Neurotoxic effects, delayed-onset

Subchronic delayed neurotoxicity The repeated daily administration of a test substance or chemical causing adverse effects, such as delayed onset of locomotor ataxia. 

Meyer A, Seidler FJ, Slotkin TA (2004) Developmental effects of chlorpyrifos extend beyond neurotoxicity Critical periods for immediate and delayed onset effects on cardiac and hepatic cell signaling. Environ Health Perspect, 112(2) 170-178. 

This patient had taken ecstasy 10 times during the year before, the last time about 3 months before the onset of symptoms. Apart from marijuana, he denied using other substances. He was treated with maximal tolerable doses of levodopa and pramipexole, without improvement. The authors reported that they had no explanation for this patient s symptoms, other than the use of ecstasy. They felt that the parkinsonian symptoms most closely resembled MPTP-induced parkinsonism. They further postulated that this could be a delayed neurotoxic effect of ecstasy in the substantia nigra and striatum and could have occurred as a result of neuronal damage by free radicals. 

Static test A test nsing aqnatic organisms in which there is no flow of the test solution. The test solution remains unchanged throughout the period of testing STEL Short-term exposure limit—the maximum amount of the test chemical substance to which a worker may be exposed for 15 minutes Subchronic delayed neurotoxicity The repeated daily administration of a test chemical substance causing adverse health effects such as delayed onset of locomotor ataxia... 

The subcommittee considered other possible toxicity end points, notably neurotoxicity, associated with GD exposure. Organophosphate compounds like GD may act directly on nerve cell receptors or, by inhibiting neural AChE, interfere with neuromuscular transmission and produce delayed-onset subjunctional muscle damage. In addition, some organophosphate compounds cause a neurotoxic effect (organophosphate-induced delayed neuropathy, or OPIDN) that is not associated with ChE inhibition. Emerging research in this area might indicate alternative... 

The development of severe neurotoxic or severe extrapyramidal adverse effects with comhinations of antipsychotics and lithium appears to be uncommon and unexplained but be alert for any evidence of toxicity if lithium is given with any of these drugs. One recommendation is that the onset of neurological manifestations, such as excessive drowsiness or movement disorders, warrants electroencephalography without delay and withdrawal of the drugs, especially as irreversible effects have been seen. A review suggests that the concurrent use of haloperidol seems to be safe if lithium levels are helow 1 mmol/L. It is not known whether this also applies to other antipsychotics. 

The time between exposure to a chemical and onset of toxic effects varies depending on the chemical and the exposure. For example, the toxic effects of carbon monoxide, sodium cyanide, and carbon disulfide are evident within minutes. For many chemicals, the toxic effect is most severe between one and a few days after exposure. However, some chemicals produce "delayed" toxicity in fact, the neurotoxicity produced by some chemicals is not observed until a few weeks after exposure. The most delayed toxic effect produced by chemicals is cancer in humans, it usually takes 10 to 30 years between exposure to a known human carcinogen and the detection of a tumor. 

---