# Bhopal, Dunsmuir and TRPA1: what they have taught us about nociception

## TL;DR

This paper reviews two chemical exposure events and their connection to a pain-sensing ion channel, TRPA1, and how they help understand health risks from toxic chemicals.

## Contribution

The paper highlights how TRPA1's role in both Bhopal and Dunsmuir incidents provides new insights into irritant-induced health effects.

## Key findings

- Methyl isocyanate and methyl isothiocyanate both target the TRPA1 ion channel.
- The TRPA1 channel's activation explains the pathogenesis of irritant-induced asthma seen in these incidents.
- Understanding TRPA1's role can help anticipate and prevent long-term health effects from chemical exposures.

## Abstract

On separate occasions nearly a decade apart, two large-scale accidental releases of industrial chemicals exposed substantial “bystander” (non-worker) populations to highly toxic air pollutants. The first of these events, occurring in Bhopal, India in 1984, generated worldwide attention and concern given its geographic scope and significant lethality. The second incident, occurring in Dunsmuir, CA in 1991 – while less publicized – yielded new insights into the pathogenesis of irritant-induced asthma. Linking these events is the fact that the toxicants involved – methyl isocyanate (MIC) in Bhopal and methyl isothiocyanate (MITC) in Dunsmuir – preferentially bind to the same TRPA1 nociceptive ion channel. This review examines each of these exposure events, including their mechanistic implications for anticipating (and potentially preventing) future long-term health effects from accidental chemical exposures.