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. GBZ 50-2002 Occupational chronic acrylamide poisoning diagnostic criteria GBZ50-2002 Standard download decompression password: www.bzxz.net

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National Occupational Health Standard of the People's Republic of China GBZ50—2002
Diagnostic Criteria of Occupational Chronic Acrylamide PoisoningPublished on April 8, 2002
Implemented on June 1, 2002
Ministry of Health of the People's Republic of China
3Published
Article 6.1 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 GB16370-1996 is inconsistent with this standard, this standard shall prevail. Chronic acrylamide poisoning may occur in occupational activities with long-term exposure to acrylamide. In order to protect the health of the contactors and effectively prevent and treat chronic acrylamide poisoning, GB16370-1996 was issued. This standard highlights the damage of acrylamide to the nervous system and makes diagnostic classifications based on the degree of damage. 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 was drafted by the Institute of Occupational Health and Poison Control of the Chinese Center for Disease Control and Prevention and the Institute of Occupational Health and Prevention 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 Ministry of Health of the People's Republic of China. Diagnostic Standard for Occupational Chronic Acrylamide Poisoning GBZ50-2002
Occupational chronic acrylamide poisoning is a disease characterized by changes in the nervous system due to close contact with acrylamide during production and use.
1 Scope
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. 2 Normative References
The clauses in the following documents become the clauses of this standard through reference in this standard. For any dated referenced document, all subsequent amendments (excluding errata) or revisions are not applicable to this standard. However, parties reaching an agreement based on this standard are encouraged to study whether the latest versions of these documents can be used. For any undated referenced document, the latest version shall apply to this standard.
3 Diagnostic principles
Diagnostic criteria for occupational acute chemical toxicity nervous system diseases 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, diagnosis can be made. 4 Observation subjects
Those who have any of the following can be listed as observation subjects: a) sweating, coldness, peeling, and erythema appear on the local skin exposed to acrylamide; b) symptoms such as numbness, tingling, weakness in the lower limbs, and drowsiness appear; c) neuro-electromyographic shows suspected neurogenic damage. 5 Diagnosis and classification standards
5.1 Mild poisoning
If the subject has any of the first two items and any of the following items, it can be diagnosed as mild poisoning: a) Disturbance of vibration sense, pain, or touch in the distal limbs, accompanied by weakened Achilles tendon reflex; b) Loss of bilateral Achilles tendon reflex;
c) Neuro-electromyography shows neurogenic damage. 5.2 Moderate poisoning
On the basis of mild poisoning, if any of the following items are present, it can be diagnosed as moderate poisoning: a) Disturbance of vibration sense, pain, or touch in the limbs to the level above the elbows and knees, accompanied by loss of Achilles tendon reflex; b) Sensory ataxia;
c) Electromyography shows neurogenic damage, and there are more spontaneous denervation potentials. 5.3 Severe poisoning
Any of the following can be diagnosed as severe poisoning: a) obvious drowsiness and cerebellar dysfunction;
b) obvious muscle atrophy of the distal limbs and affecting motor function. Treatment principles
Treatment principles
B vitamins and energy mixtures can be used, supplemented by physical therapy, physiotherapy and symptomatic treatment. Severe poisoning should also strengthen supportive therapy.
6.2 Other treatments
6.2.1 Observation subjects
Generally, they are not transferred from acrylamide work, and they are reviewed once every six months. Neuro-electromyography examinations are performed as much as possible for dynamic observation. 6.2.2 Mild poisoning
Temporarily transfer from acrylamide work during the illness, and resume the original work after recovery, and conduct regular review. 6.2.3 Moderate and severe poisoning
They should be transferred from acrylamide and other jobs that are harmful to the nervous system. After treatment, they should be arranged to rest or work according to the examination results.
7 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 personnel engaged in the production or use of acrylamide monomers, such as the production of polyacrylamide, N,N-methylenebisacrylamide, N-hydroxymethylacrylamide, etc. A.2 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. A.3 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 extends 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. A.4 After long-term exposure to low concentrations of acrylamide, the main manifestation is chronic latent multiple peripheral neuropathy. After short-term exposure to high concentrations of acrylamide, cerebellar dysfunction may occur in about a month. Although the onset is relatively fast, this standard can also be used. A.5 The cerebellar dysfunction of severely poisoned people can disappear after a few weeks of discontinuation of contact, followed by peripheral nerve damage. A.6 Vibration sense disorders in the limbs and slow Achilles tendon reflexes are early manifestations of mild poisoning. Therefore, these two signs must be carefully checked repeatedly. The Achilles tendon reflex should be checked in the prone position or with reinforcement. A.7 Ataxia caused by deep sensory (vibration sense, position sense) disorders is mainly manifested as 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 eye tremor, slurred speech like chanting, decreased muscle tension in the limbs, unstable finger-nose and Achilles tendon tests, alternating movement disorders, and gait mites. A.8 Neuro-electromyography examination is of great significance for the early diagnosis of this disease. Acrylamide poisoning is mainly characterized by peripheral nerve axonal damage, so the electromyography and sensory nerve potentials of the distal muscles of the limbs should be examined in particular. For examination methods and criteria for judging the results, see GBZ76.
A.9 It is necessary to exclude various diseases that cause peripheral neuropathy and cerebellar ataxia, such as poisoning by furans, isoniazid, arsenic, carbon disulfide, chloroene, methyl n-butyl ketone, n-hexane, and diseases such as diabetes and infectious polyneuritis. See GBZ76.
Appendix B
(Normative Appendix)
Neuro-electromyography examination methods and criteria for judging neurogenic damage
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