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Respiratory disease in grainworkers
Respiratory Medicine (1990) 84, 93-95
Respiratory disease in grainworkers Bulk storage and handling of grain is a major and expanding industry. In the United Kingdom the annual grain harvest increased from 13.2million tonnes in 1977 to 24.5million tonnes in 1986 (1), and it is estimated that up to 100000 people are occupationally exposed to grain dust. Grain is a biological mixture of great complexity. In the field it is subject to attack by a variety of moulds ('field fungi') and, when stored after harvest, may be further contaminated with storage mites such as Glycyphagus destructor, 'storage fungi' and larger insects such as the grain weevil, Sitophilus granarius (2). Endotoxin is present in substantial amounts (3) and most grain is chemically treated when in store to reduce the level of contamination. The composition of grain dust-particularly its contaminants-may vary with climatic and storage conditions. Exposure to grain dust is known to cause significant risks to health and respiratory disorders due to grain dust have been recognized for centuries. However, the diseases processes responsible for symptoms in grainworkers have not been clearly defined. There are no specific markers for grain-induced respiratory disease, and the prevalence of respiratory disability due to grain dust is largely unknown. A number of different respiratory syndromes have been described following grain dust exposure. These include occupational asthma (4-6), chronic bronchitis with airflow limitation (7,8), grain fever (which is usually associated with acute airflow limitation) (9,10) and extrinsic allergic alveolitis. There is no evidence for a byssinosis-like syndrome. Occupational asthma is the best defined of these conditions. Several reports have documented asthma developing after bronchial challenge with grain dust, extracts of grain, and with storage mites which are known to contaminate stored grain (4-6). There is no direct (bronchial challenge) evidence to support a pathogenic r01e for Sitophilus granarius or storage or field moulds but these may also be involved (11,12). The prevalence of occupational asthma in the grain industry has been difficult to establish. In many surveys, especially in those from North America, cough, sputum and chronic bronchitis are much commoner than wheeze or self-reported asthma (7,8). Asthma is of course difficult to detect in cross sectional surveys, but even where bronchial hyperresponsiveness has been measured occupational asthma can be found in only a minority of symptomatic grainworkers (5). The 0954-6111/90/020093+ 03 $03.00/0
pathogenesis of symptoms in the remainder has yet to be fully explained. Lung function tests in grainworkers usually show impaired airway calibre compared to control subjects, even allowing for the effect of smoking (13,14). There is some evidence that, at least initially, this effect is related to exposure. Seasonally employed grain handlers in both Canada and Western Australia have better lung function before the season than during the season (15-17). Cross sectional surveys have also shown a decline in FEV~ across a shift. The prevalence of this finding ranges from 2-16% (18). Some of these individuals may have occupational asthma (19), but it has also been shown that normal, previously unexposed subjects can develop acute airways obstruction when exposed to grain at very high concentrations, usually in association with grain fever (9). It has been suggested that this is caused by endotoxin, or that it is a result of direct mediator release (20), but there is no direct in vivo evidence to support these suggestions. Bronchial responsiveness is increased in grainworkers compared to controls matched for age and smoking habits (21), and occupational symptoms in grainworkers may be strongly associated with bronchial hyperresponsiveness to methacholine (5). However, the interpretation of these changes is not clear. Bronchial hyperresponsiveness cannot simply be equated with asthma, and it is possible that other inflammatory conditions of the airways may cause bronchial hyperresponsiveness. Little is known about the long term effects of grain dust exposure, because there are few prospective studies. Some Canadian grainworkers show accelerated decline in FEV~ over a 5 year period (22), and this is associated with shift-related changes in FEV I but not bronchial hyperresponsiveness (23). These changes are also associated with the duration and intensity of exposure to grain, and are significantly greater in smoking and nonsmoking grainworkers than control subjects. Information on the pathology of the lung in grainworkers is scarce (24), and there is no information on lung function changes in retired grainworkers. In any industry where labour turnover is high, long term changes are difficult to establish. Subjects who develop symptoms at an early stage may leave, with a 'survivor' population left who may be relatively resistant to the effects of grain dust. This also helps to explain why it has been difficult to establish which risk factors are important for the development 9 1990Bailli6reTindall
94
Editorial
of respiratory disease. Without prospective studies which follow-up leavers as well as those remaining employed, the effects o f such risk factors may be completely obscured. Cigarette smoking and atopy have been implicated as individual risk factors for the development of grain-induced respiratory disease, and it has been suggested that the effects of grain dust and cigarette smoking may be synergistic (25), but this has not been confirmed, Atopy, however, does appear to be an important risk factor. In West Australian seasonal grain handlers, atopic subjects are more likely to develop symptoms, and some cross sectional surveys have shown a lower prevalence of atopy in grainworkers than controls (a survivor effect?). Bronchial hyperresponsiveness, on the other hand, did not predict long term decline in FEV t in Canadian grain handlers. The respiratory effects of grain dust remain something of an enigma. This is a reflection of the complexity of this particular industrial hazard, the limited understanding of the pathology of its effects, and the lack of clearcut markers for grain-induced disease. The effects of grain dust, as a biological agent, have perhaps been neglected by comparison with the inorganic dust pneumoconioses, though numerically almost as many people are now exposed to grain dust. It is regarded as a 'nuisance dust' and permitted levels are much higher than for inorganic dusts which are known to cause respiratory disability. The task for the future is to establish precisely the ways in which biological agents such as grain dust can cause long term respiratory disability. Is it all the result of untreated and unrecognized occupational asthma, or does grain dust induce inflammatory changes in the airways which are pathologically quite distinct? What is the role of endotoxin, and the relationship between grain fever and occupational asthma? Much more work remains to be done. This year, 1990, The Health and Safety Executive is running a campaign to increase awareness of respiratory hazards in the workplace. This may create new chances to answer some of these questions; the opportunity should not be missed. A. D. BLAINEY Consultant Physician Broomfield Hospital Chelmsford E s s e x C M 1 5ET, U.K.
References 1. Aim~tal Abstract o f Statistics, 1989 ed. London: Central
Statistical Office, HMSO, 1989.
2. Lacy J. The microflora of grain dusts. In. Dosman JA, Cotton DJ, eds. Occupational Pulmonary Disease: Focus on Grain D,tst and Health. New York: Academic Press, 1980. 3. Rylander R. Lung diseasescaused by organic dusts in the farm environmen t, Am J Ind Med 1986; 81: 221-227. 4. doPico GA, Jacobs S, Flaherty D, Rankin J. Pulmonary reaction to durum wheat. Chest 1982;81: 55-61. 5. Blainey AD, Topping MD, Oilier S, Davies RJ. Allergic respiratory disease in grainworkers: the role of storage mites. J Allergy Clin lmmunol 1989; 84: 296-303. 6. Warren P, Cherniak RM, Tse KS. Hypersensitivity reactions to grain dust. J Allergy Clin h77munol 1974;53: 139 149. 7. doPico GA, Reddan W, Flaherty D, Tsiatis A, Peters M, Rao P, Rankin J. Respiratory abnormalities among grain handlers. Am Rev Res'p Dis' 1977; 115:915-927. 8. Broder I, Mintz S, Hutcheon M, Corey P, Silverman E, Davies G, Leznoff A, Peress L, Thomas P. Comparison of respiratory variables in grain elevator workers and civic outside workers of Thunder Bay, Canada. Am Rev Resp Dis 1979; 119: 193-203. 9. doPico GA, Flaherty D, Bhansali P, Chavaje N. Grain fever syndrome induced by inhalation of airborne grain dust. J Allergy Clin hnnntnol I982; 69: 435-443. I0. Cockcroft A, McDermott M, Edwards J, McCarthy P. Grain exposure-symptoms and lung function. Es J Resp Dis 1983;64: 189-196. 11. Lunn JA. Millworkers asthma: Allergic responses to the grain weevil (Sitophilus granarius). Brit J hul Med 1966; 23: 149-152. 12. Darke CS, Knowelden J, Lacey J, Milford-Ward A. Respiratory disease of workers harvesting grain. Thorax 1976; 31: 294-302. 13. Dosman JA, Cotton DJ, Graham BL, Li KYR, Froh F, Barnett GD. Chronic bronchitis and decreased forced expiratory flow rates in lifetime nonsmoking grain workers. Am Rev Resp Dis 1980; 121:11-16. 14. Chan-Yeung M, Schulzer M, MacLean L, Dorken E, Grzybowski S. Epidemiologic health survey of grain elevator workers in British Columbia. Am Rev Resp Dis 1980; 121: 329-338. 15. Cookson WOCM, Ryan G, MacDonald S, Musk AW. Atopy, non-allergic bronchial reactivity, and past history as determinants of work-related symptoms in seasonal grain handlers. Brit J lnd Med 1986; 43: 396-400. 16. James AL, Cookson WOCM, Buters G, Lewis S, Ryan G, Hockey R, Musk AW. Symptoms and longitudinal changes in lung function in young seasonal grain handlers. Brit J I n d M e d 1986;43: 587-591. 17. Broder I, Mintz S, Hutcheon M, Corey P, Kuzyk J. Effect of layoff and rehire on respiratory variables of grain elevator workers. Am Rev Resp Dis 1980; 122: 601-608. 18. CoreyP, Hutcheon M, Broder I, Mintz S. Grain elevator workers show work-related pulmonary function changes and dose-effect relationships with dust exposure. Brit J lnd Med 1982; 39: 330-337. 19. Chan-Yeung M, Wong R, MacLean L. Respiratory abnormalities among grain elevator workers. Chest 1975; 75:461-467. 20. Chan-Yeung M, Chan H, Salari H, Wall R, Tse KS. Grain dust extract induced direct release of mediators from human lung tissue. J Allergy Clin htmnmo11987; 80: 270-284.
Editorial 21. Mink JT, Gerrard JW, Cockcrofl DW, Cotton DJ, Dosman JA. Increased bronchial reactivity to histamine in nonsmoking grainworkers with normal lung ['unction. Chest 1980; 77:28---31. 22. Enarson DA, Vedal S, Chan-Yeung S. Rapid decline in FEV~ in grain handlers. Am Rev Resp Dis 1985; 132: 814-817. 23. Tabona M, Chan-Yeung M, Enarson D, MacLean L,
95
Dorken E, Schulzer M. Host factors affecting longitudinal decline in lung spirometry among grain elevator workers. Che.rt 1984; 85:782-786. 24. Cohen VL, Osgood H. Disability due to inhalation of grain dust. J Allergy 1953; 24:193-21 I. 25. Dosman JA. Chronic obstructive pulmonary disease and smoking in grainworkers. Ann Intern Med 1977; 87: 784--786.
Respiratory disease in grainworkers Bulk storage and handling of grain is a major and expanding industry. In the United Kingdom the annual grain harvest increased from 13.2million tonnes in 1977 to 24.5million tonnes in 1986 (1), and it is estimated that up to 100000 people are occupationally exposed to grain dust. Grain is a biological mixture of great complexity. In the field it is subject to attack by a variety of moulds ('field fungi') and, when stored after harvest, may be further contaminated with storage mites such as Glycyphagus destructor, 'storage fungi' and larger insects such as the grain weevil, Sitophilus granarius (2). Endotoxin is present in substantial amounts (3) and most grain is chemically treated when in store to reduce the level of contamination. The composition of grain dust-particularly its contaminants-may vary with climatic and storage conditions. Exposure to grain dust is known to cause significant risks to health and respiratory disorders due to grain dust have been recognized for centuries. However, the diseases processes responsible for symptoms in grainworkers have not been clearly defined. There are no specific markers for grain-induced respiratory disease, and the prevalence of respiratory disability due to grain dust is largely unknown. A number of different respiratory syndromes have been described following grain dust exposure. These include occupational asthma (4-6), chronic bronchitis with airflow limitation (7,8), grain fever (which is usually associated with acute airflow limitation) (9,10) and extrinsic allergic alveolitis. There is no evidence for a byssinosis-like syndrome. Occupational asthma is the best defined of these conditions. Several reports have documented asthma developing after bronchial challenge with grain dust, extracts of grain, and with storage mites which are known to contaminate stored grain (4-6). There is no direct (bronchial challenge) evidence to support a pathogenic r01e for Sitophilus granarius or storage or field moulds but these may also be involved (11,12). The prevalence of occupational asthma in the grain industry has been difficult to establish. In many surveys, especially in those from North America, cough, sputum and chronic bronchitis are much commoner than wheeze or self-reported asthma (7,8). Asthma is of course difficult to detect in cross sectional surveys, but even where bronchial hyperresponsiveness has been measured occupational asthma can be found in only a minority of symptomatic grainworkers (5). The 0954-6111/90/020093+ 03 $03.00/0
pathogenesis of symptoms in the remainder has yet to be fully explained. Lung function tests in grainworkers usually show impaired airway calibre compared to control subjects, even allowing for the effect of smoking (13,14). There is some evidence that, at least initially, this effect is related to exposure. Seasonally employed grain handlers in both Canada and Western Australia have better lung function before the season than during the season (15-17). Cross sectional surveys have also shown a decline in FEV~ across a shift. The prevalence of this finding ranges from 2-16% (18). Some of these individuals may have occupational asthma (19), but it has also been shown that normal, previously unexposed subjects can develop acute airways obstruction when exposed to grain at very high concentrations, usually in association with grain fever (9). It has been suggested that this is caused by endotoxin, or that it is a result of direct mediator release (20), but there is no direct in vivo evidence to support these suggestions. Bronchial responsiveness is increased in grainworkers compared to controls matched for age and smoking habits (21), and occupational symptoms in grainworkers may be strongly associated with bronchial hyperresponsiveness to methacholine (5). However, the interpretation of these changes is not clear. Bronchial hyperresponsiveness cannot simply be equated with asthma, and it is possible that other inflammatory conditions of the airways may cause bronchial hyperresponsiveness. Little is known about the long term effects of grain dust exposure, because there are few prospective studies. Some Canadian grainworkers show accelerated decline in FEV~ over a 5 year period (22), and this is associated with shift-related changes in FEV I but not bronchial hyperresponsiveness (23). These changes are also associated with the duration and intensity of exposure to grain, and are significantly greater in smoking and nonsmoking grainworkers than control subjects. Information on the pathology of the lung in grainworkers is scarce (24), and there is no information on lung function changes in retired grainworkers. In any industry where labour turnover is high, long term changes are difficult to establish. Subjects who develop symptoms at an early stage may leave, with a 'survivor' population left who may be relatively resistant to the effects of grain dust. This also helps to explain why it has been difficult to establish which risk factors are important for the development 9 1990Bailli6reTindall
94
Editorial
of respiratory disease. Without prospective studies which follow-up leavers as well as those remaining employed, the effects o f such risk factors may be completely obscured. Cigarette smoking and atopy have been implicated as individual risk factors for the development of grain-induced respiratory disease, and it has been suggested that the effects of grain dust and cigarette smoking may be synergistic (25), but this has not been confirmed, Atopy, however, does appear to be an important risk factor. In West Australian seasonal grain handlers, atopic subjects are more likely to develop symptoms, and some cross sectional surveys have shown a lower prevalence of atopy in grainworkers than controls (a survivor effect?). Bronchial hyperresponsiveness, on the other hand, did not predict long term decline in FEV t in Canadian grain handlers. The respiratory effects of grain dust remain something of an enigma. This is a reflection of the complexity of this particular industrial hazard, the limited understanding of the pathology of its effects, and the lack of clearcut markers for grain-induced disease. The effects of grain dust, as a biological agent, have perhaps been neglected by comparison with the inorganic dust pneumoconioses, though numerically almost as many people are now exposed to grain dust. It is regarded as a 'nuisance dust' and permitted levels are much higher than for inorganic dusts which are known to cause respiratory disability. The task for the future is to establish precisely the ways in which biological agents such as grain dust can cause long term respiratory disability. Is it all the result of untreated and unrecognized occupational asthma, or does grain dust induce inflammatory changes in the airways which are pathologically quite distinct? What is the role of endotoxin, and the relationship between grain fever and occupational asthma? Much more work remains to be done. This year, 1990, The Health and Safety Executive is running a campaign to increase awareness of respiratory hazards in the workplace. This may create new chances to answer some of these questions; the opportunity should not be missed. A. D. BLAINEY Consultant Physician Broomfield Hospital Chelmsford E s s e x C M 1 5ET, U.K.
References 1. Aim~tal Abstract o f Statistics, 1989 ed. London: Central
Statistical Office, HMSO, 1989.
2. Lacy J. The microflora of grain dusts. In. Dosman JA, Cotton DJ, eds. Occupational Pulmonary Disease: Focus on Grain D,tst and Health. New York: Academic Press, 1980. 3. Rylander R. Lung diseasescaused by organic dusts in the farm environmen t, Am J Ind Med 1986; 81: 221-227. 4. doPico GA, Jacobs S, Flaherty D, Rankin J. Pulmonary reaction to durum wheat. Chest 1982;81: 55-61. 5. Blainey AD, Topping MD, Oilier S, Davies RJ. Allergic respiratory disease in grainworkers: the role of storage mites. J Allergy Clin lmmunol 1989; 84: 296-303. 6. Warren P, Cherniak RM, Tse KS. Hypersensitivity reactions to grain dust. J Allergy Clin h77munol 1974;53: 139 149. 7. doPico GA, Reddan W, Flaherty D, Tsiatis A, Peters M, Rao P, Rankin J. Respiratory abnormalities among grain handlers. Am Rev Res'p Dis' 1977; 115:915-927. 8. Broder I, Mintz S, Hutcheon M, Corey P, Silverman E, Davies G, Leznoff A, Peress L, Thomas P. Comparison of respiratory variables in grain elevator workers and civic outside workers of Thunder Bay, Canada. Am Rev Resp Dis 1979; 119: 193-203. 9. doPico GA, Flaherty D, Bhansali P, Chavaje N. Grain fever syndrome induced by inhalation of airborne grain dust. J Allergy Clin hnnntnol I982; 69: 435-443. I0. Cockcroft A, McDermott M, Edwards J, McCarthy P. Grain exposure-symptoms and lung function. Es J Resp Dis 1983;64: 189-196. 11. Lunn JA. Millworkers asthma: Allergic responses to the grain weevil (Sitophilus granarius). Brit J hul Med 1966; 23: 149-152. 12. Darke CS, Knowelden J, Lacey J, Milford-Ward A. Respiratory disease of workers harvesting grain. Thorax 1976; 31: 294-302. 13. Dosman JA, Cotton DJ, Graham BL, Li KYR, Froh F, Barnett GD. Chronic bronchitis and decreased forced expiratory flow rates in lifetime nonsmoking grain workers. Am Rev Resp Dis 1980; 121:11-16. 14. Chan-Yeung M, Schulzer M, MacLean L, Dorken E, Grzybowski S. Epidemiologic health survey of grain elevator workers in British Columbia. Am Rev Resp Dis 1980; 121: 329-338. 15. Cookson WOCM, Ryan G, MacDonald S, Musk AW. Atopy, non-allergic bronchial reactivity, and past history as determinants of work-related symptoms in seasonal grain handlers. Brit J lnd Med 1986; 43: 396-400. 16. James AL, Cookson WOCM, Buters G, Lewis S, Ryan G, Hockey R, Musk AW. Symptoms and longitudinal changes in lung function in young seasonal grain handlers. Brit J I n d M e d 1986;43: 587-591. 17. Broder I, Mintz S, Hutcheon M, Corey P, Kuzyk J. Effect of layoff and rehire on respiratory variables of grain elevator workers. Am Rev Resp Dis 1980; 122: 601-608. 18. CoreyP, Hutcheon M, Broder I, Mintz S. Grain elevator workers show work-related pulmonary function changes and dose-effect relationships with dust exposure. Brit J lnd Med 1982; 39: 330-337. 19. Chan-Yeung M, Wong R, MacLean L. Respiratory abnormalities among grain elevator workers. Chest 1975; 75:461-467. 20. Chan-Yeung M, Chan H, Salari H, Wall R, Tse KS. Grain dust extract induced direct release of mediators from human lung tissue. J Allergy Clin htmnmo11987; 80: 270-284.
Editorial 21. Mink JT, Gerrard JW, Cockcrofl DW, Cotton DJ, Dosman JA. Increased bronchial reactivity to histamine in nonsmoking grainworkers with normal lung ['unction. Chest 1980; 77:28---31. 22. Enarson DA, Vedal S, Chan-Yeung S. Rapid decline in FEV~ in grain handlers. Am Rev Resp Dis 1985; 132: 814-817. 23. Tabona M, Chan-Yeung M, Enarson D, MacLean L,
95
Dorken E, Schulzer M. Host factors affecting longitudinal decline in lung spirometry among grain elevator workers. Che.rt 1984; 85:782-786. 24. Cohen VL, Osgood H. Disability due to inhalation of grain dust. J Allergy 1953; 24:193-21 I. 25. Dosman JA. Chronic obstructive pulmonary disease and smoking in grainworkers. Ann Intern Med 1977; 87: 784--786.