#REDIRECT [[Brain health and pollution]]
{{update|date=November 2023}}
{{R with history}}
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]].
==Air pollution==
{{See also|Particulates#Cognitive hazards and mental health}}
[[Air pollution]] is known to affect small and large [[blood vessel]]s throughout the body.
<ref name="Louwies">{{cite journal
|last1 = Louwies
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|title = Retinal Microvascular Responses to Short-Term Changes in culate Air Pollution in Healthy Adults
|journal = Environmental Health Perspectives
|volume = 121
|issue = 9
|pages = 1011–6
|year = 2013
|doi = 10.1289/ehp.1205721
|pmid = 23777785
|last2 = Int Panis
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|pmc = 3764070
}}</ref><ref name="Brook">{{cite journal
| last1 = Brook
| first1 = RD
| title = Inhalation of fine culate air pollution and ozone causes acute arterial vasoconstriction in healthy adults
| journal = Circulation
| volume = 105
| issue = 13| pages = 1534–1536
| year = 2002
| pmid = 11927516| last2 = Brook
| first2 = JR
| last3 = Urch
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| last6 = Silverman
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| doi=10.1161/01.cir.0000013838.94747.64| doi-access = free
}}</ref>
High levels of air pollution are associated with increased risk of [[stroke]]s and [[Myocardial infarction|heart attacks]].<ref>{{cite journal |url=https://pdfs.semanticscholar.org/c066/1a72abe8ffc01cad4fb6d3ab596b6bbd7c7d.pdf |doi=10.1161/01.STR.0000026865.52610.5B|s2cid=8135083 |title=Air Pollution |year=2002 |last1=Hong |first1=Yun-Chul |last2=Lee |first2=Jong-Tae |last3=Kim |first3=Ho |last4=Kwon |first4=Ho-Jang |journal=Stroke |volume=33 |issue=9 |pages=2165–2169 |pmid=12215581 |archive-url=https://web.archive.org/web/20180907071026/https://pdfs.semanticscholar.org/c066/1a72abe8ffc01cad4fb6d3ab596b6bbd7c7d.pdf |archive-date=2018-09-07 }}</ref> By permanently affecting [[vascular]] structures in the [[brain]], air pollution can have serious effects on [[nervous system|neural]] functioning and neural matter. In dogs, air pollution has been shown to cause damage to the CNS by altering the [[blood–brain barrier]], causing [[neurons]] in the [[cerebral cortex]] to degenerate, destroying [[glial cells]] found in [[white matter]], and causing [[neurofibrillary tangles]].<ref>{{cite journal | last1 = Calderon-Garciduenas | first1 = L. | last2 = Azzarelli | first2 = B. | last3 = Acuna | first3 = H. | last4 = Garcia | first4 = R. | last5 = Gambling | first5 = T. M. | last6 = Osnaya | first6 = N. | last7 = Monroy | first7 = S. | last8 = Tizapantzi | first8 = M. D. | last9 = Carson | first9 = J. L. | year = 2002 | title = Air pollution and brain damage | journal = Toxicologic Pathology | volume = 30 | issue = 3| pages = 373–389 | display-authors = etal | doi = 10.1080/01926230252929954 | pmid = 12051555 | doi-access = }}</ref><ref name="bos">{{cite journal
| last1 = Bos
| first1 = I
| title = Physical Activity, Air Pollution and the Brain
| journal = Sports Medicine
| volume = 44| issue = 11| pages = 1505–18| year = 2014
| url = https://www.researchgate.net/publication/264793941
| doi = 10.1007/s40279-014-0222-6
| pmid = 25119155| last2 = De Boever
| first2 = P
| last3 = Int Panis
| first3 = L
| last4 = Meeusen
| first4 = R
| s2cid = 207493297
}}</ref> These changes can permanently alter brain structure and [[Neurochemistry|chemistry]], resulting in various impairments and disorders. Sometimes, the effects of neural remodeling do not manifest themselves for a prolonged period of time.
===Effects in adolescents and canines===
A 2008 study compared children and dogs raised in [[Mexico City]] (a location known for high [[pollution]] levels) with children and dogs raised in [[Polotitlán de la Ilustración|Polotitlán]], Mexico (a city whose pollution levels meet the current US [[National Ambient Air Quality Standards]]).<ref>{{cite journal | last1 = Calderon-Garciduenas | first1 = L. | last2 = Mora-Tiscareno | first2 = A. | last3 = Ontiveros | first3 = E. | last4 = Gomez-Garza | first4 = G. | last5 = Barragan-Mejia | first5 = G. | last6 = Broadway | first6 = J. | last7 = Chapman | first7 = S. | last8 = Valencia-Salazar | first8 = G. | last9 = Jewells | first9 = V. | year = 2008 | title = Air pollution, cognitive deficits and brain abnormalities: A pilot study with children and dogs | journal = Brain and Cognition | volume = 68 | issue = 2| pages = 117–127 | doi = 10.1016/j.bandc.2008.04.008 | pmid = 18550243 | s2cid = 7714924 | display-authors = etal }}</ref> Children raised in areas of higher pollution were found scored lower in [[intelligence]] (i.e. on [[Intelligence quotient|IQ]] tests), and showed signs of [[lesions]] in [[MRI]] scanning of the brain. In contrast, children from the low pollution area scored as expected on IQ tests, and did not show any significant sign of the risk of brain lesions. This correlation was found to be statistically significant, and shows that pollution levels may be related to, and contribute to, brain lesion formation and IQ scores, which, in turn, manifests as impaired intellectual capacity and/or performance. Living in high pollution areas thus places adolescents at risk of premature brain [[Degeneration (medical)|degeneration]] and improper neural development. With regard to traffic related air pollution, children of mothers exposed to higher levels during the first trimester of pregnancy were at increased risk of [[allergic sensitization]] at age 1 year.<ref>{{cite journal | doi=10.1016/j.jaci.2019.07.047 | title=Prenatal exposure to traffic-related air pollution, the gestational epigenetic clock, and risk of early-life allergic sensitization | year=2019 | last1=Sbihi | first1=Hind | last2=Jones | first2=Meaghan J. | last3=MacIsaac | first3=Julie L. | last4=Brauer | first4=Michael | last5=Allen | first5=Ryan W. | last6=Sears | first6=Malcolm R. | last7=Subbarao | first7=Padmaja | last8=Mandhane | first8=Piush J. | last9=Moraes | first9=Theo J. | last10=Azad | first10=Meghan B. | last11=Becker | first11=Allan B. | last12=Brook | first12=Jeffrey R. | last13=Kobor | first13=Michael S. | last14=Turvey | first14=Stuart E. | journal=Journal of Allergy and Clinical Immunology | volume=144 | issue=6 | pages=1729–1731.e5 | pmid=31470034 | s2cid=201756930 | doi-access=free }}</ref>
===Effects in adults===
There are indications that the effects of physical activity and air pollution on neuroplasticity counteract. Physical activity is known for its health-enhancing benefits, cularly on the [[Circulatory system|cardiovascular]] system, and has also demonstrated benefits for brain plasticity processes, [[Circulatory system|cognition]] and mental health. The neurotrophine, [[BDNF|brain-derived neurotrophic factor]] (BDNF) is thought to play a key role in exercise-induced cognitive improvements. Brief bouts of physical activity have been shown to increase [[Serum (blood)|serum]] levels of BDNF, but this increase may be offset by increased exposure to [[Serum (blood)|traffic]]-related air pollution.<ref name="Bos et al. 2011">{{cite journal
| last1 = Bos
| first1 = I
| title = No exercise-induced increase in serum BDNF after cycling near a major traffic road
| journal = Neuroscience Letters
| volume = 500
| issue = 2
| pages = 129–132
|date=August 2011
| doi =10.1016/j.neulet.2011.06.019
| pmid = 21708224| last2 = Jacobs
| first2 = L.
| last3 = Nawrot
| first3 = T. S.
| last4 = de Geus
| first4 = B.
| last5 = Int Panis
| first5 = L.
| last6 = Int Panis
| first6 = L.
| last7 = Torfs
| first7 = R.
| last8 = Degraeuwe
| first8 = B.
| last9 = Meeusen
| first9 = R.
| s2cid = 411730
}}</ref>
Over longer periods of physical exercise, the cognitive improvements which were demonstrated in [[Rural area|rural]] joggers were found to be absent in [[Urban area|urban]] joggers who were partaking in the same 12-week start-2-run training programme.<ref name="Bos et al.">{{cite journal
| last1 = Bos
| first1 = I.
| title = Subclinical effects of aerobic training in urban environment
| journal = Medicine and Science in Sports and Exercise
| volume =45
| issue =3
| pages =439–47
| year = 2013
| doi =10.1249/MSS.0b013e31827767fc
| pmid = 23073213
| last2 = De Boever
| first2 = P.
| last3 = Vanparijs
| first3 = J.
| last6 = Meeusen
| first6 = Romain
| last4 = Pattyn
| first4 = N.
| last5 = Int Panis
| first5 = Luc| hdl = 1942/14628
| hdl-access = free
}}</ref>
===Epilepsy===
Researchers in [[Chile]] found statistically-significant correlations between multiple air [[pollutants]] and the risk of [[epilepsy]] using a 95% [[confidence interval]].<ref>{{cite journal | last1 = Cakmak | first1 = S. | last2 = Dales | first2 = R. E. | last3 = Vidal | first3 = C. B. | year = 2010 | title = Air pollution and hospitalization for epilepsy in Chile| journal = Environment International | volume = 36 | issue = 6| pages = 501–505 | doi=10.1016/j.envint.2010.03.008| pmid = 20452673 }}</ref> The air pollutants that the researchers attempted to correlate with increased incidence of epilepsy included [[carbon monoxide]], [[ozone]], [[sulfur dioxide]], [[nitrogen dioxide]], large [[particulates|particulate]] matter, and [[Ultrafine particle|fine particulate matter]]. The researchers tested these pollutants across seven cities and, 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 hypothesized that air pollutants increase epilepsy risk by increasing [[inflammation|inflammatory]] mediators, and by 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, the sequence of events provides a plausible mechanism by which pollution may increase epilepsy risk in individuals who are [[Genetics|genetically]] vulnerable to the disease.
==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> A study of 350 [[chemical plant]] employees exposed to a dioxin precursor for [[herbicide]] synthesis between 1965 and 1968 showed that 80 of the employees displayed signs of dioxin poisoning.<ref>{{cite journal | last1 = Urban | first1 = P. | last2 = Pelclova | first2 = D. | last3 = Lukas | first3 = E. | last4 = Kupka | first4 = K. | last5 = Preiss | first5 = J. | last6 = Fenclová | first6 = Z. | last7 = Šmerhovský | first7 = Z. | year = 2007| title = Neurological and neurophysiological examinations on workers with chronic poisoning by 2,3,7,8-tcdd: follow-up 35 years after exposure | journal = European Journal of Neurology | volume = 14 | issue = 2| pages = 213–218 | doi=10.1111/j.1468-1331.2006.01618.x| pmid = 17250732 | s2cid = 29676448 | doi-access = free }}</ref> Of these 350 employees, 15 were contacted again in 2004 to submit to neurological tests to assess the long-term effects of dioxin poisoning on neurological capabilities. The amount of time that had passed made it difficult to assemble a larger [[Cohort (statistics)|cohort]], but the results of the tests indicated that eight of the 15 subjects exhibited some [[central nervous system]] impairment, nine showed signs of [[polyneuropathy]], and [[electroencephalography]] (EEG) showed various degrees of structural abnormalities. This study suggested that the effects of dioxins were not limited to initial [[toxicity]]. Dioxins, through neuroplastic effects, can cause long-term damage that may not manifest itself for years or even decades.
==Metal exposure==
{{See also|Lead poisoning|Mercury poisoning}}
[[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"/>
Multiple sclerosis occurs when chronic inflammation leads to the compromise of [[oligodendrocyte]]s, which in turn leads to the destruction of the [[Myelin|myelin sheath]]. Then [[axon]]s begin exhibiting signs of damage, which in turn leads to neuron death. Multiple sclerosis has been correlated to living in areas with high particulate matter levels in the air.<ref>{{cite journal |last1=Oikonen |first1=M. |year=2003 |title=Ambient air quality and occurrence of multiple sclerosis relapse |journal=Neuroepidemiology |volume=22 |issue=1 |pages=95–99 |doi=10.1159/000067108 |pmid=12566960 |display-authors=1 |last2=Laippala |first2=P. |last3=Oksaranta |first3=O. |last4=Lilius |first4=E.-M. |last5=Lindgren |first5=S. |last6=Rantio-LehtimÄki |first6=A. |last7=Anttinen |first7=A. |last8=Koski |first8=K. |last9=ErÄlinna |first9=J.-P.|s2cid=26392841 }}</ref>
In Parkinson's disease, inflammation leading to depletion of [[antioxidant]] stores will ultimately lead to [[dopamine]]rgic 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 leading to the symptoms of amyotrophic lateral sclerosis (ALS, aka [[Lou Gehrig|Lou Gehrig's]] disease).
In the case of Alzheimer's disease, inflammatory processes lead to neuron death by inhibiting growth at axons and activating [[astrocytes]] that produce [[proteoglycans]]. This product can only be deposited in the [[hippocampus]] and [[Cerebral cortex|cortex]], indicating that this may be the reason these two areas show the highest levels of degeneration in Alzheimer's disease.<ref>{{cite journal |last1=Hoke |first1=A. |year=1994 |title=Regional differences in reactive gliosis induced by substrate-bound β-amyloid |journal=Exp. Neurol. |volume=130 |issue=1 |pages=56–66 |doi=10.1006/exnr.1994.1185 |pmid=7821397 |display-authors=1 |last2=Malemud |first2=Charles J. |last3=Silver |first3=Jerry|s2cid=54293885 }}</ref> [[Airborne metal particulates]] (e.g. [[manganese]]) have been shown to directly access and affect the brain through [[olfactory]] pathways, which allows a large amount of particulate matter to reach the [[blood–brain barrier]].<ref>{{cite journal |last1=Brenneman |first1=K. A. |year=2000 |title=Direct olfactory transport of inhaled manganese (<sup>54</sup>MnCl<sub>2</sub>) to the rat brain: toxicokinetic investigations in a unilateral nasal occlusion model |journal=Toxicol. Appl. Pharmacol. |volume=169 |issue=3 |pages=238–248 |doi=10.1006/taap.2000.9073 |pmid=11133346 |display-authors=1 |last2=Buccellato |first2=Matthew A. |last3=Costa |first3=Elisabeth R. |last4=Gross |first4=Elizabeth A. |last5=Dorman |first5=David C.}}</ref>
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 increased levels of inflammation. As a result, pollution can significantly contribute to various neurological disorders that are caused by inflammatory processes.
==See also==
* [[Carbon disulfide]]
* [[Manganism]]
* [[Paraquat]]
* [[Polychlorinated biphenyls]]
* [[Rotenone]]
* [[Solvent]]
* [[Toluene]]
* [[Trichloroethylene]]
* [[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]
[[Category:Pollution]]
[[Category:Neuroplasticity]]
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