Organophosphates are a class of insecticides like chlorpyrifos and soman. Sarin, used as a chemical weapon, is also an organophosphate. Many of these are neurotoxic, owing to their ability to amplify the neurotransmitter acetylcholine, which paralyzes insects and causes their death.
A recent study from medical researchers in Maryland and Pennsylvania described human toxicity from insecticide exposure in detail and explained why cannabinoids may be protective for humans. These toxic insecticides promoted a process called long-term depression (LTD), wherein the neural connections in a certain brain region are suppressed. Elevated levels of acetylcholine activate what are called muscarinic receptors, whose activity prompts endocannabinoid release, telling the neuron to calm down because its signal has been heard.
The researchers thought that endocannabinoid signaling might be dysregulated by organophosphates, allowing excessive neural activity and brain damage. When CB1 receptors were blocked, the harms were amplified — nearly all the pesticide-exposed mammals died within two hours.
This is worth noting, because a common pesticide synergist, piperonyl butoxide (PBO), is known to inhibit CB1 receptors.
PBO potentiates pesticides by strongly inhibiting cytochrome P450 enzymes, which slows pesticide metabolism in insects. But if the concentration is also high enough to block CB1 receptors, it may amplify their harms to humans as well.
California regulators have previously warned about the risks of organophosphate contamination on cannabis.
Read study: Retrograde activation of CB1R by muscarinic receptors protects against central organophosphorus toxicity
Adrian Devitt-Lee is a research scientist and longtime Project CBD contributor. © Copyright, Project CBD. May not be reprinted without permission.
