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Heavy Metals
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Mercury poisoning may cause symptoms in several organ systems, including nervous (e.g., personality changes, tremors, memory deficits, and loss of coordination), cardiovascular (e.g., increased risk of arterial obstruction, hypertension, stroke, atherosclerosis, heart attacks, and increased inflammation), and gastrointestinal (e.g., nausea, diarrhea, and ulceration) systems as well as the kidneys (failure). Mercury may also accumulate in the thyroid and skin and increase the risk of autoimmune disorders and contact dermatitis (Figure 110.1) [14–16].
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Published in Anton Sebastian, A Dictionary of the History of Medicine, 2018
Mercury [Latin: mercurius] Called quicksilver by Aristotle (384–322 BC) and liquid silver by Dioscorides (AD 40–90). It was used for treatment of syphilis by Paracelsus (1493–1541), and became a common drug for venereal diseases. Gabriele Falloppio (1523–1562) opposed its extensive use for syphilis during the mid-16th century. Mercury injections in the form of diethyl mercury was introduced as treatment for syphilis by P. Hepp of Germany in 1887, but abandoned due to toxicity. See mercury poisoning.
The quest for wellness: Public health and environmental concerns
Published in Lois N. Magner, Oliver J. Kim, A History of Medicine, 2017
During World War I, Hamilton conducted studies of war-related industries, especially factories making munitions and explosives, to establish rules for protecting workers. American factories, with little or no experience, were producing huge quantities of chemicals needed for weapons and explosives, such as dinitrobenzol, trinitrotoluol, military guncotton, fulminate of mercury, nitric acid, aniline, and rubber. Previously, America had imported many of these chemicals from Germany. In 1923, Hamilton began to study factories that produced and used mercury, one of the oldest industrial poisons. During World War I there was great demand for mercury fulminate for the detonators of high explosives. Miners were poisoned because of their exposure to mercury fumes and dust particles. Their wives were poisoned by washing clothes that were heavily contaminated with mercury. Symptoms of mercury poisoning include swelling and pain in the gums and lips, twitching limbs, tremors of the hands, fatigue, anxiety, depression, irritability, and a neurological disorder known as Mad Hatter Disease (erethism mercurialis).
Flavonoids fractions of Adansonia digitata L. fruits protects adult Wistar rats from mercury chloride-induced hepatorenal toxicity: histopathological and biochemical studies
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Wusa Makena, Yomi Samson Aribiyun, Aisha Aminu, Barka Ishaku, Ayuba Yohana, Ekwere Eke Inemesit
Heavy metals pollute the environment and are toxic to living organisms, and in their various forms, they exhibit distinct biological behavior, pharmacokinetics, and clinical manifestations [1–3]. It is commonly found in the environment and is linked to severe health issues in mammals, and exposure to mercury chloride (HgCl2) is via products like batteries, pesticides, and paints [1,4,5]. Mercury poisoning affects the nervous system, liver, kidney, and digestive system [6]. It is primarily metabolized in the liver before accumulating in the kidneys. As a result, the liver and kidneys are the organs most affected [7]. Mercury chloride poisoning has previously been shown to occur via several routes, including inhalation, ingestion, and skin absorption [8]. Mercury chloride also degrades antioxidants and reduces free radical scavenging systems like superoxide dismutase (SOD), Catalase (CAT) and reduced glutathione (GSH) [9–11]. The occurrence of lipid peroxidation is among the critical pathological factors in the sequence of events that leads to the onset of degenerative diseases due to disruptions in redox and calcium homeostasis [12,13].
Development of a Natural Product Rich in Bioavailable Omega-3 DHA from Locally Available Ingredients for Prevention of Nutrition Related Mental Illnesses
Published in Journal of the American College of Nutrition, 2020
Christina N. Charles, Hulda Swai, Titus Msagati, Musa Chacha
Fish oil is currently the major dietary source of omega-3 DHA. However, according to Lane and colleagues, there are several limitations to relying fish oils as a source of supply of omega-3 DHA (17). Some of these limitations include the undesirable odors, flavors, and tastes of fish oils which discourage consumers from consuming them in their pure forms and neither is traditional supplementation much appreciated. Furthermore, some fish contain high levels of methyl-mercury, which creates a risk of mercury poisoning to consumers (17). Also, some fish oils have been found to contain environmental contaminants such as dioxins and polychlorinated biphenyls which dissuade its use. In addition, fish oil production has reached maximum global production and its stock is decreasing throughout the world (17), thus may not be a sustainable source of DHA, especially in resource-poor countries. This calls for development of products or formulations that are rich in preformed DHA and other health promoting compounds from other sources.
Renal leukocyte chemotactic factor 2 (ALECT2)-associated amyloidosis in Chinese patients
Published in Amyloid, 2020
Dan-yang Li, Dan Liu, Su-xia Wang, Xiao-juan Yu, Zhao Cui, Fu-de Zhou, Ming-hui Zhao
Patient No. 1 died of unknown cause 8 years after diagnosis (the first reported ALECT2 amyloidosis patient in China). In addition, clinical follow-up data were available in six patients followed for a mean of 13 months (range 7–18) and are detailed in Figure 3. During follow-up, four patients received support therapy; Pt. No. 6 underwent immunosuppressive therapy by daily oral prednisone and cyclophosphamide administration; Pt. No. 7 underwent chelation therapy several times due to mercury poisoning, while another patient did not take any medication. Except for Pt. No. 6, whose serum creatinine decreased from 542 to 383 μmol/L within 1 month, there was no significant change in serum creatinine among the five patients during follow-up. The mean final follow-up serum creatinine level in six patients was 141 μmol/L (range 76–303). None of the patients had clinically evident extrarenal organ involvement during follow-up.