I now have the complete Lead Poisoning section from Park's PSM. Here is the full, well-organized answer:
Lead Poisoning - Park's Textbook of Preventive and Social Medicine (p. 910-911)
Introduction
More industrial workers are exposed to lead than to any other toxic metal. Lead is widely used in industry due to its properties:
- Low boiling point
- Mixes easily with other metals to form alloys
- Easily oxidised
- Anticorrosive
Toxicity of compounds: All lead compounds are toxic. Lead arsenate, lead oxide, and lead carbonate are the most dangerous; lead sulphide is the least toxic.
Sources of Exposure
Industrial Uses
Over 200 industries use lead, including:
- Manufacture of storage batteries
- Glass manufacture
- Ship building
- Printing and potteries
- Rubber industry and several others
Non-Occupational Sources
- Gasoline - the greatest source of environmental (non-occupational) lead; thousands of tons of lead are exhausted from automobiles every year
- Drinking water from lead pipes
- Children chewing lead paint on window sills or toys
Mode of Absorption
Lead poisoning may occur in three ways:
- Inhalation - Most cases of industrial lead poisoning result from inhalation of fumes and dust of lead or its compounds
- Ingestion - Less common. Small quantities trapped in the upper respiratory tract may be swallowed. Lead may also be ingested via contaminated hands, food, or drink
- Skin - Absorption occurs only with organic compounds of lead, especially tetraethyl lead. Inorganic compounds are NOT absorbed through the skin
Body Stores and Distribution
- Normal body store: 150 to 400 mg in the average adult
- Normal blood level: ~25 μg/100 ml
- Clinical symptoms appear at: ≥70 μg/100 ml blood lead level
- Normal daily intake: 0.2 to 0.3 mg/day (from food and beverages)
Distribution pathway:
- 90% of ingested lead is excreted in the faeces
- Absorbed lead enters circulation → 95% enters erythrocytes → transported to liver and kidneys → finally deposited in bones
- Bone lead is "metabolically inactive" but may be released to soft tissues during bone resorption
Mechanism of toxicity: Lead combines with SH-groups of certain enzymes, especially those involved in porphyrin synthesis and carbohydrate metabolism. It also affects membrane permeability, causing potassium leakage from erythrocytes.
Clinical Picture (Plumbism)
The clinical presentation differs between inorganic and organic lead exposure:
Inorganic Lead Poisoning
- Abdominal colic
- Obstinate constipation
- Loss of appetite
- Blue line on the gums (Burton's line)
- Stippling of red cells (basophilic stippling)
- Anaemia
- Wrist drop and foot drop (peripheral neuropathy)
Organic Lead Compounds (e.g., tetraethyl lead)
Toxic effects are mostly on the CNS:
- Insomnia
- Headache
- Mental confusion
- Delirium
Diagnosis
Diagnosis is based on three pillars:
1. History - History of lead exposure
2. Clinical Features - Loss of appetite, intestinal colic, persistent headache, weakness, abdominal cramps, constipation, joint and muscular pains, blue line on gums, anaemia, etc.
3. Laboratory Tests
| Test | Normal | Abnormal/Significant |
|---|
| Coproporphyrin in urine (CPU) | < 150 μg/litre | Raised = useful screening test |
| Amino levulinic acid in urine (ALAU) | - | > 5 mg/litre = indicates lead absorption |
| Lead in urine | 0.2 - 0.8 mg/litre | > 0.8 mg/litre = lead exposure |
| Blood lead | ~25 μg/100 ml | 70 μg/100 ml = clinical symptoms |
| Basophilic stippling of RBC | - | Sensitive parameter of haematological response |
Preventive Measures
- Substitution - Replace lead compounds with less toxic materials where possible
- Isolation - Enclose and segregate processes generating harmful lead dust or fumes
- Local exhaust ventilation - Adequate ventilation to remove fumes and dust promptly
- Personal protection - Approved respirators for workers
- Good housekeeping - Wet sweeping of floors, benches, and machines to control dust
- Working atmosphere - Lead concentration in workplace air must be kept below 2.0 mg per 10 cubic metres (permissible limit/threshold value)
- Periodic examination of workers - Regular medical examination including urinary lead, blood lead, RBC count, haemoglobin, CPU test, and basophilic stippling estimation. WHO Expert Committee stresses that blood lead must not exceed 70 μg/ml and ALA in urine must not exceed 10 mg/litre
- Personal hygiene - Hand-washing before eating; no food in work areas; adequate washing facilities
- Health education - Educate workers on risks and personal protection
Management
The major objectives are:
- Prevention of further absorption
- Removal of lead from soft tissues
- Prevention of recurrence
- Early recognition and removal from further exposure
- Saline purge to remove unabsorbed lead from the gut
- D-penicillamine - chelating agent; promotes lead excretion in urine (similar to Ca-EDTA)
- Ca-EDTA - chelating agent for lead excretion in urine
Important note: Lead poisoning is a notifiable and compensatable disease in India since 1924.
- Park's Textbook of Preventive and Social Medicine, pp. 910-911