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.