Cadmium mercury telluride ((Cd,Hg)Te)

Chronic Inhalation: 0.0002 mg/m3 (Mercury) (L134) Acute Inhalation: 0.00003 mg/m3 (Cadmium) (L134) Chronic Inhalation: 0.00001 mg/m3 (Cadmium) (L134) Intermediate Oral: 0.0005 mg/kg/day (Cadmium) (L134) Chronic Oral: 0.0001 mg/kg/day (Cadmium) (L134)

Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (A7, L139)

Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (L6, L7)

Cadmium and mercury may be absorbed from oral, inhalation, and dermal routes. Mercury is distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (L6, A6, L7)