Cadmium selenide

Biological Exposure Indices (BEI) [ACGIH] - Cd in urine = 5 ug/g creatinine; Cd in blood = 5 ug/L; sampling time not critical; Monitoring in blood should be preferred during the initial year of exposure and whenever changes in the degree of exposure are suspected. [ACGIH]

0.02 [mg/m3], inhalable fraction, as Se[German Research Foundation (DFG)]

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) Chronic Oral: 0.005 mg/kg/day (Selenium) (L134)

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. Chronic oral exposure to high concentrations of selenium compounds can produce a disease called selenosis. The major signs of selenosis are hair loss, nail brittleness, and neurological abnormalities (such as numbness and other odd sensations in the extremities). Animal studies have shown that selenium may also affect sperm production and the female reproductive cycle. (L619, L6)

Cadmium initially binds to metallothionein and is transported to the kidney. 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. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. Selenium readily substitutes for sulfur in biomolecules and in many biochemical reactions, especially when the concentration of selenium is high and the concentration of sulfur is low. Inactivation of the sulfhydryl enzymes necessary for oxidative reactions in cellular respiration, through effects on mitochondrial and microsomal electron transport, might contribute to acute selenium toxicity. Selenomethionine (a common organic selenium compound) also appears to randomly substitute for methionine in protein synthesis. This substitution may affect the structure and functionability of the protein, for example, by altering disulfide bridges. Inorganic forms of selenium appear to react with tissue thiols by redox catalysis, resulting in formation of reactive oxygen species and causing damage by oxidative stress. (L619, L8, A18, A19, A28)

Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. Short-term oral exposure to high concentrations of selenium may cause nausea, vomiting, and diarrhea. Brief exposures to high levels of elemental selenium or selenium dioxide in air can result in respiratory tract irritation, bronchitis, difficulty breathing, and stomach pains. Longer-term exposure to either of these air-borne forms can cause respiratory irritation, bronchial spasms, and coughing. (L619, L6)