Bangalore Medical Trust v. B. S. Muddappa


Table 1. Types of lung fibrosis caused by Asbestos

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Table 1. Types of lung fibrosis caused by Asbestos

Parenchyma

Pleural:

Visceral: Acute Chronic Asbestosis

Parietal: Hyaline Calcified Plural plaques

16. The Asbestosis has been signified at page 188 which is as follows:-

Asbestosis - The signs and symptoms of asbestosis are similar to those caused by other diffuse interstitial fibroses of the lung. Increased breathlessness on exertion is usually the first symptom, sometimes associated with aching or transient sharp pains in the chest. A cough is not usually present except in the late stages when distressing paroxysm occurs. Increased sputum is not present unless there is bronchitis, the result of smoking. The onset of symptoms (except following very heavy exposure) is usually slow and the subject may have forgotten having any contact with asbestos. Persistent dull chest pain and haemoptysis indicate the need to investigate further the diagnosis of bronchial or mesothelial cancer.

The most important physical sign is the presence of high-pitched fine crepitations (crackles) at full inspiration and persisting after coughing. They occur initially in the lower axially and extend more widely later. Agreement between skilled observers on detecting this sign is good but it may vary from day to day in the early stages. It may also be present as an isolated sign in 2-3% of otherwise normal individuals. There are now means of recording this sign on tape. Other sounds - wheezes and rhonchi - are of no help in diagnosis, but indicate associated bronchitis. Clubbing of the fingers and toes was formerly regarded as an important physical sign. There is an impression that it is now less frequently seen. Its severity does not relate well to other aspects of the diagnosis. There is poor agreement between observers except when the clubbing is very pronounced. It is possible that its presence relates to the rapidity of progression of the disease.

The chest radiograph remains the most important single piece of evidence, even though the appearances are similar to other types of interstitial fibrosis. When the radiography is classified by three or more skilled readers using the ILO 1971 scheme independently, it is found that virtually all cases of asbestosis are picked up by one or more of the readers as Category 1/0 or above. The radiographic appearances are well illustrated in the set of standard films of the ILO 1980 Classification of the radiographic appearances of the pneumoconiosis (see PnEumoconioNses, International Classification of). The classification provides a means of recording the continuum from normality to the most advanced stages on a 12 point scale of severity (profusion) and of extent (zones) affected. The earliest changes usually occur at the bases with the appearance of small irregular (liner) opacities superimposed on the normal branching architecture of the lung. As the disease advances the extent increases and the profusion of irregular opacities progressively obscures the normal structures. Shrinkage of the lung occurs, with elevation of the diaphragm. In advanced cases distortion of the lung with cysts (honeycomb lung) and bulge occur. The hilar glands are not enlarged or calcified unless exposure has been to mixtures of siliceous dusts. This may occur, for example, in making asbestos roofing shingles or pressure pipes, and in mining. The small opacities may then be rounded rather than irregular.

The pattern of lung function provides the important third component in diagnosis.

The functional changes are the result of a shrunken and non-homogeneous lung, without obstruction of the larger airways (restrictive syndrome). The total lung volume is reduced and especially the forced vital capacity (FVC), but the ventilator capacity (FEV1.0) is only reduced in proportion to the FVC, so the ratio FEV 1.0/FVC is normal or even raised. The transfer factor carbon monoxide is reduced in later stages, but in the early stage an increase of ventilation on a standard exercise test may be the only alteration indicating impairment of gas exchange. Although the restrictive syndrome is the commonest, pattern (about 40%) in about 10% of cases airway obstructions is the main feature and in the remainder a mixed pattern is seen. This is though to be largely due to the confounding effects of cigarette smoking.

Visceral pleurisy: chronic and acute - This occurs in two forms - chronic and acute.

The former is the commoner and is a usual accompaniment of parenchyma disease, but its severity does not run parallel with the parenchyma disease. The diagnosis is radiographic. In some cases on or both of the costophrenic angels are filled in but the more specific feature is the appearance of well defined shadow running parallel to the line of the lateral chest wall and separated from it by a narrow (1-2 mm) clear zone. This is due to the thickened pleura seen "edge on." It is illustrated in the ILO 1980 standard set of films. The thickening is best seen in the middle and lower third of the lateral chest wall, the apices are usually spared. It is common in those only lightly exposed to find this pleural thickening as the only radiographic feature. It is readily missed when present only over a short length of the wall and if the radiographic technique does not give a clear picture of the periphery of the lung. When the visceral pleura are greatly thickened it causes veiling of the lung field, obscuring both the normal structure and parenchyma changes. This probably the basis of the "shaggy heart" and the "ground glass" appearance described in the early accounts of asbestosis. The wide recognition that small areas of pleural thickening may be the only sign of past exposure to asbestos is recent, and it seems to be a feature of the effects of low exposure to the dust. It is likely to remain an important observation for monitoring exposure to improved conditions in the future.

Acute pleurisy affecting the base and costophrenic angles, with effusions, sometimes bloodstained, is now a recognised sequel to asbestos dust exposure. It is associated with pain, fever, leucocytosis and a raised blood sedimentation rate. It settles in a few weeks but leaves the costophrenic angles obscured. No precipitating factors have been identified. Its recognition is important. Firstly, the cause may be missed unless an adequate occupational history is taken; secondly not all effusions in asbestos workers signify the onset of an asbestos-related cancer. A few weeks of observation may be necessary to confirm the aetiology.

Summary of diagnosis - The diagnosis of asbestosis therefore depends upon-

(a) a history of significant exposure to asbestos dust rarely starting less than 10 years before examination;

(b) radiological features consistent with basel fibrosis (Category 1/0 and over, ILO 1980);

(c) characteristic bilateral crepitations;

(d) Lung function changes consistent with at least some features of the restrictive syndrome.

Not all the criteria need to be met in all cases but (a) is essential, (b) should be given greater weight than (c) or (d); however, occasionally (c) may be sole sign. Other investigations are not of much help. Asbestos bodies in the sputum indicate past exposure to asbestos but are not diagnostic of asbestosis. Their absence when there is much sputum and marked radiological changes of fibrosis suggest an alternative cause for the fibrosis.

Immunological tests may be positive but do not help in consistent separation of asbestosis from other types of fibrosis. Lung function results must be assessed in relation to appropriate standards allowing for ethnic, sex and age differences and for cigarette smoking.

Asbestos corns on the fingers-area of thickening skin surrounding implanted fibres are now much less common because much of the asbestos fibre is packed mechanically and gloves are worn. Corns do not lead to skin tumours and disappear on removal of the fibres.



17. Pleural plaques and sources of exposure to asbestos have been stated at pages 189-191, thus:-

Pleural plaques-Parietal pleural plaques alone rarely cause symptoms. They may occur alone or with asbestosis. The diagnosis in life is radiological and the appearances are more specific than in the case of parenchyma fibrosis. PA films will detect most cases, but because they are frequently thickest posteriorly their full extent is best seen using oblique views. The ILO 1980 standard films show their appearance and the scheme provides, for the first time, a separation of parietal (circumscribed) and visceral (diffuse) pleural thickening. The plaques lie along the line of the ribs, and when thick cast a well defined shadow over the lung field extending in from the lateral chest wall, where they may also be seen "edge on."

Separation from visceral thickening depends largely on a defined edge to the shadow. Both types may occur together. Dependent mostly on the length of time since first exposure, and age patchy calcification occurs in the edges. This produces a bizarre pattern of dense shadows likened to "glittering candle wax" or a "holly leaf." The onset of calcification reveals many small plaques not previously visible. When calcification occurs in a crater-shaped plaque on the dome of the diaphragm a diagnosis of past exposure to asbestos or related minerals can be made with confidence.

Sources of exposure to asbestos - Formerly it was though easy to establish past exposure to asbestos by inquiry about work in manufacturing plants, or the application of the fibre for insulation. Now it is realised that only the most detailed history of all jobs, residences and occupations of the family will reveal possible exposures to asbestos. The reasons for this change are-

(a) the much wider use of asbestos in thousands of products especially since the Second World War (see Asbestos) :

(b) the recognition that significant exposure to asbestos occurred around mines and manufacturing plants in the past:

(c) the discovery of family exposure to the dust brought home on clothing, and also that those working in an area where lagging is in progress may be affected, even though they are engaged in lagging;

(d) the finding that calcified pleural plaques, indistinguishable from those occupationally exposed, also occur in the general population in localised areas in several countries (Finland, Czechoslovakia, Bulgaria, Turkey and others).

With the discovery of such diversity of sources of possible exposure, but virtually no quantitative information about its severity, and few long-term follow up studies of those exposed, it is not surprising that there is controversy about the health hazards. However, some conclusions emerge which must be subject to revision in the future.

(1) Asbestosis is primarily occupational in origin, the result of mining, milling, manufacturing, applying, removing or transporting asbestos fibre. Exposure is much less when the fibre is bound in the product (asbestos cement and asbestos plastic and paper product). Also exposure in the past was much greater than it is today with the use of the best working practices.

(2) Asbestosis may have been caused by home exposure from dusty clothing at a time when there was no dust or hygiene control in the factories.

(3) Asbestosis does not result from the very limited exposure to which the general public is or has been subject, even though asbestos fibbers are detectable in the lungs of a high proportion of adults’ industrialised areas. The median numbers of fibres so detectable are two to three orders of magnitude less than that found in those occupationally exposed.

(4) There are and have been important differences between countries in the use of asbestos, so that exposure for the same occupation varies widely. For example, dry wall fillers (sparkling) contain asbestos in the United States but not the United Kingdom; thus standing of internal walls during construction and maintenance is a source of exposure in the former but not in the latter. On the other hand, spraying of crocodile was much more widespread in the 1940s in the United Kingdom than elsewhere.

(5) Pleural plaques can arise at levels of exposure probably much lower than required to produce asbestosis. In addition it is probable that other minerals can cause plaques. For example, among chryosotile miners in Quebec calcified plaques are limited to those who have worked in two out of the eight mines. The minerals causing the plaques in general population have not been fully established. Tremolite, an amphibole often present in deposits of asbestos may be important.

(6) Whether chrysotile and the amphiboles differ in fibrogenicity in man is uncertain, but some evidence indicates that the amphiboles may be more fibrogenic. In animals there is little difference but the amphiboles remain in the lung much longer than the chrysotile.

The relation of asbestosis to dose of dust. In only a few instances are there records of past dust sampling to relate to the prevalence or incidence of asbestosis. But the information has been exhaustively analysed for miners and millers in Quebec, a group of asbestos cement workers in the United States and asbestos textile workers in the United Kingdom, because of its relevance to setting hygiene standards. In North America the dust was measured in millions of particles/ft3, in the United Kingdom in fibres/cm3 the measurement now internationally used. All the data show a clear relation between estimated dose of dust (concentration x time of exposure) and the incidence or severity of disease, but are insufficiently precise to determine whether there is a threshold level below which asbestosis will not occur. A cautious conclusion from the North American studies is that at about 100 million particles/ft3/yr there might be a threshold or that the risk of developing asbestosis would be as low as 1% of men after 40 years exposure could be as high as 1.1 fibres/cm3 or may have to be as low as 0.3 fibres/cm3. More precise information will only become available when the dust sampling introduced widely after the mid- 1960s is related to the incidence of disease in the future.

The relation of asbestosis to lung cancer. The important question here is: firstly, is there an excess risk of bronchial cancer only in those who also have some degree of asbestosis? Secondly, if the dust exposures are low enough to eliminate asbestosis, will the excess lung cancer risk also be reduced to and acceptably low level? Neither question can be answered at present, nor so is disagreement likely. It is known that there is a close association between asbestosis and lung cancer, about 50% of those dying from or with asbestosis have a lung cancer at post mortem. Among those knowledgeable about details of the dose-response data there would probably be agreement that dust exposures low enough to eliminate asbestosis will also reduce the excess bronchial cancer risk to a very low value. This does not extend to the risk to a very low value. This nearly so closely related to that of asbestosis (see Asbestos mesothelimo and Lung cancer).

Prevention -

This depends on successful control of dust exposure and medical surveillance to protect the individual, as far as is possible, and for the detection of health trends in the group.

Engineering control - Replacement of asbestos by other material believed to be safer has been widespread since the mid-1970s. Man-made mineral fibres and other insulating materials are rapidly replacing asbestos for heat insulation. But for other uses, for example, asbestos cement, friction material and some felts and gaskets, substitution is not at present practicable.

Dust control has been gradually improved by partial or complete enclosure of plants and the wide use of well designed local exhaust ventilation. In the textile section a completely new wet process of forming the thread has greatly reduced dust level, previously difficult to control. During maintenance work on old insulation much stricter control of exposures is possible by isolation of the working areas, and by training in the use of good working practices to reduce the dust, for example damping of the insulation before removal, and the use of vacuum cleaning in place of sweeping. But removal of old insulation is likely to remain for many years a major potential source of high exposure (see also Dust control Industial).

Medical surveillance - The insidious onset of asbestosis and the lack of highly specific features indicate the need for well recorded and systematic, initial, and periodic examinations of asbestos workers. This ensures the best chance of detecting the earliest signs. Physical examination of the chest, full-sized, high technical quality chest cardiograph (sic) are the minimum required, the interval will vary from annually up to four times yearly, with more frequent visits when there are clinical reasons. There is increasing evidence that the radiological features of asbestosis are in part cigarette-smoking dependent which requires the recording of smoking histories. This and the multiplicative effects of asbestos dust and cigarette smoking on the risk of bronchial cancer provide the strongest possible grounds for stopping cigarette smoking in those potentially exposed to asbestos. Personal advice on the special dangers of smoking and limiting opportunities for smoking at work is essential steps in prevention. Full personal protective equipment will be required where dust levels cannot be lowered to the hygiene standard. The system of periodic examinations also provides, if properly analysed, essential information about the effectiveness or failure of the engineering control of the dust. Tabulation, by age and years of exposure, of the results of classifying the chest films on the ILO 1980 scheme-preferably by independent readers - gives early evidence of trends in the prevalence of asbestosis. This valuable information will be missed if the group findings are not examined in detail.

Treatment: -

There is no specific treatment for asbestosis. Where the rate of progression appears unusually rapid further special investigations, including lung biopsy, may be justified if it is likely to assist in the differential diagnosis, and influence treatment - for example the use of steroids, but these are not of proved value. The severity of past exposure is the only factor known to influence progression rate. Thus, those with some evidence of asbestosis, if young or middle-aged, should be removed from further exposure. In cases where exposure has not been heavy and asbestosis is only detected late in life, progression may be very slow and the grounds for removal from work with asbestos, under good conditions, are less compelling.

The widespread and often misleading publicity given to the hazards of exposure to asbestos may cause much anxiety to those with asbestosis, both for their own health and for that of their family. Reassurance, and the putting of the likely prognosis in true perspective, is an important part of good treatment. The special risks of continuing cigarette smoking need emphasis. Mesotheliomas are a rare complication in those exposed only to chrysotile.

Compensation:-

The conventions on the awarding of compensation of asbestosis vary in different countries. Unusual breathlessness on exertion, as a cause of disability, may be required, even though it is not essential for a confident diagnosis of asbestosis. Compensation may be limited to those with evidence of parenchyma disease; pleural fibrosis - parietal or visceral - alone may not be accepted. Lung (bronchial) cancer is usually accepted as part of the disease provided there is at least some evidence of parenchyma fibrosis, but may be rejected if there is no radiological evidence of pleural or parenchyma fibrosis. There is plenty of opportunity for disagreement, especially when a factory for uncertainty of prognosis is included. It is now established that asbestos dust alone may cause lung cancer although the absolute risk is very small compared with that from the combined effects of cigarette smoking and asbestos dust. It has not been established that pleural plaques alone result in an increased risk of bronchial or mesothelial tumours, above that for similar exposures to asbestos dust without these pleural changes. The considerable uncertainty about the likely rate of progression of the fibrosis makes assessment on first diagnosis especially difficult. Lung biopsy is not justifiable solely for compensation assessment.



Asbestos (mesothelioma and lung cancer):-

While pulmonary fibrosis due to exposure to asbestos (asbestosis) has been known for decades, the first reports of individual cases of asbestosis combined with pulmonary cancer which appeared from time to time in various countries were accepted more as a curiosity. They did not attract much attention until in 1947 a British Chief Inspector of Factories, E.R.A. Merewether reported that lung cancer was found to be the cause of death in 13.2% of persons known to have asbestosis who had died and been autopsied between 1923 and 1946. A similar high proportion of cancer deaths in asbestosis were found by other pathologists and the probability of a role of asbestos in pulmonary carcinogenesis was definitely established by an epidemiological study by Doll in 1955, and confirmed by further studies.

Soon afterwards a new surprising discovery was made in South Africa. An accumulation of cases of an otherwise very rare tumour of the pleura and peritoneum, the malignant mesothelioma, was reported by Wagner in 1959 and related to exposure to the locally mined type of asbestos, crocodile. Soon afterwards cases were identified in non-mining occupational exposures to asbestos in England, in the United States and elsewhere. In contrast with asbestosis, and in contrast with asbestos related pulmonary cancer, mesothelioma was found also in persons whose exposure was not necessarily occupational.

Bronchogenic carcinoma related to asbestos:-

Bronchogenic carcinoma of the lung. There is a disease very common in the general population. While in many countries the total mortality from cancer slowly declines, the incidence and mortality from lung cancer increases and stands as the most frequent cause of death from cancer, particularly in cigarette smokers. It begins with transformation of the mucous membrane lining the inside of the bronchus at various level and such foci of transformation may remain at their initial spot for some time shedding at times a typical; or metaplastic cells into the sputum without causing other symptoms. This is the period in which we sometimes may succeed in discovering these pre-cancerous, or the earliest cancerous changes by sputum cytology sooner than by other diagnostic methods. Some of such early alterations of cells is reversible and may spontaneously heal when the cause disappears, e.g. when the person stops smoking. When the original focus develops definite cancer cells, the focus begins to grow, to bleed and slowly to obstruct the way, a growing malignant tumour becomes visible on the radiogram, and unless it can be surgically removed as soon as confirmed, it tends to spread through growth and through dissemination by blood and by lymph and to lead eventually to death. Supporting treatment by chemotherapy and radiation successfully prolongs life and radical surgery can provide complete healing.

The various components of the bronchial lining may undergo malignant transformation and consequently the carcinoma may be composed of various cells and have various histological appearances such as adenocar-cinoma or squamous, or oat-cell carcinoma.

There are no histological or other characteristics which would specify the individual lung cancer as cancer caused by asbestos.

In many cases of asbestos-linked pulmonary cancers the lungs also show pulmonary fibrosis asbestosis microscopically, and often macroscopically, and on X-ray examination. Some scientists believe that so-called “asbestos lung cancer” can only develop on a pathologically changed terrain of asbestosis fibrosis. There is evidence of such a possibility in human pathology; the scar-carcinoma. Others believe that exposure to asbestos alone, particularly in a smoker, may provoke cancerous growth without also causing asbestosis. The decision between the two opinions is difficult to reach because in individual clinical cases of bronchogenic carcinoma we cannot distinguish what is an “asbestos cancer”, a “cigarette cancer” or lung cancer form yet another cause. Thus, in most countries bronchogenic carcinoma is considered an occupational disease due to asbestos, e.g. for workmen’s compensation only in the presence of coexisting asbestosis. If pulmonary fibrosis were a prerequisite for development of asbestos-linked lung cancer, it would follow that lowering exposures to asbestos to levels which effectively prevent asbestosis would automatically eliminate “asbestos lung cancer”.

Epidemiological data:-

In man the link of lung cancer with asbestos has been mainly epidemiological. While asbestosis cannot occur without exposure to asbestos and consequently every case of asbestosis must be linked with such exposure, with pulmonary cancer the situation is quite different. It is a rather common disease in the general population. The link with exposure to asbestos is based on finding whether in those exposed to asbestos lung cancer occurs more frequently than in those unexposed, i.e. whether in those exposed there is an excess incidence of lung cancers.

Since Doll’s study a number of other epidemiological studies, of various levels of excellence, have been carried out which confirm that indeed there is an excess of bronchogenic carcinoma in persons exposed to asbestos, under certain circumstances and thus that asbestos must be considered one of manifest a number of carcinogenic substance.

What are the circumstances of a risk of cancer in asbestos exposure? It has been established that smoking cigarettes greatly increases this risk. In fact the large majority of lung cancers attributed to asbestos exposure have occurred in smokers. A lung cancer in an asbestos-exposed non-smoker has been a rarity. Table 1 shows the effect of both exposures; together while each of the two exposures also carries a risk by itself. A particular exposure to asbestos in the reported group of workers increased the basic risk of pulmonary cancer in non smokers. However, since the risk in non-smokers was very small, its further increase still meant only very few cases if any at all.


Table 1



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