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Human Impact:

Organophosphates inhibit acetylcholinesterase (AChE), the enzyme that breaks down the neurotransmitter acetylcholine (ACh), resulting in a buildup of ACh. This build up has a detrimental effect on the nervous system, especially as it accumulates over time.

 

These effects vary from short-term physical responses to the poisoning to chronic disturbances in cognition and perception and irreversible birth defects.

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AChE inhibition leads to an increased amount of the neurotransmitter acetylcholine (ACh) in between nerve cells. This causes acetylcholine receptors on nerve cells to become overstimulated and fail to function properly. The physical effects of this disruption can be classified into three categories--muscarinic, nicotinic, and central nervous system.

 

Mild to moderate poisoning is associated with muscarinic symptoms, moderate to severe poisoning is associated with nicotinic and muscarinic symptoms, and cases of severe poisoning can result in all three categories of symptoms. In severe cases, the cause of death is most often respiratory failure. The onset time of these symptoms depends on many factors, notably level of exposure and time period over which the exposure occurs.

Nicotinic:

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Nicotinic responses are the result of disruption of nicotinic acetylcholine receptors. These receptors are found in nerve and muscle tissue throughout the body and are the main receptors that facilitate transfer of signals between muscle cells and nerve cells. Disruption of these signaling results in dysfunctional muscle contraction. Physical effects: Muscle weakness, Muscle spasms, Increased heart rate, Pupil dilation.

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Muscarinic:

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Muscarinic responses are the result of disruption of muscarinic acetylcholine receptors. These receptors facilitate signaling between ganglion, groups of nerve cells, in the parasympathetic nervous system. This section of the nervous system is associated with functions that occur while the body is at rest. Inhibition of these receptors disrupts functioning throughout the entire parasympathetic nervous system. Physical effects: Coughing/trouble breathing, Blurred vision, Uncontrolled urination/defecation, Skin discoloration, Nausea/Vomiting.

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Central Nervous System (CNS):

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CNS responses result from disruption of the central nervous system. The central nervous system is made up of the brain and the spinal cord, making it integral to many bodily functions. Physical effects: Insomnia, Anxiety, Headaches, Nightmares, Confusion, Tremor, Convulsion, Coma.

More Complicated Effects:

Birth defects:

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Numerous studies link birth defects to infants’ exposure to organophosphates while in the womb. One such study links birth defects in the brain, ears, eyes, heart, and genetalia to mothers’ exposure to chlorpyrifos during their pregnancy. These mothers were exposed to chlorpyrifos in a domestic context when it was still available for home use. However, chlorpyrifos in an agricultural context would almost certainly have similar effects on infants. Most studies on this topic only identify organophosphates as the cause of birth defects. Little is known about the exact mechanisms of disruption.

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Neurobehavioral effects:

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Because organophosphates target the nervous system, specifically the central nervous system, they can affect cognition and sensory capabilities. These responses are classified as neurobehavioral.

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A study published in 2017 monitored adolescent farm workers in Egypt for two years. They used a battery of neurobehavioral tests to assess the subjects’ memory, attention span, motor control, and visual abstraction abilities. They also monitored bio markers, compounds in the body indicative of organophosphate exposure over the sampling period. The results found higher levels of biomarkers in subjects with higher exposure, and overall decreased neurobehavioral performance in subjects with higher exposure. In addition to this correlation, researchers found that the subjects exposed to a higher concentration of the pesticide showed less improvement (from a learning effect) as they repeated the tests over the study. This is just one example of a plethora of studies with the similar findings. In fact, a review published in 2016 found that 24 out of 33 studies found an association with occupational exposure to organophosphates with neurophysical alterations which lead to neurobehavioral effects.  

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Another study published in the Journal of Neurotoxicology found that rats repeatedly exposed to chlorpyrifos demonstrated had altered functionality of the serotonergic nervous system and exhibited behavior associated with animal models of depression and anxiety.

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After reviewing recent literature it is clear that exposure to organophosphates results in neurobehavioral effects; however, most studies have not been able to identify the biological mechanisms for these abnormalities. This is due in part to the complexity of the brain and difficulty of observational studies on human subjects.

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Toxicity is age dependent:

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Intuitively, it makes sense that a toxin will have a larger effect on brains and bodies that are not fully developed. Numerous studies have found this to be the case with organophosphates.

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One such study was done in which rats of different ages were given oral doses of chlorpyrifos. Researchers found that the minimum dose that resulted in behavioral and chemical changes was five times greater in adult rats than in young rats (17 days old). Previous studies show that rats detoxify organophosphates with two classes of enzymes--carboxylesterases and A-esterases. It has also been found that young rats are deficient in both these enzymes.

 

This is a proposed reason that chlorpyrifos is significantly more toxic to young rats. The rat is the organism most often used to model human responses to pesticides. This method allows for more higher degree of experimental control and consistency than could be achieved by working with humans due to ethical limitations. However, results found with rats cannot be fully extrapolated to humans.  In any case insight to a mammal’s response to chlorpyrifos is integral to our understanding of how the pesticide affects humans.

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The effects are not equally distributed:

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The scientific findings clearly demonstrate that exposure to organophosphates is detrimental to human health. However, an analysis of the pesticides’ effect on humans would be incomplete without consideration of whom in the population is affected. The majority of studies conducted on human subjects monitor subjects in rural areas of countries in the global south--notably Ecuador, Thailand, and Egypt. This disproportionality in exposure levels is a demonstration of how worth is awarded to human lives disproportionally based on colonial power structures.

 

Historically colonized groups continue to be not only marginalized, but systematically exploited by groups that were historically colonizers. The fact that workers’ health is of little concern, and this exposure is in the context of the global agricultural system, which thrives on systematic exploitation, makes pesticide exposure a classic embodiment of colonial power dynamics. Clearly, this social dynamic exists on a global scale, but it is also very prevalent on a national scale in the US. The fact that the pesticide was banned for home use years ago, yet is still approved for agriculture is indicative of the way in which agricultural workers are regarded as less valuable than others in our national population. 

 

One literature review found that the United States and Thailand accounted for over half of the 25,000,000 reports of pesticide poisonings globally. This demonstrates that pesticide exposure is prevalent not only in countries of the global south, but also in the US. The EPA’s recent decision to reject the ban on chlorpyrifos will only solidify structurally oppressive power dynamics. Action against this decision appeals not only to ethical obligation to human life, but also to a utilitarian ethical standpoint. Banning this harmful substance will improve the overall wellbeing of our population.

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Social Impact:

“Chlorpyrifos, an organophosphate pesticide, is classified as a neurotoxin because it disrupts neurotransmission, essentially how brain cells communicate [1].”

When chlorpyrifos is metabolized, it forms a chemical that is more toxic. This chemical is called 3,5,6-trichloro-2-pyridinol (TCPy).

 

“Pregnant women in California who were exposed to organophosphates, and specifically chlorpyrifos, had up to a 60 percent increased risk for having children with autism spectrum disorders. . . [and] higher exposure was linked to mental development delays, attention problems, attention-deficit/hyperactivity disorder, and pervasive developmental problems in three-year-olds.

 

In two separate studies, the long-term effects of children with mental development delays are severe. Baker and colleagues concluded that children with cognitive delay exhibit greater behavioral problems than those without such delay. Behavioral problems, thus, caused by mental delay were a greater contribution to parental stress than cognitive delay. [2]

 

Dawson and colleagues specifically looked at the long-term effects of Autism Spectrum Disorder. They concluded that in fact “autism is associated with face recognition impairment that is manifest early in life [3].”

These long-term consequences of mental development delays suggest that affected children endure more social problems than those with normal mental development. Therefore, the link between Chlorpyrifos and children's social life is clear. The impact of Chlorpyrifos on mental health in children include social problems that could persist even after adulthood.

Human Impact (references):
  1. Carlock, L., Chen, L., Gordon, B., Killeen, C., Manley, A., Meyer, S., … Goethem, V. (1999). REGULATING AND ASSESSING RISKS OF CHOLINESTERASE-INHIBITING PESTICIDES: DIVERGENT APPROACHES AND INTERPRETATIONS. Journal of Toxicology and Environmental Health, Part B, 2(2), 105–160.

  2. https://www.sciencedirect.com/topics/neuroscience/nicotinic-acetylcholine-receptor

  3. Carlock, L., Chen, L., Gordon, B., Killeen, C., Manley, A., Meyer, S., … Goethem, V. (1999). REGULATING AND ASSESSING RISKS OF CHOLINESTERASE-INHIBITING PESTICIDES: DIVERGENT APPROACHES AND INTERPRETATIONS. Journal of Toxicology and Environmental Health, Part B, 2(2), 105–160.

  4. Carlock, L., Chen, L., Gordon, B., Killeen, C., Manley, A., Meyer, S., … Goethem, V. (1999). REGULATING AND ASSESSING RISKS OF CHOLINESTERASE-INHIBITING PESTICIDES: DIVERGENT APPROACHES AND INTERPRETATIONS. Journal of Toxicology and Environmental Health, Part B, 2(2), 105–160.

  5. Carlock, L., Chen, L., Gordon, B., Killeen, C., Manley, A., Meyer, S., … Goethem, V. (1999). REGULATING AND ASSESSING RISKS OF CHOLINESTERASE-INHIBITING PESTICIDES: DIVERGENT APPROACHES AND INTERPRETATIONS. Journal of Toxicology and Environmental Health, Part B, 2(2), 105–160.

  6. Janette D. Sherman M.D. (1996) Chlorpyrifos (Dursban) -Associated Birth Defects: Report of Four Cases, Archives of Environmental Health: An International Journal, 51:1, 5-8, DOI: 10.1080/00039896.1996.9935986

  7. Ismail, A. A., Wang, K., Olson, J. R., Bonner, M. R., Hendy, O., Rasoul, G. A., & Rohlman, D. S. (2017). The impact of repeated organophosphorus pesticide exposure on biomarkers and neurobehavioral outcomes among adolescent pesticide applicators. Journal of Toxicology and Environmental Health. Part A, 80(10-12), 542–555. http://doi.org.libproxy.berkeley.edu/10.1080/15287394.2017.1362612

  8. Muñoz-Quezada, M. T., Lucero, B. A., Iglesias, V. P., Muñoz, M. P., Cornejo, C. A., Achu, E., … Villalobos, M. (2016). Chronic exposure to organophosphate (OP) pesticides and neuropsychological functioning in farm workers: a review. International Journal of Occupational and Environmental Health, 22(1), 68–79. http://doi.org/10.1080/10773525.2015.1123848

  9. Wen-Qiang Chen, Li Yuan, Rui Xue, Yun-Feng Li, Rui-Bin Su, You-Zhi Zhang, Jin Li (2011). Repeated exposure to chlorpyrifos alters the performance of adolescent male rats in animal models of depression and anxiety. NeuroToxicology, Volume 32, Issue 4, Pages 355-361. https://doi.org/10.1016/j.neuro.2011.03.008.

  10. Padill, S., & Buzzard, J. (2000). Comparison of the role of esterases in the differential age-related sensitivity to chlorpyrifos and methamidophos. Neurotoxicology,21(1), 2nd ser., 49-56. Doi:10794384

  11. Vidair, C. A. (2004). Age dependence of organophosphate and carbamate neurotoxicity in the postnatal rat: Extrapolation to the human. Toxicology and Applied Pharmacology, 196(2), 287-302. doi:10.1016/j.taap.2003.12.016

  12. Levine, R. S., & Doull, J. (1992). Global Estimates Of Acute Pesticide Morbidity And Mortality. Reviews of Environmental Contamination and Toxicology, 29-50. doi:10.1007/978-1-4684-7106-9_3

Social Impact (references):
  1. http://civileats.com/2015/09/16/5-reasons-to-care-whether-the-epa-bans-chlorpyrifos-on-your-food/

  2. Bruce L. Baker, Jan Blacher, Keith A. Crnic, and Craig Edelbrock (2002) Behavior Problems and Parenting Stress in Families of Three-Year-Old Children With and Without Developmental Delays. American Journal on Mental Retardation: November 2002, Vol. 107, No. 6, pp. 433-444.

  3. Dawson, G. , Carver, L. , Meltzoff, A. N., Panagiotides, H. , McPartland, J. and Webb, S. J. (2002), Neural Correlates of Face and Object Recognition in Young Children with Autism Spectrum Disorder, Developmental Delay, and Typical Development. Child Development, 73: 700-717. doi:10.1111/1467-8624.00433

Photos by Kat Smith & Pexels

S Impact
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