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Lead (Pb), a grayish-white metal, has 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 is released, which rapidly oxidizes in the air to form lead suboxide, condensing into smoke and dust. As the temperature of molten lead increases, it can further oxidize into lead oxide, trilead tetroxide, and lead dioxide, but these are unstable and eventually dissociate into lead oxide and oxygen.

Industrial exposure to lead includes: mining, sintering, and refining of lead ores; smelting of lead-containing metals and alloys; battery manufacturing; type casting and plate pouring in the printing industry; cable sheathing; lead bath heat treatment in the mechanical industry; welding of water pipes, food cans, and electrical instrument components; manufacturing of bearings for trains and cars (bearing lining); production of X-ray and atomic radiation protection materials; lead spraying on radio components; and welding and cutting during the repair and dismantling of old ships and bridges. In these operations, lead is released in the form of vapor and dust.

Lead compounds, such as lead oxide (also known as red lead, litharge), lead tetroxide (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 acetate, basic lead carbonate, dibasic lead phosphate, and tribasic lead sulfate, are used in paints, pigments, rubber, glass, ceramics, glazes, pharmaceuticals, plastics, explosives, etc. These lead compounds are released as dust.

Currently, the most hazardous industries in the country are battery manufacturing, lead smelting, and ship dismantling and cutting. Mechanism of action

The primary routes of entry for lead and its compounds are the respiratory tract, followed by the digestive tract; intact skin does not absorb lead.

Respiratory tract: Lead usually enters in the form of vapor, smoke, and dust. The amount of lead inhaled varies with the size of the particles, with particles of 0.27 µm having an absorption rate of up to 54%. Generally, 70%-75% of inhaled lead is exhaled, and only 30%-50% is absorbed into the body.

Digestive tract: Mainly from eating and drinking in lead work environments. Daily intake of lead from food and beverages is about 300 mg.

After absorption in ionic form, lead enters the bloodstream and is initially distributed throughout the body, mainly as lead salts and bound to plasma proteins. After several weeks, about 95% is deposited as insoluble lead phosphate in the skeletal system and hair, with only about 5% remaining in the liver, kidneys, brain, heart, spleen, basal ganglia, cortical gray matter, and blood, and can enter the cell nucleus to form "inclusion bodies." About 95% of the lead in the blood is distributed in red blood cells, mainly in the red cell membrane, with plasma accounting for only 5%. Lead phosphate deposited in bone tissue is in a stable state, maintaining a dynamic balance with lead in the blood and soft tissues. Absorbed lead is mainly excreted through the kidneys, and can also be excreted through feces, milk, bile, menstruation, sweat glands, saliva, hair, nails, etc.

The mechanism of lead poisoning is currently understood as follows:

Lead interferes with hemoglobin synthesis: The synthesis of hemoglobin is affected by a series of enzymes. When the body is exposed to lead toxicity, some sulfhydryl enzymes in this synthesis process are inhibited, leading to the following changes:

1. Lead inhibits δ-aminolevulinic acid dehydratase (ALAD), blocking the synthesis of δ-aminolevulinic acid (ALA) into porphobilinogen (PBG), resulting in decreased ALAD activity in red blood cells and increased ALA levels in blood and urine.
2. Lead inhibits heme synthetase (ferrochelatase), preventing the combination of protoporphyrin and ferrous iron to form heme, leading to increased serum iron and accumulation of protoporphyrin in red blood cells, resulting in increased levels of erythrocyte protoporphyrin (EPP) or free erythrocyte protoporphyrin (FEP) in the blood, which combines with zinc ions to form zinc protoporphyrin (ZPP), also increasing.
3. Since lead may also inhibit coproporphyrinogen decarboxylase, it can lead to an increase in urinary coproporphyrin III (CP) content.
4. Due to the impaired utilization of iron in the bone marrow, the iron-binding capacity of red blood cells decreases, and the free iron in young red blood cells and red blood cells increases. Therefore, iron-laden young red blood cells and iron-laden red blood cells, which contain iron particles, can be observed.
5. Lead also affects the ribosomes and soluble ribonucleic acid (mRNA) in red blood cells, interfering with the synthesis of globin, resulting in an excess of ribonucleic acid for globin synthesis, which aggregates into stippling granules. Due to the aforementioned inhibitory processes, anemia ultimately results.

Lead can also directly act on red blood cells, inhibiting the activity of the red blood cell membrane Na⁺

/K⁺-ATPase, affecting water and sodium regulation, and may also inhibit pyrimidine-5'-nucleotidase in red blood cells, leading to the accumulation of large amounts of pyrimidine nucleotides in the cytoplasm, as well as the binding of lead to the red blood cell membrane, increasing mechanical fragility and affecting the stability of the red blood cell membrane, ultimately leading to hemolysis.

The effect of lead on the nervous system: Lead increases ALA, which is chemically similar to γ-aminobutyric acid (GABA), thus competitively inhibiting GABA. GABA is located in the presynaptic and postsynaptic mitochondria of Zhongshu (GV7) nerves, and its inhibition interferes with nervous system functions, such as consciousness, behavior, and neural effects. Lead can also affect the metabolism of catecholamines in the brain, significantly increasing homovanillic acid (HVA) and vanillylmandelic acid (VMA) in the brain and urine, ultimately leading to lead encephalopathy and peripheral neuropathy. Pathologically, lead encephalopathy manifests as cerebral edema, diffuse degeneration of nerve cells, and additionally, necrosis of cerebellar granular layer cells, cerebral herniation, and small focal hemorrhages in the pia mater.

Lead-induced peripheral neuropathy initially manifests as a slowing of nerve conduction velocity (NCV), with the affected nerves primarily showing changes in the nerve cell membrane and demyelination. Periaxonal changes can be observed, with myelin breaking down into granules or blocks, sometimes completely dissolving, and Schwann cell proliferation. These changes are due to lead damaging the mitochondria and microsomes within nerve cells.

The effect of lead on the kidneys: Lead damages mitochondria, affecting ATPase and interfering with active transport mechanisms, damaging the endothelial cells and function of the proximal tubules, reducing the reabsorption function of the renal tubules, and also affecting the glomerular filtration rate, leading to decreased urinary creatinine excretion, increased serum creatinine and blood urea nitrogen levels, increased urinary glucose excretion, decreased urinary γ-GT (γ-glutamyl transpeptidase) activity, and increased urinary NAG (N-acetyl-β-D-glucosaminidase) activity. Lead also affects the function of the juxtaglomerular apparatus, increasing the synthesis and release of renin, leading to vasospasm and hypertension. Lead can form intranuclear inclusion bodies in renal tubular epithelial cells, which are a lead-protein complex and a mechanism of adaptation or detoxification by the body.

Acute or subacute poisoning

is mainly caused by lifestyle factors, often due to accidental ingestion or excessive use of lead-containing folk remedies for asthma, epilepsy, deworming, early abortion, etc. These lead-containing substances include lead, minium, lead frost, litharge, Black Tin Pill, and red lead; also, the use of tin pots for brewing alcohol and tin pots for storing alcohol; and the mistaken ingestion of lead powder as sweet potato flour. Foreign children often suffer from poisoning due to the habit of eating lead-containing paint from toys, walls, furniture, and peeled plaster. This type of oral poisoning often has an incubation period, ranging from 4-6 hours, generally 2-3 days, and up to 1-2 weeks, closely related to the ingested dose and individual differences. Occupational subacute poisoning can also occur.

The clinical features include severe abdominal colicky pain, anemia, toxic liver disease, toxic nephropathy, and multiple peripheral neuropathy. Symptoms include dizziness, general weakness, muscle and joint pain, inability to eat, constipation or diarrhea, hepatomegaly, tenderness in the liver area, jaundice, and elevated blood pressure. Laboratory tests show significantly elevated lead poisoning indicators, increased bilirubin, elevated ALT; red and white blood cells in urine, positive urine porphobilinogen; decreased hemoglobin and red blood cells. Neurological examination may reveal glove-and-stocking type sensory loss in the extremities, muscle atrophy, and muscle weakness. Severe cases may develop lead palsy, such as wrist drop and foot drop; lead encephalopathy, presenting with severe headache, convulsion, delirium, seizures, stupor, and even unconsciousness. Some patients may develop paralytic ileus

.Generally speaking, recovery is rapid after lead removal treatment, and there are few sequelae except for lead encephalopathy, with a good prognosis.

Chronic poisoning

Occupational lead poisoning is mostly chronic poisoning, clinically presenting with systemic symptoms involving the nervous, digestive, and hematological systems.

Nervous system: Mainly manifests as neurasthenia, polyneuropathy, and encephalopathy.

Neurasthenia is one of the early and more common symptoms of lead poisoning, characterized by dizziness, headache, general weakness, memory loss, sleep disturbances, dreamfulness, etc., with dizziness and general weakness being the most prominent, but generally mild and functional in nature. Many early lead poisoning cases do not show obvious symptoms.

Polyneuropathy can be divided into sensory, motor, and mixed types. The sensory type is characterized by numbness in the extremities and glove-and-stocking type sensory disturbances. The motor type includes:

1. Muscle weakness, initially presenting as reduced grip strength, which appears early and is more common. Further progression leads to muscle weakness, mostly in the extensor muscles.
2. Muscle paralysis, also known as lead paralysis, commonly affects the extensor muscles of the fingers and wrist innervated by the radial nerve, leading to wrist drop, also known as wrist drop syndrome; the peroneal muscles, extensor digitorum communis, and extensor hallucis longus muscles lead to foot drop, also known as foot drop syndrome.

Encephalopathy is the most severe form of lead poisoning. Symptoms include headache, nausea, vomiting, high fever, dysphoria, convulsions, somnolence, mental disorders, unconsciousness, etc., resembling epilepsy, meningitis, cerebral edema, psychosis, or localized brain damage syndromes. Due to improved working conditions, it is less common domestically, but the incidence is high among children abroad.

Digestive system: Mild cases present with general gastrointestinal symptoms, while severe cases exhibit abdominal colicky pain.

Gastrointestinal symptoms include a metallic taste in the mouth, loss of appetite, epigastric fullness and discomfort, abdominal dull pain and constipation, with dry, bead-like stools. Lead colicky pain is often preceded by persistent constipation. The abdominal colicky pain is sudden, usually around the navel, with continuous pain and paroxysmal exacerbations, lasting from a few minutes to several hours. Due to the intense pain, patients often bend over, curl up, and press their abdomen to relieve pain. They may also have a pale complexion, cold sweating, and vomiting. Examination reveals a flat and soft abdomen, possible grade I tenderness, no fixed tender points, reduced borborygmi, and often transient hypertension and retinal artery spasm.

Hematological system: Mainly involves lead interference with hemoglobin synthesis, leading to changes in metabolic products, such as decreased blood δ-ALAD activity, increased urinary δ-ALA, increased urinary CP, increased blood FEP, ZPP, etc., ultimately leading to anemia, mostly hypochromic normocytic anemia.

Other systems: Lead-induced kidney damage is more common in acute, subacute lead poisoning, or severe chronic cases, presenting with aminoaciduria, red blood cells, white blood cells, casts, and decreased renal function, indicating toxic nephropathy, often accompanied by hypertension. Female workers are more sensitive to lead, especially pregnant and lactating women, which can cause infertility, late abortion, premature labor, dead fetus, and infant lead poisoning. Male workers may experience reduced sperm count, decreased motility, and morphological changes. Additionally, it can cause hypothyroidism. Diagnosis and differential diagnosis

Based on occupational history, occupational hygiene investigation, clinical manifestations, and laboratory results, a comprehensive analysis and judgment are made, and the diagnosis is generally not difficult. Misdiagnosis is mainly due to ingestion of lead compounds in daily life, which can be resolved by clarifying the medical history.

Diagnosis can be divided into four levels:

1. Lead absorption: Only elevated urinary or blood lead levels without clinical symptoms.
2. Grade I lead poisoning: Presence of neurasthenic syndrome and elevated urinary or blood lead levels, along with one abnormal finding in urinary CP, urinary δ-ALA, blood FEP, or blood ZPP.
3. Grade II lead poisoning: On the basis of grade I lead poisoning, if one of the following symptoms occurs: colicky abdominal pain, anemia, toxic peripheral neuropathy, toxic liver disease, or toxic nephropathy.
4. Grade III lead poisoning: lead paralysis or lead encephalopathy. The lead mobilization test can assist in diagnosis. After administering CaNa₂EDTA 0.5～1.0g, if urinary lead ≥1.45μmol/L (0.3mg/L) but <3.86μmol/L (0.8mg/L), it can be diagnosed as lead absorption; if urinary lead ≥3.86μmol/L (0.8mg/L) or 4.82μmol/24h (1.0mg/24h), it can be diagnosed as grade I lead poisoning.

Lead colicky pain should be differentiated from appendicitis, biliary ascariasis, cholelithiasis, gastric perforation, and porphyria. Treatment

for chronic lead poisoning mainly involves lead chelation therapy. The current chelating agents with confirmed efficacy, ranked by their strength in lead removal, are: CaNa₃DTPA (calcium trisodium pentetate) > CaNa₂EDTA (calcium disodium edetate) > ZnNa₃DTPA (zinc trisodium pentetate) > Na₂DMS (sodium dimercaptosuccinate), DMSA (dimercaptosuccinic acid) > 811 (chelating carboxyl phenol). The specific usage is as follows:

1. CaNa₂EDTA or CaNa₃DTPA 1.0g, administered via intravenous drip, intravenous push, or intramuscular injection (with 2ml of 2% procaine), once daily for three days, followed by a four-day break, constituting one treatment course. Generally, three courses are sufficient.
2. Na₂DMS 1.0g, administered via intravenous push or intramuscular injection (with 2ml of 2% procaine), once daily for three days, followed by a four-day break, constituting one treatment course. Generally, three courses are sufficient.
3. DMSA 0.5g, taken orally, three times daily for three days, followed by a four-day break, constituting one treatment course. Generally, three courses are sufficient.

Treatment for lead colicky pain:

1. Lead chelation therapy, CaNa₂EDTA 1.0g, administered via intravenous drip, every 12 hours until lead colicky pain is controlled; or Na₂DMS 1.0g, administered via intravenous push, every 12 hours, or every 6 hours in severe cases, until lead colicky pain is controlled. Alternatively, DMSA 1.0g, taken orally, every 6 hours until lead colicky pain is controlled, followed by the chronic lead poisoning treatment protocol.
2. Symptomatic treatment: 10% calcium gluconate 10ml, administered via intravenous injection; atropine 0.5～1.0mg or 654-2 10mg, administered via intramuscular injection; abdominal hot compress; acupuncture and moxibustion at Zusanli (ST36), Zhongwan (CV12), Neiguan (PC6), Sanyinjiao (SP6), etc.

Treatment for lead encephalopathy: Initially, BAL 2.5mg/kg administered via intramuscular injection, every 4～6 hours for the first 1～2 days; then 1～2 times daily for a total of 5～7 days. Subsequently, treat with CaNa₂EDTA according to the chronic lead poisoning treatment protocol.

Prevention

Use non-toxic or low-toxic substances to replace lead; adopt mechanized and automated production; reform product dosage forms; control lead melting temperature; enhance local ventilation and detoxification devices; strengthen personal protective measures. Regularly monitor lead concentration in the workplace. Conduct regular health surveillance, including pre-employment physical examinations and biannual or annual physical examinations. Blood lead and ZPP can be used as screening indicators to promptly identify employment contraindications and early cases of lead poisoning for timely intervention.