Alexander Law Group, LLP represents two children who suffer from autism, a disorder of neural development. The signs of autism are loss of social interaction and communication, and repetitive behavior. Autism impact information processing by changing how brain cells connect.
During her pregnancies in the 1990s, the mother of these children worked applying pesticides and was regularly exposed to Dursban, a pesticide manufactured by Dow AgroSciences.
The EPA finally banned retail sales of Dursban in 2002, but that was decades after this chemical was known to cause birth defects.
Alexander Law Group, LLP retained Dr. Theodore A. Slotkin to explain these disabling personal injuries were caused by in utero to Dursban.
Dr. Slotkin is a professor at Duke University Medical Center where he is a Professor of Pharmacology and Neurobiology, and is the Director of Graduate Studies in toxicology. He is recognized as one of the top 1% of cited scientists in the fields of pharmacology and toxicology.
At Duke, Dr. Slotkin oversees the training of students and postdoctoral fellows, and conducts research on the interaction of toxicants, drugs and hormones with developing organisms, emphasizing the fetal and neonatal nervous systems.
Dr. Slotkin has published over one hundred articles on the topic of the developmental toxicity of organophosphate insecticides, the majority of which concern chlorpyrifos.
The following information was provided by Dr. Slotkin and is shared on this website to advance the public understanding of how pesticides and insecticides cause birth defects. Any errors are mine.
The overwhelming consensus of the reported animal and human data from investigators who are independent of Dow AgroSciences is that chlorpyrifos and other organophosphates cause cellular brain damage to the developing animal fetus and newborn, leading to many abnormalities.
Animal studies have detailed damage to specific areas of the brain involved in learning and memory, as well as in emotional function, leading to defective cognitive capacity and affective disorders in children and adults exposed to organophosphates, including chlorpyrifos.
The neurotoxicity of organophosphates has been known for over fifty years, and the higher susceptibility of the developing brain to disruption by toxicant chemicals in general has been known for over forty years.
This vulnerability reflects the complexity of brain development, which involves a carefully-coordinated series of architectural, biochemical and molecular events occurring over a long span, that ultimately involve formation of millions of neural circuits that comprise the mature brain; consequently, even transient interference with the basic processes of brain development can have devastating consequences that may not emerge until much later in life, as neural circuits form.
The majority of studies in animal models of developmental organophosphate intoxication involve exposures below those necessary to elicit any notable symptoms of poisoning.
Chlorpyrifos has received the most attention in this regard. However where other organophosphates have been evaluated in a developmental context, their effects are generally similar to those of chlorpyrifos.
Chlorpyrifos interferes with the ability of developing nerve cells to reproduce themselves and also provokes a reaction called “apoptosis” that results in neural cell death. As development proceeds, neurons (the brain cells that actually communicate information) normally lose their ability to replicate, so that early deficiencies in the number of neurons can never be made up.
This is one of the main reasons that chlorpyrifos exposure during brain development elicits permanent deficits; similarly, since these effects alter the trajectory of brain development, adverse consequences continue to emerge later on, after a period of apparent normality.
These developmental effects converge to produce a syndrome where brain cells are permanently lost, where synaptic connections are missing or mis-wired, and where activity of neural pathways critical to cognitive and emotional are permanently damaged. Because chlorpyrifos misdirects the development of the brain, many of these defects can emerge after a period of apparent normality.
Studies of animals exposed to chlorpyrifos in the neonatal period indicate persistent deficits in cognitive function, as demonstrated by tests of memory performance. These effects are detectable as deficiencies in the rate of learning, but are even more notable under conditions in which the animals are challenged to respond.
In addition to impairing learning and memory, the developmental exposure to chlorpyrifos impairs the ability of the brain to adapt to changing conditions. Developmental exposure to chlorpyrifos affects emotional behaviors, evokes hyperactivity and impairs the ability to carry out social interactions. These characteristics for animal behaviors in the cognitive, emotional and social domains, all have parallel components for pervasive developmental disorders, autism and ADHD in humans.
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