ISSN 0377-4910

Vol. 29, No. 9 

September, 1999

Silicosis - An Uncommonly Diagnosed Common Occupational Disease

Pneumoconiosis resulting from exposure to free silica may be the commonest and most extensively studied occupational disease of the lung1 and even today, it continues to be among the most serious occupational diseases. The problem of silicosis is confined not only to the developing nations, but is also not uncommon in industrialized nations. For example, in 1983 more than 1 million U.S. workers were at risk of developing silicosis and 58,000 would eventually develop it2.

Importance of Silica and Silicosis

The distribution of silicon in nature is similar to the distribution of carbon in organic matters. Silicon contributes to about 28% of the earth's crust. Silicon being very reactive does not remain in the element form but combines either with oxygen alone and forms free silica (SiO2) or with oxygen and other elements and forms silicates, eg asbestos. Silica and silicates constitute the bulk of most kinds of rocks, clays and sands. The term silicosis is reserved for the lung disorder caused by inhalation of free silica, which is an untreatable progressive disease and is the commonest and most widespread of all occupational diseases. Exposure to large amount of free silica can pass unnoticed because, silica is odourless, non-irritant and does not cause any immediate noticeable effect and hence is confused with ordinary dust. Chronic exposure to silica


predisposes to tuberculosis, which is still a major public health problem in developing countries including India3. Recently crystalline silica has been classified as a human carcinogen (group I) by International Agency for Research on Cancer (IARC)4.

Occupational Exposure to Silica

Since the earth's crust contains about 12% free silica mostly in the form of quartz, mining and tunneling are the occupations most closely related to the hazard of silica exposure. The sand stone industry, stone quarrying and dressing, granite industry, grinding of metals, sand blasting, iron and steel foundries, silica milling, flint crushing and manufacture of abrasive soaps are some of the occupations related to silica exposure. Some of the occupations such as slate pencil industry and agate grinding industry which carry high risk of silicosis are peculiar to India. There are about 3 million workers at high potential risk of silica exposure. They are employed in various occupations such as mining and quarries (17 lakhs); manufacture of non-metallic products ie., refractory products, structural clay, glass, mica, etc. (6.3 lakhs) and manufacture of basic metals and alloys, ie. iron and steel, copper, ferroalloys, aluminium, etc.(6.7 lakhs)5. In addition many of the 54 lakhs construction workers are also at risk of silica exposure.



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Silica is one of the most fibrogenic material found in nature. The reason for its fibrogenicity has largely remained a matter of speculation. The early workers attributed its injurious effects to the hard and sharp edges.However Gardner6 demonstrated that particles of silicon carbide which have as sharp and hard edges as silica do not produce fibrosis in experimental animals and Gye and Purdey7 produced inflammation and necrosis with colloidal silicic acid. Of the theories so far advanced, the fibrogenic factor theory of Heppleston and styles8 is the most popular. According to this theory the macrophages after ingestion of quartz particles release a factor called macrophage fibrogenic factor (MFF), which stimulates fibroblasts to increase the production of collagen. The existence of MFF was confirmed by later investigators9-12. The MFF is a peptide, released from the lysosomes of the macrophages that have engulfed silica particles. It causes the translation of collagen from the rough endoplasmic reticulum, through the secretory vesicles to the extracellular fibrillary state in the fibroblasts of the pulmonary interstitium13. However, this theory does not take into account the immunologic factor in causation of silicosis and does not explain the high levels of anti-nuclear factors1416 and various antibodies observed in silicotics17, 18.

In summary, it may be said that the exact mechanism of the action of silica dust on the lungs is still not known, but available evidence indicates that the silica particles in some manner cause increased permeability of the digestive vacuole of alveolar macrophages leading to their autodigestion. The dying macrophages liberate a fibroblast stimulating factor, which causes increased formation of collagen tissue. Autoimmunity is probably responsible in the evolution of the later stages of silicosis.

Magnitude of the Silicosis Problem in India

Though mining and metallurgy in India were practiced much earlier than that in Europe, the first cases of silicosis in this country were described only in the 1940s in gold miners of Kolar by Caplan and Burden19. The silicosis observed among Kolar gold miners was more conspicuous by its benign nature in sharp contrast to the disease in gold miners of South Africa and Australia20. Fibrogenicity, the most important biological characteristic of free silica dust, was found lacking in the siliceous dust

of the Kolar gold fields. These findings were later confirmed by others21,22.

There are very few epidemiological studies on silicosis in India and all of them are cross sectional in nature. The results of these studies have been summarised in the table which shows a prevalence of silicosis from 3.5% in ordnance factory to 54.6% in slate pencil industry. The prevalence observed in different industries is a function of the silica concentration in the work environment, duration of work and the job demands. Since these estimates are based on cross sectional studies, they represent the surviving population only. In jobs having high physical demands such as mining, individuals suffering from silicosis/silico-tuberculosis may be missed due to sickness at the time of survey and therefore the estimates would not reflect the actual morbidity.

Table 1. Industry-wise prevalence of silicosis in India

Industry Prevalence (%) Reference
Gold mines 8.84 Caplan and Burden20
Gold mines 13.9  Gowda 22
Mica mines & mica processing industries, Bihar 34.0 Chief Advisory of Factories (CAF)23
Manganese mines 4.1 Ministry of Labour24
Lead and zinc mines 30.4 CAF25
Stone cutters 20.0 Saini et al26
Stone cutters 25.0 Sethi and Kapoor 27
Stone cutters 35.2 Gupta et al28
Foundries  27.2 Samal et al29
Ordnance factory 3.5  Viswanathan et al30
Agate workers 38.0 Sadhu et al31
Glass bangle workers  7.3 Srivastava et al32
Slate pencil workers  54.6  Saiyed et al 33
Mica mines & mica  processing  5.2 Gangopadhyay et al34
Quartz crushing 12.0 NIOH35
Stone quarry 22.0  NIOH36
Sand grinding 27.8 NIOH37
Ceramics & potteries  15.1 Saiyed et al38

The surveys have shown further that the problem of silicosis is much more severe in the unorganized sector of industries like slate pencil cutting, stone cutting, agate industry, etc. Most industries belonging to the unorganized sector do not fall under the purview of the statutory tools such as the Factories Act aimed to protect the health and safety of the working population. Moreover, the entrepreneurs lack the financial resources and technical

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know-how necessary for the safety of workers. The workers on the other hand are also not organized and lack the power of collective bargaining against exploitation.

Considering the huge population employed in mines and surface industries who are at risk of silica exposure, it can be presumed on the basis of available studies that several hundred thousand workers in India suffer from silicosis.

Clinical Features

It is important to emphasize that there may be no symptoms even when the radiographic appearances suggest fairly advanced silicosis. Dyspnoea on exertion is considered to be the most frequent and directly related symptom of silicosis. The severity of dyspnoea increases with progress of the disease. In the absence of complicating disease (eg tuberculosis), it is rarely complained of at rest. Slight unproductive cough is a symptom at the initial stages, later on the quantity of sputum increases. The symptom complex may resemble chronic bronchitis. Excessive sputum production is due to bronchial catarrh brought about by chronic dust exposure and some times it is due to secondary bacterial infection of the devitalized lungs. Chest pain and haemoptysis indicate the possibility of complication like tuberculosis.

Chest Radiography

Chest radiography is the most important tool for the diagnosis of silicosis. There appears to be a clear relationship between total dust exposure and the severity of radiographic changes. In the initial stage, there is reticulation of the lung fields due to thickening of the perivascular and inter-communicating lymphatics. The radiographic diagnosis of silicosis can be made with some degree of certainty only after the appearance of nodules. The silicotic nodules are 2-5 mm in diameter, homogenous in density and usually bilaterally symmetrical.On continued dust exposure, the nodules increase in size and number and eventually cover most parts of the lungs. Sometimes the silicotic nodules unite and form conglomerate shadows. These conglomerate shadows are sometimes described as progressive massive fibrosis (PMF), indicating the future course of disease.

Sputum Examination for Tubercle Bacilli

The recovery of tubercle bacilli in the sputum of patients suffering from silicotuberculosis is difficult. This is because of walling in of the tubercle foci by silicotic fibrosis which prevents the discharge of tubercle bacilli in the sputum. That a large number of cases of tuberculosis remain

undiagnosed during life is evidenced by the fact that a high prevalence of tuberculosis is observed in post mortem studies of industrial population occupationally exposed to high levels of silica. Gardner39 found evidence of tuberculosis in 65-75% silicotics from various industries. Yuang Ching Co40, Barras41and Schymczykicz et al42 found post mortem evidence of tuberculosis in 48, 50 and 52% silicotics respectively. James43 and Rivers et al44 found evidence of tuberculosis in 40 and 35% cases of PMF respectively at autopsy examination. However, during life, the recovery rate of tubercle bacilli from sputum of the South Wales miners with PMF was very low, ie 1.1%45 and 2.7%46.

Differential Diagnosis between Silicosis and Tuberculosis

For the diagnosis of silicosis, history of occupational exposure to silica is most important. Occurrence of silicosis in the absence of occupational exposure is rare47. Radiologically, silicosis and miliary tuberculosis closely resemble each other, however, miliary tuberculosis in adults is rare and the patient is toxaemic. The nodules in miliary tuberculosis whether small or large, are less than those in silicosis. The radiographs of patients with silicosis usually show increased translucency as against general loss of translucency in tuberculosis. In general, the severity of symptoms in a patient wih simple nodular silicosis is much less as compared to patients of miliary tuberculosis. The distinction between adult type (post-primary) tuberculosis and conglomerate (PMF) radiological shadows is some times very difficult. However, the conglomerate shadows of silicosis do not show cavitation. Associated complications like pleural effusion and distortion of the intra-thoracic organs due to fibrosis are usually not observed in conglomerate shadows.

The above description is that of classical silicosis. However, in some cases, silicosis may develop within a few months to 2 years of massive silica exposure. Dramatic dyspnoea, weakness, and weight loss are often presenting symptoms. The radiographic findings of diffuse alveolar filling differ from those in the more chronic forms of silicosis. Histologic findings similar to pulmonary alveolar proteinosis have been described, and extrapulmonary (renal and hepatic) abnormalities are occasionally reported. Rapid progression to severe hypoxaemic ventilatory failure is the usual course.

Therapy and Management of Complications of Silicosis

There is no specific treatment for silicosis, therapy being directed largely at the complications of the disease.

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Historically, the inhalation of aerosolized aluminium has been unsuccessful as a specific therapy for silicosis48. The polymers such as polyvinyl pyridine-N-oxide, and polybetaine which can prevent experimental silicosis, have not been found suitable for human disease49,50. Recent laboratory work , particularly in China, with tetrandrine has shown in vivo reduction in fibrosis and collagen synthesis in silica exposed animals treated with this drug. However, strong evidence of human efficacy is currently lacking, and there are concerns about the potential toxicity including the mutagenicity of this drug. Because of the high prevalence of disease in some countries like China, India and many other developing nations, investigations of combinations of drugs and other interventions continue. Currently, no successful approach has emerged, and the search for a specific therapy for silicosis has been unrewarding51.

Prevention and Control of Silicosis and Silico-tuberculosis

In the absence of specific therapy for silicosis, there is a need for planning a national strategy for the prevention and control of silicosis and silico-tuberculosis. Country-wide silico-tuberculosis control should consist of two major components: (i) definition of the magnitude of the problem at the national level; and (ii) implementation of actual control measures.

Definition of magnitude of the problem at national level

To plan and execute the national strategy for the prevention of silico-tuberculosis information on the total population at risk and the number of people already affected is very essential. The population at risk of silicosis can be roughly estimated on the basis of available information on industries, their location, raw material and industrial processes and employment in each of them. This should be followed by comprehensive industrial hygiene and epidemiological surveys in a sample population. After estimation of the population at risk and identification of the more vulnerable groups, the industrial and medical surveys should be carried out. The industrial hygiene survey should include measurement of the total and respirable dust at work places and the qualitative analysis of dust samples. The tools of an epidemiological survey are recording of the occupational history, clinical history and physical examination, chest radiograph, sputum examination and spirometry. Chest radiography is the most important single investigation having a high degree of specificity but relatively low sensitivity. The history and physical examination help in excluding other

respiratory diseases. Spirometry may help in appraisal of the functional loss. The results of the sample surveys will help in identifying the thrust areas. The thrust areas may be defined on the basis of the number of people at risk and the severity of the hazard. Industries having moderate risk but employing a large work force eg the mines, or highly hazardous industries employing a smaller number of workers eg slate pencil industry, agate industry, quartz grinding industry, etc., fall in this category. For the reasons already mentioned, there is a special need for looking into the problems of small scale and cottage industries.

Implementation of actual control measures

The process of the control of silicosis consists of dust control measures; and medical measures.

Dust control measures

There is no silicosis without dust exposure, and the dust levels in the work environment correlate well with the incidence as well as the severity of the disease. Therefore, elimination or suppression of dust in the work environment is the key in the control of silicosis. Each industry has its unique work process and therefore it is not possible to have a single prescription appropriate to all. The general principles of dust control measures include substitution of more hazardous substances with innocuous substances, isolation and enclosure of the sources of dust, use of wet methods wherever possible, application of local and general exhaust, humidification of the work environment, etc.

Frequently, the management is found to share the misconception of laymen that the use of dust mask is sufficient for the prevention of dust related occupational diseases in the industry. The personal protective equipments such as masks should be prescribed only when all available dust control measures have failed. In fact, the dust masks are of little value when the dust concentrations are high as the dust particles will clog the pores in the filter resulting in a choking sensation and discontinuance of the use of masks by workers. Moreover, the masks are not suited for hot and humid climate.

Medical surveillance

As per the recommendation of WHO52, the periodical medical examination of workers and the dust measurements should be integrated and pursued together so that the benefits of the dust control measures could be evaluated in terms of change in morbidity. The medical

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examination is also necessary because there exists a small susceptible population which is hypersusceptible or otherwise unusually responsive to the toxicants because of genetic factors, age and personal habits53. The medical measures for the control of silicosis and silico-tuberculosis include preemployment and periodical examinations, incorporating chest xray, sputum examination for tubercle bacilli and spirometry. The preemployment medical examination will provide the base-line data for each individual. The periodical medical examinations shall aim at early detection of cases of silicosis and tuberculosis. The success of the prevention programme will largely depend upon the active cooperation of the workers at risk. Therefore, the need for health education of the workers cannot be over emphasized.


Silicosis is an age old occupational disease and remains a major occupational health problem in India. It is responsible for high morbidity and mortality in industrial workers. Since there is no specific therapy for this progressive and irreversible disease, all steps should be taken for its prevention. The benefits of prevention include the economic benefits such as increased production by healthy workers, reduction of sickness absenteeism and less expenditure on health care and above all the alleviation of human suffering! This common occupational disease deserves greater consideration by the physicians.



1. Buechner, H.A. and Ansari A. Acute silico-proteinosis. A new pathologic variant of acute silicosis in sand blasters characterized by histologic features resembling alveolar proteinosis. Dis Chest 55: 274, 1969.

2. Shaman, M and Shaman, D. Silicosis : The occupational disease that shouldn't exist. Am Lung Assoc Bull 69: 6, 1983

3. Prabhakar, R. Tuberculosis _ The continuing scourge of India. Indian J Med Res 103: 19, 1996

4. IARC. Monograph on the Evaluation of Carcinogenic Risks to Humans _ Silica, Some Silicates, Coal Dust and Para-Aramid Fibrils.(Vol. 68) IARC, World Health Organization, Geneva. p.211, 1997

5. Indian Labour Statistics -1994. Labour Bureau, Ministry of Labour, Chandigarh, 1996

6. Gardner, L.W. Studies on the relation of the mineral dusts to tuberculosis. III. The relatively early lesions in experimental pneumoconiosis produced by carborundum inhalation and their influence on pulmonary tuberculosis. Am Rev Tuber 7: 344, 1923.

7. Gye, W.E., and Purdey, W.J. The effects of parenteral administration of large doses of colloidal silica. Br J Exp Pathol 3: 75, 1922.

8. Heppleston, A.G. and Styles, J.A. Activity of a macrophage factor in collagen formation by silica. Nature 214: 521, 1967.

9. Burrell, R. and Anderson, M. The induction of fibrogenesis by silica-treated alveolar macrophages. Environ Res 6: 389, 1973.

10. Nourse, L.D., Nourse, P.N., Botes H. and Schwartz, H.M. The effects of macrophages isolated from the lungs of guinea pigs dusted with silica on collagen biosynthesis by guinea pig fibroblasts in cell culture. Environ Res 9: 115, 1975.

11. Aalto, M. and Kulonen, E. Fractionation of connective tissueactivating factor from soluble medium of silica treated macrophages. Act Oath Microbiol Scand 87: 241, 1979.

12. Aho, S., Peltonen, J., Jalkanen, M. and Kulonen, E. Effect of silica on cultured rat peritoneal macrophages. Ann Occup Hyg 22: 285, 1979.

13. Heppleston A.G. Pathogenesis of mineral pneumoconioses. In: Occupational Lung Disorders. Ed. W.R. Parkes. Butterworth Heinmann, Oxford. p.100, 1994.

14. Jones, R.N., Turner-Warwick, M., Ziskind, M. and Weill, H. High prevalence of anti-nuclear antibodies in sand blasters' silciosis. Am Rev Respir Dis 113: 393, 1976.

15. Turner-Warwick, M., Cole, P., Weill, H., Jones, R.N. and Ziskind, M. Chemical fibrosis: The model of silica. Ann Rheum Dis 36 (Suppl.): 47, 1977.

16. Nigam S.K., Saiyed, H.N., Suthar, A.M., Karnick, A.B., Venkaiah, K. and Kashyap, S.K. Role of circulating immune complexes in the immunopathogenesis of non-occupational pneumoconiosis in villages of central Ladakh. Int J Toxicol Occup Environ Health 1: 35, 1992.

17. Wagner, J.C. and Mc Cormick, J.N. Immunological investigations of coal workers' disease. J R Coll Phys 2: 49, 1967.

18. Karnik, A.B., Saiyed, H.N. and Nigam, S.K. Humoral immunologic dysfunction in silicosis. Indian J Med Res 92: 440, 1990.

19. Caplan, A. and Burden, D.J. Proceedings of Conference on Silicosis, Pneumonconiosis and Dust Separation. Institute of Mine Engineering and Institute of Mineral Metallergy, London, Paper No.5, 1947.

20. Holt, P.F. Pneumoconiosis: Industrial Diseases of Lung Caused by Dust. Edward Arnold Ltd., London, p.131, 1957.

21. Effrench, G.E. The epidemiology of lobar pneumonia in Kolar gold field. Proc Soc Stud Industr Med 5: 19, 1983.

22. Gowda, A.M.S. Pneumoconiosis in the Kolar gold fields. Proceedings of Sixth International Conference on Pneumoconiosis (Vol.II), P.1219, 1983.

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23. Chief Advisor of Factories. Silicosis in mica mining in Bihar. Report No.3. Ministry of Labour, Govt. of India, New Delhi, 1953.

24. Report of the Manganese Poisoning Enquiry Committee, Ministry of Labour and Employment, Government of India, New Delhi, 1960.

25. Chief Advisor of Factories. Silicosis hazard in lead and zinc mines in Rajasthan. Report No.21, Ministry of Labour, Govt. of India, New Delhi 1961.

26. Saini, R.K., Yousuf, M., Allaqaband, G.Q. and Kaul, S.N. Silicosis in stone cutters in Kashmir. J Indian Med Asso 82: 198, 1984.

27. Sethi, N.K. and Kapoor, S.K. Mass-miniature radiographs vs. standard sized chest films for the detection of silicosis. Indian J Industr Med 29: 69, 1982.

28. Gupta, S.P., Bajaj, A., Jain, A.L. and Vasudeva, Y.L. Clinical and radiological studies in silicosis based on a study of the disease amongst stone-cutters. Indian J Med Res 60: 1309, 1972.

29. Samal, R.K., Reddaiah, V.P., Mukhopadhyay, S. and Nath, L.M. Prevalence of pulmonary tuberculosis among iron foundry workers. Indian J Industr Med 32: 116, 1986.

30. Viswanathan, R., Boparai, M.S., Jain, S.K. and Dash, M.S. Pneumoconiosis survey of workers in an ordnance factory in India. Arch Environ Health 25: 198, 1972.

31. Sadhu, S.G., Parikh, D.J., Sharma, Y.K., Saiyed, H.N., Rao, P.V.C., Kulkarni, P.K., and Kashyap, S.K. A follow up study of health status of small scale agate industry workers. Indian J Indust Med 41: 101, 1995.

32. Srivastava, A.K., Gupta, B.N., Harish Chandra and Mahendra, P.N. Pulmonary disease due to multimetal exposure in glass bangle workers. Indian J Industr Med 34: 20, 1988.

33. Saiyed, H.N., Parikh, D.J., Ghodasara, N.B., Sharma, Y.K., Patel, G.C., Chatterjee, S.K. and Chatterjee, B.B.: Silicosis in slate pencil workers. An environmental/medical study. Am J Industr Med 8: 127, 1985.

34. Gangopadhyay, P.K., Bhattacharya, S.K., Mazumder P.K., Ahmad, S. and Chatterjee, M.K. Occupational health problems of mica processing male workers. Indian J Industr Med 40: 8, 1994.

35. National Institute of Occupational Health. Evaluation of health hazards in quartz crushing industry and evaluation of dust control measures. Annual Report, 1985-86, p.1, 1986.

36. National Institute of Occupational Health. Pilot survey of stone quarry workers in Jakhlaun area of Lalitpur district (U.P.). Annual Report, 1986-87, p.37, 1987.

37. National Institute of Occupational Health. Study of silicosis in sand grinding workers. Annual Report, 1988-89, p.1, 1989.

38. Saiyed, H.N., Ghodasara, N.B., Sathwara, N.G., Patel, G.C., Parikh, D.J. and Kashyap, S.K. Dustiness, silicosis and tuberculosis in small scale pottery workers. Indian J Med Res 102: 138, 1995.

39. Gardner, L.W. Studies on experimental pneumoconiosis. Am Rev Tuber 20: 833, 1929.

40. Yuang Ching Co. Silicosis in gold miners. J Occupc Med 5: 46, 1963.

41. Barras, G. Silico-tuberculosis in Switzerland. Schweiz Med Wsch 100: 802, 1970.

42. Schymczykicz, K., Czuraj, H. and Kunski, H. Pneumoconiosis in iron-ore miners and ore enrichment plant personnel. Med Pracy 21: 359, 1970.

43. James, W.R.L. The relation of tuberculosis to the development of massive fibrosis in coal workers. Br J Tuber 48: 89, 1954.

44. Rivers, D., James, W.R.L., Davis, D.G. and Thomson, S. The prevalence of tuberculosis at necropsy in massive fibrosis of coal workers. Br J Industr Med 14: 39, 1959.

45. Cochrane, A.L., Cox, J.G. and Jarman, T.F. Pulmonary tuberculosis in Rhodda Fach. BMJ ii: 843, 1952.

46. Marks, J. Infective pneumoconiosis due to anonymous mycobacteria. BMJ ii: 1332., 1961

47. Saiyed, H.N., Sharma, Y.K., Sadhu, H.G., Norboo, T., Patel, P.D., Patel, T.S., Venkaiah, K. and Kashyap, S.K. Non-occupational pneumoconiosis at high altitude villages in central Ladakh. Br J Industr Med 48: 825, 1991.

48. Kennedy, M.C.S. Aluminium powder inhalation in the treatment of silicosis of pottery workers and pneumoconiosis of coal miners. Br J Industr Med 13: 85, 1956.

49. Weller, W. Long-term test on rhesus monkeys for PUNO-therapy of anthracosilicosis. In: Inhaled Particles and Vapours. IV. Ed. W.H. Walton, Pergman Press, Oxford. p.339, 1977.

50. Jindon, Z., Jingle, L. and Guizhi, L. Long-term observations of therapeutic effect of PVNO on human silicosis. Zbl Bakt Hyg Abt Orig H 178: 259, 1983.

51. John, E. Parker and Gregory R. Wagner SILICOSIS : Respiratory System in ILO Encyclopedia of Occupational Health & Safety. Ed. J.M.Stellman Vol.1(4th Edition), ILO Office, Geneva, p.101, 1998.

52. World Health Organization. Report on Control of Pneumoconiosis (Prevention, Early Diagnosis and Treatment). WHO/OCH/90.1, WHO, Geneva 1990.

53. American Conference of Governmental Industrial Hygienists (ACGIH). Threshold Limit Values for Chemical Substances and Physical Agents _ Biological Exposure Indices. ACGIH, Cincinnati, p.3, 1997.

This write-up has been contributed by Dr. H.N.Saiyed, Director, National Institute of Occupational Health. Ahmedabad.

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Some Research Projects Completed Recently

Expression of epidermal growth factor receptor, cathepsin D and p53 oncoprotein as prognostic indicators in human breast carcinoma.

The study was carried out on biopsy material from 50 patients of infiltrating ductal carcinoma obtained in the form of paraffin blocks from 2 hospitals. Morphological grading was done and epidermal growth factor receptor (EGFR), cathepsin D and p53 oncoprotein expressions were studied immunohistochemically. Efforts were also made to correlate the markers and the morphological classification of breast carcinomas and to determine their use as prognostic indicators.

Of the 50 tumours, 22 (44%) could be grouped as grade I and 14 (28%) each of grades II and III. Eleven (22%) and 25 (50%) tumours were positive for p53 and EGFR respectively, whereas all the tumours showed the expression of cathepsin D. The p53 positivity in grade I, II and III tumours was 13.6,21.4 and 35.7% respectively, whereas EGFR positivity was 18.18, 64.28 and 85.71% respectively.

The p53 positivity was found to increase with increasing histological grade not only with respect to the number of patients but also to the number of tumour cells expressing p53. The expression of EGFR also increased with higher histological grades. Of the 11 tumours positive for p53, 7 had lymph node metastases at the time of presentation, whereas of the 25 EGFR positive tumours, 17 had lymph node involvement. The tumours associated with lymph node involvement showed intense staining for cathepsin D. These observations indicated that over expression of p53 and EGFR and intense staining for cathepsin D were associated with aggressive clinical behaviour and poor prognosis of tumours.

It is concluded that immunohistochemistry is a useful technique for the detection and study of the over expression of p53, cathepsin D and EGFR.

Sudha Venkatesh
Rama Gopalan
Department of Pathology
Dr. A.L. Mudaliar Postgraduate
Institute of Basic Medical Sciences

Role of free radicals and antioxidant status and therapeutic response of Zn in age related macular degeneration.

A prospective study was carried out in 51 patients (age > 55 yr) with reduction in central visual acuity due to

age related macular degeneration (AMD) and presence of characteristic lesions in the fundus, and in 20 healthy individuals matched for age and sex to assess the status of antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) as well as other antioxidant factors like ascorbic acid, glutathione and lipid peroxidation. Efforts were also made to evaluate the effect of oral zinc supplementation on the activity of antioxidant enzymes and the clinical course of the AMD. Patients with media opacities due to any cause precluding proper fundus examination, presence of any other ocular disease causing poor vision or distorting the anatomy of the macula and patients with malignancies, diabetes mellitus, renal and chronic liver diseases were excluded from the study.

The levels of catalase, glutathione peroxidase, superoxide dismutase and glutathione and lipid peroxidation were significantly lower in the AMD patients at base-line with no difference in the levels of ascorbic acid, haemoglobin and zinc. The AMD patients were divided into 2 groups; group A included 29 patients who received zinc supplement (89.2 mg of elemental zinc given orally) and group B included 22 patients who did not receive any zinc therapy. Patients were followed up at 3 monthly intervals. At base-line, serum Zn levels were 96.73±18.62 and 99.97±13.3 mg% in groups A and B respectively. There was a significant rise in the level of Zn after 3 months of Zn supplementation, with Zn levels rising to 258±12.60 in group A vs 103.60±14.72 in group B.


There was a rise in the level of glutathione peroxidase at 3 months to 140.17±42.38 units/g Hb in group A compared to 92.36±37.22 units/g Hb in group B and this rise was maintained till 24 months. The levels of superoxide dismutase did not show any rise till 9 months after which it rose significantly. The levels of catalase showed a significant rise after 3 months of Zn administration but there after there was a gradual decrease. There was no change in the levels of glutathione, Hb and ascorbic acid in both the groups. There was no significant improvement in ocular status or visual improvement in the treatment vs non treated group.


Amod Gupta
Department of Ophthalmology
Postgraduate Institute of
Medical Education and Research

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Director-General  Dr. Lalit Kant
Dr. Bela Shah
Sh. N.C. Saxena
Dr. V. Muthuswamy
Dr. N. Medappa



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