Still working (when time permits) on the question of somehow consolidating the chronic toxicity studies, brought up late last year. The focus has been on neonics, but I came across a very interesting article (excerpted below) detailing symptoms of delayed toxic effects of organophosphates on mammals. The toxic mechanism is neuro-specific, in that an enzyme called "neurotoxic esterase" present in neurons becomes phosphorylated (read "disabled") upon exposure. This results in slow death of the neurons, starting at their distal tips (the part furthest from the cell bodies).
Excerpt below is from:
Perdrizet, J.A., J.F. Cummings, and A. de Lahunta. 1985. Presumptive organophosphate-induced delayed neurotoxicity in a paralyzed bull. The Cornell Veterinarian, vol. 75, no. 3 pp 401-410
(first part of paper described clinical signs...paresis, etc....and then neuropathology indicating extensive spinal degeneration and other neurological deterioration)
The paper's discussion is fully supported by references but I'm not typing them all in here. If someone wants a specific citation just contact me and I'll send it to you.
Discussion:
"This delayed form of neurotoxicity has been reported for various forms of triaryl organophosphates. Clinical signs usually occur 1 to 3 weeks after acute exposure to the intoxicant and after a more uncertain interval following chronic exposure. These triaryl phosphates are found in hydraulic oils, gasoline additives, flame retardants, plasticizers, pesticides and anthelmintics. Triorthoresyl phosphate is the most common form implicated clinically in cattle and has been studied extensively in cats. Haloxon, an aryl phosphate anthelmintic, has produced delayed neurotoxicity in pigs and sheep. A genetic susceptibility has been recognized in Suffolk sheep that have reduced levels of a plasma esterase that can hydrolyze the organophosphate ester before it acts as an intoxicant. The mechanism of the delayed neurotoxicity is presently thought to involve binding of phosphorylation sites on a discrete protein enzyme referred to as neurotoxic esterase and present in neuronal cell bodies and axons. ...... Because of the nature and distribution of the lesions, the history and environment of this bull were explored further for a possible exposure to organophosphates. The owner recalled that 43 days before the onset of clinical signs in this bull, most all the cattle on the farm had been treated with an aryl organophosphate insecticide...famphur (Warbex). .....The animals treated included 31 adult cows, 6 yearling heifers, 29 calves and 3 young bulls. The latter included the affected bull. The other 2 bulls of similar age were unaffected. This was the first time this insecticide had been used on this farm. Although there are studies to support the safety and efficacy of famphur in cattle, it has been observed that there is a greater sensitivity of cattle of the Brahman breed than European breeds to higher dosages of the drug and that bulls are more sensitive than heifers or steers. However, these studies only document the acute form of toxicity and not a delayed neurotoxicity. It is recognized that the delay in onset of clinical signs in this bull is more than usual."
I submit that there are many parallels between this delayed form of neurotoxicity, that strikes some animals and not others, with the delayed forms of toxicity being documented in bees. In the case of the neonics, the neurons are presumably dying because they are stressed by neonic binding to AChR. This wears them out prematurely, and that is the point....it is how neonics are used to kill insects (acutely or chronically). There are papers documenting that the immune responses of bees are suppressed after neonic exposure, making them more susceptible to viruses etc. I have not seen a mechanism proposed for this claim, however we do know that colony behavior forms a large part of the honeybee's "immune system" because it is through colony behavior that many pests and diseases are suppressed by the bees...and behavior is a role of the nervous system.
Food for thought.
Christina
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