Aluminum Salts (Final Content)

CEPA 1999 64(a) and 64 (b): Based on the available data, it is concluded that the three aluminum salts, aluminum chloride, aluminum nitrate and aluminum sulphate, are not entering the environment in a quantity or concentration or under conditions that have or may have an immediate or long-term harmful effect on the environment or its biological diversity or that constitute or may constitute a danger to the environment on which life depends.

CEPA 1999 64(c): Based on available data concerning the exposure of the Canadian population to aluminum chloride, aluminum nitrate and aluminum sulphate, and in consideration of the health effects observed in humans and in experimental animals, it is concluded that these aluminum salts are not entering the environment in a quantity or concentration or under conditions that constitute or may constitute a danger in Canada to human life or health.

It is therefore concluded that the three aluminum salts, aluminum chloride, aluminum nitrate and aluminum sulphate, do not meet the definition of “toxic” as set out in section 64 of CEPA 1999.

Footnotes

²⁵ Soil would most likely be in the form of household dust for this age group.
²⁶ A good laboratory practice (GLP) study generally following OECD and U.S. EPA Developmental Neurotoxicity guidelines, commissioned by a consortium of aluminum salt producers, is currently underway. The results, however, will not be available before mid-2009.
²⁷ Further categorization of the studies, based on salt administered, animal species, exposure vehicle and a more precisely defined exposure period, was considered but found to be not feasible. Narrowly defined subgroups did not provide an adequate number of studies with common endpoints and dose ranges. On the other hand, the comparison of pooled studies (e.g., drinking water studies vs. dietary administration studies), in order to determine the relative importance of different experimental variables, is limited by the confounding between these variables. Researchers tend to chose similar sets of experimental conditions from one experiment to another. Thus differences in the LOELs observed in a series of studies might be attributed to a particular factor (e.g., drinking water vs. diet) but could also be the result of the researchers’ choices to repeatedly use the same single dose of the same salt, in the same exposure vehicle (diet or drinking water). Likewise, evaluation of pools of single-dose studies can mask the influence of an experimental condition, as reported LOELs may be poor estimates of real effect levels.
²⁸ See discussion in section 2.4.4 on typical levels of aluminum in lab chow.
²⁹ The low-dose studies for adult exposure, in which base diet aluminum concentration is not reported, include findings of altered levels of neurotransmitters (Silva and Goncalves 2003; Dave et al. 2002; Bilkei-Gorzo 1993), of changes in the phospholipid content of synaptic plasma membrane (Pandya et al. 2001) or of increased lipid peroxidation in the brain (Kaneko et al. 2004, Pratico et al. 2002, Abd-Elghaffar et al. 2005). Some low-dose studies also documented increased neuronal damage (Varner et al. 1998, 1993; Somova et al. 1997; Abd-Elghaffar et al. 2005) and neuromotor and coordination effects (Bilkei-Gorzo 1993; Sahin et al. 1995). The low-dose prenatal/lactation exposure studies included findings of alterations in neurotransmission (Kim 2003; Ravi et al. 2000) and effects on fetal growth (Paternain et al. 1988; Domingo et al. 1987a).
³⁰ In contrast, Colomina et al. (2002) administered aluminum nitrate, enhanced with citrate, in drinking water, at an average dose of 94 mg Al/kg bw/d, to groups of male rats aged 21 days and 18 months old. The increase in whole brain aluminum concentration in the aluminum-exposed group was not statistically significant. Roig et al (2006) observed an increase of aluminum in brain regions of rats exposed to 100 mg Al/kg bw/d of aluminum nitrate with citrate in drinking water for one year. Observations were made in two-year-old rats, and increases were on the order of three- to ten-fold, depending on the brain region, and with a 22-fold increase in the striatum.
³¹ Neurofibrillary tangles in AD brains are formed from the hyperphosphorylation of tau protein.