Released on World Environment Day 2001

1. Introduction

Mankind has been using lead for over 6000 years, and solely as a result of anthropogenic activities lead has become the most ubiquitous toxic metal. Hippocrates was probably the first of the ancients to recognize lead as the cause of colic. Lead’s toxicity was recognised and recorded as early as 2000 BC and its widespread use has been a cause of endemic chronic plumbism in several societies throughout history. With the industrial expansion in the last two centuries the problem has become more serious, as evident from the Antarctic and Arctic ice core data showing presence of lead in such far off places. The last three centuries also witnessed the worst outbreaks of lead poisoning among adults which were occupational in origin, although environmental pollution also reported adverse effects of lead on health. Many reviews and references are available in literature related with health effects of exposure to lead (Pandya et al, 1983; Needleman, 1988; Parikh, 1990; Needleman, 1999). In contrast with developed countries, where lead exposure is on the decline due to implementation of environmental and occupational regulations (Howson et al, 1995), in developing countries Pb poisoning continues to be a serious problem (Romieu et al, 1997; Krishnaswamy & Kumar, 1998). Without proper corrective action, Pb exposure would remain a threat to many generations of children in the developing world.

1.1 Environmental Lead in India

India was one of the early civilization, which took to metallurgy, and the use of lead in various forms was prevalent for 3 millenia. In recent years considerable concern has been expressed regarding human risks due to environmental lead in India and several epidemiological and environmental monitoring surveys, experimental studies and case reports have appeared suggesting the gravity of the problem. Monitoring of Pb and other heavy metals has been undertaken under an Integrated Environmental Programme on Heavy Metals (IEPHM), Ganga Action Plan, and Rajiv Gandhi Drinking Water Mission. Several studies in India have revealed that the sources of Pb pollution in the air are, smelting in unorganised sector industries, refuse burning, lead and battery industries and automobiles.

The exponential rise in the number of vehicles on the Indian roads has not been matched with changes in pollution control standards. In urban areas, with congested traffic on and a high proportion of old vehicles (Samanta et al, 1995; Ramanathan, 1999) almost 90% of Pb in the atmosphere comes from burning of leaded petrol. In order to reduce the lead load in air, use of leaded gasoline has been banned with effect from February, 2000. However, exposure to lead still looms large especially due to the prevalence of home based cottage industries. These cottage industries are generally located in areas of dense population. Health of children is of particular concern since these non-regulated businesses deliver the Pb into the homes where children live or play. Children can also be exposed to Pb dust which their working parents bring from work on clothes, in hair, shoes, etc., thereby problems of occupational exposure become community problems. Traditional industrial use of lead in paints, batteries etc. also have increased considerably. In infants and young children, exposure to Pb has been shown to decrease IQ scores, slow their growth and cause hearing problems and kidney damage. These effects are persistent and interfere with school performance and are caused by exposure to such low levels of lead which were once thought to be safe. However, much data is not available in India on this.

Lead is well known to inhibit the biosynthesis of heme, and consequently of hemoglobin and to decrease the life span of circulating red blood cells (Potula, 1996). Iron deficiency and Pb toxicity can be synergistic and potentially devastating, upto 50% more Pb may be absorbed in children with iron deficiency (Hashmi et al,1978; Hashmi et al, 1989). The developing fetus is at maximum risk of lead toxicity. Exposure of pregnant women can transfer significant amount of this metal to the developing fetus which may result in premature birth, low birth weight or even abortion. Infants born to mothers exposed to high level of Pb show significant signs of neurological deficits. In countries, where a major proportion of people are prone to anemia due to a variety of reasons, Pb exposure can be more serious.

1.1.1 Efforts to reduce lead levels

The growing recognition of lead’s dangerous effects has led to a worldwide initiative to reduce lead content of gasoline (Lovei, 1998). In India, Pb levels have been reduced from 0.56 g/L in gasoline (pre 1986) to 0.013 g/L (in year 2000) (CPCB, 1997). Four metropolitan cities became Pb free in 1999 as far as exposure through gasoline is concerned. Unleaded gasoline is now available in all large cities and along highways. This transition from leaded to unleaded gasoline will reduce lead exposure in the population at large but it is also important to sum up activities to control other Pb sources too. Quantitative data on the benefit of this reduction in Pb emission and its toxicity are yet to come. In addition, monitoring of Pb levels in food materials has also been undertaken from time to time. Industrial Toxicology Research Centre at Lucknow for the last three decades has played a leading role in heavy metal toxicity. Occupational health surveys, experimental studies on the mechanism of lead intoxication, identification of factors influencing Pb toxicity and approaches for curative aspects have been undertaken alongwith monitoring of blood Pb levels of exposed population.
In fact, lead has been quantified on most environmental matrices and biological tissues, sources and exposure routes identified, and most symptom of occupational and environmental exposure detected. Interventional and restoration efforts are also underway by the regulatory agencies. In view of these, a critical appraisal of the overall issue of lead in India is attempted in this monograph. Detailed description of lead toxicity in its current international state-of-the-art is not attempted, since there are several authoritative and exhaustive documents.

2. Physical and Chemical Properties and Analytical Methods

Lead is a soft, bluish gray metal melting at 327.4 °C. It is insoluble in water and corrosion resistant, but soluble in nitric and hot sulfuric acids. The usual valence state in inorganic Pb compounds is +2. Lead also forms salts with organic acids, such as lactic and acetic acids, and stable organic compounds such as tetraethyl and tetramethyl lead. Divalent Pb can interfere with the action of other divalent cations, such as Ca2+ in biological system.
The analytical methods that are available for detecting and/or measuring and monitoring lead in environmental media and biological samples are:

  1. Spectrophotometry
  2. Stripping potentiometry
  3. Anodic stripping voltammetry
  4. Flow injection analysis coupled with various approaches
  5. Amperometry
  6. Fluorimetry
  7. X-ray fluorescence
  8. High Performance Liquid Chromatography (HPLC)
  9. Spectroscopy
  10. Differential pulse polaragraphy
  11. Complexometric titration
  12. Ion selective electrodes
  13. Flame Atomic Absorption spectrophotometry (AAS)
  14. ICP methods: ICP/AES and ICP/MS
  15. Isotopic dilution MS (IDMS)
  16. GC-MS
  17. Nutrition activation analysis
  18. Radio reagent method
  19. Hematofluorometer (for Zn protoporphyrin), etc.

The most common methods currently used for analysis of Pb in biological and environmental samples are flame atomic absorption spectrophotometry (AAS) and graphite furnace atomic absorption spectrophotometry (GFAAS), anode stipping voltametry (ASV), inductively coupled plasma atomic emission spectroscopy (ICP/AES), and inductively coupled plasma mass spectrometry (ICP/MS). For samples analysed by these methods, detection limits of 0.12 mmoles Pb/l blood (2.49 mg/dL) can be achieved. Besides environmental compartment and biological tissues, lead has been determined in several other environmental matrices including paint, fish, vegetation, crops, and various foods. Institutions in India where sampling and analysis of Pb is being carried out are:

3. Usage, Production and Consumption of Pb

In terms of tonnage used, lead ranks fourth among the non-ferrous metals. Pb is an important strategic metal because of its civil and military applications. The main use of Pb is in the automobile batteries. Consumer preference, environmental regulations, and energy conservation innovations have led to increasing use of electronic trucks at airports, hospitals, warehouses and for other delivery purposes and the trend in India for battery operated inverters as standby power in houses and offices thus further increasing the demand for Pb batteries. Lead acid traction batteries in railway application will continue to be in demand. Pb is also used as sheathing material on cables; Pb-Sb alloy bricks in nuclear power plants; in disposal of nuclear wastes; Pb-Sn solders; in construction for insulating sound; ceramic industry; lining or steel tanks and vessels for corrosion resistance; paints used in structural, marine and industrial applications

. Mines under production are Mochia, Balania, Zawarmala, Rajpura-Dariba, Agrigundala, Sargipalli, and Rangpo having lives from 9 to 27 years and plant capacity of 7840 TDP (Kothari, 1997). The per capita consumption of Pb in India has, however, continued to be low at 0.07 kg compared to USA (5.14 kg) West Germany (5.12 kg) China (0.219 kg) and Republic of Korea (1.08 kg).

Table 1: Pb consumption in India

Industrial alloys8%
Source: Kothari (1997).

3.1 Permissible Limits in Various Media

The permissible limits of lead in (a) ambient air: 0.75 mg/m3 for sensitive areas (bird sanctuaries); 1.0 mg/m3 for residential areas; 1.5 mg/m3 for industrial areas (CPCB, 1995-96), (b) Water: 0.05 mg/L for drinking water (c) Effluents: 0.10 mg/L for discharge of industrial effluents in inland surface water. These are generally in line with international standards.

3.2 Environmental Transport, Distribution and Transformation

Lead is a naturally occurring element found in the earth’s crust (about 20 mg/kg) mostly as the sulfide galena (PbS), and in all compartments of the biosphere in various chemical forms Natural sources of atmospheric Pb include geological weathering and volcanic emissions, anthropogenic emissions to the atmosphere are predominant. Pb is transferred continuously between air, water and soil by natural chemical and physical processes such as weathering, runoff, precipitation, dry deposition of dust, and river flow; however, soil and sediments seem to be important sinks for Pb. The average residence time in the atmosphere is 10 days and long distance transport may take place over this time period.
Not much deposited Pb is transported to surface or ground water as it is quite tightly bound to organic matter. Above pH 5.4, head water may contain about 30 mg Pb/l and soft water about 500 mg Pb/l. Airborne Pb can be taken up by the biota directly or through soil. Animals also can be exposed to Pb through inhalation or grazing and soil ingestion. There is little biomagnification of inorganic Pb through the food chain.

4. Sources of Human Exposure

Areas in the vicinity of Pb mines and smelters are subject to high levels of air emissions; cottage industries in ceramics, battery breaking and jewellery making often result in contamination and expose occupants and neighbouring houses to significant health risks.
Possible sources of lead exposure in India are mentioned in Table 2.

Table 2: Possible sources of lead exposure in India

  • Contaminated soil and dust
  • Mining
  • Cooking and storage vessels containing lead (tinned polish);cans
  • Ceramic pottery with painted lead glaze
  • Country liquor, beverages
  • Food adulterant in ice cream, tobacco and tobacco products
  • Toys, pencils
  • Cosmetics (sindoor, surma)
  • Herbal medicine
  • Paints, pigments
  • Industrial effluents: disposal
  • Water pipes
  • Contaminated aquifers: mining, smelting, processing, recycling
  • Occupational exposures: silver jewelry making ; battery breaking and manufacturing; welding; repairing automobile radiators; papier mache workers; etc

The evaluation of the relative contribution of sources is extraordinarily complex, and is likely to differ from one area to another, and in different population groups leading to different magnitudes of Pb toxicity. Pb is a ubiquitous pollutant causing health effects in humans and animals. Absorption of Pb is highly variable and depends on the chemical form, constituents of the diet and nutritional status, and ill health of the subjects. Pb enters humans most frequently through ingestion and inhalation, skin absorption and in utero exposures. Most individuals ingest Pb via food almost daily. Contamination of plants from atmospheric Pb is the most important pathway for Pb to enter the human food chain. It is also ingested through milk and meat. Pb content of food samples (Lalit et al, 1980) and cereal products (Srikanth et al, 1995) have been recorded.
Children with ‘pica’ (the habitual eating non food objects) are at even greater risk. Children’s gastrointestinal tracts absorbed 50% of ingested lead compared to adult absorption of 10-15%, making lead ingested through hand to mouth behaviour or dietary lead an exposure source of significant concern. Pregnant women may absorb much greater quantities of ingested lead, approximating the 50% absorption rate of children. In adults, ingestion may occur through eating, smoking, or nail biting with lead contaminated hands, particularly after renovation or hobby activities. Other ways of ingesting lead include eating or drinking food contaminated with lead. Studies of gastrointestinal absorption indicate 10-15% of dietary lead is absorbed though this can rise up to 63% in fasting conditions. Factors that increase the bioavailability and absorption of ingested lead from the gut in children and adults are:

The amount of lead inhaled depends on the lead levels in air and the amount of air being inhaled by the individual. Generally adults inhale 15 m3 of air daily while children of 2 years inhale roughly 6 m3 of air daily.
The ability of the skin to absorb certain organic lead compounds, such as tetraethyl lead found in petrol has been recognized since the 1940s. Inorganic lead compounds (e.g. lead nitrate, lead acetate and lead oxide) can also be absorbed through the skin but in very small quantities
. Lead poisoning is caused by acute or chronic environmental exposure through air, drinking water (lead soldered pipes), food (cans), paints, soil, dust. The varied and heterogenous nature of environmental exposure, is a constraint to the control, reduction, prevention, and intervention strategies implementation.

5. Environmental Levels and Human Exposures

Levels of Pb found in air, water, soil/dust and food vary widely throughout the world and depend upon the degree of industrial development, urbanisation and lifestyle factors. Vehicular emissions and effluents from battery industries had been major contributors to the excessive amounts of Pb in the Indian environment. The total estimated release of lead from vehicular traffic emissions is 640 TPY (Khandekar et al, 1987). About 50%-70% of this is expected to be released as emissions into the environment, and the rest gets deposited in the exhaust system. The annual mean values of particulate lead in ambient air during 1989-92 remained within the limits of 1000 mg/m3 as prescribed by WHO except at some places in Delhi where maximum values were 8500 ng/m2 in 1990 (CPCB, 1993). These annual mean values have come down to 350 ng/m3 in 1996 and 220 ng/m3 in 1997 as reported in CPCB annual report of 1997-98. This report also indicates highest emissions of Pb in Delhi followed by Calcutta, Mumbai and Chennai among the 4 mega cities. Congested traffic on main roads of cities and old vehicles serve as distributed source of Pb pollution (Ramanathan, 1999; Samanta et al, 1995). The total production of the lead-acid batteries in the country is about 8 million batteries per year. An estimated release of Pb from various sources in the production of 1000 such batteries is nearly 11.35 kg. Of this 11.35 kg, an estimated 5.45 kg is released as emissions and 5.90 kg as part of effluents (CPCB, 1993)
. Significant difference of ambient air lead levels have been reported from high and low exposure areas which ranges from 131-864 ng Pb/m3 147-476 ng Pb/m3 (daily average range) respectively (Parikh et al, 1999). In a study carried out on school children in Ahmedabad city, 61.6% children had Pb levels higher than the 10 mg/dL (NIOH, 1999) which is the exposure risk limit defined by Centres for Disease Control and Prevention (CDC, 1991), USA. Yiin et al (2000) have conducted studies to examine seasonal changes and relationship to blood Pb levels in preschool children. Both indoor and outdoor dust Pb levels were found to be higher in summers. Pb exposure and seasonal influences could be an important aspect in Indian conditions with tremendous variations in summer and winter temperatures.

Lead concentrations in environmental media which contribute to child lead poisoning are mentioned in Table 3.

Table 3: Lead concentrations in Environmental Media which contribute to child lead poisoning

Medium Levels that may be tolerable Levels that contribute to child lead poisoning
Drinking water 1-10 mg/L 50 mg/L
Ambient air (24 hr) 0.01-0.1 mg/m3 1 mg/m3
Dust deposition 1-5 mg/m2/day100 mg/m3/day
Soil (top 2 cm accessible to children)100-300 mg/g* 1000 mg/g
Food (whole diet average)<0.005-0.01 mg/g0.05-0.2 mg/g
*may not protect children with pica.

Survey studies on Pb levels in air in some Indian cities indicated high Pb levels in samples from industrial cities (Sadasivam et al, 1987). The highest level of Pb observed was 51.82 ug/m3 in a sample collected from Visakhapatnam, possibly due to lead smelting and transport activities and could be an exceptional case.
A survey was conducted in the vicinity (100 m-1 km) of 3 lead industries in Maharashtra which were suspected of polluting the environment and affecting the people (Nambi et al, 1997) (Table 4).

Table 4: Environmental contamination by lead industries

SampleMaximum range of Pb concentration measured near industriesTypical concentration in “normal” area in Trombay
Soil 200-3454 mg/g8.6 mg/g
Grass145-1048 mg/g1.42 mg/g
Jawar15.81 mg/g0.012 mg/g
Air 0.5– 120 mg/m30.11 mg/m3
Blood (children)23.4 – 43.47 mg/dL11.39 mg/dL
Urine (children)45.8 – 169.4 mg/l7.5 mg/l

Source: Nambi et al (1997).

Inhalation of lead from leaded petrol emissions has been an important source of lead exposure providing a generalised low dose across the general population and a more concentrated dose to those in petrol refineries, depots and service stations and high traffic areas. A screening project Lead-Free study in India sponsored by the George Foundation conducted a nationwide epidemiological study in India in 1997. Most of the cities selected for the study have high density populations where leaded petrol contributed to environmental Pb. The subjects selected were on random basis, preschool children and toddlers, slum children, children from low income groups, pregnant women and high risk adults. Initial screening for zinc protoporphyrin (ZPP) and blood Pb levels were adopted. In most cases ZnPP was higher than 35 mg/dL. 34% of the children had blood Pb levels of 10 mg/dL or higher.
Lead levels in food samples from Ahmedabad were found to range from 0.55-2.5 mg/gm in food grains, vegetables, fruits and cooked food (Pandya et al, 1983). Srikanth et al (1995) suggested that rice could be a source for higher lead intake in South Indian rural population while comparing the intake among different socio-economic groups.
In a survey by the Indian Council of Medical Research, a total of 198 samples of 20 brands of infant formula milk were collected from retail shops in and around Pune, Mumbai, Mysore, Lucknow and Ludhiana, and analysed for pesticides and metals. The study indicated high levels of metal contamination (As, Cd, Pb, Cu and Zn (ICMR, 1993).
Pb levels in most of the water sample collected from various sources and sites in India (Kaphalia et al, 1981) interestingly showed lead levels within permissible limits, from roadside urban water supply in Lucknow and Kanpur (Seth et al, 1975) to water samples from various sites of Yamuna (Israili and Khurshed, 1991) and Ganga rivers (Israili, 1991). However, higher Pb concentrations in submerged plants and fish from various sites of the Ganga river were observed only in downstream sites and in fish collected at Kanpur (NEERI, 1987). Monitoring of natural waters is important particularly in highly industrial areas. The waters of Vasai Creek (Thane, Maharashtra) carry a toxic heavy metal burden from an estimated major 18 industries which collectively release about 7 tonnes of Pb per year (Lokhande and Kelkar, 1999).
Lead content of some tap water samples in Nagpur, ranged between 0.006-0.011 mg/L (Hasan and Pande, 1978). There have been negative findings or low concentrations of Pb in Lucknow’s water supply which may be due to limited Pb in the water distribution or water that does not dissolve Pb due to hardness or alkalinity. More organised and systematic sampling of water is yet to be done. Lead has been found in the blood and milk from urban Indian cattle and buffaloes (Dwivedi & Swarup,1995; Dey & Swarup, 1996). Lead levels in bovine milk samples were significantly higher in industrial areas and those areas adjacent to highways compared with rural areas (Bhat & Krishnamachary, 1980; Bhatia & Choudhury, 1996). Milk collected from heavy traffic area contained 4.6-7.2 ppm of Pb, much higher than the permissible limit (0.3 ppm) of FDA. Pb was found in the maternal and umbilical cord blood, amniotic fluid and placenta of cows and buffaloes which caused damage to the placenta leading to fetal death (Kaur, 1989). An unexpected mortality of more than 300 cattle near a Pb reclaiming factory is attributed to toxic levels of metals in the body (Dogra et al, 1996). Investigations carried out during the 1980s in Pb mining areas of Andhra Pradesh indicate the prevalence of neurological disease in cattle due to Pb poisoning. The consumption of milk from affected cattle or the consumption of crops raised in these areas could be dangerous to humans (Bhat & Krishnamachary, 1980; Behari et al, 1986).
The shed skins of cobras and scales of wall lizards collected from heavily polluted urban area in Punjab contain Pb (Kaur, 1988) which is an indicator of environmental pollution.
Many of the above at random studies have inadequate statistical design and lack of proper controls, defects in analytical procedures especially matrix correction and possible errors in sample processing could not be ruled out . Although in a few cases attempts have been made to correlate the observed levels with sources or effects.

5.1 Non-conventional Exposure

Besides occupational and environmental exposures, there are certain non-conventional sources of lead exposures as described below:

  1. Foods or beverages stored cooked, or served in brass utensils with tinning, in lead glazed ceramics or porcelain, leaded crystal or glass, or cans with Pb soldering,
  2. Food contaminated with lead pigments or contaminated spices or colours during festivals.
  3. Bone meal calcium products.
  4. Certain ayurvedic medicines and cosmetics including surma, kohl, sindoor.
  5. Painted buttons or hair ornaments.

Potential sources of lead exposure other than occupations may vary within and between countries. In India for example, the use of cosmetics and herbal medicines containing Pb is also a source of exposure, in Mexico it is Pb for glazing pottery, and Pb solder in grinding stone of flour mills in Egypt. Therefore, in order to develop integrated programmes to control important sources of lead, it is essential to conduct more epidemiological studies to define sources better and to assess their relative importance.
In a small survey conducted by van Alphen (1999) in Indian paints, it was observed that the lower lead concentration paints are the white, blue, and brown-red paints, while in order of increasing lead concentrations are the green, red, orange and yellow paints. Of the 24 samples analysed, 17 had Pb concentrations exceeding 0.5% Pb by weight, 13 had >10% whereas 5 exceeded 10% Pb.
A 10 year survey of coloured foodstuff in U.P. revealed the use of 5 non-permitted colours containing Pb levels higher than permissible levels (Khanna et al, 1976). Some Indian paint samples tested had Pb concentrations exceeding 1% by weight, the pigment present was mostly lead chromites. Weathered lead chromate paints are toxic when ingested and have been eliminated from sale in developed countries since 1960s and 1970s. Use of white Pb (Pb(OH)2.2PbCO3) and red lead (Pb3O4) pigmented paints needs to be evaluated. While in US lead in paint had been a key source of child Pb exposure, it is not the case at present in India which could be due to the higher cost of leaded paints than alternatives.
Other sources of poisoning identified is the migration of lead from food containers. A study has reported the re coating of the inner surface of brass utensils with a mixture of Pb and tin, (“tinning”), this is widely practiced by artisans in India. The Sn-Pb alloy contained 55 to 70% lead levels, and water containing tamarind had 400-500 ug Pb/L after boiling for 5 min. Such acidic foods can leach out Pb. Lead leaching from Indian pressure cookers while cooking especially from the rubber gasket and safety valve, are minor sources of Pb concentration of cooked food (Raghunath and Nambi, 1998).
Human uptake of trace metals from foods varies geographically depending upon the dietary habits (Louenkari and Salminen, 1986) and life style. Regular consumption of alcoholic beverages also shows significant elevation of blood Pb in population not occupationally exposed to lead (Hense et al, 1992, Newton et al, 1992).
The provisional tolerable weekly intake for lead in adults, according to FAO/WHO (1984) is 50 mg/kg body weight or 3 mg/.week for a 60 kg adult. In India, the prevention for adulteration act (PFA, 1990) does not mention or recommend any permitted lead level in alcoholic beverages. In a study carried out by Srikanth et al (1995) majority of the brands of beer in India had Pb concentration of over 10 mg/L (with a mean of 13.2 mg/L). Mean Pb concentrations were found to be slightly higher than beer Pb concentration of U.K. While evaluating the genotoxic effects of a double exposure to alcohol and Pb in subjects from the printing industry, an increase in the frequently of chromosome aberrations and sister chromatid exchanges in individuals exposed to Pb was found, although not significant (Rajah and Ahuja, 1996). A study on occupational and lifestyle determinants of blood Pb levels in Chennai, India is reported in detail (Potula and Hu, 1996). Such studies even though limited have importance in risk assessment and mitigation.
Pb contamination of food could occur through the depositon of Pb petrol emissions or the use of Pb arsenate pesticides or fertilizers contaminated with Pb and other heavy metals. Particularly at risk are root vegetables grown in contaminated soil, leafy vegetarian exposed to Pb dust, food stored, cooked, reheated or served in pots “tinned: with a Pb-Sn mixture or ceramics using Pb glazes. Drinking water also may be a source of Pb. Lead pipes and corrosion of Pb plumbing material (“safeda”) in the water supply or houshold plumbing eg, lead and PVC piping, lead soldered joints in copper and brass faucets and other fittings.
Folk and herbal remedies from India have been found to contain high concentration of heavy metals and unsupervised treatment has resulted in toxicity. A patient with hepatitis was found to have lead poisoning where the source was traced to herbal medicines he had been taking for diabetes (Keen et al, 1994). A Western European developed severe anemia after ingestion of several ayurvedic drugs obtained during a trip to India. Laboratory findings showed high Blood Pb, urinary Pb concentrations and an increased urinary excretion of delta aminolevulinic acid (ALAD) (Spriewald et al, 1999). Some ayurvedic medicines containing lead are given in Table 5.

Table 5: Levels of lead in ayurvedic medicines

MedicinePb (mg/g)
Saptamrut loh5.12
Keshar gugal2.08
Punarvadi gugal1.99
Trifla gugal4.18
Bala goli25
Kandu 6.7
Trivanga bhasma261200.0
Diabline bhasma37770.4

(Modified from: Nambi et al, 1997 and JAMA report, 1984)

Surma and Kohl is an example of the use of Pb as an eye cosmetic or medicine. Surma is available as fine powder or heavy crystal mineral PbS containing 34-92% Pb w/w (Nir et al 1992; Parry and Eaton, 19910. In some market samples, adding take and other ingredients may reduce the Pb content to 1% (Gogte et al, 1991). In a study on Indian and Pakistani children using leaded eye cosmetics, 13 mg/dL mean Blood Pb level was reported compound to 4.3 mg/dL for those not using such cosmetics (Ali et al, 1978; Abdullah, 1984; Sprinke, 1995). Several studies have associated increased Blood Pb with the use of surma although studies conducted in India did not find any such links (Gogte et al, 1991; Awasthi et al, 1996). However, before concluding that this source is harmless, more detailed study is required in India which would help clarify the risk from this cosmetic. Also, the study cases are not subjected to long term followup.
Owing to the close association and common environment shared with humans, dogs are exposed to similar pollutants and have been suggested as sentinels for biohazards and for toxic pollutants (Berny et al 1995). The use of dogs as sentinels for environment quality in India was indicated by a study (Swarup et al, 2000) where considerably higher values for rural dogs (19.5±2.1 mg Pb/dL) were observed. Studies performed on dogs elsewhere too indicate that dogs can be used to monitor environmental quality of lead and cadmium as dogs exposed to these pollutants in urban areas had higher blood metal levels than their rural counterparts (Puls, 1994).

5.2 Kinetics and Metabolism in Humans

Lead has unique properties, it is persistent and accumulates where it is deposited. Lead may accumulate in the body over decades and is stored in the bones and teeth. Young children absorb it more than adults (42-48% and 8-10% respectively).
Particles between 10-70 mm diameter are commonly generated by mechanical or hand sanding and particles <40 mm are invisible to the naked eye. Fine lead dust particles smaller than 100 mm are of particular hazard to children because: they adhere more strongly to the skin they are more soluble in the gastrointestinal tract than coarser particles. Those <10 mm diameter can be readily absorbed through the respiratory tract.
Once absorbed, Pb is not homogeneously distributed throughout the body there is rapid uptake by blood and soft tissues, followed by slower redistribution to the bones. Blood Pb levels are used as a measure of body burden and absorbed doses of Pb. The half life for Pb in blood is 25-36 days but much longer in the bones (Fig. 1).

6. Effects on Humans

Lead exposure can result in a wide range of biological effects depending upon the level and duration of exposure. Occupational Pb exposure is mostly unregulated in many developing countries and little monitoring of exposures is conducted. Pb fumes and dust generated from small domestic lead scrap smelters, which are typically located within close proximity to homes, pose an exceptional health hazard to children and adults living near these operations. Other occupations where women and children are at particular risk include battery manufacturing, welding, pottery and ceramic ware production, small businesses repairing automobile radiators and artisans producing jewellery and decorative wares, papier mache workers.
The neurotoxic effects of Pb in experimental models has been extensively investigated over the last two decades. Incidence of high biliary concentration of some heavy metals including Pb may be a factor in the carcinoma of the gall bladder (Shukla et al, 1998). Populations are defined as sensitive according to intrinsic (age, sex, and genetic) and extrinsic (external exposure sources) factors or a combination of the two. Thought to be the most serious diseases of the environmental and occupational origin, lead toxicity affects the most sensitive subpopulations – infants, children fetus (via maternal exposure) and pregnant women, all of whom are at risk to the subtle adverse health effects of chronic low dose Pb exposure. Adolescents, especially carriers of porphyria genes are at a high risk to lead toxicity (Calabrese, 1978). In India, so far there has been no evidence of any genetically predisposed high risk groups vis a vis lead. By incorporating genetic markers like G-6-PD deficiency, ALAD variations, porphyria gene proteins, etc. into epidemiological studies, such persons could be identified.

6.1 Pregnant Women

Exposure to lead is of special concern among women particularly during pregnancy. Lead absorbed by the pregnant mother is readily transferred to the developing fetus (Buchet et al, 1978; Ong et al, 1985). Human evidence corroborate animal findings (Sierra & Tiffany-Castiglioni, 1992; Corpas et al, 1995; Oberley et al, 1995), linking prenatal exposure to Pb with reduced birth weight and preterm delivery (Andrews et al, 1994) and with neurodevelopmental abnormalities in offspring (Huel et al, 1992). In the developing countries, no such data is available. Deficiency of calcium, iron or zinc facilitate intestinal absorption of lead and also help in mobilising it from bones during pregnancy and lactation (Silbergeld, 1991). These nutritional and concomitant exposures play an amplification factor in lead toxicity (West et al, 1994; Bogden et al, 1995; Kristensen et al, 1995). Pregnant women can recirculate previously stored lead if they had Pb poisoning as children or have recently been exposed to Pb, or have accumulated Pb in bone stores through repeated exposure (Jacobssen et al, 1993; Rothenberg et al,1994). When the body demands more calcium for the developing fetus, it mobilizes Ca out of the bone, carrying Pb with it. A similar process occurs when the body demands more Ca during lactation (Mahaffey, 1991).
In combination with poor nutrition, infectious diseases and other disadvantages associated with poverty, the exposure to Pb threatens the normal development of children. There is ample data showing high concentrations of Blood Pb in the Indian population in various cities (Annapurna et al, 1985; Raghunath et al,1999) including female teachers (Parikh, 1990) and pregnant women (Awasthi et al, 1996; Saxena et al, 1994). A mean Blood Pb of 22.52 mg/dL was observed among pregnant women with various adverse outcomes such as preterm delivery, still birth, and spontaneous abortion (Saxena et al, 1994). A strong correlation has been observed between the maternal and cord blood Pb levels in a study carried out in Mumbai (Raghunath et al, 2000). Prenatal exposure to Pb, though low (5.1 mg/dL) was approximately 2-3 times higher than in some of the developed countries.
In a study conducted in Lucknow, mean maternal blood lead level was observed to be significantly higher in cases of abnormal delivery (22.5 mg/dL) compared to normal delivery cases (19.4 mg/dL). No significant difference in placental cord blood and foetal membrane lead levels was observed in normal and abnormal deliveries (Saxena et al, 1994).

6.2 Children

The WHO estimates that 15-18 million children in developing countries are suffering from permanent brain damage due to lead poisoning, and several millions of children and pregnant women in practically all the developing countries are exposed to elevated levels of lead (Bandyopadhyay, 1999). Intensity of Pb poisoning in children can be classified on the basis of Blood Pb levels (Table 6).

Table 6: Pb Poisoning Symptoms in Children

Intensity of poisoningBlood Pb levels
Moderate>45 mg/dL
Severe55-70 mg/dL
Medical Emergency >70 mg/dL or more

In preschool children, lead is frequently ingested through placing hands, toys and other objects, and dust or soil on those objects into their mouths. This hand to mouth behaviour is normal in pre-school children, but in an environment contaminated with Pb, in soil, household dust and paint, it poses serious threats.
Lead has been implicated in a number of health effects, ranging from severe encephalopathy and death to subtle effects on IQ (Needleman, 1996). Whereas gross pathological changes in the central nervous system may not be evident until a child’s blood level reaches 100 ug/dL, levels approximately one order of magnitude lower, or 10 mg/dL, are considered to place a child at sufficient risk of subtle developmental deficits to justify aggressive screening programmes (Bellinger, 1998). Currently, the Centre for Disease Control and Prevention (CDC) also define blood lead (Blood Pb) levels in children as elevated if they exceed 10 mg/dL.
Bone lead stores resulting from past exposures represent an endogenous or internal source of lead so that even if, exogenous exposures incurred at age 2 years are reduced, lead residing in deeper compartments can potentially be mobilized, maintaining exposure of sensitive target organs such as the CNS (Bellinger, 1998).
A correction between blood lead of children and air lead reveals that the Blood Pb in children could increase by 3.6 mg/dL for an incremental rise of 1.0 mg Pb/m3 of air (Tripathi et al, 2001).
Simple enumeration of children with overt intoxication, encephalopathy, or death from Pb exposure does not reflect the entire spectrum of biologic effects of lead. Among most insiduous effects of Pb is its effect on developing nervous system, with even low level Pb exposure, as measured by a decrease in the IQ of children (Grant and Davis, 1989). Children with elevated (>30 mg/dL) lead levels and pica exhibited fine motor dysfunction impaired concept formation, and impaired behaviour compared to subjects without pica (Kumar et al, 1998).
In a study on children directly exposed to lead through their nature of occupation, 35% children working in petrol bunks had high Blood Pb levels (>35 mg/dl), 17% engaged in bangle making industry had >30 mg/dL, and in pica eating children 47% had Blood Pb levels around 29 mg/dL (Dinesh and Krishnaswamy, 1999). In India and other countries where traditional medicine and food is very popular, it is very difficult to identify the source of Pb exposure. Parents often give these substances to their children and infants as a tonic to help their growth and development or as a medicine to treat them for minor illnesses.
Those categories of children who were exposed to Pb directly or through their nature of occupation were screened in a study carried out by NIN (1992-93). The mean blood Pb levels were found to be as follows: more than 35% children working in petrol bunks had blood Pb levels above 35 mg/dL; 17% of the 55 children engaged in bangle making industry had mean blood Pb levels more than 30 mg/dL; and in pica eating children 47% had about 29 mg/dL blood Pb levels.
In another study by NIN (1995-96), children were screened to assess the extent of Pb toxicity after some reports of cattle population deaths in Western India. Children living within the vicinity of 0-5 km of an industry engaged in preparation of packing material, the man Blood Pb levels were 35.2% mg/dL with some clinically symptoms of Pb poisoning as compared to children living further away (23-28 mg/dL).

6.3 Clinical Manifestation

Lead has been shown to have many clinical and biological manifestation. Increased levels of serum erythrocyte protoporphyrin and increased urinary excretion of copropophyrin and d–aminolaevulinic acid are observed when Pb B concentrations are elevated. Inhibition of the enzymes d–aminolaevulinic acid dehydratase and di hydrobiopterin reductase are observed at lower levels. The effects of lead on the hemopoietic system result in decreased haemoglobin synthesis, and anemia has been observed in children at PbB concentrations above 1.92 mmol/litre (40 mg/dL). For neurological, metabolic and behavioural reason, children are more vulnerable to the effects of lead than adults. Lead has been shown to be associated with impaired neurobehavioural functioning in children. Electrophysiological parameters have been shown to be useful indicators of subclinical lead effects in the CNS. Peripheral neuropathy has long been known to be caused by long term high level lead exposure at the workplace. Slowing of nerve conduction velocity has been found at lower levels. These effects have often been found to be reversible after cessation of exposure, depending on the age and duration of exposure.
Lead is known to cause proximal renal tubular damage, characterized by generalized aminoaciduria, hypophosphatemia with relative hyperphosphaturia and glycosuria accompanied by nuclear inclusion bodies, mitochondrial changes and cytomegaly of the proximal tubular epithelial cells. Tubular effects are noted after relatively short term exposures and are generally reversible, whereas sclerotic changes and interstitial fibrosis, resulting in decreased kidney function and possible renal failure, require chronic exposure to high lead levels. The reproductive effects of lead in the male are limited to sperm morphology and count. In the female, some adverse pregnancy outcomes have been attributed to lead.

6.4 Nutritional Factors and Pb Toxicity

Iron deficiency among children predisposes them to increased lead absorption thus aggravating further the detrimental effects of Pb as observed in a screening study of children carried out in Jammu city (Kaul, 1999) where there was an underlying high prevalence of iron deficiency. These children showed an increase in mean blood Pb and erythrocyte protoporphyrin (EP) levels from those in 1985; the percentage of children with higher levels of blood Pb and gt; 10 mg/dl having significantly increased. Only 33% of the children were below 10 mg/dL quot normal and quot threshold levels and 50.5% were 10-19 mg/dL, an increasing level of concern. The remaining 16.5% were in the medical intervention Pb poisoned levels between 20-87 mg/dL with corresponding EP levels between 29-160 mg/dL. Studies have shown that the consumption of certain nutrients in the diet including minerals such as Ca, P, Fe and Zn and vitamins such as vitamin C, E and thiamine can reduce absorption of dietary lead in children (Sonawane, 1999). Nutritional prophylactic studies are needed so that the exposed children can get the benefits.

6.5 Occupational Exposures

Among approximately 50,000 people residing in the vicinity of a Pb factory that produced lead ingots and lead alloys, many people especially children were affected by lead toxicity (Chatterjee and Banerjee, 1999). In employees working in various automobile garages, blood Pb levels were elevated (40.9±29 mg/dL) coupled with 4-7 fold elevated enzymuria. In 36% of these employees, some clinical symptoms were also observed (Kumar and Krishnaswamy, 1995). Small scale foundries, secondary lead smelters and Pb storage batteries are sources of Pb exposure in urban slum children in Mumbai (Shenoi et al, 1991).
Indian silver jewellery workers are exposed to high concentrations of Pb vapours in their work environment (heating silver with Pb at high temperature). They are exposed for 4-6 hrs a day without proper ventilation causing Pb poisoning (Behari et al, 1983; Flora et al, 1990) which was confirmed through clinical, hematological examinations and urinalysis (Kachru et al, 1989). Silver jewellery makers were found to have a mean blood lead level of 121 mg/dl, compared to non exposed controls with a blood lead level of 27 mg/dl. Lead exposure was assessed in a random cohort of male papier mache workers and compared with age and sex matched controls. Blood Pb levels in workers were significantly higher than in controls (Wahid et al, 1997).
Gasoline station attendants, dispensing leaded petrol to vehicles in hot summer months could aggravate inhalation of Pb also. In a study on 130 traffic constables, 60 bus drivers and 20 auto mechanics in Madras, who constantly inhaled Pb polluted air, the workshop personneal were observed to have the highest blood Pb concentrations, followed by bus drivers and traffic policemen (Green File, 1993; Potula & Hu, 1996).

7. Biomarkers for Monitoring/Screening

There is a growing consensus that Pb causes toxic injury to humans at a level of exposure that was considered safe only a decade ago. The major symptoms of Pb poisoning are not observed at prescribed safety limits of Blood Pb levels (10 mg/dL). Chronic exposure to Pb, even at very low levels, leads to slow, progressive, and most of the time, irreversible damage to the hematopoietic, nervous, and renal systems (WHO, 1986; Silbergeld, 1997). The diagnosis based on Blood Pb levels does not always give an accurate estimate of the total body burden of Pb, duration of exposure, and extent of sub-clinical toxicity which is more common than acute Pb toxicity. Therefore it is important to detect subcellular damage with the help of reliable and sensitive biochemical markers for early organ damage. Decreased erythrocytic delta amino levulinic acid dehydratase activity (ALAD) and increased urinary excretion of renal tubular lysosomal enzyme N-acetyl-B-D glucosaminidase (NAC) are sensitive indicators of early hematopoietic and renal toxicity respectively. Biomarkers in various biological media exposed to lead (Table 7).

Table 7: Biomarkers in tissues exposed to Pb

Biological media


Body fluids and tissues
(hair, nails and teeth)
Red blood cellselevated erythrocyte protoporphyrin;
delta-aminolevulinic acid dehydratase,
Blood Lead; zinc protoporphyrin
UrineLead, coproporphyrin

Studies of prenatal blood lead levels as predictors of future neurologic and behavioural development of the fetus and child are of increasing interest (Buchet et al, 1978; Huel et al, 1992). The use of Blood Pb level data has its own problems for it indexes recent rather than long term exposure, hence is not an ideal biomarker. The amount of Pb stored in the tooth provides an index of cumulative exposure. Although blood Pb is considered as an early indicator of the Pb exposure, Pb concentration in teeth and hair have been used as an indicator of long term exposure. Tissues that store Pb have an advantage of reflecting the total burden over finite time thereby offering a practical way of determining exposure. Pb is deposited in bones and teeth of which teeth having an advantage over bones as biopsy tissues; they are easy to collect and are physically stable.
Now lead can be quantified in the mitochondrial cristae by electron microprobes coupled with immuno electronic microscopy. More specific biochemical screening methods are being used by a toxicologists such as, protein kinase variants, nitric oxide, interleukin 4 (IL4) and autoantibodies in plumbism apart from gross changes stippling of erythrocytes or inhibition of amino levulinic acid dehydratase (Nag et al, 1996).
Development of biomarkers of Pb exposure has been vigorously pursued since Pb is a significant neurotoxicant. Measurement of lead in bone has been adopted as an indicator of cumulative Pb exposure, and also as a source of body lead burden that can be mobilized into the circulation. X-ray fluorescence (XRF) is used to measure skeletal lead to assess cumulative exposure. Pb in blood and bones has a clearance half time of 30 days and 15-30 years respectively (Links et al, 2001).
A molecular epidemiological approach aimed at earliest and minutest exposure and effect has to be developed and practiced. For this, the conventional methods have to be supplemented with non invasive analysis through various scanning systems and using specific molecular probes like PKC variants, glass fibre acidic proteins etc.

8. Societal and Economic Impacts

Environmental costs are partly measured in terms of health costs occuring due to growing environmental pollution. India is spending about Rs 4660 crores every year to make up for health damages caused solely by ambient air pollution (Agarwal et al, 1999). The economic disease burden can be expressed not only in costs of treatment but also in quantifying the loss of productivity.
Studies conducted at NIN, Hyderabad reveal that exposure to low levels of lead cause organ directed toxicity especially impairment of hemoglobin synthesis and renal dysfunction (NIN, 1995-96). While children in general are particularly vulnerable to Pb toxicity, ill health is aggravated among those socially and economically deprived. For, the poor live in squalor and unhygienic conditions near industries and heavy traffic, are malnutritioned and exposed to lead dust brought home by lead workers thus making them more susceptible.
Children who are probably asymptomatic and identifiable only by screening (due to low level Pb exposure) may be constituting a large percentage. This would be directly proportional to a lot of human potential being wasted away ultimately leading to society’s loss. This could be an entirely preventable condition if proper strategies are worked out as in the developed world.

8.1 Treatment Strategies

There is ample evidence that vitamins, essential minerals and trace elements play a preventive role in reducing lead poisoning in humans (Calabrese, 1978) and animals (Flora et al, 1982; Flora & Tandon, 1990). Considerable research has been directed towards investigating whether ascorbic acid could prevent lead toxicity in animal models (Flora and Tandon, 1986). In a study it was observed that depletion of vitamin C and associated decline in heme synthesizing enzymes could be responsible for impaired drug metabolism found in lead exposed animals (Vij et al, 1998). From this study a conclusion was drawn that either lead interferes with the bioavailability of antioxidants like vitamin C and thiol compounds or exacerbates its demand in the body and that even self synthesizing species like rats under toxicant stress, are benefited by exogenous supplementation of vitamin C which by its sparing effect on sulfhydryl could confer protection against toxic insult.
A pilot study on mono-castors suggests that the daily administration of thiamine (50-100 mg) not only restored 30-50% of the basal ALAD activity and reversed the urinary NAG activity, but also reduced blood Pb levels by 25-30% in a span of 9-10 month (Kumar et al, 1994). Thiamine, which is non toxic and economically viable, may be recommended for prevention/treatment of the toxic effects of Pb. It is not clear, whether the effect is through Pb chelation or enhanced metabolism. Eversince milk supplementation of lead paint workers was suggested a century back, the benefical effect of Ca and proteins against Pb was known.
Pb exposure is usually asymptomatic below 45 mg/dL in children and 60 mg/dL in adults (Table 8). If a person has an elevated body burden of a metal, then administration of a chelating agent should cause a short term increase in the urinary excretion of the metal. The most commonly used chelation challenge test has been Ethylenediamine tetraacetic acid (EDTA) administration following lead exposure. The clinically recommended form is calcium disodium salt of EDTA although British Anti Lewisite and penicillamine have also been used. Oral therapy with D-penicillamine for 7 days led to significant improvement in patients (Kachru et al, 1989). More recently, attention has focussed on dimercaptosuccinic acid (DMSA) or succimer, approved chelating agent for the treatment of pediatric lead toxicity. DMSA induced excretion of Pb peaks within 2 hrs and since it acts quickly DMSA chelation challenge could be a convenient, safe approach to assessing the biological burden of lead. Drug treatment with succimer lowered blood lead faster than placebo but treating lead exposed 2 year-olds did not improve scores on psychological, behavioural and IQ tests in followups until age 5 years (Rogan, 2001).

Table 8: Normal ranges for reporting Pb

Lab testNormal range
Blood lead0.30 mg/dL
Urine lead 0-50 mg/dL
Liver lead 0.21-0.55 mg/g
Kidney lead0.1-0.6 mg/g
Urine coproporphyrin0.04-0.26 mg/L
[Source: Colgrove et al, 1984]

Venous blood samples should be used to determine treatment, blood Pb levels being the reflection of poisoning. 60 mg/dL is the Indian standard for danger level requiring chelation therapy and 40 mg/dL is the return level and acceptable limit to resume work. Lead encephalopathy is a medical emergency and requires prompt diagnosis and treatment. Acute signs include coma, seizures, bizarre behaviour, ataxia, apathy, incoordination, vomiting, alteration in consciousness, and subtle loss of recently acquired skills (Piomelli et al, 1984). One or more of the above signs and a blood lead concentration of 70 mg/dL or higher are sufficient for diagnosis. At 50 mg/dL blood Pb poisoning can produce the following symptoms: decreased play activity, lethargy, anorexia, sporadic vomiting, intermittent abdominal pain, and constipation. Currently the Centres for disease control and Prevention (CDC) define blood Pb levels in children as elevated if they exceed 10 mg/dL. There is an urgent need for devisory a standard protocol for diagnosis and treatment of human cases of chronic Pb poisoning.
Policies for prevention and elimination of childhood lead poisoning should focus on identification and treatment of Pb poisoned children through increased childhood lead screening and follow up by medical practitioners and public programmes. Lead exposure could be decreased by reducing environmental sources of Pb. Preventing Pb exposures is of paramount importance because Pb is significantly toxic at subclinical levels, and treating patients elevated blood levels is different. Public Health measures must continue to be directed at the reduction and prevention of exposure to lead by reducing the use of lead and lead compounds, and by minimizing lead containing emissions, that result in human exposures.

9. Prevention and Intervention Strategies

A whole hearted effort is required for the implementation of a comprehensive programme to eliminate Pb poisoning.

For better understanding and control for the low dose health effects of lead the major needs are:
  1. Better and less expensive measurement techniques for both research and screening.
  2. Better understanding of the molecular basis of toxicity
  3. Avoid Pb based pipe fittings for water especially soft or acidic water.
  4. Better techniques for abatement and treatment of lead intoxication.
  5. A longitudinal study is needed for monitoring the human foodchain.
  6. Rigid QA/QC programe to be followed by labs.

    10. Conclusions

    It is clear from the foregoing that exposure to lead from occupational and community environment, contaminated food and consumer items, and water is of major concern. Apart from these, buildup of Pb in the environmental compartments is still an issue of high exposure risk in India inspite of the relatively lesser organised production and use of Pb as compared to the developed countries. The cottage industries engaged in lead acid batteries, scrap, smelting and refining of non ferrous etc. dotted in urban slums make it difficult for the authorities to implement mitigation programmes of environmental Pb poisoning in India. The Pb exposure is not confined to certain hot spots alone, such as high traffic zones, industrial complexes or urban slums but is manifested almost throughout the country. Though generally the environmental levels are reasonably within the prescribed limits and classical cases of lead poisoning are rare to find, it is the subtle, chronic low-dose long term exposure which is of concern. Efforts in the direction of detection and analysis of Pb in various matrices, as a function of human exposure and earliest effects, is a priority need. Hence, it is essential to have standard operating procedures from sampling to analysis which ought to be uniformly used aided by lesser invasive techniques and specific biomarkers. Similarly, runoffs from hazardous solid wastes or dumping sites, dry river bed agriculture zones, polluted drinking water sources in acidic soil zones have to be identified and lead emissions controlled.
    The issue of traditional medicines and cosmetics containing lead have been examined and regulated but acceptable limits are yet to be fixed. Prioritizing identification, monitoring of sources and implementation of regulatory norms is the need of the hour. There has been a ban on leaded gasoline and change of technology in the printing sector initiating a considerable decline in lead burden as reported from developed countries. But in India, other sources like battery use is on the rise as an alternative to frequent electricity failures. The Pb emission standards are not fully implemented in the small scale/cottage/traditional industries, which lead to pockets of high Pb levels.
    Food processing has become a high technology organised industry where domestic and export norms are practiced but the raw material, that is the horticultural/agricultural produce, has to be of quality so that the major export commodities like sea foods, rice, tea, spices, and crude herbal drugs could meet user country standards. Hence, corrective measures to clean up soil along with prevention of further releases have to be implemented.
    The influence of nutritional factors have been well studied in India and gross protein and calorie malnutrition is being taken care of in the country with the help of several nutritional programmes being carried out by government and non government organisations. However, persons suffering from iron deficiency and other forms of anaemia could continue among the weaker strata who are most vulnerable, need to be protected from Pb toxicity.
    A lot of international data are available on childhood exposures and brain functions but only a beginning has been made in India. Well designed surveys are required in different parts of the country preferably including effects of seasonal variations. Any correlation between background levels in various environmental compartments and food, with that in blood and brain, and IQ levels should be found out although lead in tissues and umbilical cord blood has been correlated to air Pb levels in some studies. Once the early toxic effects are detected before the onset of irreversible changes, the potential victims can be saved. Thus, lead poisoning is preventable and with proper concerted efforts a lead-free society can be envisaged.

    Current Status of Lead Poisoning in India

    Farhat N Jaffery

    Exposure to lead from occupational and community environment, contaminated food and consumer items, and water are of major concern in India. Apart from these, buildup of lead in the environmental compartments is still an issue of high exposure risk inspite of the relatively lesser organized production and use of lead as compared to the developed countries. The cottage industries engaged in lead acid batteries, scrap, smelting and refining of non ferrous alloys etc. dotted in urban slums make it difficult for the authorities to implement mitigation programmes of environmental lead poisoning in India. The lead exposure is not confined to certain hot spots alone, such as high traffic zones, industrial complexes or urban slums but is manifested almost throughout the country. The transition from leaded to unleaded gasoline will reduce the lead burden to a large extent but,quantitative data on the impact of this reduction in lead levels and its toxicity are yet to come.Though generally the environmental levels are reasonably within the prescribed limits and classical cases of lead poisoning are rare to find, it is the subtle, chronic low-dose long term exposure which is of concern. Lead has already been quantified on most environmental matrices and biological tissues,sources and exposure routes identified,and most symptoms of occupational and environmental exposures detected. Intervention and restoration efforts are also underway by regulatory agencies.In view of these a critical appraisal of the overall issue of lead poisoning in India will be attempted.


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