Lead poisoning

Introduction to lead poisoning Lead poisoning is a non-infectious chronic disease caused by the cumulative absorption of lead. Typical symptomatic children with lead poisoning are not common. Most children have no signs of brain lesions but have persistent behavioral and cognitive problems. , seriously affecting health and learning. When it is characterized by irritability, loss of appetite, personality change, abdominal cramps, etc., its blood lead level is generally around 50g/dL, which is already a serious lead poisoning, but these symptoms are easily thought to be caused by other causes. If it is not realized at this stage, blood lead can easily rise above 100 g / dL, when the symptoms of children usually increase intracranial pressure, causing radioactive vomiting, sensory changes, convulsions, etc., which is extremely heavy lead Poisoned. Adults who continue to lead poisoning at a blood lead concentration of 50-60 g/dL can cause renal failure, unresponsiveness, peripheral nervous system disorders, gout, and the like. Lead poison is not easy to cure, and its harm to the human body will last for a long time even after the blood lead content is reduced. basic knowledge Sickness ratio: 0.5% Susceptible people: more common in children Mode of infection: non-infectious Complications: ataxia, coma, liver, jaundice, hemiplegia

Lead poisoning cause

Causes:

Environmental pollution (35%):

1. In the atmosphere, it mainly refers to lead emissions from industrial production, life and transportation. Lead poisoning is caused by unavoidable industrial waste gas, leaded gasoline, automobile exhaust, coal burning, steel metallurgy, and chemical plant emissions.

2. In soil and dust, in general, the soil contains lead 10~50mg/kg, but in urban areas, the lead content in the soil may be hundreds or even thousands of times higher. Indoor lead dust is also an important source of lead exposure in children.

3. In the water, wastewater contaminated drinking water can cause an increase in lead content in the water. Studies have shown that children's absorption rate of lead can be as high as 50% or more.

Ingestion of excess lead (20%):

Other (20%):

Pathophysiology

1. Absorption, distribution and discharge of lead

Normal people enter 300g of lead per day from the diet, about 10% of which can be absorbed. About 40% of the lead inhaled by the respiratory tract can be absorbed. After the lead is absorbed, it enters the blood and is distributed in soft tissues such as liver, spleen, kidney, brain, etc. After that, lead is redistributed in the body. 90%-95% of the lead is stored in the bones. The lead absorbed into the body is mainly excreted by the kidneys, and a small part is excreted by feces, saliva, sweat, milk, etc., and the daily lead absorption exceeds 0. 5mg can accumulate and become toxic.

Lead in blood and soft tissues is transportable lead, which is biologically active. Its amount exceeds normal, but it is lead absorption when there is no poisoning symptom. Excess lead can cause toxicity. Lead in bone is stored as lead, no biological activity, blood lead, Soft tissue lead and bone lead are in a state of dynamic equilibrium. In the case of infection, drinking, acidosis, etc., lead transport in the bone to the blood and soft tissue can cause poisoning.

2, poisoning mechanism

The toxicity of lead and its inorganic compounds is related to the amount of lead in the body. Lead compounds with small particles are easily inhaled by the respiratory tract. Lead compounds with high solubility are easily absorbed into the body, which is highly toxic, and lead is easily combined with sulfhydryl groups of proteins in the body. It can inhibit thiol-containing enzymes, especially several enzymes related to heme synthesis. Lead inhibits erythrocyte delta--amino-r-ketovalerate dehydratase (ALAD), which increases serum and urinary -amino-r-ketovaleric acid (ALA), and lead inhibits coproporphyrinogen decarboxylase, causing urine in the feces. Increased porphyrin, lead inhibits heme synthase, interferes with iron and protoporphyrin to form heme, and affects hemoglobin production, resulting in accumulation of iron (forming ring-shaped iron granules) and free protoporphyrin (FEP) in young red blood cells The free protoporphyrin is chelated with zinc to form zinc protoporphyrin (ZPP).

Lead poisoning can increase the number of rainbow cells, which is because lead inhibits erythrocyte pyrimidine-5-nucleotide plum, which causes the degradation of pyrimidine nucleotides in erythrocytes, and also hinders the degradation of ribosomal RNA. Degraded pyrimidine nucleotides and ribosomal RNA form basophilic spots.

Lead is attached to the erythrocyte membrane, interfering with Na+, K+ATPase, and making red blood cells fragile and easy to hemolyze.

In recent years, ALA has been found to pass the blood-brain barrier. A large amount of ALA entering the brain tissue during lead poisoning can cause various behavioral and neurological effects. The mechanism may be that ALA is similar in structure to r-aminobutyric acid (GABA) and can compete with GABA for postsynaptic membrane. The GABA receptor affects the function of GABA.

Some aspects of the pathogenesis of lead poisoning have not yet been elucidated.

Lead poisoning prevention

1. Improve production conditions and reduce lead concentration in the air: The production equipment should be mechanized and automated, minimize the contact of lead dust and lead smoke, and the place where lead dust and lead smoke are generated should be sealed, and ventilation equipment should be installed to control the melting. The lead temperature is used to reduce the generation of lead smoke. The process of lead dust can be carried out by wet operation, technological innovation, and the use of non-toxic substances instead of lead. For example, pigments in paint replace titanium dioxide with titanium dioxide, and lead red is replaced by iron red. . Various technical measures are adopted to reduce the lead concentration in the air, and the test is carried out periodically so that the lead concentration in the air of the workshop is not the maximum allowable concentration, the lead smoke is 0.03 mg/m3, and the lead dust is 0.05 mg/m3.

2. Strengthen worker's personal protection and medical supervision: lead workers should wear overalls when working, wear filter-type anti-lead masks, work clothes should not enter the canteen, dormitory, work and washing before meals, smoking in the workshop, eating, regular worker health Monitoring.

3, to avoid accidental intake of excessive lead compounds: food and beverages to prevent lead contamination, the use of lead-containing drugs should be strictly controlled dose, not excessive.

Lead poisoning complications Complications, ataxia, coma, hepatic rhubarb, hemiplegia

Lead poisoning encephalopathy may have ataxia, convulsions, coma; liver enlargement, jaundice, oliguria or anuria, circulatory failure; gastrointestinal bleeding and paralytic ileus may cause dyspnea or even respiratory failure; Can cause mental retardation, blindness and hemiplegia.

Symptoms of lead poisoning Common symptoms The wrist of the distal part of the limb appears

1. Acute poisoning: Within a few days after entering the large amount of lead compound from the digestive tract or respiratory tract, there may be metallic taste, nausea, vomiting, constipation, diarrhea and stubborn abdominal cramps. Hepatic diseases, peripheral neuropathy, hemolysis may also occur in critically ill patients. Anemia and high blood pressure, etc. Children can develop toxic encephalopathy, coma, convulsions, and timely treatment can quickly recover.

Second, chronic poisoning: long-term exposure to low-level lead dust or lead smoke caused by occupational lead poisoning is mostly chronic poisoning, due to the improvement of working conditions, patients are mostly mild.

(1) mild poisoning

1, neurasthenia syndrome: symptoms appear earlier, more common, headache, dizziness, fatigue, limb pain.

2, indigestion: the patient's mouth has a metallic taste, abdominal pain, constipation, a small number of patients in the gingival margin mucosa can be seen in the formation of "lead line" formed by the deposition of lead sulfide particles, dark gray or blue banded or irregular spots Blocks are often seen in a few poor oral hygiene.

(2) Moderate poisoning

1, abdominal cramps: abdominal pain is severe and unbearable at the time of attack, in the umbilical cord, lower abdomen or other parts, pain with colic nature, abdominal pain bursts, each time lasts for several minutes to several hours, pale face when abdominal pain occurs, out Cold sweat, irritability, tender parts are not fixed.

2, anemia: may have mild anemia, pale complexion.

3, peripheral neuropathy: most of the multiple neuropathy, limbs have lightning-like pain, paralysis, numbness, sensory obstacles in the distal parts of the limbs, weakness.

(3) Severe poisoning

1, sputum: mainly involving the extensor muscle, in the upper limbs as a vertical wrist, in the lower limbs as a vertical foot.

2, encephalopathy: begin to have a slight disorder of feeling, memory, mood, sleepiness, convulsions, mania, ataxia in months, weeks, and finally tremors, coma, convulsions, this situation is rare .

Lead poisoning inspection

First, the determination of lead in the human body

1, blood lead: is the recent absorption index, the upper limit of normal blood lead is 2.4mol / L (50g / dl).

2, urine lead: can reflect the absorption of lead, the upper limit of normal urine lead value is 0.39mol / L (0.08mg / L).

3. Diagnostic lead-driving test: its urine lead 1.45mol/L (0.3mg/L) is the upper limit of normal value, and urine lead exceeds 3.86mol/L (0.8mg/L) or 4.82mol/L (1mg/d). Can diagnose lead poisoning.

4, urinary porphyrin (uric brown pigment): urinary excrement of porphyrin is also seen in hematoporphyria, liver disease and alcoholism and barbiturate poisoning, urinary fecal porphyrin semi-quantitative ++ is positive.

5, red blood cell free protoporphyrin (FEP), red blood cell zinc protoporphyrin (ZPP) are sensitive indicators of lead absorption, ZPP measured by blood fluorometer, rapid operation, easy to on-site inspection, the upper limit of FEP normal value is 0.72 - 1.78 mol/L (40-100 g/dl). The upper limit of the normal value of ZPP is 0.9-1.79 mol/L (4.0-8.0 g/gHb). The increase in both is also seen in iron deficiency anemia.

6, red blood cell ALAD: ALAD activity reduction is a very sensitive indicator of lead exposure, sometimes blood lead in the normal range, ALAD activity has been significantly reduced, and therefore can not be used as a diagnostic indicator.

Second, blood test

1, hemoglobin, red blood cell count: chronic lead severe anemia is mostly mild, is a hypopigmentation anemia, acute lead poisoning may have hemolytic anemia.

2, reticulocytes and alkaline red blood cells: these two red blood cells can be significantly increased in lead poisoning anemia, but not unique to lead severity, also seen in other types of anemia, such cells in the health survey of workers are not detected High, but for the diagnosis of severe lead poisoning, there is a reference value of the upper limit of normal value, 300 red blood cells / million red cells, or 10-15 / 50 fields of view.

Diagnosis and identification of lead poisoning

diagnosis

1. History of lead exposure: Occupational lead poisoning should have a professional history of exposure to excessive lead. A detailed understanding of the type of work, the age of workers, the concentration of lead in the environment, and the protection of the lead. The history of exposure to lead poisoning is sometimes unclear. Clinically, if there are typical multi-system symptoms, the possibility of lead poisoning may often be suggested. Ask about the possibility of food or drink contaminating lead, such as drinking from a tin jug or taking lead-containing drugs in the near future.

2, the clinical manifestations of lead poisoning: the human body's effect on lead has a certain relationship with the dose of lead, acute lead poisoning onset, acute abdominal cramps, liver disease, hemolytic anemia, peripheral neuropathy, toxic encephalopathy, chronic lead severity Can be divided into light, medium and heavy three levels.

3. Laboratory evidence for lead absorption: Increased blood lead and urinary lead indicate that the body has absorbed excessive lead, and urine ALA, urinary porphyrin, and red blood cell ZPP increase, reflecting the biochemical reaction caused by pre-absorption, such as according to occupational history and doubt. There is heavy lead, but the lead in urine does not exceed the upper limit of normal value. The lead-discharge test can be used to assist the diagnosis. The method is to use intravenous injection or intravenous drip of 1.0 g of disodium edetate or 0.5 g of intramuscular injection. The urine lead does not exceed 1.45 mol/L within 24 hours after administration, and the lead in the lead poisoning often exceeds 3.86 mol/L or 4.82 mol/d.

With clinical manifestations of lead poisoning, combined with exposure history, and laboratory positive findings for comprehensive analysis, can diagnose lead poisoning, lead exposure history, blood lead or increased urine lead, but lead-free poisoning symptoms are diagnosed as lead absorption, The diagnosis of occupational lead severity should be carried out in accordance with the "Principles of Occupational Chronic Severity Diagnostic Criteria" (GB11504-89) approved by the Ministry of Health.

Differential diagnosis

1, lead toxic abdominal cramps, need to be identified with other acute abdomen, lead colic pain frequent, long duration, the site below the main abdomen, but not fixed, no abdominal distension, abdominal muscles can relax during pain relief, peripheral There are more red blood cells in the blood, and there may be other symptoms associated with lead. The acute intermittent hematoporphyria is similar to lead cramps. The point of identification is that the urinary biliary tract is increased in a large amount during the onset of the former. Long, and there is no obvious evidence of lead absorption.

2, lead toxic anemia: acute anemia should be identified with other hemolytic anemia, chronic anemia should be differentiated from other iron granulocyte anemia, erythrocyte pyrimidine 5 'nucleotidase deficiency. Mainly rely on lead exposure history, evidence of lead absorption and other symptoms of lead poisoning.

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