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 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 disorders. Both air pollution and heavy metal pollution have been implicated as having negative effects on central nervous system (CNS) functionality. The ability of pollutants to affect the neurophysiology of individuals after the structure of the CNS has become mostly stabilized is an example of negative neuroplasticity.
Air pollution
During exercise, traffic-related air pollution air pollution can reduce the beneficial effects of that exercise.[1]
Dioxin poisoning
Organohalogen compounds, such as dioxins, are commonly found in pesticides or created as by-products of pesticide manufacture or degradation. These compounds can have a significant impact on the neurobiology of exposed organisms. Some observed effects of exposure to dioxins are altered astroglial intracellular calcium ion (Ca2+), decreased glutathione levels, modified neurotransmitter function in the CNS, and loss of pH maintenance.[2] 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.[3] 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, 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
Heavy metal exposure can result in an increased risk of various neurological diseases. Research indicates that the two most neurotoxic heavy metals are mercury and lead. The impact that these two heavy metals will have is highly dependent upon the individual due to genetic variations. Mercury and lead are particularly neurotoxic for many reasons: they easily cross cell membranes, 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 sulfhydryl groups.[4] Organomercury is a particularly damaging form of mercury because of its high absorbability[5] Lead also mimics calcium, a very important mineral in the CNS, and this mimicry leads to many adverse effects.[6] 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.[7] Lead's ability to imitate calcium allows it to cross the blood–brain barrier. Lead also upregulates glutathione.[8]
Autism
Heavy metal exposure, when combined with certain genetic predispositions, 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 stressors such as pollution, as found in a 2010 study.[9] There have been reports of autism outbreaks occurring in specific locations.[10] 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.[11] 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.[11]
See also
- Carbon disulfide
- Epigenetics
- Exposome
- Manganism
- Pesticide | Paraquat | Rotenone
- Polychlorinated biphenyls
- Solvent | Toluene | Trichloroethylene
- Substance-induced psychosis
- Welding
References
- ^ Bos I, De Boever P, Int Panis L, Meeusen R (November 2014). "Physical activity, air pollution and the brain". Sports Med (Review). 44 (11): 1505–18. doi:10.1007/s40279-014-0222-6. PMID 25119155.
- ^ 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. doi:10.1016/j.freeradbiomed.2010.07.028. PMID 20696237.
- ^ Urban, P.; Pelclova, D.; Lukas, E.; Kupka, K.; Preiss, J.; Fenclová, Z.; Šmerhovský, Z. (2007). "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. doi:10.1111/j.1468-1331.2006.01618.x. PMID 17250732. S2CID 29676448.
- ^ 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. doi:10.1016/j.mrrev.2010.06.003. PMID 20601101.
- ^ Ng, D. K.-K.; Chan, C.-H.; SOO, MAN-Ting; Lee, R. S.-Y. (2007). "Low-level chronic mercury exposure in children and adolescents: Meta-analysis". Pediatrics International. 49 (1): 80–87. doi:10.1111/j.1442-200X.2007.02303.x. PMID 17250511. S2CID 24367277.
- ^ Bridges, C. C.; Zalups, R. K. (2005). "Molecular and ionic mimicry and the transport of toxic metals". Toxicol. Appl. Pharmacol. 204 (3): 274–308. doi:10.1016/j.taap.2004.09.007. PMC 2409291. PMID 15845419.
- ^ Liu, J.; Lei, D.; Waalkes, M. P.; Beliles, R. P.; Morgan, D. L. (2003). "Genomic analysis of the rat lung following elemental mercury vapor exposure". Toxicol. Sci. 74 (1): 174–181. doi:10.1093/toxsci/kfg091. PMID 12730625.
- ^ Stacchiotti, A.; Morandini, F.; Bettoni, F.; Schena, I.; Lavazza, A.; Grigolato, P. G.; Apostoli, P.; Rezzani, R.; Aleo, M. F.; et al. (2009). "Stress proteins and oxidative damage in a renal derived cell line exposed to inorganic mercury and lead". Toxicology. 264 (3): 215–224. doi:10.1016/j.tox.2009.08.014. PMID 19720107.
- ^ Herbert, M. R. (2010). "Contributions of the environment and environmentally vulnerable physiology to autism spectrum disorders". Current Opinion in Neurology. 23 (2): 103–110. doi:10.1097/wco.0b013e328336a01f. PMID 20087183. S2CID 17280526.
- ^ Baron-Cohen, S.; Saunders, K.; Chakrabarti, S. (1999). "Does autism cluster geographically? A research note". Autism. 3: 39–43. doi:10.1177/1362361399003001004. S2CID 146452563.
- ^ a b Campbell, A. (2004). "Inflammation, Neurodegenerative Diseases, and Environmental Exposures". Annals of the New York Academy of Sciences. 1035 (1): 117–132. Bibcode:2004NYASA1035..117C. doi:10.1196/annals.1332.008. PMID 15681804. S2CID 21762775.