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AMOSITE ASBESTOS AND MESOTHELIOMA
1397
Encephalitis lethargica was first described in Austria and France in 1917 when von Economo saw numerous patients with a strange variety of symptoms in a Viennese clinic.2,3 By 1918 the disease had spread throughout France, Austria, and England, and had appeared in Germany and North America. In 1919 it had overrun Europe and spread to Canada, Central America, India, and later Japan and Africa. The clinical and pathological features were typical of viral infection with microscopic foci of inflammation mainly in the grey matter of the mid-brain and basal ganglia. Although no causal organism was isolated, the disease was thought to be due to an airborne infective agent, filter passible, and it was transmitted to monkeys by injection of brain tissue from infected patients.5 Children and young adults were mainly affected. The death rate was high, between 30% and 40%, and only about a quarter recovered completely.6 Infectivity was very slight and transmission by contact was never observed in 1156 cases in Vienna. Encephalitis lethargica occurred in the same years as a great influenza pandemic, but the two conditions were clearly different in prevalence, clinical features, infectivity, and after-effects. Other neurotropic viral illnesses which were later recognised, including the St Louis, Californian, and eastern and western equine varieties of encephalitis, mostly arise in the summer and spread by mosquitoes, unlike encephalitis lethargica which was a disease of the winter months, except in Japan. Encephalitis lethargica may have been the first to be recognised of a new class of diseases, due to slow virus infection of the nervous
system.8 The clinical features of encephalitis lethargica were very variable despite common features in most epidemics. In the acute phase lethargy, headache, and fever lasted days, weeks, or months, and were accompanied by pupillary changes and ocular palsies in 75% of patients. Other cranial nerve palsies, dysphagia, and hemiplegia were frequent. Somnolence, stupor, coma, sleep reversal, and narcolepsy occurred during both acute and chronic phases of illness and, in later
epidemics, fits, myoclonus, hiccup, chorea, respiratory diabetes insipidus, and sweating were common. During the acute illness or after apparent recovery for as long as three or four years, and in a fashion reminiscent of syphilis, unexpected features could first appear, the strangest of which was parkinsonism. This was often something more than paralysis agitans, with oculogyric crises, involuntary movements, compulsive behaviour, disturbed sleep, and sometimes psychic disorders. These
psychotic behaviour, and crime were not uncommon. 3,11,12 Hoffstadt13 described 21 children with wild nocturnal excitement, arising with remarkable punctuality, with or
ceaseless activity, talking, singing, shouting, and restlessness. More than one instance of homicide by young children came before the criminal courts such as a boy of 10 who knifed his mother, threatened to cut his brother up, and took a hatchet to his sister. 14 Should encephalitis lethargica be relegated to history? In endemic form the disease is difficult to diagnose with certainty on account of the variable clinical picture and absence of specific diagnostic tests. However, the occurrence of encephalitis with lethargy, eye signs, changes in behaviour, and parkinsonism, accompanied by oculogyric crises, is sufficiently distinct to indicate the likely diagnosis. Although
parkinsonism may follow encephalitis with serological evidence of poliomyelitis, Coxsackie B2, and echo virus infection,15,16 these rarely produce chronic or severe motor disability and have different pathological features from encephalitis lethargica. Rail, Scholtz, and Swash have lately observed eight patients with clinical features similar to those of the encephalitis lethargica pandemic of 60 years ago. 17 The disease was acquired after 1960 in six patients. Other similar isolated cases, sometimes with onset at the time of epidemic influenza, are described from year to year. 18-20 The problem of diagnosis is greatest in patients presenting with psychiatric symptoms alone, although many such patients were seen in 1917-27 in whom ophthalmoplegia or parkinsonism developed later. Hunter and Jones21,22 described six patients presenting with psychiatric syndromes, hypomania, depression, or anxiety, in all of whom oculopupillary abnormalities later appeared. Although it is sometimes difficult
to
evaluate these cases, there
seems
little doubt that
encephalitis lethargica still occurs in endemic form throughout the world and is still responsible for occasional new cases of parkinsonism as well as mental disturbance.
disturbances,
could take many bizarre forms. Schwab
et
al. mention
a
patient with episodic paranoia localised to one side of the body and occurring during oculogyric crises, and the rise of National Socialism in Germany, with the violent aggressive behaviour and gesticulation of Hitler, may have been due, at least partly, to encephalitis lethargica. 10 Acute psychiatric disturbances with overactivity, antisocial, cruel, destructive, 2. Cruchet JR, Moutier F, Calmettes A. Quarante cas d’encéphalo-myélite subaigue. Bull Soc Méd Hôp Paris 1917; 41: 614-16. 3. von Economo C. Encephalitis lethargica: Its sequelae and treatment. Translated by KO Newman. London: Oxford University Press, 1931. 4. Abrahamson I. Lethargic encephalitis. New York; 1935. 5. Levaditi C, Harvier P. Recherches experimentales sur l’encéphalite épidémique C R Soc Biol Paris 1921; 84: 388. 6. Hall AJ. Epidemic encephalitis. Bristol: John Wright, 1924. 7. Hoff H. In: Hall AJ, ed. Epidemic encephalitis. Bristol: John Wright, 1924. 8. Kakulas BA, Adams RD. Viral infection of the nervous system. In: Isselbacher KJ, Adams RD, Braunwald E, Petersdorf RG, Wilson JD, eds. Harrison’s principles of internal medicine. New York: McGraw-Hill, 1980; 1970. 9. Schwab RS, Fabing MD, Prichard JD Psychiatric symptoms and syndromes in Parkinson’s disease Am JPsychiatry 1951; 107: 901-07. 10. Stolk PJ. Adolph Hitler: His life and his illness. Psychiatria Neurologia Neurochirurgia 1968; 71: 381-98.
AMOSITE ASBESTOS AND MESOTHELIOMA THREE types of asbestos have been used commercially in the United Kingdom-the serpentine chrysotile (white asbestos) and the amphiboles crocidolite (blue) and amosite (brown). The last of these is the least understood in terms of its health effects in man. One of the difficulties is that there are few human populations which have been been exposed to amosite but not to other forms of asbestos. Mesothelioma is clearly much com11. Lishman WA Organic psychiatry. Oxford: Blackwell, 1978; 411-22. 12. Fairweather DS. Psychiatric aspects of the post-encephalitic syndrome. 1947; 93: 201-54.
J Ment
Sci
13. Hofstadt F. Ueber eine eigenartige Form von schlafstörung im kindesalter als spätschaden nach encephalitis epidemica. Munch Med Schr 1980; 67: 1400-02. 14. MacPhail HD. Mental disorder from encephalitis lethargica. J Ment Sci 1922; 68: 169-71. 15. Thieffry S. Enterovirus (Poliomyelite, Coxsackie, ECHO) et maladies du systeme nerveux. Revision critique et experience personelle. Rev Neurol 1963; 105: 753-76. 16. Poser CM, Huwley CJ, Poland JD. Paraencephalitic parkinsonism. Report of an acute case due to coxsackie virus type Bx and re-examination of the aetiologic concepts of post-encephalitic parkinsonism. Acta Neurol Scand 1969, 45: 199-215. 17. Rail D, Scholtz C, Swash M Post-encephalitic parkinsonism: current experience J 3 Neurol Neurosurg Psychiatry 1981; 44: 670-76 18. Leigh AD. Infection of the nervous system occurring during an epidemic of influenza B. Br Med J 1946; ii 936-38. 19 Bickerstaff ER, Cloake PCP Mesencephalitis and rhombencephalitis. Br Med J 1951; ii. 77-81. 20. Espir MLE, Spalding JMK. Three recent cases of encephalitis lethargica Br Med J
1956; i: 1141-44. 21. Hunter
R, Jones M. Acute lethargica-type encephalitis. Lancet 1966; ii: 1023-24. Encephalitis of lethargica type in a mental hospital. Lancet 1966; ii: 1014-15.
22. Editorial.
1398 in crocidolite minersl,2 than in chrysotile miners:3,4 in exhaustive study of Quebec chrysotile miners and millers, only 7 mesotheliomas definitely attributable to chrysotile could be found in more than 4500 deaths. The position of amosite may be intermediate between chrysotile and crocidolite.
moner an
Marine insulation block manufactured from amosite was made in a New Jersey factory during and after the 1939-45 war and 933 union members who worked in this factory have been followed up by Selikoff and his colleagues.5By 1973 11 deaths from mesothelioma had been reported in these men (5 pleural, 6 peritoneal) and 4 others had occurred in members of their families exposed to dust brought home on their clothes.6 Pleural and peritoneal mesotheliomas have also been common in American pipe-fitters who have been exposed principally to mixtures of amosite and chrysotile.’ In contrast, mesothelioma is almost unknown in process workers exposed to chrysotile alone in the manufacture of friction materials and textiles.
Experimental work in animals shows that the physical configuration of mineral fibres is an important determinant of carcinogenicity. It is possible to prepare samples of chrysotile fibre which are at least as carcinogenic as amosite both in inhalation experiments9 and after introduction of the fibre directly into the pleural space. The much lower rate of mesothelioma in men exposed to chrysotile is probably due to differences between samples of fibre prepared for experimental use and those used in commerce.
On p. 1403 Professor Acheson and his colleagues report the mortality from mesothelioma in a workforce exposed to a mixture containing 97% amosite and 3% chrysotile in the manufacture of insulation board. By the end of 1980 5 deaths had occurred in which mesothelioma had been recorded as the underlying cause (4 pleural and 1 peritoneal) and mesothelioma contributed to death in 2 others. Even though not more than about 700 of the men have so far been followed for twenty or more years since first exposure to asbestos, this number far exceeds what might have been expected as a result of exposure to chrysotile. 3,7 It is now two years since the British Advisory Committee on Asbestos recommended a stricter control limit in the workplace for amosite (0’5fibre per ml) than for chrysotile (1fibre per ml). 11 The principal basis for this recommendation was
the evidence that in man exposure to amosite has been associated with a higher risk of mesothelioma than to chrysotile. The evidence for this view has subsequently been strengthened by studies from both sides of the Atlantic and the Government should reconsider its plan 12 to reject this recommendation.
OCCUPATIONAL ASTHMA OCCUPATIONAL lung diseases are usually classified according to the provoking agent, such as gases, fumes, mineral dusts, and organic dusts (see p. 1429). Another way is to subdivide them according to the major clinicopathological response, such as asthma, alveolitis, pulmonary fibrosis, and malignant change. Some agents can induce more than one responselung fibrosis and malignancy in asbestos workers; or alveolitis and interstitial fibrosis after exposure to beryllium fumes. In coalworkers’ pneumoconiosis years of exposure are necessary before disease shows itself clinically, progressive lung fibrosis is uncommon if exposure to coal-dust ceases, and regular chest radiography can reveal disease long before symptoms develop. The position with occupational asthma is very different. Symptoms may follow a short exposure and the subject may not always recover fully when exposure ceases. Moreover, because asthma is so common, a connection with work is often not thought of, and the patient becomes chronically ill. Once the diagnosis has been entertained proof can come from the combination of a careful history, lung function tests at home and work, and inhalation challenge under strict supervision, although immunological tests are also occasionally helpful. In such a way Blainey and coworkers’ investigated asthma and rhinitis in two men working with western red cedar. Asthma was induced by bronchial provocation with fine dust from western red cedar but not other woods with which they worked, and both patients improved symptomatically and on peak flow
recordings when away from work. of State for Social Services has the recommendation of the Industrial Injuries Advisory Council on Occupational Asthma (defined as asthma which develops after a variable period of symptomless exposure to a sensitising agent encountered at work) that asthma due to certain agents-platinum salts, isocyanates, epoxy resin curing agents, colophony fumes, proteolytic enzymes, animals and insects in laboratories, and dust from grain and flour-should be a prescribed disease which may allow the payment of disablement benefits through the existing pneumoconiosis panels. The Council suggests that 5-30% of the workforce exposed to these agents may have occupational asthma and that a substantial ninority have to give up work for this reason. In Britain the
Secretary
lately2 accepted Wagner JC, Sleggs CA, Merchand P. Diffuse pleural mesothelioma and asbestos exposure in the North Western Cape Province. Br J Ind Med 1960; 17: 260-71. 2. Hobbs MST, Woodward SD, Murphy B, Musk AW, Elder JE. The incidence of pneumoconiosis, mesothelioma and other respiratory cancer in men engaged in mining and milling crocidolite in Western Australia. In: Wagner JC, ed. Biological effects of mineral fibres (IARC Sci Publ no. 30), IARC: Lyon, 1980: 615. 3. McDonald JC. In: Glen HW, ed. Proceedings of Asbestos Symposium, Johannesburg, Oct. 3-7, 1977. Randburg: National Institute for Metallurgy, 1978: 67-79. 4. Gilson JC. Asbestos cancer; past and future hazards. Proc Roy Soc Med 1973; 66: 395. 5. Selikoff IJ, Hammond EC. Multiple risk factors in environmental cancer. In: Fraumeni JF, ed. Persons at high risk of cancer: An approach to cancer aetiology and control. London: Academic Press, 1975: 467. 6. Anderson HA, Lilis R, Daum SM, Fischbein AS, Selikoff IJ. Household contact asbestos neoplastic risk. Ann NY Acad Sci 1976; 271: 311. 7. Selikoff IJ, Hammond EC, Chung J. Mortality experiences in asbestos insulation workers 1943-68. In: Shapiro HA, ed. Pneumoconiosis. Proceedings of the International Conference, Johannesburg, 1969, Cape Town: Oxford Press, 1970. 8. Wagner JC, Berry G, Pooley FD. Carcinogenesis and mineral fibres. Br Med Bull 1980; 1.
36: 53-56. 9. 10.
Wagner JC, Berry G, Skidmore JW, Timbrell V. The effects of the inhalation of asbestos in rats. Br J Cancer 1974; 29: 252. Davis JMG, Beckett ST, Bolton RE, Collings P, Middleton AP. Mass and number of fibres in the pathogenesis of asbestos related lung disease in rats. Br J Cancer 1978; 37: 673.
11.
Advisory Committee on Asbestos: Final report. London: HM Stationery Office,
1979.
12. Hansard (House of Commons), Oct. 22, 1981, col. 457. 1. Blainey AD, Graham VAL, Phillips MJ, Davies RJ. Respiratory tract reactions to western red cedar. Human Toxicol 1981; 1: 41-51. 2. Industrial Injuries Advisory Council, Department of Health and Social Security. Occupational asthma. London: H.M. Stationery Office, 1981.
Encephalitis lethargica was first described in Austria and France in 1917 when von Economo saw numerous patients with a strange variety of symptoms in a Viennese clinic.2,3 By 1918 the disease had spread throughout France, Austria, and England, and had appeared in Germany and North America. In 1919 it had overrun Europe and spread to Canada, Central America, India, and later Japan and Africa. The clinical and pathological features were typical of viral infection with microscopic foci of inflammation mainly in the grey matter of the mid-brain and basal ganglia. Although no causal organism was isolated, the disease was thought to be due to an airborne infective agent, filter passible, and it was transmitted to monkeys by injection of brain tissue from infected patients.5 Children and young adults were mainly affected. The death rate was high, between 30% and 40%, and only about a quarter recovered completely.6 Infectivity was very slight and transmission by contact was never observed in 1156 cases in Vienna. Encephalitis lethargica occurred in the same years as a great influenza pandemic, but the two conditions were clearly different in prevalence, clinical features, infectivity, and after-effects. Other neurotropic viral illnesses which were later recognised, including the St Louis, Californian, and eastern and western equine varieties of encephalitis, mostly arise in the summer and spread by mosquitoes, unlike encephalitis lethargica which was a disease of the winter months, except in Japan. Encephalitis lethargica may have been the first to be recognised of a new class of diseases, due to slow virus infection of the nervous
system.8 The clinical features of encephalitis lethargica were very variable despite common features in most epidemics. In the acute phase lethargy, headache, and fever lasted days, weeks, or months, and were accompanied by pupillary changes and ocular palsies in 75% of patients. Other cranial nerve palsies, dysphagia, and hemiplegia were frequent. Somnolence, stupor, coma, sleep reversal, and narcolepsy occurred during both acute and chronic phases of illness and, in later
epidemics, fits, myoclonus, hiccup, chorea, respiratory diabetes insipidus, and sweating were common. During the acute illness or after apparent recovery for as long as three or four years, and in a fashion reminiscent of syphilis, unexpected features could first appear, the strangest of which was parkinsonism. This was often something more than paralysis agitans, with oculogyric crises, involuntary movements, compulsive behaviour, disturbed sleep, and sometimes psychic disorders. These
psychotic behaviour, and crime were not uncommon. 3,11,12 Hoffstadt13 described 21 children with wild nocturnal excitement, arising with remarkable punctuality, with or
ceaseless activity, talking, singing, shouting, and restlessness. More than one instance of homicide by young children came before the criminal courts such as a boy of 10 who knifed his mother, threatened to cut his brother up, and took a hatchet to his sister. 14 Should encephalitis lethargica be relegated to history? In endemic form the disease is difficult to diagnose with certainty on account of the variable clinical picture and absence of specific diagnostic tests. However, the occurrence of encephalitis with lethargy, eye signs, changes in behaviour, and parkinsonism, accompanied by oculogyric crises, is sufficiently distinct to indicate the likely diagnosis. Although
parkinsonism may follow encephalitis with serological evidence of poliomyelitis, Coxsackie B2, and echo virus infection,15,16 these rarely produce chronic or severe motor disability and have different pathological features from encephalitis lethargica. Rail, Scholtz, and Swash have lately observed eight patients with clinical features similar to those of the encephalitis lethargica pandemic of 60 years ago. 17 The disease was acquired after 1960 in six patients. Other similar isolated cases, sometimes with onset at the time of epidemic influenza, are described from year to year. 18-20 The problem of diagnosis is greatest in patients presenting with psychiatric symptoms alone, although many such patients were seen in 1917-27 in whom ophthalmoplegia or parkinsonism developed later. Hunter and Jones21,22 described six patients presenting with psychiatric syndromes, hypomania, depression, or anxiety, in all of whom oculopupillary abnormalities later appeared. Although it is sometimes difficult
to
evaluate these cases, there
seems
little doubt that
encephalitis lethargica still occurs in endemic form throughout the world and is still responsible for occasional new cases of parkinsonism as well as mental disturbance.
disturbances,
could take many bizarre forms. Schwab
et
al. mention
a
patient with episodic paranoia localised to one side of the body and occurring during oculogyric crises, and the rise of National Socialism in Germany, with the violent aggressive behaviour and gesticulation of Hitler, may have been due, at least partly, to encephalitis lethargica. 10 Acute psychiatric disturbances with overactivity, antisocial, cruel, destructive, 2. Cruchet JR, Moutier F, Calmettes A. Quarante cas d’encéphalo-myélite subaigue. Bull Soc Méd Hôp Paris 1917; 41: 614-16. 3. von Economo C. Encephalitis lethargica: Its sequelae and treatment. Translated by KO Newman. London: Oxford University Press, 1931. 4. Abrahamson I. Lethargic encephalitis. New York; 1935. 5. Levaditi C, Harvier P. Recherches experimentales sur l’encéphalite épidémique C R Soc Biol Paris 1921; 84: 388. 6. Hall AJ. Epidemic encephalitis. Bristol: John Wright, 1924. 7. Hoff H. In: Hall AJ, ed. Epidemic encephalitis. Bristol: John Wright, 1924. 8. Kakulas BA, Adams RD. Viral infection of the nervous system. In: Isselbacher KJ, Adams RD, Braunwald E, Petersdorf RG, Wilson JD, eds. Harrison’s principles of internal medicine. New York: McGraw-Hill, 1980; 1970. 9. Schwab RS, Fabing MD, Prichard JD Psychiatric symptoms and syndromes in Parkinson’s disease Am JPsychiatry 1951; 107: 901-07. 10. Stolk PJ. Adolph Hitler: His life and his illness. Psychiatria Neurologia Neurochirurgia 1968; 71: 381-98.
AMOSITE ASBESTOS AND MESOTHELIOMA THREE types of asbestos have been used commercially in the United Kingdom-the serpentine chrysotile (white asbestos) and the amphiboles crocidolite (blue) and amosite (brown). The last of these is the least understood in terms of its health effects in man. One of the difficulties is that there are few human populations which have been been exposed to amosite but not to other forms of asbestos. Mesothelioma is clearly much com11. Lishman WA Organic psychiatry. Oxford: Blackwell, 1978; 411-22. 12. Fairweather DS. Psychiatric aspects of the post-encephalitic syndrome. 1947; 93: 201-54.
J Ment
Sci
13. Hofstadt F. Ueber eine eigenartige Form von schlafstörung im kindesalter als spätschaden nach encephalitis epidemica. Munch Med Schr 1980; 67: 1400-02. 14. MacPhail HD. Mental disorder from encephalitis lethargica. J Ment Sci 1922; 68: 169-71. 15. Thieffry S. Enterovirus (Poliomyelite, Coxsackie, ECHO) et maladies du systeme nerveux. Revision critique et experience personelle. Rev Neurol 1963; 105: 753-76. 16. Poser CM, Huwley CJ, Poland JD. Paraencephalitic parkinsonism. Report of an acute case due to coxsackie virus type Bx and re-examination of the aetiologic concepts of post-encephalitic parkinsonism. Acta Neurol Scand 1969, 45: 199-215. 17. Rail D, Scholtz C, Swash M Post-encephalitic parkinsonism: current experience J 3 Neurol Neurosurg Psychiatry 1981; 44: 670-76 18. Leigh AD. Infection of the nervous system occurring during an epidemic of influenza B. Br Med J 1946; ii 936-38. 19 Bickerstaff ER, Cloake PCP Mesencephalitis and rhombencephalitis. Br Med J 1951; ii. 77-81. 20. Espir MLE, Spalding JMK. Three recent cases of encephalitis lethargica Br Med J
1956; i: 1141-44. 21. Hunter
R, Jones M. Acute lethargica-type encephalitis. Lancet 1966; ii: 1023-24. Encephalitis of lethargica type in a mental hospital. Lancet 1966; ii: 1014-15.
22. Editorial.
1398 in crocidolite minersl,2 than in chrysotile miners:3,4 in exhaustive study of Quebec chrysotile miners and millers, only 7 mesotheliomas definitely attributable to chrysotile could be found in more than 4500 deaths. The position of amosite may be intermediate between chrysotile and crocidolite.
moner an
Marine insulation block manufactured from amosite was made in a New Jersey factory during and after the 1939-45 war and 933 union members who worked in this factory have been followed up by Selikoff and his colleagues.5By 1973 11 deaths from mesothelioma had been reported in these men (5 pleural, 6 peritoneal) and 4 others had occurred in members of their families exposed to dust brought home on their clothes.6 Pleural and peritoneal mesotheliomas have also been common in American pipe-fitters who have been exposed principally to mixtures of amosite and chrysotile.’ In contrast, mesothelioma is almost unknown in process workers exposed to chrysotile alone in the manufacture of friction materials and textiles.
Experimental work in animals shows that the physical configuration of mineral fibres is an important determinant of carcinogenicity. It is possible to prepare samples of chrysotile fibre which are at least as carcinogenic as amosite both in inhalation experiments9 and after introduction of the fibre directly into the pleural space. The much lower rate of mesothelioma in men exposed to chrysotile is probably due to differences between samples of fibre prepared for experimental use and those used in commerce.
On p. 1403 Professor Acheson and his colleagues report the mortality from mesothelioma in a workforce exposed to a mixture containing 97% amosite and 3% chrysotile in the manufacture of insulation board. By the end of 1980 5 deaths had occurred in which mesothelioma had been recorded as the underlying cause (4 pleural and 1 peritoneal) and mesothelioma contributed to death in 2 others. Even though not more than about 700 of the men have so far been followed for twenty or more years since first exposure to asbestos, this number far exceeds what might have been expected as a result of exposure to chrysotile. 3,7 It is now two years since the British Advisory Committee on Asbestos recommended a stricter control limit in the workplace for amosite (0’5fibre per ml) than for chrysotile (1fibre per ml). 11 The principal basis for this recommendation was
the evidence that in man exposure to amosite has been associated with a higher risk of mesothelioma than to chrysotile. The evidence for this view has subsequently been strengthened by studies from both sides of the Atlantic and the Government should reconsider its plan 12 to reject this recommendation.
OCCUPATIONAL ASTHMA OCCUPATIONAL lung diseases are usually classified according to the provoking agent, such as gases, fumes, mineral dusts, and organic dusts (see p. 1429). Another way is to subdivide them according to the major clinicopathological response, such as asthma, alveolitis, pulmonary fibrosis, and malignant change. Some agents can induce more than one responselung fibrosis and malignancy in asbestos workers; or alveolitis and interstitial fibrosis after exposure to beryllium fumes. In coalworkers’ pneumoconiosis years of exposure are necessary before disease shows itself clinically, progressive lung fibrosis is uncommon if exposure to coal-dust ceases, and regular chest radiography can reveal disease long before symptoms develop. The position with occupational asthma is very different. Symptoms may follow a short exposure and the subject may not always recover fully when exposure ceases. Moreover, because asthma is so common, a connection with work is often not thought of, and the patient becomes chronically ill. Once the diagnosis has been entertained proof can come from the combination of a careful history, lung function tests at home and work, and inhalation challenge under strict supervision, although immunological tests are also occasionally helpful. In such a way Blainey and coworkers’ investigated asthma and rhinitis in two men working with western red cedar. Asthma was induced by bronchial provocation with fine dust from western red cedar but not other woods with which they worked, and both patients improved symptomatically and on peak flow
recordings when away from work. of State for Social Services has the recommendation of the Industrial Injuries Advisory Council on Occupational Asthma (defined as asthma which develops after a variable period of symptomless exposure to a sensitising agent encountered at work) that asthma due to certain agents-platinum salts, isocyanates, epoxy resin curing agents, colophony fumes, proteolytic enzymes, animals and insects in laboratories, and dust from grain and flour-should be a prescribed disease which may allow the payment of disablement benefits through the existing pneumoconiosis panels. The Council suggests that 5-30% of the workforce exposed to these agents may have occupational asthma and that a substantial ninority have to give up work for this reason. In Britain the
Secretary
lately2 accepted Wagner JC, Sleggs CA, Merchand P. Diffuse pleural mesothelioma and asbestos exposure in the North Western Cape Province. Br J Ind Med 1960; 17: 260-71. 2. Hobbs MST, Woodward SD, Murphy B, Musk AW, Elder JE. The incidence of pneumoconiosis, mesothelioma and other respiratory cancer in men engaged in mining and milling crocidolite in Western Australia. In: Wagner JC, ed. Biological effects of mineral fibres (IARC Sci Publ no. 30), IARC: Lyon, 1980: 615. 3. McDonald JC. In: Glen HW, ed. Proceedings of Asbestos Symposium, Johannesburg, Oct. 3-7, 1977. Randburg: National Institute for Metallurgy, 1978: 67-79. 4. Gilson JC. Asbestos cancer; past and future hazards. Proc Roy Soc Med 1973; 66: 395. 5. Selikoff IJ, Hammond EC. Multiple risk factors in environmental cancer. In: Fraumeni JF, ed. Persons at high risk of cancer: An approach to cancer aetiology and control. London: Academic Press, 1975: 467. 6. Anderson HA, Lilis R, Daum SM, Fischbein AS, Selikoff IJ. Household contact asbestos neoplastic risk. Ann NY Acad Sci 1976; 271: 311. 7. Selikoff IJ, Hammond EC, Chung J. Mortality experiences in asbestos insulation workers 1943-68. In: Shapiro HA, ed. Pneumoconiosis. Proceedings of the International Conference, Johannesburg, 1969, Cape Town: Oxford Press, 1970. 8. Wagner JC, Berry G, Pooley FD. Carcinogenesis and mineral fibres. Br Med Bull 1980; 1.
36: 53-56. 9. 10.
Wagner JC, Berry G, Skidmore JW, Timbrell V. The effects of the inhalation of asbestos in rats. Br J Cancer 1974; 29: 252. Davis JMG, Beckett ST, Bolton RE, Collings P, Middleton AP. Mass and number of fibres in the pathogenesis of asbestos related lung disease in rats. Br J Cancer 1978; 37: 673.
11.
Advisory Committee on Asbestos: Final report. London: HM Stationery Office,
1979.
12. Hansard (House of Commons), Oct. 22, 1981, col. 457. 1. Blainey AD, Graham VAL, Phillips MJ, Davies RJ. Respiratory tract reactions to western red cedar. Human Toxicol 1981; 1: 41-51. 2. Industrial Injuries Advisory Council, Department of Health and Social Security. Occupational asthma. London: H.M. Stationery Office, 1981.