Postgrad Med J: first published as 10.1136/pgmj.69.808.129 on 1 February 1993. Downloaded from Postgrad Med J (1993) 69, 129- 135 © The Fellowship of Postgraduate Medicine, 1993

Occupational Medicine Occupational lung diseases other than asthma* P.H. Wright Benefits Agency, Department ofSocial Security, Olympic House, Olympic Way, Wembley, Middlesex, HA9 ODL, UK

Introduction To cover this topic completely would need a book anatomy briefly in order from the nose downwards. too heavy to handle and too expensive to buy. The nose and pharynx warm and humidify the Moreover, others have discussed some aspects so incoming air. Particles are caught by nasal hairs, or well that I could not better their work. Instead, I impact on the walls of the pharynx and are shall try to describe the classic occupational lung swallowed.4 The nose is so efficient that the diseases in a wider context to help those app- difference between breathing through it or the roaching the A.F.O.M. or M.R.C.P. diplomas mouth can determine whether exposure leads to understand and remember them, and give a back- disease. Airways down to terminal bronchioles ground for assessing new ideas. I shall be dogmatic, (that is, not involved in gas exchange and without citing research references and review articles for gas exchanging areas opening directly offthem) are wider discussions of the issues, and ignoring many lined by ciliated epithelium. This is covered by a fascinating minor or rare disorders. I can layer of supply a mucus from secreting lining cells (and copyright. fuller list of references for anyone who wants to mucous glands in the walls ofthe bronchi), which is check the provenance ofthe assertions I shall make. swept up to the pharynx and swallowed.5 The I recommend two and a half textbooks: Morgan largest airways (bronchi) have cartilage in their and Seaton' for general reading. It is, however, walls, so they cannot be closed by muscular action somewhat uneven and may not cover particular alone, unlike the smaller bronchioles without car- topics sufficiently. Parkes' tome2 is like the Bible; tilage or mucous glands. Muscular action, excess comprehensive but impossible to read from cover secretions and inflammatory changes can narrow to cover without fervent enthusiasm. It is encyc- them. Pathology at this level is the principal cause lopaedic, but tends to summarize every published of airflow limitation. Smaller airways still (respira- paper without fully reviewing them; it is ideal for a tory bronchioles) have flimsy walls with little http://pmj.bmj.com/ one-stop overview of the literature, but leaves you muscle. They lie within the lung and are kept open to digest some ofit for yourself. For the occasional by the elastic pull of the surrounding tissue.6 If this query about long forgotten hazards in long dead pull is reduced, as by the lung destruction of industries, try Hunter's classic text (not the edition emphysema, they narrow. They are not lined by written since his death).3 mucus; their defence is phagocytes,7 and immuno- Beginning with some background anatomy and globulins.8 Large airways therefore have defence physiology should help explain the diseases, and mechanisms (mucus, cilia) ideal for large particles; make the usual lists easier to learn. the more distal regions have mechanisms (phagocy- on October 2, 2021 by guest. Protected tosis, immunoglobulins) better for smaller par- ticles. The response ofthe lung to injurious substances: the effect of anatomy The fate of an inhaled particle' The site of an insult to the lungs is one important determinant of the effect. I shall discuss applied This depends on its aerodynamic properties, which are in turn determined by its shape, size and Correspondence: P.H. Wright, M.Sc., M.R.C.P., density. A long, thin, light particle behaves M.F.O.M. differently from a short, fat, heavy one, will end up Accepted: 13 August 1992 in a different place in the lung, and meet different *Views expressed in this review are those of the author defence mechanisms. Ifparticles carry an electrical and do not necessarily reflect those of the Department of charge, or change size by adsorbing water from Social Security or its Benefits Agency. intra-pulmonary air, their fate is also affected. Postgrad Med J: first published as 10.1136/pgmj.69.808.129 on 1 February 1993. Downloaded from 130 P.H. WRIGHT

Human factors such as smoking, the rate of iron miners developed it. The basic radiographic airflow, the depth of breathing and the size of the abnormality is pin-point round opacities, though lungs are important; those with larger lungs retain they may coalesce into lesions up to 2 mm across. more particles, and familial factors affect clear- Septa and the hilar glands can be outlined, but are ance. Nevertheless, some idea ofwhere particles are normal. Tin produces a similar picture, but the likely to land and go can be given. Large particles in lesions are more radio-dense, and outlining com- an airstream will tend to impact by inertia on the moner; there may be a few UK cases left in old walls where the airstream bends or turns. The nose people's homes. Antimony, barium (baritosis), and pharynx trap most particles over 10 Elm in this zirconium, hafnium, rare earth elements, chromite way. Most between 10 gm and 5 tm veer out ofthe and titanium produce similar changes. Sometimes airstream by inertia and impact on to the walls of the dose of a harmful substance is too low to the large airways. Smaller particles will continue produce disease; asbestos fibres occur in the lungs forwards where airways divide, and impinge on to of town dwellers, and even more are found if the the walls and the mucociliary escalator. Still smaller town has an asbestos mine, but disease need not ones sediment on to airway walls below the necessarily result." escalator where airflow is far slower, and are phagocytosed by alveolar macrophages migrating Asthma up to it. Particles between 3 gm and 5 Elm reach the alveoli, cross to the alveolar wall and are This was considered elsewhere in this series.'2 phagocytosed by lining macrophages which pene- Remember that occupational asthma can become trate the alveolar wall and go to the lung lym- chronic despite ending exposure, and can lead to phatics. Particles under 3 glm leave the lung in the chronic airflow limitation and present as such. expired air with few deposited in the lung at all. Those smaller than 0.5 gm diffuse to the alveolar Chronic bronchitis wall by Brownian movement, so proportionally more are deposited. Substances which irritate the larger airways and

their mucus glands can produce chronic bronchitis,copyright. defined as persistent cough and sputum produc- Assessing the pathogenicity of a substance tion. Such chronic bronchitis itself does not cause airflow limitation with death from respiratory The following therefore determine the effect of a failure. However, they often occur together as the substance on the lung: commonest cause of chronic bronchitis, smoking, 1. Its chemistry and toxicology; particularly whe- produces both effects;'3 possibly from different ther it is irritant, a carcinogen or capable of fractions of the fume. Chronic bronchitis increases stimulating allergy or fibrosis. the likelihood of chest infections; important in an 2. Its physical state; heat or cold can damage the occupational setting if they produce absence from

lung and determine whether the substance is a work! Chronic bronchitis has been seen as a http://pmj.bmj.com/ solid, fluid, or gas; and its solubility and charge. harmless concomitant of exposure to smoking, air 3. Its size and shape if it is particulate, and so pollution, or occupational atmospheric pollution. where it goes in the lungs. However, first, it acts as a marker oftoxic exposure; 4. Whether it is pure or contaminated; mixtures as anyone exposed to one toxin is probably more can produce different pictures from a simple likely to meet others, it is likely to be associated sum of the effects of each component. with increased morbidity and mortality. Secondly, an irritant gas may worsen the effects of a concur- rent occupational exposure or of asthma. Thirdly, on October 2, 2021 by guest. Protected The response ofthe lung to insults: pathological just as tobacco smoke can cause airflow limitation pictures as well as producing chronic bronchitis, so may occupational exposures. The symptoms of chronic Nopathological change bronchitis should, therefore, not be ignored. A harmless metal of high molecular weight may Acute lung damage simply produce an abnormal chest radiograph without damaging the lung. The only such 'benign This was described well on the Western Front in the pneumoconiosis' likely to occur in clinical practice First World War. Basically two pictures result: is in welders inhaling iron fume; one survey found pulmonary irritants (for example, chlorine and 7% of arc welders in a factory were affected.'0 A phosgene) produce pulmonary oedema with rapid- similar picture used to occur in steel workers, and ly developing dyspnoea; if basic lung structure is polishers of steel or silver who used iron oxide. undamaged, and gas transfer is not too severely Occasionally foundry workers, boiler scalers, and impaired, subjects can recover though many die Postgrad Med J: first published as 10.1136/pgmj.69.808.129 on 1 February 1993. Downloaded from OCCUPATIONAL LUNG DISEASES OTHER THAN ASTHMA 131 and there may be permanent sequelae. Probably sure has been associated with emphysema in man, the most important such occupational exposure is and cadmium chloride aerosol exposure gives rats to oxides ofnitrogen produced in farm silos. These centrilobular emphysema. This elegant occupa- are not particularly irritant to the upper respiratory tional pathogenesis, often reproduced in textbooks, tract, though very damaging to the lungs; workers unfortunately has no adequate epidemiology to may not be aware that they are receiving lethal support it. More interesting are the lung function exposures. Vesicants, such as nitrogen mustard, changes in workers heavily exposed to the pro- damaged epithelial surfaces with effects appearing teolytic enzyme alcalase; they could represent early after 2-4 hours. Death occurred between 2 and 14 emphysema.'6 days from sloughing of the lung lining, or from delayed bronchopneumonia. Finally, some metal Fibrosis fumes, notably cadmium, may produce metalfume fever, a 'flu-like illness, worse with the first (a) Silica Continuing inflammation produces exposure of the working week, occurring some fibrosis. The commonest substance involved is hours after it, but neither serious nor fatal. silica, though it produces various clinical pictures. Heavy, acute, relatively pure quartz exposure leads An oddity-byssinosis to a severe illness like alveolar proteinosis with an alveolitis; mortality is high."7 Silicosis is now exces- Somewhere between asthma and bronchitis comes sively rare in workers doing occupations known to the curious disorder byssinosis produced by cotton involve exposure, because they are strictly con- dust. Workers complain of chest tightness and trolled. Occasionally, procedures are not recog- breathlessness, initially worse on returning to work nized as risky, high exposures occur, and an acute after the weekend break, then extending gradually form of silicosis with fever and dyspnoea follows through the working week, and finally becoming which may be fatal; sandblasting without adequate permanent.14 They may show airflow limitation protection (outlawed in the UK), compulsive with these symptoms, and are more likely to do so inhalation of'Ajax' scouring powder and repairing as worsen. as they Finally, the symptoms become the tracery of cathedral windows'8 are recently copyright. constant so do airflow limitation and dyspnoea. reported causes. The classic lesions of 'silicosis' The disease was said to have caused deaths in the produced by low-level long-term exposure to past. The radiographic changes, lung function tests quartz or flint are nodules of hyaline collagenous and histopathology are indistinguishable from fibrosis, predominantly in the upper lung fields, chronic bronchitis and emphysema, though the appearing as well-defined rounded opacities of disease existed before cigarette smoking was com- 1-3 mm on the chest radiograph and without mon. Diagnosis is therefore by history; unique symptoms, though lung function tests may be amongst disorders for which the government pays mildly abnormal. Since the tests correlate better compensation, and making research difficult. with the amount of dust inhaled than with the

There is no evidence of allergy; all kinds of toxins radiographic change, they may be due to chronic http://pmj.bmj.com/ can be extracted from cotton, but none completely silica obstructive bronchitis (which certainly oc- reproduces the disorder. Moreover, a number of curs) rather than fibrosis. With increasing exposure different disorders follow work with cotton, and opacities multiply and extend down the radio- must be distinguished from each other, and from graph. Septa, the pleura and hilar glands may be byssinosis.'5 Reduction of cotton dust levels, and outlined and calcify. The upper lobe lesions may decline of the industry, mean that it is now difficult conglomerate into masses called progressive mas- to find cases in countries where the disease could be sive fibrosis (PMF), causing enough shrinkage to fully investigated. produce dyspnoea but rarely cavitating unless on October 2, 2021 by guest. Protected there is tuberculosis. The incidence of tuberculosis Emphysema is increased; ingested silica damages alveolar mac- rophages so they cannot kill the tubercle bacillus. A Particles which are not destroyed after phagocy- diffuse fibrosis of the alveolar walls and spaces tosis may damage cells scavenging them so that without nodules 'fibrosing alveolitis' follows inhal- they leak enzymes. Emphysema, local fibrosis, or ing calcined diatomaceous earth-'diatomite pneu- generalized lung fibrosis may result. Iflung tissue is moconiosis'. It predominantly affects the upper destroyed, alveoli are lost, the elastic properties of lobes and there is obvious dust in lung sections. the lung decrease and emphysema occurs. Natural a-l antitrypsin counteracts the most potent ofthese (b) Mixtures of silica and other dusts, including enzymes. Subjects congenitally lacking it, who coal The picture changes with mixed dusts. Foun- smoke, develop basal emphysema. Cadmium dry workers and iron miners more commonly show blocks its action, and seems to concentrate in 'mixed-dust disease' from inhaling silica and iron emphysematous smokers' lungs. Cadmium expo- than classical silicosis; defined nodules are replaced Postgrad Med J: first published as 10.1136/pgmj.69.808.129 on 1 February 1993. Downloaded from 132 P.H. WRIGHT by irregular stellate opacities, and upper lobe PMF of lung function, and irregular radiographic opac- (defined as opacities over 3 cm in size) is common. ities, but there is furious controversy over whether Silica and aluminium, in plants producing abra- dust alone, without smoking, can produce sives from bauxite, cause Shaver's disease,'9 with sufficient impairment in the absence of silicosis to upper lobe fibrosis and emphysema, leading to produce disabling dyspnoea.20 If it does, no-one honeycombing, pleural emphysematous blebs and knows how to quantify the contributions of the pneumothorax. Another major disorder from silica different possible causes in an individual claiming mixtures is the pneumoconiosis of coal workers, benefit.2' perhaps the most complex of all occupational lung No M.R.C.P. student can forget Caplan's syn- diseases to describe. Coal is basically rotten vegeta- drome. Classically,22 this was the occurrence of tion, sandwiched between layers of sandstone. The multiple well-defined round opacities 0.5-5 cm in time and temperature of the rotting may vary in diameter distributed throughout the lung fields but different locations affecting the composition of the particularly at the periphery, in miners with slight coal, as do variations in the sandstone. A rough or absent simple pneumoconiosis and rheumatoid classification is by the 'rank' of coal which does arthritis. The lesions came in crops, often with relate to the disease produced. The role ofa worker exacerbations ofthe arthritis, and could cavitate so will determine the balance of coal and sandstone mimicking PMF. As redefined,23 the syndrome was (silica) exposure; those making or maintaining the of an increased incidence of rheumatoid arthritis, tunnels of a deep mine will meet more silica than both clinical and detectable only by serological coal as opposed to miners (though some of these tests, in coal miners with radiographic shadowing changedjobs in their careers). The picture is further either like simple pneumoconiosis and/or nodules. complicated because miners smoked, kept pigeons, It rarely occurs with other minerals, such as heated their homes with free coal from their asbestos. employers so polluting them with fumes, met nitrous fumes from diesel engines and explosives in (c) Asbestos This contains silicates, but produces the mines, and got tuberculosis; all contributing to various disorders quite different from those already their undoubted respiratory ill health. described. Most of the asbestos used was blue

Many copyright. epidemiologists spent useful careers failing to asbestos (crocidolite), or white asbestos (chry- elucidate the respiratory problems of miners; with sotile); some brown (amosite) was also used, and the current decline in the industry it may well be chrysotile from some Canadian mines is con- that breathless miners will disappear from the UK taminated with a further variant, tremolite, which before their problems are understood. In brief(and also occurs in talc. A little anthophyllite has been I shall not try to give references for a vast literature used commercially. A given asbestos firm might full of controversies), miners suffer from chronic knowingly mix the different types, or use the same bronchitis, emphysema, and pneumoconiosis. The but from different mines and so with different pneumoconiosis is similar to silicosis, but the compositions; many mixed loads indiscriminately. nodules range up to 5 mm, and are less well- Asbestos users, such as laggers and sprayers, were http://pmj.bmj.com/ defined. PMF develops, and the lesions may often not sure exactly what type they had worked cavitate, the contents are then expectorated, and with. Even if they were, processing changes the the lesions refill, without tuberculosis (the fibre geometry modifying the biological effects; incidence of which is increased) necessarily being flake-like tremolite produces no disease, fine-fibred present. Simple pneumoconiosis (that is, without produces mesothelioma, and coarse-fibred pleural PMF) is not associated with significant reduction plaques.24 Toxic or carcinogenic oils may be of pulmonary function or loss of life expectancy; adsorbed during milling and grinding. Never- the presence of PMF is. Since the risk of PMF theless, studies ofminers and users ofone fibre type on October 2, 2021 by guest. Protected increases with the profusion of simple pneu- allow some classification of the disorders pro- moconiosis, regular chest radiography has been duced. used to identify all miners developing simple 1. Asbestos corns, lesions resulting from fibres disease so they can be removed from further penetrating the skin and resolving after their exposure. This policy meant most working miners removal, were simply a sign of heavy exposure. had normal radiographs. Although PMF is rare 2. Pleural plaques which may calcify, characteris- amongst them, it does occur and the group is so tically appearing at least 20 years after ex- large that it now includes most new PMF cases, posure, are found with other mineral exposures though affected miners have had higher dust including silicosis. They have not been shown to exposures. Mine dust produces chronic bronchitis, cause significant functional impairment and which may be associated with impairment of dyspnoea, but they are a marker ofexposure. In pulmonary function, and there is good patholog- one series for example, 4.5% developed clinical ical evidence that coal miners develop emphysema. asbestosis within 10 years.25 There is a relationship between dust exposure, loss 3. Asbestos pleural effusions, which can be fol- Postgrad Med J: first published as 10.1136/pgmj.69.808.129 on 1 February 1993. Downloaded from OCCUPATIONAL LUNG DISEASES OTHER THAN ASTHMA 133

lowed by pleural fibrosis and disability, may iated with circulating precipitins, so producing type occur during exposure or after it has ceased. The III Arthus type reactions (as well as the possibility fibre type and mechanism are unknown, but the oftype II), and mast cell involvement. The result is relative rarity of new cases, and the regular extrinsic allergic alveolitis; a misnomer for 'an mention of pleural fibrosis in reports of post acute granulomatous interstitial pneumonitis' with mortems on cases of asbestosis 60 years ago, alveolitis and bronchiolitis. There is a long list of suggest it may reflect intermittent high ex- such disorders (Table I); they are commoner in posure; an idea supported by more recent non-smokers. The multiple immune mechanisms studies.26 Pericardial effusions occasionally oc- involved are reflected in the variety of clinical cur. courses. There may be multiple acute episodes with 4. Asbestosis is a fibrosing alveolitis. In the 1920s, 'flu-like symptoms and minimal dry cough. The it was an acute condition leading to death within chest radiograph will show a fine ground-glass a few years. More recent cases follow lower opacification, which may be difficult to detect, exposures after some latency, and are chronic; sometimes with larger patchy shadows. As expo- indeed, only 20% ofcases diagnosed in Medical sure continues, a chronic stage with multiple small Boarding Centres (Respiratory Diseases) die of irregular opacities like fibrosing alveolitis may it now, though 68% die of an asbestos-induced develop. Like all such opacities, these seem more disorder.27 Current exposures should never pro- dense at the bases because the rays for a PA film duce it. pass through more lung there than at the apices. As 5. There is clear evidence of an excess of lung the disease progresses, this shadowing lessens but cancer in asbestos workers, but the relationship bands of apical fibrosis appear, the lungs shrink, to smoking and asbestosis is unclear (see below). and persistent dyspnoea develops. Sometimes this There is some evidence for an increased inci- chronic stage appears to develop insidiously, with- dence ofother tumours in men28 but not in every out acute episodes. Conversely, some pigeon fan- series studied, and of the ovary.29 ciers seem to lose symptoms and live happily with 6. Crocidolite, amosite and tremolite, but rarely their pigeons and their precipitins. The significance

chrysotile, produce a serosal tumour (meso- of precipitins depends on the condition and the copyright. thelioma) 20 years or more after exposure. method used to detect them; in general, budgerigar Usually this is pleural, but it can occur in the precipitins are always associated with lung disease30 peritoneum or pericardium; factors determining but perhaps only a third of those with pigeon ones the site are unknown. show disease.3' By far the commonest extrinsic allergic alveolitis is 'farmer's lung', due to inhaling Granulomatosis mouldy hay. The problems ofprecipitin testing are well seen in this disorder. A survey of 9132 Devon A type IV allergic reaction producing granulomata farmers found 23% had precipitins against mouldy can follow an occupational exposure. The com- hay. Eighteen per cent of the men (23) reported monest is berylliosis. Allergy may be detected by breathlessness; the proportion with precipitins was http://pmj.bmj.com/ skin tests analogous to the Mantoux (the beryllium similar to that in those not reporting breathless- patch test), or by in vitro lymphocyte testing. The ness. Precipitins seemed best correlated with a disease pictures are as follows. picture of attacks of breathlessness, fever and 1. Granulomata in beryllium-contaminated wounds shivering; of ten such cases, five already had been preventing them healing until all the metal is diagnosed as having the disease, but five without removed. Casualty officers should remember precipitins had not. In Somerset, only 43% of that beryllium is not radio-opaque. clinically diagnosed patients had precipitins.33 A 2. Conjunctivitis, corneal ulceration, allergic ble- Canadian study in which precipitin tests were on October 2, 2021 by guest. Protected pharitis, contact dermatitis, an acute tracheo- repeated after 4 years showed farmers losing and bronchitis and pneumonitis from irritant gaining precipitins, and that symptoms were not beryllium vapour. The last may be fatal, resolve related to them.34 The absence ofprecipitins may be or go on to chronic granulomatous disease. because the particular organism has not been tested 3. A chronic granulomatous disorder clinically for, or because the wrong antigen of it has been rather like sarcoidosis after a latency ofup to 20 used. Sometimes, the alternative pathway ofcomp- years in up to 5% of those exposed to lower lement activation not involving precipitins may be levels of fume, contamination from workers' involved in a particular case. overalls, or from neighbouring factories. Rarely, the presenting problem may be renal colic following hypercalcaemia, and all berylliotics Carcinogenesis should be screened for hypercalciuria and renal tract disease. Any lung fibrosis can give rise to tumours, be it More usually a type IV reaction is also assoc- local scars, or cryptogenic fibrosing alveolitis Postgrad Med J: first published as 10.1136/pgmj.69.808.129 on 1 February 1993. Downloaded from 134 P.H. WRIGHT

Table I Types of extrinsic allergic alveolitis Name Agent Farmer's lung Fungi in mouldy hay Bird fancier's lung Avian protein Bagassosis Mouldy sugar cane Mushroom workers' lung Fungi in compost dust Malt worker's lung Fungi on mouldy barley Suberosis Fungi on mouldy cork dust Maple bark strippers' lung Fungi on mouldy bark Wood pulp workers' disease Fungi on mouldy bark Humidifier disease Organisms growing in the water Sewage sludge disease Bacteria in the sludge Sauna-takers' disease Contaminated steam Sequoiosis Mouldy giant redwood sawdust Cheese washers' lung Fungal dust Dry rot lung Mould dust Wheat weevil lung Mite antigen Animal handlers' lung Serum and urine protein Fish meal workers' lung Fish protein Diisocyanate 'alveolitis' TDI and HDI Pyrethrum 'alveolitis' Insecticide aerosol Pituitary snuff taker's lung Pig or ox protein Tobacco worker's lung Tobacco dust

where the risk interacts with that of smoking and life-long non-smoking, and their statements maycopyright. the cell types produced are indistinguishable. A well be inaccurate. An increased incidence of lung substance producing lung fibrosis is therefore likely cancer can be demonstrated where the carcinogen to increase the incidence ofcancer even ifit is not a is not fibrogenic, but these are all rare. The carcinogen. Deciding whether a substance (such as commonest involve miners working on rocks con- asbestos) can cause cancer without fibrosis is taminated with radioactive elements. therefore difficult. An attempt was made on the basis that tumours occur at asbestos exposure levels below those associated with fibrosis, though Conclusions

this has been disputed; cases are few and measure- http://pmj.bmj.com/ ments of low-level fibre exposure particularly diffi- Much ofmy survey will seem rather historical, and cult. Sorting out the carcinogenic effects of asbestos only the imminence of exams is likely to make a and smoking is equally difficult. Attempts to show young physician try to remember baritosis-but whether the cell type of tumours associated with this was true of tuberculosis before AIDS. Apart asbestos differ from those associated with smoking from such unforseen developments, I suggest show the proportion of adenocarcinomas may be knowing something about the classic occupational higher, but it is not certain that this is a real lung diseases is worthwhile because of the follow- difference as proper groups for comparison are ing. on October 2, 2021 by guest. Protected difficult to find." The simplest extrapolation of 1. They show the patterns of disease the lung can observed facts to try and link cause and effect is produce, and these can occur with other hazardous; smoking can affect the clearance of exposures, such as to drugs. asbestos from the lung by increasing the retention 2. It will be increasingly rare for workers to enter of short fibres; the pathological effects of smoking an industry on leaving school at 15 and work vary between subjects for unknown reasons; until 65 in the same fumes. We will probably studies are difficult because workers with more never understand any occupational diseases as disease may stop smoking or leave the industry; well as the classic occupational lung diseases, asbestos may adsorb carcinogens from tobacco and most of our knowledge of the relationships smoke and carry them into cells; chrysotile in between occupational exposure and disease textile mills seems to produce more tumours than comes from them. In the future, we will often chrysotile mining or milling. Finally, most surveys only be able to extrapolate from that knowledge rely upon the workers to identify themselves as to new disorders where the data will be even less, smokers and non-smokers since there is no test for and all the pressure will be to close down a Postgrad Med J: first published as 10.1136/pgmj.69.808.129 on 1 February 1993. Downloaded from OCCUPATIONAL LUNG DISEASES OTHER THAN ASTHMA 135

process suspected of being unsafe before ade- practitioners, and deserve to be diagnosed com- quate epidemiology can be done. The classical petently. Some will have symptoms of disease diseases will be the only guide to the new ones and will expect them to be explained. Others we shall certainly be seeing. Most branches of may have findings irrelevant to their com- medicine include some occupational disorders, plaints; unnecessarily doing computerized but few have so many as well investigated as tomography or biopsying the lungs of a man those affecting lungs; even an orthopaedic with welder's siderosis is wasteful and bad surgeon wanting to investigate work-related practice; a good chest radiograph, a good bone andjoint disorders could best learn how to history, and a doctor with a good memory is do so from studying occupational lung diseases what is needed. An occupational diagnosis will and their epidemiology! always impress the patient, particularly if com- 3. Workers with occupational lung diseases do pensation can be obtained! appear in the clinics of physicians and general

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