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Basic dataStandard ID: GBZ 5-2016 (GBZ5-2016)Description (Translated English): Diagnosis of occupational fluorine and inorganic compound poisoning Sector / Industry: National Standard Classification of Chinese Standard: C60 Classification of International Standard: 13.100 Word Count Estimation: 9,978 Date of Issue: 2016-01-18 Date of Implementation: 2016-07-01 Older Standard (superseded by this standard): GBZ 5-2002 Quoted Standard: GB/T 16180; GBZ 51; GBZ 73; GBZ 74; GBZ/T 228; WS/T 30; WS/T 212 Regulation (derived from): National Guard (2016) on the 1st Issuing agency(ies): General Administration of Quality Supervision, Inspection and Quarantine of the People's Republic of China Summary: This standard specifies the occupational fluorine and its inorganic compound poisoning diagnosis and treatment principles. This standard is applicable to the diagnosis and treatment of occupational fluorine and its inorganic compound poisoning. This standard does not apply to acute organic fluoride poisoning and endemic fluorosis diagnosis and treatment. GBZ5-2016: Diagnosis of occupational fluorine and inorganic compound 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 fluorine and inorganic compound poisoning ICS 13.100C60 National Occupational Health Standards GBZ 5-2016 replaces GBZ 5-2002 Diagnosis of occupational fluoride and its inorganic compound poisoning Published on.2016-01-18 2016-07-01 implementation People's Republic National Health and Family Planning Commission released ForewordThis standard is formulated in accordance with the Law of the People's Republic Chapter 6 of this standard is recommended and the rest are mandatory. This standard was drafted in accordance with the rules given in GB/T 1.1-2009. This standard replaces GBZ 5-2002 "Diagnostic Standard for Industrial Fluorosis"; compared with GBZ 5-2002, the main technical changes are as follows. --- The standard name was changed from "Diagnostic Standard for Industrial Fluorosis" to "Diagnosis of Occupational Fluoride and Its Inorganic Compound Poisoning"; --- Amend the "Diagnostic Principles of Industrial Fluorosis" to "Diagnostic Principles of Chronic Poisoning"; --- Amend the "segmentation of bone X-ray changes" to "chronological diagnosis of chronic poisoning"; --- Deleted the observation object; --- Increased the diagnosis and treatment of acute fluoride and its inorganic compound poisoning. This standard is drafted by. Shanghai Chemical Occupational Disease Prevention and Treatment Institute. Participated in the drafting of this standard. Shanghai Municipal Center for Disease Control and Prevention, Chongqing Municipal Hospital for Occupational Diseases, and Hunan Provincial Hospital for Occupational Diseases. The main drafters of this standard. Li Sihui, Liu Wen, Han Yuzhen, Wang Yongyi, Lai Yan, Wang Jie, He Wei, Yan Lili, Hu Xunjun. The previous versions of the standards replaced by this standard are. ---GB 3234-1982; ---GBZ 5-2002. Diagnosis of occupational fluoride and its inorganic compound poisoning1 ScopeThis standard specifies the principles for the diagnosis and treatment of occupational fluorine and its inorganic compound poisoning. This standard applies to the diagnosis and treatment of occupational fluorine and its inorganic compound poisoning. This standard does not apply to the diagnosis and treatment of acute organofluorine poisoning and endemic fluorosis.2 Normative referencesThe following documents are indispensable for the application of this document. For dated references, only the dated version applies to this article. Pieces. For undated references, the latest edition (including all amendments) applies to this document. GB/T 16180 Labor ability appraisal employee injury and occupational disease disability level GBZ 51 diagnostic criteria for occupational chemical skin burns GBZ 73 Occupational acute chemical toxicity diagnostic criteria for respiratory diseases GBZ 74 Diagnostic criteria for occupational acute chemical toxicity heart disease GBZ /T 228 diagnostic criteria for sequelae of occupational acute chemical poisoning WS/T 30 method for determination of ion selective electrode in urine WS/T 212 Determination of fluoride in serum - Ion selective electrode method3 Diagnostic principles3.1 Acute poisoning According to the occupational history of exposure to higher concentrations of fluoride and its inorganic compounds in the short term, acute respiratory damage and symptomatic hypocalcemia are The main clinical manifestations, combined with laboratory blood (urine) fluoride and blood calcium and other test results, refer to the job site occupational health information, exclude other reasons After a similar disease, a comprehensive analysis can be diagnosed. 3.2 Chronic poisoning According to the occupational history of close contact with fluorine and its inorganic compounds for 5 years and above, the clinical manifestations based on skeletal damage, combined with experiments The results of blood (urine) fluoride test, refer to occupational health information on the job site, and exclude other diseases caused by other causes, comprehensive analysis diagnosis.4 contact reactionAfter short-term exposure to a large amount of fluorine and its inorganic compounds, one of the following manifestations occurred and was significantly reduced or disappeared within 72 hours of disengagement. a) eye pain, tearing, photophobia, cough, sore throat, chest tightness and dizziness, fatigue, palpitations and other symptoms; b) Blood calcium is reduced but has no clinical manifestations.5 diagnostic rating5.1 Acute poisoning 5.1.1 Mild poisoning Short-term exposure to higher concentrations of inorganic fluoride, dizziness, fatigue, cough, sore throat, palpitations, chest tightness, nausea, vomiting and other symptoms and blood (urine) fluoride Increased and has one of the following performances. a) acute tracheal-bronchitis (see GBZ 73); b) 1 degree to 2 degrees of laryngeal edema (see GBZ 73); c) ECG shows prolonged QT interval or abnormal ST-T changes; d) Paroxysmal supraventricular tachycardia or single-source ventricular premature contraction (see GBZ 74). 5.1.2 Moderate poisoning Based on 5.1.1, it has one of the following performances. a) acute bronchial pneumonia or interstitial pulmonary edema (see GBZ 73); b) 3 degree laryngeal edema (see GBZ 73); c) paroxysmal ventricular tachycardia or multi-source ventricular premature contraction (see GBZ 74); d) Repeated convulsions. 5.1.3 Severe poisoning Based on 5.1.2, it has one of the following performances. a) alveolar pulmonary edema (see GBZ 73); b) acute respiratory distress syndrome (see GBZ 73); c) 4 degrees of laryngeal edema or asphyxia (see GBZ 73); d) hypocalcemia crisis (ventricular tachycardia, ventricular fibrillation and epileptic seizures); e) Sudden death. 5.2 Chronic poisoning 5.2.1 mild poisoning Long-term close contact with fluorine and its inorganic compounds, and one of the following manifestations. a) The trunk bone (pelvis and lumbar vertebrae) are mainly changed; the bone density is increased; the trabecular bone is thickened and thickened, and it is "gauze-like"; b) There is a clear calcification or ossification of the periorbital bone (osteophyseal, interosseous membrane) of the ulna, ulna or iliac crest. 5.2.2 Moderate poisoning The bone density of the trunk was significantly increased; the trabecular bone was significantly thickened, showing a "sack pattern"; accompanied by a defined change in the periosteum and periosteum of the long bone. 5.2.3 Severe poisoning Most of the bones in the body are involved; the bone density is significantly increased, the trabecular bone is blurred, and it is "marble-like"; the long bone cortex is thickened and the medullary cavity is changed. Narrow; periosteal changes are more obvious, bone bridges can form between the vertebral bodies.6 Processing principles6.1 Principles of treatment 6.1.1 Acute poisoning 6.1.1.1 Keep the airway open and perform a tracheotomy if necessary. 6.1.1.2 Dynamic monitoring of blood fluoride, blood calcium, myocardial enzymes and electrocardiogram. 6.1.1.3 Early intravenous supplementation of a sufficient amount of calcium. 6.1.1.4 Other symptomatic and supportive treatments, protection of cardiopulmonary and other multi-organ function. 6.1.1.5 Burning skin should be treated with wounds in the early stage (see GBZ 51). a) The wound is wet or soaked with calcium and magnesium suspension and sodium bicarbonate solution; b) Deep burn wounds, early implementation of cutting (shaving) sputum surgery. 6.1.2 Chronic poisoning Strengthen nutrition, supplement vitamin D and other preparations, and also appropriate calcium supplementation, and give symptomatic treatment and strengthen bone function exercise. 6.2 Other treatment If there are sequelae, it can be carried out in accordance with GBZ /T 228. If you need a labor ability appraisal, deal with it according to GB/T 16180.7 Instructions for the correct use of this standardSee Appendix A.Appendix A(informative appendix) Instructions for the correct use of this standard A. 1 Acute fluorosis A. 1.1 The most common fluorides causing occupational acute fluoride and its inorganic compounds poisoning are hydrogen fluoride and hydrofluoric acid, followed by elemental fluorine, three Boron fluoride, silicon tetrafluoride, fluorosilicic acid, oxygen difluoride, nitrogen trifluoride, sulfur pentafluoride, sulfur hexafluoride, sulfur hexafluoride and uranium hexafluoride. A. 1.2 Fluoride mainly invades the human body through the skin mucosa and respiratory tract, leading to poisoning. The clinical manifestations of fluorosis caused by different invasive pathways are endless. the same. a) Inhalation poisoning in the respiratory tract alone. Most of them are caused by inhalation of hydrogen fluoride or hydrofluoric acid mist, and the clinical manifestations are acute respiratory damage. Mainly harmful. Immediately after inhalation, there are irritation such as cough, sore throat, and shortness of breath. Severe cases have a lot of foam, and both lungs can smell wet. Arpeggio, chest X-ray images of bronchitis, chemical pneumonia or pulmonary edema, severe acute respiratory distress Combined. b) Simple burns the skin to absorb poisoning. Mostly caused by hydrofluoric acid burns, clinical manifestations of acute cardiovascular system caused by hypocalcemia Damage is dominant. Some may have repeated convulsions. Mild symptoms can increase myocardial enzyme activity index or muscle calcium egg within 48 hours after injury White positive. Electrocardiogram mainly shows QT interval prolongation and ST-T abnormal changes; severe cytotoxicity due to fluoride ion And hypocalcemia, electrocardiogram showed T wave low level and conduction block, frequent premature beats, severe ventricular tachycardia, ventricular fibrillation and other arrhythmias, Or epilepsy-like convulsions, or even sudden death. c) Burning skin absorption and inhalation poisoning. Mostly found in hydrofluoric acid burn concentration > 40% and there is a burn in the face and neck. Illness The degree is often severe, and the rate of sudden death is high. Even a small area (< 3%) of II to III degree burns can cause death. When burns occur at the same time Symptoms such as coughing, hoarseness, and difficulty in breathing should be considered for combined inhalation injury, and should be alert to serious illness. d) The main cause of sudden death from acute inorganic fluorosis is laryngeal edema or sudden cardiac death. A. 1.3 Acute inorganic fluorosis can cause acute laryngeal edema, manifested as cough, inhalation dyspnea, hoarseness, and loss of sound. Lighter Gradually relieved after contact; severe suffocation can occur, cyanosis is a precursor of suffocation, and three concave symptoms suggest serious condition. See the classification of laryngeal edema GBZ 73. A. 1.4 Hypocalcemia refers to a serum calcium concentration of less than 2.2 mmol/L when the serum protein concentration is normal. Symptomatic hypocalcemia is mainly caused by tendon. Early refers to (toe) numbness, which leads to clinical manifestations of increased nerve and muscle excitability such as larynx, wrist and foot, bronchi, etc. And cardiovascular system conduction block, tachycardia, severe hypocalcemia crisis manifested as ventricular tachycardia, ventricular fibrillation and other arrhythmias and epilepsy It is like convulsions and even sudden death. The typical electrocardiogram is characterized by a significant prolongation of the QT interval and ST segment with or without arrhythmia. Blood calcium value The level may not be exactly the same as the severity of the disease, but it is related to the rate of blood calcium decline. The degree and speed of blood calcium reduction is determined by correcting low calcium The blood is fast and slow. There are often laboratory tests with significant low calcium, but no clinical symptoms. A. 1.5 Increased urinary fluoride is an important indicator reflecting the excessive exposure of fluoride to current workers, but the level of urinary fluoride and the severity of acute fluorosis The degree is not completely parallel and is an auxiliary diagnostic indicator, which is helpful for differential diagnosis (see WS/T 30 for determination of fluoride in urine). A. 1.6 Early monitoring of blood fluoride has clinical value in the prevention and treatment of fluorosis. If calcium supplementation and wound treatment are performed when high fluoride period has not occurred, It can avoid or reduce the fatal hypocalcemia caused by fluorosis (see WS/T 212 for the determination of fluoride in serum). A. 1.7 The main points of treatment for acute fluorosis include three aspects. early intravenous supplementation of sufficient calcium to prevent and correct the onset of hypocalcemia. Health and development; protect heart and lung function, closely observe vital signs, timely support, symptomatic comprehensive treatment, prevent sudden death; When the skin is damaged by poisoning, the wound should be treated as soon as possible to prevent fluoride ions from penetrating into deep tissues. A. 2 chronic fluorosis A. 2.1 Fluoride which causes occupational chronic fluorosis in industrial production is mainly derived from fluorite (CaF2), cryolite (Na3AlF3) and phosphate ash. Stone [3Ca3(PO4)2·CaF2]. The fluorine-containing components produced are elemental fluorine, hydrogen fluoride, calcium fluoride, sodium fluoride, potassium fluoride, aluminum fluoride, and fluorination. Gas, vapor and dust of fluorides such as magnesium and lithium fluoride. Chronic fluorosis is caused by prolonged exposure to excessive levels of inorganic fluoride and must be sustained for more than 5 years in a high concentration of fluorine. History of occupational exposure. A. 2.2 Classification of bone X-ray changes in chronic fluorosis (see Appendix B for bone X-ray film requirements). a) Bone changes (bone density changes). The bones are thickened due to the deposition of large amounts of fluoride and calcium on the bone, and the cortex is thickened and the density is increased. therefore X-rays showed an increase in bone density. In severe cases, the cortical bone and the medullary cavity, medulla and cancellous could not be distinguished, and it became an unstructured white scorpion. Bone changes often start from the torso, especially in the pelvis and lumbar vertebrae; b) Bone structure changes (trabecular trabecular changes). trabecular bone thickening and thickening, can be fused to each other in the form of unstructured sand, also has trabecular trabeculae The thick crosses are in the form of a coarse mesh, which is “gauze-like”, and the heavy one is “sack-like”. The above changes are more obvious with the increase of time. Unclear marble c) Perivascular changes (calcification/ossification). perivascular hyperplasia, most of which occur in the pelvis, obturator, posterior tibial and humerus And other parts. The shape is a mound, a thorn, a brush, and in severe cases, a waxy shape. A. 2.3 Due to the skeletal system damage and bone X-ray changes only have relative specificity, it should be noted that it has a similar performance His diseases, such as endemic fluorosis, rheumatoid arthritis, ankylosing spondylitis, osteopetrosis, bone metastases and renal bone disease. A. 2.4 The effect of chronic fluorosis on bone is mainly osteoporosis, and osteoporosis is rare. Normal people grow up with age after age 40 The bone is gradually loose and the cortex is thin. If the bone X-ray signs of the fluorine workers in this age group show that the bones are hard and the density is high, they need to be Consider skeletal fluorosis. And should pay attention to the identification of endemic fluorosis. A. 2.5 The urinary fluoride value before the shift can reflect the fluoride load in the working workers. Taking into account the natural fluctuations of urinary fluoride, it should be sent continuously for more than 3 times. Take the average value as a basis for measuring the level of urinary fluoride. A. 2.6 Blood fluoride value has a positive correlation with urine fluoride value and can be used as a recent indicator of fluoride exposure. Blood fluoride has the advantages of less interference factors and accurate data. It can also avoid the shortage of specimens to collect pollution, so it is recommended that those with conditions should also detect blood fluoride and urinary fluoride.Appendix B(normative appendix) Bone X-ray film requirements B. 1 Using an X-ray diagnostic machine with a frequency of.200 mA or more, the focus size is not more than 2.0 mm × 2.0 mm, preferably a rotating anode bulb. B. 2 Photographing parts. The basic requirements are pelvic anteroposterior, one side iliac crest, ulnar anteroposterior and ipsilateral iliac crest, tibia positive and lateral radiographs; Department and lumbar vertebrae. B. 3 The requirements for the conditions of the investment are shown in Table B. 1. Table B. 1 Requirements for investment conditions Film location target distance cm Exposure mAs Tube voltage kV filter Pelvis 100 100~150 Thickness (cm)×2+(30~40) + 桡, ulna 100 25 ~ 30 thickness (cm) × 2+ (30 ~ 40) - 胫, 腓 bone 100 30 ~ 40 thickness (cm) × 2+ (30 ~ 40) - Lumbar spine 100 100 ~ 150 thickness (cm) × 2+ (30 ~ 40) + Chest 150 20 ~ 25 thickness (cm) × 2+ (30 ~ 40) - Note. X-ray film is best used with a blue base. B. 4 Photographic quality requirements. The position of the film is accurate, the contrast is good, the direct exposure area is black, the soft tissue is gray, the layers are distinct, the cortex and The trabecular bones are clearly displayed. ......Tips & Frequently Asked Questions:Question 1: How long will the true-PDF of GBZ5-2016_English be delivered?Answer: Upon your order, we will start to translate GBZ5-2016_English as soon as possible, and keep you informed of the progress. The lead time is typically 1 ~ 3 working days. 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