| DiamondPeel had previously sold Aluminum-Oxide (also known as Aluminium-Oxide or Al2O3) based microdermabrasion machines. We switched over to crystal-free systems because of the numerous studies published by various Health Journals and the US government about the health hazards with long-term exposure to fine Aluminum-Oxide dust. One thing to note for people who hesitate purchasing the DiamondPeel because of a fear of the metal wands touching the face of your patients. Our wands are made out of surgical-grade steel which is used in most medical instruments. Not only this, but the patient's skin will hardly be touching the metal since the diamond coating will be what is in contact with the skin at all times. Do keep in mind that Aluminum-Oxide crystals are also a metal substance (made out of Aluminum), though in the form of small crystals. The biggest danger being the small particulates entering the lungs through breathing the contaminated air. Not to mention possible damage to the eyes from any loose crystals accidentally going inside them. We have included a number of papers and websites that can be studied by yourself to better understand the dangers inherent in using Aluminum-Oxide, Sodium-Bicarbonate, and Organic crystals to exfoliate the skin. We think that after looking at all the evidence on the subject, you yourself will reach a similar conclusion to the problems associated with all crystal-based machines |
* A 4-page report of OSHA's study on Aluminum-Oxide dust on workers * A US Government CDC report on Aluminum toxicity |
Problems associated with Aluminum-Oxide use:
| Additional Federal and State Regulations (If you live in the following states, then you face additional Health regulations): Illinois toxic substances disclosure to employee act: Aluminum oxide Rhode Island RTK hazardous substances: Aluminum oxide Minnesota: Aluminum oxide Massachusetts RTK: Aluminum oxide New Jersey: Aluminum oxide New Jersey spill list: Aluminum oxide California Director's list of Hazardous Substances: Aluminum oxide TSCA8(b) inventory: Aluminum oxide SARA 313 toxic chemical notification and release reporting: Aluminum oxide Other Regulations: EINECS: This product is on the European Inventory of Existing Commercial Chemical Substances. |
One of the most fundamental arguments in this debate is the presence of elevated aluminum levels in the
brain tissue and the surrounding cerebralspinal fluid (CSF). Collectively, a majority of all the reviewed
studies concurrred with the conclusion that the concentration of aluminum was greater in the brains of AD
patients than those not afflicted with the disease. For example, a study led by M. Hollosi showed that the
aluminum levels in AD patients ranged between 6 and 12 parts per million (ppm) in lesion containing areas
and between 0 and 15 ppm in areas that had not gone through any noticeable degeneration, which is much
higher than the amount found in non-Alzheimer disease brains1.
Another study, led by P. Evans, states that, "of the various environmental factors that have been
implicated, the one with the greatest amount of supportive evidence is aluminum"2. In the studies found
that opposed the majority's consensus, methodological practices were cited as the major cause of
discrepancies between the two conclusions, such as not taking into account the taclum powder inside
latex examination gloves. M. Lovell and his group showed that samples analyzed and corrected for multiple
substances that interfered with the measurement of the aluminum level reflected a nonexistent to minimal
elevation in the concentration of aluminum in AD patients, also citing other groups that had failed to find a
difference in aluminum amounts3.
Also contradicting the norm is a study focusing on the concentration of aluminum in the CSF, led by E.
Kopaki. This group pointed out the controversial argument dealing with poor sampling and handling of
samples and inferior analysis procedures for the level of aluminum present in previous studies of CSF.
Being careful to follow a strict procedure to avoid contamination of samples and a control group with which
to compare the results, the Kopaki group concluded that any possible increase in the aluminum
concentration level in the brain is not evident in the CSF4.
concentration level in the brain is not evident in the CSF4.
1 Hollosi, Miklos et al. "Stable Intrachain and Intrachain complexes of neurofilament peptides: A putative
link between Al and Alzheimer disease." Proceedings of the National Academy of Sciences of the United
States of America. 91 (1994): 4902-4906.
2 Evans, Peter H. "Aluminum and Trace Element Oxidative Interactions in the Etiopathogenesis of
Alzheimers Disease."
3 Lovell, M.A. et al. "Laser Microprobe Analysis of Brain Aluminum in Alzheimers Disease." Annals of
Neurology. 33 (1993): 36-42.
4 Kopaki, E.N. et al. "Cerebralspinal Fluid Aluminum Levels in Alzheimers Disease." Biological Psychiatry.
33 (1993): 679-681.
Can Aluminum Pass the Blood Brain Barrier?
An additional area dealing with aluminum in the brain that is currently in question is the extent to which
aluminum present in the bloodstream is able to cross into the brain tissue. Aluminum is thought to cross
the blood-brain barrier (BBB) by using the iron transport and storage systems because the solution
chemistries of aluminum and iron are very similar. The hypothesis is supported by the gradual buildup of
aluminum in bone and brain tissue1.
A possible mechanism for crossing the BBB has been suggested as a "Trojan horse" method of transport
for aluminum, where aluminum is mistaken for iron, once again because of their similar properties, and
brought into the brain from the bloodstream by hematogenous macrophages and monocytes2. It has also
been hypothesized that the increased absorption of aluminum in the brain is enhanced by the possible
increase in permeability of the BBB as a result of the development of AD.
1 Clauberg M., and Joshi, J.G. "Regulationof serine protease activity by aluminum: Implications for
Alzhemer disease." Proceedings of the National Academy of Sciences of the United States of America. 90
(1993) 1009-12.
2 Evans, Peter H. "Aluminum and Trace Element Oxidative Interactions in the Etiopathogenesis of
Alzheimers Disease."
An additional area dealing with aluminum in the brain that is currently in question is the extent to which
aluminum present in the bloodstream is able to cross into the brain tissue. Aluminum is thought to cross
the blood-brain barrier (BBB) by using the iron transport and storage systems because the solution
chemistries of aluminum and iron are very similar. The hypothesis is supported by the gradual buildup of
aluminum in bone and brain tissue1.
A possible mechanism for crossing the BBB has been suggested as a "Trojan horse" method of transport
for aluminum, where aluminum is mistaken for iron, once again because of their similar properties, and
brought into the brain from the bloodstream by hematogenous macrophages and monocytes2. It has also
been hypothesized that the increased absorption of aluminum in the brain is enhanced by the possible
increase in permeability of the BBB as a result of the development of AD.
1 Clauberg M., and Joshi, J.G. "Regulationof serine protease activity by aluminum: Implications for
Alzhemer disease." Proceedings of the National Academy of Sciences of the United States of America. 90
(1993) 1009-12.
2 Evans, Peter H. "Aluminum and Trace Element Oxidative Interactions in the Etiopathogenesis of
Alzheimers Disease."
Involved in the ongoing debate is the speculation that aluminum somehow affects neurofibrillary tangles.
Initially, the scientific community believed that the high concentration of aluminum in NFTs was an
irreparable event in a dying neuron1. Presently, it is believed that aluminum plays a role in NFT formation
covalent shift of the triphosphate group from adenosine triphosphate (ATP) to tau. Aluminum, having a
Because tau contains multiple phosphorylation sites, aluminum acts as a catalyst for the nonenzymatic
positive charge of three, bonds with three phosphates of ATP, each having a negative charge, because the
triphosphates have a higher affinity for aluminum than the adenosine. From there, the phosphates, having a
greater affinity for the tau protein than the aluminum, are transferred to the protein, causing its
precipitation. When this occurs, the entire triphosphate group is transferred to the protein and results in the
aggregation of tau2.
Also, evidence of aluminum induced NFT formation in animals has been provided as support that aluminum
does affect neurofibrillary tangles. In 1965, Klatzo and coworkers reported that the injections of aluminum
salts in the brains of rabbits caused NFT formation3. Later, it was found that in cultured rat neurons,
aluminum treatment prompts the formation of NFTs2. In opposition, Lovell et al. argued that no significant
differences in aluminum levels were found in "NFT-bearing neurons compared with NFT- free neurons" in
AD patients4. In a study performed by M.P. Mattson and colleagues, data indicated that neuronal damage
and an alteration of tau did not occur with increases in aluminum5. The data collected in this same study
indicated that the collection of aluminum alone in neurons cannot perpetuate NFTs, the tell-tale features of
Alzheimers disease5.
1 McLachlan. D.R. "The possible relationship between aluminium and Alzheimersdisease and the
mechanisms of cellular pathology." Alzheimers Disease and the Environment. 26 (1991): 42-52.
2 Ghany, M.A. et al. "Aluminum-induced Nonenzymatic Phospho-incorporation into Human Tau and Other
Proteins." The Journal of Biological Chemistry. 268 (1993): 11976- 11981.
3 Klatzo. I. et al. "Experimental production of neurofibrillary degeneration: I. Light microscopic
observations." Journal Neuropathol Exp Neurol. 24 (1965):187-199.
4 Lovell, M.A. et al. "Laser Microprobe Analysis of Brain Aluminum in Alzheimers Disease." Annals of
Neurology. 33 (1993): 36-42.
5 Mattson, M.P. "Comparison of the effects of elevated intracellular aluminum and calcium levels on
neuronal survival and tau immunoreactivity." Brain Research. 602 (1993): 21-31.
Initially, the scientific community believed that the high concentration of aluminum in NFTs was an
irreparable event in a dying neuron1. Presently, it is believed that aluminum plays a role in NFT formation
covalent shift of the triphosphate group from adenosine triphosphate (ATP) to tau. Aluminum, having a
Because tau contains multiple phosphorylation sites, aluminum acts as a catalyst for the nonenzymatic
positive charge of three, bonds with three phosphates of ATP, each having a negative charge, because the
triphosphates have a higher affinity for aluminum than the adenosine. From there, the phosphates, having a
greater affinity for the tau protein than the aluminum, are transferred to the protein, causing its
precipitation. When this occurs, the entire triphosphate group is transferred to the protein and results in the
aggregation of tau2.
Also, evidence of aluminum induced NFT formation in animals has been provided as support that aluminum
does affect neurofibrillary tangles. In 1965, Klatzo and coworkers reported that the injections of aluminum
salts in the brains of rabbits caused NFT formation3. Later, it was found that in cultured rat neurons,
aluminum treatment prompts the formation of NFTs2. In opposition, Lovell et al. argued that no significant
differences in aluminum levels were found in "NFT-bearing neurons compared with NFT- free neurons" in
AD patients4. In a study performed by M.P. Mattson and colleagues, data indicated that neuronal damage
and an alteration of tau did not occur with increases in aluminum5. The data collected in this same study
indicated that the collection of aluminum alone in neurons cannot perpetuate NFTs, the tell-tale features of
Alzheimers disease5.
1 McLachlan. D.R. "The possible relationship between aluminium and Alzheimersdisease and the
mechanisms of cellular pathology." Alzheimers Disease and the Environment. 26 (1991): 42-52.
2 Ghany, M.A. et al. "Aluminum-induced Nonenzymatic Phospho-incorporation into Human Tau and Other
Proteins." The Journal of Biological Chemistry. 268 (1993): 11976- 11981.
3 Klatzo. I. et al. "Experimental production of neurofibrillary degeneration: I. Light microscopic
observations." Journal Neuropathol Exp Neurol. 24 (1965):187-199.
4 Lovell, M.A. et al. "Laser Microprobe Analysis of Brain Aluminum in Alzheimers Disease." Annals of
Neurology. 33 (1993): 36-42.
5 Mattson, M.P. "Comparison of the effects of elevated intracellular aluminum and calcium levels on
neuronal survival and tau immunoreactivity." Brain Research. 602 (1993): 21-31.
Kuroda and colleagues performed a study on this relationship and concluded that aluminum promoted the
aggregation of synthetic beta-amyloid protein. Because the aggregation of beta-amyloid protein results in
neurotoxicity, the elevated presence of aluminum in the brain accelerates the aggregation of beta-amyloid
protein in the brain tissue, therefore, accelerating the development of senile plaques and AD (Kuroda et al.
3).
A differing idea relating aluminum to the protein has been presented by M. Clauberg and J.G. Joshi, who
speculate that aluminum could have an effect on the production of beta-amyloid protein by suppressing the
inhibitor domain, making the cell incapable of suspending the production of the protein when there is an
excess amount in the cell. Without anything to hold its level of production within a normal range, the
beta-amyloid protein accumulates and increases the rate at which senile plaques are formed (Clauberg and
Joshi 1009). In opposition to both of these ideas are many scientists who have failed to find a considerable
elevation in aluminum levels in senile plaques. A group led by H. Jacqmin and associates concurs with the
conclusion that there is no reliable evidence for aluminum in senile plaques (Jacqmin et al. 48).
1 Kuroda, Y. et al. "Application of Long-Term Cultured Neurons in Aging and Neurological Research:
Aluminum Neurotoxicity, Synaptic Degeneration and Alzheimers Disease." Gerontology. 41 (1994): 2-6.
2 Clauberg M., and Joshi, J.G. "Regulationof serine protease activity by aluminum: Implications for
Alzhemer disease." Proceedings of the National Academy of Sciences of the United States of America. 90
(1993) 1009-12.
3 Jacqmin, Helene et al. "Components of Drinking Water and Risk of Cogitive Impairment in the Elderly."
American Journal of Epidemiology. 139 (1994): 48-57.
Glossary of Terms
acetylcholine: A chemical found in vertebrate neurons that carries information across the synaptic cleft, the
space between two nerve cells.
Alzheimers Disease: A progressive, neurodegenerative disease characterized by loss of function and death
of nerve cells in several areas of the brain leading to loss of cognitive function such as memory and
language. The cause of nerve cell death is unknown. Alzheimer's disease is the most common cause of
dementia.
axon: The threadlike extensions on a neuron, or nerve cell which conducts nerve impulses.
dementia: Loss of intellectual functions, (such as thinking, remembering, and reasoning) of sufficient
severity to interfere within an individual's daily functioning.
dendrite: A long extension of the cytoplasm of a neuron with thin, treelike branches. It receives nerve
signals an transmits them to the main body of the cell (called the cyton).
enzymes: Proteins that act as catalysts, speeding the rate at which biochemical reactions proceed but not
altering the direction or nature of the reactions.
leukocyte: A pale, nucleated cell that acts as a part of the immune system by destroying invading cells
and removing debris.
monocyte: A type of large, round leukocyte that engulfs and breaks down debris and invading cells.
Monocytes are formed in bone marrow and have round or kidney-shaped nuclei.
macrophage: A type of large leukocyte that travels in the blood but can leave the bloodstream and enter
tissue; like other leukocytes, it protects the body by digesting debris and foreign cells.
neuritic plaque: Abnormal cluster of dead and dying nerve cells, other brain cells, and protein. Neuritic
plaques are one of the characteristic structural abnormalities found in the brains of Alzheimer's disease
(AD) patients. Upon autopsy, the presence of neuritic plaques and neurofibrillary tangles is used to
positively diagnose AD.
neurodegenerative disorder: A type of neurological disease marked by the loss of nerve cells.
neurofibrillary tangle: Accumulation of twisted protein fragments inside nerve cells. Neurofibrillary tangles
are one of the characteristic structural abnormalities found in the brains of Alzheimer's disease (AD)
patients. Upon autopsy, the presence of neuritic plaques and neurofibrillary tangles is used to positively
diagnose AD.
neuron: A nerve cell; it receives and conducts electrical impulses from the brain. It consists of a cell body
called the cyton, an axon, axon terminals, and dendrites.
Parkinson's disease (parkinsonism): A progressive, neurodegenerative disease characterized by the death
of nerve cells containing the neurotransmitter dopamine in a specific area of the brain; the cause of nerve
cell death is unknown. Parkinson's patients have such symptoms as tremors, speech impediments,
movement difficulties, and often dementia.
protein: A large molecule composed of one or more chains of amino acids in a specific order; the order is
determined by the base sequence of nucleotides in the gene coding for the protein. Proteins are required
for the structure, function, and regulation of the bodys cells, tissues, and organs, and each protein has
unique functions. Examples are hormones, enzymes, and antibodies.
acetylcholine: A chemical found in vertebrate neurons that carries information across the synaptic cleft, the
space between two nerve cells.
Alzheimers Disease: A progressive, neurodegenerative disease characterized by loss of function and death
of nerve cells in several areas of the brain leading to loss of cognitive function such as memory and
language. The cause of nerve cell death is unknown. Alzheimer's disease is the most common cause of
dementia.
axon: The threadlike extensions on a neuron, or nerve cell which conducts nerve impulses.
dementia: Loss of intellectual functions, (such as thinking, remembering, and reasoning) of sufficient
severity to interfere within an individual's daily functioning.
dendrite: A long extension of the cytoplasm of a neuron with thin, treelike branches. It receives nerve
signals an transmits them to the main body of the cell (called the cyton).
enzymes: Proteins that act as catalysts, speeding the rate at which biochemical reactions proceed but not
altering the direction or nature of the reactions.
leukocyte: A pale, nucleated cell that acts as a part of the immune system by destroying invading cells
and removing debris.
monocyte: A type of large, round leukocyte that engulfs and breaks down debris and invading cells.
Monocytes are formed in bone marrow and have round or kidney-shaped nuclei.
macrophage: A type of large leukocyte that travels in the blood but can leave the bloodstream and enter
tissue; like other leukocytes, it protects the body by digesting debris and foreign cells.
neuritic plaque: Abnormal cluster of dead and dying nerve cells, other brain cells, and protein. Neuritic
plaques are one of the characteristic structural abnormalities found in the brains of Alzheimer's disease
(AD) patients. Upon autopsy, the presence of neuritic plaques and neurofibrillary tangles is used to
positively diagnose AD.
neurodegenerative disorder: A type of neurological disease marked by the loss of nerve cells.
neurofibrillary tangle: Accumulation of twisted protein fragments inside nerve cells. Neurofibrillary tangles
are one of the characteristic structural abnormalities found in the brains of Alzheimer's disease (AD)
patients. Upon autopsy, the presence of neuritic plaques and neurofibrillary tangles is used to positively
diagnose AD.
neuron: A nerve cell; it receives and conducts electrical impulses from the brain. It consists of a cell body
called the cyton, an axon, axon terminals, and dendrites.
Parkinson's disease (parkinsonism): A progressive, neurodegenerative disease characterized by the death
of nerve cells containing the neurotransmitter dopamine in a specific area of the brain; the cause of nerve
cell death is unknown. Parkinson's patients have such symptoms as tremors, speech impediments,
movement difficulties, and often dementia.
protein: A large molecule composed of one or more chains of amino acids in a specific order; the order is
determined by the base sequence of nucleotides in the gene coding for the protein. Proteins are required
for the structure, function, and regulation of the bodys cells, tissues, and organs, and each protein has
unique functions. Examples are hormones, enzymes, and antibodies.
References
Crapper D R, Krishnan S S and Quittkat S (1976) 'Aluminium, neurofibrillary degeneration and Alzheimer's
disease'. Brain 99: 67-80
Flaten T P and Odegård M (1988) 'Tea, aluminium and Alzheimer's disease'. Food and Chemical
Toxicology 26 (11-12): 959-60
Gitelman H J ed (1988) Aluminium and health, a critical review, London: CRC Press
Gomez M, Esparza J L, Domingo J L, Singh PK and Jones M M (1998) 'Comparative aluminium mobilizing
actions of deferoxamine and four 3-hydroxypyrid-4-ones in aluminium-loaded rats'. Toxicology 130 (2):
175-81 (7)
Klatzo I, Wisniewski H and Streicher E (1965) 'Experimental production of neurofibrillary pathology: 1. Light
microscopic observations'. Journal of Neuropathology and Experimental Neurology 24: 187-99
Massey RC and Taylor D eds (1989) Aluminium in food and the environment. London: Royal Society of
Chemistry Netter P, Kessler M, Gaucher A and Bannwarth B 'Does aluminium have a pathogenic role in
dialysis associated arthropathy?' Annals of the Rheumatic Diseases 49 (8): 573-75
Rao J K S and Rao V G (1995) 'Aluminium leaching from utensils - a kinetic study'. International Journal of
Food Science and Nutrition 46: 31-38
Terry R D and Pena C (1965) 'Experimental production of neurofibrillary pathology: electron microscopy,
phosphate histochemistry and electron probe analysis'. Journal of Neuropathology and Experimental
Neurology 24: 200-10
Trapp G A, Miner G D, Zimmerman R L, Mastri A R, Heston L L (1978) 'Aluminum levels in brain in
Alzheimer's disease'. Biological Psychiatry 13 (6): 709-18
Crapper D R, Krishnan S S and Quittkat S (1976) 'Aluminium, neurofibrillary degeneration and Alzheimer's
disease'. Brain 99: 67-80
Flaten T P and Odegård M (1988) 'Tea, aluminium and Alzheimer's disease'. Food and Chemical
Toxicology 26 (11-12): 959-60
Gitelman H J ed (1988) Aluminium and health, a critical review, London: CRC Press
Gomez M, Esparza J L, Domingo J L, Singh PK and Jones M M (1998) 'Comparative aluminium mobilizing
actions of deferoxamine and four 3-hydroxypyrid-4-ones in aluminium-loaded rats'. Toxicology 130 (2):
175-81 (7)
Klatzo I, Wisniewski H and Streicher E (1965) 'Experimental production of neurofibrillary pathology: 1. Light
microscopic observations'. Journal of Neuropathology and Experimental Neurology 24: 187-99
Massey RC and Taylor D eds (1989) Aluminium in food and the environment. London: Royal Society of
Chemistry Netter P, Kessler M, Gaucher A and Bannwarth B 'Does aluminium have a pathogenic role in
dialysis associated arthropathy?' Annals of the Rheumatic Diseases 49 (8): 573-75
Rao J K S and Rao V G (1995) 'Aluminium leaching from utensils - a kinetic study'. International Journal of
Food Science and Nutrition 46: 31-38
Terry R D and Pena C (1965) 'Experimental production of neurofibrillary pathology: electron microscopy,
phosphate histochemistry and electron probe analysis'. Journal of Neuropathology and Experimental
Neurology 24: 200-10
Trapp G A, Miner G D, Zimmerman R L, Mastri A R, Heston L L (1978) 'Aluminum levels in brain in
Alzheimer's disease'. Biological Psychiatry 13 (6): 709-18
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