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Special Issue "Environmental Neurotoxicology"

A special issue of International Journal of Environmental Research and Public Health (ISSN 1660-4601).

Deadline for manuscript submissions: closed (31 March 2017)

Special Issue Editor

Guest Editor
Prof. Dr. Peter S. Spencer

Department of Neurology, School of Medicine, and Oregon Institute for Occupational Health Sciences, Oregon Health & Science University, Portland, OR 97239, USA
E-Mail
Phone: 503 209-0986
Interests: neurotoxinology (plant, fungal); neurotoxicology; systems biology; human disease Contribution: Special Issue: Neurotoxins: Health Threats and Biological Tools

Special Issue Information

Dear Colleagues,

Definitive evidence of cause and effect in human environmental neurotoxic disease is rare, in part because chemical exposures are diverse, focus is usually placed on a narrow subset, disease incubation may be prolonged, and experimental studies for assessing individual substances are time-consuming and expensive. Furthermore, the results obtained from laboratory models may be challenging to extrapolate to humans. These limitations notwithstanding, this research provides the opportunity to discover which and how natural and synthetic chemical substances cause neurological illness, both in individuals and in populations. The discovery of causation can lead to primary disease prevention. When this logic is applied to human sporadic neurodegenerative disorders, where the current research focus is placed on treatments for delaying clinical expression and advance, the human health and financial impacts of primary disease prevention become apparent. While this is an important component of environmental neurotoxicology, researchers are more often more focused on assessing the health risks from exposure to agents that are known or perceived to have neurotoxic potential, with uncertain extrapolations made from laboratory animal and human health. Finally, as much as neurotoxicology is concerned with the adverse affects of chemical agents on the nervous system, once the chemical culprits are convincingly identified and the mechanisms of attack understood, the same chemicals become valuable tools for the basic neuroscientist to probe nervous system function and dysfunction.

The present collection of invited papers reflects the above biases, approaches, and contributions. Importantly, the net is spread widely, in that the term “environment” is interpreted to include the totality of exogenous chemicals to which humans are exposed, whether in the air, food or water. Substances used in medicine are omitted, even though many have the potential to cause nervous system damage or dysfunction. These include drugs that are used in treating cancer and epilepsy, in anesthesia and psychiatry, and in the treatment of infections and parasites. Other deliberate omissions from this volume are chemicals used to induce euphoria, including alcohol and certain drugs, which also have significant neurotoxic potential. The public health impact from the neurotoxic effects of medicines and drugs is substantial, but beyond the focus of this volume.

Prof. Peter S. Spencer 
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Environmental Research and Public Health is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Neurotoxins
  • Neurotoxicants
  • Neurologic disease
  • Neurodegenerative disorders

Published Papers (5 papers)

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Research

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Open AccessCommunication Chronic Exposure to Uranium from Gestation: Effects on Behavior and Neurogenesis in Adulthood
Int. J. Environ. Res. Public Health 2017, 14(5), 536; doi:10.3390/ijerph14050536
Received: 29 March 2017 / Revised: 5 May 2017 / Accepted: 13 May 2017 / Published: 17 May 2017
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Abstract
Uranium exposure leads to cerebral dysfunction involving for instance biochemical, neurochemical and neurobehavioral effects. Most studies have focused on mechanisms in uranium-exposed adult animals. However, recent data on developing animals have shown that the developing brain is also sensitive to uranium. Models of
[...] Read more.
Uranium exposure leads to cerebral dysfunction involving for instance biochemical, neurochemical and neurobehavioral effects. Most studies have focused on mechanisms in uranium-exposed adult animals. However, recent data on developing animals have shown that the developing brain is also sensitive to uranium. Models of uranium exposure during brain development highlight the need to improve our understanding of the effects of uranium. In a model in which uranium exposure began from the first day of gestation, we studied the neurobehavioral consequences as well as the progression of hippocampal neurogenesis in animals from dams exposed to uranium. Our results show that 2-month-old rats exposed to uranium from gestational day 1 displayed deficits in special memory and a prominent depressive-like phenotype. Cell proliferation was not disturbed in these animals, as shown by 5-bromo-2′deoxyuridine (BrdU)/neuronal specific nuclear protein (NeuN) immunostaining in the dentate gyrus. However, in some animals, the pyramidal cell layer was dispersed in the CA3 region. From our previous results with the same model, the hypothesis of alterations of neurogenesis at prior stages of development is worth considering, but is probably not the only one. Therefore, further investigations are needed to correlate cerebral dysfunction and its underlying mechanistic pathways. Full article
(This article belongs to the Special Issue Environmental Neurotoxicology)
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Open AccessArticle Sub-Acute Toxicity Study of Graphene Oxide in the Sprague-Dawley Rat
Int. J. Environ. Res. Public Health 2016, 13(11), 1149; doi:10.3390/ijerph13111149
Received: 1 July 2016 / Revised: 17 October 2016 / Accepted: 7 November 2016 / Published: 17 November 2016
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Abstract
Graphene oxide (GO) is an oxidized derivative of graphene used in biotechnology and medicine. The safety of GO is uncertain, so we evaluated its toxicity in male rats. Rat tail veins were injected with 2.5, 5, or 10 mg/kg GO for seven days
[...] Read more.
Graphene oxide (GO) is an oxidized derivative of graphene used in biotechnology and medicine. The safety of GO is uncertain, so we evaluated its toxicity in male rats. Rat tail veins were injected with 2.5, 5, or 10 mg/kg GO for seven days and behavioral patterns, pathology, and tissue morphology were assessed. Data show that behaviors were not altered according to an open field test and a functional observational battery test, but histopathological analysis indicated that GO caused inflammation of the lung, liver, and spleen. GO also reduced cholesterol, high density lipoprotein (HDL), and low density lipoprotein (LDL). No other organs were modified. Thus, high concentrations of GO are toxic for the lung, liver, and spleen, but the mechanism by which this occurs requires more study. Full article
(This article belongs to the Special Issue Environmental Neurotoxicology)
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Figure 1

Open AccessArticle In Utero Exposure to Diethylhexyl Phthalate Affects Rat Brain Development: A Behavioral and Genomic Approach
Int. J. Environ. Res. Public Health 2015, 12(11), 13696-13710; doi:10.3390/ijerph121113696
Received: 9 August 2015 / Revised: 25 September 2015 / Accepted: 2 October 2015 / Published: 28 October 2015
Cited by 6 | PDF Full-text (1148 KB) | HTML Full-text | XML Full-text
Abstract
Diethylhexyl phthalate (DEHP) is one of the most widely utilized phthalate plasticizers. Previous studies have demonstrated that gestational or postnatal DEHP exposure induced adverse effects on rat brain development and function. In this study, we investigated the effects of gestational DEHP exposure on
[...] Read more.
Diethylhexyl phthalate (DEHP) is one of the most widely utilized phthalate plasticizers. Previous studies have demonstrated that gestational or postnatal DEHP exposure induced adverse effects on rat brain development and function. In this study, we investigated the effects of gestational DEHP exposure on gene expression profiling in neonatal rat brain and cognitive function change at adulthood. Adult Sprague Dawley dams were orally treated with 10 or 750 mg/kg DEHP from gestational day 12 to 21. Some male pups were euthanized at postnatal day 1 for gene expression profiling, and the rest males were retained for water maze testing on postnatal day (PND) 56. DEHP showed dose-dependent impairment of learning and spatial memory from PND 56 to 63. Genome-wide microarray analysis showed that 10 and 750 mg/kg DEHP altered the gene expression in the neonatal rat brain. Ccnd1 and Cdc2, two critical genes for neuron proliferation, were significantly down-regulated by DEHP. Interestingly, 750 mg/kg DEHP significantly increased Pmch level. Our study demonstrated the changed gene expression patterns after in utero DEHP exposure might partially contribute to the deficit of cognitive function at adulthood. Full article
(This article belongs to the Special Issue Environmental Neurotoxicology)
Open AccessArticle Altered Hippocampal Lipid Profile Following Acute Postnatal Exposure to Di(2-Ethylhexyl) Phthalate in Rats
Int. J. Environ. Res. Public Health 2015, 12(10), 13542-13559; doi:10.3390/ijerph121013542
Received: 3 September 2015 / Revised: 14 October 2015 / Accepted: 20 October 2015 / Published: 27 October 2015
Cited by 2 | PDF Full-text (1314 KB) | HTML Full-text | XML Full-text
Abstract
Slight changes in the abundance of certain lipid species in the brain may drastically alter normal neurodevelopment via membrane stability, cell signalling, and cell survival. Previous findings have demonstrated that postnatal exposure to di (2-ethylhexyl) phthalate (DEHP) disrupts normal axonal and neural development
[...] Read more.
Slight changes in the abundance of certain lipid species in the brain may drastically alter normal neurodevelopment via membrane stability, cell signalling, and cell survival. Previous findings have demonstrated that postnatal exposure to di (2-ethylhexyl) phthalate (DEHP) disrupts normal axonal and neural development in the hippocampus. The goal of the current study was to determine whether postnatal exposure to DEHP alters the lipid profile in the hippocampus during postnatal development. Systemic treatment with 10 mg/kg DEHP during postnatal development led to elevated levels of phosphatidylcholine and sphingomyelin in the hippocampus of female rats. There was no effect of DEHP exposure on the overall abundance of phosphatidylcholine or sphingomyelin in male rats or of lysophosphatidylcholine in male or female rats. Individual analyses of each identified lipid species revealed 10 phosphatidylcholine and six sphingomyelin lipids in DEHP-treated females and a single lysophosphatidylcholine in DEHP-treated males with a two-fold or higher increase in relative abundance. Our results are congruent with previous work that found that postnatal exposure to DEHP had a near-selective detrimental effect on hippocampal development in males but not females. Together, results suggest a neuroprotective effect of these elevated lipid species in females. Full article
(This article belongs to the Special Issue Environmental Neurotoxicology)

Review

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Open AccessReview Environmental Exposures and Parkinson’s Disease
Int. J. Environ. Res. Public Health 2016, 13(9), 881; doi:10.3390/ijerph13090881
Received: 6 May 2016 / Revised: 29 August 2016 / Accepted: 30 August 2016 / Published: 3 September 2016
Cited by 7 | PDF Full-text (321 KB) | HTML Full-text | XML Full-text
Abstract
Parkinson’s disease (PD) affects millions around the world. The Braak hypothesis proposes that in PD a pathologic agent may penetrate the nervous system via the olfactory bulb, gut, or both and spreads throughout the nervous system. The agent is unknown, but several environmental
[...] Read more.
Parkinson’s disease (PD) affects millions around the world. The Braak hypothesis proposes that in PD a pathologic agent may penetrate the nervous system via the olfactory bulb, gut, or both and spreads throughout the nervous system. The agent is unknown, but several environmental exposures have been associated with PD. Here, we summarize and examine the evidence for such environmental exposures. We completed a comprehensive review of human epidemiologic studies of pesticides, selected industrial compounds, and metals and their association with PD in PubMed and Google Scholar until April 2016. Most studies show that rotenone and paraquat are linked to increased PD risk and PD-like neuropathology. Organochlorines have also been linked to PD in human and laboratory studies. Organophosphates and pyrethroids have limited but suggestive human and animal data linked to PD. Iron has been found to be elevated in PD brain tissue but the pathophysiological link is unclear. PD due to manganese has not been demonstrated, though a parkinsonian syndrome associated with manganese is well-documented. Overall, the evidence linking paraquat, rotenone, and organochlorines with PD appears strong; however, organophosphates, pyrethroids, and polychlorinated biphenyls require further study. The studies related to metals do not support an association with PD. Full article
(This article belongs to the Special Issue Environmental Neurotoxicology)
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