Related Articles

BACKGROUND:

In patients with asthma, smoking has been associated with accelerated decline in pulmonary function, poor disease control and reduced responsiveness to corticosteroids.

OBJECTIVE:

To assess the influence of current and former smoking on self-reported asthma control and health care use in a large population of asthma patients.

METHODS:

The present analysis was conducted following a telephone survey of adult Canadians aged 18 to 54 years who had physician-diagnosed asthma and a smoking history of less than 20 pack-years.

RESULTS:

Of 893 patients, 268 were former smokers and 108 were current smokers. Daytime and nighttime symptoms, absenteeism from work or school, emergency care use for asthma in the past year, and use of a short-acting bronchodilator without controller medication were reported more frequently by current smokers than non-smokers and former smokers. Former smokers were not significantly different from nonsmokers with respect to most asthma outcomes.

CONCLUSIONS:

Current smokers with asthma show evidence of poorer asthma control and greater acute care needs than lifelong nonsmokers or former smokers. These observations stress the importance of smoking cessation to help achieve asthma control.

Background

Although it is recognised that smoking is a major risk factor for subjects with chronic obstructive pulmonary disease and is associated with respiratory symptoms, there is less agreement concerning the relationship between asthma and smoking. This study aims to examine the relationship between cigarette smoking and asthma prevalence.

Method

Data were used from two postal questionnaire surveys (1999 and 2001) in two general practice populations, using a respiratory questionnaire based on the ECRHQ and a generic quality of life questionnaire (EQ-5D). Only subjects less than 45 years old were included in the survey. An empirical definition of likely asthma was used based on respiratory questionnaire responses. Smoking was examined according to three categories, current smoker, ex smoker and never smoker.

Results

Almost 3500 subjects were included in the analyses. Current smokers had a higher prevalence of likely asthma compared to never smokers, odds ratio (OR) 1.59 (95% confidence interval (CI) 1.24 to 2.04). and also compared to ex smokers OR 1.79 (CI 1.25 to 2.56), but there was no difference between ex smokers and never smokers (OR 1.00 (0.75–1.35)). Current smoking was also positively associated with all symptoms but not with a history of hayfever/eczema.

Conclusion

Although the positive association found between current smoking and obstructive airways disease is likely to be due to the effect of cigarettes on asthma, it could reflect an association with early COPD (GOLD stages 0 or 1). Smoking cessation has a beneficial effect on the prevalence of respiratory symptoms and is therefore of paramount importance among these young adults.

Dutch workers have proposed that people with asthma and those smokers who develop chronic airflow obstruction share a common allergic constitution. To study whether smoking itself is associated with indicators of allergy, we have examined 237 men aged 51-61 years (120 smokers, 73 ex-smokers, and 44 non-smokers) who were recruited to a long term study of lung function in 1974, at which time men with a clinical diagnosis of asthma were excluded. Smokers, ex-smokers, and non-smokers did not differ in personal or family history of allergic disease, but the prevalence of positive responses to skinprick tests was greater in ex-smokers (59%) than in the other two groups (33% and 34%). In men with negative responses to skinprick tests total serum IgE was greater in smokers (log10 mean 1.41 IU/ml) and in ex-smokers (log10 mean 1.53 IU/ml) than in non-smokers (log10 mean 1.12 IU/ml). In men with positive skin test responses serum IgE was similar in the three groups (log10 mean ranging from 1.68 to 1.78 IU/ml). Geometric mean total white cell counts in the peripheral blood were higher in smokers (7.34 X 10(9)/l) than in non-smokers (5.82 X 10(9)/l); the value in ex-smokers (6.16 X 10(9)/l) was intermediate. Absolute blood eosinophil counts were increased in smokers disproportionately to the increase in total white cell count. Thus smoking is associated with small increases in some markers of allergy. These changes are probably acquired after the onset of smoking but sequential studies are required to amplify these cross sectional observations. Smokers whose skin test responses are positive appear more likely to give up smoking.

Background

Studies on the associations between smoking and allergic diseases have mostly focused on asthma. Epidemiological studies in adults on the effects of smoking on allergic diseases other than asthma, such as eczema and rhinoconjunctivitis, have been limited, and the information that is available has been inconsistent. The aim of this study was to investigate the association between smoking status and environmental tobacco smoke (ETS) exposure and the prevalence of allergic diseases.

Methods

Study subjects were 1743 pregnant Japanese women. The definitions of wheeze and asthma were based on criteria from the European Community Respiratory Health Survey whereas those of eczema and rhinoconjunctivitis were based on criteria from the International Study of Asthma and Allergies in Childhood. Adjustment was made for age; region of residence; family history of asthma, atopic eczema, and allergic rhinitis; household income; and education.

Results

Compared with never smoking, current smoking and ≥ 4 pack-years of smoking were independently positively associated with the prevalence of wheeze. There were no associations between smoking status and the prevalence of asthma, eczema, or rhinoconjunctivitis. When subjects who had never smoked were classified into four categories based on the source of ETS exposure (never, only at home, only at work, and both), exposure occurring both at home and at work was independently associated with an increased prevalence of two outcomes: wheeze and rhinoconjunctivitis. No relationships were observed between exposure to ETS and the prevalence of asthma or eczema.

Conclusions

Our results provide evidence that current smoking and ETS exposure may increase the likelihood of wheeze. The possibility of a positive association between ETS exposure and rhinoconjunctivitis was also suggested.

Asthma and rhinitis are often co-morbid conditions. As rhinitis often precedes asthma it is possible that effective treatment of allergic rhinitis may reduce asthma progression.

The aim of our study is to investigate history of allergic rhinitis as a risk factor for asthma and the potential effect of allergen immunotherapy in attenuating the incidence of asthma.

Hospital-referred non-asthmatic adults, aged 18–40 years between 1990 and 1991, were retrospectively followed up until January and April 2000. At the end of follow up, available subjects were clinically examined for asthma diagnosis and history of allergen specific immunotherapy, second-hand smoking and the presence of pets in the household. A total of 436 non-asthmatic adults (332 subjects with allergic rhinitis and 104 with no allergic rhinitis nor history of atopy) were available for final analyses.

The highest OR (odds ratio) associated with a diagnosis of asthma at the end of follow-up was for the diagnosis of allergic rhinitis at baseline (OR, 7.8; 95%CI, 3.1–20.0 in the model containing the covariates of rhinitis diagnosis, sex, second-hand smoke exposure, presence of pets at home, family history of allergic disorders, sensitization to Parietaria judaica; grass pollen; house dust mites; Olea europea: orchard; perennial rye; and cat allergens). Female sex, sensitization to Parietaria judaica and the presence of pets in the home were also significantly predictive of new onset asthma in the same model. Treatment with allergen immunotherapy was significantly and inversely related to the development of new onset asthma (OR, 0.53; 95%CI, 0.32–0.86).

In the present study we found that allergic rhinitis is an important independent risk factor for asthma. Moreover, treatment with allergen immunotherapy lowers the risk of the development of new asthma cases in adults with allergic rhinitis.

Persistent obstruction was assessed in 630 asthmatic subjects by measurement after bronchodilator of the maximum potential peak flow rate and forced vital capacity. Persistent obstruction was directly related to duration of asthma. The fit was slightly better after logarithmic transformation, suggesting that the early stages of asthma may be as important as the later ones in the development of persistent obstruction. On multivariate analysis age was an additional factor in males, but made no significant difference to females. Atopy did not prove relevant. Measurements of peak flow suggested a more rapid deterioration in males of social classes III, IV and V than classes I and II. Although current smokers had lower peak flow rate and vital capacity than non-smokers, there was no evidence of a steeper decline in smokers than non-smokers suggesting that the effect of cigarette smoking was at most additive to that of duration of asthma.

Background

Severe asthma is a heterogeneous condition. Airway remodelling is a feature of severe asthma and can be determined by the assessment of high-resolution computed tomography (HRCT) scans. The aim of this study was to assess whether airway remodelling is restricted to specific subphenotypes of severe asthma.

Methods

A retrospective analysis was performed of HRCT scans from subjects who had attended a single-centre severe asthma clinic between 2003 and 2008. The right upper lobe apical segmental bronchus (RB1) dimensions were measured and the clinical and sputum inflammatory characteristics associated with RB1 geometry were assessed by univariate and multivariate regression analyses. Longitudinal sputum data were available and were described as area under the time curve (AUC). Comparisons were made in RB1 geometry across subjects in four subphenotypes determined by cluster analysis, smokers and non-smokers, and subjects with and without persistent airflow obstruction.

Results

Ninety-nine subjects with severe asthma and 16 healthy controls were recruited. In the subjects with severe asthma the RB1 percentage wall area (%WA) was increased (p=0.009) and lumen area (LA)/body surface area (BSA) was decreased (p=0.008) compared with controls but was not different across the four subphenotypes. Airway geometry was not different between smokers and non-smokers and RB1 %WA was increased in those with persistent airflow obstruction. RB1 %WA in severe asthma was best associated with airflow limitation and persistent neutrophilic airway inflammation (model R2=0.27, p=0.001).

Conclusions

Airway remodelling of proximal airways occurs in severe asthma and is associated with impaired lung function and neutrophilic airway inflammation.

Introduction

The purpose of this study was to determine the effect of cigarette smoking on the risk of hip fracture for postmenopausal women living in rural and urban areas of Northwest Texas.

Methods

Using an unmatched case-control design, we compared postmenopausal women who had recently experienced osteoporotic hip fracture with women who had not. Both study groups completed a questionnaire on demographic, clinical, and behavioral risk factors for osteoporotic hip fracture. We categorized smoking status as never smoked, former smoker, and current smoker. Covariates included age, weight, age at menopause, physical activity, estrogen replacement, calcium supplementation, and rurality. We used univariate and multivariate logistic regressions to test the associations between hip fracture and the independent variables of interest.

Results

We found an increased risk of hip fracture for former smokers (adjusted odds ratio [OR], 2.27; 95% confidence interval [CI], 1.22–4.21) and current smokers (adjusted OR, 3.72; 95% CI, 1.59–8.70). Residence in a rural county (population <100,000) also was associated with increased risk (adjusted OR, 2.71; 95% CI, 1.48–4.95).

Conclusion

Former and current smoking increased the risk of hip fracture in this population of postmenopausal women.

Objective To assess the risk of lung cancer in smokers of medium tar filter cigarettes compared with smokers of low tar and very low tar filter cigarettes.

Design Analysis of the association between the tar rating of the brand of cigarette smoked in 1982 and mortality from lung cancer over the next six years. Multivariate proportional hazards analyses used to assess hazard ratios, with adjustment for age at enrolment, race, educational level, marital status, blue collar employment, occupational exposure to asbestos, intake of vegetables, citrus fruits, and vitamins, and, in analyses of current and former smokers, for age when they started to smoke and number of cigarettes smoked per day.

Setting Cancer prevention study II (CPS-II).

Participants 364 239 men and 576 535 women, aged ≥ 30 years, who had either never smoked, were former smokers, or were currently smoking a specific brand of cigarette when they were enrolled in the cancer prevention study.

Main outcome measure Death from primary cancer of the lung among participants who had never smoked, former smokers, smokers of very low tar (≤ 7 mg tar/cigarette) filter, low tar (8-14 mg) filter, high tar (≥ 22 mg) non-filter brands and medium tar conventional filter brands (15-21 mg).

Results Irrespective of the tar level of their current brand, all current smokers had a far greater risk of lung cancer than people who had stopped smoking or had never smoked. Compared with smokers of medium tar (15-21 mg) filter cigarettes, risk was higher among men and women who smoked high tar (≥ 22 mg) non-filter brands (hazard ratio 1.44, 95% confidence interval 1.20 to 1.73, and 1.64, 1.26 to 2.15, respectively). There was no difference in risk among men who smoked brands rated as very low tar (1.17, 0.95 to 1.45) or low tar (1.02, 0.90 to 1.16) compared with those who smoked medium tar brands. The same was seen for women (0.98, 0.80 to 1.21, and 0.95, 0.82 to 1.11, respectively).

Conclusion The increase in lung cancer risk is similar in people who smoke medium tar cigarettes (15-21 mg), low tar cigarettes (8-14 mg), or very low tar cigarettes (≤ 7 mg). Men and women who smoke non-filtered cigarettes with tar ratings ≥ 22 mg have an even higher risk of lung cancer.

The objective of this study was to assess disparities in health care utilization, by smoking status, among adults in the United States. We used 1999–2004 National Health and Nutrition Examination Survey (NHANES) data from 15,332 adults. Multivariate logistic regressions were used to examine the relationship between smoking status (current, former, and never smoker), with health care utilization. After controlling for demographic characteristics, current smokers and former smokers who quit either <2 years or ≥10 years prior to the survey were more likely to have had inpatient admission in the past year than never smokers. Current smokers did not differ from never smokers on whether they had an outpatient visit in the past year. They were, however, more likely than never smokers to have ≥4 outpatient visits. Smokers who quit either <2 years ago or ≥10 years ago were more likely to have had an outpatient visit than never smokers. Former smokers were more likely than never smokers to have ≥4 outpatient visits regardless of when they quit. Our results show that cigarette smoking is associated with higher health care utilization for current and former smokers than for never smokers. Frequent hospitalization and outpatient visits translate into higher medical costs. Therefore, more efforts are needed to promote interventions that discourage smoking initiation and encourage cessation.

Objective. Among current smokers, the proportion of Nondaily smokers is increasing. A better understanding of the characteristics and smoking behaviors of Nondaily smokers is needed. Methods. We analyzed data from the New York City (NYC) Community Health Survey to explore Nondaily smoking among NYC adults. Univariate analyses assessed changes in Nondaily smoking over time (2002–2010) and identified unique characteristics of Nondaily smokers; multivariable logistic regression analysis identified correlates of Nondaily smoking in 2010. Results. The proportion of smokers who engage in Nondaily smoking significantly increased between 2002 and 2010, from 31% to 36% (P = 0.05). A larger proportion of Nondaily smokers in 2010 were low income and made tax-avoidant cigarette purchases compared to 2002. Smoking behaviors significantly associated with Nondaily smoking in 2010 included smoking more than one hour after waking (AOR = 8.8, 95% CI (5.38–14.27)); buying “loosies” (AOR = 3.5, 95% CI (1.72–7.08)); attempting to quit (AOR = 2.3, 95% CI (1.36–3.96)). Conclusion. Nondaily smokers have changed over time and have characteristics distinct from daily smokers. Tobacco control efforts should be targeted towards “ready to quit” Nondaily smokers.

Background: Childhood exposure to environmental tobacco smoke has been extensively associated with childhood respiratory illness; fewer studies have addressed the effects on adults.

Methods: Childhood environmental tobacco smoke exposure in relation to chronic cough, phlegm, and asthma diagnosis was studied in never smokers from a cohort of Singaporeans of Chinese ethnicity aged 45–74 years at enrolment from 1993 to 1998. From 1999 to 2004 subjects were interviewed regarding environmental tobacco smoke exposure before and after the age of 18 and the presence and duration of current symptoms of chronic cough and phlegm production and asthma diagnosis.

Results: Among 35 000 never smokers, fewer had smoking mothers (19%) than fathers (48%). Although few subjects currently lived (20%) or worked (4%) with smokers, 65% reported living with a daily smoker before the age of 18 years. Living with a smoker before the age of 18 increased the odds of chronic dry cough (149 cases, odds ratio 2.1, 95% CI 1.4 to 3.3) and, to a lesser extent, phlegm, after adjustment for age, sex, dialect group, and current and past exposure to smokers at home and at work after the age of 18. Associations strengthened with higher numbers of smokers in childhood. There was no association with asthma or chronic bronchitis. There was evidence to suggest a stronger association among subjects with a lower adult intake of fibre which has previously been found to be protective for respiratory symptoms.

Conclusions: In this large study of non-smokers, living with a smoker in childhood was associated with chronic dry cough and phlegm in adulthood, independent of later exposures to environmental tobacco smoke.

Objective: To assess whether starting to smoke in childhood increases the risk of obstructive airways disease (OAD) in adult life.

Methods: A retrospective cohort analysis was undertaken of 12 504 current and ex-smokers in the EPIC-Norfolk cohort. The main exposure was starting to smoke during childhood (age <16 years). Three definitions of OAD were used: doctor diagnosed asthma, doctor diagnosed bronchitis/emphysema, and "any OAD" (doctor diagnosed asthma or bronchitis/emphysema, or taking medication used in the treatment of OAD).

Results: Childhood smokers had significantly more pack years of exposure and poorer lung function than subjects who started to smoke in adulthood (⩾16 years). Compared with starting in adulthood, starting to smoke in childhood was associated with a greater risk of bronchitis/emphysema in female smokers (OR 1.79, 95% CI 1.25 to 2.56) and ex-smokers of both sexes (OR 1.29, 95% CI 1.07 to 1.55 in men and OR 1.40, 95% CI 1.05 to 1.85 in women), and of "any OAD" in female smokers (OR 1.72, 95% CI 1.24 to 2.38) and male and female ex-smokers (OR 1.20, 95% CI 1.03 to 1.40 in men and 1.34, 95% CI 1.07 to 1.57 in women). After adjustment for pack years, childhood smoking was associated with poorer lung function (FEV1 92.3% predicted in adult smokers and 89.5% in childhood smokers, p = 0.03) and a greater risk of bronchitis/emphysema (adjusted OR 1.55, 95% CI 1.08 to 2.24) and for "any OAD" (OR 1.54, 95% CI 1.10 to 2.13) in female smokers but not in male and female ex-smokers.

Conclusion: Starting to smoke in childhood is associated with an increased risk of airways disease because of the extra pack years smoked. In women, childhood smoking is itself an independent risk factor for the development of airways disease.

BACKGROUND--Previous studies investigating the effect of cigar or pipe smoking on the occurrence of chronic cough and chronic phlegm have reported prevalences among cigar and pipe smokers lying between those of non-smokers and current cigarette smokers. This study uses data on previous cigarette consumption, current cigar or pipe consumption, and biochemical markers of smoking to provide a detailed analysis of chronic cough and chronic phlegm among cigar and pipe smokers. METHODS--A total of 10,359 men and women aged 40-59 years were sampled for the Scottish Heart Health Study between 1984 and 1986. Prevalence of chronic cough and chronic phlegm among male cigar and pipe smokers (non-cigarette smokers) was compared with those who had never smoked, between ex-smokers of cigarettes and those who had never smoked cigarettes, between cigar-only and pipe-only smokers, and by cigar or pipe consumption levels. RESULTS--In all, 463 ex-smokers of cigarettes and 154 who had never smoked cigarettes were cigar or pipe smokers; 1080 had never smoked any form of tobacco. Ex-cigarette smokers smoked and inhaled more than those who had never smoked cigarettes. Among the ex-cigarette smokers, cigar or pipe smokers had 1.63-1.71 times the prevalence of both chronic cough and chronic phlegm than those who had never smoked (1.31-1.36 among cigar only smokers; 2.23-2.84 among pipe only smokers). A strong positive dose-response effect was found between the prevalence of symptoms and cigar or pipe consumption. CONCLUSIONS--Cigar and pipe smokers have a higher prevalence of chronic cough and phlegm than those who have never smoked, and the difference is more marked in pipe-only smokers than in cigar-only smokers. Both categories show a positive dose-response effect. Among cigar and pipe smokers, ex-cigarette smokers have a higher prevalence of symptoms than those who have never smoked cigarettes, which may be because they inhale more or may be attributable to previous cigarette smoking.

Objectives

Cigarette smoking is a modifiable risk factor for cardiovascular disease. Bilirubin is a potent antioxidant and its concentration decreases in smokers. However, studies about the association between cigarette smoking and bilirubin are scarce and most are limited to total bilirubin. Additionally, bilirubin is highly related to hemoglobin. Therefore, this study evaluates the association between bilirubin subtypes and cigarette smoking in healthy Korean men independently of hemoglobin.

Methods

This study included 48 040 Korean men aged 30 to 87 years who visited the Korea Medical Institute for routine health examinations from January to December, 2007. The association of smoking with total, direct, and indirect bilirubin was assessed by logistic regression analysis taking into consideration differences in subjects and smoking characteristics.

Results

Current smokers had lower bilirubin concentrations than never-smokers and ex-smokers. Smoking amount and duration were inversely significantly associated with total, direct, and indirect bilirubin. In a multivariable adjusted model, compared to never-smokers, the odds ratios (ORs) and 95% confidence intervals (CIs) of current smokers with the highest number of pack-years were 1.7 (1.6 to 1.9) for total, 1.5 (1.4 to 1.6) for direct, and 1.7 (1.6 to 1.9) for indirect bilirubin. After further adjustment for hemoglobin, this association became stronger (OR [95% CI], 2.1 [1.9 to 2.2] for total; 1.9 [1.8 to 2.0] for direct; 2.0 [1.9 to 2.2] for indirect bilirubin).

Conclusions

In this study, bilirubin subtypes are inversely associated with smoking status, smoking amount, and smoking duration in healthy Korean men independently of hemoglobin. Further studies are needed to investigate this association in healthy Korean women.

The prevalence and incidence of asthma in relation to cigarette smoking habits was studied in a population of 14,729 Finnish adult men and women who participated in a postal health survey in 1975. Of those invited to participate in a new survey in 1981, 89.7% replied. Asthma was diagnosed on the basis of self reporting of asthma diagnosed by a physician and by record linkage to a national register of hospital admissions to all general and tuberculosis hospitals during 1972 and 1983. The prevalence of diagnosed asthma in 1975 was significantly higher among male smokers than among male non-smokers (relative risk (RR) = 1.73); no significant difference was observed for women (RR = 1.33). People with asthma were slightly but not significantly more likely to stop smoking during the six year follow up period (RR = 1.23). The incidence of asthma among those who had neither reported asthma in 1975 nor been admitted to hospital for asthma before the 1975 questionnaire study was not significantly higher among smokers than among non-smokers during follow up. Although possible mechanisms exist to explain how smoking could have a role in the aetiology of asthma, this study suggests that smoking is not a strong risk factor for asthma.

Background

Severe asthma subjects have increased physiologically measured air trapping. However, a similar study using CT measures of air trapping has not been performed. This study was designed to address two hypotheses: 1) air trapping, measured by multi-detector CT quantitative methodology, would be a predictor of a more severe asthma phenotype; and 2) historical, clinical, allergic, or inflammatory risk factors could be identified via multivariate analysis.

Methods

Multi-detector CT scanning of a subset of the Severe Asthma Research Program subjects was performed at functional residual capacity. Air trapping was defined as 9.66% or more of the lung tissue less than −850 HU. Subjects who were defined as air trappers were then compared to non-trappers on clinical and demographic factors using both univariate and multivariate statistical analysis.

Results

Air trappers were significantly more likely to have a history of asthma-related hospitalizations, ICU visits and/or mechanical ventilation. Duration of asthma (OR 1.42, 95% CI 1.08–1.87), history of pneumonia (OR 8.55, 95% CI 2.07–35.26), high levels of airway neutrophils (OR 8.67, 95% CI 2.05–36.57), air flow obstruction (FEV1/FVC) (OR 1.61, 95% CI 1.21–2.14) and atopy (OR 11.54, 95% CI 1.97–67.70), were identified as independent risk factors associated with the air trapping phenotype.

Conclusions

Quantitative CT determined air trapping in asthmatic subjects identifies a group of individuals with a high risk of severe disease. Several independent risk factors for the presence of this phenotype were identified, perhaps most interestingly history of pneumonia, neutrophilic inflammation, and atopy.

OBJECTIVES

To analyze the association between cigarette smoking and biochemical recurrence (BCR) after radical prostatectomy among men from the Shared Equal Access Regional Cancer Hospital (SEARCH) cohort.

METHODS

We performed a retrospective analysis of 1267 subjects from the SEARCH cohort treated from 1998 to 2008 with smoking status available from the preoperative notes. A comparison of the baseline patient and disease characteristics between the current smokers and nonsmokers (past and never smokers combined) was performed using the chi-square and rank sum tests. The univariate and multivariate associations between smoking status and BCR-free survival were analyzed using Kaplan-Meier plots, the log-rank test, and Cox proportional hazard models.

RESULTS

Of the 1267 patients, 408 (32%) were active smokers and 859 (68%) were nonsmokers at surgery. The current smokers were younger (P < .001), more likely to be black (P < .001), and had a lower body mass index (P < .001), a greater percentage of positive biopsy cores (P = .039), a greater preoperative prostate-specific antigen level (P = .003), more extracapsular extension (P = .003) and seminal vesicle invasion (P = .029), and lower prostate volumes (P = .002). On univariate analysis, smokers had a risk of BCR similar to that of nonsmokers (hazard ratio 1.19, P = .129). On multivariate analysis, smoking was associated with an increased risk of BCR when adjusted for body mass index only (hazard ratio 1.37, P = .008). However, after adjustment for multiple preoperative characteristics, the association was attenuated and no longer statistically significant (hazard ratio 1.12, P = .325). After additional adjustment for postoperative features, such as tumor grade and stage, smoking was unrelated to the risk of BCR (hazard ratio 0.91, P = .502).

CONCLUSIONS

Among patients undergoing radical prostatectomy in the SEARCH cohort, cigarette smoking was associated with slightly more advanced disease but a similar risk of BCR.

Rationale: Although involuntary exposure to maternal smoking during the in utero period and to secondhand smoke are associated with occurrence of childhood asthma, few studies have investigated the role of active cigarette smoking on asthma onset during adolescence.

Objectives: To determine whether regular smoking is associated with the new onset of asthma during adolescence.

Methods: We conducted a prospective cohort study among 2,609 children with no lifetime history of asthma or wheezing who were recruited from fourth- and seventh-grade classrooms and followed annually in schools in 12 southern California communities. Regular smoking was defined as smoking at least seven cigarettes per day on average over the week before and 300 cigarettes in the year before each annual interview. Incident asthma was defined using new cases of physician-diagnosed asthma.

Measurements and Main Results: Regular smoking was associated with increased risk of new-onset asthma. Children who reported smoking 300 or more cigarettes per year had a relative risk (RR) of 3.9 (95% confidence interval [95% CI], 1.7–8.5) for new-onset asthma compared with nonsmokers. The increased risk from regular smoking was greater in nonallergic than in allergic children. Regular smokers who were exposed to maternal smoking during gestation had the largest risk from active smoking (RR, 8.8; 95% CI, 3.2–24.0).

Conclusions: Regular smoking increased risk for asthma among adolescents, especially for nonallergic adolescents and those exposed to maternal smoking during the in utero period.

The effects of smoking on the development of work related asthma and on the production of specific IgE and IgG antibodies to antigen from a contaminated humidifier are described for a sample of 258 workers from a printing factory. Current smoking was associated with low production of IgG antibody but with higher production of IgE antibody. No dose response for either antibody was found when numbers of cigarettes or pack-years smoked were considered. Work related asthma was detected in 12 workers by peak flow recordings. Six were current smokers and one was an ex-smoker. One subject with work related asthma had a high (and one a marginal) concentration of specific IgE to humidifier antigen.

Introduction

A number of personality traits have been associated with cigarette smoking. Current smokers generally show higher levels of negative emotionality and lower levels of behavioral constraint than former smokers and those who never smoked. However, prior investigations have not examined thoroughly whether these smoking–personality associations are unique to smoking status or simply reflect the fact that these personality traits tend to be elevated across numerous forms of psychopathology. Likewise, prior studies have not addressed whether personality shows differential associations with smoking based on the presence or absence of lifetime psychiatric disorders.

Methods

The present study examined these questions using data from 472 current, 311 former, and 324 never-smokers aged 34–44 years.

Results

Current smokers reported being more reactive to stress, more aggressive, more alienated, and less harm avoidant than both former smokers and never-smokers, whereas former smokers and never-smokers showed similar personality profiles overall. Psychiatric disorder history did not interact with smoking status in predicting personality. Controlling for differences in four major lifetime psychiatric disorders (major depression, alcohol dependence, drug dependence, and conduct disorder) reduced the differences in personality traits associated with smoking status. However, smoking status continued to relate uniquely and significantly to higher levels of negative emotionality and behavioral undercontrol with the most robust effect observed for trait alienation.

Discussion

These results provide the most comprehensive depiction to date of interrelations among personality, psychopathology, and smoking and suggest an important role of personality in smoking that is not redundant with or conditional upon lifetime psychopathology.

The associations between cigarette smoking, plasma leucocyte elastase concentration, peripheral leucocyte count and FEV1 were examined in 148 men, 72 of whom were current cigarette smokers, 40 of whom were ex-smokers, and 36 who had never smoked. All men were part of a long-term survey. Smokers had significantly higher plasma leucocyte elastase concentrations than ex-smokers or those who had never smoked. Mean current FEV1 was lower, and the annual decline in FEV1 in the preceding 10 years was faster in smokers than the other two groups. A few smokers had slight increases in serum C-reactive protein concentrations. Although peripheral blood leucocyte counts were higher in smokers than in non-smokers or ex-smokers, no association was found in any of the three groups of men between plasma elastase concentration and peripheral leucocyte count, nor between either of these two variables and annual decline in FEV1 or current level of FEV1. There was also no relation between plasma elastase concentration and reported daily cigarette consumption or mixed expired carbon monoxide in smokers. The results indicate that some male smokers have increased in vivo release of elastase from peripheral blood neutrophils at a time when there is no evidence of acute infection. Because leucocyte elastase is a strong candidate for pulmonary tissue damage, further studies of the mechanisms that increase plasma concentrations are indicated.

BACKGROUND: Exposure to chromium during electroplating is a recognised though poorly characterised cause of occupational asthma. The first series of such patients referred to a specialist occupational lung disease clinic is reported. METHODS: The diagnosis of occupational asthma was made from a history of asthma with rest day improvement and confirmed by specific bronchial provocation testing with potassium dichromate and nickel chloride. RESULTS: Seven workers had been exposed to chrome and nickel fumes from electroplating for eight months to six years before asthma developed. One subject, although exposed for 11 years without symptoms, developed asthma after a single severe exposure during a ventilation failure. This was the only subject who had never smoked. The diagnosis was confirmed by specific bronchial challenges. Two workers had isolated immediate reactions, one a late asthmatic reaction, and four a dual response following exposure to nebulised potassium dichromate at 1-10 mg/ml. Two of the four subjects were also challenged with nebulised nickel chloride at 0.1-10 mg/ml. Two showed isolated late asthmatic reactions, in one at 0.1 mg/ml, where nickel was probably the primary sensitising agent. Four workers carried out two hourly measurements of peak expiratory flow over days at and away from work. All were scored as having occupational asthma using OASYS-2. Breathing zone air monitoring was carried out in 60 workers from four decorative and two hard chrome plating shops from workers with similar jobs to those sensitised. No measurement exceeded the current occupational exposure standard for chromate or nickel, the mean levels of chromate exposure for jobs similar to those of the affected workers were 9-15 micrograms/m3. CONCLUSION: Chrome used in electroplating is a potential cause of occupational asthma. Sensitivity to chrome in electroplaters may occur in situations where exposure levels are likely to be within the current exposure standards. There may be cross reactivity with nickel. Inhalation challenge with nebulised potassium dichromate solution is helpful in making the specific diagnosis where doubt exists. 




Purpose

Rhinitis and asthma usually occur together. There are increasing evidences that allergic rhinitis (AR) may influence the clinical course of asthma. The aim of this study is to evaluate clinical parameters and therapeutic response in patients with between asthma and asthma with AR.

Methods

Four-hundred eighty-five patients with asthma and 428 asthmatics with AR, who had lesser than 50 years old and smoked less than 10 pack-years were recruited. We compared FEV1 and FEV1/FVC following bronchodilator, atopy, IgE, emphysema on HRCT, and aspirin intolerance between two groups. Also we compared physiologic fixed airway obstruction defined using FEV1/FVC and FEV1 less than 75% following anti-asthmatic drug for 1 year.

Results

46.8% (428/913) asthmatics suffered from AR. There were no differences of total IgE, body mass index, PC20, sputum eosinophils and emphysema on HRCT between two groups. The age in asthmatics was higher than that in those with AR. FEV1/FVC was lower in asthmatics than in those with AR. The prevalence of atopy was higher in asthmatics with AR than in asthmatics. Aspirin intolerance was higher in asthmatics with AR than in asthmatics (42/218 vs 13/109, P=0.001). Fixed airway obstruction were more observed in asthmatics than in those with AR (39/319 vs 28/355, P=0.001) after anti-asthmatic drug for 1 year.

Conclusions

Asthmatics with AR had more atopy and aspirin intolerance than asthmatics, and asthmatics had poor response to anti-inflammatory drugs than those with concurrent rhinitis, indicating that asthmatics have more fixed airway obstruction than those with concurrent rhinitis.

OBJECTIVE--To determine whether tobacco smoking causes increased DNA modification (adducts) in human cervical epithelium. DESIGN--Comparison of DNA adducts measured by the technique of postlabelling with phosphorus-32 in normal ectocervical epithelium of smokers and non-smokers. A questionnaire on smoking habit and a urinary cotinine assay were used to identify smokers and non-smokers. SETTING--Cytology unit in large teaching hospital. SUBJECTS--39 women (11 current smokers, seven former smokers, and 21 who had never smoked) undergoing gynaecological treatment (colposcopy or hysterectomy). Nineteen members of staff who did not smoke as controls. INTERVENTIONS--Biopsy of normal ectocervical epithelium. Urine sample. MAIN OUTCOME MEASURES--Measurement of DNA adducts in cervical epithelial tissue of smokers and non-smokers. Smoking habit derived from results of questionnaire and urinary cotinine:creatinine ratio. Proportion of adducts in women with abnormal and normal results of cervical smear test. RESULTS--DNA samples from smokers (identified from questionnaire) had significantly higher median proportions of DNA adducts that non-smokers (4.62 (95% confidence interval 4.04 to 7.74) v 3.47 (2.84 to 4.78) adducts/10(8) nucleotides; p = 0.048). Exclusion of women whose urinary cotinine:creatinine ratio did not confirm their self reported smoking habit (smoker or non-smoker) increased this difference (4.7 (3.85 to 8.08) v 3.52 (2.32 to 4.95) adducts/10(8) nucleotides; p = 0.03). Women who had abnormal results of cervical smear tests had significantly higher proportions of adducts than those with normal results (4.7 (3.90 to 8.13) v 3.47 (3.06 to 5.36) adducts/10(8) nucleotides; p = 0.03). CONCLUSIONS--Tobacco smoking by women leads to increased modification of DNA in cervical epithelium, suggesting biochemical evidence consistent with smoking as a cause of cervical cancer.

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