Nickel, Intoxication and cancer
* by
Dr Rita MONSIEUR
The nickel is 24th abundant natural element in the earth's crust and widely distributed in the environment.
The major deposits of nickel ore are located in Australia, Canada, Cuba, Indonesia, New Caledonia, and Russia.
The natural sources of atmospheric nickel are the dust from volcanic emissions, the erosion of rocks and soils, the burning of fuels, emission during mining and refining.
The high consumption of products containing nickel inevitably leads to environmental pollution by nickel and its derivatives at all stages of production, use and distribution.
Human and Environmental contamination summary
The nickel leached locations of landfills and contributes to the contamination of the aquifer coat. The acid rain has a tendency to mobilize nickel from soil and increase the nickel concentration of groundwater with an increased consumption of the plants, microorganisms and animals.
The nickel exposure occurs primarily by inhalation and ingestion particularly high, among metallurgical workers.
The implantation of endoprosthesis containing nickel such as artificial limb, dental bridges, prosthetic heart valves, thread of cardiac pacemakers and also tooth fillings which can cause immunological disturbances around the implants read the Pratikadent.
The administration of contaminated medications by nickel (albumin, produce of radiocontrast, produces of hemodialysis) increases the parenteral exposure significantly. The dermal absorption of the nickel, can occur by wearing jewelry, handling coins or tools made of amalgam containing nickel.
The ingestion of nickel in diets rich in oatmeal, cocoa, walnuts, soy products can reach 900µg per day.
In big cities and industrial regions, the concentration of atmospheric nickel is related with volatile ashes from the combustion of fuel and waste, and can reach 120-170 ng/m3 compared to 6-17ng/m3 in urban areas.
Cigarette smoke may also increase the inhaled nickel.
Another source of contamination is the consumption of plant products which can achieve until 1mg Ni /kg.
Contamination effects summary
The risks of respiratory cancers are secondary to exposure to soluble nickel concentrations beyond 1mg/m3 and insoluble beyond 10mg/m3.
Contrary to the insoluble compounds, such as the NiO, the soluble salts are easily absorbed by the lung and digestive tracts, and less by the skin.
The volatility and the lipo-solubility of carbonyl nickel Ni (CO) 4 allows it to penetrate into the membranes of the cells, and its reducing reactivity contributes to its high toxicity.
The carbonyl nickel inhaled is quickly absorbed by lungs and gets into the red blood cells where it is converted in Ni2+ and CO.
In the human plasma , Ni2+ is bound to ultrafilterable constituents : albumin, histidine, nickeloplasmin, an alpha 2 - macroglobulin. In the cytosol of tissues, nickel is bound to several proteins and peptides.
Carcinogenic effects in humans (dose dependent or not) summary
The propensity of nickel workers to develop cancers of the nasal cavities was first reported by Bridge in 1933. Since several decades experimental results have been confirmed by numerous epidemiological studies in humans and carcinogenesis bioassays in animals.
The epidemiological studies show an increased mortality among workers in nickel refineries by carcinomas, lung and nasal cavities, linked to chronic exposure of dusts and vapors of Ni during the roasting and melting.
Also, the weld of alloy of Ni, (for example the stainless steel) can be a source of such vapors.
During years we believed that only the insoluble dust particles in the water (Ni3S2, NiO) were carcinogenic. However, more recent epidemiological data, clearly indicate that the inhalation of the compounds of hydrosoluble NiSO4, during electrorefining are also carcinogenic and dose-dependent manner.
The interaction between smoking and nickel exposure seems to be additive rather than multiplicative.
Among 100 sino-nasal cancers of these refineries studied by Sunderman, 48 % were carcinomas of squamous cells, 39 % undifferentiated carcinomas and 6 % of adenocarcinomas.
Of the 259 cases of lung tumors 67% are squamous cell carcinomas.
There is no obvious epidemiological risk of cancer by the general environment or exposure by Ni food.
Other increased risks, such as, carcinomas of the larynx , kidney, prostate, stomach and sarcomas of soft tissue were noted, but the statistical significance of these results is doubtful.
Besides the fact of professional exposure - the nickel released from endoprosthesis, plates and screws for bone repair and other medical materials, and amalgams containing some nickel - were suspected of being the cause of sporadic local tumors, but this is not proven.
In general, the implantation of foreign body, metallic cobalt, metallic nickel, an alloy powder consisting of 66-67% , chromium of 13-16% and iron of 7 % was recently classified as '' probably carcinogenic to humans '' ( group2B ) by the Committee of IARC/CIRC (International Agency for Research on Cancer) supported by the fundamental concept that nickel compounds can release ions in critical sites of the target cells.
The evaluation of the IARC concluded :
‘‘there is a sufficient evidence in humans for the carcinogenicity of nickel sulphate and combinations of sulphides and oxides in the nickel refining industry (Group I), there is an unsatisfactory evidence in humans for the carcinogenicity of Ni metallic and nickel alloys (Group 2B).'' Global evaluation : Ni compounds are carcinogenic to humans (Group 1).
The metallic nickel is probably carcinogen to humans (Group 2 B).
Action Strategy summary
The effects of genetic and epigenetic of Ni2+ are the indirect result of the binding of Ni2+ with molecular components of the cell including proteins of chromatin, and not a direct effect of additive mutagenic formation of DNA.
The co-administration of Ni3S2 and essential metals such as Mg2+, Mn2+, Zn2+, Fe3+ (in experimental animals), results in a decrease in carcinogenesis.
This competition of Ni with essential metals for common ligands and their binding sites can be on the base of the inhibition observed of the experimental nickel carcinogenesis by Mg 2+, Mn2+, Zn2+ and also in some cases Fe2+ and Ca2+.
However, the broadest possible range of effects relevant to carcinogenesis, results from redox activity of Ni2+ complexes with certain cellular ligands, including amino acids, peptides, proteins, and other molecules but not the DNA.
The free radicals (superoxide anion : O2 - ; hydrogen peroxide : H2O2 and the hydroxyl radical : OH ) released by the reaction of these complexes with ambient oxygen, are capable of causing damages in ligands and other molecules. And so if the metallic complex is situated in the chromatin, it is the case of histone H3 and H2A, ROS can be generated near the DNA and produce the different types of oxidative DNA damage.
The epigenetic hypothesis of nickel carcinogenesis, can result only through the formation of silent genes such as suppressor genes and of senescence, even in the absence of mutation.
This interesting hypothesis in the activity (tumor-promoting ) of low doses of nickel, is typical of the soluble form.
The genotoxic and mutagenic capacity, responsible for the alteration of DNA at higher intracellular doses of Ni2 +, are better delivered by phagocytosis.
The target cell in Ni2+ included the immune system among others by the system NF-kB.
In this activation observed by the inflammatory response to Ni2+, the oxidative stress may be increased. Also, the inhibition of lymphocytic cells NK (natural killer) by the metal, can suppress the recognition and elimination of mutated cells.
The prevalence of contact dermatitis in Ni is in significant growth in women and there is a relationship between pearcing and induction of nickel allergy.
The mode of pearcing anticipates the increase of prevalence in humans.
Nickel allergy associated with SFC with or without autoimmunity is described for the first time by professor Stejskal in 1999 ( http://www.melisa.org/ ), by examining the hypersensitivity in heavy metals in patients with complicated various pathologies of SFC and or FM.
The dermatitis of contact, contact stomatitis, periodontitis, lichen planus, resistance to antibiotics, are described after sensitization to heavy metals.
The resulting inflammation, may occur elsewhere in the body where heavy metals are deposited.
In these patients with CFS the lymphocytic reaction is increased significantly.
The improvement in many patients is observed after replacement of tooth fillings and metal elimination; there is no correlation between the intensity, complaints and the number of amalgam.
The dental amalgam are in contact with mucous membranes of the dental cavity during many years. The practitioner must choose the least corrosive, corrosion which is increased by the acidity, the dental plaque, the intra oral flora.
It is an immunological basis rather than toxicological and genetically linked.
Not only the corrosion of dental amalgam, but also orthopedic implants, may cause rejection, a dermatitis or poor healing in sensitized patients and could cause systemic reactions and general symptoms.
The stainless metal (austenitic: Cr, Mo, Ni), represent a resistant group to corrosion. The metal released by ionization, can be deposited in the surrounding tissues where metalose,from then on, the Ni, phagocytosed by macrophages plays a central role in inflammatory process.
The inhalation of cigarette smoke and absorption of nickel food may trigger an allergy of type 4 and contribute to the SFC and muscular pains.
The allergy in Ni with regard to general and diffuse symptoms such as CFS and FM is not completely understood and probably underestimated.
The patch test can aggravate the existing allergy.
Therapeutic Applications summary
A strategy detection of all immunological disturbances, as allowed the Melisa test, accompanied by a therapeutic action to aiming concomitantly to ...
- of metallic detoxication (WITHOUT DEMINERALIZING !),
- inhibition of carcinogenesis
- And a high anti-oxidizing activity
Take NKL Action Program Which groups together in a single package and for a full month of use, the various products and substances necessary to achieve these objectives
The human exposure to nickel pollution has the potential to create a variety of pathological effects such as, skin allergies, lung fibrosis, cardiovascular and renal diseases, which the most serious is linked to the carcinogenic activity.
The fibromyalgia (FM) and the Chronic Fatigue Syndrome (CFS) are also implicated.
The exact mechanism of carcinogenesis induced by nickel is not known and has been the subject of numerous experimental and epidemiological investigations. The nickel particularly at high dose has an obvious property of mutagenic and genotoxic activity.
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