Respiratory symptoms and pulmonary function in Saskatchewan farmers.
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Biomedical subjects
Publications and source records attributed to J A Dosman.
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The six workshops in this subgroup--Injuries, Respiratory Diseases, Acute Chemical Toxicity, Cancer, and Health Surveillance--competently outlined the principal health and safety issues in agriculture, documenting the increased and unacceptable morbidity and mortality in farmers and their families. It became evident that although research knowledge is just now unfolding, sufficient data exist to permit comprehensive program planning for research and prevention. It is necessary that farmers and their families be considered an occupational grouping and that specific programs aimed at ongoing risk assessment and early diagnosis are important. At the same time, a more broadly based approach to rural family life enhancement is essential, including the following: 1) education; 2) prevention; 3) family life enhancement; and 4) research. Because of the scope and nature of the problem, program development should include a multidisciplinary approach that involves the local community, state government, university (professional) resources, farm/organizations, and industry.
The idea that increases in airways responsiveness--either as a result of exposure to cigarette smoke and/or pre-existing increases in bronchial responsiveness, possibly genetically mediated--might be causal in the pathogenesis of the development of COPD in cigarette smokers presents an attractive hypothesis. The fact that a relatively small proportion of cigarette smokers develop COPD begs for specific susceptibilities as an explanation of selective pathogenesis. In our view, the evidence for modest increases in airways responsiveness in cigarette smokers who do not have asthma or allergies is convincing. Such increases in bronchial responsiveness are modest when compared to patients with asthma and may have a different mechanism. However, the demonstration by Verma et al that two types of patients with cigarette smoke-induced COPD, "bronchitis" patients and "emphysematous" patients, have virtually identical alterations in bronchial responsiveness, and that these alterations appear to be a function of airways caliber, has led us to believe that the changes in airways tone in patients with COPD may be reflective more of changes in airways geometry imposed by the development of disease rather than a measurement of a risk factor in the development of COPD. Of the epidemiologic studies that have emerged throughout the 1980s, problems of possible inclusion of asthmatic subjects in the study groups and of baseline airflow rates as a function of bronchial responsiveness have limited the ability of data to implicate increases in airways responsiveness as a risk factor in the development of COPD.(ABSTRACT TRUNCATED AT 250 WORDS)
Airways obstruction as a result of occupational exposure may be divided into two categories on the basis of whether or not occupational asthma is present. The first category, nonspecific airways obstruction, takes place in the absence of occupational asthma, and demonstrates only modest changes in airways responsiveness. The second category, occupational asthma, usually has a causal relationship to exposure, and demonstrates marked changes in airways responsiveness. These distinctions are of use in diagnosis, treatment, and disability assessment.
The frequencies of GC phenotypes in 104 patients with chronic obstructive airways disease (COAD) were compared with those in 413 control subjects. The distributions were significantly different with fewer patients with the GC 2 allele than expected (relative risks = 0.8, 0.7 and 0.5 for 2-2, 2-1S and 2-1F, respectively) and more 1F-1F patients than expected (relative risk = 4.8). These data suggest that the GC 2 allele exerts a protective effect, whereas 1F, when homozygous, increases the risk of developing COAD.
In order to evaluate the determinants of cell type in patients with primary lung cancer, we compared smoking characteristics in 1,939 patients (1,474 men and 465 women). Patients with squamous cell carcinomas, adenocarcinomas, or small-cell carcinomas were eligible. This study did not consider smoking as a risk factor for lung cancer, as all subjects had a confirmed diagnosis. We were interested in smoking history and the pattern of smoking among those whose risk was 100 percent. Among these patients, we confirmed that a larger subset of nonsmoking individuals developed adenocarcinomas than squamous cell or small-cell carcinomas; however, the duration and intensity of cigarette smoking, as measured by pack-years, were not determinants of tumor cell type in male patients. Small-cell carcinomas in women were more strongly associated with cigarette smoking than either squamous cell carcinomas or adenocarcinomas. More than 3,500 different substances have been measured in tobacco smoke, including tumor initiators, promoters, and those involved in tumor progression. These data confirm the hypothesis that factors other than cigarette smoking are more likely to be involved in the initiation of adenocarcinomas than other cell types. Endogenous and exogenous factors related to gender may be more important than the duration or intensity of cigarette smoking.
Ascertaining cases from a population-based tumor registry in which registration of primary lung cancer is virtually complete, we have consistently found that 40% to 50% of male lung cancer patients were farmers. We interviewed 273 newly diagnosed men and compared their occupational exposures, medical history and smoking characteristics to those of 187 male randomly selected community control subjects. We found that more of the control subjects were farmers (53.5% v 41.4%), that the control subjects tended to have larger farms (P less than .05), and that more control subjects spilled chemicals on their hands or clothing (47% v 28%, P less than .01) and had an accidental inhalation of a chemical directly into the lung (54% v 33%, P less than .005). We report an absence of correlation of lung cancer risk with occupational exposure to any specific pesticide or pesticides grouped by chemical composition. Adjusting for smoking pack-years or extent of pesticide use did not alter our preadjustment conclusions.
We examined the extrinsic and intrinsic characteristics of patients with primary lung cancer diagnosed at early ages and compared them with those of older patients. Significant differences in gender distribution and histologic cell type were present. Cigarette smoking was an important etiologic factor in both groups.
Allergy prick skin testing was performed on 137 newly diagnosed patients with primary lung cancer and 137 age-(+/- 3 years) and sex-matched randomly selected control subjects. We also compared 38 patients with lung cancer and 38 of their closest in age, same-sex siblings. Demographic data, personal, medical, smoking and occupational histories were obtained by personal interview. We skin tested these individuals with a standard battery of seven common allergens and a diluent control. Fewer patients (35.8 percent) than control subjects (58.4 percent) responded with one or more positive skin reactions (p less than .005). There was no significant difference between patients (27.8 percent) and control subjects (37.2 percent) responding to more than one allergen. Fewer of the 38 sibling-matched patients had one or more positive skin tests (23.7 percent) than did their siblings (55.3 percent) (p less than .01). There were fewer patients with greater than one positive skin test (15.8 percent) than sibling control subjects (42.1 percent) (p less than .025). There were no differences in smoking pack-years between patients and siblings. Historic evidence of allergy was greater in both control groups compared to their matched cancer groups; p less than .05 for community controls, p less than .005 for sibling control subjects. These findings raise the possibility that atopy, by either immunologic or nonimmunologic means, protects against development of lung cancer, or alternately, that lung cancer affects immunologic status as gauged by (type 1) skin sensitivity.
Airway responsiveness to inhaled histamine was examined in two groups of carefully selected patients with nonasthmatic chronic obstructive airways disease (COAD). Twelve patients with chronic bronchitis and airflow obstruction but little emphysema and 13 with predominantly emphysema and airflow obstruction but little bronchitis were selected based on history, chest roentgenogram, and diffusing capacity for carbon monoxide (Dsb). Emphysema patients had less cough, less sputum, less chronic bronchitis, lower Dsb, and more radiographic evidence of vascular deficiency. There was no difference in anthropometric features, smoking history, atopic skin sensitivity, hemoglobin, blood eosinophilia, PaO2, PaCO2, ECG, lung volumes, or expiratory flow rates. The two groups had similar airway responsiveness to inhaled histamine; the geometric mean provocation concentrations producing a 20 percent FEV1 fall (PC20) was 0.56 mg/ml for the bronchitis patients and 0.28 mg/ml for the emphysema patients (p greater than 0.20). Regression of log histamine PC20 vs percent predicted FEV1 showed a high correlation in both groups (r = 0.73, p less than 0.01 in bronchitis and r = 0.79, p less than 0.001 in emphysema). The regression lines were almost identical. These data suggest that in COAD bronchial responsiveness to inhaled histamine is mainly due to the altered airway geometry, and that there is no difference in histamine responsiveness between patients with emphysematous COAD and nonemphysematous COAD with chronic bronchitis.
To determine whether farmers who produced swine in animal confinement chambers in Saskatchewan were at increased risk of developing respiratory dysfunction, we carried out a respiratory health questionnaire and spirometric pulmonary function test measurements, including forced expired volume in 1 second (FEV1), forced vital capacity (FVC), and the ratio of FEV1 to FVC (FEV1/FVC x 100), on 504 farmers who indicated that they raised swine, and 448 rural-dwelling nonfarming control subjects. Swine producers had lower values for FVC and FEV1 than did the control subjects. However, FEV1/FVC x 100 was somewhat higher in the swine producers. The reduction in FEV1 with retained FEV1/FVC ratio is suggestive of restrictive disease. However, the fact that the FEV1/FVC ratio is only modestly higher in swine producers than in control subjects suggests that there may be a mixed restrictive/obstructive condition in these workers.
We conducted a retrospective questionnaire study concerning farming and exposure to chemicals on 165 male lung cancer patients, mean age +/- SE, 64.2 +/- 1.0 years, and 165 closest in age male siblings, mean age 64.5 +/- 0.7 years. The patients were diagnosed as having primary lung cancer between January 1, 1979, and November 1, 1983. Among the lung cancer patients, 38.5% had a same-sex sibling eligible for inclusion and of these, 62.0% responded to the questionnaire. Mean pack-years of smoking for patients was 41.0 +/- 2.2 (n = 135) and among the siblings 36.9 +/- 2.4 (118) (P less than .002). The occupation of farming was present in 47.8% of 163 patients with known occupations as compared to 37.6% of 155 siblings with known occupations (not significant). Patients were consistently exposed more frequently to herbicides (P = .05), grains (P less than .015), and diesel fuels (P less than .005), and were consistently exposed to greater numbers of chemicals than were siblings (P less than .005). These findings raise the possibility that, in addition to smoking, farming and related exposures could be implicated in the etiology of lung cancer in men.
This report is based on responses to a mailed questionnaire from 927 patients with lung cancer (730 men, 197 women), or their next of kin, and information obtained from the Saskatchewan Cancer Foundation Tumour Registry. Women were diagnosed at an earlier mean age than males (means +/- SE, 63.5 +/- 0.85 years versus 67.6 +/- 0.37 years, P less than 0.001), a finding which was consistent for each major histologic type. Women were more frequently diagnosed before age 60 years (42.0%) than were men (25.6%) (P less than 0.001). Female patients were significantly more likely to be lifetime nonsmokers of cigarettes than male patients (23% versus 3.7%, P less than 0.001). Among current smokers, women started smoking at an older age (19.3 +/- 0.69 versus 16.5 +/- 0.21 years, P less than 0.001), smoked for fewer years (41.0 +/- 1.2 years versus 47.4 +/- 0.57 years, P less than 0.001) and smoked slightly fewer cigarettes per day than male patients (23.6 +/- 1.0 versus 26.7 +/- 0.63, P less than 0.05). Similar results were found for the duration of the smoking habit and number of cigarettes smoked among exsmokers. When current smokers and exsmokers were combined, the distribution of pack years by gender was significantly different. A higher percentage than expected of women as compared to men, are clustered in the lower pack-year categories (P less than 0.0003). No occupational exposure or familial factors which might act in synergism with cigarette smoking were identified. Thus, women developed primary lung cancer at an earlier age while smoking for fewer years than men.
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A questionnaire was given to 1,824 farmers and 556 control subjects in Saskatchewan to assess respiratory health and pulmonary function tests. With data corrected for age and smoking, farmers were found to have increased prevalences of the respiratory symptoms of phlegm, wheeze, shortness of breath, and the condition of chronic bronchitis. In addition, farmers had significantly lower values for the pulmonary function test variables forced vital capacity (FVC), forced expired volume in one second (FEV1) and maximum midexpiratory flow rate. However, the FEV1/FVC ratio was slightly but significantly greater in farmers than in control subjects. These findings suggest an increase in respiratory symptoms in farmers compared with rural control subjects who are not farmers and a decrease in lung volume and expired flow rates. The slightly high FEV1/FVC ratio may indicate a mixed obstructive and restrictive picture.
51.4% of 1,954 grain elevator workers surveyed in 1978 and 1979 complained of pruritus following exposure to grain dusts. 95% of 796 grain elevator workers surveyed in 1985 noted that pruritus following exposure to grain dust was of short duration. Exposure to barley dust and oat dust provoked the greatest number of complaints. Those with a past history of infantile eczema were significantly more likely to complain. Younger workers were more likely to complain than older workers. 13.1% of those surveyed in 1985 complained of a rash following exposure, in 35% of whom it lasted more than 1 day. Nasal congestion, ocular and oropharyngeal irritation were also frequent complaints.
In a community survey of 953 adults we identified 40 who reported having had psoriasis. Eight of these cases were subsequently documented from physicians' records. alpha 1-Antitrypsin (alpha 1-AT) phenotyping identified 35 MZ individuals, 4 (11.4%) of whom reported psoriasis. Among the 918 non-MZ individuals 36 (3.9%) reported psoriasis, yielding a relative incidence of 3.2 (p less than 0.05). This is consistent with previous reports suggesting an association between moderate alpha 1-AT deficiency and psoriasis.
Increasing concentrations of inhaled aerosolized histamine acid phosphate were administered to 31 heavy cigarette smokers from a smoking cessation clinic. Nineteen of 31 smokers (mean age +/- ISD: 39.6 +/- 11.5 yrs; pack years 25.5 +/- 13.5) failed to reduce forced expired volume in one second (FEV1) while inhaling histamine and were labelled nonresponders. In 12 of 31 smokers (age 38.4 +/- 9.4 yrs; pack years 23.0 +/- 10.5), extrapolated provocation concentration of inhaled histamine required to reduce forced expired volume in one second (FEV1) by 10 percent (PC10) could be determined and these smokers were labelled responders. We also measured maximum expiratory flow volume curves with air and also a mixture of 80 percent helium and 20 percent oxygen (HeO2) to determine the percentage of increase in maximal flow at 50 percent vital capacity breathing HeO2 as compared to air (delta Vmax50), and the slope of phase III of the single breath oxygen test (delta N2/L). In the responders, PC10 ranged from 1.4 mg/ml to 10.2 mg/ml (mean 5.5 +/- 3.3 mg/ml) and delta Vmax50 ranged from 7.1 percent to 68.4 percent (mean 39.6 +/- 18.3 percent). There was a significant positive correlation between PC10 and delta Vmax50 (r = 0.77, p less than 0.01), and a significant negative correlation between PC20 and delta N2/L (r = -.61, p less than 0.01). There was no difference between responders and nonresponders in mean values for lung function tests, allergy skin tests, or symptoms. These results suggest that there may be two fundamentally different groups of smokers with peripheral airways dysfunction: one group in which dysfunction is associated with, or related to, airways reactivity, and one group in which dysfunction is related to other factors.