This book reviews the scientific literature and the authors’ own research linking aluminum neurotoxicity with cognitive impairment and Alzheimer’s disease (AD). It focuses on aluminum levels in the brain, region-specific and subcellular distribution, and its relation to neurofibrillary tangles and amyloid beta. Further, the book stresses the importance of aluminum’s complex speciation chemistry in relation to biology, and details aluminum’s mechanism in oxidative stress and cell death, especially in connection with apoptosis and necroptosis. The electrophysiological variation and synaptic plasticity induced by aluminum are covered, while the metal’s debatable role in AD and the cross-talk between aluminum and genetic susceptibility are also discussed. In closing, the book reviews the neurotoxic effects of aluminum and its important role in the pathogenesis of AD. Given its depth of coverage, the book provides readers with a systematic summary of aluminum neurotoxicity.
Aluminum is the third most abundant element in the Earth's crust. In many of the previous experimental, epidemiological, pathohistological, biochemical and other research studies, aluminum, accumulated from the environment has been recognized as a very harmful substance to the human body. Aluminum intake usually happens unintentionally due to the fact that people know little about its prevalence in water, factory-processed foods, medicines, cosmetics, etc. When accumulated in human organs, it can cause severe damage, and even lead to chronic neurodegenerative diseases. Both oxidative and nitrosative stress can be the leading cause or contribute to its toxic effects in humans and animals. All of this is supported by the fact that mitochondrial dysfunction is the earliest stage of aluminum neurotoxicity. When oxidative damage occurs under the effects of free radicals, together with the decreased antioxidant protection due to the decreased production of the chemical energy molecule (adenosine triphosphate) as well as reducing equivalents (both in and out of mitochondria) then the conditions for the occurrence of a vicious circle in aluminum neurotoxicity are created. Aluminum also significantly interferes with the main steps of the synaptic neurotransmission, which may lead to the progression of neuropathies. The glutamate-glutamine pathway and numerous neurotransmitter transporters are affected as well. Oxidative stress and the disruption of neurotransmission do not only exist when adult individuals are exposed to this neurotoxin, but also in individuals prenatally exposed to it as well, and these are expressed after birth. Numerous research studies, both in animals and humans, ex vivo and in vitro, quite clearly showed that aluminum can be associated with chronic neurodegenerative diseases. Additionally, there is a positive correlation between the exposure to aluminum and the pathophysiology of Alzheimer's, Parkinson's, Huntington's disease, amyotrophic lateral sclerosis, and so on. One of the possible mechanisms for the generation/development of these diseases could be the disturbed homeostasis of essential metals and the appearance of unfolded or misfolded proteins that are mostly specific for a particular disease. In those research studies, the influence of aluminum on the generation of beta-amyloid, alpha synuclein, etc. was satisfactorily examined. It is very difficult, however, to suppress aluminum neurotoxicity, as well as development and progression of the diseases caused by or associated with aluminum. This is the result of some complex mechanisms through which aluminum causes its deleterious effects, and which are also responsible for the existence of multiple targets for aluminum. It is, therefore, necessary to know how these mechanisms induce the damage, in order to be able to prevent or treat the damage once it occurs. A large number of substances, including active components in traditional medicine, medical drugs and substances which are used only experimentally, have been examined so far. The results of studies conducted so far are inconclusive and they require further research. According to all the aforementioned findings, it may be concluded that well-planned, prospective and randomized clinical trials are necessary in order to use any of these substances in humans.
Trace minerals and metals such as zinc, copper, and magnesium are accepted as a "natural" part of the human system. Interactions of some elements and/or disturbances in trace-metal or mineral homeostasis can, however, be toxic to the central nervous system (CNS). Mineral and Metal Neurotoxicology describes a wide range of basic and clinical issues
Aluminium is a chemical element present in earth’s crust and it is a known environmental toxin which has been found to be associated with various neurological disorders. Aluminium has been found to be a very strong risk factor for the development of Alzheimer’s disease. Biochemical Mechanisms of Aluminium Induced Neurological Disorders explains the association of aluminium with neurological disorders. The book introduces the reader to sources of aluminium exposure, followed by an explanation of pharmacokinetics of aluminium and the different biochemical pathways that cause neurological effects. Chapters cover the typical mechanisms associated with aluminium neurotoxicity such as synaptic impairment as well as recent topics of interest such as the role of aluminum in impairing blood-brain barrier functions. Separate chapters which cover clinical evidence of aluminium toxicity and its management are also included in the book. Biochemical Mechanisms of Aluminium Induced Neurological Disorders is a concise, yet informative reference on the subject of aluminium neurotoxicity for all readers, whether they are students of biochemistry, pharmacology and toxicology, clinical neurologists, environmentalists interested in metal pollution or general readers who want to learn about the toxic effects of aluminium in humans.
Parents have come to depend on vaccines to protect their children from a variety of diseases. Some evidence suggests, however, that vaccination against pertussis (whooping cough) and rubella (German measles) is, in a small number of cases, associated with increased risk of serious illness. This book examines the controversy over the evidence and offers a comprehensively documented assessment of the risk of illness following immunization with vaccines against pertussis and rubella. Based on extensive review of the evidence from epidemiologic studies, case histories, studies in animals, and other sources of information, the book examines: The relation of pertussis vaccines to a number of serious adverse events, including encephalopathy and other central nervous system disorders, sudden infant death syndrome, autism, Guillain-Barre syndrome, learning disabilities, and Reye syndrome. The relation of rubella vaccines to arthritis, various neuropathies, and thrombocytopenic purpura. The volume, which includes a description of the committee's methods for evaluating evidence and directions for future research, will be important reading for public health officials, pediatricians, researchers, and concerned parents.
Most people associate fluoride with the practice of intentionally adding fluoride to public drinking water supplies for the prevention of tooth decay. However, fluoride can also enter public water systems from natural sources, including runoff from the weathering of fluoride-containing rocks and soils and leaching from soil into groundwater. Fluoride pollution from various industrial emissions can also contaminate water supplies. In a few areas of the United States fluoride concentrations in water are much higher than normal, mostly from natural sources. Fluoride is one of the drinking water contaminants regulated by the U.S. Environmental Protection Agency (EPA) because it can occur at these toxic levels. In 1986, the EPA established a maximum allowable concentration for fluoride in drinking water of 4 milligrams per liter, a guideline designed to prevent the public from being exposed to harmful levels of fluoride. Fluoride in Drinking Water reviews research on various health effects from exposure to fluoride, including studies conducted in the last 10 years.
Scientists agree that exposure to toxic agents in the environment can cause neurological and psychiatric illnesses ranging from headaches and depression to syndromes resembling parkinsonism. It can even result in death at high exposure levels. The emergence of subclinical neurotoxicity-the concept that long-term impairments can escape clinical detection-makes the need for risk assessment even more critical. This volume paves the way toward definitive solutions, presenting the current consensus on risk assessment and environmental toxicants and offering specific recommendations. The book covers: The biologic basis of neurotoxicity. Progress in the application of biologic markers. Reviews of a wide range of in vitro and in vivo testing techniques. The use of surveillance and epidemiology to identify neurotoxic hazards that escape premarket screening. Research needs. This volume will be an important resource for policymakers, health specialists, researchers, and students.
Exposure to toxic chemicalsâ€"in the workplace and at homeâ€"is increasing every day. Human behavior can be affected by such exposure and can give important clues that a person or population is in danger. If we can understand the mechanisms of these changes, we can develop better ways of testing for toxic chemical exposure and, most important, better prevention programs. This volume explores the emerging field of neurobehavioral toxicology and the potential of behavior studies as a noninvasive and economical means for risk assessment and monitoring. Pioneers in this field explore its promise for detecting environmental toxins, protecting us from exposure, and treating those who are exposed.
Ignition of upholstered furniture by small open flames from matches, cigarette lighters, and candles is one of the leading causes of residential-fire deaths in the United States. These fires accounted for about 16% of civilian fire deaths in 1996. On average, each year since 1990, about 90 deaths (primarily of children), 440 injuries, and property losses amounting to 50 million dollars have resulted from fires caused by the ignition of upholstered furniture by small open flames. Certain commercial seating products (such as aircraft and bus seats) are subject to flammability standards and sometimes incorporate FR-treated upholstery cover materials, but there is no federal-government requirement for residential upholstered furniture, and it is generally not treated with FR chemicals. It is estimated that less than 0.2% of all U.S. residential upholstery fabric is treated with flame-retardant (FR) chemicals. The Consumer Product Safety Act of 1972 created the U.S. Consumer Product Safety Commission (CPSC) as an independent federal regulatory agency whose mission is to protect the public from unreasonable risks of injury and death associated with consumer products. CPSC also administers the Flammable Fabrics Act, under which it regulates flammability hazards and the Federal Hazardous Substances Act (FHSA), which regulates hazardous substances including chemicals. In 1993, the National Association of State Fire Marshals petitioned CPSC to issue a performance-based flammability standard for upholstered furniture to reduce the risk of residential fires. The Commission granted that portion of the petition relating to small open flame ignition risks. In response to concerns regarding the safety of FR chemicals, Congress, in the fiscal year 1999 appropriations report for CPSC, requested that the National Research Council conduct an independent study of the health risks to consumers posed by exposure to FR chemicals that are likely to be used in residential upholstered furniture to meet a CPSC standard. The National Research Council assigned the project to the Committee on Toxicology (COT) of the Commission on Life Sciences' Board on Environmental Studies and Toxicology. COT convened the Subcommittee on Flame-Retardant Chemicals, which prepared this report. Subcommittee members were chosen for their recognized expertise in toxicology, pharmacology, epidemiology, chemistry, exposure assessment, risk assessment, and biostatistics. Toxicological Risks of Selected Flame-Retardant Chemicals is organized into 18 chapters and two appendices. Chapter 2 describes the risk assessment process used by the subcommittee in determining the risk associated with potential exposure to the various FR chemicals. Chapter 3 describes the method the subcommittee used to measure and estimate the intensity, frequency, extent, and duration of human exposure to FR chemicals. Chapters 4-19 provide the subcommittee's review and assessment of health risks posed by exposure to each of the 16 FR chemicals. Data gaps and research needs are provided at the end of these chapters.
