk of being HPV DNA-positive was significantly higher in CIN 2 and 3 as compared with CIN 1 (p = 0.037). Importantly, the prevalence of high-risk HPV types was significantly higher in cigarette smokers than in non-smokers (p = 0.046). Conclusions. The results indicate that the severity of CIN lesions was clearly related to two fundamental risk factors: 1) high-risk HPV types, and 2) current cigarette smoking. These two risk factors were closely interrelated in that the high-risk HPV types were significantly more frequent in current smokers than in non-smokers, suggesting the possibility of a synergistic action between these two risk factors in cervical carcinogenesis.

Association between solitary keratoacanthoma and cigarette smoking: A case-control study

Solitary keratoacanthoma (KA) is a common benign epithelial tumor of the skin characterized by rapid growth and a tendency toward spontaneous regression. The exact etiology and classification of KA are a matter of debate. Smokers also seem to be more affected than persons who never smoke. The objective of this study was to evaluate the association between solitary KA and smoking habit. A case-control study involving 78 patients diagnosed with KA and 199 controls from the related community was performed to evaluate the association between cigarette smoking and KA. A higher smoking prevalence was noted in cases (69.2 %) than controls (21.6 %) and the odds ratio adjusted for sex and age was 9.1 (95 % CI 4.9 to 17.1, p< 0.01). The mean tumoral diameter at surgery and the site of involvement was not statistically related to smoking. These findings suggest that cigarette smoking is associated with the development of KA. © 2006 Dermatology Online Journal.

Effects of Cigarette Smoking Intensity on the Mucociliary Clearance of Active Smokers

Background: Smoking impairs mucociliary clearance and increases respiratory infection frequency and severity in subjects with and without smoking-related chronic lung diseases. Objective: This study evaluated the effects of smoking intensity on mucociliary clearance in active smokers. Methods: Seventy-five active smokers were grouped into light (1-10 cigarettes/day; n = 14), moderate (11-20 cigarettes/day; n = 34) and heavy smokers (≥21 cigarettes/day; n = 27) before starting a smoking cessation programme. Smoking behaviour, nicotine dependence, pulmonary function, carbon monoxide in exhaled air (exCO), carboxyhaemoglobin (COHb) and mucociliary clearance measured by the saccharin transit time (STT) test were all evaluated. An age-matched non-smoker group (n = 24) was assessed using the same tests. Results: Moderate (49 ± 7 years) and heavy smokers (46 ± 8 years) had higher STT (p = 0.0001), exCO (p < 0.0001) and COHb (p < 0.0001) levels compared with light smokers (51 ± 15 years) and non-smokers (50 ± 11 years). A positive correlation was observed between STT and exCO (r = 0.4; p < 0.0001), STT and cigarettes/day (r = 0.3, p = 0.02) and exCO and cigarettes/day (r = 0.3, p < 0.01). Conclusion: Smoking impairs mucociliary clearance and is associated with cigarette smoking intensity. Copyright © 2013 S. Karger AG, Basel.

Does cigarette smoking modify the association between change in body mass index during young adulthood and risk of coronary mortality during middle-age in men? Twenty-five year follow-up results from the Chicago Western Electric Study

Many persons in the U.S. gain weight during young adulthood, and the prevalence of obesity has been increasing among young adults. Although obesity and physical inactivity are generally recognized as risk factors for coronary heart disease (CHD), the magnitude of their effect on risk may have been seriously underestimated due to failure to adequately handle the problem of cigarette smoking. Since cigarette smoking causes weight loss, physically inactive cigarette smokers may remain relatively lean because they smoke cigarettes. We hypothesize cigarette smoking modifies the association between weight gain during young adulthood and risk of coronary heart disease during middle age, and that the true effect of weight gain during young adulthood on risk of CHD can be assessed only in persons who have not smoked cigarettes. Specifically, we hypothesize that weight gain during young adulthood is positively associated with risk of CHD during middle-age in nonsmokers but that the association is much smaller or absent entirely among cigarette smokers. The purpose of this study was to test this hypothesis. The population for analysis was comprised of 1,934 middle-aged, employed men whose average age at the baseline examination was 48.7 years. Information collected at the baseline examinations in 1958 and 1959 included recalled weight at age 20, present weight, height, smoking status, and other CHD risk factors. To decrease the effect of intraindividual variation, the mean values of the 1958 and 1959 baseline examinations were used in analyses. Change in body mass index ($\Delta$BMI) during young adulthood was the primary exposure variable and was measured as BMI at baseline (kg/m$\sp2)$ minus BMI at age 20 (kg/m$\sp2).$ Proportional hazards regression analysis was used to generate relative risks of CHD mortality by category of $\Delta$BMI and cigarette smoking status after adjustment for age, family history of CVD, major organ system disease, BMI at age 20, and number of cigarettes smoked per day. Adjustment was not performed for systolic blood pressure or total serum cholesterol as these were regarded as intervening variables. Vital status was known for all men on the 25th anniversary of their baseline examinations. 705 deaths (including 319 CHD deaths) occurred over 40,136 person-years of experience. $\Delta$BMI was positively associated with risk of CHD mortality in never-smokers, but not in ever-smokers (p for interaction = 0.067). For never-smokers with $\Delta$BMI of stable, low gain, moderate gain, and high gain, adjusted relative risks were 1.00, 1.62, 1.61, and 2.78, respectively (p for trend = 0.010). For ever-smokers, with $\Delta$BMI of stable, low gain, moderate gain, and high gain, adjusted relative risks were 1.00, 0.74, 1.07, and 1.06, respectively (p for trend = 0.422). These results support the research hypothesis that cigarette smoking modifies the association between weight gain and CHD mortality. Current estimates of the magnitude of effect of obesity and physical inactivity on risk of coronary mortality may have been seriously underestimated due to inadequate handling of cigarette smoking. ^

Cigarette smoking and Ecuadorian adolescents: A cross-sectional survey and policy review

This study investigates the relationship between cigarette smoking and adolescents in Ecuador, South America. Using the Social Learning Theory as a basis, the cross-sectional survey focuses attention on such social influences as the smoking habits of family members and peers as well as, the role of cigarette advertisements. Actual use prevalence, access to cigarettes and knowledge and attitudes about smoking are also obtained.^ The survey was conducted in both urban and rural areas, with 50 schools in 40 different communities participating. Two thousand four hundred and fifty-seven adolescents aged 9 to 15 years completed a self-administered questionnaire. This part of the study was conducted in collaboration with the international health organization Amigos de las Americas (AMIGOS). Staff assigned to the AMIGOS Ecuador projects worked with local health and education officials to implement the cross-sectional survey in the field.^ The key informant survey and subsequent policy review were designed to illuminate the social, cultural and institutional environment for anti-smoking activities and interventions in Ecuador. Key individuals involved with this issue on both national and local levels were interviewed. A review of past legislative efforts and present anti-smoking laws was also conducted.^ The current smoking prevalence among the study population was 8.6 percent. Findings from the cross-sectional survey revealed significant positive associations between the smoking habits of siblings and peers and the smoking behavior of the adolescents surveyed. Significant age and gender differences were also found in association with several different variables.^ The policy review found an unfavorable environment for anti-smoking efforts. Several factors contribute to this including, most importantly, lack of funding and lack of public support. The present anti-smoking law is often vague and lacks important provisions, such as a prohibition on selling tobacco products to minors.^ Together, the two surveys provide comprehensive information for the purpose of designing smoking prevention interventions. Using the results from the two surveys, recommendations for intervention are proposed. ^

[Smoking and digestive tract: a complex relationship. Part 2: Intestinal microblota and cigarette smoking]

The digestive tract is colonized from birth by a bacterial population called the microbiota which influences the development of the immune system. Modifications in its composition are associated with problems such as obesity or inflammatory bowel diseases. Antibiotics are known to influence the intestinal microbiota but other environmental factors such as cigarette smoking also seem to have an impact on its composition. This influence might partly explain weight gain which is observed after smoking cessation. Indeed there is a modification of the gut microbiota which becomes similar to that of obese people with a microbiotical profile which is more efficient to extract calories from ingested food. These new findings open new fields of diagnostic and therapeutic approaches through the regulation of the microbiota.