|
|
|
| Year : 1986 | Volume
: 32
| Issue : 4 | Page : 185-91 |
|
Medical survey of methyl isocyanate gas affected population of Bhopal. Part II. Pulmonary effects in Bhopal victims as seen 15 weeks after M.I.C. exposure.
SR Naik, VN Acharya, RA Bhalerao, SS Kowli, HH Nazareth, AA Mahashur, SS Shah, AV Potnis, AC Mehta
Correspondence Address:
S R Naik
How to cite this article:
Naik S R, Acharya V N, Bhalerao R A, Kowli S S, Nazareth H H, Mahashur A A, Shah S S, Potnis A V, Mehta A C. Medical survey of methyl isocyanate gas affected population of Bhopal. Part II. Pulmonary effects in Bhopal victims as seen 15 weeks after M.I.C. exposure. J Postgrad Med 1986;32:185-91
|
How to cite this URL:
Naik S R, Acharya V N, Bhalerao R A, Kowli S S, Nazareth H H, Mahashur A A, Shah S S, Potnis A V, Mehta A C. Medical survey of methyl isocyanate gas affected population of Bhopal. Part II. Pulmonary effects in Bhopal victims as seen 15 weeks after M.I.C. exposure. J Postgrad Med [serial online] 1986 [cited 2023 Sep 26 ];32:185-91
Available from: https://www.jpgmonline.com/text.asp?1986/32/4/185/5325 |
Full Text
INTRODUCTION
A large amount (40 tonnes) of MIC gas leaked from the storage tank of the factory of Union Carbide Co. Ltd., Bhopal, into the atmosphere on the night of 2/3 December 1984, killing a few thousand people and leaving several thousand disabled. In the absence of adequate literature it was difficult to predict and prevent long-term effects of MI.C gas on human beings. In order to assess the extent and nature of lung damage a study was undertaken. This article describes in detail the effects on the respiratory system at the end of three and half months.
MATERIAL AND METHODS
The material consisted of two groups [Group I (n = 446) and group It (n = 123)]. The selection of these two groups has been described earlier.[9] Each individual was assessed for his/her lung function.
Pulmonary function tests consisted of forced expiratory spirography with the help of a Vitalograph (UK) and peak expiratory flow rates (PEFR) measured with the help of Wright's Mini Peak Flowmeter. After explaining the procedure, each subject was made to blow in the vitalograph and a forced expiratory spirogram was recorded. Each subject repeated the performance thrice and the best graph was selected.[6] From this graph, the forced vital capacity (FVC), forced expiratory volume in one second (FEV1), FEV1/FVC ratio and mid expiratory flow rates (MEFR) were calculated. On the basis of these tests, the pulmonary function disability was classified as restrictive or obstructive in nature. Subjects with FVC of 80% below the predicted values6 were labelled as having restrictive disability, they were further, classified into mild (FVC 60-80% of predicted), moderate (FVC 40-60% of predicted) and severe (FVC< 40% of predicted). Similarly, obstruction was further classified on the basis of FEV1/FVC ratio.[6] In those subjects showed airway obstruction, the tests were repeated after giving a bronchodilator aerosol. Pulmonary function tests could not be done in children below the age of seven years because of lack of cooperation.
Routine chest films were taken in subjects with respiratory symptoms and signs, and in those who had abnormal pulmonary functions. Precaution was taken to maintain the consistency of technique to achieve a good comparative standard. Radiographs were reviewed by three independent observers who looked for certain predetermined findings which were noted in accordance with the earlier study from this institute. The zones affected were noted as per the criteria followed by Tuberculosis Chemotherapy Centre.[13]
RESULTS
Demographic patterns in both the groups have already been discussed earlier.[9]
Clinical features
In Group I, all subjects who were interrogated gave a history of burning of nose and throat and dry cough on the night of 2-3 December immediately after exposure to MIC gas. The symptoms gradually improved with the treatment they received. [Table 1] shows residual symptoms and signs in both the groups at the time of the survey (104-109 days later). In Group I, the cough was dry in 107 (23.8%) and productive in 217. In 202 subjects (45%), the sputum was small in quantity and the patients had a lot of difficulty to bring it out. The chest pain was continuous and dull-aching in nature and used to be aggravated by coughing and deep breathing. In this group, 52 (11.6%) subjects were smoking more than 5-10 bidees/cigarettes per day.
In Group 41, the cough was dry, in 13 and productive in 8 subjects. In this group, 28 (22.8%) subjects were smokers smoking more than 10 cigarettes/bidees per day.
Pulmonary function tests
Group I [Table 2] Pulmonary function tests could be done in only 326 subjects of Group I. Restrictive disability was present in 160. The details regarding severity of restriction and/or obstruction are presented in [Table 2] and [Table 3] which are self-explanatory.
Chest radiography
Chest radiography was done in 306 of Group I and 81 of Group II subjects. The details are given in [Table 4].
DISCUSSION
The most notable respiratory symptoms were cough and dyspnoea, which were present in all subjects in Group I immediately after exposure. These symptoms gradually improved after treatment, the details of which were not known. However, even as late as 100 days, both these symptoms were still predominant in 72.6% and 66% subjects respectively. In contrast, of Group II, only 17% subjects had cough and 9% had dyspnoea. Pulmonary function tests revealed predominantly moderate to severe restrictive disability. The radiographs in Group I showed deposits and correlated well with the pulmonary function pattern; 49% subjects showed restrictive pattern and 57% subjects had abnormal X-rays. Our results suggest, therefore, that residual effects of MIC were present in both the Group I and Group 11 areas, but Group I subjects were affected much more.
The present knowledge of chronic human damage by isocyanate has been based on two studies in 35 firemen exposed to toluene diisocyanate (TDI).[1] Similar to our observations, those subjects manifested with nose and throat irritation. Chest symptoms in them were worse during the first three days and subsided later. Simple lung function tests showed a persistent decline. Other analogues of isocyanates such as phenyl isocyanate, hexyl diisocyanate (HDI), hexyl isocyanate (HI) are less potent than TDI but show similar effects on the lung.[11], [12] Workers exposed to isocyanates develop episodic asthma due to nonspecific effect on the airway smooth muscle.[14] The underlying cause of isocyanate asthma is not understood. Specific reaginic and complement fixing antibodies to TDI have been found in some affected people,[3], [7], [8] and lymphocyte transformation has been observed.[2] However, these results have not yet been confirmed by other workers. Workers exposed to TDI had nonspecific irritability of the airway.
In our subjects, there was no episodic asthma probably because all our subjects had acute but short exposure. The lung reaction to TDI varied with the concentration and the duration of exposure. High concentration of the vapour of isocyanates which may occur in accidental spillage causes rhinitis, cough, wheezing and crepitations4 and in severe cases there may be bronchopneumonia or pulmonary edema. In our series, wheezing was present in 18.6% and rales in 24.9% as late as after 100 days. Sometimes; acute exposure to isocyanates can cause acute extrinsic allergic alveolitis.
Reduced values of VC and diffusion of carbon monoxide compared with the control group have been reported in workers after a prolonged exposure to isocyanates in plastics industry and it is suggested that this may indicate diffuse interstitial pulmonary fibrosis.[11] There are no relevant radiographic abnormalities except in cases of pulmonary oedema or acute extrinsic allergic alveolitis. In our subjects the VC was low in the majority of subjects. Although the diffusion test could not be per. formed, the clinical functional and radiological observations suggest that these subjects had a picture of acute extrinsic allergic bronchiolo-alveolitis,[10] due to exposure to MIC, which has gone into the chronic phase of extrinsic allergic bronchiolo-alveolitis.
In Group I, 38 subjects had non-specific abnormalities like overinflation, prominent pulmonary conus etc. in X-rays. Of these, only 16 subjects had abnormal pulmonary functions and 15 were abnormal clinically, whereas in Group II, 18 subjects had nonspecific X-ray changes out of which 10 had abnormal lung functions. This means that the abnormal pulmonary functions were largely due to specific abnormalities, as seen in X-rays. We recommend that all subjects during follow-up must have their pulmonary function tests and chest radiographs done, as only clinical examination is not adequate. Prolonged follow-up studies with more specific tests like diffusion studies, flow-volume loop and arterial blood gas studies are evidently necessary to know the course of the damage to lungs due to isocyanate.
ACKNOWLEDGEMENT
This survey was made possible due to untiring efforts of Nagarik Rahat and Punarvas Committee (NRPC) and Voluntary Health Association of India (VHAI). We are most thankful to them.
We are grateful to Shri Jamshed Kanga, the Municipal Commissioner, Shri V. D. Vaidya, Deputy Municipal Commissioner and Drs. G. B. Parulkar and B. R. Kalke, the Deans of two medical institutions, for their administrative and other help to enable us to carry out the survey and for their permission to use the various departments of K.E.M. Hospital and Seth G. S. Medical College to further scrutinise the material in depth after the survey.
References
| 1 | Axford, A. T., McKerrow, C. B., Jones, A. P. and LeQuesne, P. M.: Accidental exposure to isocyanate fumes in a group of firemen. Brit. J. Industr. Med., 33: 6571, 1976. |
| 2 | Bruckner, H. C., Avery, S. B., Stetson, D. M., Dodson, V. S. and Ranayne, J. J.: Clinical and immunological appraisal of workers exposed to düsocyanates. Arch. Environ. Hlth., 16: 619-625, 1968. |
| 3 | Butcher, B. T., Jones, R. N., O'Neil, C. E., Glindmeyer, H. W., Diem, J. E., Dharmarajan, V., Weill, H. and Salvaggio, J. R.: Longitudinal study of workers employed in the manufacture of toluenedüsocyanate. Amer. Rev. Resp. Dis., 116: 411-421, 1977. |
| 4 | Hama, G. M.: Symptoms of workers exposed to isocyanates. Arch. Ind., Hyg., 16: 232-233, 1957. |
| 5 | Kamat, S. R., Mahashur, A. A., Tiwari, A. K. B., Potdar, P. V., Gaur, M., Kolhatkar, V. P., Vaidya, P., Parmar, D., Rupawate, R., Chatterjee, T. S., Jain, K. B., Kelkar, M. D. and Kinare, S. G.: Early observations on pulmonary changes and clinical morbidity due to the isocyanate gas leak at Bhopal. J. Postgrad. Med., 31: 63-72, 1985. |
| 6 | Kammat, S. R., Sarma, B. S., Raju, V. R. K., Venkataraman, C., Balkrishnan, M., Bhavsar, R. C., Kulkarni, S. T. and Malhotra, M. S.: Indian norms for pulmonary functions. J. Assoc. Phys. India, 25: 531-540, 1977. |
| 7 | Karol, M. H., Isoet, H. H. and Alarie, Y. C.: Tolylspecific IgE antibodies in workers with hypersensitivity to toluene düsocyanate. Amer. Ind. Hyg. Assoc. J. 39: 454-458, 1979, |
| 8 | Karol, M. H., Sandberg, T., Riley, E. J. and Alarie, Y.: Longitudinal study of tolyl-reactive IgE antibodies in workers hypersensitive to TDI. J. Occ. Med, 21: 354-358, 1979. |
| 9 | Naik, S. R., Acharya, Vidya N., Bhalerao, R. A,, Kowli, S. S. Nazareth, H., Mahashur, A. A., Shah, S., Potnis, A. V. and Mehta, Arundhati C.: Medical survey of methyl isocyanate gas affected population of Bhopal. Part I-General medical observations 15 weeks following exposure, J. Postgrad, Med., 32: 175-184, 1986. |
| 10 | Parkes, W.R.: Disorders caused by organic agents (excluding occupational asthma). In, "Occlusive Lung Disorders." 2nd edition. Editor: W,R. Parkes, Butterworths, London, Boston, Sydney, Wellington, Durban and Toronto, 1982, pp. 358-414, |
| 11 | Pham, O. T., Cavelier, C., Mereau, P., Mur, J. M. and Cicolella, A.: Isocyanates and respiratory functions: a study of workers producing polyurethane foam moulding. Ann. Occup. Hyg., 21: 121-129, 1978, |
| 12 | Sangha, G. K. and Alarie, Y.: Sensory irritation by toluene diisocyanate in single and repeated exposures. Toxicol. and Appl. Pharmacol., 50: 533-547, 1979. |
| 13 | Tuberculosis Chemotherapy Centre: A concurrent expansion of isoniazid plus PAS with three-regimens of isoniazid alone in the domicilliary treatment of pulmonary tuberculosis in South India, Bull, World. Hlth. Org., 23: 535-585, 1960. |
| 14 | White, W. G., Morris, M. J., Sugden, E. and Zapata, E.: Isocyanate-induced asthma in a car factory. Lancet, 1: 756-760, 1980. |
| 15 | |
|
