Proper help for nickel poisoning. Nickel water poisoning
Nickel content in earth's crust is 8-10-3% (by weight). It is mainly found in the form of copper-nickel sulfide, oxidized silicate and arsenic ores. Nickel is used to produce highly plastic and corrosion-resistant alloys (with iron, chromium, copper, etc.); for nickel plating of medical instruments, car parts, bicycles, chemical equipment, production of batteries; in the fat and perfume industry; for the preparation of catalysts; in the production of organic compounds.
Main sources of pollution environment nickel - enterprises of the mining industry, non-ferrous metallurgy, mechanical engineering, metalworking, chemical, instrument making and others that use various nickel compounds in technological processes; thermal power plants operating on fuel oil and coal; motor transport.
Nickel pollution is most often local: biogeochemical “provinces” are formed with increased nickel content in soil, water, air and local food products of plant and animal origin.
Nickel can enter water through weathering from bedrock and leaching from soil. Significant quantities nickel enters water bodies from wastewater industrial enterprises.
Pollution atmospheric air nickel compounds occur as a result of emissions from enterprises producing and processing it; when burning solid and liquid fuels. Nickel enters the air with vehicle exhaust gases in quantities depending on the type of fuel used, as well as in the form of wear products. car tires and car parts.
Sea water contains about 10-5% nickel, fresh waters- 10-6 -10-7%, in underground - up to 10-5%.
The toxicity of nickel and its compounds depends on the route of entry into the body and solubility. The toxicity of water-soluble nickel compounds (sulfate and chloride) is approximately 30 times higher than that of poorly soluble nickel compounds (oxide and sulfite).
Nickel chloride in concentrations of 0.1-1.5 mg/l causes the death of a number of algae; at a concentration of 0.7 mg/l and above - the death of daphnia. At a concentration of 4.0-4.5 mg/l it causes the death of minnows and carp after 200 hours, and at a concentration of 8.1 mg/l - after a few hours.
At a concentration of 1 mg/l, nickel causes chlorosis of oats; at higher concentrations, growth retardation of vegetable and grain crops and a significant increase in nickel content in plants are observed.
Nickel enters the body mainly through the respiratory tract. gastrointestinal tract and skin.
Different species of animals have different sensitivity to air pollution by nickel compounds. At high concentrations of nickel (for this species) in the air, intoxication developed in the very first hours, which was accompanied by the appearance of shortness of breath, apathy, loss of appetite, vomiting, diarrhea and symptoms of damage nervous system; signs pulmonary insufficiency increased until the animals died after a few hours. At chronic exposure, as in acute cases, the first violations occurred in the lung tissue.
Intoxication with nickel and its compounds is also observed when it enters the body with food or water.
Chronic exposure of humans to nickel chloride (up to 8.6 mg/kg) for 3 months resulted in clinical symptoms intoxication: lethargy, ataxia (disorder of coordination of movements), respiratory failure, decreased body temperature, salivation, strabismus, constipation. The balance and absorption of calcium, magnesium and phosphorus, copper decreased, iodine fixation decreased (impact on the functional state thyroid gland), signs of the development of protein dystrophy were noted.
Absolutely lethal dose metallic nickel (a suspension of metal dust) for rats and mice is 1200 mg/kg, the minimum lethal dose is 500 mg/kg. The animals exhibited a decrease in body weight, leukocytosis, increased body temperature, changes in skin vascular permeability, impaired liver and kidney function, and changes in the ECG. In most cases, the animals died 3-5 days after the administration of nickel.
The following MPCs have been established for nickel and its salts.
- 1. For reservoirs for sanitary water use - 0.1 mg/l.
- 2. For atmospheric air in populated areas: soluble salts nickel - 0.0002 mg/m3; metallic nickel and nickel oxide - 0.001 mg/m3.
- 3. For air working area: nickel carbonyl - 0.0005 mg/m 3 ; nickel salts in the form of hydroaerosol in terms of nickel - 0.005 mg/m 3 ; metallic nickel, its oxides, sulfide and mixtures of these compounds in terms of nickel - 0.05 mg/m 3.
Poisoning of animals with thalia compounds.
Thallium is a soft colored metal butter, quickly oxidizes in air. Thallium compounds are satellites of sulfur and are presented in the form of chloride, sulfate, acetate, and nitrate. They have rodenticidal, insecticidal and fungicidal effects. Waist acetate is used as an epilator. Trivalent thallium compounds: bromide and iodide are less toxic - LD50 for animals 35-40 mg/kg than thallium chloride and acetate (LD50 9-27 mg/kg, for humans 14 mg/kg). Sheep and young animals of all types of animals are most sensitive to thallium compounds.
Causes of poisoning. Intake of thallium compounds with water and feed; eating baits to control ants and rats.
Toxicodynamics. Thallium compounds penetrate well through the skin and mucous membranes and are evenly distributed in the body with the exception of the liver and kidneys; there it accumulates 10 times more. They are highly toxic protoplasmic poisons that affect the central nervous system, including the striopalidal region; cause the breakdown of the myelin sheath; affects ectodermal organs, gastrointestinal tract and kidneys. Thallium competes with potassium ion in biochemical processes. Accumulates in mitochondria and has a general cellular effect toxic effect. Thallium compounds block the sulfhydryl groups of Na+K+ dependent ATPase, causing membrane depolarization. Blockade of thiol enzymes disrupts different kinds metabolism. Causes riboflavin deficiency. Up to 1 month and more is excreted from the body.
Clinical signs. Clinical manifestations toxicosis depend on the dose of poison, type of exposure and route of entry. In acute cases, agitation is noted, profuse drooling, difficulty swallowing, rapid pulse, muscle tremors, urge to vomit, vomiting with blood. Hemorrhagic gastroenteritis, later constipation develops. In subacute cases of toxicosis, muscle twitching, conjunctivitis, polyneuritis, disturbance functional state central nervous system, liver, kidneys, paresis and paralysis develop. The number of red blood cells and hemoglobin, lymphocytosis, and eosinopenia decrease. Damage to the kidneys and liver is noted, and jaundice occurs. In case of chronic poisoning, usually 20-25 days from the moment of poisoning, baldness and increasing muscle weakness with atrophy, peripheral neuropathy, retrobulbar toxic neuritis. The root color of the hair changes, it turns black and falls out; the horny processes are deformed. A turquoise line appears on the gums near the tooth sockets.
Pathological changes. Catarrhal inflammation of the mucous membranes oral cavity, stomach and intestines. Fatty degeneration liver. Granular dystrophy kidneys and myocardium. Hemorrhagic diathesis. Alopecia.
Diagnostics. Complex.
Treatment. Rinse the stomach with a 0.5% solution of sodium thiosulfate and potassium chloride. Saline laxatives, astringents and enveloping agents are prescribed. A specific antidote is potassium ferrocyanide (yellow blood salt). It is prescribed for the first two days of toxicosis, orally at a dose of 0.06-0.07 g/kg. It promotes the immobilization of intracellular thallium with its subsequent redistribution into the gastrointestinal tract. Infusion therapy carried out with multicomponent drugs. Potassium chloride or potassium iodide 0.01-0.02 g/kg is prescribed orally up to 6 times a day; sodium chloride 0.15 g/kg 3-4 times a day. Potassium chloride is also administered intravenously at a dose of 0.01 g/kg 3 times a day in the form of a 4% solution. During potassium ferrocyanide therapy, potassium salts should be discontinued. Sodium thiosulfate is administered intravenously at a dose of 0.1 g/kg of animal weight. Diacarb is given orally at a dose of 0.03 g/kg, once every two days, 4 times. Shown are vitamins B1, B2, B6, PP and C; proserine, galantamine hydrobromide. Lipoic acid prescribed orally at 0.0005-0.0015 g/kg three times a day for 20-30 days. Available in tablets of 0.012 and 0.025 g. Can be administered intramuscularly in the form of a 0.5% solution at a dose of 0.0005 g/kg; ampoules of 2.0 ml. Methionine is prescribed orally at a dose of 0.01-0.025 g/kg 3-4 times a day, and sulfur.
VSE. At negative results In laboratory tests, meat is used as conditional meat.
Prevention. Regular monitoring of thallium levels in environmental objects, feed and feed additives.
Cobalt. Vitamin B12 contains cobalt. Without vitamin B12, metabolism does not occur. propionic acid and the amount of ATP decreases (remember the Krebs cycle). A decrease in the amount of ATP reduces the transfer of energy to cells, which in turn leads to a general weakening of the entire organism. Excess propionic acid in the blood reduces appetite. Since there are many places in the world where soils lack cobalt, cobalt deficiency is not that uncommon. Cobalt deficiency is accompanied by decreased appetite and slower growth. Further development general weakness, quick loss weight, fatty liver degeneration, weakening of the cytolytic function of white blood cells (neutrophils), decreased resistance to infections, pale mucous membranes. Unfortunately, the symptoms of cobalt poisoning are exactly the same! To distinguish cobalt deficiency from its excess, it is necessary to measure the cobalt content in the liver.
The intestinal microflora of ruminants also requires cobalt for the synthesis of vitamin B12. Therefore, ruminants (goats and sheep) require more cobalt than rabbits and horses. The latter need less cobalt, since their microflora does not synthesize cobalt compounds, as do the intestinal microorganisms of ruminants. Ruminants are also more metabolically dependent fatty acids than animals in which food is digested in the caecum (rabbits, horses, Guinea pigs). Rabbits absorb vitamin B 12 more efficiently than humans, rats or sheep because they are coprophagous and eat their own droppings. Cobalt can be given to animals as part of mineral supplements, or add cobalt sulfate or carbonate to food. For food for large animals cattle cobalt is added using glass capsules containing cobalt or a mixture of cobalt oxide and iron.
Nickel (Niccolum, Ni) is chemical element VIII group. Serial number 28, atomic weight 58.71. Nickel is a silvery-white metal, melting point 1455°, density 8.9, soluble in dilute nitric acid. It is used in the production of high-quality steels, alloys, nickel catalysts, and in electroplating for nickel plating of products. Nickel compounds are used in the ceramics industry and as a poison for pest control.
Nickel carbonyl is very toxic - Ni(CO) 4. Nickel and its compounds enter the body through the lungs with inhaled air in the form of dust, fog, and vapor.
In industry, chronic poisoning mainly occurs. However, when exposed to high concentrations of nickel compounds, acute poisoning can occur. Symptoms of acute poisoning include weakness, headache, . In case of mild poisoning, all symptoms disappear within fresh air. In severe cases, pulmonary edema may develop. In case of chronic poisoning, frequent nosebleeds, impaired sense of smell, damage to the mucous membrane of the upper respiratory tract such as laryngitis, tracheitis, bronchitis, development bronchial asthma, possibly the nasal septum. Contact with nickel compounds can lead to skin lesions - “nickel”, or “nickel”. These diseases occur in nickel workers and people involved in electrolytic production.
Treatment. First aid for acute nickel poisoning: remove the patient from the room contaminated with nickel compounds, heat, absolute rest for 3-5 days after poisoning, and for shortness of breath - inhalation pure oxygen, according to indications, as an antispasmodic - (0.2 g orally 2-3 times a day or intramuscularly 2-3 ml of a 12% solution); every 6 hours. during the first two days and twice a day for the next 8 days, intramuscular administration of the antidote dimercaptol at 3-5 mg per 1 kg of patient weight; intravenous infusion of 5-10 ml of 10% chloride solution and 10-20 ml of 40% glucose solution; bloodletting; according to indications - cardiac.
Prevention. Identify persons with hypersensitivity and not allow them to work with nickel. Preventing skin contact of workers with nickel compounds. Mechanization of loading and removal of products during nickel plating. The use of special protective coatings for baths in the electrolytic production of nickel. Using special gloves, aprons, lubricating the skin of the hands protective ointments. Sealing of equipment with appropriate local mechanical exhaust ventilation. The maximum permissible concentration of nickel compounds in the air of industrial premises is 0.5 mg/m 3 .
All those working with nickel compounds undergo periodic examinations once every six months by a committee consisting of a therapist, neurologist, dermatologist, and radiologist.
Nickel in the blood
Determination of nickel concentration in blood serum used for the diagnosis of acute and chronic poisoning nickel
Synonyms Russian
Nickel in blood serum.
English synonyms
Nickel (Ni), Blood.
Research method
Atomic adsorption spectrometry (AAS).
Units
μg/L (micrograms per liter).
What biomaterial can be used for research?
Venous blood.
How to properly prepare for research?
- Do not eat for 2-3 hours before the test; you can drink clean still water.
- Do not smoke for 30 minutes before the test.
General information about the study
Nickel is a heavy metal whose compounds are toxic when accumulated in the body. Normally, it is present in humans in very low concentrations, but physiological role not installed.
The main ways nickel enters the body are through water and food, which contain increased concentrations of this metal. It is found in foods such as tea, coffee, chocolate, beans, hazelnuts, cabbage, spinach and potatoes. Every day a person consumes about 175 mcg of nickel in food, which, however, is not enough to develop any symptoms of intoxication. Another source of nickel is polluted air. A non-smoking person inhales 0.1-0.25 mcg of nickel per day (for workers at metallurgical plants this figure can exceed 1 mcg). Inhalation is the main route of intoxication at work. Smoking increases nickel intake by 0.0004 mcg per day. Also important is the penetration of this element through the skin and mucous membranes during prolonged contact with nickel-containing jewelry, coins, and stainless steel items. Elemental nickel does not penetrate intact skin, but the absorption of nickel chloride and sulfate is 77%.
To diagnose nickel poisoning, its concentration in the blood is measured. Since the level of nickel and other heavy metals, even when exceeded normal values- these are just nanograms per milliliter; the ultrasensitive method of atomic adsorption spectrometry is used for analysis. At the same time, the accuracy of blood testing for diagnosing nickel poisoning is inferior to urine testing. In addition, the analysis does not allow identifying the source of poisoning (that is, it does not differentiate between sulfides, oxides or elemental nickel).
The timing of symptoms and severity of nickel poisoning depends on physiological state body, the route and rate of nickel intake, the presence concomitant diseases and some other reasons. The damaging effect of nickel is based on its ability to bind oxygen molecules, thus interfering with the process of oxidative phosphorylation, and sulfhydryl groups, reducing the activity of certain enzymes. The resulting ATP deficiency is accompanied by dysfunction of many organs (lungs, kidneys, hematopoietic tissue), but tissues with a high degree of metabolism - the liver and brain - are primarily affected. Acute poisoning occurs when inhaling nickel carbonyl, one of the most toxic substances to humans. Nickel carbonyl is widely used in petroleum refining, oil hydrogenation, and the production of metal alloys and plastics. Symptoms of poisoning with this substance include shortness of breath, cough, headache, nausea and vomiting, abdominal pain, bleeding, pulmonary edema, pneumonia, cerebral edema, delirium, convulsions and depression of consciousness up to coma. The disease develops within 12-120 hours after inhalation of nickel carbonyl vapor. The study of nickel concentration in the blood is complemented by others laboratory research to assess the function of vital organs.
Most patients with chronic nickel poisoning are workers exposed to nickel sulfides and oxides in glass, ceramics, and paint production. Chronic nickel intoxication is accompanied by symptoms of upper respiratory tract irritation (nasal congestion, cough, rhinorrhea) and can lead to asthma. In addition, nickel has a carcinogenic effect and is associated with the development malignant tumors nasopharynx and lungs. In this group of patients also great importance has a percutaneous route of nickel entry and the development of occupational nickel dermatitis.
It should be noted that clinical picture acute and chronic nickel poisoning is not specific to this heavy metal. Similar symptoms have intoxication with cadmium, chromium, cobalt, copper, selenium and zinc. Therefore, diagnosing heavy metal poisoning in a patient with occupational hazards- it's always comprehensive examination, including a study of the concentration of all necessary elements to determine the specific source of poisoning.
When interpreting a study result, one should pay attention Special attention for a history of contact with nickel compounds (primarily nickel carbonyl). Since clinically significant nickel poisoning is very rare in the general population, an increase in nickel concentration in a patient without occupational hazards is more likely to indicate false positive result due to sample contamination. An increase in the concentration of nickel in the blood is observed in patients undergoing hemodialysis, which, however, is not accompanied by any signs of intoxication and has no diagnostic value.
What is the research used for?
For the diagnosis of acute and chronic nickel poisoning in patients whose work involves a certain risk (oil refining, production of metal alloys, glass, ceramics).
When is the study scheduled?
For symptoms:
- acute poisoning with nickel (nickel carbonyl): shortness of breath, cough, headache, nausea and vomiting, abdominal pain, bleeding, pulmonary edema, pneumonia, cerebral edema, delirium, convulsions and depression of consciousness up to coma;
- chronic nickel poisoning: feeling of nasal congestion, runny nose, cough, attacks of shortness of breath or suffocation, malignant neoplasms of the nasopharynx and lungs.
What do the results mean?
Reference values: 0.6 - 7.5 µg/l.
Reasons for increased nickel levels in the blood:
- acute or chronic nickel intoxication;
- hemodialysis.
Decreased nickel levels in the blood has no diagnostic value.
What can influence the result?
- Nickel concentrations may increase during hemodialysis.
- After using iodine- or gadolinium-containing contrast agents The study is recommended to be carried out no earlier than after 4 days.
Important Notes
- When interpreting the result, special attention should be paid to a history of exposure to nickel compounds (nickel carbonyl).
- A positive test result in a patient without occupational hazards was most likely obtained due to contamination of the sample.
Price: 600 rub.
Material: Blood
Pickup time: 7:00-12:00 Sat. 7:00-11:00
Output of results: up to 6 working days
Conditions for preparing for analysis:
Strictly on an empty stomach
Nickel in the blood
Nickel is a heavy metal whose compounds are toxic when accumulated in the body. It is normally present in humans in very low concentrations, but its physiological role has not been established.
The main ways nickel enters the body are through water and food, which contain increased concentrations of this metal. It is found in foods such as tea, coffee, chocolate, beans, hazelnuts, cabbage, spinach and potatoes. Every day a person consumes about 175 mcg of nickel in food, which, however, is not enough to develop any symptoms of intoxication. Another source of nickel is polluted air. A non-smoking person inhales 0.1-0.25 mcg of nickel per day (for workers at metallurgical enterprises this figure can exceed 1 mcg). Inhalation is the main route of intoxication at work. Smoking increases nickel intake by 0.0004 mcg per day. Also important is the penetration of this element through the skin and mucous membranes during prolonged contact with nickel-containing jewelry, coins, and stainless steel items. Elemental nickel does not penetrate intact skin, but the absorption of nickel chloride and sulfate is 77%.
To diagnose nickel poisoning, its concentration in the blood is measured. Since the level of nickel and other heavy metals, even when exceeding normal values, is only nanograms per milliliter, the ultrasensitive method of atomic adsorption spectrometry is used for analysis. At the same time, the accuracy of blood testing for diagnosing nickel poisoning is inferior to urine testing. In addition, the analysis does not allow identifying the source of poisoning (that is, it does not differentiate between sulfides, oxides or elemental nickel).
The time of onset of symptoms and the severity of nickel poisoning depends on the physiological state of the body, the route and rate of nickel intake, the presence of concomitant diseases and some other reasons. The damaging effect of nickel is based on its ability to bind oxygen molecules, thus interfering with the process of oxidative phosphorylation, and sulfhydryl groups, reducing the activity of certain enzymes. The resulting ATP deficiency is accompanied by dysfunction of many organs (lungs, kidneys, hematopoietic tissue), but tissues with a high degree of metabolism - the liver and brain - are primarily affected. Acute poisoning occurs when inhaling nickel carbonyl, one of the most toxic substances to humans. Nickel carbonyl is widely used in petroleum refining, oil hydrogenation, and the production of metal alloys and plastics. Symptoms of poisoning with this substance include shortness of breath, cough, headache, nausea and vomiting, abdominal pain, bleeding, pulmonary edema, pneumonia, cerebral edema, delirium, convulsions and depression of consciousness up to coma. The disease develops within 12-120 hours after inhalation of nickel carbonyl vapor. The study of nickel concentration in the blood is complemented by other laboratory tests to assess the function of vital organs.
Most patients with chronic nickel poisoning are workers exposed to nickel sulfides and oxides in glass, ceramics, and paint production. Chronic nickel intoxication is accompanied by symptoms of upper respiratory tract irritation (nasal congestion, cough, rhinorrhea) and can lead to asthma. In addition, nickel has a carcinogenic effect and is associated with the development of malignant tumors of the nasopharynx and lungs. In this group of patients, the percutaneous route of nickel exposure and the development of occupational nickel dermatitis are also of great importance.
It should be noted that the clinical picture of acute and chronic nickel poisoning is not specific to this heavy metal. Intoxication with cadmium, chromium, cobalt, copper, selenium and zinc has similar symptoms. Therefore, diagnosing heavy metal poisoning in a patient with occupational hazards is always a comprehensive examination, including a study of the concentration of all necessary elements to establish the specific source of poisoning.
When interpreting the test result, special attention should be paid to a history of contact with nickel compounds (primarily nickel carbonyl). Since clinically significant nickel poisoning is very rare in the general population, an increase in nickel concentration in a patient without occupational hazards is more likely to indicate a false positive result due to sample contamination. An increase in the concentration of nickel in the blood is observed in patients undergoing hemodialysis, which, however, is not accompanied by any signs of intoxication and has no diagnostic value.
