The Chemistry of Human Exposure to Aluminium (Part Two)
Let's examine rule number two
This is the second instalment of my trilogy concerning the chemistry of human exposure to aluminium. Please read in the context of what was explained in Part One. The final part of the trilogy will finish with a take home summary of this critical analysis of the toxicity of aluminium in humans.
Rule Number Two
The binding of Al3+(aq) is determined by both thermodynamic and kinetic constraints.
While Al3+(aq) is biologically reactive (and is avidly bound by biochemically important functional groups) for Al3+(aq) to be defined as biologically available, its binding should bring about some recognisable response in participating biochemistry and/or underlying physiology.
In short it should bring about toxicity.
The thermodynamic properties of any aluminium complex will dictate strength of binding (sometimes referred to as a stability constant) and can be thought of as competition between rate of formation and dissolution of the complex.
Since Al3+(aq) is a relatively small and highly electropositive cation, it will be strongly bound by many biological ligands and especially oxygen-based functional groups. Generally, this means that the rate of formation will be preferred over the rate of dissolution, and, therefore, Al3+(aq) will remain bound.
However, to both remain bound and to bring about a biochemical response (toxicity), the delivery of Al3+(aq) to target groups must also be optimal. Significant numbers of Al3+(aq) cations must remain bound over a particular timeframe to produce a biochemical response.
The delivery of Al3+(aq) to its binding sites in significant amounts over a specific timeframe is governed by kinetic constraints. To further understand these kinetic parameters, let’s consider a small but significant change to Equation 1 (See Rule Number One).
Al3+(aq) ↔ AlOH2+(aq) ↔ Al(OH)2+(aq) ↔ Al(OH)3(s) ↔ Al(OH)4-(aq) (Equation 3)
In any system where the solubility of aluminium hydroxide is exceeded, aluminium will be precipitated as amorphous Al(OH)3(s) (Equation 3), and the formation and dissolution of this solid phase will determine the availability of the soluble monomeric hydrolytic aluminium ions including Al3+(aq).
Under any condition which favours the formation of Al(OH)3(s), it will be the dissolution of this phase which determines the rate of delivery of Al3+(aq) to possible target sites for binding.
The rate of dissolution of Al(OH)3(s) will depend upon the avidity with which Al3+(aq) is bound by competitive ligands and, importantly, the stability of Al(OH)3(s) with newly formed amorphous precipitates of this sparingly soluble phase dissolving more rapidly than aged, semi-crystalline forms such as gibbsite (see Equation 4).
Al(OH)3(amorphous) ↔ Al(OH)3(gibbsite) (Equation 4)
In those environments where the precipitation of aluminium is favoured, thermodynamic constraints upon the biological reactivity of Al3+(aq) may give way to kinetic constraints in much the same way as a grain of sand (silica:SiO2) does not immediately dissolve to give silicic acid (Si(OH)4) upon being dropped into a glass of pure water. Thermodynamically the grain of sand should immediately dissolve to give Si(OH)4, while kinetically it remains as SiO2 .
The occurrence of a solid phase as an intermediate in a delivery chain for Al3+(aq) will be rate-limiting and might also be the difference between a biological burden of aluminium (AlB) being biologically reactive (AlBR) and also biologically available (AlBA).
AlB ↔ AlBR ↔ AlBA (Equation 5)
This concept is more often than not ignored in the scientific literature regardless of periodic published warnings. For example, stock solutions of aluminium salts are regularly prepared by researchers by simply dissolving the salt in a solvent such as water. These stocks are invariably super-saturated with respect to aluminium hydroxide or aluminium hydroxyphosphate (where phosphate-buffered saline is the solvent), and no thought is given to the evolution or ageing of their aluminium content over time.
During these ageing processes, condensation reactions and aggregation phenomena affect the equilibria depicted in Equation 5 and almost always ensure that the biological availability of aluminium will be different in freshly prepared as opposed to aged stock preparations.
One simple example of this can be found when aluminium salts are dissolved in an experimental animal’s drinking water which the animal then proceeds to imbibe over hours, days, or even weeks in some instances. The biological availability of the aluminium being ingested from water which is 1 week old will be significantly different to the same water when it was only hours old. The exposure regime has changed and concomitant differences in the biological response should be expected.
This is rule number two. I know that this information is not simple per se and may be difficult to understand in isolation. Stick with me and by the end of Part Three I am confident that you will have a better understanding of why aluminium is toxic and why we need to think carefully about how we live in the aluminium age.
Is there any justification for injecting this crap into an infant during his first few days of life and then continuing for another decade?
Looking forward to part 3. As I read I'm wondering how to construct a Freedom of Information request to our Therapeutic Goods Regulator to find out on what studies they rely on to determine injecting Al adjuvanted vaccines ( or using it in the control groups for some clinical trials) is "safe". I'm fairly confident the studies were never done...just grandfatheres in alum.