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Metal Exposure and Toxic Responses
Published in Stephen K. Hall, Joana Chakraborty, Randall J. Ruch, Chemical Exposure and Toxic Responses, 2020
Arsine (AsH3) is the most toxic arsenic compound. It is a colorless gas with a slight garlic-like odor and can be generated by side reactions or unexpectedly. Once absorbed, arsine is gradually oxidized in the body to arsenic trioxide. During this oxidation the protein of the red blood cells is denatured, resulting in hemolysis. Invariably, the first sign observed is hemoglobinuria, coloring the urine a port wine hue. Jaundice starts at the second or third day and rapidly spreads over the whole body. As a result of the rapid destruction of the red blood cells, large quantities of free hemoglobin block the renal tubules with hemoglobin crystals and fragments of cells. This is manifested by increasing oliguria, followed by anuria, leading to uremia and death.
Occupational toxicology of the kidney
Published in Chris Winder, Neill Stacey, Occupational Toxicology, 2004
There are a number of clinical signs in patients with renal injury (Schrier 1999), as follows: anuria (no urine output), oliguria (decreased urine output) or less commonly polyuria (increased urine output)oedema from severe hypoalbuminaemia due to glomerular dysfunction (nephrotic syndrome)hypertensionanaemiaabnormalities of the urine.
Toxicology
Published in Martin B., S.Z., of Industrial Hygiene, 2018
Arsine (AsH3) is the most toxic arsenic compound. It is a colorless gas with a slight garlic-like odor generated by side reactions. Once absorbed, arsine is gradually oxidized in the body to arsenic trioxide. During this oxidation the protein of the red blood cells is denatured, resulting in hemolysis. Invariably, the first sign observed is hemoglobinuria, coloring the urine up to port wine hue. Jaundice starts at the second or third day and rapidly spreads over the whole body. As a result of the rapid destruction of the red blood cells, large quantities of free hemoglobin block the renal tubules with hemoglobin crystals and fragments of cells. This is manifested by increasing oliguria, followed by anuria, leading to uremia and death.
Heavy metal concentrations in commercially valuable fishes with health hazard inference from Karnaphuli river, Bangladesh
Published in Human and Ecological Risk Assessment: An International Journal, 2020
Mir Mohammad Ali, Mohammad Lokman Ali, Ram Proshad, Saiful Islam, Zillur Rahman, Tanmoy Roy Tusher, Tapos Kormoker, Mamun Abdullah Al
In the recent years, world consumption of fish has increased because of their nutritional and therapeutic benefits. In addition to being an important source of protein, fish typically have rich contents of essential minerals, vitamins, protein (Fish fulfil 60% protein requirement) and unsaturated fatty acids (Medeiros et al. 2012; Hossen et al. 2018; DoF 2019). But it has been proved that different severe diseases occurred due to consumption of toxic metal contaminated fish. Several examples, chromium (Cr) causes anuria, nephritis and extensive lesions, kidney lesions by contaminated fish (Rahman and Islam 2010; Proshad et al. 2018). Poor reproductive capacity, kidney dysfunction, tumours, hypertension and hepatic dysfunction are caused by Cadmium toxicity (Rahman and Islam 2010; Al-Busaidi et al. 2011); Liver damage and renal failure are caused by lead (Luckey and Venugopal 1977; Lee et al. 2011). Again, fish skin and gills may be potential sources of heavy metal accumulation in fish (Al-Busaidi et al. 2011).
From small molecules to polymeric probes: recent advancements of formaldehyde sensors
Published in Science and Technology of Advanced Materials, 2022
Swagata Pan, Subhadip Roy, Neha Choudhury, Priyanka Priyadarshini Behera, Kannan Sivaprakasam, Latha Ramakrishnan, Priyadarsi De
Formaldehyde (FA, HCHO), is the simplest aldehyde, and its 40% aqueous solution is known as formalin. It is a colorless, poisonous gas with a strong smell, that causes severe damage to our central nervous system (CNS) and immune system [1]. It is generally used in the making of many resins, polymers, wood products [2], and protein cross-linkers for tissue fixation [3]. The thermal and chemical decomposition of construction materials such as particleboard and urea-formaldehyde foam insulation heavily release FA in the atmosphere [1]. FA is well known for its toxicity and carcinogenic nature [4]. In humans, formaldehyde transforms into formic acid, giving rise to breathing difficulties, hypothermia, blood acidity, and coma or death [5]. Recently, International Agency for Research on Cancer (IARC) has announced formaldehyde as one of the main Group 1 carcinogenic organic compounds in the World [6]. The World Health Organization (WHO) declared the limit of exposure to formaldehyde as 80 parts per billion (ppb) as standard for 30 min [7]. Occupational Safety and Health Administration (OSHA) fixed standard value for permissible exposure limit at 750 ppb, while maximum exposure value for Immediately Dangerous to Life or Health (IDLH) is considered as 20 parts per million (ppm) [8,9]. US Environmental Protection Agency has determined the maximum reference dosage of FA is 0.15–0.2 mg/kg body weight/day [10]. In the brains of healthy individuals, the concentration of FA is in the 0.2–0.4 mM range [11]. In body tissues, FA reacts with biomolecules like amino acids, proteins, nucleic acids and nucleotides, and produces unstable assemblies which transport FA to distant tissues from the respiratory tract [12]. Consumed FA causes damage in liver and kidney (Figure 1b), which leads to albuminuria, jaundice, haematuria and acidosis, anuria, or inactivity in central nervous system leading to depression, and even causing heart failure [5,13]. Even a low level of FA harms the respiratory organs, nose, eyes, and originates allergies, commonly identified as sick house syndrome [14]. Ingestion of 30 mL of 37% HCHO solution is reported to cause death in humans [15]. Moreover, FA is toxic to neuronal cells and is able to disrupt the neuronal networks through τ protein polymerization and induction of hyperphosphorylation [16].
Fetal surgery: how recent technological advancements are extending its applications
Published in Expert Review of Medical Devices, 2019
The first example is the use of fetoscopy to map and guide the fulguration of placental anastomoses in twin-to-twin transfusion syndrome (TTTS) [2]. TTTS occurs in 10–20% of monochorionic pregnancies with the natural history showing a mortality rate of near 90%. In TTTS, abnormal vascular communications lead to an unbalanced blood flow from one twin (the donor) to the other twin (the recipient) [2]. This can cause anuria, oligohydramnios and poor fetal growth in the donor twin due to hypovolemia, as well as polyuria, polyhydramnios, heart failure, and hydrops in the recipient twin due to hypervolemia. Fetoscopic selective laser coagulation (FSLC) of the placental anastomoses has become the standard-of-care treatment in severe TTTS [2]. Essentially, a 1-3 mm endoscope is introduced into the polyhydramniotic sac of the recipient twin and a laser fiber is used to cauterize the placental anastomoses. Originally, the photocoagulation of the anastomoses was done in a non-selective laser ablation of placental anastomoses, meaning that all vessels crossing the intertwin membranes were targeted by the laser [3]. However, research indicated that non-selective photocoagulation of placental anastomoses was associated with higher frequency of donor twin demise [3]. Therefore, a selective laser ablation was developed that endoscopically identifies all anastomoses and occludes only such connections avoiding ablating important vessels to the twins that are not causing TTTS. Residual anastomosis leading to twin anemia polycythemia sequence (TAPS) and recurrent TTTS were found to be an issue with this technique in up to 33% of cases. In order to minimize the risk of residual anastomoses that are invisible to the naked eye, the Solomon technique was introduced. After selectively ablating the anastomoses, we ablate the area between the anastomoses making a line on the placental vascular equator, with the objective of occluding small anastomoses that are usually not seen through fetoscope. The Solomon technique is different than the non-selective technique initially described since we follow the placental vascular equator where the anastomoses are really located, preserving important vessels to both twins. Solomonization not only coagulates all identified anastomotic vessels, but it also creates a continuous line of coagulation on the chorionic plate [3]. Recent studies demonstrated that this approach significantly reduces the incidence of TAPS and recurrent TTTS in comparison to the selective laser method and may improve survival and neonatal outcome [3]. Fortunately, because of the technological advancements, outcomes for fetoscopic laser surgery have significantly improved over the past 25 years, with up to 70% overall double survival and >80% single survival rates [1]. Flexible mini-telescopes have recently been applied to allow for better visualization of the vascular equator in anterior placentas, especially in cases where anastomoses are close to the insertion site of the fetoscope [3].