Natural killer cell activity in cigarette smokers and asbestos workers

In order to evaluate the effects of cigarette smoking and asbestos exposure on cellular immunity, we tested a group of cigarette smokers and asbestos workers for natural killer (NK) activity in the peripheral blood. The mean NK activity in cigarette smokers was lower than in normal subjects (13.7 +/- 1.6 versus 29.0 +/- 3%; p less than 0.05). As a group, the mean NK activity for the asbestos-exposed group was also reduced compared with that of the nonsmoking control group (22.6 +/- 3.2%; p less than 0.05). When divided according to the smoking status, the asbestos workers who were nonsmokers or ex-smokers showed similar decreases in NK activity compared with normal subjects (19.5 +/- 6.2 and 21.2 +/- 4.5%, respectively; p less than 0.05). A subgroup of asbestos-exposed subjects who currently smoked showed no decrease in NK activity. The data show that NK activity is reduced in the peripheral blood of cigarette smokers and asbestos workers. The relatively normal NK activity found in asbestos workers who also smoked is unexplained. Impairment of NK activity is a potential mechanism for the increased incidence of infection and cancer in smokers and neoplasia in asbestos workers.     

Severity of pulmonary asbestosis as classified by International Labour Organisation profusion of irregular opacities in 8749 asbestos-exposed American workers. Those who never smoked compared with those who ever smoked.

The profusion of irregular opacities on chest roentgenograms by International Labour Organisation pneumoconiosis criteria was used to assess the severity of asbestosis in 8749 asbestos-exposed active and retired American workers. Seventy-eight percent had no asbestosis (category 0/0 or 0/1), 18.6% had slight asbestosis (1/0 to 1/2), 3% had moderate asbestosis (2/1 to 2/3), and 0.3% had advanced disease (3/2 or greater). Significantly more current smokers had asbestosis than did those who had never smoked, and their average profusion of opacities was higher. The mean age of current smokers with asbestosis was 60 years, whereas subjects with the disease who had never smoked had a mean age of 64 years, a significant difference. Cigarette smoking and asbestosis appear to act synergistically to produce irregular opacities on chest roentgenograms of asbestos-exposed American workers.     

Smoking Prevalence Among General Practitioners' Patients

The prevalence of smoking is reported in a representative sample of 2,616 patients attending the surgeries of 28 General Practitioners (GPs) in London. 43% of the men and 34 % of the women were current cigarette smokers. These figures are substantially lower than those of the general population due to a higher proportion of ex-smokers rather than those who have never smoked. Daily cigarette consumption of current smokers, at 19 per day for men and 16 per day for women, was similar to the general population. The excess of ex-smokers was comprised mainly of those who had stopped smoking recently possible due to the current illness causing their attendance at the surgery, and who under natural circumstances would be likely to start smoking again after recovery. Besides current cigarette smokers, this group of recent ex-smokers would seem an ideal target for preventive intervention by GPs.     

Association of cigarette smoking with decreased numbers of circulating natural killer cells

To investigate the relationship between cigarette smoking and the level of circulating natural killer (NK) cells, we studied 282 subjects from a population-based, stratified random sample of healthy persons. NK cells were enumerated by flow cytometry using the monoclonal antibody anti-Leu 11A. Cigarette smokers had a significantly lower proportion of NK cells than did subjects who had never smoked (5.5 +/- 0.3% versus 7.4 +/- 0.4% of lymphoid cells; p = 0.0002). NK cells were also decreased among ex-smokers (5.6 +/- 0.4%; p = 0.002), including subjects who had not smoked for more than 20 yr. The white blood cell and lymphocyte counts were increased in smokers compared with those in never smokers (p less than 0.0001). In contrast to NK cells, the smoking-related changes in leukocyte count were not present in ex-smokers, even those who had stopped smoking within the past year. Multivariate analysis confirmed that both current and past smokers had significant decreases in both the number and proportion of NK cells after controlling for age, sex, and lymphocyte count. These data indicate that cigarette smoking is associated with a decrease in the number and proportion of circulating NK cells, and that this effect is present many years after smoking cessation. This quantitative NK cell deficit may contribute to the elevated risk of malignancy in this population.     

Lung function and exercise performance in smoking and nonsmoking asbestos-exposed workers

Evaluation of impairment caused by exposure to an occupational toxin can be complicated by additional exposure to other injurious agents. Because cigarette smoking is common and cigarettes are implicated in obstructive lung disease and cardiovascular diseases, we assessed the contribution of smoking to functional abnormalities in a group of asbestos-exposed shipyard workers. Seventy-three workers who never smoked were paired with 73 current smokers by age and asbestos exposure. Pulmonary function and performance during cycle incremental exercise were compared between the 2 groups. Nonsmokers had significantly higher VC, FEV1, FEV1/VC, and diffusing capacity for carbon monoxide than did smokers. Only 3 of the 73 nonsmokers but 23 of the 73 smokers had a FEV1/VC below the 95% confidence limit of predicted value. The FEF25-75%, on the other hand, failed to identify additional subjects with obstruction not found by the FEV1/VC. During exercise, despite no difference in maximal heart rate, the maximal O2 uptake (VO2max) and oxygen-pulse were lower among smokers. In addition, smokers more frequently had abnormal AaPO2 at maximal exercise. Of 33 smokers who had a VO2max less than 80% of predicted, 16 were judged to have cardiac disease, whereas only 2 appeared to be limited by obstruction. Only 15 of the 73 nonsmokers had a VO2max less than 80%. We conclude that cigarette smoking was the major contributing factor to the obstructive lung disease observed in asbestos workers, and it also had a strong influence on the occurrence, nature, and magnitude of exercise limitation. The history of cigarette smoking has an important effect on the assessment of impairment from asbestos.     

Natural killer cell activity in asbestos workers. Interactive effects of smoking and asbestos exposure

Both the numbers and function of natural killer (NK) cells in 60 were evaluated in asbestos cement workers grouped by smoking history and chest roentgenogram findings (ILO profusion scores less than 1/0 or greater than or equal to 1/0, or isolated pleural plaques). Worker and control subjects who smoked had smoking histories of less than 27 pack-years, a level of smoking lower than that previously determined to adversely affect NK function. Asbestos workers who did not smoke had percentages and total numbers of NK cells and NK function not different from that of nonsmoker control subjects. Workers who smoked and had evidence of asbestosis (ILO profusion category greater than or equal to 1/0) had significantly lower total numbers of NK cells and mononuclear cell NK activity than did smoker control subjects or smokers with pleural plaques only (p less than or equal to 0.05). Numbers of NK cells and NK cell function were not decreased in either of the asbestos-exposed smoking groups without asbestosis when compared to nonsmoker controls. We conclude that smoking and asbestos exposure interact to decrease mononuclear cell NK function in workers with levels of asbestos exposure sufficient to induce asbestosis. This finding may explain in part the previously reported synergistic effect of smoking and asbestos exposure on the risk of lung cancer. Furthermore, the data presented here clarify previous conflicting reports on NK function where asbestos exposed groups have not been stratified for analysis of data.     

Outpatient endoscopic survey of smoking and peptic ulcer.

A survey of the smoking habits of 1217 outpatients undergoing upper gastrointestinal endoscopy was carried out over an 18 month period. Six hundred and twenty four were current smokers, 248 ex-smokers and 345 non-smokers. 11.9% of smokers had gastric ulcers, 7.7% of ex-smokers (p less than 0.025) and 4.6% of non-smokers (p less than 0.001). 2.8% of smokers had duodenal ulcers, 6.8% of ex-smokers (p less than 0.01) and 6.1% of non-smokers (p less than 0.001). There was a dose response effect between the number of cigarettes smoked and duodenal and gastric ulceration. Gastric cancer was also more frequent in smokers than non-smokers (p less than 0.01), but macroscopic oesophagitis less frequent (p less than 0.001). The results confirm the association between smoking and peptic ulcer.     

Smoking, lung function, and rheumatoid factors.

Positive rheumatoid factor (RF) reactions commonly precede the onset of clinically manifest rheumatoid arthritis (RA). Thus if items associated with RF reactions were traced at the community level this might provide clues to the cause of RA. The relations between smoking and lung functions and the occurrence of RA and RFs in a population sample representative of the adult Finnish population were studied. Rheumatoid factor testing was performed for 7124 subjects (89% of the sample) by the sensitised sheep cell agglutination test. Forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) were measured with spirometry. 'False positive' RF reactions occurred twice as often in current smokers and ex-smokers than in those who had never smoked. The prevalence of high titres was fourfold greater among current smokers than among those who had never smoked. These associations were statistically significant and independent of age, FVC, and FEV1 in both sexes. The women with airflow limitation (FEV1/FVC less than 70%) had a significantly increased occurrence of RFs which was independent of their smoking history, but no such relationship was found in men. The results suggest an impact of smoking on RF production; a follow up study may show whether the raised RF titers in smokers will be reflected as an increased incidence of RA.     

Increased alveolar plasminogen activator in early asbestosis

Alveolar macrophage-derived plasminogen activator (PA) activity is decreased in some chronic interstitial lung diseases such as idiopathic pulmonary fibrosis and sarcoidosis but increased in experimental models of acute alveolitis. Although asbestos fibers can stimulate alveolar macrophages (AM) to release PA in vitro, the effect of chronic asbestos exposure of the lower respiratory tract on lung PA activity remains unknown. The present study was designed to evaluate PA activity of alveolar macrophages and bronchoalveolar lavage (BAL) fluid in asbestos-exposed sheep and asbestos workers. Forty-three sheep were exposed to either 100 mg UICC chrysotile B asbestos in 100 ml phosphate-buffered saline (PBS) or to 100 ml PBS by tracheal infusion every 2 wk for 18 months. At Month 18, chest roentgenograms were analyzed and alveolar macrophage and extracellular fluid PA activity were measured in samples obtained by BAL. Alveolar macrophage PA activity was increased in the asbestos-exposed sheep compared to control sheep (87.2 +/- 17.3 versus 41.1 +/- 7.2 U/10(5) AM-24 h, p less than 0.05) as was the BAL fluid PA activity (674.9 +/- 168.4 versus 81.3 +/- 19.7 U/mg alb-24 h, p less than 0.01). Among the asbestos-exposed sheep, 10 had normal chest roentgenograms (Group SA) and 15 had irregular interstitial opacities (Group SB). Strikingly, whereas Group SA did not differ from the control group in BAL cellularity or PA activity, Group SB had marked increases in alveolar macrophages (p less than 0.005), AM PA activity (p less than 0.02), and BAL PA activity (p less than 0.001) compared to the control group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Increased content of thiobarbituric acid-reactive substances and hydrogen peroxide in the expired breath condensate of patients with stable chronic obstructive pulmonary disease: no significant effect of cigarette smoking.

The imbalance between oxidants and antioxidants is known to play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cigarette smoking is the most frequent factor responsible for development of COPD by leading to oxidant overload in the lower airways, due to presence of its own oxidants and to recruitment and activation of pulmonary phagocytes. We aimed to determine whether (1) patients with stable COPD have higher thiobarbituric acid-reactive substances (TBARs, an end-product of lipid peroxidation) and H2O2 levels in expired breath condensate than healthy subjects who have never smoked; (2) COPD subjects who are current smokers exhale more TBARs and H2O2 than COPD ex-smokers and those who have never smoked; and (3) concentration of TBARs correlates with H2O2 levels in the breath condensate of COPD patients. The TBAR and H2O2 content in expired breath condensate of 17 healthy nonsmoking subjects and 44 patients (11 current smokers, 20 ex-smokers and 13 who had never smoked) with stable COPD [forced expiratory volume in 1 s (FEV1) 63.3 +/- 16.3% and FEV1 reversibility 5.2 +/- 4.3% predicted value] was measured spectrofluorimetrically by the thiobarbituric acid and homovanillic acid methods, respectively. The mean concentrations of TBARs and H2O2 in the expired breath condensate of COPD subjects were 12 (0.48-0.86 microM vs. 0.04 +/- 0.14 microM; P < 0.05) and 10 times (0.48 +/- 0.67 microM vs. 0.05 +/- 0.07 microM; P < 0.005) higher than in healthy controls. Current smokers with COPD did not exhale more H2O2 than COPD ex-smokers and those who had never smoked. TBARs levels shared only a tendency to be higher in the breath condensate of smoking COPD subjects than in that of ex-smokers (0.92 +/- 1.49 microM vs. 0.35 +/- 0.44 microM) and of COPD subjects who had never smoked (0.92 +/- 1.49 microM vs. 0.30 +/- 0.53 microM). No correlation was found between TBAR and H2O2 levels in the whole COPD group. These variables did not correlate with cigarette smoking status and the time from smoking cessation. Subjects with stable COPD exhibit increased lipid peroxidation and H2O2 generation in the airways. Current cigarette smoking does not distinguish COPD subjects with respect to TBARs and H2O2 exhalation.     

Small airways changes in workers exposed to asbestos

Although restriction is considered the classic pulmonary function profile of asbestosis, studies suggest that obstruction of the peripheral airways not revealed by standard spirometry is equally frequent and indicative of peribronchiolar fibrosis. We recorded flows and volumes from maximal expiratory flow volume (MEFV) curves, closing volume data and the phase III slope of the alveolar plateau for 610 litigants, 575 men and 35 women, exposed to asbestos for varying periods in a single workplace in northern New Jersey. Smokers (260) included current smokers and subjects who had stopped within the previous 10 years; nonsmokers (350) had either never smoked or had given up for more than 10 years. Analyses were made for both groups according to years worked. Compared to predicted, smokers and nonsmokers had significantly higher closing capacities (p less than 0.01) and delta N2% (p less than 0.001) means, and lower forced vital capacity (FVC), forced expiratory volume for the first second (FEV1.0, maximal expiratory flow rate (MEFR) and peak expiratory flow rate (PEFR) functions (p less than 0.05); the flow rate after 75% of the FVC had been exhaled (FEF75%) values were significantly reduced (p less than 0.01) only for workers exposed for more than 30 years. The change from predicted was significantly more rapid for smokers, compared with nonsmokers, for FVC, FEV1.0, PEFR, MEFR and FEF75% means, while the increase in closing capacity (CC) was twice as rapid for nonsmokers and the two groups did not differ in their mean rates of rise for delta N2%. CC and the slope of the alveolar plateau appeared to be the measures best able to discriminate between the data for both smoking and nonsmoking asbestos workers and their lung function prediction means.(ABSTRACT TRUNCATED AT 250 WORDS)     

Depressive symptoms and smoking among Hong Kong Chinese adolescents

AIMS: To examine associations among depressive symptoms, smoking, smoking trajectories and quitting smoking in Hong Kong. DESIGN: Prospective longitudinal design, with wave 1 at baseline (T1) and wave 2 (T2) 12 months later. SETTING AND PARTICIPANTS: Form 1 (equivalent to 7th grade in the United States) students, mean age = 12.7 years, n = 1894. MEASUREMENTS: Self-reported smoking status, attempts to quit and depressive symptoms. FINDINGS: At both waves, current as well as ex-smokers had higher depressive symptoms than never smokers. T1 smoking predicted T2 depressive symptoms among those with low baseline depressive symptoms. Depressive symptoms at T1 predicted smoking at T2 among non-smokers at T1. Trajectories were defined by separating participants who were never smokers at both waves ('non-smokers'), those who smoked at both waves ('persistent smokers'), those who smoked at one time but were not smoking at either wave ('past smokers), and those who had never smoked at T1 but reported smoking a year later ('new smokers'). Persistent, past and new smokers had higher depressive symptoms at both waves than non-smokers. Smokers who reported not wanting or trying to quit and those who had been unsuccessful at quitting had higher depressive symptoms at T2 than those who successfully quit. CONCLUSION: Our results suggest that depressive symptoms promote tobacco use in Asian adolescents by making it more likely that an adolescent will begin smoking and less likely that she or he will quit. These findings elucidate risk factors in Hong Kong for two important public health concerns for adolescents: smoking and depression.     

Smoking and the risk of systemic lupus erythematosus

This study aims to study the association of smoking with the development of systemic lupus erythematosus (SLE). The study included 223 SLE patients (92 % women, mean age 47 years) and 1,538 population controls of similar age and socioeconomic status living in the metropolitan area of Finland. The history of smoking in patients and controls was obtained by personal interview. The prevalence of current and past smoking was more common in patients with SLE than in controls. In women with a history of daily smoking for more than 1 year, the odds ratio (OR) for SLE was 1.45 (95 % CI 1.07–1.97), in current daily smokers as compared to never smokers, the OR was 1.55 (1.00–2.40), and in ex-smokers versus never smokers 1.80 (1.15–2.83). The number of men with SLE, who had smoked more than 100 cigarettes during their lifetime was higher than in male controls (p?=?0.026). A history of smoking is significantly though modestly associated with the development of SLE.     

Evaluation of breathlessness in asbestos workers. Results of exercise testing

We studied 120 asbestos-exposed workers seeking compensation for asbestos-related ventilatory impairment who were referred to us for evaluation of their complaint of dyspnea. We reviewed history, chest radiographs, pulmonary function studies, and exercise tests. The workers were 59.9 +/- 9.5 (mean +/- SD) yr of age and their first asbestos exposure had been 34.4 +/- 10 yr prior to the study; 63% were smokers, 19% were ex-smokers, and 18% were nonsmokers. Chest radiographs were normal in 4%, showed only pleural disease in 35%, only parenchymal diseases in 5%, and pleuroparenchymal disease in 56%. Restrictive pulmonary function abnormalities were present in 25% of the workers, and obstructive abnormalities were present in 27%. Because the impairment of one of several organ systems (i.e., ventilatory, cardiac, pulmonary vascular, or peripheral circulatory) may limit exercise performance, we designed an exercise test score in an attempt to identify the system causing the limitation. No abnormal limitation was detectable in half (49.2%) of the subjects. Only 26% had a ventilatory limitation, which was much more frequent in smokers (32%) than in nonsmokers (9%) (p less than 0.05). Unexpectedly, rather more (37%) had a cardiac rather than a ventilatory limitation. We conclude that the complaint of dyspnea in these asbestos-exposed workers was usually not caused by a ventilatory dysfunction.     

Relationship between the duration of the preoperative smoke-free period and the incidence of postoperative pulmonary complications after pulmonary surgery

STUDY OBJECTIVE: To examine the relationship between the duration of the preoperative smoke-free period and the development of postoperative pulmonary complications (PPCs) in patients who underwent pulmonary surgery, and the optimal timing of quitting smoking. DESIGN: Retrospective cohort study. SETTING: Osaka Medical Center for Cancer and Cardiovascular Diseases, Osaka, Japan. PATIENTS: Two hundred eighty-eight consecutive patients who underwent pulmonary surgery between January 1997 and December 1998. Measurements and results: We collected information on the preoperative characteristics, intraoperative conditions, and occurrence of PPCs by reviewing the medical records. Study subjects were classified into four groups based on their smoking status. A current smoker was defined as one who smoked within 2 weeks prior to the operation. Recent smokers and ex-smokers were defined as those whose duration of abstinence from smoking was 2 to 4 weeks and > 4 weeks prior to the operation, respectively. A never-smoker was defined as one who had never smoked. The incidence of PPCs among the current smokers and recent smokers was 43.6% and 53.8%, respectively, and each was higher than that in the never-smokers (23.9%; p < 0.05). The moving average of the incidence of PPCs gradually decreased in patients whose smoke-free period was 5 to 8 weeks or longer. After controlling for sex, age, results of pulmonary function tests, and duration of surgery, the odds ratios for PPCs developing in current smokers, recent smokers, and ex-smokers in comparison with never-smokers were 2.09 (95% confidence interval [CI], 0.83 to 5.25), 2.44 (95% CI, 0.67 to 8.89), and 1.03 (95% CI, 0.47 to 2.26), respectively. CONCLUSIONS: These findings indicate that preoperative smoking abstinence of at least 4 weeks is necessary for patients who undergo pulmonary surgery, to reduce the incidence of PPCs.     

Effects of cessation of smoking on serum lipids and high density lipoprotein-cholesterol

This study examined the effect of cessation of smoking on serum lipid and lipoprotein levels. Twenty-six females who smoked a minimum of 20 cigarettes per day for the past 5 years served as volunteers. Twelve subjects abstained from smoking for a period of 60 days (ex-smokers). Six stopped smoking for 30 days then resumed smoking for an additional 30 days (re-smokers). Eight subjects continued to smoke for the entire 60 days (smokers). Additionally, 10 females who had never smoked served as non-smoking controls (non-smokers). Pre-cessation HDL-C levels for all smoker groups were 15-20% (P less than 0.05) below those of non-smokers. By day 30 of cessation HDL-C levels of ex-smokers and re-smokers significantly increased by 5.7 and 10.5 mg/dl, respectively, and were significantly higher than those of smokers. At day 60, HDL-C of ex-smokers increased another 6.8 mg/dl to 63.9 mg/dl while levels of re-smokers returned to pre-cessation levels (50.7 mg/dl). The findings of this study suggest that low levels of HDL-C associated with smoking in females do not appear to be cumulative and can be reversed in as little as 30 days.     

Effects of smoking habits on pulmonary function. Cross-sectional and longitudinal studies in male subjects on medical check-up]

Cross-sectional and longitudinal studies were done to evaluate effects of cigarette smoking and smoking cessation on age-related pulmonary function decline. Data on pulmonary function from 11,875 healthy asymptomatic men between the ages of 35 and 74 years were analyzed on the basis of smoking habits in each age group. Longitudinal changes in pulmonary function during a 5-yr period were also assessed in relation to smoking habits in 1888 healthy men. Cross-sectional studies showed that the difference of FEV1 between man current smokers and men who had never smoked is small at younger ages but increases with increases in age. A beneficial effect on FEV1 decline was observed in former smokers, even in less than 1 year after smoking cessation. Longitudinally, current smokers showed a more rapid decline in FEV1 in 5 years than nonsmokers. The men who quitted smoking had lower rates of decline in FEV1 than those who continued to smoke. These results indicate that cigarette smoking is associated with reduced pulmonary function and that smoking cessation may have a beneficial effect on FEV1 decline. Provision of a smoking cessation program for all smokers, especially those with a rapid decline of FEV1, should be considered a very important strategy to prevent progression of COPD.     

The association of cigarette smoking with disease outcome in patients with early inflammatory polyarthritis

OBJECTIVE: Cigarette smoking is known to increase rheumatoid factor (RF) and nodule formation in patients with rheumatoid arthritis (RA). In this study, we examined the influence of smoking on disease outcome at 3 years among patients newly presenting with inflammatory polyarthritis (IP). METHODS: We studied 486 patients with IP who were referred to the Norfolk Arthritis Register, of whom 323 (67%) satisfied the American College of Rheumatology 1987 criteria for RA. Smoking status was assessed at baseline. Disease outcome was assessed at 3 years, using measures of joint inflammation, functional disability, and radiologic damage. The influence of smoking on disease outcome was explored using logistic regression techniques, with patients who had never smoked as the referent group. Results are expressed as odds ratios (ORs), with their 95% confidence intervals (95% CIs). RESULTS: Current smokers were significantly more likely to be RF positive at baseline (47%) than were ex-smokers (34%) and never smokers (31%). After 3 years, rheumatoid nodules were significantly more common in smokers (13%) compared with ex-smokers/never smokers (4%), a relationship which persisted after adjusting for age and sex (OR 4.07, 95% CI 1.38-12). In contrast, after adjusting for age and sex, current smokers had significantly fewer swollen joints (OR 0.61, 95% CI 0.37-0.98). However, smoking status had no influence on the development of erosions or functional disability. CONCLUSION: Despite smokers being more likely to develop nodules and to be RF positive, current smokers did not have higher levels of radiologic damage, and had fewer swollen joints. We hypothesize that this could be due to either the effect of cigarette smoking on the inflammatory response or other factors (e.g., reduced physical activity in smokers) which may limit joint inflammation and damage.     

A clinical study of serum IgE concentrations in elderly patients with bronchial asthma and chronic obstructive pulmonary disease]

We tested the hypothesis that serum IgE concentrations may be influenced by the severity of respiratory symptoms, impairment of pulmonary functions, and smoking history in elderly patients with bronchial asthma and/or chronic obstructive pulmonary disease (COPD). A total of 325 elderly outpatients aged over 65 years were enrolled in the study: 112 (22 men, 90 women) with bronchial asthma (BA), 135 (118 men, 17 women) with COPD, and 78 (56 men, 22 women) with both COPD and asthma (COPD/BA). The mean ages for the 3 groups were 74.3,76.0 and 76.6 years, respectively; the age differential was not significant. As a group, the male subjects displayed higher serum IgE concentrations than the female subjects. Also, ex-smokers and current smokers showed higher serum IgE concentrations than patients who had never smoked, and patients in the BA group had higher serum IgE concentrations than those in the COPD or COPD/BA groups. Although serum IgE concentrations were increased in BA patients with decreased FEV1.0 levels, the reverse was observed in the COPD patients. Peripheral blood eosinophil counts for men and women were higher in the BA group than in the COPD group. A positive correlation between serum IgE concentration and eosinophil count was observed in the BA group. Although bronchial asthma and COPD in the elderly have been considered to be pathologically similar, the findings of our study suggested they are probably different in terms of serum IgE concentration, pulmonary function, and smoking history.     

Combined effect of smoking habits and occupational exposure to hard metal on total IgE antibodies.

A survey was made within a population of workers (n = 706) exposed to hard metal dust (an alloy including cobalt), an agent known to cause occupational allergy. Twenty-seven (4 percent) of 733 workers were eliminated from consideration in this study because of atopic status identified prior to starting work in the plant. Using a Phadebas PRIST, the subjects' total IgE levels were determined and related to their smoking and exposure status. Nonexposed male smokers (n = 135) had a higher geometric mean IgE level (39.7 IU/ml) than did nonexposed subjects who had never smoked (33.1 IU/ml; n = 99); those with a higher Brinkman index (greater than 300), a smoking index obtained by multiplying the number of cigarettes per day by the duration of smoking in years, had significantly (p less than 0.05) decreased IgE levels. Although ex-smokers (n = 72) had a higher geometric mean IgE level (73.3 IU/ml) than did those who had never smoked, their serum IgE level declined with age since the time they quit smoking, regardless of their hard metal exposure status. Hard metal (cobalt) exposure may play a significant role as an adjuvant in the production of total IgE. A multivariate analysis demonstrated that hard metal exposure and a smoking habit together arithmetically (p less than 0.05) increased total IgE levels. These two factors may be preventable risk factors for occupational allergy in hard metal workers.