Aluminiumantimonid

Warning

H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]

P261, P264, P270, P271, P273, P301+P317, P304+P340, P317, P330, P391, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 5 reports by companies from 2 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Following oral exposure to antimony, administer charcoal as a slurry (240 mL water/30 g charcoal). Following inhalation exposure, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. In case of eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. Following dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists. (T36)

Aluminum targets the nervous system and causes decreased nervous system performance and is associated with altered function of the blood-brain barrier. The accumulation of aluminum in the body may cause bone or brain diseases. High levels of aluminum have been linked to Alzheimer's disease. A small percentage of people are allergic to aluminium and experience contact dermatitis, digestive disorders, vomiting or other symptoms upon contact or ingestion of products containing aluminium. Dermal exposure to antimony can cause antimony spots (papules and pustules around sweat and sebaceous glands). Antimony poisoning can also lead to pneumoconiosis. Alterations in pulmonary function and other effects including chronic bronchitis, chronic emphysema, inactive tuberculosis, pleural adhesions, and irritation can result from inhalation of antimony. Increased blood pressure can also result from antimony poisoning. Myocardial depression, vasodilation and fluid loss may cause shock with hypotension, electrolyte disturbances and acute renal failure. Cerebral oedema, coma, convulsions, and death are possible. (L741, L739, L740)

The main target organs of aluminum are the central nervous system and bone. Aluminum binds with dietary phosphorus and impairs gastrointestinal absorption of phosphorus. The decreased phosphate body burden results in osteomalacia (softening of the bones due to defective bone mineralization) and rickets. Aluminum's neurotoxicity is believed to involve several mechanisms. Changes in cytoskeletal protein functions as a results of altered phosphorylation, proteolysis, transport, and synthesis are believed to be one cause. Aluminum may induce neurobehavioral effects by affecting permeability of the blood-brain barrier, cholinergic activity, signal transduction pathways, lipid peroxidation, and impair neuronal glutamate nitric oxide-cyclic GMP pathway, as well as interfere with metabolism of essential trace elements because of similar coordination chemistries and consequent competitive interactions. Aluminum can also interact with estrogen receptors, increasing the expression of estrogen-related genes and contributing to the progression of breast cancer. Certain aluminum salts induce immune responses by activating inflammasomes. The inhalation data suggest that the myocardium is a target of antimony toxicity. It is possible that antimony affects circulating glucose by interfering with enzymes of the glycogenolysis and gluconeogenesis pathways. The mechanism of action of antimony remains unclear. However, some studies suggest that antimony combines with sulfhydryl groups including those in several enzymes important for tissue respiration. The antidotal action of BAL depends on its ability to prevent or break the union between antimony and vital enzymes. Moreover, the The cause of death is believed to be essentially the same as that in acute arsenic poisoning. (T18, L741, A238, L739, A235, A236)

Inhalating aluminum dust causes coughing and abnormal chest X-rays. A small percentage of people are allergic to aluminium and experience contact dermatitis, digestive disorders, vomiting or other symptoms upon contact or ingestion of products containing aluminium. Abdominal pain, vomiting, diarrhea can result from inhalation of antimony. Dyspnea, headache, vomiting,cough, conjunctivitis, and bloody purulent discharge from nose can result from inhalation exposure. Skin or eye contact can cause pain and redness of the exposed surface. (T64, L741, L739, L740)

Aluminum is poorly absorbed following either oral or inhalation exposure and is essentially not absorbed dermally. The bioavailability of aluminum is strongly influenced by the aluminum compound and the presence of dietary constituents which can complex with aluminum and enhance or inhibit its absorption. Aluminum binds to various ligands in the blood and distributes to every organ, with highest concentrations found in bone and lung tissues. In living organisms, aluminum is believed to exist in four different forms: as free ions, as low-molecular-weight complexes, as physically bound macromolecular complexes, and as covalently bound macromolecular complexes. Absorbed aluminum is excreted principally in the urine and, to a lesser extent, in the bile, while unabsorbed aluminum is excreted in the faeces. Antimony is widely distributed throughout the body. The hair and skin contain the highest levels of antimony. The adrenal glands, lung, large intestine, trachea, cerebellum, and kidneys also contain relatively high levels of antimony. Blood is the main vehicle for the transport of absorbed antimony to various tissue compartments of the body. Antimony is a metal and, therefore, does not undergo catabolism. Antimony can covalently interact with sulfhydryl groups and phosphate, as well as numerous reversible binding interactions with endogenous ligands (e.g., proteins). It is not known if these interactions are toxicologically significant. Antimony is excreted via the urine and feces. Some of the fecal antimony may represent unabsorbed antimony that is cleared from the lung via mucociliary action into the esophagus to the gastrointestinal tract. (L741, L739)