Eddleston, Michael. "Organophosphorus and carbamate pesticides."
- Organophosphorus (OP) or carbamate poisoning cannot be considered as homogenous single entities since there are significant intra-class differences between pesticides.
- Result in highly variable clinical syndromes, response to therapy, and outcome.
- Important to determine which of the 100-200 OP or carbamate pesticides has caused the poisoning.
- Many OP pesticides have a sulphur atom attached to the phosphorus atom (P=S) and are termed thions. This sulphur must be replaced with an oxygen (P=O) to make the active oxon. OP pesticides already in the oxon form (eg. monocrotophos) are active as soon as they are absorbed; thion OPs must be activated by enzymes in the gut wall or liver. The speed of onset of poisoning therefore depends upon whether the OP is an oxon or, if not, how quickly the thion is converted to an oxon. For some thion OPs (eg. methylparathion), this is extremely quick with symptoms occurring within minutes; for others (such as dimethoate) it can be relatively slow and take hours.
- Carbamates do not need activating and therefore cause symptoms relatively quickly.
- Most OPs can be divided into two groups based on their chemical structure:
- those with two [-O-CH3] groups (dimethyl OPs)
- those with two [-O-C2H5] groups (diethyl OPs) attached to the phosphorus
- a few have atypical side groups (eg [-S-C3H7] in profenofos).
- classification is important for determining responsiveness to oximes.
- Marked variation in fat solubility of the OPs.
- Some are very soluble (log Kow of 4.0-5.0; eg. fenthion)
- rapidly distributed into fat and leach out slowly over days. This can result in mild or absent acute cholinergic features on admission with subsequent cholinergic crises as OP comes out of the fat
- Others relatively insoluble (log Kow <1.0; eg. dimethoate)
- small volumes of distribution producing high blood OP concentrations. These will reduce the effectiveness of oximes
view full text here