Cotton dust exposure, across-shift drop in FEV1, and five-year change in lung function.

Christiani, David C.; Ye, Tingting; Wegman, David H.; Eisen, Ellen A.; Dai, Helian; Lu, P L

doi:10.1164/ajrccm.150.5.7952548

Cited by 84 publications

(51 citation statements)

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“…The result was consistent with that observed in male grain workers, in which annual losses in FEV1 were 28.7 mL for nonsmokers, and 41.7 mL for current smokers [13]. Overall, the data provide further supportive evidence for the chronic effects of exposure to cotton dust, which has been suggested by the current authors' previous observations [8,9] and by other cohort studies [4,5].…”

Section: Discussionsupporting

confidence: 91%

“…The initial cohort was established in 1981, and consisted of 447 cotton and 472 silk textile workers who were recruited in Shanghai, China [8]. The four follow-up surveys were undertaken in 5-yr intervals.…”

Section: Methodsmentioning

confidence: 99%

“…The results of a cohort study that followed a group of Chinese textile workers exposed chronically to cotton dust have been reported previously [8,9]. One of the features of the cohort was that .50% of the workers were nonsmoking females, which allowed an assessment of the effects of cotton-dust exposure without confounding by smoking.…”

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confidence: 99%

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A 20-year follow-up study on chronic respiratory effects of exposure to cotton dust

Wang¹

2005

European Respiratory Journal

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In order to evaluate chronic effects of long-term exposure to cotton dust on respiratory health, and the role of dust and endotoxin, longitudinal changes in lung function and respiratory symptoms were observed prospectively from 1981 to 2001 in 447 cotton textile workers, along with 472 silk textile controls.The results from five surveys conducted over the 20-yr period are reported, including standardised questionnaires, pre-and post-shift spirometric measurements, work-area inhalable dust sample collections and airborne Gram-bacterial endotoxin analysis.Cotton workers had more persistent respiratory symptoms and greater annual declines in forced expiratory volume in one second (FEV1) and forced vital capacity as compared with silk workers. After exposure cessation, in the final 5-yr period, the rate of FEV1 decline tended to slow in nonsmoking males, but not in nonsmoking females. Workers who reported byssinotic symptoms more persistently suffered greater declines in FEV1. Chronic loss in lung function was more strongly associated with exposure to endotoxin than to dust.In conclusion, the current study suggests that long-term exposure to cotton dust, in which airborne endotoxin appears to play an important role, results in substantial adverse chronic respiratory effects.

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Section: Discussionsupporting

confidence: 91%

Section: Methodsmentioning

confidence: 99%

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A 20-year follow-up study on chronic respiratory effects of exposure to cotton dust

Wang¹

2005

European Respiratory Journal

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“…In this study, we demonstrate that in a murine model mimicking the weekday cycle of occupational endotoxin exposure in cotton textile workers (34), increased airflow resistance and airway hyperreactivity ( Figure 1) are accompanied by increased lung neutrophils with longer durations of exposure (Figures 2 and 4). These findings are associated with a striking inversion of the ratio of macrophages to DCs, with an increase in lung proinflammatory DCs after 8 weeks of LPS exposure (Figures 4-6).…”

Section: Discussionmentioning

confidence: 58%

Chronic Endotoxin Exposure Produces Airflow Obstruction and Lung Dendritic Cell Expansion

Lai

Fresco

Pinilla

et al. 2012

Am J Respir Cell Mol Biol

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Little is known about the mechanisms of persistent airflow obstruction that result from chronic occupational endotoxin exposure. We sought to analyze the inflammatory response underlying persistent airflow obstruction as a result of chronic occupational endotoxin exposure. We developed a murine model of daily inhaled endotoxin for periods of 5 days to 8 weeks. We analyzed physiologic lung dysfunction, lung histology, bronchoalveolar lavage fluid and total lung homogenate inflammatory cell and cytokine profiles, and pulmonary gene expression profiles. We observed an increase in airway hyperresponsiveness as a result of chronic endotoxin exposure. After 8 weeks, the mice exhibited an increase in bronchoalveolar lavage and lung neutrophils that correlated with an increase in proinflammatory cytokines. Detailed analyses of inflammatory cell subsets revealed an expansion of dendritic cells (DCs), and in particular, proinflammatory DCs, with a reduced percentage of macrophages. Gene expression profiling revealed the up-regulation of a panel of genes that was consistent with DC recruitment, and lung histology revealed an accumulation of DCs in inflammatory aggregates around the airways in 8-week-exposed animals. Repeated, low-dose LPS inhalation, which mirrors occupational exposure, resulted in airway hyperresponsiveness, associated with a failure to resolve the proinflammatory response, an inverted macrophage to DC ratio, and a significant rise in the inflammatory DC population. These findings point to a novel underlying mechanism of airflow obstruction as a result of occupational LPS exposure, and suggest molecular and cellular targets for therapeutic development.Keywords: airway resistance; inhalation; neutrophils; macrophages; dendritic cells; endotoxin Endotoxin (lipopolysaccharide, or LPS) is a cell-wall component of Gram-negative bacteria, and is ubiquitous in the environment. Occupational settings in which the ambient concentration of endotoxin is markedly increased include swine farms, sewage treatment plants, humidified buildings, and the processing of organic materials (in particular, cotton), where exposure levels can exceed 5,900 EU/m 3 (1). Endotoxin is also an important component of indoor air pollution in homes burning biomass fuel (2).Human studies have demonstrated a relationship between occupational endotoxin exposure and the development of airflow obstruction, and suggest that sufficient endotoxin exists in cotton dust to cause respiratory symptoms (often as part of a syndrome termed "byssinosis") and a decline in pulmonary function test results (3, 4). Importantly, the endotoxin concentration in cotton dust, and not the dust concentration, is correlated with the decline in lung function (5). Although most studies in humans examined the acute response to airborne endotoxin, some studies suggest that long-term exposure to cotton dust is associated with a loss of lung function, with symptoms and pulmonary function test results similar to those observed in chronic obstructive CLINICAL RELEVANCEOccupat...

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“…There is also a set of pulmonary reactions that occur only after chronic exposure. These include the dassical chest tightness (21), a greater than predicted annual decline in FEVi (31,32), and bronchitis (33).…”

Section: Introductionmentioning

confidence: 99%

Pulmonary Reactions to Organic Dust Exposures: Development of an Animal Model

Castranova¹,

Robinson²,

Frazer³

1996

Environmental Health Perspectives

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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. Environ Health Perspect 104(Suppl 1): 41-53 (1996)

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Cotton dust exposure, across-shift drop in FEV1, and five-year change in lung function.

Cited by 84 publications

References 0 publications

A 20-year follow-up study on chronic respiratory effects of exposure to cotton dust

A 20-year follow-up study on chronic respiratory effects of exposure to cotton dust

Chronic Endotoxin Exposure Produces Airflow Obstruction and Lung Dendritic Cell Expansion

Pulmonary Reactions to Organic Dust Exposures: Development of an Animal Model

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