Abstract
In a previous study assessing respiratory symptoms in individuals employed in wool textile mills in the north of England relations between symptoms of chronic bronchitis, breathlessness and wheeze, and rhinitis and current exposure to airborne mass concentration of dust were shown. As preliminary steps in defining the potential hazard associated with dust from the air of wool mills the ability of inspirable dust, collected from the air of wool textile mills, to cause inflammation when injected into the lungs of rats was determined. Dusts were collected from the beginning of wool processing (opening) in one factory and from the middle (combing) and late (backwinding) stages of the process in two other factories. Ability of the dusts to cause inflammation was assessed by instillation into the lungs of rats followed by bronchoalveolar lavage. All the dusts caused some inflammation which peaked on day 1 and did not persist beyond one week. A distinctive aggregation response of mononuclear cells in the lavage, however, had a different time course, peaking at day 7. An attempt was made to determine how the wool mill dusts caused inflammation and experiments showed that the dusts themselves had no inherent chemotactic activity but that they did have a pronounced ability to generate chemotaxins in serum and so could activate complement in lung fluid. In addition, dust collected from ledges in the mills had the ability to injure epithelial cells in vitro which could also contribute to inflammation. A role for endotoxin in the inflammatory activity of the dusts was not discounted and a leachate of the dust had the ability to cause inflammation when injected into the lungs of rats. Wool mill dust is likely to be a complex mixture of materials and these experiments represent a preliminary approach to understanding the biological activity of the whole unfractionated dust and further studies are in progress to define more accurately the toxic material(s) in the dust.
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Selected References
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- Ayars G. H., Altman L. C., O'Neil C. E., Butcher B. T., Chi E. Y. Cotton dust-mediated lung epithelial injury. J Clin Invest. 1986 Dec;78(6):1579–1588. doi: 10.1172/JCI112750. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Donaldson K., Bolton R. E., Jones A., Brown G. M., Robertson M. D., Slight J., Cowie H., Davis J. M. Kinetics of the bronchoalveolar leucocyte response in rats during exposure to equal airborne mass concentrations of quartz, chrysotile asbestos, or titanium dioxide. Thorax. 1988 Jul;43(7):525–533. doi: 10.1136/thx.43.7.525. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Donaldson K., Brown G. M. Assessment of mineral dust cytotoxicity toward rat alveolar macrophages using a 51Cr release assay. Fundam Appl Toxicol. 1988 Feb;10(2):365–366. doi: 10.1016/0272-0590(88)90322-3. [DOI] [PubMed] [Google Scholar]
- Donaldson K., Slight J., Brown G. M., Bolton R. E. The ability of inflammatory bronchoalveolar leucocyte populations elicited with microbes or mineral dust to injure alveolar epithelial cells and degrade extracellular matrix in vitro. Br J Exp Pathol. 1988 Jun;69(3):327–338. [PMC free article] [PubMed] [Google Scholar]
- Dosman J. A., Cotton D. J., Graham B. L., Li K. Y., Froh F., Barnett G. D. Chronic bronchitis and decreased forced expiratory flow rates in lifetime nonsmoking grain workers. Am Rev Respir Dis. 1980 Jan;121(1):11–16. doi: 10.1164/arrd.1980.121.1.11. [DOI] [PubMed] [Google Scholar]
- Gellert A. R., Langford J. A., Winter R. J., Uthayakumar S., Sinha G., Rudd R. M. Asbestosis: assessment by bronchoalveolar lavage and measurement of pulmonary epithelial permeability. Thorax. 1985 Jul;40(7):508–514. doi: 10.1136/thx.40.7.508. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Hoidal J. R., Niewoehner D. E. Pathogenesis of emphysema. Chest. 1983 Apr;83(4):679–685. doi: 10.1378/chest.83.4.679. [DOI] [PubMed] [Google Scholar]
- Issekutz A. C., Megyeri P., Issekutz T. B. Role for macrophage products in endotoxin-induced polymorphonuclear leukocyte accumulation during inflammation. Lab Invest. 1987 Jan;56(1):49–59. [PubMed] [Google Scholar]
- Love R. G., Smith T. A., Gurr D., Soutar C. A., Scarisbrick D. A., Seaton A. Respiratory and allergic symptoms in wool textile workers. Br J Ind Med. 1988 Nov;45(11):727–741. doi: 10.1136/oem.45.11.727. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Martin T. R., Raghu G., Maunder R. J., Springmeyer S. C. The effects of chronic bronchitis and chronic air-flow obstruction on lung cell populations recovered by bronchoalveolar lavage. Am Rev Respir Dis. 1985 Aug;132(2):254–260. doi: 10.1164/arrd.1985.132.2.254. [DOI] [PubMed] [Google Scholar]
- Mundie T. G., Boackle R. J., Ainsworth S. K. In vitro alternative and classical activation of complement by extracts of cotton mill dust: a possible mechanism in the pathogenesis of byssinosis. Environ Res. 1983 Oct;32(1):47–56. doi: 10.1016/0013-9351(83)90190-1. [DOI] [PubMed] [Google Scholar]
- Ozesmi M., Aslan H., Hillerdal G., Rylander R., Ozesmi C., Baris Y. I. Byssinosis in carpet weavers exposed to wool contaminated with endotoxin. Br J Ind Med. 1987 Jul;44(7):479–483. doi: 10.1136/oem.44.7.479. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Rylander R., Vesterlund J. Airborne endotoxins in various occupational environments. Prog Clin Biol Res. 1982;93:399–409. [PubMed] [Google Scholar]
- Von Essen S. G., Robbins R. A., Thompson A. B., Ertl R. F., Linder J., Rennard S. Mechanisms of neutrophil recruitment to the lung by grain dust exposure. Am Rev Respir Dis. 1988 Oct;138(4):921–927. doi: 10.1164/ajrccm/138.4.921. [DOI] [PubMed] [Google Scholar]
- Warheit D. B., George G., Hill L. H., Snyderman R., Brody A. R. Inhaled asbestos activates a complement-dependent chemoattractant for macrophages. Lab Invest. 1985 May;52(5):505–514. [PubMed] [Google Scholar]
