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GBZ32-2015 English PDF

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GBZ32-2015: Diagnosis of occupational chloroprene poisoning
Status: Valid

GBZ32: Evolution and historical versions

Standard IDContents [version]USDSTEP2[PDF] delivered inStandard Title (Description)StatusPDF
GBZ 32-2015English129 Add to Cart 3 days [Need to translate] Diagnosis of occupational chloroprene poisoning Valid GBZ 32-2015
GBZ 32-2002English199 Add to Cart 3 days [Need to translate] Diagnostic Criteria of Occupational Chloroprene Poisoning Obsolete GBZ 32-2002

PDF similar to GBZ32-2015


Standard similar to GBZ32-2015

GBZ 57   GBZ 20   GBZ 49   GBZ 27   GBZ 23   GB/T 32.1   

Basic data

Standard ID GBZ 32-2015 (GBZ32-2015)
Description (Translated English) Diagnosis of occupational chloroprene poisoning
Sector / Industry National Standard
Classification of Chinese Standard C60
Classification of International Standard 13.1
Word Count Estimation 6,611
Date of Issue 2015-04-21
Date of Implementation 2015-11-01
Older Standard (superseded by this standard) GBZ 32-2002
Quoted Standard GB/T 16180; GBZ 59; GBZ 73; GBZ 76
Regulation (derived from) State-Health-Communication 2015 No.6
Issuing agency(ies) National Health and Family Planning Commission
Summary This Standard specifies the principles of diagnosis and treatment of occupational chloroprene poisoning. This Standard applies to the diagnosis and treatment of occupational chloroprene poisoning.

GBZ32-2015: Diagnosis of occupational chloroprene poisoning

---This is a DRAFT version for illustration, not a final translation. Full copy of true-PDF in English version (including equations, symbols, images, flow-chart, tables, and figures etc.) will be manually/carefully translated upon your order.
Diagnosis of occupational chloroprene poisoning ICS 13.100 C60 People's Republic of China National Occupational Health Standards Replacing GBZ 32-2002 Diagnosis of occupational chloroprene poisoning 2015-04-21 release 2015-11-01 implementation People's Republic of China National Health and Family Planning Commission released

Foreword

According to the "People's Republic of China Occupational Disease Prevention Law" to develop this standard. Chapter 6 of this standard is recommended and the remainder is mandatory. This standard is drafted in accordance with the rules given in GB/T 1.1-2009. This standard replaces GBZ 32-2002 "diagnostic criteria for occupational chloroprene poisoning". Compared with GBZ 32-2002, the main modifications are as follows. - "diagnostic principle" is divided into "acute poisoning" and "chronic poisoning" in two parts; The principle of chronic poisoning diagnoses the minimum time limit for long-term close contact with chlorobutadiene; --- increase the "contact response" and its related content; --- delete the "observation object" and its related content; --- will be diagnosed by mild, severe poisoning secondary to mild, moderate, severe poisoning three; - other processing, an increase of "labor ability identification" of the treatment; - Appendix A adds a description of the relevant information on the diagnosis of chlorampheneolated toxic liver disease. This standard is responsible for drafting units. Shanghai Chemical Industry Occupational Disease Prevention and Control Institute. The standard to participate in the drafting unit. China Center for Disease Control and Prevention Occupational Health and Poison Control, Tongji University, Shanghai pulmonary medicine Hospital, Chongqing Municipal Occupational Disease Prevention and Control Hospital, Fujian Province Occupational Disease Prevention and Control Hospital, Wuxi City People's Hospital. The main drafters of this standard. Li Sihui, Huang Jinxiang, Yan Lili, Sun Daoyuan, Hu Xunjun, Wang Yongyi, Lin Liying, Yang Hong The previous version of the standard replacement standard issued by this standard is. --- GB 8790-1988; --- GBZ 32-2002. Diagnosis of occupational chloroprene poisoning

1 Scope

This standard specifies the principles of diagnosis and treatment of occupational chloroprene poisoning. This standard applies to the diagnosis and treatment of occupational chloroprene poisoning.

2 normative reference documents

The following documents are indispensable for the application of this document. For dated references, only the dated edition applies to this article Pieces. For undated references, the latest edition (including all modifications) applies to this document. GB/T 16180 Labor capacity - Identification of workers' injury and occupational disease Diagnostic criteria for occupational toxic liver disease GBZ 73 Occupational acute chemicals - Criteria for the diagnosis of toxic respiratory diseases GBZ 76 Occupational acute chemical poisoning Nervous system disease diagnostic criteria

3 diagnostic principles

3.1 acute poisoning According to the short-term exposure to higher concentrations of chlorobutadiene occupational history, to the central nervous system and/or respiratory damage mainly in the Pro Bed performance, combined with laboratory findings and workplace occupational health survey data, a comprehensive analysis, excluding other reasons similar to After the disease, can be diagnosed. 3.2 chronic poisoning With more than 1 year (including 1 year) close contact with chlorobutadiene occupational history, liver, nervous system damage-based clinical manifestations, combined with laboratory Inspection results and workplace occupational health information, a comprehensive analysis, excluding other causes of similar diseases, can be diagnosed.

4 contact reaction

Short-term exposure to higher concentrations of chloroprene, the emergence of dizziness, headache, or tears, throat pain, cough, chest tightness, shortness of breath, nausea and other symptoms, No positive signs, no abnormal chest X-ray, and 72 hours from the contact with the symptoms were significantly reduced or disappeared.

5 diagnostic grading

5.1 acute poisoning 5.1.1 mild poisoning Short-term exposure to higher concentrations of chloroprene, the emergence of dizziness, headache, fatigue, nausea, vomiting, chest tightness, shortness of breath and other symptoms, and conjunctival filling Blood, pharyngeal congestion and other signs, and have one of the following manifestations. a) acute mild toxic encephalopathy, such as mild disturbance of consciousness, gait staggering (see GBZ 76); b) Acute tracheal-bronchitis (see GBZ 73). 5.1.2 moderate poisoning One of the following manifestations. a) acute moderate toxic encephalopathy, such as moderate disturbance of consciousness, ataxia and other performance (see GBZ 76); b) acute bronchial pneumonia or interstitial pulmonary edema (see GBZ 73). 5.1.3 severe poisoning One of the following manifestations. a) acute severe encephalopathy, such as severe disturbance of consciousness (see GBZ 76); b) alveolar pulmonary edema (see GBZ 73). 5.2 Chronic poisoning 5.2.1 mild poisoning With more than 1 year (including 1 year) chloroprene occupational exposure history, there dizziness, headache, fatigue, fatigue, insomnia, irritability, memory loss Retreat and other clinical symptoms, and have one of the following manifestations. a) moderate to severe alopecia and neurasthenia syndrome; b) chronic mild toxic liver disease (see GBZ 59), may be associated with serum protein electrophoresis β globulin ratio before and after comparison to reduce their 20% the above. 5.2.2 moderate poisoning Chronic moderate toxic liver disease (see GBZ 59). 5.2.3 severe poisoning Chronic severe toxic liver disease (see GBZ 59).

6 Principles of handling

6.1 Principles of treatment 6.1.1 acute poisoning immediately from the poisoning scene, clean contaminated eyes and skin, replace contaminated clothing, keep quiet, warm, oxygen. Acute attention to bed rest, symptomatic and supportive treatment, if necessary, given glucocorticoid treatment. 6.1.2 chronic poisoning during the treatment of chloroprene from the operation, appropriate rest, strengthen nutrition, symptomatic treatment. 6.2 Other treatments 6.2.1 acute poisoning Light and moderate poisoning can be cured after treatment, severe poisoning as the disease from the original job or engaged in light work. 6.2.2 Chronic poisoning Light and moderate poisoning can be restored after the original work. Severe poisoning is no longer engaged in chloroprene operation, depending on the condition of rest or engaged in light industry For. For labor identification, according to GB/T 16180 treatment.

7 Correctly use the instructions in this standard

See Appendix A.

Appendix A

(Informative) Correctly use the instructions in this standard A.1 Chlorobutadiene (2-chloro-1,3-butadiene) is a liquid monomer for the production of chloroprene rubber and can be copolymerized with styrene, acrylonitrile, isoprene, Production of various synthetic rubber; also other chloroprene products, such as neoprene latex and neoprene asphalt monomer. Where engaged in the production of neoprene Diene and a variety of chloroprene monomer containing chloroprene rubber and latex, adhesive and other production and processing, are likely to occur chloroprene Poisoning. A.2 acute chloroprene poisoning clinical manifestations of the central nervous system and acute respiratory tract and respiratory damage. Since chloroprene has hemp Drunk, after inhalation can make patients quickly paralyzed into a coma, from the scene after most of the 5min ~ 10min sober. Higher concentration Inhalation can quickly inhibit the respiratory center, can occur early in the onset of breathing difficulties or respiratory arrest. A.3 chronic chloroprene poisoning first appeared in the performance of neurasthenic syndrome, followed by liver damage. Neurasthenic syndrome is nonspecific Sexual, objectivity is poor, it is not listed as a separate classification index, but because of its high incidence and as a prerequisite for the diagnosis of chronic poisoning. A.4 hair loss is the clinical characteristics of chronic poisoning of chloroprene, not all contacts can occur. The degree of hair loss is divided into. a) mild hand gently wipe the head, that is, more hair off; b) moderate hair loss to obvious sparse degree; c) severe hair basic stripping, may be associated with eyebrows, armpit hair, pubic hair off. From the contact after the gradual recovery of their own. A.5 nail color change often in contact with chloroprene 15d ~ 30d appear. From the root of the nail began to appear purple brown, often involving the bilateral or one Side of the thumb nails. 3 weeks after the operation, the stain fades, with the nail growth, purple brown to the distal propulsion, a root and normal nails color. If the contact is nail color, but also repeated, so nail color can be used as contact with chlorinated butadiene. A.6 serum protein electrophoresis β-globulin ratio is one of the characteristics of chloroprene toxic liver disease. β globulin ratio before and after their own More than 20% lower than the determination of poisoning diagnostic limit. Their own contrast methods are. a) exposure to chlorobutadiene before and after operation of β globulin ratio of their own comparison; b) out of contact with chloroprene operation after 1 to 2 months, the β globulin ratio of their own comparison. From the contact of chloroprene after the β-ball Protein ratio can return to normal, re-contact and rapid decline. A.7 chloroprene toxic liver disease and other chronic liver disease clinical manifestations are not exactly the same. First of all, the former early onset of gastrointestinal symptoms can be Not obvious, and often accompanied by neurasthenic syndrome and the occurrence of varying degrees of hair loss and nail color and other characteristics; and other liver disease early digestive tract Symptoms and abnormal liver function. Second, serum protein electrophoresis test results are inconsistent, the former showed an increase in albumin ratio, β globulin The ratio of α and γ globulin did not change significantly; other liver disease on the contrary, the serum protein electrophoresis showed a decrease in albumin ratio, white (A/G) decreased or inverted, γ-globulin ratio increased.

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