A study conducted by Tyler, C.R., et.al (2014) states thatarsenic can alter a multitude of systems in the brain. HPA axis dysregulation that may underliebehavioral deficits, particularly related to the hippocampus.
Arsenic canaffect in the alterations of adult neurogensis and Ras-MAPK/ERK signaling. It also have an impact on cholinergic andmonoaminergic signaling, though the mechanisms are not well understood at thispoint. A study on Rodents have provided useful document of the epidemiological evidence suggestingthat a number of mechanisms could cause cognitive deficits and mood disorders.More research focused on the dynamics of epigenetics, particularly onmechanisms of learning and memory and mood, will be important for understandingthe impact of arsenic on the brain.
Studies on the mechanisms of arsenic-inducedtoxicity have established that arsenic alters learning and memory in behavioralassays and impacts multiple neurobiological processes including those ofneurogenesis and cholinergic, glutamatergic, and monoaminergic signalingpathways. Work using animal models has revealed potent changes in hippocampalfunction, morphology, and signaling leading to change in cognitive behaviorafter arsenic exposure. According to Hong, Y.-S.
, et.al (2014) Arsenic is the onlycarcinogen known to cause cancer through respiratory exposure andgastrointestinal exposure . The International Agency for Research on Cancer(IARC) officially recognized it as carcinogenicsubstance . Studies conducted in the United States, Taiwan, Bangladesh,India, Argentina, and Chile further examined this association, and the resultssupported those of previous reports . It states that inorganic arseniccompounds can be categorized as clear carcinogens (group 1) or potential carcinogens(group 2B) such as DMA and MMA, while arsenobetaine and other organoarsenicalshave not been categorized as carcinogens (group 3).
Toxic mechanism behindarsenic have been suggested, including induced chromosome abnormalities,altered growth factors, altered DNA repair, oxidative stress, altered DNAmethylation patterns, enhanced cell proliferation, suppression of p53, and geneamplification. International Agency for Research on Cancer has confirmed theassociation of arsenic exposure with cancers of the skin, lungs, and bladder,while reports on the relationship with the liver, kidney, and prostate cancerremain limited. Key epidemiological evidence regarding the carcinogenicity ofarsenic stems from studies from those in Taiwan , Bangladesh , Chile , andArgentina , who consume drinking water containing high concentrations ofarsenic (150 ?g/L).
However, despite the well-established toxicity ofarsenic, studies regarding the association between chronic exposure to lowconcentrations of arsenic and the development of cancer are lacking; furtherstudy is needed to support effective public health management. A study conducted by Lin, H.J., et.al (2013) shows the results ofa 20-year retrospective cohort study on liver cancer patients (802 male and 301female) from 138 communities in Taiwan found a significant increase in livercancer incidence in both genders at a arsenic concentration above 0.64 mg/L,but no association was found at exposure levels lower than lower 0.64 mg/L.
Hopenhayn-Rich et al. observed a significant increase in lung cancer-relateddeaths with arsenic intake. Moreover, numerous studies have investigated thedose-dependent relationship between arsenic intake and lung cancer incidence,making lung cancer the most well-known cancer associated with arsenic exposure.In a recent study conducted in Taiwan, a high mortality rate and standardizedmortality ratio of lung cancer was observed among patients who consumedhigh-arsenic concentrated drinking water for the past 50 years.