Lead sulphide or galena is the main source of lead. About four million tons of this metal is produced in the world each year. It is the most ubiquitous toxic metal and can be detected in practically all components of the environment as well as of the biosphere. Lead is toxic to most of the living beings while it has no known function within a biological system.

Lead finds wide application in industries and effluents from these units contain a good quantity of this element. Lead may come from pipes carrying water, combustion of fossil fuels and from exhausts of automobiles run on petrol containing lead compounds which are added as anti-knock agents.

Plants growing near busy highways are regularly exposed to fumes and smoke discharged from automobiles containing plenty of lead. It has been estimated that almost 450 tons of lead are emitted annually into the atmosphere in Bombay alone through automobile exhausts (Khandekar et al, 1980).

There is little absorption of lead through root system of plants. It gains entry through stomata and is absorbed by the tissues within. Leafy vegetables, therefore, are likely to possess a higher lead concentration as compared to others. Lead is also accumulated by green plants and is passed on to higher trophic levels.


In animals including man, gastro-intestinal absorption of lead ranges between 5-15% of the total amount ingested. Only about 4-5% of the lead thus abosrbed is retained. The rest of it is excreted. However, children have been shown to absorb much more, about 40% of lead ingested with food and water and retain almost 30% of it (Goyer, 1986). Absorption of lead through lungs is rather more efficient and almost complete. Vapours of tetra-ethyl-lead, used as an additive to petrol, may be absorbed through intact skin as it is strongly lipophilic in nature.

More than 90% of the lead absorbed goes to blood where it can be detected in red blood cell associated with its membrane and haemoglobin (Barltop and Smith, 1971). Later it is distributed to liver, kidney and bones including teeth. It is finally deposited in bones. About 90% of the metal organism. Its concentration in bones increases with age of the individual.

Any subsequent disturbance resulting in osteolysis, tends to mobilize the deposit of lead in bones reading ultimately to its toxic action. Acute toxicities of lead are of rare occurrence. It may occur only in cases where intake is deliberate. Ingestion of large quantities of lead salts such as lead acetate produces burning pain in mouth, throat and stomach.

This is followed by abdominal pain accompanied by constipation of diarrhoea and often bleeding in severe cases. Finally there may be failure of blood circulation and termination of liver and kidney functions. The patient passes into coma followed by respiro-cardiac failure.


Chronic lead toxicity is marked by a general feeling of unwellness, fatigue and pain in limbs Anaemia is usually the first symptom in animals including man following low level lead intake over long durations. It has been shown that lead inactivates aminolevulinic acid dehydratase and porphyrobilinogen decarboxylase which cause suppression of haem-synthesis.

However the toxic effects of lead are probably more significant in terms of human agility and performance. Degenerative changes in motor nerves and ganglia occur which result in decreased speed of conductance of nerve impulses to and from the muscles.

The individual becomes dull, slow and inactive. In growing chilli degeneration of intellect and mental retardation may occur (Rutter and Jones, 1983, Needleman, 1980). Excretory mechanism of kidney is affected by this metal which may cause discharge of proteins and even blood through urine. Irreversible lead induced chronic kidney pathology is; characterised by deganeration of tubular cells, interstitial fibrosis, glomerular schlerosis etc.

Lead reduces uric acid excretion and chronic lead toxicities have been associated with development of gouty conditions in the hapless patients. Hypertension has also been found to be associated with a high percentage of lead in blood stream.


Severe lead toxicites have long been associated with sterility and gameto-toxic effects in both male and female animals. Lead is capable of passing through the placenta to foetus to cause developmental anomalies and still births. Some clinical studies have found increased chromosomal defects in workers with high levels of lead in blood (Deknudt et al, 1977). Suppression of immune system has been observed in laboratory animals even at such low doses which do not cause any apparent symptoms of toxicity (Koller et al, 1983).

Lead poisoning usually causes the presence of characteristic nuclear inclusions which appear as dense, homogenous eosinophilic bodies under light microscope while cells containing them are usually swollen. Under electron microscope these bodies are seen to possess a dense coreandat outer fibrillary region. They are composed of lead-protein complex and contain a large amount of aspartic and glutamic acids and a little cystine (Moore et al, 1973).

Experimental studies have pointed out that nuclear inclusion bodies are earliest evidence of lead exposure which may be observed before any of the functional changes of intoxication in the system are detectable. It is thought that the sequestering of lead in these bodies is helpful in protecting other susceptible organelles.

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