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Human Health Studies
Published in Barry L. Johnson, Impact of Hazardous Waste on Human Health, 2020
Neurotoxicity is the capacity of chemical, biologic, or physical agents to cause adverse functional or structural changes in the nervous system. Massive neurologic injury can result in incoordination, dementia, convulsions, paralysis, and coma. Even slight damage to the nervous system can produce memory loss, impaired ability to reason, motor dysfunction, and communication problems. Children and developing fetuses are of special concern because damage to the developing nervous system can cause great functional consequences and be long-lasting. Fetal Alcohol Syndrome is an example of neurotoxic damage caused to a fetus by a toxicant (ethanol) and which has profound consequences in lowered birth weight or in more extreme cases, of mental retardation.
Risk Assessment for Occupational Neurotoxicants
Published in Lucio G. Costa, Luigi Manzo, Occupatinal Neurotoxicology, 2020
Occupational risk assessment refers to the use of toxicological data to define the relationship between an occupational exposure and adverse health outcome. The goal is to develop a quantitative estimate of the probability that a given health outcome results from a specific exposure experienced at one’s workplace, for a particular length of time, by a particular route.1 Neurotoxicity may be defined as any adverse effect on the structure or function of the central and/or peripheral nervous system by a biological, chemical, or physical agent. Neurotoxic effects may be permanent or reversible, produced by neuropharmacological or neurodegenerative properties of a neurotoxicant, or the result of direct or indirect actions on the nervous system. Adverse effects can include both unwanted effects and any alteration from baseline that diminishes the ability of an organism to survive, reproduce, or adapt to its environment.2-3 So to put them together, occupational neurotoxicity risk assessment seeks to define the relationship between adverse health outcome and an occupational exposure to an agent that affects the structure or function of the nervous system.
Indoor Air Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
On most jet turbine aircraft, unfiltered engine bleed air is fed into the cabin, providing oxygen and heat for those aboard.140 Exposure of passengers and crew to some level of TAPs occurs in approximately 23% of monitored flights,141,142 whereas higher levels of exposure can occur when engine seals wear or fail. Symptoms of aerotoxic syndrome resulting from such exposures can include extreme mental impairment,143 an acute flight safety issue when crew exposure to contaminated air is significant. Material safety data sheets for synthetic jet lubricants list TAP contents of 1%–10%. Acute as well as long-term effects have been shown in the form of neurotoxicity resembling Parkinson's disease.
Application of molecular imaging technology in neurotoxicology research
Published in Journal of Environmental Science and Health, Part C, 2018
Xuan Zhang, Qi Yin, Marc Berridge, Che Wang
Neurotoxicity can be defined as adverse functional or structural changes in the central or peripheral nervous system. Neurotoxic effects that are caused by exposure to neurotoxins can be permanent or reversible. Neurotoxic substances, including biological, chemical, or physical agents, may disturb protein synthesis in neurons, alter the production of specific neurotransmitters, and cause cell death. Symptoms may appear immediately after exposure or be delayed. They may include sensory or motor malfunction, learning and memory process disruption, and detrimental behavioral effects.[1,2] Neurotoxin-induced biochemical and molecular events in the nervous system of animals may provide clues for exploring underlying mechanisms and serve as markers for early neurotoxicity detection.[2,3] Approaches that have been developed for neurotoxicology are designed to identify toxicants, investigate toxic effects, clarify the mechanism involved in toxicity, and provide protective strategy against neurotoxicity.
Chemical characterization and neuroprotective properties of copper nanoparticles green-synthesized by nigella sativa L. seed aqueous extract against methadone-induced cell death in adrenal phaeochromocytoma (PC12) cell line
Published in Journal of Experimental Nanoscience, 2020
Wen Yan, Yutang Liu, Shirin Mansooridara, Atoosa Shahriyari Kalantari, Nastaran Sadeghian, Parham Taslimi, Akram Zangeneh, Mohammad Mahdi Zangeneh
Methadone is an opioid pain medication used to treat moderate to moderately severe pain. It is a synthetic opioid that suppresses the pain signaling through the opioid and the non-opioid receptor pathways in humans and animals [1, 2]. The affinity of methadone for opioid receptors is lower than other opioids, such as morphine and heroin, and there is no specificity in binding this substance to μ, κ, and δ opioid receptors [1–3]. Methadone abuse leads to destructive effects on different cells of the body, especially neurons [4, 5]. Degeneration of red neurons was observed in the brain of rats exposed to chronic use of this substance. These observations indicate that the cerebra does not act properly in the central nervous system of abuser rats [6]. It adversely affects the central nervous system, cardiovascular, and gastrointestinal systems [6–8]. Therefore, the importance of alternative pathways increases in analgesic effects of methadone compared to the opioid pathway [9]. The metabolism of methadone occurs in the liver and inactive metabolites are excreted through the kidneys. Therefore, in the case of high dose and chronic use, these organs suffer from toxic effects caused by methadone [8–10]. Reducing opioid effects and low addiction potential has charmed the use of this drug compared with the other opioid analgesics [9, 10]. Among the effects of methadone abuse, fatal intoxications and respiratory depression can be mentioned as well as the development of lesions in the brain [6, 7]. These effects may lead to neurotoxicity and dysfunction in central nervous cells. So, studying the effects of this substance on the nervous system seems to be necessary in order to reduce its adverse effects [5]. Previous studies have shown that lipid peroxidation plays a major role in the production of methadone-dependent cytotoxicity, as it has been observed in the chronic consumption of heroin and cocaine. It induces apoptosis through increasing the oxidative stress [6, 7]. Also, similar studies revealed that many mechanisms such as inadequate neurogenesis, apoptotic processes, mitochondrial dysfunction, and oxidative stress are important in neurotoxicity of methadone [5, 6]. One group of materials that can remove the neurotoxicity activities of the psychedelic drugs is the metallic nanoparticles [11].