GBZ 52-2002 Diagnostic criteria for occupational acute carbamate pesticide poisoning
Some standard content:
ICS13.100
National Occupational Health Standard of the People's Republic of China GBZ52-2002
Diagnostic Criteria of Occupational Acute Carbamate Insecticides PoisoningPublished on April 8, 2002
Implemented on June 1, 2002
Ministry of Health of the People's Republic of China
Article 4.1 of this standard is recommended, and the rest are mandatory. This standard is formulated in accordance with the "Law of the People's Republic of China on the Prevention and Control of Occupational Diseases". From the date of implementation of this standard, if the original standard GB16372-1996 is inconsistent with this standard, this standard shall prevail. Acute poisoning may occur in occupational activities involving contact with carbamate insecticides. In order to protect the health of the contactors and effectively prevent and control acute carbamate insecticide poisoning, GB16372-1996 was issued. This standard is a revised version. In view of the fact that acute carbamate insecticide poisoning has an acute onset, rapid recovery, and relatively mild symptoms, no observation subjects are set. Appendix A of this standard is an informative appendix, and Appendix B is a normative appendix. This standard is proposed and managed by the Ministry of Health of the People's Republic of China. This standard is drafted by the Institute of Occupational Health and Poison Control of the Chinese Center for Disease Control and Prevention, and the Department of Occupational Diseases of Xi'an Central Hospital, Jiangsu Provincial Center for Disease Control and Prevention, Xuzhou Municipal Health and Epidemic Prevention Station, Zhenjiang Municipal Health and Epidemic Prevention Station, and Wuxi Municipal Health and Epidemic Prevention Station participated in the drafting.
This standard is interpreted by the Ministry of Health of the People's Republic of China..comDiagnostic Standard for Occupational Acute Carbamate Insecticide Poisoning GBZ52-2002
Acute carbamate insecticide poisoning is a systemic disease with muscarinic, nicotinic and central nervous system symptoms caused by decreased cholinesterase activity in the body after short-term close contact with carbamate insecticides. 1 Scope
This standard specifies the diagnostic criteria and treatment principles for occupational acute carbamate insecticide poisoning. This standard applies to the diagnosis and treatment of occupational acute carbamate pesticide poisoning. 2 Diagnostic principles
According to the occupational history of short-term exposure to large amounts of carbamate pesticides, the corresponding clinical manifestations appear quickly, combined with the timely determination of whole blood cholinesterase activity results, and reference to the on-site labor hygiene survey data, a comprehensive analysis is conducted, and other causes are excluded before diagnosis can be made.
3 Diagnosis and grading standards
3.1 Mild poisoning
After short-term close contact with carbamates, milder muscarinic and central nervous system symptoms appear, such as dizziness, headache, fatigue, blurred vision, nausea, vomiting, salivation, sweating, pupil constriction, etc., and some may be accompanied by nicotinic symptoms such as fasciculations, which generally return to normal within 24 hours. Whole blood cholinesterase activity is often below 70%. 3.2 Severe poisoningbzxz.net
In addition to the aggravation of the above symptoms, if any of the following is present, severe poisoning can be diagnosed: a) pulmonary edema;
b) coma or cerebral edema.
The activity of whole blood cholinesterase is generally below 30%. 4 Treatment principles
4.1 Treatment principles
4.1.1 Leave the poisoning site quickly, take off contaminated clothes, and thoroughly wash contaminated skin, hair and nails with soap and warm water.
4.1.2 Specific antidote:
For mild poisoning, specific antidote may not be needed. Atropine may be taken orally or intramuscularly if necessary, but atropine is not necessary. a)
b) For severe poisoning, atropine should be used according to the condition and atropineization should be achieved as soon as possible. No rejuvenating agent is needed for simple carbamate insecticide poisoning. c)
..com4.1.3 The principle of symptomatic treatment is the same as that of internal medicine. 4.2 Other treatments
After the poisoning is cured, the patient can still do the original work.
Instructions for the correct use of this standard
See Appendix A (Informative Appendix) and Appendix B (Normative Appendix). Appendix A
(Informative Appendix)
Instructions for the correct use of this standard
A.1 This standard applies to acute poisoning of various personnel involved in the production, packaging, processing, handling and use of carbamate insecticides. Commonly used varieties in China include furadan, carbaryl, cypermethrin, chlorpyrifos, chlorpyrifos, chlorpyrifos, chlorpyrifos, etc. Acute poisoning by living carbamate insecticides can also refer to this standard. Thio (or dithio) carbamate herbicides or fungicides have no inhibitory effect on the body's cholinesterase. The diagnosis and treatment of poisoning cannot be based on this standard. A.2 The clinical characteristics of acute carbamate pesticide poisoning are rapid onset, rapid recovery, relatively mild condition, and no delayed neuropathy after the poisoning is cured.
A.3 The diagnostic classification of acute poisoning is mainly based on clinical manifestations, and the timely determination of blood cholinesterase activity can be used as a reference indicator. If the whole blood cholinesterase determination is not possible according to Appendix B, the hydroxy iron colorimetric method can be used. A.4 The diseases that need to be differentially diagnosed mainly include acute organophosphorus poisoning, heat stroke, acute gastroenteritis and food poisoning. It is generally not difficult to make a distinction based on the contact history, clinical characteristics, blood cholinesterase determination and dynamic observation. If necessary, the content of carbamate pesticides or their metabolites in biological materials can be determined. A.5 At present, pesticide compounding is widely used, and the problem of mixed poisoning of carbamate and organophosphorus or other pesticides may exist at the same time: attention should be paid to diagnosis and differential diagnosis. A.6 Mild poisoning is relieved quickly after the contact is broken. Treatment can be treated with atropine 0.6-0.9 mg orally or 0.5-1.0 mg intramuscularly. Repeat 1-2 times if necessary. Atropine is not necessary. Severe poisoning should be atropine as soon as possible, but the total dose required is generally smaller than that of organophosphorus poisoning. The interval between medications can be appropriately extended and the maintenance time is relatively short. ..comB.1 Principle
Appendix B
(Normative Appendix)
Determination of cholinesterase activity in whole blood, red blood cells and plasmaAcetylthiocholine is hydrolyzed into thiocholine and acetate under the action of cholinesterase. Thiocholine reacts with dithiobis-nitrobenzoic acid to form a yellow compound and then is quantified by colorimetry. The amount of thiocholine produced by hydrolysis reflects the activity value of cholinesterase. B.2 Instruments
a. Constant temperature water tank (37±0.5℃);
b. Centrifuge;
C. Spectrophotometer.
B.3 Reagents
a: Thioacetyl iodide choline solution (matrix); weigh 75 mg of thioacetyl iodide choline, dissolve it in double distilled water, dilute to 10 mL, and store it in a refrigerator (4℃). Dilute 10 times with double distilled water before use. b. Dithiobis-nitrobenzoic acid solution (color developer): weigh 100 mg of dithiobis-nitrobenzoic acid, dissolve it in 50 mL of normal saline, and then add it to 50 mL of 1/15 mol phosphate buffer (pH8.0). Store it in a refrigerator. Dilute 10 times with equal volumes of normal saline and 1/15 mol phosphate buffer before use. c. Physostigmine salicylate (inhibitor): Weigh 10 mg of physostigmine salicylate, dissolve it in double distilled water and dilute to 10 mL. Store in a refrigerator.
B.4 Operation steps
B.4.1 Take 10 μL of ear (or finger) blood and add it to a centrifuge tube containing 10 mL of dithiobis-nitrobenzoic acid solution, and mix gently.
B.4.2 Take out 4.0 mL and put it in test tube A as a tube for whole blood cholinesterase activity determination. Centrifuge the remaining solution at 3000 r/min for 5 minutes, and transfer 4.0 mL of the supernatant to test tube B as a tube for plasma cholinesterase activity determination. Take another 4.0 mL of dithiobis-nitrobenzoic acid solution and add it to test tube C as a blank tube. B.4.3 Add 1.0 mL of thioacetyl iodocholine to each tube A, B, and C, mix well, and record the time. B.4.4 After keeping the temperature in a 37°C constant temperature water bath for 6 minutes, add 2 drops of salicylic acid physostigmine solution to each of the above tubes and mix quickly.
B.4.5 Centrifuge tube A at 3000r/min for 5 minutes to precipitate the blood cells. B.4.6 Use 1cm colorimetric cups to measure the absorbance of the supernatant of tube A and tube B at a wavelength of 420nrn, and adjust the zero point with a blank tube.
B.5 Calculation
Substitute the measured absorbance of tubes A and B into formula (A1) to calculate the cholinesterase activity of whole blood and plasma. The difference between the two is the cholinesterase activity value of red blood cells,
Absorbance
1.36×104
×10°×2.6×=×
Absorbance×7.97-
Where: 1.6X104-The absorbance coefficient of nitrobenzoate ions formed in the enzyme assay. The number of nitrobenzoate ions is the same as the amount of thiocholine produced.
The result of the cholinesterase activity assay is based on the production of 1um thiocholine per minute per milliliter of whole blood (plasma or red blood cells) as 1 unit.
Precautions
a. Before blood collection, it is necessary to pay attention to cleaning the skin surface to prevent contamination, and accurately draw 10μL with a heparin-treated hemoglobin tube.
b. Both the matrix and the sample need to be preheated to ensure the reaction temperature. The preheating time depends on the room temperature during the assay, generally 2 to 5 minutes. c. The insulation time of each sample must be strictly controlled at 6 minutes, that is, the time from adding the matrix to terminating the enzyme reaction must be consistent in each tube.
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