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Depressive Symptoms and Smoking Cessation Among Adolescents and Young Adults Who Smoke: A Prospective Cohort Study.

PURPOSE: This study examined the bidirectional prospective associations between depressive symptoms and smoking cessation among adolescent and young adults who smoke. METHODS: Data on 1,151 participants aged &#x2264;25 years who smoke and receive peer-led quitline counseling in Hong Kong (2016-2022) were analyzed. Exposures included baseline depressive symptoms and smoking cessation (self-reported 7-day abstinence) at 1, 3, and 6 months; Outcome measures included smoking cessation at 1, 3, and 6 months and depressive symptoms at 6 months. Depressive symptoms were assessed using the Center for Epidemiologic Studies Depression Scale, with a score &#x2265;16 indicating at risk for depression. RESULTS: More severe baseline depressive symptoms were associated with lower odds of smoking cessation at 1, 3, and 6 months, which reversely was associated with lower depressive symptoms at 6 months (all p < .05). Similarly, being at risk for depression at baseline was associated with lower odds of smoking cessation at 1 (adjusted odds ratio [aOR] .66, 95% confidential interval [CI] .47-.93) and 3 months (aOR .71, 95% CI .52-.97). Conversely, smoking cessation at 1 (aOR .40, 95% CI .23-.69), 3 (aOR .58, 95% CI .37-.92), and 6 months (aOR .44, 95% CI .29-.69) was associated with lower odds of at risk for depression at 6 months. DISCUSSION: More severe depressive symptoms were prospectively associated with lower odds of smoking cessation, while smoking cessation was associated with lower depressive symptoms and risk for depression. Integrated interventions simultaneously addressing psychological needs and smoking are warranted, when delivered in smoking cessation programs or embedded within mental health services for youth who smoke.

Humans

Relationships Between Risky Substance Use and Irritable Bowel Syndrome (IBS) Severity, Mental Health, and Smoking-Related Processes in Adults with IBS Who Smoke.

Objective: Irritable Bowel Syndrome (IBS) is a debilitating chronic pain condition that presents a major and growing public health burden. Combustible cigarette smoking plays a role in the maintenance of IBS, and the co-occurrence of these conditions warrants greater focus. Moreover, given that smoking co-occurs with other substance use behaviors, the impact of these comorbid behaviors on physical and mental health-related outcomes among individuals with IBS who smoke is warranted. The goal of the present cross-sectional study was to assess relationships of risky alcohol, cannabis, and opioid use with IBS severity, anxiety and depression, and smoking-related processes among adults with IBS who smoke. Methods: In total, 263 adults who met Rome IV criteria for IBS and who smoked combustible cigarettes were included in the study. Hierarchical regression analyses were conducted to examine the influence of risky substance uses on IBS symptom severity, IBS-related quality of life, anxiety, depression, perceived barriers for smoking cessation, and cigarette dependence. Results: Results indicated that opioid use was statistically related to all criterion variables, whereas alcohol use was specifically associated with depression and anxiety. Cannabis use showed a statistically significant association only with anxiety symptoms. Conclusions: The present investigation is among the first to explore the role of risky substance use in terms of a wide array of IBS, mental health, and smoking processes among adults with IBS who smoke. The findings suggest that substance use should be a focal point of screening and intervention for the IBS population to optimize outcomes beyond the reach of medical therapies.

Irritable bowel syndrome

The effect of smoking cessation on pulmonary function: a 30-month follow-up of two smoking cessation clinics.

To obtain further information about the effects of cessation of smoking on pulmonary function, we followed subjects who attended 2 smoking cessation clinics during a period of 30 months. This paper reports the results from 15 persons who succeeded in stopping smoking for the full 30-month period and from 42 who did not succeed for more than one month. Testing included a respiratory questionnaire, spirometry, and the single-breath N2 test. Standardized methods, the same equipment, and the same experienced personnel were used throughout the study. We found that forced vital capacity, one-second forced expiratory volume, closing volume as a percentage of vital capacity, closing capacity as a percentage of total lung capacity, and the slope of the alveolar plateau of the single-breath N2 test all improved significantly in the subjects who stopped smoking. This improvement continued for as long as 6 to 8 months, and then remained stable. There was no sex difference in the response to smoking cessation, nor could we find a threshold of function below which cessation did not result in improvement. On the contrary, those subjects with the greatest impairment initially showed the greatest improvement. Respiratory symptoms virtually disappeared in those who stopped smoking. Subjects who continued to smoke showed an initial improvement in some function tests, probably due to a marked decrease in consumption, but no significant improvement during the whole period. We concluded from this study that cessation of smoking results in definite improvement in pulmonary function, that there is greater improvement in persons who begin with impaired function than in those whose function is initially normal, that respiratory symptoms disappear rapidly.

Adult

Does smoking kill workers or working kill smokers? OR The mutual relationship between smoking, occupation, and respiratory disease.

Evidence accumulated since 1964 appears to show that occupation, not cigarette smoking, may be the primary cause of lung disease, especially of cancer and chronic obstructive disease. Comparisons of groups of individuals who smoke more with those who smoke less actually serve to contrast groups with a high proportion of blue-collar workers exposed to toxic fumes and a low proportion of professionals, managers, and proprietors with groups having lower proportions of blue-collar workers and higher proportions of professionals, managers, and proprietors. Thus, many diseases associated with smoking actually may be of occupational origin. Indeed, more than a dozen recent investigations of lung cancer epidemics among industrial workers have failed to find smoking to be a major cause (in some, not even a contributing cause). This evidence is strengthened further by shifts in the incidence of lung cancer that follow in time shifts in industrial employment patterns. Yet a worker's past smoking habits seem to play a key role in decreasing compensation awards for injuries that actually may be due to occupational exposure rather than personal habits. Thus, the relationship between smoking, occupation, and disease needs serious clarification. Smoking appears to have been used to divert attention away from the effects of occupational and environmental exposures to toxic substances.

Adult

Impaired adaptation to smoke-derived phenolic compounds in Listeria monocytogenes CC204 from smoked salmon and trout.

Listeria monocytogenes is a major foodborne pathogen in ready-to-eat smoked fish products. This study evaluated whether clonal complex affiliation contributes to variability in growth responses to stresses representative of smoked salmon and trout processing. Ten strains were studied, including strains from CC121, CC26 and CC204, the three major clonal complexes reported in the French smoked salmon and trout sectors, together with the EGDe reference strain. Strains were exposed to salt, cold, smoke-derived phenolic compounds and combined stress conditions. Growth responses were compared with whole-genome-based phylogeny, and the impaired phenotype observed under phenolic exposure was further investigated using viable counts, live/dead microscopy and comparative genomics. Growth profiles were partly structured by clonal complex, with strains from the same clonal complex showing similar behaviour across stress conditions. Salt and cold reduced growth globally, while smoke-derived phenolic compounds were the most discriminating conditions. CC204 strains showed markedly lower growth rates under phenolic exposure than CC121, CC26 and EGDe. This phenotype was not associated with loss of cultivability or significant loss of membrane integrity. Comparative genomics did not identify a clear gene-content determinant explaining the CC204 phenotype. These results suggest that CC204 has an impaired adaptive response to smoke-derived compounds, likely involving regulatory or physiological mechanisms.

Listeria monocytogenes

Biological activity of tobacco smoke and tobacco smoke-related chemicals.

Exposure to whole cigarette smoke from reference cigarettes results in the prompt (peak activity is 6 hrs), but fairly weak (similar to 2 fold), induction of murine pulmonary microsomal monooxygenase activity. This activity can be detected by using as substrates either benzo(a)pyrene or ethoxyresorufin, and can be inhibited by treatment with cycloheximide or actinomycin D. Unlike the induction of pulmonary monooxygenases following intratracheal administration of 3-methylcholanthrene, these cigarette smoke-induced increases were not unequivocally linked to the Ah locus. Whole smoke condensate and fractions derived from these condensates can; a) induce pulmonary monooxygenase activity, b) inhibit benzo(a)pyrene metabolism in vitro, c) be metabolized to forms mutagenic to Salmonella typhimurium tester strains TA153, or TA98, d) transform C3H 10T1/2 cells in vitro, and e) enhance the carcinogenicity of benzo(a)pyrene in murine pulmonary tissue. A potentially important observation is that whereas hepatic tissue is capable of activating whole cigarette smoke condensate to mutagenic forms in vitro, murine pulmonary tissue does not seem capable of such activation. Although these pulmonary-derived tissue homogenates have significant AHH activity and can metabolize Aflatoxin B1, 2-aminofluorene and 7, 8-dihydro-7,8-dihydroxybenzo(a)pyrene to mutagenic forms, these homogenates fail to activate both cigarette smoke condensate and the pro-mutagen, 6-aminochrysene. These results are discussed with reference to the concept that whole cigarette smoke may be both a potential "initiator" and "promotor" of lung cancer in mice, and that this latter property may be the most important in determining cancer risk.

Animals

Inhalation bioassay chemistry--Walton Horizontal Smoking Machine for inhalation exposure of rodents to cigarette smoke.

Studies of experimental tobacco smoke carcinogenesis have suffered from the lack of a conveniently available and well-characterized device for exposing animals to tobacco smoke for inhalation. The Walton Horizontal Smoking Machine, a commercially available system designed to expose up to 20 mice to the smoke of a single cigarette, may fulfill this need. This system produced a uniform smoke aerosol of predictable concentration and appropriate composition for cigarettes with high delivery of nicotine (40 mg total particulate matter, 2.6 mg nicotine, and 17 cm3 carbon monoxide per cigarette) and with low delivery of nicotine (30 mg total particulate matter, 0.3 mg nicotine, and 17 cm3 carbon monoxide). In this experiment C57BL and DBA/2Bd strains of mice were used. Limitations of the concept of exposing animals to standing smoke were defined.

Animals

Clinical methods in smoking cessation: description and evaluation of a stop smoking clinic.

This study reports the results of the Kaiser-Permanente Stop Smoking Clinic and describes the philosophy and methods employed by the clinic in treating addictive smoking behavior. Of the 1,128 clients who registered for the group program, 57 per cent are abstinent six months after quitting smoking and 47 per cent are abstinent at one year. The clinic methods used are described in detail. They attempt to relate smoking behavior to the larger phenomenon of addiction.

Adult

[Experimental studies on the rumorigenic activity of cigarette smoke condensate on mouse skin. VI. Fractionation of cigarette smoke condensate (author's transl)].

This experiment has been performed to clarify the question to which extent fractions containing polycyclic aromatic hydrocarbons (PAH) or other carcinogenic compounds are responsible for the biological activity of cigarette smoke condensate. With chromatographic procedures using organic gels it was possible to separate quantitatively polar compounds from the PAH-fraction and to obtain fraction IX representing 0.4% of the whole condensate. In this fraction the PAH were enriched 250fold. Significant losses of tumorigenic effects by this fractionation method could not be observed. This PAH-containing fraction showed 50% of activity compared with the overall activity of whole smoke condensate of a reference cigarette. A so-called PAH-free fraction showed with 7% of the overall activity of the whole smoke condensate a weak carcinogenic effect. The importance of PAH for the tumorigenic effect of cigarette smoke is emphasized by these results.

Animals

Cigarette smoking among secondary schoolchildren in 1975. Prevalence of respiratory symptoms, knowledge of health hazards, and attitudes to smoking and health.

A questionnaire relating to smoking habits, respirator symptoms, and health attitudes was administered to 10 498 secondary schoolchildren in 1975. The results reported in this paper indicate that children who smoke regularly have a higher prevalence of upper respiratory tract infections and a higher incidence of the respiratory symptoms, cough, phlegm production with a cold, and shortness of breath, compared with non-smokers. Children are aware of the risks of lung cancer when smoking, but less aware of the other more immediate health risks, and this is particularly so in the younger age groups. It is suggested that health education should be directed towards younger children and that more use should be made of the fact that smoking clearly makes them less healthy.

Adolescent

Organ specificity of induction of activating and inactivating enzymes by cigarette smoke and cigarette smoke condensate.

Inhalation of cigarette smoke specifically induces the rat lung and kidney aryl hydrocarbon hydroxylase (AHH) in less than 4 h. The epoxide hydratase (EH) and the glutathione S-transferase are not significantly modified by a similar treatment in any of the rat tissues. Compared to the kidney AHH, the lung hydroxylase is 3--4 times more sensitive to small concentrations of cigarette smoke and seems to have a longer biological half-life. In both tissues, the induced AHH presents the same in vitro sensitivity to various inhibitors as a polycyclic hydrocarbon induced AHH. In primary fetal rat liver cell culture, the cigarette smoke condensate fractions (CSCF) induce both the AHH and EH activity. Nevertheless, the AHH activity responds faster and to lower concentrations of CSCF than the EH activity. The liver cell culture constitutes a unique tool for a comparative study of the AHH and EH induction mechanism. Low concentration (10 muM) of benz(a)anthracene induces only the AHH activity while trans-stilbene oxide enhances selectively the EH activity. Appropriate concentrations of CSCF or of phenobarbital (PB) determine a parallel induction of both enzymes. The results are discussed on the basis of (a) the existence of specific mechanisms of AHH regulation in the lung and in the kidney and (b) the existence of coordinated or independent biochemical control of the AHH and EH activity.

Animals

An investigation into the effect on cigarette smoking of a new anti-smoking chewing gum.

A preparation claimed to help patients to break the habit of smoking has recently been introduced. Material released in the mouth from a chewing gum causes an unpleasant taste when tobacco smoke is inhaled. This claim has been investigated in a double-blind trial on sixty subjects, thirty of whom took the active chewing gum and thirty the placebo chewing gum. The subjects each used one piece of chewing gum four times a day over a period of two weeks. This investigation clearly indicates that the active chewing gum is effective as an anti-smoking preparation, when used over a period of two weeks and the effect is still demonstrable one month later, although to a lesser extent.

Acetates

Reported physiological and psychological symptoms of tobacco smoke pollution in nonsmoking and smoking college students.

A 147-item questionnaire concerning the relevance of the nonsmokers' right movement to college and university campuses was administered to 307 University of New Hampshire undergraduates. The fourth section of the questionnaire consisted of 28 questions on symptoms caused by smoke pollution. Responses to these questions were given on a five-category frequency of occurrence scale. Frequencies, descriptive statistics, and t tests contrasting current smokers from nonsmokers were presented. Generally sizable percentages of nonsmokers reported adverse physiological and psychological symptoms from tobacco smoke pollution. Smokers reported a similar pattern of responding but at lower frequencies of occurrence.

Adolescent

Influence of heavy smoking upon the bone mineral content of the radius of the aged and effect of tobacco smoke on the sensitivity to calcitonin of rats.

Using Norland-Cameron Bone Mineral Analyzer BMA 178 Type, it has been found that bone mineral content of the radius is considerably less in male heavy smokers aged 61 to 75 and 76 to 90, then in nonsmokers with similar age. Less difference was found within the group of 61 to 75 year old women. Furthermore, also it has been pointed out that the sensitivity to calcitonin of rats inhaling tobacco smoke is considerably less, than that of control rats. It is possible that smoking promotes the decrease in mineral content of bones i.e. the aggravation of osteoporosis, by the means of calcitonin resistance. The authors recommend tobacco abstinence to patients with osteoporosis and to persons who are particularly endangered by osteoporosis (e.g. in menopause, in post-gastrectomic state ect.).

Age Factors