By Wan Zainal Azman Wan Abdullah
The Sun, December 5, 1995
By Wan Zainal Azman Wan Abdullah
The Sun, December 5, 1995
Aluminium is the most widely used metal in the world after iron. Comprising about 8% of the earth's crust, it is the third most common element. It has a great affinity for oxygen and therefore occurs only in the oxidized form, mainly as alumina. It is found in almost 300 different minerals and widely distributed in rocks, clay and soils.
The sources of aluminium are largely unknown to the public. As well as occuring naturally in food and water, aluminium may be found in many processed foods, cosmetics, toothpaste, antiperspirants and adjuvants in various parenteral preparations. It could also be found in different amounts in vegetation and animals according to its presence in the environment.
Because of the widespread distribution of aluminium compounds through food and drink intake and the air that we breathe in, exposure to it is unavoidable. Daily intake of aluminium for people in the general population has been reported to range from 9 mg/day to 36 mg/day, with an average of 20 mg/day.
Normal ingestion of aluminium in the diet is about 3mg/day to 5 mg/day, of which only about 15 microgram is absorbed through the wall of the gastrointestinal tract. In humans, this small amount is usually excreted through the kidneys. However, with intakes of greater than 1000 mg/day, retention does occur.
The most common foods that contain substantial amounts of aluminium-containing additives include processed cheeses, baking powders, cake mixes, frozen dough's, pancake mixes, self-raising flours and pickled vegetables.
Some forms of aluminium, like insoluble aluminium compounds that constitute aluminium hydroxide mixture are poorly absorbed from the gastrointestinal tract. Certain organic ligands of aluminium, such as aluminium citrate, pass very rapidly from the food chain into the blood. Once absorbed, aluminium is bound extensively to protein.
Aluminium compounds can also affect absorption of other elements in the gastrointestinal tract and alter intestinal function. Aluminium inhibits fluoride absorption and may decrease the absorption of calcium and iron compounds. It possibly hinders the absorption of cholesterol too by forming an aluminium-pectin complex that binds fats to nondigestible vegetable fibers.
Aluminium salts are found in some common medicines as well. These include analgesics (buffered aspirins), antacids, anti-diarrhoeal products, anti-haemorroidal preparations.
Buffered aspirins may be used over prolonged periods and in high dosage by elderly arthritic patients. Three to 9gm of aspirin daily could lead to the ingestion of 126mg to 728mg aluminium daily from this source. As for antacids, the aluminium content per dose may range from 35mg to 208mg. If taken at the maximum dosage, 24 tablets could lead to a possible daily intake of between 840mg and 5,000mg, resulting in acute toxicity.
Another important route of exposure to aluminium is through the contamination of fluids used in parenteral nutrition therapy, particularly in patients with renal impairment.
Aluminium retention in the body results in its accumulation in the bone and decreased mineralisation. The principal sources of aluminium contamination in typical total parenteral nutrition (TPN) formulations are potassium phosphates, amino acids, and calcium gluconate, gluceptate or glubionate salts.
The chronic use of medicines and fruit juices containing citrates should also be avoided in patients with impaired renal function, especially if prescribed together with antacids containing aluminium hydroxide because they are greatly increase absorption of aluminium.
The most serious problem of aluminium toxicity involves patients with end-stage chronic renal failure managed by long-term intermittent hemodialysis. It can cause neurological disturbance known as dialysis encephalopathy syndrome (DES).
The symptoms include memory loss, malaise, tremor, jerking movements, depression and anxiety. A toxin in the untreated tap water used for dialysis is suspected to be the cause.
Children can also be exposure to aluminium poisoning, particularly children with chronic renal failure. This could be due to the use of aluminium contaminated dialysate or orally administered aluminium-containing phosphate binders.
Milk products are high in phosphorus. Relatively large amounts of phosphate binders are required to maintain normal serum phosphate levels and they may be a major factor in raised aluminium levels.
Other clinicians have confirmed that infant formulae contain aluminium and its concentration is generally higher than that of cow or human milk.
Other contributing factors could be the immature gastrointestinal tracts of newborns and infants that could absorb an increased amount of orally administered aluminium as well as growing bones that could be especially exposed to its accumulation.
Aluminium poisoning has also been linked to Alzheimer's disease, a progressive neurodegenerative disorder associated with dementia. Higher concentrations of aluminium have been found in brain tissue of patients dying of Alzheimer's disease. The use of aluminium-based chemicals in the treatment is its treatment is believed to have caused that.
Occupational exposure also occurs in workers exposed to aluminium in the work place. Coughing, increased phlegm production and a sense of irritation are noted in this group of workers. These effects are believed to be related to increased aluminium dust concentration in the environment.
Chronic inhalation of fine aluminium dust or vapors has resulted in fibrosis of the lung, asthma, dyspnea, cough and pneumothorax.
In this aspect, prevention of toxicity is the major objective of the public health policies As such, environmental and occupational hygienic programmes must be monitored and maintained.
The writer is a Science Officer at the National Poison Centre, Universiti Sains Malaysia, Penang.