LECTURE
Theme of lecture:
NEUROTOXICOSIS
(MERCURY POISONING. TETRAETHYLLEAD POISONING. MANGANESE POISONING).
INTOXICATION BY LEAD.
І.Mercury poisoning
l Industrial uses.
l Pathogenesis of Mercury poisoning.
l Clinical picture. Diagnosis.
l Treatment.
ІІ. Tetraethyllead poisoning
l Industrial uses.
l Pathogenesis of Tetraethyllead poisoning.
l Clinical picture. Diagnosis.
l Treatment.
ІІІ. Manganese poisoning
l Industrial uses.
l Pathogenesis of Manganese poisoning.
l Clinical picture. Diagnosis.
l Treatment.
LEAD POISONING
l Lead properties.
l Industrial uses.
l Pathogenesis of lead poisoning.
l Clinical picture. Diagnosis.
l Preventive measures.
l Management of lead poisoning.
І. MERCURY POISONING
Mercury has been used commercially and medically for centuries. In the past it was a common constituent of many medications. It is still used in hospitals in thermometers and blood-pressure cuffs and commercially in batteries, switches, and fluorescent light bulbs. Large quantities of metallic mercury are employed as electrodes in the electrolytic production of chlorine and sodium hydroxide from saline. These uses still give rise to accidental and occupational exposures.
Today, however, exposure of the general population comes from three major sources: fish consumption, dental amalgams, and vaccines. Each has its own characteristic form of mercury and distinctive toxicologic profile and clinical symptoms. Dental amalgams emit mercury vapor that is inhaled and absorbed into the bloodstream. Dentists and anyone with an amalgam filling are exposed to this form of mercury. Liquid metallic mercury (quicksilver) still finds its way into homes, causing a risk of poisoning from the vapor and creating major cleanup costs. Humans are also exposed to two distinct but related organic forms, methyl mercury (CH3Hg+) and ethyl mercury (CH3CH2Hg+).
Fish are the main if not the only source of methyl mercury, since it is no longer used as a fungicide. In many countries, babies are exposed to ethyl mercury through vaccination, since this form is the active ingredient of the preservative thimerosal used in vaccines. Whereas removal of certain forms of mercury, such as that in blood-pressure cuffs, will not cause increased health risks, removal of each of the three major sources described in this article entails health risks and thus poses a dilemma to the health professional. Exposure to mercury from dental amalgams and fish consumption has been a concern for decades, but the possible risk associated with thimerosal is a much newer concern. These fears have been heightened by a recent recommendation by the Environmental Protection Agency (EPA) that the allowable or safe daily intake of methyl mercury be reduced from 0.5 μg of mercury per kilogram of body weight per day, the threshold established by the World Health Organization in 1978, to 0.1 μg of mercury per kilogram per day.
Table 1 summarizes the clinical toxicologic features of mercury vapor and methyl and ethyl mercury. It also includes data on inorganic divalent mercury, since this is believed to be the toxic species produced in tissues after inhalation of the vapor. It is also responsible for kidney damage after exposure to ethyl mercury, since ethyl mercury is rapidly converted to the inorganic form. Inorganic mercury as both mercuric and mercurous salts was also the chief cause of acrodynia, a childhood disease that is now mainly of historical interest. The clinical symptoms of acrodynia consist of painful, red, swollen fingers and toes in association with photophobia, irritability, asthenia, and hypertension. It is believed to be a hypersensitivity reaction.
MERCURY VAPOR FROM DENTAL AMALGAMS
Dental amalgams have been in use for over 150 years. They are inexpensive and thought to be more durable and easier to use than other types of fillings. The amalgam consists of approximately 50 percent mercury combined with other metals such as silver and copper. Since their introduction, dental amalgams have been a source of controversy because of the assumed health risks of mercury. The arguments between the protagonists and antagonists have been referred to as the “amalgam wars” and became more heated around 1970 with the discovery that amalgams can release mercury vapor into the oral cavity in concentrations that are higher than those deemed safe by occupational health guidelines. Subsequently, it was realized that the actual inhaled dose was small, owing to the small volume of the oral cavity. Nevertheless, amalgam fillings are the chief source of exposure to mercury vapor in the general population. Brain, blood, and urinary concentrations correlate with the number of amalgam
Higher urinary concentrations are found in persons who chew a great deal. For example, the long-term use of nicotine chewing gum will raise urinary concentrations close to occupational health limits. The removal of amalgam fillings can also cause temporary elevations in blood concentrations, since the process transiently increases the amount of mercury vapor inhaled.
What is the health risk from such exposures? Cases of poisoning from inhalation of mercury vapor have been recognized for centuries. Severe cases are characterized by a triad of intentional tremor, gingivitis, and erethism (Table 1). Erethism consists of bizarre behavior such as excessive shyness and even aggression. Today’s occupational exposures, such as in the dental office, are lower and may lead to mild, reversible effects on the kidney or mild cognitive changes and memory loss. However, urinary concentrations in people with amalgams (about 2 to 4 μg of mercury per liter) are well below concentrations found in people who are occupationally exposed to mercury (20 to 50 μg of mercury per liter) unless they are also excessive chewers. Current concern arises from claims that long-term exposure to low concentrations of mercury vapor from amalgams either causes or exacerbates degenerative diseases such as amyotrophic lateral sclerosis, Alzheimer’s disease, multiple sclerosis, and Parkinson’s disease. Speculation has been most intense with respect to Alzheimer’s disease after a report that the brains of patients with Alzheimer’s disease had elevated mercury concentrations. However, several epidemiologic investigations failed to provide evidence of a role of amalgam in these degenerative diseases, including a long-term study of 1462 women in Sweden, an ongoing Swedish twin study involving 587 subjects, and a study of 129 nuns 75 to 102 years of age, which included eight tests of cognitive function. Nevertheless, in vitro studies have indicated that mercury can affect the biochemical processes believed to be involved in Alzheimer’s disease. The problem is that mercury can inhibit various biochemical processes in vitro without having the same effect in vivo. Patients who have questions about the potential relation between mercury and degenerative diseases can be assured that the available evidence shows no connection. Some will ask whether their mercury fillings should be removed. They should be reminded that the process of removal generates mercury vapor and that blood concentrations will subsequently rise substantially before they eventually decline. There is no clear evidence supporting the removal of amalgams.
METHYL MERCURY
Among humans, the sole source of exposure to methyl mercury is the consumption of fish and sea mammals. Methyl mercury is produced environmentally by biomethylation of the inorganic mercury present in aquatic sediments (Fig. 1). It accumulates in the aquatic food chain and reaches its highest concentrations in long-lived, predatory fish such as swordfish and shark in the oceans and pike and bass in fresh water. Concentrations of mercury in ambient air and water are too low to pose a serious risk to the general population.
EXPOSURE IN ADULTS
Cases of severe, even fatal, methyl mercury poisoning date back to the 1860s in England, when such mercurials were first synthesized. Subsequent cases arose through occupational and dietary exposures. Several large outbreaks were caused by the consumption of bread mistakenly made from methyl mercury–coated seed grain; for example, an outmercury
The Global Cycle of Mercury. Iature, mercury vapor (Hg0), a stable monatomic gas, evaporates from the earth’s surface (both soil and water) and is emitted by volcanoes (Panel A). Anthropogenic sources include emissions from coal-burning power stations and municipal incinerators. After approximately one year, mercury vapor is converted to a soluble form (Hg2+) and returned to the earth in rainwater. It may be converted back to the vapor form both in soil and in water by microorganisms and reemitted into the atmosphere. Thus, mercury may recirculate for long periods. Mercury attached to aquatic sediments is subject to microbial conversion to methyl mercury (MeHg), whereupon it enters the aquatic food chain. It reaches its highest concentrations in long-lived predatory fish, such as sharks. Panel B indicates the routes of transformation to methyl mercury as originally suggested by Jernelov. Panel C depicts the increase in mercury concentrations in feathers of fish-eating birds in Sweden. The period covered by these data corresponds approximately to the growth of industrialization in Sweden. Break in 1971 and 1972 in
The brain is the primary target tissue. Adults present with paresthesias of the circumoral area and hands and feet, followed by visual-field constriction and ataxia. Neuropathological examination reveals regional destruction of neurons in the visual cortex and cerebellar granule cells. There is usually a latent period of weeks or months between exposure and the onset of symptoms.
Several studies have reported statistical associations between cardiovascular disease and mercury, mostly in the form of methyl mercury. One study found a direct relation between mercury concentrations and the risk of myocardial infarction, whereas a nested case–control study of more than 300,000 health professionals found no such association. A third study, from eastern Finland, where the consumption of saturated animal fat is high, found an association, but the authors suggested that their finding might be specific to the region. A fourth study among seven-year-old children on the Faeroe Islands found that blood pressure was increased when the blood mercury concentration was below 10 μg per liter but not when it was higher. “Contrary to expectation,” as the authors stated, “this association occurred within an exposure range characteristic of communities not depending on marine food” such as the United States. They also pointed out that “the average birth weight in this fishing community is the highest in the world and therefore the community may represent a unique setting.” Thus, firm conclusions about cause and effect cannot be yet made, since cardiovascular disease has multiple risk factors (e.g., family history, stress, dietary habits, smoking, alcohol use, diabetes, and socioeconomic status). The researchers themselves recognize this complication and use extensive statistical measures to correct for these factors. Prospective studies are needed to settle this issue.
PRENATAL EXPOSURE
The fetal brain is more susceptible than the adult brain to mercury-induced damage. Methyl mercury inhibits the division and migration of neuronal cells and disrupts the cytoarchitecture of the developing brain. In the past 15 years or so, epidemiologic studies have focused on the effects of prenatal exposure. As a consequence of these epidemiologic data, the EPA reduced the allowable intake of methyl mercury from 0.5 to 0.1 μg of mercury per kilogram per day. This threshold is lower than those used by other regulatory agencies. Moreover, it translates into a weekly consumption of one 198-g (7-oz) can of tuna for an adult. Given that canned tuna is the cheapest and most widely consumed fish in the United States and is approved by the American Heart Association as part of a diet low in saturated fat and cholesterol, the debate over the safety of tuna and fish in general will continue with some intensity.
It is reassuring that the only clinical reports of mercury poisoning from fish consumption are those from Japan in the 1950s and 1960s. The EPA guideline is derived from reports of subtle and small neuropsychological changes in children in the Faeroe Islands study, whose exposure was mainly from whale consumption. A similar study in the Seychelles found no adverse effects from fish consumption alone. The majority of the general population in the United States has levels of exposure well below the EPA guideline, but 8 percent or so have levels that are slightly higher. Although a National Academy of Sciences committee reported that 60,000 children in the United States were at risk as a result of prenatal exposure, they failed to provide any justification or explanation for that conclusion.
Fish consumption has clear health benefits, and the risk posed by exposure to mercury is currently speculative. The Food and Drug Administration has recommended that pregnant women, nursing mothers, and young children avoid eating fish with a high mercury content (>1 ppm), such as shark, swordfish, tilefish, and king mackerel. Because whale meat contains up to 3 ppm of mercury, about half of which is in the form of methyl mercury, consumption of whale meat should also be discouraged.
THIMEROSAL IN VACCINES
Thimerosal has been used as a preservative in many vaccines since the 1930s. At concentrations found in vaccines, thimerosal meets the requirements for a preservative set forth by the U.S. Pharmacopeia — that is, it kills the specified challenge organisms and can prevent the growth of the challenge fungi. It contains the ethyl mercury radical (CH3CH2Hg+) attached to the sulfur group of thiosalicylate and is believed to behave toxicologically like other ethyl mercury compounds. Early toxicity studies found no adverse health effects; recently, however, Ball et al. reevaluated thimerosal by applying the revised EPA guideline for methyl mercury to ethyl mercury. They calculated that infants undergoing the usual U.S. program of vaccines from birth to six months of age would receive more than 0.1 μg of mercury per kilogram per day. Steps were rapidly taken to remove thimerosal from vaccines by switching to single-dose vials that did not require any preservative. This process is now virtually complete in the United States. The decision itself is remarkable, and the speed of execution even more so, however, the EPA guideline is based on epidemiologic data on prenatal exposure to methyl mercury rather than postnatal exposure to ethyl mercury. Ethyl mercury has some similarities to methyl mercury. They are closely related chemically, have a similar initial distribution in the body, and cause similar types of damage to the brain in toxic doses.
They also have differences. Methyl mercury is more potent. Ethyl mercury is metabolized more rapidly to inorganic mercury; perhaps this is why ethyl mercury, unlike methyl mercury, causes kidney damage in humans. Of greater importance is the recent finding that the half-life of ethyl mercury in the body is much shorter. The half-life of methyl mercury in blood, which is assumed to indicate the total body burden, is usually assumed to be about 50 days. In contrast, in children receiving thimerosal in vaccines, the half-life of ethyl mercury in blood was 7 to 10 days, or 1/7 to 1/5 as long as that of methyl mercury. Therefore, in the two-month periods between vaccinations (at birth and at two, four, and six months), all of the mercury should have been excreted, so that there is no accumulation. Given the short half-life of ethyl mercury, any risks of its damaging either the brain or kidneys would seem remote. A World Health Organization advisory committee recently concluded that it is safe to continue using thimerosal in vaccines. This is especially important in developing countries, where the use of a preservative is essential in multidose vials. The known risk of infectious diseases far exceeds that of the hypothetical risk of thimerosal. Claims have been made that thimerosal in vaccines may be a cause of autism and related disorders, but studies testing that theory have yet to be performed. All forms of mercury have adverse effects on health at high doses. However, the evidence that exposure to very low doses of mercury from fish consumption, the receipt of dental amalgams, or thimerosal in vaccines has adverse effects is open to wide interpretation. Moreover, attempts to reduce such exposure may pose greater health risks than those hypothesized to occur from mercury.
Clinical picture.
Acute mercury poisoning occurs rarely. It arises up after contact with large quantities of mercury. The main symptoms of the acute poisoning are hypersalivation, inflammation and formation of ulcers of mucous of the mouth, swelling of salivary glands, increase of submandibular lymph nodes, inflammation of gums, nausea and vomiting, diarrhea, tenesmus, intestinal colic. The signs of respiratory tracts affection appear at the same time (acute bronchitis, pneumonia). Necrotizing nephrosis with acute renal failure often develops. Very often liver, nervous system are affected. In blood: hemolysis, leukocytosis, increase of ESR (to 30-50 mm/h), increase of blood protein, nitrogen.
Chronic poisoning occurs after contact with mercury during 8-10 years. Clinical symptoms of poisoning develop gradually and are characterized by affection of the nervous system. According to the degree of expressiveness of pathological process chronic poisoning is divided into 3 stages: initial (functional), moderate and severe.
Diagnosis. Early typical symptoms: irritability, weakness, gingivitis and stomatitis. Confirmation of diagnosis is mercury determination in urine and feces. Presence of mercury in urine without proper clinical symptoms indicates a “mercury carriage”.
Treatment. To destroy mercury and excrete it from organism antidotes are recommend: Unitiol, Sucsimer, sodium thiosulphate. Most effective is Unitiol (sodium 2,3-dymercaptopropansulfonat) – 5% 5-10 ml (0,05 g or 5% 1 ml per 10 kg of patient’s weight); 1 day – 2-4 injections, next 6-7 days –1 injection/ day. Its sulfhydryl groups form untoxic complexes with poison and are excreted with urine.
ІІ. TETRAETHYLLEAD POISONING
A tetraethyllead (TEL) is an oily transparent liquid which contains a 64,07 % of lead, well dissolves in organic solvents (ether, alcohol, benzol, petrol and other) and in fats. ТЕL is applied as antidetonate. A dangerous contact with TEL may occur at its producing, mixing with a fuel, at cleaning of petrol cisterns.
Tetraethyllead is a strong neurotrop poison.
Acute poisoning: in 1-3 hours after a contact with ТЕL the first symptoms of the acute poisoning appear. According to the degree of expressiveness of clinical manifestations there are three stages of the acute poisoning by ТЕL: initial, preculmination, and culmination.
Chronic TEL poisoning is observed in workers who worked in contact with ТЕL during long period. A clinic develops gradually and can be poorly expressed.
According to the degree of expressiveness of clinical manifestations there are three stages of the chronic poisoning: I-st (initial), II-nd and III-rd.
Treatment.
To wash up skin (with warm water and soap), to make gastric washing, to use absorbents.
Patients with acute TEL poisoning need complete rest, hypnotic medicines from the group of barbituratus (phenobarbital, barbital sodium or etaminal sodium).
At hyperexcitability barbamil (i/m or i/v) or hexenal are prescribed.
hypertensive solution of glucose i/v, Vitamine therapy.
Warm baths are recommended before sleep.
Treatment of patients with the chronic form of TEL poisoning is appointed taking into account expressiveness of clinical manifestations. For such patients drugs which influence on a tissue metabolism (glutamine acid, glucose, vitamins C, B1, B2, ATF, riboxin), tranquilizers (Diasepam, Tazepam) are recommended.
ІІІ. MANGANESE POISONING.
The occupational manganese poisoning occurs among workers who work on the manganese mines, in metallurgical industry at steel making , special alloys producing (ferromanganese – to 80 % of manganese, mirror cast-iron – to 15 % of manganese), at making of electrodes and gumboils which are used for the electric welding, in chemical and lacquer-paint industry, in agriculture (stain of seed for stimulation of plant growth), in rubber industry. Most dangerous is ground and sifting of pound ore, because a lot of small disperse dust of manganese appear.
Into the organism manganese penetrates through the organs of breathing, rarer through a gastrointestinal tract and skin. The oxides of manganese are quickly absorbed. In blood manganese circulates as an unsteady complex with plasma proteins. Manganese is deposited in bones, cerebrum, parenchyma organs. It is excreted from the organism with feces and urine. Manganese may cause bronchial asthma and eczema because of its allergic influence.
Pathogenesis. Manganese, as a microelement, takes part in biological processes of organism. It influences on metabolic processes, depresses cholinesterase activity, affects metabolism of serotonin. At the protracted and systematic getting into the organism it has a direct influence oervous tissue, and causes vascular violations, increase capillary permeability. It changes activity of enzymes of nervous cells, depresses the biosynthesis of catecholamines, intensifies protein metabolism. The action of manganese is divided into two phases.
The first phase – cholinergic – is characterized by predominance of cholinergic influence.
Second phase – phase of areactivity – injury of acetylcholinoreactive structures.
A manganese influences on the function of thyroid, cardiovascular system, gastrointestinal tract, liver and other.
Clinical picture.
Acute poisoning. In industry acute manganese poisoning occurs rarely. It arises up at breathing in a large quantities of dust which contains manganese. Manganese poisoning causes severe disorders of blood circulation, dyspnea, frequent syncopes. In easy cases of poisoning irritation of the mucous of respiratory tracts, cough, and headache are observed.
Сhronic manganese poisoning. Symptoms of chronic intoxication develop gradually, that causes difficulty of diagnosis of the initial stages. The basic symptoms of poisoning are functional violations of central nervous system, which have a tendency to progress and can pass to the stage of organic changes. Affection of the striopallidar system is specific for chronic manganese poisoning, it is characterized by akinetic-stiff syndrome and phenomena of parkinsonism.
Besides neurological symptoms, violations of the cardiovascular system, gastrointestinal tract and liver occur.
Clinical picture of the chronic manganese poisoning is characterized by three stages.
The special feature of clinical course of chronic manganese poisoning is inclination to its progress after stopping contact with a metal.
Diagnosis. Special attention is paid to early diagnosis of chronic manganese poisoning. It’s necessary to find out a professional route, sanitary description of labor conditions (manganese concentration in the workplace, duration of contact during work day, experience of work, influence of other harmful professional factors), to analyse results of biochemical investigations (level of manganese in blood, urine, saliva, milk).
A decline of patient activity, dormancy of psychical processes, insufficient critical relation to the state of organism predetermine the late appeal of patients for medical help.
Treatment: Glucose 40 % + Vit.C (300-500 mg) i/v, vitamin B1 (40-50 mg), 0,25 % novocaine 10-15 ml (15-20 injections). At appearance of Parkinsonism signs it is necessary to prescribe antiparkinsonism cholinolytics (Cyklodol, Norakin, Amedin, Tropacin, tab. “Korbella”).
Tropacinum – is effective antiparkinsonism cholinolytical drug (10-20 mg 1-2 times per a day after meal). “Karbella” decrease tremor and diminish tonus of muscles (1 tablet before sleep).
LEAD POISONING
More industrial workers are exposed to lead than to any other toxic metal. Lead is used widely in a variety of industries because of its properties : (1) low boiling point (2) mixes with other metals easily to form alloys (3) easily oxidised and (4) anticorrosive. All lead compounds are toxic – lead arsenate, lead oxide and lead carbonate are the most dangerous; lead sulphide is the least toxic.
INDUSTRIAL USES : Over 200 industries are counted where lead is used – manufacture of storage batteries; glass manufacture; ship building; printing and potteries; rubber industry and several others.
NON-OCCUPATIONAL SOURCES : The greatest source of environmental (non-occupational) lead is gasoline. Thousands of tons of lead every year is exhausted from automobiles. Lead is one of the few trace metals that is abundantly present in the environment. Lead exposure may also occur through drinking water from lead pipes; chewing lead paint on window sills or toys in case of children.
Lead has multiple toxic health effects—haematological, renal, and neurological—although at typical levels of exposure in the environment, neuropsychological impacts are the main concern, especially for developing children. Aside from local contamination or pollution, exposure to lead has been quite widespread from dissolution into drinking water from lead piping, use of lead in paint in old houses, and airborne exposure from leaded petrol. In addition, people have been exposed via their food from the use of lead solder for sealing cans, although this has now been completely phased out. However, the other sources still lead to exposure. Although the use of lead additive in petrol has virtually ceased, there is still much dust on roadsides from past use and this is resuspended or picked up by children; lead present in paint in older houses remains an important source as it is chipped off through normal wear and tear; again in older dwellings, lead pipes in the home or connecting with the main water supply can be a source, with solubility depending on the chemistry and pH of the water supply. Research into the effects of lead exposure on children’s neurological development measures their intelligence quotient and emotional and behavioural development.
Children are more vulnerable to occupational disease—they are smaller, have the potential to be exposed for many years, and their tissues are more sensitive. They are also more likely to be exploited and, being less aware, more accident prone.
MODE OF ABSORPTION : Lead poisoning may occur in three ways : (1) INHALATION : Most cases of industrial lead poisoning is due to inhalation of fumes and dust of lead or its compounds. (2) INGESTION : Poisoning by ingestion is of less common occurrence. Small quantities of lead trapped in the upper respiratory tract may be ingested. Lead may also be ingested in food or drink through contaminated hands (3) SKIN : Absorption through skin occurs only in respect of the organic compounds of lead, especially tetraethyl lead Inorganic compounds are not absorbed through the skin.
DISTRIBUTION IN THE BODY: Ninety per cent of the ingested lead is excreted in the faeces. Lead absorbed from the gut enters the circulation, and 95 per cent enters the erythrocytes. It is then transported to the liver and kidneys and finally transported to the bones where it is laid down with other minerals. Although bone lead is thought to be ‘metabolically inactive’, it may be released to the soft tissues again under conditions of bone resorption. Lead probably exerts its toxic action by combining with essential SH-groups of certair enzymes, for example some of those involved in prophyrin synthesis and carbohydrate metabolism. Lead has an effect on membrane permeability and potassium leakage has been demonstrated from erythrocytes exposed to lead.
CLINICAL PICTURE : The clinical picture of lead poisoning or plumbism is different in the inorganic and organic lead exposures. The toxic effects of inorganic lead exposure are abdominal colic, obstinate constipation, loss of appetite, dermatitis, blue-line on the gums, stippling of red cells, anaemia, wrist drop and foot drop. The toxic effects of organic lead compounds are mostly on the central nervous system – insomnia, headache, mental confusion, delirium, etc.
DIAGNOSIS. Diagnosis of lead poisoning is based on : (1) HISTORY: as history of lead exposure (2) CLINICAL FEATURES : such as loss of appetite, intestinal colic, persistent headache, weakness. abdominal cramps and constipation, joint and muscular pains, blue line on gums, anaemia, etc. (3) LABORATORY TESTS : (a) Coproporphyrin in urine (CPU) : Measurement of CPU is a useful screening test. Ion-exposed persons, it is less than 150 microgram/litre. (b) Amino levulinic acid in wine (ALAU): If it exceeds 5 mg/litre, it indicates clearly lead absorption. (c) Lead in blood and urine: Measurement of lead in blood or urine requires refined laboratory techniques. They provide quantitative indicators of exposure. Lead in urine over 0.8 mg/litre (normal is 0.2 to 0.8 mg) indicates lead exposure and lead absorption. A blood level of 70 μg/ 100 ml is assosiated with clinical symptoms, (d) Basophilic stiplng of RBC : is a sensitive parameter of the heamatological response.
PREVENTIVE MEASURES : (1) Substitution : That is, where possible lead compounds should be substituted by less toxic materials. (2) Isolation : All processes which give rise to harmful concentration of lead dust or fumes should be enclosed and segregated. (3) Local exhaust ventilation: There should be adequate local exhaust ventilation system to remove fumes and dust promptly (4) Personal protection : Workers should be protected by approved respirators. (5) Good housekeeping : Good housekeeping is essential where lead dust is present. Floors, benches, machines should be kept clean by wet sweeping. (6) Working atmosphere : Lead concentration in the working atmosphere should be kept below 2.0 mg per 10 cu. metres of air, which is usually the permissible limit or threshold value. (7) Periodic examination of workers : All workers must be given periodical medical examination. Laboratory determination of urinary lead, blood lead, red cell count, haemoglobin estimation and coproporphyrin test of urine should be done periodically. Estimation of basophylic stippling may also be done. An Expert Committee of the WHO states that in the case of exposure to lead, it is not only the average level of lead in the blood that is important, but also the number of subjects whose blood level exceeds a certain value (e.g., 70μg/ml or whose ALA in the urine exceeds 10 mg/litre) (8) Personal hygiene : Hand-washing before eating is an important measure of personal hygiene. There should be adequate washing facilities in industry. Prohibition on taking food in work places is essential. (9) Health education : Workers should be educated on the risks involved and personal protection measures.
MANAGEMENT : The major objectives in management of lead poisoning are the prevention of further absorption, the removal of lead from soft tissues and prevention of recurrence. Early recognition of cases will help in removing them from further exposure. A saline purge will remove unabsorbed lead from the gut. The use of d-penicillamine has been reported to be effective. Like Ca-EDTA, it is a chelating agent and works by promoting lead excretion in urine.
