Neurodevelopmental disabilities, including autism, attention-defi cit hyperactivity disorder, dyslexia, and other cognitive impairments, aff ect millions of children worldwide, and some diagnoses seem to be increasing in frequency. Industrial chemicals that injure the developing brain are among the known causes for this rise in prevalence. In 2006, we did a systematic review and identifi ed fi ve industrial chemicals as developmental neurotoxicants: lead, methylmercury, polychlorinated biphenyls, arsenic, and toluene. Since 2006, epidemiological studies have documented six additional developmental neurotoxicants—manganese, fl uoride, chlorpyrifos, dichlorodiphenyltrichloroethane, tetrachloroethylene, and the polybrominated diphenyl ethers. We postulate that even more neurotoxicants remain undiscovered. To control the pandemic of developmental neurotoxicity, we propose a global prevention strategy. Untested chemicals should not be presumed to be safe to brain development, and chemicals in existing use and all new chemicals must therefore be tested for developmental neurotoxicity. To coordinate these eff orts and to accelerate translation of science into prevention, we propose the urgent formation of a new international clearinghouse.

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Neurobehavioural effects of developmental toxicity

Purpose—To critically review and evaluate the science behind individual eligibility criteria (indication/inclusion and contraindications/exclusion criteria) for intravenous recombinant tissue-type ...

Scientific Rationale for the Inclusion and Exclusion Criteria for Intravenous Alteplase in Acute Ischemic Stroke: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association

Cadmium (Cd), a by-product of zinc production, is one of the most toxic elements to which man can be exposed at work or in the environment. Once absorbed, Cd is efficiently retained in the human body, in which it accumulates throughout life. Cd is primarily toxic to the kidney, especially to the proximal tubular cells, the main site of accumulation. Cd can also cause bone demineralization, either through direct bone damage or indirectly as a result of renal dysfunction. In the industry, excessive exposures to airborne Cd may impair lung function and increase the risk of lung cancer. All these effects have been described in populations with relatively high exposures to Cd in the industrial or in heavily polluted environments. Recent studies, however, suggest that the chronic low environmental exposure to Cd now prevailing in industrialized countries can adversely affect the kidneys and bones of the general population. These studies show consistent associations between various renal and bone biomarkers and the urinary excretion of Cd used to assess Cd body burden. The public health impact of these findings are still unknown. Further research is needed to ascertain that these associations are truly causal and not secondary to parallel changes in Cd metabolism and in the bone or kidney function occurring because of ageing or diseases unrelated to Cd exposure.

Cadmium & its adverse effects on human health.

Cadmium (Cd) is a heavy metal that has received considerable concern environmentally and occupationally. Cd has a long biological half-life mainly due to its low rate of excretion from the body. Thus, prolonged exposure to Cd will cause toxic effect due to its accumulation over time in a variety of tissues, including kidneys, liver, central nervous system (CNS), and peripheral neuronal systems. Cd can be uptaken from the nasal mucosa or olfactory pathways into the peripheral and central neurons; for the latter, Cd can increase the blood brain barrier (BBB) permeability. However, mechanisms underlying Cd neurotoxicity remain not completely understood. Effect of Cd neurotransmitter, oxidative damage, interaction with other metals such as cobalt and zinc, estrogen-like, effect and epigenetic modification may all be the underlying mechanisms. Here, we review the in vitro and in vivo evidence of neurotoxic effects of Cd. The available finding indicates the neurotoxic effects of Cd that was associated with both biochemical changes of the cell and functional changes of central nervous system, suggesting that neurotoxic effects may play a role in the systemic toxic effects of the exposure to Cd, particularly the long-term exposure.

https://downloads.hindawi.com/journals/omcl/2013/898034.pdf

Cadmium and Its Neurotoxic Effects

Nanocomposite membranes for water separation and purification: Fabrication, modification, and applications

In countries such as India, the silver jewelry industry is an important cottage industry. Silver is mixed with cadmium and then used to make silver jewelry. During this process there is a formation of cadmium fumes, and the workers inhale the fumes. Cadmium is a neurotoxic and nephrotoxic heavy metal, and there are no national policies to prevent exposure to such chemicals. We will present a case of cadmium induced peripheral neuropathy, nephropathy, and decreased bone density.

/pdf/cadmium-exposure-health-hazards-of-silver-cottage-industry-16ag6zttfh.pdf

Cadmium exposure: Health hazards of silver cottage industry in developing countries

Visual agnosia they could see, but were unable to recognise familiar objects or their use. Oral tendencies they would examine their surroundings with their mouths instead of their eyes. Hypermetamorphosis a desire to explore everything. Emotional changes emotion was dulled and facial movements and vocalisations were far less expressive. They lost fear where it would normally occur. Even after being attacked by a snake, they would casually approach it again. This was called 'placidity'. Hypersexuality a dramatic increase in overt sexual behaviour, including masturbation. They may even attempt copulation with inanimate objects.

Kluver Bucy syndrome.

Levetiracetam is a commonly used broad-spectrum anticonvulsant efficacious in both partial and generalized seizures. It has an extremely favorable side effect profile with few drug-drug interactions, low potential for hematological and hepatic toxicity, and thus has rapidly become the preferred drug in patients with traumatic brain injuries who need seizure prophylaxis. We report, here, a patient who was started on levetiracetam for seizure prophylaxis after developing large bifrontal-parietal traumatic subdural hematomas (SDH) following a fall from a horse necessitating bifrontal craniotomies for evacuation. The patient developed an asymptomatic elevation of the liver enzymes. The liver enzymes trended back to normal after levetiracetam was stopped, and topiramate was initiated in its place.

Asymptomatic elevation of liver enzymes due to levetiracetam: a case report.

Cysticercosis is a common parasitic infection caused by encysted larvae of the helminth Taenia solium (pork tapeworm). The central nervous system (CNS) is the most important primary site of infection and the disease can present with solitary or multiple space occupying lesions. Less common presentations in the CNS include the racemose variety with macroscopic groups of cysticerci in the subarachnoid space giving the appearance of a cluster of grapes and basal or ventricular cysticercosis causing obstructive hydrocephalus. Involvement of other organs: skeletal muscle, eyes, myocardium and the lungs has also been reported. Cases of cysticercosis presenting as isolated muscle mass (pseudotumours) without involvement of the CNS have also been recently described in the literature. We present a case of a 43-year-old woman who complained of subacute onset of left temporal pain and headache. Magnetic resonance imaging (MRI) showed characteristic imaging findings suggestive of cysticercosis of the temporalis muscle.

https://link.springer.com/content/pdf/10.1007%2Fs10194-007-0410-y.pdf

Prahlad K. Sethi

Papers

Cadmium exposure: Health hazards of silver cottage industry in developing countries

Kluver Bucy syndrome.

Asymptomatic elevation of liver enzymes due to levetiracetam: a case report.

Cysticercosis of temporalis muscle: an unusual cause of temporal headaches. A case report

Central nervous system fungal infections: Observations from a large tertiary hospital in northern India