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John H. Lange, Environmental and Occupational Consultant Envirosafe Training and Consultants, Inc., U. Fedeli and G. Mastrangelo
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john.pam.lange{at}worldnet.att.net John H. Lange, et al.
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Is mushroom workers’ chronic cough the same as byssinosis and what should the occupational exposure limit be for endotoxin? Tanaka and his colleagues’ (1) reported that most of the mushroom workers in their study group are experiencing chronic cough which they further characterized as organic dust toxic syndrome, hypersensitivity pneumonitis (HP), runny nose (postnasal drip syndrome), cough variant asthma, and eosinophilic bronchitis. These diseases (except two cases of HP) were not defined on an etiological ground. Some cases of asthma or rhinitis could be due to an immunologic mechanism, but the authors’ did not measure IgE against Hypsizigus marmoreus (commonly called Jade Gill mushrooms) spores. The remaining cases could be an irritant effect from airborne fungal spores, mycotoxin, organic dust, or endotoxin. We suggest that the mushroom workers’ chronic cough is the same (or a variant) disease as reported in cotton textile workers, byssinosis (2). The following supports the basis of endotoxin being the agent of chronic cough in mushroom workers: First, symptoms reported by those with “chronic cough” were observed “to improve or disappear after weekend holidays.” This is similar to the reported Monday-morning effect experienced by those in the cotton textile industry, which has associated endotoxin as the causative agent (2). Second, the rapid occurrence of chronic cough in this population of workers is similar to that in cotton textile workers, in whom Wang et al., (3) reported a rapid decline in FEV1 for newly hired, non-smoking, female cotton dust workers after three months of exposure; Third, since 71.4% of workers reporting chronic cough developed symptoms within 3 months after employment, sensitization to fungal spores is an unlikely responsible factor. Endotoxin (lipopolysaccharide - LPS) air concentrations in the harvesting (three samples) and packing rooms (three samples) were reported (Table 1) to be well above the suggested no-observed effect level (NOEL) for airway inflammation (10 ng/m3) (4), although a range from 9 to 170 ng/m3 has been reported (5). In the cultivating room the LPS concentration was below the NOEL, but above the level observed to cause acute decrease in airway function (53 EU/m3 or ~5 ng/m3) (6), reduce lung function (4 ng/m3) (7) and elicit a physiological response (2 ng/m3) (8,9). Since airborne endotoxins are highly variable, the relatively low levels of LPS reported by Tanaka require confirmation before these findings can be fully accepted. LPS concentrations should be expressed in EU/m3 and not as ng/m3 (5,10). Reporting endotoxin values as ng/m3 does not allow an accurate comparison with other measurements (10). Additional data might be useful in the establishment of an Occupational Exposure Limit (OEL) for endotoxin that minimizes occupational disease (5). It is proposed here that the OEL (8 hour average – time weighted average) be established between the concentration reported for reducing lung function and physiologic response (20 to 50 EU/m3). This will provide some margin of safety in protecting the majority of people. This proposed value is similar to the suggested OEL (50 EU/m3/8 hours or about 4.5 ng/m3) initially proposed by the National Health Council in the Netherlands (5,10), which was a health based standard (11), although a higher value was finally adopted 200 EU/m3 (11). The study by Tanaka et al., illustrates the diversity of industries (5,6,10-14) where workers have exposure to levels of endotoxin sufficient to cause respiratory diseases. Endotoxin may even be one of the major causes of health effects from outdoor pollutant particulates (15). It should be mentioned that there have been suggested beneficial effects of LPS as a result of occupational exposure, notably reduced lung cancer rates (16,17). Thus, occupational exposure may be a two-edged sword. It is suggested that beneficial effects of occupational exposure also be reported in studies rather than dismissing these results as bias or some form of the healthy worker effect (18). References 1. Tanaka H, Saikai T, Sugawara H, Takeya I, Tsunematsu K, Matsuura A, Abe S. Workplace-related chronic cough on a mushroom farm. Chest 2002; 122: 1080-1085. 2. Musgrave KJ, McCawley MA. Respiratory health risks in agriculture. In. Environmental Respiratory Diseases, eds Cordasco EM, Demeter SL, Zenz C. Van Nostrand Reinhold, New York, 1995, Pages 263- 294 3. Wang X-R, Pan LD, Zhang H-X, Sun B-X, Dai H, Christiani DC. Follow -up study of respiratory health of newly-hired female cotton textile workers. Am J Ind Med 2002; 41: 111-118. 4. Rylander R (editor). Endotoxins in the environment – a criteria document. Int J Occup Environ Med 1997; 3: S1-S48. 5. Heederik D, Douwes J. Towards an occupational exposure limit for endotoxins? Ann Agric Environ Med. 1997;4:17-19. 6. Zock JP, Hollander A, Heederik D, Douwes J. Acute lung function changes and low endotoxin exposures in the potato processing industry. Am J Ind Med 1998; 33: 384-391 7. Milton DK, Wypij DW, Kriebel D, Walters MD, Hammond K, Evans JS, Endotoxin exposure-response in a fiberglass manufacturing facility. Am J Ind Med 1996; 29: 3-13. 8. Wolff SM. Biological effects of bacterial endotoxins in man. In. Kass EH, Wolff SM, eds., Bacterial lipopolysaccharides, Chicago, University of Chicago Press, 1973, pp. 251-256. 9. Post W, Heederik D, Houba R. Decline in lung function related to exposure and selection processes among workers in the grain processing and animal feed industry. Occup Environ Med 1998;55:349-55. 10. Conference Report. Respiratory health hazards in agriculture. Am J Respir Crit Care Med 1998; 158: S1-S76. 11. Thorn J, Beijer L, Honsson T, Rylander R. Measurements strategies for the determination of airborne bacterial endotoxin in sewage treatment plants. Ann Occup Hyg 2002;46:549-54. 12. Vogel PF, van der Gulden JW, Folgering H, Kolk JJ, Heederik D, Preller L, Tielen MJ, van Schayck CP. Endotoxin exposure as a major determinant of lung function decline in pig farmers. Am J Respir Crit Car Med 1998; 157: 15-18. 13. Eduard W, Douwes J, Mehl R, Heederik D, Melbostad E. Short term exposure to airborne microbial agents during farm work: exposure-response relations with eye and respiratory symptoms. Occup Environ Med 2001; 58: 113-118. 14. Rylander R. Endotoxin in the environment – exposure and effects. J Endotoxin Res 2002; 8:241-252. 15. Becker S, Fenton MJ, Soukup JM. Involvement of microbial components and toll-like receptors 2 and 4 in cytokine responses to air pollution particles Am. J. Respir. Cell Mol. Biol. 2002; 27: 611-618 16. Mastrangelo G, Marzia V, Marcer G. Reduced lung cancer mortality in diary farmers: is endotoxin exposure the key factor? Am J Ind Med 1996; 30: 601-9. 17. Enterline PE, Sykora JL, Keleti G, Lange JH. Endotoxin, cotton dust and cancer. Lancet 1985; 2: 934-5. 18. Lange JH. Reduced cancer rates in agricultural workers: a benefit of environmental and occupational endotoxin exposure. Med Hypotheses 2000; 55: 383-385 |
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