Following a request from the Commission, the Panel on Food Additives, Flavourings, Processing Aids and Food Contact Materials (AFC) was asked to provide a scientific opinion on the safety of aluminium from all sources of dietary intake. In the event the estimated exposure for a particular sub-group(s) is found to exceed the Provisional Tolerable Weekly Intake, a detailed breakdown by exposure source should be provided.
Aluminium occurs naturally in the environment and is also released due to anthropogenic activities such as mining and industrial uses, in the production of aluminium metal and other aluminium compounds.
A variety of aluminium compounds are produced and used for different purposes, such as in water treatment, papermaking, fire retardant, fillers, food additives, colours and pharmaceuticals. Aluminium metal, mainly in the form of alloys with other metals, has many uses including in consumer appliances, food packaging and cookware.
The major route of exposure to aluminium for the general population is through food. Aluminium in drinking water represents another, minor, source of exposure. Additional exposures may arise from the use of aluminium compounds in pharmaceuticals and consumer products.
Most unprocessed foods typically contain less than 5 mg aluminium/kg. Higher concentrations (mean levels 5 to 10 mg/kg) were often found in breads, cakes and pastries (with biscuits having the highest levels), some vegetables (with mushrooms, spinach, radish, swiss card, lettuce and corn salad having the highest levels), glacé fruits, dairy products, sausages, offals, shellfish, sugar-rich foods baking mixes, and a majority of farinaceous products and flours. Foods with very high mean concentrations included tea leaves, herbs, cocoa and cocoa products, and spices.
Under normal and typical conditions the contribution of migration from food contact materials would represent only a small fraction of the total dietary intake. However, the Panel noted that in the presence of acids and salts, the use of aluminium-based pans, bowls, and foils for foods such as apple puree, rhubarb, tomato puree or salted herring could result in increased aluminium concentrations in such foods. Also, the use of aluminium vessels and trays for convenience and fast food in might moderately increase the aluminium concentrations, especially in foods that contain tomato, different types of pickles, and vinegar.
Total dietary exposure to aluminium from all sources has been estimated from duplicate diet studies (the Netherlands, Hungary, Germany, Sweden, and Italy), and market basket and total diet studies (UK, Finland, and France). Mean dietary exposure from water and food in non-occupational exposed adults showed large variations between the different countries and, within a country, between different surveys. It ranged from 1.6 to 13 mg aluminium per day, corresponding to 0.2 to 1.5 mg/kg body weight (bw) per week in a 60 kg adult. Children generally have higher food intake than adults when expressed on a body weight basis, and therefore represent the group with the highest potential exposure to aluminium per kg body weight.. Large individual variations in dietary exposure to aluminium can occur. In children and young people the potential estimated exposure at the 97.5th percentile ranged from 0.7 mg/kg bw/week for children aged 3-15 years in France to 2.3 mg/kg bw/week for toddlers (1.5-4.5 years) and 1.7 mg/kg bw/week for those aged 4-18 years in the UK. Cereals and cereal products, vegetables, and beverages appeared to be the main contributors (>10%) to the dietary aluminium exposure in the general population.
In infants aged 0-3, 4-6, 7-9 and 10-12 months, potential dietary exposures from infant formulae and other foods manufactured specially for infants were estimated to be respectively 0.10, 0.20, 0.43 and 0.78 mg/kg bw/week.
Potential exposure to aluminium in 3-month infants from a variety of infant formulae was estimated by the Panel. At the mean it was up to 0.6 mg/kg bw/week for milk-based formulae and was 0.75 mg /kg bw/week for soya-based formulae; at high percentiles of exposure it was up to 0.9 mg/kg bw/week for milk-based formulae and was 1.1 mg /kg bw/week for soya-based formulae.
The Panel noted that in some individual brands of formulae (both milk-based and soya-based) the aluminium concentration was around 4 times higher that the mean concentrations estimated above, leading to a 4 times higher potential exposure in brand-loyal infants.
Potential exposure in breast-fed infants was estimated to be less than 0.07 mg/kg bw/week.
The oral bioavailability of the aluminium ion in humans and experimental animals from drinking water has been estimated to be in the range of 0.3%, whereas the bioavailability of aluminium from food and beverages generally is considered to be lower, about 0.1%. However, it is likely that the oral absorption of aluminium from food can vary at least 10-fold depending on the chemical forms present. Although the degree of water solubility of an aluminium compound appears to increase the bioavailability of the aluminium ion, the presence or absence in the intestines of dietary ligands may either increase (e.g. citrate, lactate, and other organic carboxylic acid complexing agents, fluoride), or decrease the absorption (e.g. phosphate, silicon, polyphenols).
After absorption, aluminium distributes to all tissues in animals and humans and accumulates in some, in particular bone. The main carrier of the aluminium ion in plasma is the iron binding protein, transferrin. Aluminium can enter the brain and reach the placenta and fetus.
Aluminium may persist for a very long time in various organs and tissues before it is excreted in the urine. Although retention times for aluminium appear to be longer in humans than in rodents, there is little information allowing extrapolation from rodents to the humans.
Although at high levels of exposure, some aluminium compounds may produce DNA damage in vitro and in vivo via indirect mechanisms, the Panel considered this unlikely to be of relevance for humans exposed to aluminium via the diet.
The database on carcinogenicity of aluminium compounds is limited. In the most recent study no indication of any carcinogenic potential was obtained in mice given aluminium potassium sulphate at high levels in the diet. Overall the Panel concluded that aluminium is unlikely to be a human carcinogen at dietary relevant doses.
Aluminium has shown neurotoxicity in patients undergoing dialysis and thereby chronically exposed parenterally to high concentrations of aluminium. It has been suggested that aluminium is implicated in the aetiology of Alzheimer’s disease and associated with other neurodegenerative diseases in humans. However, these hypotheses remain controversial. Based on the the available scientific data, the Panel does not consider exposure to aluminium via food to constitute a risk for developing Alzheimer’s disease.
The Panel noted that several compounds containing aluminium have the potential to produce neurotoxicity (mice, rats) and to affect the male reproductive system (dogs). In addition, after maternal exposure they have shown embryotoxicity (mice) and have affected the developing nervous system in the offspring (mice, rats). The Panel also noted that there are very few specific toxicological data for food additives containing aluminium. Thus the Panel considered it prudent to take these effects into account when setting a tolerable intake for all dietary sources. The available studies have a number of limitations and do not allow any dose-response relationships to be established. The Panel therefore based its evaluation on the combined evidence from several studies in mice, rats and dogs that used dietary administration of aluminium compounds. In these studies the lowest-observed-adverse-effect levels (LOAELs) for effects on neurotoxicity, testes, embryotoxicity, and the developing nervous system were 52, 75, 100, and 50 mg aluminium/kg bw/day, respectively. Similarly, the lowest no-observed-adverse-effect levels (NOAELs) for effects on these endpoints were reported at 30, 27, 100, and for effects on the developing nervous system, between 10 and 42 mg aluminium/kg bw per day, respectively.
In view of the cumulative nature of aluminium in the organism after dietary exposure, the Panel considered it more appropriate to establish a tolerable weekly intake (TWI) for aluminium rather than a tolerable daily intake (TDI). Based on the combined evidence from the above-mentioned studies, the Panel established a TWI of 1 mg aluminium/kg bw/week.
The estimated daily dietary exposure to aluminium in the general population, assessed in several European countries, varied from 0.2 to 1.5 mg/kg bw/week at the mean and was up to 2.3 mg/kg bw/week in highly exposed consumers.
The TWI of 1 mg/kg bw/week is therefore likely to be exceeded in a significant part of the European population. Cereals and cereal products, vegetables, beverages and certain infant formulae appear to be the main contributors to the dietary aluminium exposure.
Due to the design of the human dietary studies and the analytical methods used, which only determine the total aluminium content in food, and not the individual aluminium compounds or species present, it is not possible to conclude on the specific sources contributing to the aluminium content of a particular food, such as the amount inherently present, the contributions from use of food additives, and the amounts released to the food during processing and storage from aluminium-containing foils, containers, or utensils. Thus a detailed breakdown by exposure source is not possible.