Organohalogen compounds, such as dioxins, are commonly found in pesticides or created as byproducts of pesticide manufacturing or degradation. These compounds can have a significant impact on the neurobiology of exposed organisms. Some effects observed from dioxin exposure are altered intracellular astroglial calcium (Ca2+) ions, low glutathione levels, modified neurotransmitter function in the CNS, and loss of pH maintenance.[10] A study conducted between 1965 and 1968 of 350 employees of a chemical plant, exposed to a dioxin precursor for the synthesis of herbicides, showed that 80 of those employees showed signs of poisoning by the dioxins.[11] Of these 350 employees, 15 were contacted in 2004 to submit neurological examinations to assess whether dioxin poisoning had any long-term effects on neurological abilities. The amount of time that had passed made it difficult to assemble a larger cohort, however test results indicated that eight of the 15 subjects showed some central nervous system impairment, nine presented signs of polyneuropathy, and the electroencephalogram (EEG) showed varying degrees of structural abnormalities. This study suggests that the effect of dioxins was not limited to initial toxicity. Dioxins, through neuroplastic effects, can cause long-term damage, which may not manifest for years or even decades.

La exposición a metales puede resultar en un aumento del riesgo de varias enfermedades neurológicas. Las investigaciones indican que los dos metales pesados más neurotóxicos son el mercurio "Mercurio (elemento)") y el plomo. El efecto que estos dos metales tendrán depende mayormente del individuo debido a variaciones genéticas. El mercurio y el plomo son particularmente neurotóxicos debido a muchas razones: pueden atravesar fácilmente las membranas celulares, tienen efectos oxidativos en las células, reaccionan con azufre en el cuerpo (dando lugar a alteraciones en las diversas funciones que dependen de los grupos sulfhidrilo), y reducen los niveles de glutatión dentro de las células. El Metilmercurio, particularmente, tiene una extrema afinidad por los grupos sulfhidrilo.[12]​ El organomercurio es una forma característica perjudicial del mercurio por su alta capacidad de absorción.[13]​ El plomo también imita al calcio, un mineral muy importante en el SNC, y este mimetismo conduce a muchos efectos adversos.[14]​ Los mecanismos neuroplásticos del mercurio trabajan al afectar a la producción de proteínas. Un nivel elevado de mercurio incrementa los niveles de glutatión al afectar la expresión génica, y esto en consecuencia afecta dos proteínas (MT1 y MT2-2) que están contenidas en los astrocitos y neuronas.[15]​ La habilidad del plomo por imitar al calcio le permite cruzar la barrera hetamoencefálica. El plomo también retroalimenta positivamente al glutatión.[16]​.

Autism

Exposure to heavy metals, combined with certain genetic predispositions, can put individuals at risk of developing autism. Many examples of CNS pathophysiology, such as oxidative stress, neuroinflammation, and mitochondrial dysfunction, could be byproducts of environmental stressors such as pollution. Cases of autism outbreaks occurring in specific locations have been reported. Since these cases of autism are related to geographic location, the implication is that something in the environment is complementing a risk genotype that causes autism in these vulnerable individuals. Both mercury and Lead contributes to inflammation, leading scientists to speculate that these heavy metals could play a role in autism. These results are controversial, however, a significant number of researchers think that the increased rates of autism are a consequence of screening and diagnostic methods, and are not due to any type of environmental factor.[19]​.

Neuroinflammation is associated with increased rates of neurodegeneration.[20] Inflammation tends to increase naturally with age. Consequently, by facilitating inflammation, pollutants such as air particles and heavy metals cause faster aging of the CNS. Many late-onset diseases are caused by neurodegeneration. Diseases such as multiple sclerosis, Parkinson's disease, amyotrophic lateral sclerosis (ALS), and Alzheimer's disease are believed to be aggravated by inflammatory processes, resulting in individuals showing symptoms of the diseases at an earlier age than expected.[20]​.

Multiple sclerosis occurs when chronic inflammation leads to the compromise of oligodendrocytes, which in turn leads to the destruction of myelin sheaths. Consequently, the axons begin to exhibit signs of damage, which leads to the death of the neurons. Multiple sclerosis has been correlated to living in areas with high levels of suspended particles.[21]​.

In Parkinson's disease, inflammation, which leads to a depletion of antioxidant reserves, will ultimately lead to the degeneration of dopaminergic neurons; causing a shortage of dopamine and contributing to the formation of Parkinson's disease. Chronic glial activation as a result of inflammation causes the death of motor neurons and compromises astrocytes; These factors lead to the symptoms of amyotrophic lateral sclerosis (ALS, aka Lou Gehrig's disease).

In the case of Alzheimer's, inflammatory processes lead to neuronal death by inhibiting growth in axons and activating astrocytes that produce proteoglycans. This product can only be deposited in the hippocampus "Hippocampus (anatomy)") and cortex, indicating that this may be the reason why these two areas show the highest levels of degeneration in Alzheimer's disease.[22] It has been shown that airborne metal particles can directly access and affect the brain through the olfactory pathways, allowing a large amount of particulate material to reach the barrier. hematoencephalic.[23]​.

These facts, together with the relationship of air pollution to neurofibrillary tangles and vascular changes observed in dogs, suggest that the negative neuroplastic effects of pollution may result in an increased risk for Alzheimer's disease, and may also implicate pollution as the cause of early-onset Alzheimer's through multiple mechanisms. The overall effect of pollution is to increase inflammation levels. As a result, pollution can significantly contribute to different neurological disorders that are caused by inflammatory processes.

Organohalogen compounds, such as dioxins, are commonly found in pesticides or created as byproducts of pesticide manufacturing or degradation. These compounds can have a significant impact on the neurobiology of exposed organisms. Some effects observed from dioxin exposure are altered intracellular astroglial calcium (Ca2+) ions, low glutathione levels, modified neurotransmitter function in the CNS, and loss of pH maintenance.[10] A study conducted between 1965 and 1968 of 350 employees of a chemical plant, exposed to a dioxin precursor for the synthesis of herbicides, showed that 80 of those employees showed signs of poisoning by the dioxins.[11] Of these 350 employees, 15 were contacted in 2004 to submit neurological examinations to assess whether dioxin poisoning had any long-term effects on neurological abilities. The amount of time that had passed made it difficult to assemble a larger cohort, however test results indicated that eight of the 15 subjects showed some central nervous system impairment, nine presented signs of polyneuropathy, and the electroencephalogram (EEG) showed varying degrees of structural abnormalities. This study suggests that the effect of dioxins was not limited to initial toxicity. Dioxins, through neuroplastic effects, can cause long-term damage, which may not manifest for years or even decades.

La exposición a metales puede resultar en un aumento del riesgo de varias enfermedades neurológicas. Las investigaciones indican que los dos metales pesados más neurotóxicos son el mercurio "Mercurio (elemento)") y el plomo. El efecto que estos dos metales tendrán depende mayormente del individuo debido a variaciones genéticas. El mercurio y el plomo son particularmente neurotóxicos debido a muchas razones: pueden atravesar fácilmente las membranas celulares, tienen efectos oxidativos en las células, reaccionan con azufre en el cuerpo (dando lugar a alteraciones en las diversas funciones que dependen de los grupos sulfhidrilo), y reducen los niveles de glutatión dentro de las células. El Metilmercurio, particularmente, tiene una extrema afinidad por los grupos sulfhidrilo.[12]​ El organomercurio es una forma característica perjudicial del mercurio por su alta capacidad de absorción.[13]​ El plomo también imita al calcio, un mineral muy importante en el SNC, y este mimetismo conduce a muchos efectos adversos.[14]​ Los mecanismos neuroplásticos del mercurio trabajan al afectar a la producción de proteínas. Un nivel elevado de mercurio incrementa los niveles de glutatión al afectar la expresión génica, y esto en consecuencia afecta dos proteínas (MT1 y MT2-2) que están contenidas en los astrocitos y neuronas.[15]​ La habilidad del plomo por imitar al calcio le permite cruzar la barrera hetamoencefálica. El plomo también retroalimenta positivamente al glutatión.[16]​.

Autism

Exposure to heavy metals, combined with certain genetic predispositions, can put individuals at risk of developing autism. Many examples of CNS pathophysiology, such as oxidative stress, neuroinflammation, and mitochondrial dysfunction, could be byproducts of environmental stressors such as pollution. Cases of autism outbreaks occurring in specific locations have been reported. Since these cases of autism are related to geographic location, the implication is that something in the environment is complementing a risk genotype that causes autism in these vulnerable individuals. Both mercury and Lead contributes to inflammation, leading scientists to speculate that these heavy metals could play a role in autism. These results are controversial, however, a significant number of researchers think that the increased rates of autism are a consequence of screening and diagnostic methods, and are not due to any type of environmental factor.[19]​.

Neuroinflammation is associated with increased rates of neurodegeneration.[20] Inflammation tends to increase naturally with age. Consequently, by facilitating inflammation, pollutants such as air particles and heavy metals cause faster aging of the CNS. Many late-onset diseases are caused by neurodegeneration. Diseases such as multiple sclerosis, Parkinson's disease, amyotrophic lateral sclerosis (ALS), and Alzheimer's disease are believed to be aggravated by inflammatory processes, resulting in individuals showing symptoms of the diseases at an earlier age than expected.[20]​.

Multiple sclerosis occurs when chronic inflammation leads to the compromise of oligodendrocytes, which in turn leads to the destruction of myelin sheaths. Consequently, the axons begin to exhibit signs of damage, which leads to the death of the neurons. Multiple sclerosis has been correlated to living in areas with high levels of suspended particles.[21]​.

In Parkinson's disease, inflammation, which leads to a depletion of antioxidant reserves, will ultimately lead to the degeneration of dopaminergic neurons; causing a shortage of dopamine and contributing to the formation of Parkinson's disease. Chronic glial activation as a result of inflammation causes the death of motor neurons and compromises astrocytes; These factors lead to the symptoms of amyotrophic lateral sclerosis (ALS, aka Lou Gehrig's disease).

In the case of Alzheimer's, inflammatory processes lead to neuronal death by inhibiting growth in axons and activating astrocytes that produce proteoglycans. This product can only be deposited in the hippocampus "Hippocampus (anatomy)") and cortex, indicating that this may be the reason why these two areas show the highest levels of degeneration in Alzheimer's disease.[22] It has been shown that airborne metal particles can directly access and affect the brain through the olfactory pathways, allowing a large amount of particulate material to reach the barrier. hematoencephalic.[23]​.

These facts, together with the relationship of air pollution to neurofibrillary tangles and vascular changes observed in dogs, suggest that the negative neuroplastic effects of pollution may result in an increased risk for Alzheimer's disease, and may also implicate pollution as the cause of early-onset Alzheimer's through multiple mechanisms. The overall effect of pollution is to increase inflammation levels. As a result, pollution can significantly contribute to different neurological disorders that are caused by inflammatory processes.