: Of, F: 3, O'KeUy OBE, FFCM, F.

FQM;

Introduction
A recent report of three cases by Morgan and Ong 1 appears to be the first diagnosis of byssinosis in Hong Kong. The active local textile industry must have involved the exposure of personnel to cotton dust over the years and experience in other countries suggests that further cases are probable, A description of the disease may not be amiss in promoting awareness, refreshing memory and facilitating diagnosis, History Byssinosis was first recognised by Ramazzini in 1713 2 and seems to have affected textile worker in Europe in the eighteenth and nineteenth centuries3 Although described as 'spinnersphthisis' in 1831 it did not receive much attention in Britain until surveys of the cotton industry started about thirty years ago. The "disease was then thought to be mostly confined to Lancashire, the centre of the British cotton industry5 but it has since been reported from most countries where raw cotton is handled.

Aetiology
The airborne cotton dust responsible consists of broken cotton fibres, plant debris, minerals, bacteria and fungi. The aetiological agent has not been determined but some constituent of the dust seems to cause histamine release by pharmacological rather than immunoiogical mechanisms at bronchiolar level. Signs and symptoms The characteristic earliest symptoms of byssinosis occur in the first day on return to work after a break. There may be chest tightness, cough and/or difficulty in breathing. The symptoms may first be noted after iongish holidays but later on they usually occur after week-ends -the socalled 'Monday fever' in Western countries. The early symptoms disappear shortly after leaving the workplace. The onset may be a few months after starting work in a mill or be delayed for several years. As the disease progresses the chest tightness and breath I essness become more marked and extend to the second and subsequent days after a break from work until eventually the worker may become seriously affected with permanent effort intolerance and impaired ventiiatory capacity which is not improved by removal from dust exposure. in the final stage the picture is one severe obstructive airways disease.

Nature of the disease Byssinosis is a respiratory disease occurring among cotton flax and soft hemp workers exposed to dust during the cleaning and processing of fibres. It embraces a gradation of symptoms ranging from acute dyspnoea with cough and chest tightness, reversible by bronchodiiators, on one or more days after a break from work up to permanent obstructive airways disease of varying degrees of severity.

of

Chest X-rays show no specific changes, but it is advisable to eliminate other diseases.

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Pathology
No specific abnormalities have been identified. The lungs are often dust pigmented infiltration of bronchial and bronchialar walls but no fibrosis.

Grading of byssinosis
A system of grading the symptoms of byssinosis In general use is as foliows:Grade CO No symptoms of byssinosis. Occasional chest tightness or difficulty in breathing'on the first day of the working week. Chest tightness or difficulty on the first day of every working week.

Grade C1/2 -

Lung function tests

Exposure to cotton dust causes both temporary and permanent changes in ventilatory capacity. The most commonly used measurement is the Forced Expiratory Volume measured in one second (FEV-j}. The acute effect is measured by the fall in FEVi from the beginning to the end of the work shift on the first day after a break is classified as follows: Less than 0.06 litre-no acute effect 0.06 - 0.20 litre - slight acute effect, over 0.20 litre definite acute effect.
Grade C1 -

Grade C2 - Chest tightness or difficulty on breathing on the first day and other days of the working week. Grade C3 Grade 2 symptoms accompanied by evidence of permanent incapacity from diminished effort tolerance or reduced ventilatory capacity.

A functional grading recommended' for changes in ventilatory capacity is as follows:

Grade F. O - No demonstrable acute effect of the dust on ventilatory capacity. No evidence of chronic ventilatory impairment. Grade F1/2 - Slight acute effect of dust on ventilatory capacity. No evidence of chronic ventilatory impairment. Grade F. 1 - Definite acute effect of dust on ventilatory capacity. No evidence of chronic ventilatory impairment. Grade F. 2 Evidence moderate pairment capacity. of a slight to irreversible imof ventilatory

Chronic ventilatory impairment may be measured by the FEV-| in the absence of dust exposure for a normal person of the same sex, race, age and height. The results may be classified: Over 80% of predicted valueno chronic ventilatory 60%-80% of predicted valueslight to moderate chronic ventilatory impairment. Less than 60% of predicted valuemoderate to severe chronic ventilatory impairment. impairment.

Grade F. 3 Evidence of a moderate to severe irreversible impairment of ventilatory capacity.

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Diagnosis The diagnosis of grade C1/2 to C2 rests on occupational exposure to cotton dust, a history of these clinical grades and a fall in FEV-| during the working shift. In practice the objective evidence of FEV-j at the time of symptoms may be difficult to obtain and the diagnosis may have to depend on the reliability of the patient's history. Smokers and others may have chronic bronchitis, evidenced by cough and sputum unrelated to periods of dust exposure. In such patients byssinosissymptoms following exposure to dust can be differentiated and an acute fall of the already impaired FEV-j can confirm the diagnosis. The diagnosis of grade C3 disease rests upon the occupational history, a history of progressive development of the clinical grades of respiratory symptoms and evidence of irreversible airway obstruction. Prognosis Recovery from grades C1/2 and C1 disease occurs of dust exposure is stopped and this usually occurs in grade C2, although slight to moderate impairment of ventilatory capacity may remain in some cases. Worsening of grade C3 may be prevented by removal from dust exposure otherwise the disease may end in pulmonary heart disease and congestive failure. Prognosis in grade C2 and C3 is worsened by smoking.

trations or removal from areas of exposure is the treatment of choice for patients with evidence of byssinosis. The airway obstruction of grades C1/2 to C2 can usually be relieved by bronchodilators but therapeutic measures are no substitute for prevention.

Prevention
The prevention of byssinosis depends on reducing the inhalation of dangerous levels of cotton dust which may oe achieved by the following methods:(a) Dust control in the place of work - control depends mainly on machine design complemented by adequate ventilation and dust exhaust systems with good housekeeping provision. In the cotton industry, as in many other industries, achievement of the ideal dust free atmosphere cannot be guaranteed and "Threshold Limit Values" (TLV) for airborne dust concentrations have, been set as workplace controls to minimise health hazards. A TLV of 0.5 mg cotton dust per cubic metre of air is the present standard in the United Kingdom. Environmental monitoring should ensure that dust levels do not exceed the TLV. (b) Personal protection suitable face-masks are effective in reducing dust inhalation but user resistence is not uncommon. The use of respiratory protection is particularly desirable in any areas where dust exposure reaches unusually high levels such as in certain machine maintenance operations. Medical surveillance Until such time as the workplace environment is completely dust free (and this is not yet in sight in the cotton
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Treatment
Reduction of inhaled dust concenTHE HONG KONG PRACTITIONER, MARCH 1982

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industry),medical surveillance is desirable. Ideally it should include both initial and periodic examinations. The initial examination should aim to exclude from dust exposure persons who have a history of atopic asthma, chronic non-specific lung disease, tuberculosis or any specific lung disease in which respiratory disability is a feature. Those who will be exposed to dust should be discouraged from smoking. The periodic medical examination should detect workers who are susceptible to byssinosis and they should be removed to less dusty areas before they develop substantial disability. In addition the systematic examination of groups of workers is a valuable method of checking the adequacy of dust control and detecting those areas where tjghter control is needed. The standard respiratory symptom questionnaire as recommended by the Medical Research Council is a useful basis for the routine medical assessment of cotton workers.

possibility of occupation affecting health and underlines the need to determine the occupational history and consider possible hazards at work when investigating the patient. The Industrial Health Division, telephone number 3688111 extension 422 is available to advise on any problems which may arise from byssinosis or any other occupational health matter and approach from doctors would be welcomed. Reference: 1) Morgan P G M and Ong S G - "The First Report of Byssinosis in Hong Kong" B J I M 1981; 38:290-2. 2) Ramazzini B -"Diseases of Workers". Latin text of 1713. Translated by W C Wright, Chicago University Press 1940. Patissier P - "Traite des Maladies des Artisans". 1827 Paris. Kay J P - "Observations and experiments on spinners phthisis". N England 1:348-363. 5) Med Surg J 1831;

3) 4)

Mill fever
Mill fever is another illness which occurs among cotton workers on first employment in a mill. It is characterised by the onset of a short dry cough, sneezing, headaches and a raised temperature. Complete recovery within a few days is usual. This should be distinguished from byssinosis which does not normally appear until some months or years after starting in a mill.

Schilling R S F "Byssinosis in Cotton and Other Textile Workers". Lancet 1956; 2:261-5 ; 319-24. Schilling R S F et al - "Proceedings of the XIV International Congress on Occupational Health". Madrid, 1963; Excerpt Medic Int Congress Series. 62:137, Bouhuys A et al Archives of Environmental Health. 1970; 21:475.
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6)

Conclusion
Byssinosis is a good example of the
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What I Read
Chasing The Wind Through The Bones Are the so-called "herbal medicines" more effective in the treatment of some diseases than are the so-called "Western medicines"? Do herbal medicines contain as yet unidentified compounds which could prove to be "wonder drugs"? (Quinine was found in cinchona bark, a salicylate related compound was found in willow bark and digitalis was found in common foxglove plant there are numerous other examples.) Are we overlooking valuable additions to our repertoire of Western medicines? The answer may come from researchers at the Chinese University of Hong Kong who are apparently investigating the content of the herbal medicines. I have seen little so far published in the medical press. Has anything been discovered? Are the people of Hong Kong being duped into parting with their hard-earned dollars in exchange for expensive mixtures with dubious unstandardised effects? In the British Medical Journal of 4th August 1979 appeared a short paper entitled "Chuei-Fong-Tou-Geu-Wan in rheumatoid arthritis" which reported the remarkable response of a 44-year-old Dutch housewife in Birmingham, England to that clumsily named preparation. At the time that she began selfodministering it (at the suggestion of friends in Holland} she was already under .treatment with non-steroidal anti-inflammatory drugs which were having little effect fust two days after starting the preparation all pain had gone! The authors wrote "Her improvement was so impressive that we agreed to her continuing." A wonder drug? Sorry, dear readers, but the almost magical effect was attributable simply to dexamethasone and indomethacin! The authors were astute for they quickly observed that "the effect of the drug on her symptoms and acute-phase serum proteins suggested that it contained corticosteroids or synthetic analogues." Three months later she began to look Cushingnoid. Finally the preparation was stopped and the patient is "now well taking prednisolone 3. 75 mg daily. " This tale has sinister aspects - the authors recorded that in the San Francisco Bay area the preparation, with the same name, but this time containing amino' pyrine and phenylbutazone, was implicated in four cases of agranulocytosis one of which was fatal. Why were these potent drugs apparently added to a "herbal medicine " and by whom and where? Why was the preparation permitted to be sold? Are powerful and potentially lethal preparations available without control to our unsuspecting public in Hong Kong? How do we inform them about the possible danqers? How many cases of agranulocytosis have been unwittingly self-induced in Hong Kong? How many have died as a result? J. ForsterP ] G etal. Dudley Road Hospital, Birmingham B18 7QH

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