Regional specific groundwater arsenic levels and neuropsychological functioning: a cross-sectional study

Edwards, Melissa; Johnson, Leigh; Mauer, Cortney B.; Barber, Robert C.; Hall, James; O’Bryant, Sid

doi:10.1080/09603123.2014.883591

Cited by 22 publications

(12 citation statements)

References 49 publications

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“…In recent years, many studies have focused on neural injury after arsenic exposure including hippocampal function (Liu et al, 2012 ), increased Alzheimer’s-associated pathologies (Gharibzadeh and Hoseini, 2008 ; Gong and O’Bryant, 2010 ; Edwards et al, 2014 ), and adult neurogenesis (Tyler and Allan, 2013 ). These potential mechanisms are closely related with apoptosis of nerve cells.…”

Section: Discussionmentioning

confidence: 99%

Sodium Arsenite-Induced Learning and Memory Impairment Is Associated with Endoplasmic Reticulum Stress-Mediated Apoptosis in Rat Hippocampus

Sun

Yang

Shao

et al. 2017

Front. Mol. Neurosci.

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Chronic arsenic exposure has been associated to cognitive deficits. However, mechanisms remain unknown. The present study investigated the neurotoxic effects of sodium arsenite in drinking water over different dosages and time periods. Based on results from the Morris water maze (MWM) and morphological analysis, an exposure to sodium arsenite could induce neuronal damage in the hippocampus, reduce learning ability, and accelerate memory impairment. Sodium arsenite significantly increased homocysteine levels in serum and brain. Moreover, sodium arsenite triggered unfolded protein response (UPR), leading to the phosphorylation of RNA-regulated protein kinase-like ER kinase (PERK) and eukaryotic translation initiation factor 2 subunit α (eIF2α), and the induction of activating transcription factor 4 (ATF4). Arsenite exposure also stimulated the expression of the endoplasmic reticulum (ER) stress markers, glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and the cleavage of caspase-12. Furthermore, exposure to arsenite enhanced apoptosis as demonstrated by expression of caspase-3 and TUNEL assay in the hippocampus. The results suggest that exposure to arsenite can significantly decrease learning ability and accelerate memory impairment. Potential mechanisms are related to enhancement of homocysteine and ER stress-induced apoptosis in the hippocampus.

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Section: Discussionmentioning

confidence: 99%

Sodium Arsenite-Induced Learning and Memory Impairment Is Associated with Endoplasmic Reticulum Stress-Mediated Apoptosis in Rat Hippocampus

Sun

Yang

Shao

et al. 2017

Front. Mol. Neurosci.

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“…In a case-control study measuring heavy metal serum levels in 89 Ad patients and 188 cognitively normal controls, there was no difference in serum arsenic levels between the AD group and controls [171]. Another study conducted by Edwards et al, with a cohort consisting of 733 AD patients, 127 individuals with mild cognitive impairment, and 530 individuals of normal cognition, found that exposure to low level arsenic exposure from groundwater was found to be associated with poorer neuropsychological performance [172]. A cross-sectional study by Shuie (2015), using NHANES 2011-2012 data, found that individuals who has problems remembering had higher levels of urinary arsenic [125].…”

Section: Epidemiologic and Experimental Evidence Of Brain Health Dmentioning

confidence: 99%

Estrogenic Endocrine Disrupting Chemicals Influencing NRF1 Regulated Gene Networks in the Development of Complex Human Brain Diseases

Preciados

Yoo

Roy

2016

IJMS

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During the development of an individual from a single cell to prenatal stages to adolescence to adulthood and through the complete life span, humans are exposed to countless environmental and stochastic factors, including estrogenic endocrine disrupting chemicals. Brain cells and neural circuits are likely to be influenced by estrogenic endocrine disruptors (EEDs) because they strongly dependent on estrogens. In this review, we discuss both environmental, epidemiological, and experimental evidence on brain health with exposure to oral contraceptives, hormonal therapy, and EEDs such as bisphenol-A (BPA), polychlorinated biphenyls (PCBs), phthalates, and metalloestrogens, such as, arsenic, cadmium, and manganese. Also we discuss the brain health effects associated from exposure to EEDs including the promotion of neurodegeneration, protection against neurodegeneration, and involvement in various neurological deficits; changes in rearing behavior, locomotion, anxiety, learning difficulties, memory issues, and neuronal abnormalities. The effects of EEDs on the brain are varied during the entire life span and far-reaching with many different mechanisms. To understand endocrine disrupting chemicals mechanisms, we use bioinformatics, molecular, and epidemiologic approaches. Through those approaches, we learn how the effects of EEDs on the brain go beyond known mechanism to disrupt the circulatory and neural estrogen function and estrogen-mediated signaling. Effects on EEDs-modified estrogen and nuclear respiratory factor 1 (NRF1) signaling genes with exposure to natural estrogen, pharmacological estrogen-ethinyl estradiol, PCBs, phthalates, BPA, and metalloestrogens are presented here. Bioinformatics analysis of gene-EEDs interactions and brain disease associations identified hundreds of genes that were altered by exposure to estrogen, phthalate, PCBs, BPA or metalloestrogens. Many genes modified by EEDs are common targets of both 17 β-estradiol (E2) and NRF1. Some of these genes are involved with brain diseases, such as Alzheimer’s Disease (AD), Parkinson’s Disease, Huntington’s Disease, Amyotrophic Lateral Sclerosis, Autism Spectrum Disorder, and Brain Neoplasms. For example, the search of enriched pathways showed that top ten E2 interacting genes in AD—APOE, APP, ATP5A1, CALM1, CASP3, GSK3B, IL1B, MAPT, PSEN2 and TNF—underlie the enrichment of the Kyoto Encyclopedia of Genes and Genomes (KEGG) AD pathway. With AD, the six E2-responsive genes are NRF1 target genes: APBB2, DPYSL2, EIF2S1, ENO1, MAPT, and PAXIP1. These genes are also responsive to the following EEDs: ethinyl estradiol (APBB2, DPYSL2, EIF2S1, ENO1, MAPT, and PAXIP1), BPA (APBB2, EIF2S1, ENO1, MAPT, and PAXIP1), dibutyl phthalate (DPYSL2, EIF2S1, and ENO1), diethylhexyl phthalate (DPYSL2 and MAPT). To validate findings from Comparative Toxicogenomics Database (CTD) curated data, we used Bayesian network (BN) analysis on microarray data of AD patients. We observed that both gender and NRF1 were associated with AD. The female NRF1 gene network is completely ...

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“…To date, most of human studies about As and AD are focused on the association between As exposure in drinking water and the risk of cognitive deficit [13][14][15]. The current study aimed to investigate the possible association between As exposure in soil and the mortality from AD.…”

Section: Introductionmentioning

confidence: 99%

Positive association between soil arsenic concentration and mortality from alzheimer’s disease in mainland China

Zhan

Zheng

et al. 2020

Journal of Trace Elements in Medicine and Biology

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Objectives: The current study was designed to investigate the relationship between the soil arsenic (As) concentration and the mortality from Alzheimer's disease (AD) in mainland China. Study design: Ecological study. Methods: Twenty-two provinces and 3 municipal districts in mainland China were included in this study. The As concentrations in soil in 1990 was obtained from the China State Environmental Protection Bureau; the data on annual mortality of AD from 1991 to 2000 were obtained from the National Death Cause Surveillance Database of China. Using these data, we calculated the spearman correlation coefficient between soil As concentration and AD mortality, and the relative risk (RR) between soil As levels and AD mortality by quartile-dividing study groups. Results: The spearman correlation coefficient between As concentration and AD mortality was 0.552 (p = 0.004), 0.616 (p = 0.001) and 0.622 (p = 0.001) in the A soil As (eluvial horizon), the C soil As (parent material horizon), and the Total soil As (A soil As + C soil As), respectively. When the A soil As concentration was over 9.05 mg/kg, 10.40 mg/kg and 13.10 mg/kg, the relative risk was 0.835 (95 % CI: 0.832, 0.838), 1.969 (95 %CI: 1.955, 1.982), and 2.939 (95 % CI: 2.920, 2.958), respectively; when the C soil As reached 9.45 mg/kg, 11.10 mg/kg and 13.55 mg/kg, the relative risk was 4.349 (95 % CI: 4.303, 4.396), 6.108 (95 % CI: 6.044, 6.172), and 9.125 (95 %CI: 9.033, 9.219), respectively. No correlation was found between lead, cadmium, and mercury concentration in the soil and AD mortality. Conclusion: There was an apparent soil As concentration dependent increase in AD mortality. Results of this study may provide evidence for a possible causal linkage between arsenic exposure and the death risk from AD.

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Regional specific groundwater arsenic levels and neuropsychological functioning: a cross-sectional study

Cited by 22 publications

References 49 publications

Sodium Arsenite-Induced Learning and Memory Impairment Is Associated with Endoplasmic Reticulum Stress-Mediated Apoptosis in Rat Hippocampus

Sodium Arsenite-Induced Learning and Memory Impairment Is Associated with Endoplasmic Reticulum Stress-Mediated Apoptosis in Rat Hippocampus

Estrogenic Endocrine Disrupting Chemicals Influencing NRF1 Regulated Gene Networks in the Development of Complex Human Brain Diseases

Positive association between soil arsenic concentration and mortality from alzheimer’s disease in mainland China

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