Neuroplastic effects of pollution: Difference between revisions

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Brain health and pollution

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+#REDIRECT [[Brain health and pollution]]
-{{multiple issues|
-{{Merge to|Brain health and pollution|discuss=Talk:Neuroplastic_effects_of_pollution#Scope|date=April 2024}}
-{{notability|date=March 2024}}
-{{update|date=November 2023}}
-{{medref|date=March 2024}}
-{{duplication|date=March 2024}}
-}}
-Research indicates that living in areas of high [[pollution]] has serious long term health effects. Living in these areas during [[childhood]] and [[adolescence]] can lead to diminished [[Intelligence|mental capacity]] and an increased risk of [[brain damage]]. People of all ages who live in high pollution areas for extended periods place themselves at increased risk of various [[neurological disorder]]s. Both [[air pollution]] and [[Heavy metal (chemistry)|heavy metal]] pollution have been implicated as having negative effects on [[central nervous system]] (CNS) functionality. The ability of [[pollutant]]s to affect the [[neurophysiology]] of individuals after the structure of the CNS has become mostly stabilized is an example of negative [[neuroplasticity]].
-==Dioxin poisoning==
-[[Organohalogen]] compounds, such as [[dioxins]], are commonly found in [[pesticide]]s or created as by-products of pesticide manufacture or [[Biodegradation|degradation]]. These compounds can have a significant impact on the [[Neuroscience|neurobiology]] of exposed organisms. Some observed effects of exposure to dioxins are altered [[Astrocyte|astroglial]] intracellular [[Astrocyte|calcium]] ion (Ca<sup>2+</sup>), decreased [[glutathione]] levels, modified [[Astrocyte|neurotransmitter]] function in the CNS, and loss of [[pH]] maintenance.<ref>{{cite journal | last1 = Mates | first1 = J. | last2 = Segura | first2 = J. | last3 = Alonso | first3 = F. | last4 = Marquez | first4 = J. | year = 2010 | title = Roles of dioxins and heavy metals in cancer and neurological diseases using ros-mediated mechanisms | journal = Free Radical Biology and Medicine | volume = 49 | issue = 9| pages = 1328–1341 | doi=10.1016/j.freeradbiomed.2010.07.028| pmid = 20696237 }}</ref>
-==Metal exposure==
-{{See also|Lead poisoning|Mercury poisoning}}
-[[Heavy metals|Heavy metal]] exposure can result in an increased risk of various neurological diseases. Research indicates that the two most [[Neurotoxicity|neurotoxic]] heavy metals are [[mercury (element)|mercury]] and [[lead]]. The impact that these two [[heavy metals]] will have is highly dependent upon the individual due to [[genetic variation]]s. Mercury and lead are particularly neurotoxic for many reasons: they easily cross [[cell membrane]]s, have oxidative effects on cells, react with [[sulfur]] in the body (leading to disturbances in the many functions that rely upon [[sulfhydryl]] groups), and reduce [[glutathione]] levels inside cells. [[Methylmercury]], in particular, has an extremely high affinity for [[Thiol|sulfhydryl]] groups.<ref>{{cite journal | last1 = Gundacker | first1 = C. | last2 = Gencik | first2 = M. | last3 = Hengstschlager | first3 = M. | year = 2010 | title = The relevance of the individual genetic background for the toxicokinetics of two significant neurodevelopmental toxicants: mercury and lead | journal = Mutation Research/Reviews in Mutation Research | volume = 705 | issue = 2| pages = 130–140 | doi=10.1016/j.mrrev.2010.06.003| pmid = 20601101 }}</ref>  [[Organomercury]] is a particularly damaging form of mercury because of its high absorbability<ref>{{cite journal | last1 = Ng | first1 = D. K.-K. | last2 = Chan | first2 = C.-H. | last3 = SOO | first3 =  MAN-Ting| last4 = Lee | first4 = R. S.-Y. | year = 2007 | title = Low-level chronic mercury exposure in children and adolescents: Meta-analysis | journal = Pediatrics International | volume = 49 | issue = 1| pages = 80–87 | doi = 10.1111/j.1442-200X.2007.02303.x | pmid = 17250511 | s2cid = 24367277 }}</ref> Lead also mimics [[calcium]], a very important mineral in the CNS, and this mimicry leads to many adverse effects.<ref>{{cite journal | last1 = Bridges | first1 = C. C. | last2 = Zalups | first2 = R. K. | year = 2005 | title = Molecular and ionic mimicry and the transport of toxic metals | journal = Toxicol. Appl. Pharmacol. | volume = 204 | issue = 3| pages = 274–308 | doi=10.1016/j.taap.2004.09.007| pmid = 15845419 | pmc = 2409291 }}</ref> Mercury's neuroplastic mechanisms work by affecting [[protein]] production. Elevated mercury levels increase glutathione levels by affecting [[gene expression]], and this in turn affects two proteins (MT1 and MT2) that are contained in [[astrocytes]] and neurons.<ref>{{cite journal | last1 = Liu | first1 = J. | last2 = Lei | first2 = D. | last3 = Waalkes | first3 = M. P. | last4 = Beliles | first4 = R. P. | last5 = Morgan | first5 = D. L. | year = 2003 | title = Genomic analysis of the rat lung following elemental mercury vapor exposure | journal = Toxicol. Sci. | volume = 74 | issue = 1| pages = 174–181 | doi=10.1093/toxsci/kfg091| pmid = 12730625 | doi-access = free }}</ref> Lead's ability to imitate calcium allows it to cross the blood–brain barrier. Lead also [[Downregulation and upregulation|upregulates]] glutathione.<ref>{{cite journal | last1 = Stacchiotti | first1 = A. | last2 = Morandini | first2 = F. | last3 = Bettoni | first3 = F. | last4 = Schena | first4 = I. | last5 = Lavazza | first5 = A. | last6 = Grigolato | first6 = P. G. | last7 = Apostoli | first7 = P. | last8 = Rezzani | first8 = R. | last9 = Aleo | first9 = M. F. | year = 2009 | title = Stress proteins and oxidative damage in a renal derived cell line exposed to inorganic mercury and lead | journal = Toxicology | volume = 264 | issue = 3| pages = 215–224 | doi=10.1016/j.tox.2009.08.014| pmid = 19720107  | display-authors = etal  }}</ref>
-===Autism===
-{{main|Causes of autism}}
-{{See also|Epigenetics of autism}}
-Heavy metal [[exposome|exposure]], when combined with certain [[genetic predisposition]]s, can place individuals at increased risk for developing [[autism]]. Many examples of CNS [[pathophysiology]], such as [[oxidative stress]], [[neuroinflammation]], and [[mitochondrial]] dysfunction, could be by-products of environmental [[stressor]]s such as [[pollution]], as found in a 2010 study.<ref>{{cite journal | last1 = Herbert | first1 = M. R. | author-link = Martha Herbert | year = 2010 | title = Contributions of the environment and environmentally vulnerable physiology to autism spectrum disorders | journal = Current Opinion in Neurology | volume = 23 | issue = 2| pages = 103–110 | doi=10.1097/wco.0b013e328336a01f | pmid=20087183| s2cid = 17280526 }}</ref> There have been reports of [[autism outbreaks]] occurring in specific locations.<ref>{{cite journal | last1 = Baron-Cohen | first1 = S. | last2 = Saunders | first2 = K. | last3 = Chakrabarti | first3 = S. | year = 1999 | title = Does autism cluster geographically? A research note | journal = Autism | volume = 3 | pages = 39–43 | doi=10.1177/1362361399003001004| s2cid = 146452563 }}</ref> 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.
-==Accelerated neural aging==
-[[Neuroinflammation]] is associated with increased rates of [[neurodegeneration]].<ref name="CAMPBELL, A. 2004">{{cite journal | last1 = Campbell | first1 = A. | year = 2004 | title = Inflammation, Neurodegenerative Diseases, and Environmental Exposures | journal = Annals of the New York Academy of Sciences | volume = 1035 | issue = 1| pages = 117–132 | doi = 10.1196/annals.1332.008 | pmid = 15681804 | bibcode = 2004NYASA1035..117C | s2cid = 21762775 }}</ref> Inflammation tends to increase naturally with age. By facilitating inflammation, pollutants such as air particulates and heavy metals cause the CNS to age more quickly. Many late-onset diseases are caused by neurodegeneration. [[Multiple sclerosis]], [[Parkinson's disease]], [[amyotrophic lateral sclerosis]] (ALS), and [[Alzheimer's disease]] are all believed to be exacerbated by inflammatory processes, resulting in individuals displaying signs of these diseases at an earlier age than is typically expected.<ref name="CAMPBELL, A. 2004"/>
-==See also==
-* [[Carbon disulfide]]
-* [[Epigenetics]]
-* [[Exposome]]
-* [[Manganism]]
-* [[Pesticide]] | [[Paraquat]] | [[Rotenone]]
-* [[Polychlorinated biphenyls]]
-* [[Solvent]] | [[Toluene]] | [[Trichloroethylene]]
-* [[Substance-induced psychosis]]
-* [[Welding]]
-==References==
-{{reflist|2}}
-==Further reading==
-* [https://factor.niehs.nih.gov/2022/12/feature/4-feature-parkinsons-disease Environmental exposures and Parkinson’s disease: connecting the dots] (NIEHS)
-* [https://pubmed.ncbi.nlm.nih.gov/22309908/ Industrial toxicants and Parkinson's disease]
-* [https://pubmed.ncbi.nlm.nih.gov/33061891/ The Inflamed Brain in Schizophrenia: The Convergence of Genetic and Environmental Risk Factors That Lead to Uncontrolled Neuroinflammation]
-[[Category:Pollution]]
-[[Category:Neuroplasticity]]