Presentation on theme: "LEAD POISONING By F.Ahmadzadeh occupational medicine especialist."— Presentation transcript:
1LEAD POISONINGBy F.Ahmadzadehoccupational medicine especialist
2Lead is an ancient metal Lead is an ancient metal. Because of its malleability and low melting point, humans have used lead since prehistoric times to make statues, jewelry, water pipes, and drinking vessels.In the mid-1970s, nearly 200,000 tons of lead were consumed annually in gasoline in the United States.Virtually all of this lead was emitted into the environment from vehicles in a finely particulate form and caused widespread contamination of air, dust,soil, drinking water and food crops.
3OCCUPATIONAL LEAD EXPOSURE In the United States more than 3 million workers are estimated by NIOSH to be potentially exposed to leadin their work.Occupational exposure to lead is regulated in the UnitedStates by the OSHA lead standard, first promulgated in 1978.This standard sets limits on air-borne lead exposure as well ason permissible levels of lead in blood.
4Major occupations associated with risk of inorganic lead poisoning
5A major industrial group that previously had been exempted from the protection of the United States leadstandard were construction workers. Major outbreaks oflead poisoning were observed among workers who cut leadpainted steel structures such as bridges with oxyacetylene torches and among renovation workers who remove lead paint from older homes.In 1993, the OSHA lead standard was extended to cover theconstruction and demolition trades.
6Measurement of occupational exposure Assessment of occupational exposure to inorganic leadrequires measurement of lead levels in both air and blood.The OSHA standard (1993) for the permissible exposurelevel of lead in workplace air is 50 micrograms/m3,expressed as an 8-hour time-weighted average .This standard can no longer be considered adequatelyprotective of workers’ health, because lead toxicityhas been observed in workers whose lead exposures donot exceed the current OSHA standard.Fetal lead poisoning can occur in the offspring of female lead workers well below this level .
7Measurement of the blood lead level complements determination of lead levels in air.By the OSHA lead standard, anyone found to have a bloodlead level of 50 micrograms/dl or above must be removed fromthe high-exposure job (termed ‘medical removal protection’).A worker is not allowed to return to a high-exposurejob until the blood lead level has fallen to below 40 µGr/dl.
8ENVIRONMENTAL LEAD EXPOSURE Air:Air lead standard in the United States is 1.5 µgr/m3Motor vehicles were the major contributor of lead emissions to the air (TEL).MTBE (Methyl tert-butyl ether)Ethanol
9and lead paint is a major route of lead exposure in children Some lead compounds are colorful and are used widely in paintsand lead paint is a major route of lead exposure in childrenSoilMay be caused by:broken-down lead paint,residues from lead-containing gasoline,used engine oilPesticides used in the pastfrom nearby industries such as foundries or smelters
10Water1.From the atmosphere or soil ( end up in groundwater and surface water.)2.from plumbing and fixtures (chloramines , which were adopted as a substitute for chlorine disinfectant due to fewer health concerns, increase corrositivity )In the US, 14–20% of total lead exposure is attributed to drinking water .safe drinking water standard for leadis 0.15 mg/l (15 parts per billion).
11Lead-containing products Lead can be found in products such as kohl, an ancient cosmetic.from some toys. In 2007, millions of toys made in China were recalled from multiple countries owing to safety hazards including lead paint.Lead is commonly incorporated into herbal remedies such as Indian Ayurvedic.preparations and remedies of Chinese origin.
12Who is most Vulnerable to the Effects of Lead? In the general population, children are the group most heavily exposed and most susceptible to the toxic effects of lead.
13Exposure to lead can cause behavior problems and learning disabilities in young children and can also affect the health of adults.Imported toys tainted with lead have made news recently. The lead can be both in the paint and in the plastic itself. Sucking or chewing on the toy -- or getting lead on the hands -- can be enough to poison a child.
14The mean blood lead level of children in the United States is about 3 micrograms/dl.A decline of 90% in bloodlead levels occurred amongAmerican children from 1976 to 1997 as a consequenceof removal of lead from gasoline.According to the Centers for Disease Control and Prevention(CDC), blood lead levels of 10 micrograms/dl and higher inchildren indicate excessive exposure.Blood leadlevels of 10 µg/dl and above are associated withsubclinical lead toxicity in children.
16Lead-based paint is the major concentrated, high-dose source of lead for American children. Since 1979, themaximum allowable concentration of lead in domesticpaint has been regulated by the United States ConsumerProduct Agency at 0.06 parts per million.The new dust standard :40 micrograms/ft2 for floors250 micrograms/ft2on window sillsBelow 400 ppm in soil of play areas1200 ppm average for bare soil in the rest of the yard.
18CLINICAL EFFECTS IN ADULTS Acute inorganic lead toxicityIntense occupational exposure to lead over a brief periodof time .Signs and symptomsabdominal colic,constipation,fatigue,hemolytic anemia,peripheral neuropathy,alteration of central nervoussystem function
19gingival lead lineacute encephalopathy with coma,convulsions, and papilledema may occur;
20only fatigue, headache or personality changes may be evident In milder cases :only fatigue, headache or personality changes may be evidentas manifestations of the neurologic toxicity of lead.Mild liver involvement, limited to modest elevations inserum glutamic-oxaloacetic transaminase (SGOT).musculoskeletal pains and arthritic.Basophilic stippling in the redblood cells.(occur in blood lead level 70 micrograms/dl or more)
21Chronic inorganic lead toxicity Signs and symptomsArthralgiasMyalgiasHeadacheWeaknessDepressionloss of libido, impotence,Vague gastrointestinal difficulties.Thyroid and adrenal function often are depressed.HypertensionSperm counts can be depressed in menand fertility reduced in women.
22Renal function may reveal impairment of glomerular clearance; decreased tubular urate clearanceresulting in hyperuricemia is common.Late effects of inorganic lead intoxication include :chronic renal failure, gout,chronic encephalopathy, and hypertension.Subclinical toxicity( low-dose exposure )May cause harmful effects to health in the absence ofsymptoms and signs that are evident on the standardClinical examination.
23The effects of lead on organ system Function 1.Hematologic toxicityAnemia :presence of anemia is not required for a diagnosis of leadpoisoningThe severity and prevalence of lead-induced anemia are correlated directly with the blood lead level in both adults and children.
24Lead-induced anemia is the result of multiple mechanisms: impairment of heme biosynthesis :1.Inhibition of the cytoplasmic enzyme, d-aminolevulinicacid dehydratase (ALA-D).2.The mitochondrial enzyme ferrochelatase.That results accumulation of zinc protoporphyrin [ZPP]) inthe erythrocytes.Acceleration of red blood cell destruction.inhibition of erythopoietin production in the kidney.
252.Neurologic toxicity(Neurologic toxicity of lead in adults)Peripheral motor neurologic toxicity:1. Extensor muscle palsy with wrist drop or ankle drop2. AsymmetryUnlike other toxic neuropathies, thismotorneuropathy may show left–right asymmetry.
28Mild to moderate sensory dysfunction also may be evident in lead neuropathy, and in such cases the clinical picture isone of mixed motor–sensory neuropathy, often withasymmetric features.In the central nervous system( high-dose acute exposure to lead )causes encephalopathy characterized clinically by obtundationcoma, and convulsionsAmong persons who recover from acute lead encephalopathy, ahigh proportion are left with significant neuropsychologicdeficits, including reduced intelligence, shortened attentionspan, and instability of mood.
29Impairment in central neurologic function in adults at doses insufficient to produce clinical encephalopathy:-Fatigue-Short-term memory loss-Depressed mood
303.Renal toxicity Acute Fanconi syndrom Vit .D defficiency At blood lead levels below 25 µgm/dl, leadinhibits the metabolic activation (hydroxylation) of vit. DAt blood lead levels of 40–80 µgm/dl, lead induces theformation of dense intranuclear inclusion bodies consistingof a lead protein complex in cells lining the proximal tubules.
31Hyperuremic goutresulting from increased reabsorption of uric acid by thetubular cells.Chronic nephropathy, which may progress to kidney failure.Chronic low-level lead exposure:abnormal urinary excretion of n-acetyl glucosaminidase (NAG)4. hypertensionlong-term, high-dose exposure to lead associated with an increased incidence of hypertension and cerebrovascular disease
325.Reproductive toxicity of lead Decreased sperm counts, abnormal spermmorphology, and decreased sperm motility when lead levelswere above 40 micrograms/dl.increased incidence in spontaneous abortion among femalelead workers as well as in the wives of male lead workers.lead may cause neurologic damage to the fetus at blood levelsas low as 5–10 micrograms/dl, substantially below the currentOSHA standard for blood levels of lead in Workers.
33The prevention of fetal lead encephalopathy requires that blood lead levels of prospective mothers be kept below10 micrograms/dl, not only during pregnancy but also inthe years preceding conception.If a woman who has previously had elevated blood leadlevels wishes to become pregnant, it may be reasonable torecommend either an x-ray Fluorescence examination of boneto determine body burden of lead .
346.Carcinogenicitygroup 2A – probable human carcinigenRenal cancerBrain tumor
35Organic leadTEL use as antiknock in gasolineTEL produce a syndrom difrenet from inorganic lead poisoningCause : insomnia, anorhexia, muscle irritability,aggitatedencephalopathy,tremor and ataxia
36Clinical evaluation Clinical evaluation strategy for adult The diagnosis of in organic lead intoxication in adults requires:1- demonstration of excess lead absorption2-documentation of impairment in an organ system consistentwith the effect of lead3-exclution of other cause of impairment
37Lead Distribution in human body Lead is not distributed homogeneously in the humanbody It is dispersed amonge several physiologicallydistinct compartment.Blood leadSingle best indicator of recent lead absorptionhalf life 36 days1% of body burdenNormal adult lead level is below 10µgr/dlClinical symptom appear at µgr /dlAt 50 µgr /dl worker must immediately remoev fromexposure and they can not return to work their levelhave fallen below 40 µg/dl
38Lead in calcified tissue of skeleton and teeth: 90-99% of absorpted lead ( 70% in children) .Half life →15-20 years.blood lead level appears principally to reflect release of stored fromdeep tissue compartment to blood .K-shell x-ray fluorescence (XRF) analysis is a accurate, non-invasiveand relatively rapid assessment of chronic lead exposure.
41Zinc protoporphyrinZinc protoporphyrin (ZPP) or free erythrocyte protoporphyrin(FEP) levels reflect the toxic effect of lead on the erythrocyticenzyme ferrochelatase.A combination of normal FEP value and high blood leadlevel indicates very recent exposure that has not yet hadopportunity to poison heme metabolism.Because the ZPP level remains elevated long after theblood lead level has fallen, this test does not discriminatebetween recent and past exposure.
42Anemia:the diagnosis of lead poisoning cannot await the appearance of anemiaBasophilic stippling:Basophilic stippling in the red blood cells is seen in mostpatients with acute hemolysis and occasionally in patientswith chronic hemolytic syndromes; it is not specific tolead poisoning.Lead lines:Lead lines on the gums are uncommon except in cases ofsevere poisoning and may be difficult to recognize in patientswith poor dental hygiene.
43Complete blood counts and routine blood chemistry should be performed as baseline in asymptomatic workers.Other baseline tests include creatinine clearance,BUN, anduric acid.Blood pressure should be measured regularly.Blood lead levels should be obtained on a periodically.If the whole blood lead levelexceeds 40 micrograms/dl,tests should be repeatedmonthly; blood lead levels over50 micrograms/dl require immediate removal of workersfrom lead-exposure, andthey may not return to work in alead-exposed job untilthere have been two lead-levelsbelow 40 micrograms/dl
44urine leadMeasurement of the urine lead level is of little value inmonitoring populations exposed to inorganic lead; the testis too highly variable to be reliable.Hair leadhair lead analysis is not considered reliable for monitoring purposes.
45Clinical evaluation strategy: organic lead Organic lead (TEL) intoxication is difficult to diagnosewithout a history of exposure.Blood or urine lead levels and FEP levels are not predictablyelevated in TEL poisoning.
46MANAGEMENT Management of acute lead poisoning in adults: Immediate removal from exposure to lead.chelation (intravenous calcium EDTA and Oral chelationwith DMSA ).Chelation should be considered for blood levels greaterthan 80 micrograms/dl, especially when there arecentral or peripheral nervous system effects.For blood lead levels of 60–80 micrograms/dl, decisionsregarding chelation should be made on a case-by-casebasis.
47Management of chronic lead Intoxication Studies are needed to confirm whether chelation therapy ofadults with chronic lead intoxication results in amelioration oflong-term effects such as gout, hypertension or renalinsufficiency,The administration of chelating agents to persons with chroniclead intoxication must be approached with great care, becausethey often have impairment of renal function.Chronic administration of oral chelation agents to workerswho continue to be exposed to unacceptably high levels oflead in their work has been used by some unscrupulousemployers as a means of reducing blood lead levels whilenot reducing levels of lead in air in the workplace.
48Management of organic lead poisoning The treatment for TEL poisoning is primarily support;chelation with calcium EDTA has been tried with variableefficacy. Sedation and careful observation are required insevere cases, often for prolonged periods.
49Prevention of occupational lead Poisoning Air-born exposure to both organic and inorganic lead inthe workplace must be strictly limited by enclosure ofhazardous processes, ventilation, and other engineeringcontrols.OSHA lead standard mandates that occupational exposuresto lead be held below 50 µgr/m3 of air, expressed as an 8-hour,TWA.However, studies have shownclearly that toxic adverse effectscan occur in lead workers at levels of exposure below thisstandard.
50clinical or subclinical toxic effects can occur at and below the current biologic exposure limitof 50 micrograms/dl of whole blood.A physician may remove a worker with a lower blood level if leadPoisoning is diagnosed and restrict the worker from return toExposure until approved by the physician.