Acute toxicity of organophosphorus compounds

Morris, CM; Savy, C; Judge, SJ; Blain, PG

doi:10.1007/978-1-4471-5625-3_3

Acute toxicity of organophosphorus compounds

Lookup NU author(s): Dr Christopher Morris, Claire Savy, Dr Sarah Judge, Professor Peter Blain

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Abstract

© Springer-Verlag London 2014. Whilst a useful group of insecticides, organophosphorus (OP) pesticides represent a major cause of toxicity and mortality in individuals experiencing acute high-level exposure. The use of several OP compounds (OPs) with extremely high toxicity as chemical warfare agents has also highlighted the dangers of these compounds. OP toxicity is predominantly explained by their major mode of action in inhibiting the enzyme acetylcholinesterase (AChE) and promoting accumulation of the neurotransmitter acetylcholine, predominantly at peripheral nicotinic and muscarinic synapses. This promotes cholinergic hyperstimulation with pupillary miosis and lacrymation, hypersalivation, diarrhoea and loss of bladder control, bradycardia and bronchospasm being prominent features of muscarinic receptor stimulation. Nicotinic receptor hyperstimulation leads to muscle spasm and hypercontractions with eventual paralysis. Central nervous system effects are also present with confusion, nausea and dizziness with eventual coma and seizures and centrally mediated cardiac and respiratory arrest. An intermediate syndrome also occurs, which typically happens 24-96 h after an acute cholinergic crisis and is characterised by distal limb neuropathy and weakness, along with respiratory muscle paralysis requiring ventilatory support. Recovery is generally good following acute OP toxicity with appropriate medical support. There are, however, indications that even in the absence of acute symptoms, exposure to OPs at low levels may cause subtle central nervous system effects since several studies in humans have found nerve conduction and neuropsychiatric problems, notably depression and anxiety. This chapter will therefore discuss the signs and symptoms of acute OP toxicity and the physiological and pathological changes that follow.