Occupation and Bronchitis
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235 Occupation and Bronchitis VISITORS to factories and mines often find that the atmosphere makes them cough. Although the workers seem oblivious of the problem and indeed may show no particular sickness absence due to acute respiratory illness, it is hard for the visitors to believe that such daily exposure does no harm. On analogy with the cigarette smoker the worker must get used to the irritants but may be doing irreparable damage to his bronchial mucosa and lung parenchyma. Serious crippling lung disease does result from some occupations, notably those entailing exposure to dusts containing silica or asbestos. The damage is principally to the paren- chymal part of the lung rather than airways and the levels of exposure which cause serious disease are often well below those noticed by visitors. In the unaccustomed visitor less toxic dusts such as coal dust and gases such as sulphur dioxide and ammonia can cause symptoms due to irritation of the airways. The question is whether such irritants, although well tolerated by the worker, cause dis- abling bronchitis after long-term exposure. Early studies on coal workers showed that serious dis- ability did not arise until massive lesions had devel- oped in the lung parenchyma. There was no in- creasing disability with increasing radiological change of the simple pneumoconiosis type, though miners with X-ray changes were a little more breathless and had a lower ventilatory capacity than miners without X-ray changes. 1 In the early investigations other factors leading to airways disease such as cigarette smoking and 1 Gilson JC, Hugh Jones P. Lung Function in coal-workers pneumoconiosis. Med Res Coun Spec Rep no. 290. 1955: 98-99 general atmospheric pollution were not analysed separately. Airways disease was always fourid to in- crease with age, but a year of life or "age" was admitted to include a year’s exposure to cigarettes and all the other extrinsic causes of airways disease except that measured in the study. Long-term fol- low-up of British coalminers confirms that airways disease increases with "age". Although- the men in dustier jobs show slightly more airways abnor- mality than do others of the same age this differ- ence is constant and does not increase with age. By contrast, cigarette smoking does increase the rate of development of airways disease with age in all dust-exposure groups. In a more detailed analysis JACOBSEN3 has shown that smoking is the main cause of symptoms and disability in miners without massive lesions. One major study of foundrymen disclosed some evidence of bronchitis related to occupation independent of smoking but the find- ings were not all statistically significant. 4 In a study of two large steelworks in South Wales, LowE and his colleagues5 found no evidence of occupationally related bronchitis. Many other stu- dies of single occupational groups have been done, often with equivocal results, but no major effort has been made to answer the general question as to whether occupation is a substantial factor in caus- ing the bronchitis for which Britain is famous. In Western Germany, as part of a research pro- gramme initiated by the Health and Safety Direc- torate of the Commission of the European Com- munities, standardised survey methods have been applied to factories and mines in various locations. A report on the first stage has been published, and an English translation is available.6 The popula- tion of 6700 includes workers in coalmines, steel- works, heavy engineering works, cement works, asbestos factories (textiles, board, and cement), and in plants making ceramics and refractory ware. They include workers of all age-groups and both sexes and some pensioners. Each worker answered a modified Medical Research Council questionnaire including smoking habits and gave an occupational history. A clinical examination, electrocardiogram and chest X-ray were followed by measurement of vital capacity, one-second forced expiratory volume, airways resistance, and arterial blood gases. In each factory or mine dust and other air- borne contaminants were measured and workers 2. Rogan JM, Attfield MD, Jacobsen, M, Rae S, Walker DD, Walton WH. Role of dust in the working environment in development of chronic bronchitis in British coal miners. Br J Ind Med 1973; 30: 217-26. 3. Jacobsen M. Dust exposure, lung disease and coal miners’ mortality. PH.D thesis. Edinburgh, 1976. 4. Lloyd Davies TA. Respiratory disease in foundrymen. London: H.M. Stationery Office, 1971: 34. 5. Lowe CR, Campbell H, Khosla T. Bronchitis in two integrated steel works. III Respiratory symptoms and ventilatory capacity related to atmospheric pollution. Br J Ind Med 1970; 27: 121-29. 6. Deutsche Forschungsgemeinschaft. Research report on chronic bronchitis and occupational dust exposure. Harald Boldt Verlag, 1978.
Transcript of Occupation and Bronchitis
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Occupation and BronchitisVISITORS to factories and mines often find that
the atmosphere makes them cough. Although theworkers seem oblivious of the problem and indeedmay show no particular sickness absence due toacute respiratory illness, it is hard for the visitorsto believe that such daily exposure does no harm.On analogy with the cigarette smoker the workermust get used to the irritants but may be doingirreparable damage to his bronchial mucosa andlung parenchyma. Serious crippling lung diseasedoes result from some occupations, notably thoseentailing exposure to dusts containing silica or
asbestos. The damage is principally to the paren-chymal part of the lung rather than airways andthe levels of exposure which cause serious diseaseare often well below those noticed by visitors. Inthe unaccustomed visitor less toxic dusts such ascoal dust and gases such as sulphur dioxide andammonia can cause symptoms due to irritation ofthe airways. The question is whether such irritants,although well tolerated by the worker, cause dis-abling bronchitis after long-term exposure. Earlystudies on coal workers showed that serious dis-
ability did not arise until massive lesions had devel-oped in the lung parenchyma. There was no in-creasing disability with increasing radiologicalchange of the simple pneumoconiosis type, thoughminers with X-ray changes were a little morebreathless and had a lower ventilatory capacitythan miners without X-ray changes. 1
In the early investigations other factors leadingto airways disease such as cigarette smoking and
1 Gilson JC, Hugh Jones P. Lung Function in coal-workers pneumoconiosis.Med Res Coun Spec Rep no. 290. 1955: 98-99
general atmospheric pollution were not analysedseparately. Airways disease was always fourid to in-crease with age, but a year of life or "age" wasadmitted to include a year’s exposure to cigarettesand all the other extrinsic causes of airways diseaseexcept that measured in the study. Long-term fol-low-up of British coalminers confirms that airwaysdisease increases with "age". Although- the men industier jobs show slightly more airways abnor-mality than do others of the same age this differ-ence is constant and does not increase with age. Bycontrast, cigarette smoking does increase the rateof development of airways disease with age in alldust-exposure groups. In a more detailed analysisJACOBSEN3 has shown that smoking is the maincause of symptoms and disability in miners withoutmassive lesions. One major study of foundrymendisclosed some evidence of bronchitis related to
occupation independent of smoking but the find-ings were not all statistically significant. 4 In a
study of two large steelworks in South Wales,LowE and his colleagues5 found no evidence ofoccupationally related bronchitis. Many other stu-dies of single occupational groups have been done,often with equivocal results, but no major efforthas been made to answer the general question as towhether occupation is a substantial factor in caus-ing the bronchitis for which Britain is famous.
In Western Germany, as part of a research pro-gramme initiated by the Health and Safety Direc-torate of the Commission of the European Com-munities, standardised survey methods have beenapplied to factories and mines in various locations.A report on the first stage has been published, andan English translation is available.6 The popula-tion of 6700 includes workers in coalmines, steel-works, heavy engineering works, cement works,asbestos factories (textiles, board, and cement), andin plants making ceramics and refractory ware.They include workers of all age-groups and bothsexes and some pensioners. Each worker answereda modified Medical Research Council questionnaireincluding smoking habits and gave an occupationalhistory. A clinical examination, electrocardiogramand chest X-ray were followed by measurement ofvital capacity, one-second forced expiratoryvolume, airways resistance, and arterial blood
gases. In each factory or mine dust and other air-borne contaminants were measured and workers
2. Rogan JM, Attfield MD, Jacobsen, M, Rae S, Walker DD, Walton WH. Roleof dust in the working environment in development of chronic bronchitisin British coal miners. Br J Ind Med 1973; 30: 217-26.
3. Jacobsen M. Dust exposure, lung disease and coal miners’ mortality. PH.Dthesis. Edinburgh, 1976.
4. Lloyd Davies TA. Respiratory disease in foundrymen. London: H.M.Stationery Office, 1971: 34.
5. Lowe CR, Campbell H, Khosla T. Bronchitis in two integrated steel works.III Respiratory symptoms and ventilatory capacity related to atmosphericpollution. Br J Ind Med 1970; 27: 121-29.
6. Deutsche Forschungsgemeinschaft. Research report on chronic bronchitisand occupational dust exposure. Harald Boldt Verlag, 1978.
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were classified into three groups according to expo-sure-—high, moderate, or low. Account was takenof the length of time each worker had been exposedand those with previous exposure to other respira-tory hazards were excluded. Each factory or groupof factories has been analysed separately so that in-ternal comparisons can be made. The standardisedmethod of analysis also permits comparisonsbetween geographical areas within an industry orbetween one industry and another. The results arepresented so that the reader can compare theeffects of smoking, occupational exposure, and ageon the symptoms and the physiological findings.
Within each industry age and smoking habits arethe most important factors in determining the inci-dence of bronchitic symptoms and airwayschanges. Indices of emphysema seem less clearlydefined and cannot be so closely related to the threefactors analysed. Dust and other air contaminantsare usually least important, although dust is impor-tant in causing the symptoms of bronchitis in theyoungest age-group in some occupations. When theseparate effects of smoking, age, and dust are
added together their combined effect should equalthe sum of the separate effects. This additive
phenomenon holds true for most of the young andmiddle-aged working groups. But in those near theretiring age with a high level of abnormality thecombined effect was less than the sum of the separ-ate effects. These older workers seemed to havereached the limit of their ability to respond todamaging agents. In the asbestos industry, smokersshow a striking relation between dust exposure andsymptoms of bronchitis but the respiratory-func-tion tests reveal no evidence of permanent changesassociated with either bronchitis or emphysema.Impressive differences between the figures from dif-ferent industries suggest that dust and other in-haled agents are more important in causingobstructive airways disease and the symptoms ofbronchitis than is indicated by the within-industrycomparisons. Coalminers are the most severelyaffected and the German workers point out that allcoalminers are exposed to high levels. Another pos-- sibility is that, outside as well as inside the work-place, the air they breathe tends to be heavily pol-luted. In the working population as a whole, theprevalence of the symptoms of bronchitis was high,rising from an average of about 20% in the under35s to about 50% in those over 55. But the preva-lence of definite airways narrowing and permanentimpairment of lung function is low-about 20% inthe over-55 age-group. This German survey wascross-sectional and did not include workers whohad left the industries because of chest illness. Noattempt was made to measure the effect of atmos-
pheric pollution outside the working environment.Nevertheless, it does provide a sound basis for thefollow-up studies which were started at the same
time. The first report on these, expected this year,should establish the contribution of occupationalexposure to the burden of chronic bronchitis and
emphysema in the West German population today.Health authorities will then be able to select themost effective means of prevention. The presentreport indicates that the most effective measurewould be a drastic reduction in cigarette smoking.
Towards the Prevention ofIntraventricular Hæmorrhage
INTRAVENTRICULAR haemorrhage (IVH) is an im-portant cause of handicap and a major cause ofdeath among low birthweight infants. What is itthat makes the low birthweight infant susceptibleto this form of haemorrhage? Since IVH is almostinvariably a postnatal event we can take it that
postnatal circulatory changes are causally impor-tant. Identification of the source of the htmor-
rhage is the first step towards understanding its
pathogenesis. HAMBLETON and WIGGLESWORTH2have provided evidence that the origin of the bleed-ing is the rich network of thin capillaries in the ger-minal layer overlying the caudate nucleus; whilePAPE and WIGGLESWORTH3 point out that, as a vas-cular watershed, this territory is particularly sus-ceptible to ischsemic hypoxia.
Further insight into the pathogenesis of IVH hascome from timing of the onset. EMERSON et a1.4examined the ventricular clots in 10 preterm in-fants who had died of IVH after receiving multipletransfusions of adult blood. They compared theconcentration of fetal hxmoglobin in the clots withvalues measured sequentially in the systemic circu-lation during life. IVH seemed to have occurredbetween 3 hours and 96 hours after birth. The im-
portance of this timing has been in delineation ofclinical events antedating IVH. FuJiMURA et a1.5have recorded the results with this technique in 5infants who died with IVH; and they compared theclinical course of these babies with that of 6 othersof similar birthweight (less than 1500 g) or ges-
1. Papile LA, Burstein J, Burstein R, Koffler H. Incidence and evolution of sub-ependymal haemorrhage: the study of infants with birth weight less than1500 grams. J Pediat 1978; 92: 529-34.
2. Hambleton G, Wigglesworth JS. Origin of IVH in newborn infants. Arch DisChildh 1976; 51: 651-59.
3. Pape KE, Wigglesworth JS. Haemorrhage, ischaemia and the perinatalbrain. Clinics in developmental medicine nos 69/70. London: HeinemannMedical Books, Philadelphia: JB Lippincott. 1979: 12.
4. Emerson P, Fujimura M, Howat P, Howes D, Keeling J, Robinson RO.Salisbury D, Tizard JPM. Timing of intraventricular haemorrhage ArchDis Childh 1977; 52: 183-87.
5. Fujimura M, Salisbury DM, Robinson RO, Howat P, Emerson P, KeelingJW, Tizard JPM. Clinical events leading to intraventricular haemorrhagein the newborn. Arch Dis Childh 1979; 54: 409-14.
