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Lead (lead, Pb) is a gray-white metal with an atomic weight of 207.20, a specific gravity of 11.34, a melting point of 327.5°C, and a boiling point of 1620°C. When heated to 400-500°C, a large amount of lead vapor escapes and is rapidly oxidized into lead oxide in the air. , and agglomerates into smoke. As the temperature of molten lead increases, it can be further oxidized into lead oxide, lead trioxide, and lead trioxide, but they are all unstable, and finally dissociate into lead oxide and oxygen.

Industrial lead exposure includes: mining, sintering and refining of lead ores; smelting of lead-containing metals and alloys; battery manufacturing; letter casting and pouring in the printing industry; lead coating in cables; lead bath heat treatment in the machinery industry; tap water pipes and food cans And welding of electrical instrument components; manufacturing bearings (hanging tiles) for trains and cars; manufacturing X-ray and atomic radiation protection materials; lead spraying of radio components; welding and cutting when repairing and dismantling old ships and bridges. During the above operations, lead escapes in the form of vapor and smoke.

Lead compounds, such as lead oxide (also known as red lead, litharge), lead trioxide (also known as hydrargyri oxydum rubrum), lead dioxide, lead trioxide, lead sulfide, lead sulfate, lead chromate ( Also known as chrome yellow), lead nitrate, lead silicate, lead vinegar, basic lead carbonate, dibasic lead phosphate, tribasic lead sulfate, etc. are used in paints, pigments, rubber, glass, ceramics, glazes, etc. Lead compounds from pharmaceuticals, plastics, explosives, etc. are released in the form of dust.

At present, the most harmful industries in China are battery manufacturing, lead smelting and old ship scrapping and cutting. Mechanism of action

The entry route of lead and its compounds is mainly the respiratory tract, followed by the digestive tract, and cannot be absorbed by intact skin.

Respiratory tract: Usually enters in the form of steam, smoke and dust. The amount of lead inhaled varies with the size of the dust particles. For example, the absorption rate of dust particles with a diameter of 0.27Hm reaches 54%. Generally speaking, 70% to 75% of the inhaled lead is still excreted with exhalation, and only 30% to 50% is absorbed into the body.

Digestive tract: Mainly from food intake and fluid retention water in lead workplaces. The daily intake of lead in daily food and fluid retention materials is about 300mg.

Lead enters the blood circulation after being absorbed in an ionic state. It is initially distributed in various tissues of the body in the form of lead salts and combined with plasma proteins. After a few weeks, about 95% is deposited in the skeletal system and hair as insoluble lead phosphate. Only about 5% of lead remains in the liver, kidney, brain, heart, spleen, basal ganglia, cortical gray and white matter and other organs and blood, and can enter the cell nucleus to form "inclusion bodies". About 95% of the lead in blood is distributed in red blood cells, mainly in the red blood cell membrane, and only 5% is in plasma. The lead phosphate deposited in the bone tissue is in a stable state and maintains a dynamic balance with the lead in the blood and soft tissues. The absorbed lead is mainly excreted through the kidneys, but can also be excreted through feces, milk, gallbladder, menstruation, sweat glands, saliva, hair, nails and other channels.

The mechanism of disease caused by lead poisoning is relatively clear at present:

Lead's obstacle to hemoglobin synthesis: The synthesis process of hemoglobin is affected by a series of enzymes. When the body is affected by lead poisoning, this synthesis Some thiol-containing enzymes in the process are inhibited, and the following changes occur:

1. Because lead inhibits δ-aminoγ-levulinic acid dehydratase (ALAD), δ-aminoγ-levulinic acid (ALA) ) synthesis of BPG is blocked, resulting in reduced ALAD activity in red blood cells and increased ALA content in blood and urine.
2. Because lead inhibits heme synthase (ferrous synthase), it prevents protoprin from combining with divalent iron to form heme, which increases serum iron and protoprin in the abdominal mass of red blood cells, resulting in red blood cells in the blood. The amount of EPP or free erythrocyte purine (FEP) increases, and the latter combines with zinc ions to form zinc purine (ZPP).
3. Because lead may also inhibit fecal pollen decarboxylase, resulting in increased urine fecal pollen III (CP) content.
4. Due to the obstruction of the utilization of iron in the bone marrow, the amount of iron binding in red blood cells decreases, and the free iron in red blood cells and red blood cells increases. Therefore, sideroblasts and sideroblast red blood cells, that is, iron-containing eggs, can be seen.
5. Lead also affects ribonucleosomes and soluble ribonucleic acid (mRNA) in red blood cells, and interferes with the synthesis of globin, resulting in a relatively excessive amount of ribonucleic acid for the synthesis of globin and aggregation into pointillist particles. Due to the above inhibitory process, anemia finally results.

Lead can also directly act on red blood cells, inhibit the activity of membrane Na⁺/K⁺-ATPase in red blood cells, affect the regulation of water and sodium, and may also Inhibits erythrocyte pyrimidine-5'-nucleosylase, causing a large amount of pyrimidine nucleotides to accumulate in the cytoplasm. The combination of lead and erythrocyte membrane increases mechanical fragility, affects the stability of erythrocyte membrane, and finally leads to hemolysis.

The effects of lead on the nervous system: Lead increases ALA. ALA has a similar chemical structure to γ-aminobutyric acid (GABA), so it has a competitive inhibitory effect with GABA. GABA is located in the presynaptic and synaptic areas of Zhongshu (GV7) nerves. In the postsynaptic mitochondria, GABA inhibition interferes with nervous system functions, such as changes in consciousness, behavior, and neural effects. Lead can also affect the metabolism of Black Catechu phenolic amines in the brain, causing a significant increase in homovanillic acid (HVA) and vanillylmandelic acid (VMA) in the brain and urine, ultimately leading to lead toxic encephalopathy and peripheral neuropathy. The pathological manifestations of lead toxic encephalopathy are brain edema and diffuse degeneration of nerve cells. In addition, cerebellum granular layer cell necrosis, cerebral herniation and small focal hemorrhage of the leptomens membrane can also be seen.

Lead toxic peripheral neuropathy first manifests as slowing of nerve conduction velocity (NCV), and damaged nerves are mainly changes in nerve cell membranes and demyelination. Changes around the axon can be seen, myelin disintegrates into granules or blocks, sometimes completely dissolves, and Schwann cells proliferate. These changes are caused by lead damaging mitochondria and microsomes in nerve cells.

The effects of lead on the kidneys: Lead damages mitochondria, affects ATPase, interferes with the active operating mechanism, damages proximal tubule endothelial cells and their functions, reduces tubular reabsorption, and also affects glomerular filtration. The rate decreases, resulting in decreased urinary creatinine excretion, increased blood creatinine and blood urea nitrogen levels, increased urinary glucose excretion, decreased urinary γ-GT (γ-glutaminophen transpeptidase) activity, and urinary NAG (N-2acyl-β- D-glucosaminidase) activity is increased. Lead also affects the function of the juxtaglomerular apparatus, causing increased renin synthesis and release, leading to vasospasm and hypertension. Lead can form intranuclear inclusion bodies in renal tubular epithelial cells. It is a lead-protein complex and is an adaptation or toxin removing mechanism of the body.

Acute or subacute poisoning

Mainly caused by daily life, mostly caused by accidental or excessive intake of folk prescriptions containing lead compounds to treat asthma, epilepsy, roundworms, early abortion, etc. These lead compounds such as lead, Minium, lead cream, litharge, Black Tin Pill, camphor, etc.; tin pots are also used to make wine and tin pots are used to hold wine; and lead-powder is mistaken for potato powder and taken by mistake. Foreign children often suffer from poisoning due to their habit of eating toys containing lead paint and peeling plaster from walls and furniture. The onset of oral poisoning often has an incubation period, which can be as short as 4 to 6 hours, generally 2 to 3 days, or as long as 1 to 2 weeks, which is closely related to the dose taken and individual differences. Occupational subacute poisoning can also occur.

The clinical characteristics are severe abdominal colicky pain, anemia, toxic liver disease, toxic nephropathy, and multiple peripheral neuropathy. Symptoms include dizziness, general weakness, sore muscles and joints, inability to eat, constipation or diarrhea, enlarged liver, tenderness in the liver area, jaundice, and elevated blood pressure. Laboratory tests: In addition to significantly elevated lead poisoning indicators, elevated bilirubin and elevated ALT High; red blood cells, white blood cells, and urinary bilegen positivity can be seen in the urine; hemoglobin and red blood cells are both decreased. Nervous system examination may reveal glove-sock-type hypoesthesia at the end of the limbs, muscle atrophy and muscle weakness. Severe cases may lead to lead paralysis, namely wrist drop and foot drop; lead toxic encephalopathy, severe headache, convulsion, delirium, convulsions, stupor and even unconsciousness. Individual patients may develop paralytic intestinal obstruction

Generally speaking, they can recover quickly after lead exorcism treatment. Except for lead toxic encephalopathy, there are few sequelae and the prognosis is good.

Chronic poisoning

Occupational lead poisoning is mostly chronic poisoning, with clinical symptoms of neurological, digestive, blood and other systems.

Nervous system: The main manifestations are neurasthenia, polyneuropathy and encephalopathy.

Nervous failure is one of the early and more common symptoms of lead poisoning, manifesting as dizziness, headache, general weakness, memory loss, sleep disorders, dreamfulness, etc. Among them, dizziness and general weakness are the most obvious, but they are generally Mild, functional symptoms. There are still many people with early lead poisoning whose symptoms are not obvious.

Polyneuropathy can be divided into sensory, motor and mixed types. The sensory type is characterized by numbness of the extremities and glove-sock-type sensory impairment at the end of the limbs. The symptoms of sports type include:

1. Muscle weakness, starting with loss of grip strength, appears earlier and is more common. It further develops into muscle weakness, mostly extensor muscle weakness.
2. Muscle paralysis, also known as lead paralysis, is more common in the extensor muscles of the fingers and wrists innervated by the radial nerve, causing wrist ptosis, also known as wrist ptosis; the peroneal muscles, common extensor digitorum muscles, and extensor digitorum extensor myotomes exhibit foot ptosis, also known as foot drop. It's called foot drop.

Encephalopathy is the most serious form of lead poisoning. Symptoms include headache, nausea, vomiting, high fever, dysphoria, convulsion, somnolence, mental disorder, unconsciousness and other symptoms, which are similar to syndromes such as epileptic seizures, encephalitis, cerebral edema, psychosis or local brain damage. Due to the improvement of working conditions in China, it occurs less frequently, but the incidence rate among children abroad is very high.

Digestive system: Mild cases will show general digestive tract symptoms, while severe cases will show abdominal colicky pain.

Digestive tract symptoms include metallic taste in the mouth, loss of appetite, upper abdominal distension and discomfort, abdominal dull pain and constipation, dry and hard stools in the shape of abacus beads, and stubborn constipation as a precursor before the onset of lead colicky pain. Abdominal colicky pain is a sudden attack, mostly around the umbilicus, with persistent pain that worsens in paroxysms, and each attack lasts from several minutes to several hours. Because the pain is severe and unbearable, I often bend my waist and knees, toss and turn restlessly, and press my hands on my abdomen to relieve the pain. At the same time, the complexion is pale, with cold sweating all over the body and possibly vomiting. On examination, the abdomen is flat and soft, with grade I tenderness, no fixed tender points, decreased bowel sounds, and is often accompanied by a temporary increase in blood pressure and stirred pulse spasm in the fundus.

Blood system: Mainly lead interferes with the hemoglobin synthesis process and causes changes in its metabolites, such as reduced blood δ-ALAD activity, increased urinary δ-ALA, increased urinary CP, increased blood FEP and ZPP, etc., which ultimately leads to anemia, mostly for Hypochromic normocytic anemia.

Other systems: Lead damage to the kidneys is more common in cases of acute or subacute lead poisoning or severe chronic sexually transmitted disease. The presence of amino acid proteinuria, red blood cells, white blood cells and casts and decreased renal function indicates toxic nephropathy, accompanied by Have high blood pressure. Female workers are more sensitive to lead, especially pregnant women and lactating women, which can cause infertility, late abortion, premature labor, dead fetus and infant lead poisoning. Male labor can cause a decrease in sperm count, weakened activity and changes in morphology. In addition, it can cause hypothyroidism. Diagnosis and differential diagnosis

Based on comprehensive analysis and judgment based on occupational history, labor hygiene investigation, clinical manifestations and laboratory test results, generally speaking, diagnosis is not difficult. The main reason for misdiagnosis is the daily consumption of lead compounds, which can be solved by asking about the medical history.

The diagnosis can be divided into four levels:

1. Lead absorption: only elevated urinary lead or blood lead but no clinical symptoms.
2. Grade I lead poisoning: In addition to neurasthenic syndrome and elevated urinary lead or blood lead, there is also an abnormality in urinary CP, urinary δ-ALA, blood FEP, and blood ZPP.
3. Grade II lead poisoning: On the basis of grade I lead poisoning, if there is any one of abdominal colicky pain, anemia, toxic peripheral neuropathy, toxic liver disease, and toxic nephropathy.
4. grade III lead poisoning: lead paralysis or lead encephalopathy. The lead removal test can assist diagnosis. After using CaNa₂EDTA 0.5~1.0g, if the urine lead is ≥1.45μmol/L (0.3mg/L) and 3.86μmol/L (0.8mg/L) It can be diagnosed as lead absorption; if the urine lead is ≥3.86μmol/L (0.8mg/L) or 4.82μmol/24h (1.0mg/24h), it can be diagnosed as grade I lead poisoning.

Those with lead colicky pain should be differentiated from Lanwei (EX-LE7) inflammation, biliary ascariasis, cholelithiasis, gastric perforation, hemorrhagic disease, etc. Treatment

Lead removal treatment is mainly used for chronic lead poisoning. The current status of the lead-removing effect of complexing agents that have certain effects: CaNa₃DTPA (calcium excretion-stimulating agent) > CaNa₂EDTA (sodium calcium edetate)> ZnNa₃DTPA (zinc excretion-stimulating agent) > Na₂DMS (sodium dimercaptosuccinate), DMSA (dimercaptosuccinic acid) > 811 (chelate (combined carboxyphenol). The specific usage is as follows:

1. CaNa₂EDTA or CaNa₃DTPA 1.0g, intravenous drip or intravenous push or intramuscular injection (add 2% Prunusin Caine 2ml), once a day, three consecutive days of drug withdrawal and four days as a course of treatment, usually three courses are enough.
2. Na₂DMS 1.0g, intravenous injection or intramuscular injection (plus 2% procaine 2ml), once a day, three days of continuous use and four days of drug withdrawal constitute a course of treatment, usually three One course of treatment is enough.
3. DMSA 0.5g, taken orally, three times a day, three days of continuous use and four days of non-medication constitute a course of treatment. Generally, three courses of treatment are enough.

Lead colicky pain treatment:

1. Lead removal treatment, CaNa₂EDTA 1.0g, intravenous drip, once every 12 hours until lead colicky pain is controlled; or Na ₂DMS 1.0g, intravenous injection, once every 12 hours, in severe cases, once every 6 hours until colicky pain is controlled. Or DMSA 1.0g, orally, once every 6 hours until the lead colicky pain is controlled, and then follow the chronic lead poisoning treatment plan.
2. Symptomatic treatment: 10% calcium gluconate 10ml, intravenous injection; atropine 0.5~1.0mg or 654-2 10mg, intramuscular injection; abdominal hot compress; acupuncture and moxibustion Zusanli (ST36), Zhongwan (CV12), Neiguan (PC6) , Sanyinjiao (SP6) et al.

Treatment of lead encephalopathy: First, intramuscular injection of BAL 2.5 mg/kg, once every 4 to 6 hours on the 1st to 2nd day; then 1 to 2 times a day for a total of 5 to 7 days. Then treat with CaNa₂EDTA, and the usage should be according to the treatment plan for chronic lead poisoning.

Prevention

Replace lead with non-toxic or low-toxic substances; adopt mechanized and automated production; reform product dosage form; control the temperature of molten lead; strengthen local ventilation and detoxification devices; strengthen personal protection measures. Regularly monitor lead concentrations in the workplace. Regular health monitoring, including pre-employment physical examination and regular physical examination every six months or one year, blood lead and ZPP can be used as screening indicators to promptly detect employment contraindications and early detection of lead poisoning patients for timely treatment.