Fluoride acute effects

The acute pulmonary toxicity of inhaled uranium is dependent on the chemical form of the uranium. Uranium hexafluoride is the only uranium compound that has been associated with acute effects after inhalation. Two accidents involving uranium hexafluoride have resulted in the deaths of three workers in the US uranium processing industry. However, the lethal effects were due to liberated hydrogen fluoride rather than the uranium. 

Workers exposed to an airborne fluoride concentration of 5mg/m complained of eye and respiratory tract irritation and nausea. The lethal oral dose of sodium fluoride for humans has been estimated to be 32-65 mg F/kg of body weight. Effects from ingestion are diffuse abdominal pain, diarrhea, and vomiting excessive salivation, thirst, and perspiration painful spasms of the limbs and sometimes albuminuria." Gastrointestinal effects produced after the acute ingestion of toxic amounts of fluoride likely arise from the corrosive action of hydrofluoric acid, which is produced within the acidic environment of the stomach. Cardiac arrest after accidental exposure to high levels of fluoride has been attributed to the development of hypocalcemia and/or hyperkalemia. ... 

Already in 1937 Roholm [40], originator of modern fluoride research, distinguished between chronic and acute toxicity of inorganic fluorides. Chronic toxicity is the result of continuous or repeated exposure of an organism to a toxic substance. Acute toxicity involves harmful effects in an organism through a single or short-term exposure to a toxic substance. 

Animal studies tend to confirm the dermal/ocular effects reported for humans. Bis(tributyltin)oxide is a severe irritant to the skin and an extreme eye irritant in rabbits (Sheldon 1975). By contrast, tributyltin fluoride and triphenyltin fluoride produced only minimal skin irritation but were also extreme eye irritants (Sheldon 1975). Other acute studies have likewise demonstrated the skin irritating potential of bis(tributyltin)oxide and triphenyltin acetate in rats (Klimmer 1969 Pelikan and Cerny 1968). 

Inhalation of beryllium compounds can cause acute chemical pneumonitis, a very rapidly progressing condition in which the entire respiratory tract, including nasal passages, pharynx, tracheobronchial airways, and alveoli, develops an inflammatory reaction. Beryllium fluoride is particularly effective in causing this condition, which has proven fatal in some cases. 

Acute symptoms of injury from various pollutants in different horticultural and agronomic groups are visible on the affected plant. Symptom expressions produced include chlorosis, necrosis, abscission of plant parts, and effects on pigment systems. Major pollutants which produce these injuries include sulfur dioxide, peroxyacetyl nitrate (PAN), fluorides, chlorides, nitrogen dioxide, ozone, and particulate matter minor pollutants are ethylene, chlorine, ammonia, and hydrogen chloride. Symptoms of acute injury are often used to identify pollutant source and to estimate agricultural damage. 

Two types of publications are presented herein. The first set outlines the toxic effects of aluminum compounds on various living systems. The second set, comprised of two papers, deals with the formation and activity of aluminum fluoride compounds. The Volume begins with a chapter by Berend Acute Aluminum Intoxication that outlines the myriad toxic effects aluminum can have once it has by-passed an organisms protective barriers. This occurs in humans, for example, when aluminum salts are used in medicine (a practice that has now been eradicated). The in-depth coverage of this topic provides an excellent background for understanding the chemical interactions associated with aluminum that are described subsequently in Chapters 2-4. 

Renal effects can be produced in animals after acute-duration inhalation exposures to uranium. A 10-minute exposure to 637 mg U/m as uranium hexafluoride produced severe degeneration of the cortical tubules 5-8 days later in rats (Spiegl, 1949). These same effects were observed in dogs 1-3 days after a 1-hour exposure to 250 mg U/m as uranyl fluoride (Morrow et al. 1982). Proteinuria and glucosuria were also observed in rats after 2-10-minute exposures to uranium hexafluoride (Leach et al. 1984). 

The major toxicological effects of beryllium are on the lung. Acute exposure to soluble beryllium compounds (e.g., fluoride, an intermediate in the ore extraction process) irritates the entire respiratory tract, may produce acute chemical pneumonitis, and can result in fatal pulmonary edema. Hypersensitivity, which appears to be mediated by the immune system, may also occur following exposure. This means that future exposure to beryllium may produce health effects at concentrations lower than those generally associated with the effect (the individual becomes much more sensitive to beryllium). 

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