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A follow-up study of respiratory function in cotton textile workers was performed 10 yr after the original cross-sectional study (1975 to 1985). There were 35 nonsmoking female and 31 smoking male textile workers restudied from the original group of 116. The majority of those lost to follow-up had left the industry. The prevalence of byssinosis among the female workers at the time of follow-up was 15/35 (42.9%) compared with 8/35 (22.9%) at the time of the initial study (p = 0.063). For men the byssinosis prevalence at follow-up was 16/31 (51.6%) compared with 8/31 (22.9%) at the time of the initial study (p = 0.03). Similarly, the prevalence of almost all other respiratory symptoms was significantly higher at the follow-up than at the time of the initial study. Significant across-shift decrements in FEV1 and FVC were documented at both surveys. The mean annual decline in ventilatory capacity was greater than expected for both female (FVC: -0.036 +/- 0.005 L/yr; FEV1: -0.059 +/- 0.009 L/yr) and male workers (FVC: -0.059 +/- 0.008 L/yr; FEV1: -0.068 +/- 0.006 L/yr) (Mean +/- SE). The mean total airborne dust concentration measured at the time of the follow-up study was 3.95 mg/m3 with an average respirable dust concentration of 0.97 mg/m3. We conclude that continued exposure to high dust concentrations in the cotton textile industry is associated with an increasing prevalence of respiratory symptoms and progressive impairment of lung function. The increase in respiratory impairment was seen both in smokers and nonsmokers.

Most healthy subjects challenged with cotton bract extract demonstrate some degree of bronchospasm. This response has been associated with the endogenous production of histamine by the inhalation of cotton bract extract. We examined whether this responsiveness reflects increased sensitivity to histamine. Thirty-one healthy subjects were screened for sensitivity to cotton bract extract administered by nebulization. Pulmonary function was measured using partial expiratory flow-volume curves on which flows at 60% of the control vital capacity below total lung capacity were measured (MEF40%(P)). Responders were defined as subjects who exhibited a 20% or greater decrease in MEF40%(P) after 10 min inhaling cotton bract extract. Of those screened, 10 subjects were responders. From the remaining nonresponders, 11 consecutive subjects were selected. The maximal decrease in MEF40%(P) in responders was 40.5 +/- 5.1%, compared to 10.9 +/- 2.2% in nonresponders. The dose-response relationship for histamine was measured in all subjects, using inhalations of progressively more concentrated histamine solutions. The mean +/- SEM threshold for the responders was 38.4 +/- 7.4 mg of histamine per ml, compared to 42.2 +/- 6.8 mg of histamine per ml for responders (difference not significant). The percentage decrease in MEF40%(P) at the threshold dose was 27.6 +/- 3.7% for responders and 32.4 +/- 5.2% for nonresponders (difference not significant). We conclude that healthy subjects sensitive to cotton bract extract do not exhibit increased reactivity to histamine. This suggests that responders are not, in general, subclinical asthmatics, and that the difference between responders and nonresponders to CBE is not due to increased histamine sensitivity among responders.

This study examined nonspecific airway responsiveness to methacholine (MC) after inhalation of cotton bract extract (CBE). In a randomized double-blind, crossover trial, 13 healthy volunteers underwent an MC inhalation challenge test prior to inhalation of CBE and normal saline solution (NSS) aerosol sham as well as 2, 8, 24, and 168 h (7 days) later. The response parameter was the concentration of MC required to induce a 25% decrement in the maximal expiratory flow at 40% of the vital capacity below total lung capacity on the partial expiratory flow-volume curve (PC25MEF40%(P]. Five of 13 subjects demonstrated a ventilatory response to CBE with a 20% or larger decrement in the MEF40%(P); no subject demonstrated such change with NSS. For the group, the maximal decrement in MEF40%(P) was to 76.5 +/- 20.3% of baseline (mean +/- SD), occurring approximately 60 to 90 min after provocation, whereas the largest decrement after normal saline was to 88 +/- 10.6% of baseline, occurring immediately after inhalation. Changes in airway responsiveness to MC were transient. For example, the PC25MEF40%(P) for the group (mean +/- SD) was 51.3 +/- 41.1 mg/ml at baseline and 25.8 +/- 30.3 and 52.2 +/- 57.3 mg/ml at 2 and 8 h. After a pre-sham baseline of 50.4 +/- 43.2 mg/ml, PC25MEF40%(P) was 57.6 +/- 83.8 and 153.8 +/- 148 mg/ml at 2 and 8 h. Repeated measures ANOVA on these acute, same-day changes (i.e., 2 and 8 h after provocation) demonstrated a statistically significant effect of CBE on airway responsiveness (p = 0.048). These data demonstrate that inhalation of CBE, in addition to bronchospasm, causes a transient increase in airway responsiveness.

Byssinosis is characterized by an obstructive bronchitis in some workers exposed to cotton dust. Mechanisms of airway alterations induced by cotton dust are unknown. To study mechanisms of these alterations, we administered an aqueous extract of cotton bract (CBE) to normal human subjects. After CBE inhalation, we demonstrated reproducible reductions in flow rates of variable magnitude. The percentage of polymorphonuclear leukocytes (PMN) recovered by bronchoalveolar lavage (BAL) and total PMN per milliliter BAL fluid were increased after challenge with CBE, and these parameters were correlated (r = 0.556 and r = 0.553, respectively) with the degree of bronchoconstriction induced by CBE. In addition, chemotactic factors for PMN were noted in BAL fluid and in supernatant from BAL cell cultures. The degree of BAL fluid chemotactic activity correlated with the degree of bronchoconstriction induced by CBE. Assessment of molecular sieve column effluent demonstrated BAL fluid to have 3 distinct peaks of chemotactic activity (approximate molecular weight, greater than 25,000, 10,000, and less than 1,000 daltons) and cell culture supernatant to contain 1 peak (approximate MW, 10,000 daltons). Complement activation as one source of BAL chemotactic activity was suggested by almost complete inhibition of BAL chemotactic activity after incubation with antibody to the fifth component of complement (C5) and detection of C5a des Arg in BAL fluid from some subjects challenged with CBE. These findings suggest that exposure of volunteer subjects to CBE results in a bronchoalveolar inflammatory response related to both complement activation and chemotactic factor synthesis by luminal cells.

Reversible airway obstruction has been shown to be a characteristic finding of early byssinosis. In the chronic phase of this disease, the patterns of respiratory abnormalities have not been well defined. We examined the lung function of a cohort of 383 older (45 yr of age or more), active and retired, cotton textile workers seen both in 1973 and in 1979 in Columbia, South Carolina. A group of control subjects consisted of 277 white community residents of comparable age from Lebanon, Connecticut. Using data at follow-up, 25% of the male and 14% of the female cotton textile workers had moderate to severe obstructive airway abnormalities, as opposed to 13 and 5% for male and female control subjects (p less than 0.01). There were fewer persons with restrictive than with obstructive lung patterns among cotton textile workers and control subjects, but again, abnormalities were more prevalent among cotton textile workers. Overall, 50% of male cotton textile workers and 37% of female cotton textile workers had some abnormality of lung function, as opposed to 29% of male and 20% of female control subjects (p less than 0.001). More abnormalities were present in cotton textile workers than in control subjects when only lifetime nonsmokers were examined. We conclude that there is an increased prevalence of both obstructive and restrictive lung function abnormalities among cotton textile workers when compared with control subjects, with the most common pattern being obstructive.

We explored the relationship between a number of respiratory symptoms or symptom complexes (e.g., cough, recent wheeze, byssinosis) and lung function in white cotton textile workers (CTW) and control subjects 45 yr of age or older. The CTW were studied in 1973 and in 1979 in Columbia, South Carolina, and the control subjects were studied in 1972 and in 1978 in Lebanon, Connecticut. The CTW had a high prevalence of byssinosis (18%) and other symptoms. For each symptom or symptom complex, among persons with the symptom, CTW had lower lung function on the average than did control subjects. Also, among persons without the particular symptom, CTW had lower lung function than did control subjects. This pattern also occurred for persons without any respiratory symptoms (i.e., asymptomatic). Moreover, persons (CTW or control subjects separately) reporting the presence of a particular symptom had, in general, lower lung function than did those without the symptom. Among nonsmokers, all these same patterns usually held, but differences were often not statistically significant because of the small numbers of persons with symptoms. We conclude that on a group basis, respiratory function is more impaired in CTW than in control subjects with respiratory symptoms, that respiratory function is more impaired in persons (CTW or control subjects) with symptoms than in those without, and that even asymptomatic CTW have significantly greater lung function impairment than do control subjects.

A 25-year-old woman survived a fulminant epidose of rapidly progressive renal failure with severe hemoptysis initially suspected of being Goodpasture's syndrome. Four years later the patient was diagnosed as having Wegener's granulomatosis.

We studied the white residents of Lebanon, Connecticut, a rural community, cross-sectionally in 1972 and a follow-up survey in 1978. In this community, we examined prospectively the growth and decay of lung function and the prevalence, attack, and remission of respiratory symptoms in 1,262 persons. These longitudinal findings were related to sex, age, and smoking habits. Respiratory symptoms and 3 lung function variables were examined: forced expiratory volume in one second (FEV1) and maximal expiratory flow rates at 50 and 25% of vital capacity (Vmax50 and Vmax25). The representativeness of the follow-up population was examined by an extensive analysis of the respondents and nonrespondents based on their cross-sectional characteristics. These analyses did not, in general, reveal any consistent results indicating that a healthier population was followed. The longitudinal data showed that lung growth continued into early adulthood (25 to 34 yr of age) with a leveling off and decline beginning at 35 yr and older. This is in contrast to cross-sectional studies of growth and decay of lung function, which show less growth among the young and more decay among adults. The rates of growth in both males and females were affected by their smoking status, with smokers having less growth and greater decline than nonsmokers. In particular, lung function growth was impaired in young smokers as early as 15 to 24 yr of age, and an actual decline was seen in the females of this age group.

In a cross-sectional survey of 3 separate communities, we studied the white residents 7 year of age and older in order to determine the relation between cigarette smoking and lung function. We identified 2,817 nonsmokers, 664 ex-smokers, and 1,209 smokers who were further classified as light smokers (1 to 20 cigarettes per day) and heavy smokers (greater than 20 cigarettes per day). Residual lung function (observed-predicted) was examined in these groups for forced expiratory volume in one second (rFEV1) and for maximal expiratory flow rates at 50% and 25% of the vital capacity (rVmax50% and rVmax 25%). Mean residuals by sex, age, and smoking category were compared and revealed an increasing progression of lung function loss with advancing age in males and females in all smoking categories. These age-related trends were due primarily to the amount smoked by persons in each group. The age of onset of these abnormalities was found to be as early as the age group 15 to 24 yr. Abnormalities were greater in smokers than ex-smokers, even when the amount smoked was taken into account. This is suggested improvement in lung function after cessation of smoking. Men and women were found to experience the same relative degree of gain. Also, the contribution of the various smoking habits to lung function loss was assessed using regression analyses and accounted for no more than 15% of the variation of the residual lung function. Combinations of variables were found to explain only slightly more variation than a single variable. The two most important variables were duration of smoking and pack-years. Inhalation and use of filters were not significant. Although the same amount of variation explained by the smoking variables after accounting for age, height, weight, and sex was small, this variation accounted for almost all of the decrease, over age, in residual lung function for smokers and ex-smokers.

A 63-year-old woman was demonstrated to have a hyperlucent lung in a hemithorax irradiated 9 years previously for carcinoma of the breast. This is the second reported concurrence of these events.