GB 16370-1996 Diagnostic criteria and treatment principles for occupational chronic acrylamide poisoning
time:
2024-08-06 05:38:41
- GB 16370-1996
- in force
Standard ID:
GB 16370-1996
Standard Name:
Diagnostic criteria and treatment principles for occupational chronic acrylamide poisoning
Chinese Name:
职业性慢性丙烯酰胺中毒诊断标准及处理原则
Standard category:
National Standard (GB)
-
Date of Release:
1996-05-23 -
Date of Implementation:
1996-01-02
Standard ICS number:
Medical and Health Technology >> 11.020 Medical Science and Healthcare Devices ComprehensiveChina Standard Classification Number:
Medicine, Health, Labor Protection>>Health>>C60 Occupational Disease Diagnosis Standard
Release date:
1996-05-23Review date:
2004-10-14Drafting Organization:
Chinese Academy of Preventive MedicineFocal point Organization:
Ministry of HealthPublishing Department:
State Administration of Technical Supervision Ministry of Health of the People's Republic of ChinaCompetent Authority:
Ministry of Health
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Summary:
This standard specifies the diagnostic criteria and treatment principles for occupational chronic acrylamide poisoning. This standard applies to the diagnosis and treatment of occupational chronic acrylamide poisoning. GB 16370-1996 Diagnostic criteria and treatment principles for occupational chronic acrylamide poisoning GB16370-1996 Standard download decompression password: www.bzxz.net
Some standard content:
National Standard of the People's Republic of China
Occupational chronic acrylamide poisoning
Diagnostic criteria and principles of management ofoccupational chronic acrylamide poisoningGB16370--1996
Occupational chronic acrylamide poisoning is a disease characterized by changes in the nervous system caused by close contact with acrylamide during production and use Subject Content and Scope of Application
This standard specifies the diagnostic criteria and management principles of occupational chronic acrylamide poisoning. This standard applies to the diagnosis and treatment of occupational chronic acrylamide poisoning. 2 Reference Standards
GB4865 Diagnostic Criteria and Management Principles of Occupational Chronic Allyl Chloride Poisoning 3 Diagnostic Principles
Based on the occupational history of close contact with acrylamide, symptoms and signs of multiple peripheral nerve damage and neuro-electromyographic changes or cerebellar dysfunction, combined with on-site hygiene investigation, and excluding similar diseases caused by other causes, the diagnosis can be made. 4 Diagnosis and classification standardsbzxz.net
4.1 Observation subjects
Those who have any of the following items can be listed as observation subjects: hyperhidrosis, dampness, peeling, and erythema on the local skin exposed to acrylamide. a.
b. Numbness, tingling, weakness in the lower limbs, drowsiness and other symptoms appear. c.
Neuro-electromyography shows suspected neurogenic damage. 4.2 Mild poisoning
Those who have any of the first two items of the observation subjects and any of the following items can be diagnosed as mild poisoning: vibration sensation or pain sensation and tactile sensation in the distal limbs are impaired, accompanied by weakened Achilles tendon reflex. i.
b. Bilateral Achilles tendon reflex disappears
Neuro-electromyography shows neurogenic damage. 4.3 Moderate poisoning
On the basis of mild poisoning, if any of the following items are present, moderate poisoning can be diagnosed: a.
The level of motor or pain and tactile disturbance in the limbs reaches above the elbow and knee, accompanied by the disappearance of tendon reflexes. Sensory ataxia.
c. Electromyography shows neurogenic damage and there are many spontaneous denervation potentials. 4.4 Severe poisoning
Approved by the State Administration of Technical Supervision on May 23, 1996, and implemented on December 1, 1996
GB16370—1996
If any of the following items are present, severe poisoning can be diagnosed: a. Obvious drowsiness and cerebellar dysfunction.
Obvious muscle atrophy in the distal limbs, affecting motor function. b.
5 Treatment principles
You can use B vitamins, energy mixtures, and supplement with physical therapy, physiotherapy and symptomatic treatment. Severe poisoning should also strengthen supportive therapy. 6 Work capacity assessment
6.1 Observation subjects
Generally, they are not transferred from acrylamide operations, and they are reexamined once every six months. Neuro-electromyography examinations are performed as much as possible. Dynamic observation is carried out. 6.2 Mild poisoning
Temporarily transfer from acrylamide operations during the illness, and can resume the original work after recovery, and reexamine regularly. 6.3 Moderate and severe poisoning
Should be transferred from acrylamide and other operations that are harmful to the nervous system, and after treatment, they should be arranged to rest or work according to the examination results. 7 Health examination requirements
7.1 Acrylamide workers should undergo pre-employment physical examinations, including internal medicine and neurology examinations. 7.2 Workers engaged in acrylamide operations shall undergo a physical examination once a year. In addition to the same examination items as the pre-employment physical examination, a neuro-electromyographic examination shall be performed when conditions permit.
8 Contraindications to occupational drugs
Organic diseases of the central and peripheral nervous systems; diabetes;
Allergic skin diseases and other serious skin diseases. See Appendix A of GB4865.
GB16370—1996
Appendix A
Methods for neuro-electromyographic examination
and the criteria for judging neurogenic damage
(Supplement)
Appendix B
Instructions for the correct use of the standard
(Reference)
B1 This standard applies to personnel engaged in the production or use of acrylamide monomers, such as the production of polyacrylamide, N,N-methylenebisacrylamide, N-hydroxymethylacrylamide, etc.
B2 Skin contact is the main route of occupational acrylamide poisoning. Therefore, close contact with acrylamide mainly refers to the degree of skin contamination, followed by the concentration of workshop air. B3 Mild and moderate acrylamide poisoning is mainly manifested by peripheral nerve damage. The classification boundary between the two is that in moderate poisoning, the range of sensory impairment expands to the elbow and knee level or ataxia caused by deep sensory impairment occurs; when there is obvious atrophy of the distal muscles of the limbs and affects motor function or cerebellar dysfunction (whether it is the first manifestation or occurs on the basis of existing peripheral neuropathy), it should be diagnosed as severe poisoning. B4 After long-term exposure to low concentrations of acrylamide, the main manifestation is chronic predatory multiple peripheral neuropathy. After short-term exposure to high concentrations of acrylamide, cerebellar dysfunction may occur in about a month. Although the onset is faster, this standard can also be used as a reference. B5 The cerebellar dysfunction of severely poisoned people can subside after a few weeks of discontinuation of contact, followed by peripheral nerve damage. 6 Impairment of vibration sense in the limbs and slow Achilles tendon reflex are early manifestations of mild poisoning. Therefore, these two signs must be checked repeatedly and carefully. The Achilles tendon reflex should be checked in the prone position with the knees bent or by using the reinforcement method. B7 Ataxia caused by deep sensory (vibration sense, position sense) disorders is mainly manifested by the inability to walk in a straight line with both feet, the inability to stand on one foot, and difficulty standing with eyes closed. The manifestations of cerebellar dysfunction include horizontal tremor of the eyeballs, slurred speech like chanting, decreased muscle tension in the limbs, unstable finger-nose and heel-knee-shin tests, alternating movements, and sluggish gait. B8 Neuro-electromyography examination is of great significance for the early diagnosis of this disease. Acrylamide poisoning is mainly characterized by peripheral nerve axonal damage. Therefore, the electromyography and sensory nerve potential of the distal muscles of the limbs should be checked in particular. For the examination methods and the criteria for judging the results, please refer to Appendix A of GB4865. B9 It is necessary to exclude various diseases that cause peripheral neuropathy and cerebellar ataxia, such as furan, isocyanate, arsenic, carbon disulfide, allyl chloride, methyl n-butyl ketone, n-hexane poisoning, diabetes, infectious polyneuritis and other diseases. Additional notes:
This standard is proposed by the Ministry of Health of the People's Republic of China. This standard was drafted by the Institute of Labor Hygiene and Occupational Diseases, Chinese Academy of Preventive Medicine and the Occupational Prevention Institute of Shandong Qilu Petrochemical Company, and Zhejiang Academy of Medical Sciences and Heilongjiang Institute of Labor Hygiene and Occupational Diseases participated in the drafting. This standard is interpreted by the Institute of Labor Hygiene and Occupational Diseases, Chinese Academy of Preventive Medicine, the technical coordination unit entrusted by the Ministry of Health. 267
Tip: This standard content only shows part of the intercepted content of the complete standard. If you need the complete standard, please go to the top to download the complete standard document for free.
Occupational chronic acrylamide poisoning
Diagnostic criteria and principles of management ofoccupational chronic acrylamide poisoningGB16370--1996
Occupational chronic acrylamide poisoning is a disease characterized by changes in the nervous system caused by close contact with acrylamide during production and use Subject Content and Scope of Application
This standard specifies the diagnostic criteria and management principles of occupational chronic acrylamide poisoning. This standard applies to the diagnosis and treatment of occupational chronic acrylamide poisoning. 2 Reference Standards
GB4865 Diagnostic Criteria and Management Principles of Occupational Chronic Allyl Chloride Poisoning 3 Diagnostic Principles
Based on the occupational history of close contact with acrylamide, symptoms and signs of multiple peripheral nerve damage and neuro-electromyographic changes or cerebellar dysfunction, combined with on-site hygiene investigation, and excluding similar diseases caused by other causes, the diagnosis can be made. 4 Diagnosis and classification standardsbzxz.net
4.1 Observation subjects
Those who have any of the following items can be listed as observation subjects: hyperhidrosis, dampness, peeling, and erythema on the local skin exposed to acrylamide. a.
b. Numbness, tingling, weakness in the lower limbs, drowsiness and other symptoms appear. c.
Neuro-electromyography shows suspected neurogenic damage. 4.2 Mild poisoning
Those who have any of the first two items of the observation subjects and any of the following items can be diagnosed as mild poisoning: vibration sensation or pain sensation and tactile sensation in the distal limbs are impaired, accompanied by weakened Achilles tendon reflex. i.
b. Bilateral Achilles tendon reflex disappears
Neuro-electromyography shows neurogenic damage. 4.3 Moderate poisoning
On the basis of mild poisoning, if any of the following items are present, moderate poisoning can be diagnosed: a.
The level of motor or pain and tactile disturbance in the limbs reaches above the elbow and knee, accompanied by the disappearance of tendon reflexes. Sensory ataxia.
c. Electromyography shows neurogenic damage and there are many spontaneous denervation potentials. 4.4 Severe poisoning
Approved by the State Administration of Technical Supervision on May 23, 1996, and implemented on December 1, 1996
GB16370—1996
If any of the following items are present, severe poisoning can be diagnosed: a. Obvious drowsiness and cerebellar dysfunction.
Obvious muscle atrophy in the distal limbs, affecting motor function. b.
5 Treatment principles
You can use B vitamins, energy mixtures, and supplement with physical therapy, physiotherapy and symptomatic treatment. Severe poisoning should also strengthen supportive therapy. 6 Work capacity assessment
6.1 Observation subjects
Generally, they are not transferred from acrylamide operations, and they are reexamined once every six months. Neuro-electromyography examinations are performed as much as possible. Dynamic observation is carried out. 6.2 Mild poisoning
Temporarily transfer from acrylamide operations during the illness, and can resume the original work after recovery, and reexamine regularly. 6.3 Moderate and severe poisoning
Should be transferred from acrylamide and other operations that are harmful to the nervous system, and after treatment, they should be arranged to rest or work according to the examination results. 7 Health examination requirements
7.1 Acrylamide workers should undergo pre-employment physical examinations, including internal medicine and neurology examinations. 7.2 Workers engaged in acrylamide operations shall undergo a physical examination once a year. In addition to the same examination items as the pre-employment physical examination, a neuro-electromyographic examination shall be performed when conditions permit.
8 Contraindications to occupational drugs
Organic diseases of the central and peripheral nervous systems; diabetes;
Allergic skin diseases and other serious skin diseases. See Appendix A of GB4865.
GB16370—1996
Appendix A
Methods for neuro-electromyographic examination
and the criteria for judging neurogenic damage
(Supplement)
Appendix B
Instructions for the correct use of the standard
(Reference)
B1 This standard applies to personnel engaged in the production or use of acrylamide monomers, such as the production of polyacrylamide, N,N-methylenebisacrylamide, N-hydroxymethylacrylamide, etc.
B2 Skin contact is the main route of occupational acrylamide poisoning. Therefore, close contact with acrylamide mainly refers to the degree of skin contamination, followed by the concentration of workshop air. B3 Mild and moderate acrylamide poisoning is mainly manifested by peripheral nerve damage. The classification boundary between the two is that in moderate poisoning, the range of sensory impairment expands to the elbow and knee level or ataxia caused by deep sensory impairment occurs; when there is obvious atrophy of the distal muscles of the limbs and affects motor function or cerebellar dysfunction (whether it is the first manifestation or occurs on the basis of existing peripheral neuropathy), it should be diagnosed as severe poisoning. B4 After long-term exposure to low concentrations of acrylamide, the main manifestation is chronic predatory multiple peripheral neuropathy. After short-term exposure to high concentrations of acrylamide, cerebellar dysfunction may occur in about a month. Although the onset is faster, this standard can also be used as a reference. B5 The cerebellar dysfunction of severely poisoned people can subside after a few weeks of discontinuation of contact, followed by peripheral nerve damage. 6 Impairment of vibration sense in the limbs and slow Achilles tendon reflex are early manifestations of mild poisoning. Therefore, these two signs must be checked repeatedly and carefully. The Achilles tendon reflex should be checked in the prone position with the knees bent or by using the reinforcement method. B7 Ataxia caused by deep sensory (vibration sense, position sense) disorders is mainly manifested by the inability to walk in a straight line with both feet, the inability to stand on one foot, and difficulty standing with eyes closed. The manifestations of cerebellar dysfunction include horizontal tremor of the eyeballs, slurred speech like chanting, decreased muscle tension in the limbs, unstable finger-nose and heel-knee-shin tests, alternating movements, and sluggish gait. B8 Neuro-electromyography examination is of great significance for the early diagnosis of this disease. Acrylamide poisoning is mainly characterized by peripheral nerve axonal damage. Therefore, the electromyography and sensory nerve potential of the distal muscles of the limbs should be checked in particular. For the examination methods and the criteria for judging the results, please refer to Appendix A of GB4865. B9 It is necessary to exclude various diseases that cause peripheral neuropathy and cerebellar ataxia, such as furan, isocyanate, arsenic, carbon disulfide, allyl chloride, methyl n-butyl ketone, n-hexane poisoning, diabetes, infectious polyneuritis and other diseases. Additional notes:
This standard is proposed by the Ministry of Health of the People's Republic of China. This standard was drafted by the Institute of Labor Hygiene and Occupational Diseases, Chinese Academy of Preventive Medicine and the Occupational Prevention Institute of Shandong Qilu Petrochemical Company, and Zhejiang Academy of Medical Sciences and Heilongjiang Institute of Labor Hygiene and Occupational Diseases participated in the drafting. This standard is interpreted by the Institute of Labor Hygiene and Occupational Diseases, Chinese Academy of Preventive Medicine, the technical coordination unit entrusted by the Ministry of Health. 267
Tip: This standard content only shows part of the intercepted content of the complete standard. If you need the complete standard, please go to the top to download the complete standard document for free.
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