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Prenatal exposure to a common pesticide linked with brain abnormalities

Virginia A. Rauh, et al. published in PNAS (Early Edition Articles) this week that prenatal exposure to chlorpyrifos (CPF), a widely-used organophosphate insecticide, is associated with neurobehavioral deficits in humans. 


WTF are CPF?

CPF have a shady history, to say the least, starting in 1965 (Dow Chemical Company) when CPF was first registered as a home and garden insecticide. In 2001, the Enivornmental Protection Agency (EPA) set regulatory action to phase out residential use; however, despite reports of chronic exposure to CPF being linked with neurological effects, developmental disorders, and autoimmune disorders – this product is still widely used in agriculture. 

For more history: go here


In high-doses CPF works by inhibiting acetylcholinesterase (AChE), an enzyme required to hydrolyze the neurotransmitter acetylcholine. AChE is important mainly to terminate synaptic transmission and inhibitors of AChE lead to muscular paralysis, convulsions, bronchial constriction, and death by asphyxiation. CPF, a class of organophosphates, are a class of irreversible AChE inhibitors. 


AChE mechanism of action. (via)



CPF are the same type of AChE inhibitors used in nerve gases during chemical warfare (ex: Sarin and Soman). High exposure (such as an insect on an apple) to AChE-inhibiting CPF will result in death, however humans receive only low doses. 


That begs the question:


What happens to animals and humans when exposed to "real" doses of CPF?

Me? (via)
Previous animal models (most likely carried out to assess exposure and safety) have shown that low-level exposure to CPF during developmental stages lead to developmental and neurobehavioral abnormalities. Developmentally-challenged neonatal rats anyone?


Interestingly, a very large component of the toxicity found in these studies is likely unrelated to the inhibition of AChE (yes, it does other horrible, nasty things in low-doses as well).
Instead, CPF additionally disrupt cellular machinery that control neuronal replication, differentiation, apoptosis, axon formation, synaptogenesis, and neural circuit formation – all of which sound pretty important for healthy development of a baby if you ask me. With this horrifying information, researchers have recently looked to study if low-levels of CPF exposure had similar consequences in children.


Unfortunately it is known that CPF is detectible in amniotic fluid and readily crosses the placental barrier, and prenatal exposures have been linked to smaller head sizes, lower birth weights, attention problems, and results in lower IQs (references all included in the primary article, let me know if you’d like it).


So what does this study show?

Despite all of this evidence for neurodevelopmental toxicity of CPF, specific effects on brain structure that could lead to behavorial or cognitive differences in humans, have not been studied.
Virginia A. Rauh, et al. was studying a cohort of children from 5.9-11.2 years of age that were prenatally exposed to low-doses of CPF. She found that this low-exposure to CPF caused damage in the brain regions that deal with mood, behavior and cognition (septal nucleus, striatum, somatosensory cortex, and hippocampus). 


This damage came in many forms including: general glial cell numbers (glial cells are non-neuronal cells that provide support and protection for neurons in the brain), changes in number and types of neurons, and delayed alterations in hippocampal cell number along with swelling and early stages of glial scarring (that occurs in response to cellular injury).


What does this mean for us?

In her discussion at the end of the article Virginia Rauh discusses the public health implications of her findings. She mentions that the neurotoxic effects are not only harmful in utero, but have long-term effects extending (at least) into the early school years. Additionally, these studies mimick previous animal model data, suggesting that the neural damage is irreversible.


The big and scary end of the story is that current safety limits are set according to levels needed to achieve inhibition of cholinesterase (mentioned above), because it has been long-assumed that only high-levels of CPF can cause toxicity. However, this study and previous animal studies have shown that low-levels of CPF result in neuronal damage (independent of inhibition of cholinesterase) that result in these horrifying brain abnormalities.


Therefore it’s high time we adjust “toxicity” levels of CPF based on something other than inhibition of cholinesterase. Either that or eat organic foods (that’s my only PSA for the year, I swear).


 -Brooke N.



ResearchBlogging.orgRauh, V., Perera, F., Horton, M., Whyatt, R., Bansal, R., Hao, X., Liu, J., Barr, D., Slotkin, T., & Peterson, B. (2012). Brain anomalies in children exposed prenatally to a common organophosphate pesticide Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.1203396109


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    Prenatal exposure to a common pesticide linked with brain abnormalities - Blog - Smaller Questions
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    In spite of the greater part of this confirmation for neuro developmental harmfulness of CPF, particular consequences for cerebrum structure that could prompt behavorial or intellectual contrasts in people, have not been mulled over.
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Reader Comments (3)

This is a great article, and a great topic to explore. Thanks for sharing.

May 5, 2012 | Unregistered CommenterHealth site

Pesticides have ill effects on human health and can cause damage to the brain too. CPFs are found to be harmful for animals and human beings that can even reach to the fetus brain and lower the size of brain and lessen the IQ level. I think the use of such pesticides should be banned and completely avoided in residential areas. eating organic food is the only option we are left with.

April 19, 2013 | Unregistered CommenterStephen Luther

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June 1, 2014 | Unregistered CommenterEssac

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