Aluminium is the third most abundant element in the Earth’s crust and the most abundant
metal. Bauxite is the most important raw material used to produce Aluminium. It contains
about 55% of Al in the form of aluminium oxide (Al2O3). Production of Al from bauxite is
associated with its emission to the environment, which may become a potential threat to the
entire ecosystem. However, aluminium has been traditionally regarded as non-toxic metal
that induces clinical changes only in very specific conditions, e.g., long-term dialysis due to
renal failure or occupational exposure to Al dusts, fumes and its oxides (Sinczuk-Walczak,
Szymczak, Razniewska, Matczak, Szymczak, 2003).
Aluminium is now a known neurotoxin. Aluminium is therefore the component of interest in
bauxite in determining the possible link with Alzheimer’s disease. As a result of the
neurotoxicity of Aluminium and the prevalence of neurological diseases the Aluminium
Hypothesis was developed. The Aluminium Hypothesis (AH) promotes the theory that
aluminium exposure is involved in the aetiology of Alzheimer disease (AD) (Wesdock &
Arnold, 2014). Alzheimer’s disease is characterized by a general loss of cognitive function,
including memory. A particularly compelling neurological syndrome highlighting the
potential role of aluminium in Alzheimer’s disease arose with descriptions of “dialysis
associated encephalopathy” (DAE). In this disorder, patients with insufficient kidney function
had sometimes inadvertently received dialysis fluids containing high levels of aluminium.
DAE showed many of the characteristics of Alzheimer’s disease, both behaviourally and
pathologically. Conversely, those affected showed rapid improvement when aluminium was
removed from the dialysis fluid. It is highly significant that DAE as a clinical syndrome
vanished once aluminium was removed from dialysis solutions (The Alzheimer’s disease
fund).
In a study to determine the effects of occupational exposure to aluminium on nervous system,
neurological and electroencephalographic studies reveal that occupational exposure to Al
present in the ambient air at work posts of smelters and auxiliary workers, employed in the Al
production with Al2O3 concentrations, ranging between 0.13 and 1.95 mg/m3 does not induce
organic lesions in the central or peripheral nervous system that could provide grounds for
clinical diagnosis of encephalopathy or polyneuropathy. This means that occupational
exposure to Al could not lead to a diagnosis of Alzheimer’s disease. However, the study
reported that Al seems to be responsible for sub-clinical effects on the nervous system such
as vertigo, increased emotional irritability, concentration difficulties, sleep disturbance and
anxiety (Sinczuk-Walczak, Szymczak, Razniewska, Matczak, Szymczak, 2003).
Therefore, to answer the question of the chance of the young man developing Alzheimer’s
disease as a result of working in the bauxite industry the answer is maybe. He is at a greater
risk of developing some neurological diseases due to the neurotoxicity of Aluminium.
Though scarce, available research provide evidence that occupational exposure to Al and its
components generates harmful effects on the workers’ nervous system as well as induces
disorders of mental processes and motor activities. However, no single finding supports a
hypothesis that occupational exposure to Al directly causes Alzheimer’s disease.
In this review, we have summarized the properties associated with various aspects of Al
neurotoxicity. There is growing evidence for a link between Al and AD, and between other
metals and AD. Nevertheless, because the precise mechanism of AD pathogenesis remains
unknown, this issue is controversial. However, it is widely accepted that Al is a recognized
neurotoxin, and that it could cause cognitive deficiency and dementia when it enters the brain
and may have various adverse effects on CNS. In general, the absorption of metals by the
gastrointestinal tract is widely variable and is influenced by various factors including an
individual difference, age, pH, stomach contents [173]. Recent studies using mass
spectrometry of 26Al have demonstrated that small, but a considerable amount of Al crosses
the blood brain barrier, enters into the brain, and accumulates in a semi-permanent manner
[174, 175]. Therefore, Al can cause severe health problems in particular populations,
including infants, elderly people, and patients with impaired renal functions, and unnecessary
exposure to Al should be avoided for such patients [176].
Despite growing interest in Al neurotoxicity, the published findings on occupational exposure
to Al and its compounds are rather scarce. The available reports provide evidence that
occupational exposure to Al and its components generates harmful effects on the workers’
nervous system as well as induces disorders of mental processes and motor activities.
However, no single finding supports a hypothesis that occupational exposure to Al affects
cognitive mechanisms.
Rate of fatal injuries
Rate of loss-time injuries
2011
0
165.88
2012
0
1.86
2013
1
139.43
2014
1
131.98
2015
0
20.40
Total
2
556.57
Wesdock, J. C., & Arnold, I. M. (2014). Occupational and environmental health in the
aluminum industry: key points for health practitioners. Journal of Occupational and
Environmental Medicine, 56(5 Suppl), S5.
Sinczuk-Walczak, H., Szymczak, M., Razniewska, G., Matczak, W., & Szymczak, W.
(2003). Effects of occupational exposure to aluminum on nervous system: clinical and
electroencephalographic findings. International journal of occupational medicine and
environmental health, 16(4), 301-310.
The Alzheimer’s Disease Fund (n.d.). Aluminum in Alzheimer’s disease and 0ther
neurological disorders. Retrieved from http://www.alzdisease.org/downloads/Aluminum1.pdf