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Individual differences |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |
Biological: Behavioural genetics · Evolutionary psychology · Neuroanatomy · Neurochemistry · Neuroendocrinology · Neuroscience · Psychoneuroimmunology · Physiological Psychology · Psychopharmacology (Index, Outline)
Recent research indicates that living in areas of high pollution has serious long term implications. Living in these areas during childhood and adolescence can lead to diminished mental capacity and increased risk for brain damage. People of all ages who live in high pollution areas for extended periods place themselves at increased risk for various neurological disorders. Both air pollution and heavy metal pollution have been implicated as having negative effects on central nervous system functionality. Pollution's ability to affect individuals' neurophysiology after central nervous system structure is fairly stabilized is an example of negative neuroplasticity.
Air pollution is known to have serious vascular effects throughout the body; high levels of air pollution are associated with increased risk for strokes and heart attacks. By permanently affecting vascular structure in the brain, air pollution can have serious effects on neural functioning. Air pollution can also seriously affect neural matter. Currently, air pollution is known to cause damage to the central nervous system by altering the blood-brain barrier, causing neurons in the cerebral cortex to degenerate, destroying glial cells found in white matter, and by causing neurofibrillary tangles . These changes can permanently alter brain structure and chemistry, resulting in various impairments and disorders. Sometimes, the effects of neural remodeling do not manifest for a prolonged period of time.
Effects in adolescents and caninesEdit
A recent study from 2008 compared children and dogs raised in Mexico City, an area known for its high pollution, with children and dogs raised in Polotitlán, a city whose pollution levels meet the current USA National Ambient Air Quality Standards. According to this study, children raised in areas of higher pollution scored lower on IQ tests and showed signs of brain lesions when they underwent an MRI. The children from the low pollution area scored as expected on IQ tests and did not show any signs of being significantly at risk for brain lesions. This correlation was found to be statistically significant and shows that there is a relation between pollution levels and brain lesion formation and also a relation between IQ scores and pollution levels. The implication of these findings is that high pollution levels contribute to brain lesion formation which in turn manifests visibly as impaired intellectual capability. Living in high pollution areas thus places adolescents at risk of premature brain degeneration and improper neural development; these findings could have significant implications for future generations. Dogs which spent their lives in high pollution areas showed signs of restructured blood flow in the subcortical region of their brains when compared to dogs living in low pollution areas. The kind of restructuring that was observed was similar to that seen in Alzheimer's patients, suggesting that air pollution could possibly increase an individual's risk for Alzheimer's Disease or speed up the rate at which the disease progresses in already afflicted individuals. Unfortunately, it is impossible to be certain that the difference in lesion formation is only due to pollution; other variations between the two tested locations could serve as confounding factors leading to incorrect conclusions; correlation does not imply causation.
Researchers in Chile found statistically significant correlations between multiple air pollutants and risk for epilepsy using a 95% confidence interval. These air pollutants that the researchers attempted to correlate with increased incidence of epilepsy were Carbon Monoxide, Ozone, Sulfur Dioxide, Nitrogen Dioxide, large particulate matter, and fine particulate matter. The researchers tested these pollutants across seven cities; in all but one case a correlation was found between pollutant levels and the occurrence of epilepsy. All of the correlations found were shown to be statistically significant. The researchers hypothesize that air pollutants increase epilepsy risk by providing inflammatory mediators and providing a source of oxidative stress. They believe that these changes eventually alter the functioning of the blood-brain barrier, causing brain inflammation. Brain inflammation is known to be a risk factor for epilepsy; thus this sequence of events provides a plausible mechanism by which pollution may increase epilepsy risk in individuals who are genetically vulnerable to the disease.
Organohalogen compounds, commonly used in pesticides, can have significant impacts on neurobiology. Some observed effects of Dioxin exposure are altered astroglial intracellular Ca2+, decreased Glutathione levels, modified neurotransmitter functions in the central nervous system, and loss of pH maintenance . A study on 350 chemical plant employees exposed to a dioxin precursor for herbicides between 1965 and 1968 showed that 80 of the employees displayed signs of initial dioxin poisoning  15 of these 350 employees were contacted once again in 2004 to come in for neurological tests to assess whether the dioxin poisoning had any long term effects on neurological capability. The amount of time that had passed made it difficult to assemble a larger cohort. The results of the tests indicated that 8 of the 15 subjects exhibited central nervous system impairment and 9 showed signs of polyneuropathy. Electroencephalography showed various degrees of structural abnormalities. This study showed that the effects of dioxins were not limited to initial dysfunction. Dioxins, through neuroplastic effects, can cause long term damage that may not exhibit for years.
Heavy metal exposure can result in increased risk for various neurological diseases. Current research indicates that the two most neurotoxic heavy metals are mercury and lead. The impact that these two metals will have is highly dependent upon the individual. This is due to genetic variation amongst individuals. There are many reasons that mercury and lead are particularly neurotoxic. Mercury and lead easily cross cell membranes and have oxidative effects on cells; both metals also react with sulfur in the body leading to disturbances in the many bodily functions that rely upon sulfhydryl groups and reduce glutathione levels inside cells. Methylmercury, in particular, has an extremely high affinity for sulfhydrl groups.. Organomercury is a particularly damaging form of mercury because of its high absorbability  Lead also mimics calcium, a very important mineral in the central nervous system. This mimicry has many adverse effects upon the central nervous system . Mercury's neuroplastic mechanisms work by affecting protein production. Elevated mercury levels increases glutathione levels by affecting gene expression and this in turn affects two proteins, MT1 and MT2, that are contained in astrocytes and neurons. Lead's ability to imitate Calcium allows it to cross the blood-brain barrier. Lead also upregulates glutathione .
Heavy metal exposure, when combined with certain genetic predispositions, can place individuals at increased risk for developing autism. Many examples of central nervous system pathophysiology, such as oxidative stress, neuroinflammation, and mitochondrial dysfunction, could be byproducts of environmental stressors such as pollution. There have been reports of autism outbreaks occurring in specific locations . Since these cases of autism are related to geographic location, the implication is that something in the environment is complementing an at risk genotype to cause autism in these vulnerable individuals. Mercury and lead both contribute to inflammation, leading scientists to speculate that these heavy metals could play a role in autism. These findings are controversial, however, with many researchers believing that increasing rates of autism are a byproduct of more accurate screening methods and not any sort of environmental factor.
Accelerated neural agingEdit
Neuroinflammation is associated with increased rates of neurodegeneration . Inflammation tends to increase naturally with age. By facilitating inflammation, pollutants such as air particulates and heavy metals cause the central nervous system to age more quickly. Many late onset diseases are caused by neurodegeneration. Multiple Sclerosis, Parkinson's Disease, Amyotrophic Lateral Sclerosis,and Alzheimer's are all believed to be exacerbated by inflammatory processes, resulting in individuals displaying signs of these disease at an earlier age than is typically expected.. Multiple Sclerosis occurs when chronic inflammation leads to the compromise of oligodendrocytes. This in turn leads to the destruction of the myelin sheath. After this, axons will began exhibiting signs of damage, which in turn will lead to neuron death. Multiple Sclerosis has been correlated to living in areas with high particulate matter levels in the air . In Parkinson's Disease, inflammation leading to depletion of antioxidant stores will ultimately lead to dopaminergic neuron degeneration, causing a shortage of dopamine and contributing to the formation of Parkinson's Disease. Chronic glial activation as a result of inflammation causes motor neuron death and compromises astrocytes; these factors lead to the symptoms of Amyotrophic Lateral Sclerosis. In the case of Alzheimer's, inflammatory processes lead to neuron death by inhibiting growth at axons and activating astrocytes that produce proteoglycans; this product can only be deposited at the hippocampus and cortex, indicating that this may be the reason these two areas show the highest levels of degeneration in Alzheimer's.. Airborne metal particulates have been shown to directly access and affect the brain through olfactory pathways; this direct access allows a large amount of particulate matter to reach the blood-brain barrier . These facts, coupled with air pollution's link to neurofibrillary tangles and the observed subcortical vascular changes observed in dogs, imply that the negative neuroplastic effects of pollution could result in increased risk for Alzheimer's disease and could also implicate pollution as a cause of early onset Alzheimer's disease through multiple mechanisms. The general effect of pollution is to increase levels of inflammation levels. By doing this, pollution can significantly contribute to various neurological disorders that are caused by inflammatory processes.
- ↑ Hong et al., 2002 Y.C. Hong, J.T. Lee, H. Kim and H.J. Kwon, Air pollution: a new risk factor in ischemic stroke mortality, Stroke 33 (9) (2002), pp. 2165–2169
- ↑ Calderon-Garciduenas, L.,Azzarelli, B.,Acuna, H.,Garcia, R.,Gambling, T. M.,Osnaya, N.,Monroy, S.,Tizapantzi, M. D.,Carson, J. L.,Villarreal-Calderon, A.,Rewcastle, B. (2002). Air pollution and brain damage. Toxicology Pathology 30 (3), 373-389.
- ↑ Calderon-Garciduenas, L., Mora-Tiscareno, A., Ontiveros, E., Gomez-Garza, G., Barragan-Mejia, G., Broadway, J., Chapman, S., Valencia-Salazar, G., Jewells, V., Maronpot, R., Henriquez-Roldan, C., Perez-Guille, B., Torres-Jardon, R., Herrit, L., Brooks, D., Osnaya-Brizuela, N., Monroy, M., Gonzalez-Maciel, A., Reynoso-Robles, R., Villareal-Calderon, R., Solt, A.., Engle, R. (2008). Air pollution, cognitive deficits and brain abnormalities: A pilot study with children and dogs. Brain and Cognition, 68(2), 117-127. doi: 10.1016/j.bandc.2008.04.008
- ↑ Cakmak, S., Dales, R. E., Vidal, C. B. (2010). Air pollution and hospitalization for epilepsy in Chile. [Article]. Environment International 36(6) 501-505.
- ↑ Mates, J., Segura, J., Alonso, F., & Marquez, J. (2010). Roles of dioxins and heavy metals in cancer and neurological diseases using ros-mediated mechanisms.Free Radical Biology and Medicine,49(9), 1328-1341
- ↑ Urban, P., Pelclova, D., Lukas, E., Kupka, K., & Preiss, J. neurological and neurophysiological examinations on workers with chronic poisoning by 2,3,7,8-tcdd: follow-up 35 years after exposure. European Journal of Neurology, 14(2), 213-218.
- ↑ Gundacker, C., Gencik, M., & Hengstschlager, M. (2010). The relevance of the individual genetic background for the toxicokinetics of two significant neurodevelopmental toxicants: mercury and lead. MUTATION RESEARCH-REVIEWS IN MUTATION RESEARCH , 705(2), 130-140.
- ↑ NG, D. K.-K., CHAN, C.-H., SOO, M.-T. and LEE, R. S.-Y. (2007), Low-level chronic mercury exposure in children and adolescents: Meta-analysis. Pediatrics International, 49: 80–87. doi: 10.1111/j.1442-200X.2007.02303.x
- ↑ C.C. Bridges and R.K. Zalups, Molecular and ionic mimicry and the transport of toxic metals, Toxicol. Appl. Pharm. 204 (2005), pp. 274–308.
- ↑ J. Liu, D. Lei, M.P. Waalkes, R.P. Beliles and D.L. Morgan, Genomic analysis of the rat lung following elemental mercury vapor exposure, Toxicol. Sci. 74 (2003), pp. 174–181.
- ↑ A. Stacchiotti, F. Morandini, F. Bettoni, I. Schena, A. Lavazza, P.G. Grigolato, P. Apostoli, R. Rezzani and M.F. Aleo, Stress proteins and oxidative damage in a renal derived cell line exposed to inorganic mercury and lead, Toxicology 264 (2009), pp. 215–224.
- ↑ Herbert, M.R. (2010). Contributions of the environment and environmentally vulnerable physiology to autism spectrum disorders. Current Opinions in Neurology, 23(2), 103-110.
- ↑ Baron-Cohen, S., Saunders, K., & Chakrabarti, S. (1999). Does autism cluster geographically? A research note. Autism, 3, 39–43
- ↑ Wing, L. and Potter, D. (2002), The epidemiology of autistic spectrum disorders: is the prevalence rising?. Mental Retardation and Developmental Disabilities Research Reviews, 8: 151–161. doi: 10.1002/mrdd.1002
- ↑ 15.0 15.1 CAMPBELL, A. (2004), Inflammation, Neurodegenerative Diseases, and Environmental Exposures. Annals of the New York Academy of Sciences, 1035: 117–132. doi: 10.1196/annals.1332.008
- ↑ Oikonen, M. et al. 2003. Ambient air quality and occurrence of multiple sclerosis relapse. Neuroepidemiology 22: 95–99.
- ↑ Hoke, A. et al. 1994. Regional differences in reactive gliosis induced by substrate-bound β-amyloid. Exp. Neurol. 130: 56–66.
- ↑ Brenneman, K.A et al. 2000. Direct olfactory transport of inhaled manganese (54MnCl2) to the rat brain: toxicokinetic investigations in a unilateral nasal occlusion model. Toxicol. Appl. Pharmacol. 169: 238–248.
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