Iron poisoning

Most iron salts and compounds may be safely handled following common safe laboratory practices. Some compounds are irritants. A more serious threat is ingestion of massive quantities of iron salts which results in diarrhea, hemorrhage, fiver damage, heart damage, and shock. A lethal dose is 200 250 mg/kg of body weight. The majority of the victims of iron poisoning are children under five years of age. 

Siderophores like desferrioxamine may, therefore, find increasing applications not only in the treatment of iron poisoning and iron-overloaded disease states but also as chemotherapeutic agents, although the possible problems noted above cannot be ignored. 

Oral iron poisoning Cigarette-smoke effects... 

Iron is an essential element, for humans and for many forms of life, but even a modest excess can be toxic as the human body does not have an effective iron excretion mechanism. It is therefore necessary to maintain an appropriate level of iron in the body, to supply iron in absorbable form if it is deficient (anemia) and to remove iron if present in excess. Inorganic coordination chemistry plays an important role in dealing with these complementary conditions of deficiency and of excess. The latter condition is much more common than often supposed, for there are a number of conditions, such as hemochromatosis and thallasemia, where the build-up of iron in essential organs is eventually lethal. Mild iron poisoning is not infrequent in children, while even iron fortification of foodstuffs can have adverse effects. Mild iron poisoning can be treated with bicarbonate or phosphate, which presumably complex and precipitate the iron. ... 

Mechanism of Action An antidote that binds with iron to form complex. Therapeutic Effect Promotes urine excretion of acute iron poisoning. 

Severe iron poisoning is manifested as vomiting, severe abdominal pain, diarrhea, and dehydration, followed by hyperventilation, pallor or cyanosis, and cardiovascular collapse. 

When injected, it forms a stable water-soluble iron complex (ferrioxamine) that prevents the iron from entering into further chemical reactions and is readily excreted in the urine giving the urine a characteristic reddish colour. Some of it is also excreted in the faeces via the bile. It can also chelate aluminium and thus is useful in aluminium overload. It is primarily a chelator used in acute iron poisoning and chronic iron overload as in thalassemia patients needing multiple transfusions. 

It is an orally active iron chelator. It is useful in acute iron poisoning, iron overload in cirrhosis, transfusion siderosis in thalassemia patients. Adverse effects are anorexia, vomiting, altered taste, joint pain and neutropenia. 

Deferoxamine (see also Chapters 58 and 59) Chelates excess iron Reduces the toxicity associated with acute or chronic iron overload Treatment of acute iron poisoning and for inherited or acquired hemochromatosis that is not adequately treated by phlebotomy Preferred route of administration is IM or SC Toxicity Rapid IV administration may cause hypotension acute respiratory distress has been observed with long infusions neurotoxicity and increased susceptibility to certain infections has occurred with longterm use... 

Exactly the opposite problem may occur for plants whose roots are growing in anaerobic media. In Hooded soils the roots may be exposed to high levels of irontll). posing potential problems of iron toxicity. Rice plants and water lilies with roots in anaerobic soils transport dioxygen (from the air or photosynthesis, or both) to the periphery of the roots where it oxidizes the iron(II) to irondll). In (his case the insolubility of Irondll) hydroxide is utilized to protect the plant from iron poisoning.113 A similar problem from too much iron occurs in parts of sub-Saharan Africa. 

The stability constants of the FeIU siderophore complexes are some of the largest known, e.g. the ferrichrome and ferrioxamine E complexes have log values of the order 29 and 32 respectively as compared to a value of 25 for Fe(edta). So strong are these complexes that microbes have been observed to leach iron from stainless steel vessels. Not surprisingly the siderophores also find use in treating cases of iron poisoning and for the elimination of iron from cases of thalassaemia.84 Complexation of Fe11 is considerably weaker than that of FeIU and this is probably utilized for the release of the iron within the cells. 

Sudden excessive uptake of soluble iron salts, especially by young children, can lead to acute iron poisoning, characterised by the highly corrosive action of iron... 

The mechanism of hydrogen evolution has been investigated by impedance measurements [371] and hydrogen-tritium kinetic isotope effects [375]. The effect of halides dissolved in solution has been studied [372, 376] these ions increase the overpotential in the sequence Cl- Adsorption isotherms for halides have been derived. They conform to the Temkin adsorption model with partial charge transfer. The lateral interaction between adsorbed particles has been calculated. It is higher for Br- than for I- and increases with overpotential on account of the weakening in the metal-halide bond. Thus, halides are substantial poisons for hydrogen evolution on iron. Poisons also include metal ions such as Cd2+, Zn2+, and Mn2+ [26]. 

Iron poisoning is characterized by vomiting, abdominal pain, gastroenteritis, and shock, and if not properly treated, severe acidosis, coma, and death ensue. Deferoxamine, which binds iron, is used as the preferred chelator in treating iron poisoning. The metabolic acidosis may be appropriately... 

Deferoxamine is isolated from Streptomycespilosus. It binds iron avidly but essential trace metals poorly. Furthermore, while competing for loosely bound iron in iron-carrying proteins (hemosiderin and ferritin), it fails to compete for biologically chelated iron, as in microsomal and mitochondrial cytochromes and hemoproteins. Consequently, it is the chelator of choice for iron poisoning (Chapters 33 and 59). Deferoxamine plus hemodialysis may also be useful in the treatment of aluminum toxicity in renal failure. Deferoxamine is poorly absorbed when administered orally and may increase iron absorption when given by this route. It should therefore be administered intramuscularly or, preferably, intravenously. It is believed to be metabolized, but the pathways are unknown. The iron-chelator complex is excreted in the urine, often turning the urine an orange-red color. 

Dose. In acute iron poisoning 5 g of desferrioxamine mesylate by mouth, with 2 g intramuscularly, and up to 15 mg/kg/hour by intravenous infusion. 

High doses of iron salts by mouth can cause severe gastrointestinal irritation and even necrosis of the mucous membrane. Autopsy shows severe damage to brain and liver. Iron poisoning is particularly dangerous in children. Sustained-release forms are safer in homes where heedless parents live with small children. Ferrous sulphate is the most toxic. 

Typically acute oral iron poisoning has the following phases ... 

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