Sequential respiratory, psychologic, and immunologic studies in relation to methyl isocyanate exposure over two years with model development.

Abstract

Of 113 methyl isocyanate (MIC)-exposed subjects studied initially at Bhopal, India, 79, 56, 68, and 87 were followed with clinical, lung function, radiographic, and immunologic tests at 3, 6, 12, 18, and 24 months. Though our cohort consisted of subjects at all ages showing a varied severity of initial illness, fewer females and young subjects were seen. Initially all had eye problems, but dominant symptoms were exertional dyspnea, cough, chest pain, sputum, and muscle weakness. A large number showed persistent depression mixed with anxiety, with disturbances of personality parameters. The early radiographic changes were lung edema, overinflation, enlarged heart, pleural scars, and consolidation. The persistent changes seen were interstitial deposits. Lung functions showed mainly restrictive changes with small airway obstruction; there was impairment of oxygen exchange. Oxygen exchange improved at 3-6 months, and spirometry improved at 12 months, only to decline later. The expiratory flow rates pertaining to large and medium airway function improved, but those for small airways remained low. There were changes of alveolitis in bronchoalveolar lavage fluid on fiber optic bronchoscopy, and in 11 cases positive MIC-specific antibodies to IgM, IgG, and IgE were demonstrated. On follow up, only 48% of the subjects were clinically stable, while 50% showed fluctuations. Thirty-two percent of the subjects had lung function fluctuations. Detailed sequential behavior over 2-4 years was predicted for dyspnea, forced vital capacity, maximum expiratory flow rate (0.25-0.75), peak expiratory flow rate, VO2, and depression score. A model for clinical behavior explained a total variance of 52.4% by using the factors of cough, PCO2 and X-ray zones in addition to above five parameters. The behavior of the railway colony group (1640 patients) revealed a similar pattern of illness. When this observed pattern of changes was transferred to the affected Bhopal city sections (with an equitable age-sex distribution), our model results were again validated. Thus the picture of MIC-induced disease seems similar despite the differences for age-sex and initial severity of illness in our cohort and in the population of Bhopal city as predicted by our model.ImagesFIGURE 1.FIGURE 2.

Respiratory morbidity 10 years after the Union Carbide gas leak at Bhopal: a cross sectional survey

“…They did not attempt to correlate their findings with a measure of exposure. Kamat and colleagues followed 113 subjects who had been initially admitted to hospital 12. Over two years they found no improvement in respiratory symptoms or in basic spirometry, but 42% of the group had evidence consistent with deteriorating small airways function.…”

Persistent effects of chlorine inhalation on respiratory health

“…Hundreds of thousands of people were exposed to methyl isocyanate as a result of an accidental release in Bhopal, India in 1984. Long‐term follow‐up of this population was difficult, but some evidence was obtained for persistent effects, such as respiratory symptoms, lung function impairment (including both obstructive and restrictive changes), inflammation, and histological abnormalities (including airway inflammation and fibrosis) . Animal studies have shown long‐lasting effects of acute methyl isocyanate exposure on airway structure .…”

Methyl Isocyanate

“…It would thus appear that the lethal effects of MIC were caused by pulmonary complications. It was also found that a single exposure to MIC can produce long-lasting pulmonary complications (Ferguson and Alarie, 1991;Kamat et al, 1992;ICMR, 2004).…”

“…Since the prevalence of compromise in lung function was higher in the population closer to the Union Carbide plant than in the population farther away, it is very likely that this occurred as a result of exposure to the toxic gases rather than preexisting bronchitis, tuberculosis, or emphysema. A follow-up of 113 exposed patients revealed worsening of pulmonary symptoms 2 years later, forced expiratory flow (FEF) between FEF 25% and FEF 75% of forced vital declined progressively over a 2-year period (Kamat et al, 1985(Kamat et al, , 1992Patel et al, 1987), a 1-to 7-year period (Vijayan et al, 1989;Vijayan and Kuppurao, 1993;Vijayan and Sankaran, 1996) and a 10-year period (Acquilla et al, 1996;. Likewise, other researchers have found a direct relationship between pulmonary function compromise and inflammatory alveolitis and the severity of exposure (Vijayan et al, 1989).…”