ACHE and acute respiratory distress syndrome: There is increasing evidence that mechanisms other than AChE inhibition may contribute to the high toxicity of OP (Eyer et al. 2010; Xie et al. 2000), e.g. the formation of lung edema, tissue destruction and alterations in the immune response leading to an acute respiratory distress syndrome (Perkins et al. 2011; Lotti 2001).