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PURPOSE OF REVIEW: Although, in the industrialized world, there is a significant decline in the prevalence of cotton dust lung diseases, studies show an increasing incidence in the developing world. With rapid industrialization of the developing world, cotton dust-induced lung diseases are poised to become a global health problem. Discovery of other vegetable dusts causing similar conditions and appreciation of a wider variety of clinical features also make this an opportune time to review this topic. RECENT FINDINGS: In addition to chronic exposure-related byssinosis and less common forms of acute byssinosis, recent reports describe the rare occurrence of cotton dust-induced pulmonary fibrosis. New data also relate long-term cotton dust exposure to symptoms and physiologic changes of chronic obstructive pulmonary disease. There have also been new developments relating the pathogenesis of cotton dust airway disease to endotoxin lipopolysaccharide found in cotton dust and bract extracts. SUMMARY: Establishment of an association between prolonged exposure to cotton and other vegetable dusts and symptoms of chronic obstructive pulmonary disease widens the clinical implication of cotton dust exposure. In addition, accumulating knowledge of endotoxins will bring about promising new developments reshaping industrial safety standards and measures to prevent cotton dust exposure.

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Air samples from various processing areas of an Indian jute mill were examined for endotoxin. The authors assessed work-related respiratory symptoms and pulmonary function changes in the dust-exposed workers from the different processing areas using a standard questionnaire and spirometry. Endotoxin was estimated in water extract of jute dust from 3 milling areas, and in outside air, by the Limulus amebocyte lysate gel clot technique. The batching, spinning, and weaving areas of the jute mill showed endotoxin levels of 0.22-4.42 microg/m3, 0.04-1.47 microg/m3, and 0.01-0.07 microg/m3, respectively, values similar to those found in Indian cotton mills. Respiratory morbidities among the workers included typical byssinotic symptoms, along with acute changes in postshift forced expiratory volume in 1 s (FEV1.0) (31.8%). Results of this study demonstrated that increased exposure to bacterial endotoxin in airborne dust is related to byssinotic symptoms among Indian jute mill workers. Findings were similar to those reported previously for workers in the cotton, flax, and hemp industries.

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Byssinosis as a nonspecific chronic respiratory disease in textile workers exposed to cotton, flax, jute, hemp and sisal is described. Opinions about aetiopathogenesis are presented. The following chapters are focused on clinical symptoms and functional lung changes. Classification of the disease is described afterwards. Finally, the necessity of medical and technical measures to prevent the development of this disease in textile workers is emphasised.

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Acute inhalation of organic dusts such as cotton, hay, silage, grain, animal confinement, or compost dust can result in illness characterized by fever, pulmonary inflammation, chest tightness, and airway obstruction. These agricultural materials are complex mixtures of plant, bacterial, and fungal products. Elucidation of the time course of disease onset, the mechanisms of disease progression, and the identity of etiologic agents is essential for effective prevention and treatment. Toward this end, animal models for acute organic dust-induced reactions have been developed and characterized. Information concerning the applicability of various animal models to humans and progress toward elucidation of causative agents and mechanisms of action is presented.

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Cotton dust has been found to cause acute pulmonary inflammation and fever in humans and in a guinea pig model of byssinosis. Following 3 h inhalation of cotton dust particles, guinea pig macrophages were found to release ex vivo a factor(s) toxic to WEHI fibrosarcoma cells. The cytotoxic factor(s) was also present in the bronchoalveolar fluid. We sought to investigate the mechanism of the inflammatory response to determine whether the factor was TNF. Antibodies to murine TNF were produced by immunizing sets of rabbits using two protocols. All animals produced anti-TNF antibodies with titers of 1/1000-1/25,000. Sera from one set of animals completely neutralized the cytotoxicity of murine TNF toward the WEHI cell line. The antisera neutralized up to 93% of the cytotoxicity of guinea pig samples but only 54% of human recombinant TNF. These results identify TNF in pulmonary tissues of guinea pigs following exposure to cotton dust. Moreover, the studies indicate that rabbit antibodies to murine TNF can be used to detect the guinea pig cytokine.

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A study was conducted in a cotton spinning mill to assess the prevalence of respiratory impairment in 189 asymptomatic workers and 133 byssinotics drawn from various sections of the plant exposed to airborne cotton dust in the work environment. Eight-four healthy controls belonging to the same socioeconomic status and ethnic group having never been exposed to cotton dust or any other pollutant was also studied for the purpose of comparison. Of the 189 asymptomatic workers, 13 (6.8%) suffered from bronchial obstruction whereas only 2 (2.3%) among the control showed obstructive pulmonary impairment. The byssinotics showed a significantly higher prevalence (15.7%) of bronchial obstruction than that (6.8%) observed among the asymptomatic cotton workers (P less than 0.005). Byssinotics (grade II) showed significantly higher prevalence (31.5%) of bronchial obstruction than that (9.4%) observed in acute byssinotics (grade I). The effect of smoking on the prevalence of bronchial obstruction in the asymptomatic and byssinotics was quite discernible as smokers showed significantly higher prevalence than that observed among the nonsmokers (P less than 0.05). The asymptomatic cotton workers and those with different grades of byssinosis having more than 10 years of exposure showed significantly higher prevalence of bronchial obstruction than that observed in the group with less than 10 years of exposure (P less than 0.005). The healthy cotton workers and byssinotics engaged in the preparatory section (card, blow, and waste plant rooms) showed an insignificant higher prevalence of bronchial obstruction (11.3 and 24.4%, respectively) than among those who worked in the spinning, reeling, and winding sections of the mill. The mechanism responsible for causing ventilatory obstruction in the textile workers is discussed.

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Reported epidemiological findings of the state of blonchopulmonary apparatus using a questionnaire, physical and functional examination of workers allowed to reveal chronic bronchitis, mainly of stage I and initial signs of byssinosis in those working at enterprises on processing of low-quality cotton growth. Results of hygienic evaluation of the dust factor dictate the necessity of extending the existing method during examination of enterprises engaged in processing of fibrous vegetal dusts. The necessity is also substantiated of perfecting medical screening of this category of workers.

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Inhalation of cotton mill dust or condensed tannin, a major botanical component of cotton mill dust, induces an acute pulmonary inflammatory response characterized by a rapid influx of neutrophils into the airways. The development of neutrophil alveolitis caused by tannin inhalation is accompanied by the accumulation of low molecular weight neutrophil chemotactic factor (NCF) in the airways. To determine if the alveolar macrophage is the source of this NCF, the ability of tannin to induce the secretion of NCF from rabbit alveolar macrophages was examined in vitro. Tannin did promote the secretion of NCF from alveolar macrophages in a time- and dose-dependent manner. Secretion began immediately after challenge and was maximal after 4 to 5 h. Maximal secretion occurred at a tannin concentration of 50 micrograms/ml. Comparison with the dose response for NCF secretion by cotton dust extract indicated that tannin was the major component in the dust responsible for NCF secretion from alveolar macrophages in the time period examined. The NCF had an apparent molecular weight of greater than 800 as determined by gel chromatography. The NCF could be extracted into organic solvents, suggesting it was a lipid. Its secretion, however, could not be prevented by treatment of the macrophages with the 5-lipoxygenase inhibitor, nordihydroguaretic acid, demonstrating that the NCF was not leukotriene B4. These data indicate that the action of tannin on resident alveolar macrophages results in the secretion of a NCF that may be responsible for the acute neutrophil alveolitis associated with inhalation of cotton dust.

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Anesthetized, intubated, and mechanically ventilated rabbits were exposed to aerosolized saline, cotton dust extract (CDE), or tannin for 5 minutes and lavaged 4 hours after exposure. Cell numbers and types present in the bronchoalveolar lavage fluid (BALF) were determined and the concentrations of thromboxane A2 (TxA2) and prostaglandin F2-alpha (PGF2-alpha) in the BALF were also analyzed. The saline control animals had increased numbers and percentage of polymorphonuclear leukocytes (PMN) in the BALF as well as increased levels of TxB2 and PGF2-alpha compared with unexposed animals. Exposure to CDE further increased the number and percentage of PMN and the level of PGF2-alpha but had no effect on TxA2 levels when compared with control animals. Tannin exposure increased PGF2-alpha levels to the same extent as CDE exposure. PMN also increased but to a lesser extent than with CDE. These results indicate that the inflammatory response to CDE is only partially due to the tannin present in CDE.

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To determine if constituents of cotton plants might play a role in byssinosis by injuring pulmonary epithelium, we added extracts of cotton dust, green bract, and field-dried bract to human A549 and rat type II pneumocytes. Injury was measured as pneumocyte lysis and detachment, and inhibition of protein synthesis. Extracts of cotton dust and field-dried bract produced significant dose- and time-dependent lysis and detachment of both target cells, while green bract extract was less damaging. Extracts treated with polyvinylpolypyrrolidone to remove tannins produced significantly less injury. In contrast, purified 5,7,3',4'-tetrahydroxy-flavan 3,4-diol (THF), a tannin in cotton dust and bract, caused substantial cell damage. Field-dried bract extract and THF also produced dose-dependent inhibition of pneumocyte protein synthesis. Endotoxin levels did not correlate with observed injury. THF added to rat tracheal explants caused epithelial disruption and desquamation, whereas endotoxin did not. Instillation of cotton dust and field-dried bract extract in rat lungs produced disruption of bronchial epithelium and smooth muscle constriction, while polyvinylpolypyrrolidone-treated cotton dust extract produced no injury. These findings suggest that extracts of cotton plants are toxic to alveolar, tracheal, and bronchial epithelium and that THF or other tannins may be the responsible agents.

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In this study we describe, through stereological methods, the lung morphology following inhalation exposure of guinea pigs to 21 mg/m3 cotton dust (CD) for 1 year. Various stereological parameters were determined on semithin histological sections, through a multistage sampling approach, to study the reaction of the whole lung, alveolar parenchyma, and bronchioles to CD inhalation. After 1 year of exposure, the lung volume was increased. Two distinct patterns of lung response were identified among the exposed animals. In type I responders, most of the morphometric parameters measured to describe the alveolar parenchymal reaction were within control value limits (means +/- 2 SD). In type II responders, the volume density (Vv) of the parenchymal zone was decreased, while the Vv, mean thickness, and absolute volume of the alveolar septa were increased. These changes caused the surface density (Sv) of alveolar epithelium to decrease, and an estimate of the percentage of alveolar septa remaining functional for gas exchange was also significantly lowered in these animals. In both types of responders, fifth to ninth orders of bronchioles had a raised wall to lumen ratio; the Vv and mean thickness of the bronchiolar epithelium were markedly increased, denoting hyperplastic changes. Thus, chronic exposure to cotton dust induced definite morphological changes on the peripheral conducting airways in most of the exposed animals, and induced pronounced changes at the alveolar level in 8 of 17 CD-exposed guinea pigs.

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Changes in respiratory function (FEV1) and polymorphonuclear neutrophils (PMN) on nasal epithelium were studied in 68 students and 39 cotton mill workers in an experimental cardroom. The exposure was characterised by the vertical elutriator dust and endotoxin levels. A dose related decrease was found for FEV1 which was more pronounced in smoking workers. The thresholds for no FEV1 reaction were 0.58 mg/m3 dust and 0.17 micrograms/m3 endotoxin for students and 0.43 mg/m3 and 0.08 micrograms/m3 for smoking workers. The PMN increased in most of the experiments but no dose response relationship could be shown. In experiments with smoking workers or when washed cotton was carded a better correlation was obtained between FEV1 decrease and endotoxin levels than for dust levels.

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The proportions of gland, muscle and cartilage were measured in the named bronchi of 43 byssinotics, and compared with the proportions in normal subjects and chronic bronchitics. The smoking habits and symptomatology of the byssinotics were also investigated. In the byssinotics the proportions of gland, muscle and cartilage were higher than in the normal, non-smoking subject at all levels in the bronchial tree, and were similar to those in chronic bronchitics. The increase was not confined to the lobar bronchi as the results of a previous investigation had suggested. It is concluded that although exposure to cotton dust is a factor in the pathogenesis of chronic byssinosis, anatomical changes in the bronchi of Lancashire cotton workers are non-specific, and are confounded by other environmental factors. Smoking has a deleterious effect on the natural history of the disease, but no morphological difference between smokers and non-smokers was found.

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