Most of the individual and/or amalgamated compounds present in the atmospheric air are not known for their toxicologic potential and impact on human health. The toxicologic strength of methyl isocyanate (MIC) gas was unknown till its accidental leakage that instantly claimed thousands of lives. Cytogenetic study showed increased chromosome aberrations (CA) and sister chromatid exchanges (SCEs) and delayed cell replication index (RI) in a multicentre genetic screening program on gas victims immediate post-disaster. A surveillance study after 30 years displayed reduction in CA compared to the initial status in survivors of the severely and moderately exposed strata. Altogether, cytogenetic damage was significantly predominant in the severely exposed population. Stable and replicable aberrations and chromatid exchanges were detected in both studies, which collectively indicate genetic instability. The variation in individual cytogenetic spectrum from similar exposure status could be the result of inter-individual response to the external factors over 30 years post-disaster. The spectrum of CA detected after 30 years might be the cumulative effect of occupational, environmental and life-style factors at a background of one episode of acute MIC exposure. Had MIC's toxicologic potential was known before, fatality and health effects could have been averted. In vitro assessment of toxicity of tin showed a positive correlation with dose and age of exposure, which was aggravated by smoking. Age has shown a significant effect on CA in the general population. The present report recommends evaluation of toxicity prior to use, and reduction of pollution at source for a maintaining a sustainable environmental context.
Keywords: Cytogenetic alterations in MIC gas victims; Cytogenetic effects of tin; Environmental pollution; Methyl isocyanate (MIC).
© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.