Bahaya Timah Hitam

Timah Hitam

Timah Hitam atau Bahasa Inggerisnya Plumbum atau Lead seringkali digunakan dalam bateri. Tetapi orang kita tidak kisah membuang bateri di belakang rumah. Bateri ini pula dibakar lalu mengeluarkan “lead fume’. Tiada siapa yang kisah…. Ada aku kisah???  Sila anda ikuti betapa tidak sihatnya timah hitam seperti di bawah.  Untuk pautan sila tuan ke HSDB dan Toxnet.

LEAD COMPOUNDS
CASRN: NO CAS RN

This record contains general information for lead ions and compounds, including statements in the literature referenced to lead compounds, lead salts, etc. For compound-specific information, refer to the appropriate individual records as listed in the RELATED HSDB RECORDS field; for information on the metal itself, refer to the LEAD, ELEMENTAL record.
For other data, click on the Table of Contents

Human Toxicity Excerpts:
LEAD IS POISONOUS IN ALL FORMS. IT IS ONE OF THE MOST HAZARDOUS OF THE TOXIC METALS BECAUSE THE POISON IS CUMULATIVE & THE TOXIC EFFECTS ARE MANY & SEVERE. /LEAD CMPD/
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-226]**PEER REVIEWED**

Acute lead poisoning is relatively infrequent and occurs from ingestion of acid soluble lead compounds or inhalation of lead vapors. Local actions in the mouth produce marked astringency, thirst, and a metallic taste. Nausea, abdominal pain, and vomiting ensue. The vomitus may be milky from the presence of lead chloride. Although the abdominal pain is severe, it is unlike that of chronic poisoning. Stools may be black from lead sulfide, and there may be diarrhea or constipation. If large amounts of lead are absorbed rapidly, a shock syndrome may develop as the result of massive gastrointestinal loss of fluid. Acute symptoms of the central nervous system incl paresthesia, pain, and muscle weakness. An acute hemolytic crisis sometimes occurs and causes severe anemia and hemoglobinuria. The kidneys are damaged, and oliguria and urinary changes are evident. Death may occur in 1 or 2 days. If the patient survives the acute episode, characteristic signs & symptoms of chronic lead poisoning are likely to appear. /Inorganic lead compounds/
[Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1651]**PEER REVIEWED**

Signs & symptoms of chronic lead poisoning (plumbism) can be divided into 6 categories: gastrointestinal, neuromuscular, CNS, hematological, renal, & other. They may occur separately or in combination. The neuromuscular & CNS syndromes usually result from intense exposure, while the abdominal syndrome is a more common manifestation of a very slowly & insidiously developing intoxication. The CNS syndrome is usually more common among children, while the GI syndrome is more prevalant in adults. /Inorganic lead compounds/
[Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1651]**PEER REVIEWED**

... /IN CHRONIC LEAD POISONING/ THE ABDOMINAL SYNDROME OFTEN BEGINS WITH VAGUE SYMPTOMS, SUCH AS ANOREXIA, MUSCLE DISCOMFORT, MALAISE, AND HEADACHE. CONSTIPATION IS USUALLY AN EARLY SIGN, ESP IN ADULTS, BUT DIARRHEA OCCASIONALLY OCCURS. A PERSISTENT METALLIC TASTE APPEARS EARLY IN THE COURSE OF THE SYNDROME. AS INTOXICATION ADVANCES, ANOREXIA AND CONSTIPATION BECOME MORE MARKED. INTESTINAL SPASM, WHICH CAUSES SEVERE ABDOMINAL PAIN, OR LEAD COLIC, IS THE MOST DISTRESSING FEATURE OF THE ADVANCED ABDOMINAL SYNDROME. THE ATTACKS ARE PAROXYSMAL AND GENERALLY EXCRUCIATING. THE ABDOMINAL MUSCLES BECOME RIGID, & TENDERNESS IS ESP MANIFESTED IN THE REGION OF THE UMBILICUS. /INORGANIC LEAD COMPOUNDS/
[Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1651]**PEER REVIEWED**

THE NEUROMUSCULAR SYNDROME OR LEAD PALSY NOW IS RARE IN THE UNITED STATES. IT IS A MANIFESTATION OF ADVANCED SUBACUTE POISONING. MUSCLE WEAKNESS & EASY FATIGUE OCCUR LONG BEFORE ACTUAL PARALYSIS AND MAY BE THE ONLY SYMPTOMS. WEAKNESS OR PALSY MAY NOT BECOME EVIDENT UNTIL AFTER EXTENDED MUSCLE ACTIVITY. THE MUSCLE GROUPS INVOLVED USUALLY ARE THE MOST ACTIVE ONES (EXTENSORS OF THE FOREARM, WRIST, & FINGERS & EXTRAOCULAR MUSCLES). WRIST DROP &, TO A LESSER EXTENT, FOOT DROP WITH APPROPRIATE HISTORY OF EXPOSURE HAVE BEEN CONSIDERED ALMOST PATHOGNOMONIC FOR LEAD POISONING. THERE IS USUALLY NO SENSORY INVOLVEMENT. DEGENERATIVE CHANGES IN MOTONEURONS & THEIR AXONS HAVE BEEN DESCRIBED. /INORGANIC LEAD COMPOUNDS/
[Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1651]**PEER REVIEWED**

THE CNS SYNDROME HAS BEEN TERMED LEAD ENCEPHALOPATHY. IT IS THE MOST SERIOUS MANIFESTATION OF LEAD POISONING, AND IS MUCH MORE COMMON IN CHILDREN THAN IN ADULTS. THE EARLY SIGNS OF THE SYNDROME MAY BE CLUMSINESS, VERTIGO, ATAXIA, FALLING, HEADACHE, INSOMNIA, RESTLESSNESS, AND IRRITABILITY. AS THE ENCEPHALOPATHY DEVELOPS, THE PATIENT MAY FIRST BECOME EXCITED AND CONFUSED; DELIRIUM WITH REPETITIVE TONIC-CLONIC CONVULSIONS OR LETHARGY & COMA FOLLOW. VOMITING, A COMMON SIGN, IS USUALLY PROJECTILE. VISUAL DISTURBANCES ARE ALSO PRESENT. ... TREATMENT FOR CEREBRAL EDEMA MAY BECOME NECESSARY. THERE MAY BE APROLIFERATIVE MENINGITIS, INTENSE EDEMA, PUNCTATE HEMORRHAGES, GLIOSIS AND AREAS OF FOCAL NECROSIS. ... THE MORTALITY RATE AMONG PATIENTS WHO DEVELOP CEREBRAL INVOLVEMENT IS ABOUT 25%. WHEN CHELATION THERAPY IS BEGUN AFTER THE SYMPTOMS OF ACUTE ENCEPHALOPATHY APPEAR, APPROXIMATELY 40% OF SURVIVORS HAVE NEUROLOGICAL SEQUELAE, SUCH AS MENTAL RETARDATION, EEG ABNORMALITIES OR ... SEIZURES, CEREBRAL PALSY, OPTIC ATROPHY, OR DYSTONIA MUSCULORUM DEFORMANS. /INORGANIC LEAD COMPOUNDS/
[Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1651]**PEER REVIEWED**

EXPOSURE TO LEAD OCCASIONALLY PRODUCES ... PROGRESSIVE MENTAL DETERIORATION IN CHILDREN. THE HISTORY OF THESE CHILDREN INDICATES NORMAL DEVELOPMENT DURING THE FIRST 12-18 MONTHS OF LIFE OR LONGER, FOLLOWED BY A STEADY LOSS OF MOTOR SKILLS & SPEECH. THEY MAY HAVE SEVERE HYPERKINETIC AND AGGRESSIVE BEHAVIOR DISORDERS & A POORLY CONTROLLED CONVULSIVE DISORDER. THE LACK OF SENSORY PERCEPTION SEVERELY IMPAIRS LEARNING. CONCN OF LEAD IN BLOOD EXCEED 60 UG/DL OF WHOLE BLOOD, & X-RAY MAY SHOW HEAVY, MULTIPLE BANDS OF INCR DENSITY IN THE GROWING LONG BONES. ... AN INCREASED INCIDENCE OF HYPERKINETIC BEHAVIOR & A STATISTICALLY SIGNIFICANT, ALTHOUGH MODEST, DECREASE IN IQ HAVE BEEN SHOWN IN CHILDREN WITH BLOOD LEAD CONCN OF 30-50 UG/DL. /INORGANIC LEAD COMPOUNDS/
[Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1652]**PEER REVIEWED**

When the blood lead concn is near 80 ug/dl or greater, basophilic stippling (the aggregation of ribonucleic acid) occurs in erythrocytes. This is thought to result from the inhibitory effect of lead on the enzyme, pyrimidine-5'-nucleotidase. Basophilic stippling is not ... pathognomonic of lead poisoning. A more common hematological result of chronic lead intoxication is a hypochromic microcytic anemia, which is more frequently observed in children and is morphologically similar to that which results from iron deficiency. The anemia is thought to result from two factors: a decreased life span of the erythrocytes & an inhibition of heme synthesis. Very low concn of lead influence the synthesis of heme. ... Lead clearly inhibits heme formation at several ... /enzymatic steps/. /Inorganic lead compounds/
[Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1652]**PEER REVIEWED**

Renal toxicity occurs in two forms: a reversible renal tubular disorder (usually seen after acute exposure of children to lead) and an irreversible interstitial nephropathy (more commonly observed in chronic industrial lead exposure). Clinically, a Fanconi-like syndrome is seen with proteinuria, hematuria, and casts in the urine. Hyperuricemia with gout occurs more frequently in the presence of chronic lead nephropathy than in any other type of chronic renal disease. Histologically, lead nephropathy is revealed by a characteristic nuclear inclusion body, composed of a lead-protein complex; this appears early & resolves after chelation therapy. Such inclusion bodies have been reported in the urine of workers exposed to lead in an industrial setting. /Inorganic lead compounds/
[Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1652]**PEER REVIEWED**

OTHER SIGNS & SYMPTOMS OF PLUMBISM ARE ASHEN COLOR OF THE FACE & PALLOR OF LIPS; RETINAL STIPPLING; APPEARANCE OF "PREMATURE AGING," WITH STOOPED POSTURE, POOR MUSCLE TONE, & EMACIATION; & BLACK, GRAYISH, OR BLUE-BLACK SO-CALLED LEAD LINE ALONG THE GINGIVAL MARGIN. ... THE HUMAN CARCINOGENICITY IS NOT WELL ESTABLISHED, BUT IT HAS BEEN SUGGESTED, & SEVERAL CASE REPORTS OF RENAL ADENOCARCINOMA IN LEAD WORKERS HAVE BEEN PUBLISHED. /INORGANIC LEAD COMPOUNDS/
[Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1652]**PEER REVIEWED**

THERE IS NO EVIDENCE TO SUGGEST THAT EXPOSURE TO LEAD SALTS CAUSES CANCER OF ANY SITE IN MAN. HOWEVER, ONLY ONE EPIDEMIOLOGICAL STUDY OF THE RELATIONSHIPS BETWEEN EXPOSURE TO LEAD & THE OCCURRENCE OF CANCER HAS BEEN REPORTED. ... THE LEVEL OF HUMAN EXPOSURE EQUIVALENT TO THE LEVEL OF LEAD ACETATE PRODUCING RENAL TUMORS IN RATS IS 810 MG/DAY (550 MG PB). THIS LEVEL APPEARS TO EXCEED BY FAR THE MAX TOLERATED DOSE FOR MAN. /INORGANIC LEAD COMPOUNDS/
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V1 48 (1972)]**PEER REVIEWED**

A few clinical studies have found increased chromosomal defects in workers with blood lead levels above 60 ug/dl. /Inorganic lead compounds/
[Klaassen, C.D., M.O. Amdur, Doull J. (eds.). Casarett and Doull's Toxicology. The Basic Science of Poisons. 5th ed. New York, NY: McGraw-Hill, 1995., p. 708]**PEER REVIEWED**

RESIDUAL NEUROLOGICAL SEQUELAE MAY AFFECT AS HIGH AS 82% OF SURVIVORS. /INORGANIC LEAD COMPOUNDS/
[PERLSTEIN; CLINICAL PED 5: 292 (1966)]**PEER REVIEWED**

IN MANY CASES THERE IS NO MACROSCOPIC OR MICROSCOPIC EVIDENCE OF BRAIN EDEMA. EDEMA IS RARELY THE CAUSE OF DEATH. /INORGANIC LEAD COMPOUNDS/
[KRIGMAN ET AL; EXP CLIN NEUROTOXICOLOGY, WILLIAMS & WILLIAMS (1980)]**PEER REVIEWED**

MICROCYTOSIS & ANEMIA EVIDENTLY OCCUR MUCH LESS COMMONLY THAN PREVIOUSLY REPORTED IN CHILDHOOD LEAD POISONING UNCOMPLICATED BY OTHER HEMATOLOGIC DISORDERS. /INORGANIC LEAD COMPOUNDS/
[COHEN AR ET AL; PEDIATRICS 67 (6): 904-6 (1981)]**PEER REVIEWED**

... The incidence of premature fetal membrane rupture in term and preterm infants is much higher (17%) 30 to 50 miles west of a lead mining area of Missouri than in a Missouri urban area remote from lead mining activities (0.41%). Maternal and fetal blood lead levels (PbB) at birth also differed significantly for normal births vs births with premature membrane rupture. Maternal and fetal blood lead levels for the normal deliveries were about 14 and 4 ug/dl respectively, whereas they were about 26 and 13 ug per dl for mothers and infants with membrane rupture. /Inorganic lead compounds/
[USEPA; Ambient Water Quality Criteria Doc: Lead p.C-67 (1980) EPA 440/5-80-057]**PEER REVIEWED**

INCREASED SERUM ARGINASE ACTIVITY MAY INDICATE LIVER DAMAGE, WHILE DECR KALLIKREIN ACTIVITY MAY INDICATE KIDNEY DAMAGE IN WORKERS EXPOSED TO LEAD. /INORGANIC LEAD COMPOUNDS/
[CHMIELNICKA J ET AL; BR J IND MED 38 (2): 175-8 (1981)]**PEER REVIEWED**

Blood lead values in children ranging from 40 to 80 ug/100 ml seem to be associated with adverse neuropsychological effects. Landrigan and coworkers ... compared a group of 70 children, aged 3 to 15 years (mean blood lead 48 ug/100 ml). They found that higher lead levels were associated with decreased intelligence and slowing in a finger wrist tapping test. /Inorganic lead compounds/
[NIOSH; Criteria Document: Inorganic Lead p.XI-56 (1978) DHEW Pub. NIOSH 78-158]**PEER REVIEWED**

The reproductive ability of men was ... shown to be adversely affected by moderate absorption of lead. Concn of lead in blood greater than 52 ug/100 ml were associated with a high frequency of altered spermatogenesis. Disorders of sexual dynamics were evident with blood lead values greater than 41 ug/100 ml. Among the workers with the highest concn of lead in blood (mean 74.50 + or - 26 ug/100 ml), 75% were judged to be hypofertile, 50% being even infertile. It was not possible, however, to demonstrate a reliable association between lead absorption in these men and the number of normal pregnancies per couple, or the frequency of miscarriages, ectopic pregnancies, or premature births. Nevertheless, these results were interpreted to indicate that lead clearly has a direct toxic action on the male gonads at relatively low levels of absorption. /Inorganic lead compounds/
[NIOSH; Criteria Document: Inorganic Lead p.XI-52 (1978) DHEW Pub. NIOSH 78-158]**PEER REVIEWED**

... WHEN AN EXCESSIVE AMT OF LEAD HAS BEEN DEPOSITED IN BONE, EITHER FROM INGESTION OR FROM INDUSTRIAL EXPOSURE, & HAS REMAINED IMMOBILIZED FOR YEARS, INTERCURRENT FACTORS CAUSING MOBILIZATION MAY CAUSE A SUDDEN OUTBREAK OF CLINICAL SYMPTOMS OF LEAD POISONING. /INORGANIC LEAD COMPOUNDS/
[Browning, E. Toxicity of Industrial Metals. 2nd ed. New York: Appleton-Century-Crofts, 1969., p. 174]**PEER REVIEWED**

... In rural Scotland, four people developed clinical lead poisoning and others showed biochemical evidence of grossly elevated lead exposure. Pb concn in the domestic water supply was 2-3 mg/l. In this case the reason for the extreme contamination was that the water was stored in lead tanks. /Inorganic lead/
[WHO; Environ Health Criteria: Lead p.49 (1977)]**PEER REVIEWED**

... In humans, lead decreased glucose-6-phosphate dehydrogenase activity and thus decreased the gluthathione level in red blood cells. /Lead cmpd/
[Nat'l Research Council Canada; Effects of Lead in the Canadian Envir p.572 (1978) NRCC No 16736]**PEER REVIEWED**

ON BASIS OF CLINICAL OBSERVATION ... DISTURBANCES /OCCUR IN/ VISUAL CORTEX & SUPRAGENICULATE PATHWAY; OPTIC NERVE ... RETROBULBAR & BULBAR; RETINA; INTRAOCULAR MUSCLE; LENS; & EXTRAOCULAR MUSCLE. INDIVIDUAL PORTION OF VISUAL SYSTEM MAY BE AFFECTED ... MORE /OFTEN/ SEVERAL PORTIONS. ... /LEAD CMPD/
[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 551]**PEER REVIEWED**

... Lead levels were elevated in the liver of individuals having liver siderosis or other diseases involving altered iron metabolism. ... Hemosiderin induced by high levels of iron, may act as a binding agent not only for iron but for Pb as well. Thus these diseases may incr Pb retention in the body and especially in the liver. The Pb(+2) may later be released by being replaced with Fe(+3). /Inorganic lead/
[Nat'l Research Council Canada; Effects of Lead in the Canadian Envir p.572 (1978) NRCC No.16736]**PEER REVIEWED**

Lead containing particles in ambient air have an aerodynamic diameter of approx 0.1-1.0 um, & the predicted deposition in the airway is about 35%. This is questionable for smaller particles (< 0.1 um) which are mainly deposited by diffusion. Actual measurements of deposition in human volunteers gave results that differed considerably depending on the physical & chemical properties of the inhaled aerosol. ... A deposition of approx 25% /was observed/ after exposure to particles with a mass median aerodynamic diameter of 0.25 um. ... A deposition in the resp tract of about 60% /was observed/ in persons close to a motorway, where particles were about 0.03 um in diameter. This figure is consistent with lab expt carried out by the same authors, in which subjects inhaled radioactively labeled particles of about the same size. When volunteers inhaled lead particles near urban roads where the particle size was larger (0.2-2.0 um), deposition was about 50%. Based on available data, it seems reasonable to conclude that the rate of deposition of airborne lead in the general population is approx 30-50%, depending on particle size & ventilation rates. /Inorganic lead compounds/
[Friberg, L., Nordberg, G.F., Kessler, E. and Vouk, V.B. (eds). Handbook of the Toxicology of Metals. 2nd ed. Vols I, II.: Amsterdam: Elsevier Science Publishers B.V., 1986., p. V2 311]**PEER REVIEWED**

Recent research work on the clinical effects of lead has focused on the subtle neuropsychiatric, reproductive, & renal effects of chronic low dose lead exposure. Children are particularly susceptible to lead induced impairment of neuropsychological development because of their reduced ability to excrete lead & their enhanced absorption of lead compared to adults. Death in children from undetected lead poisoning may be greater than heretofore suspected. /Inorganic lead/
[Ellenhorn, M.J. and D.G. Barceloux. Medical Toxicology - Diagnosis and Treatment of Human Poisoning. New York, NY: Elsevier Science Publishing Co., Inc. 1988., p. 1030]**PEER REVIEWED**

Lead systemic poisoning can cause a wide variety of visual & ocular disturbances according to many case reports during the past 3.5 centuries. Much of what ... /is known/ of the clinical aspects of ocular effects comes from early literature which has been condensed in several reviews. ... Of 172 eye cases surveyed by Lewin & Guillery /& reported in 1913/, 79 had colic, 52 had headache, 47 had convulsions, delirium, stupor, or coma, & 27 had paralysis of extensor muscles. In general ocular disturbances appeared most commonly after many months or years of chronic poisoning, & at least after several weeks of poisoning. As a rule, ocular involvement was not among the early symptoms in adults, although it could be one of the first symptoms, esp in children. On the basis of clinical & exptl observations, it has been possible to recognize disturbances of the following sites: visual cortex & suprageniculate pathways; optic nerve, both retrobulbar & bulbar; retina; intraocular muscles; & extraocular muscles. Unfortunately many reports describing visual symptoms provide insufficient information for determination of site or mechanism. /Inorganic lead/
[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 550]**PEER REVIEWED**

... Studies correlating elevated blood lead levels to hypotension are conflicting. Concern exists over possibility that soft acid water increases the solubility of lead & that elevated levels account for the increased incidence of hypertension & cardiovascular mortality in areas with soft-water supplies. The contribution of increased lead absorption to gout, hypertension, nephropathy, & neurotoxicity remains to be determined. /Inorganic lead/
[Ellenhorn, M.J. and D.G. Barceloux. Medical Toxicology - Diagnosis and Treatment of Human Poisoning. New York, NY: Elsevier Science Publishing Co., Inc. 1988., p. 1030]**PEER REVIEWED**

Although per day children ingest less lead in their diets and inhale less Pb than do adults, on a dose per body weight basis children may have 2-3 times the exposure. Furthermore children because of their poor oral hygiene are more likely than adults to absorb Pb from extraneous sources: ingestion of foreign objects, dust, paint chips, inhalation of resuspended settled dusts. Preliminary data indicate that children absorb 50% of ingested Pb, ie at a rate 5 times greater than adults. Animal studies support the hypothesis that the young retain more of a Pb dose than do adults and that this is reflected in soft tissue Pb levels. The portions of the Pb body burden found in soft tissues of children and adults are 27.5% and 5% respectively. Hence, a higher fraction of a child's body burden of Pb is available to produce toxic effects in soft tissues. /Inorganic lead/
[USEPA; Ambient Water Quality Criteria Doc: Lead p.C1-9 (1984) EPA 440/5-84-027]**PEER REVIEWED**

SYMPTOMATOLOGY: A. Acute poisoning by ingestion only. 1) An astringent and metallic taste in the mouth, dry throat, thirst. 2) Burning abdominal pain, nausea, and vomiting. The vomitus may appear milky due to the presence of lead chloride. The abdominal pain may become colicky and severe. 3) Sometimes diarrhea, less often constipation. The stools may be bloody, or black due to the presence of lead sulfide. 4) Peripheral circulatory collapse. 5) Neuromuscular symptoms include muscular weakness, pain, and cramps, especially in the legs. 6) Central nervous system manifestations include headache, insomnia, paresthesias, depression, coma, and death. 7) Though usually of secondary concern, kidney damage may result in oliguria, albuminuria, and cylindruria. The renal lesion may be due to the mildly nephrotoxic action of lead, to disturbances in kidney circulation, or to the products of intravascular hemolysis. Renal lesions may assume increased importance if edetate calcium disodium therapy is instituted. 8) An acute hemolytic crisis sometimes develops and results in anemia and hemoglobinuria. 9) Death may occur within 1 or 2 days, but recovery is the rule. Convalescence is slow and may be interrupted by episodes like those seen in typical chronic poisoning. /Lead cmpd/
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-232]**PEER REVIEWED**

SYMPTOMATOLOGY: B. Lead encephalopathy in chronic lead poisoning. 1) Headache and insomnia. 2) Persistent vomiting, which is sometimes projectile. A typical lead colic may or may not be present. 3) Visual disturbances, choked optic disks. 4) Irritability, restlessness, delirium, hallucinations. 5) Convulsions and coma. 6) The intracranial pressure is characteristically high. The cerebrospinal fluid is generally unremarkable except for and elevation of total protein. 7) Death from exhaustion and respiratory failure. The mortality rate is high; Recovery is slow and frequently incomplete. /Lead cmpd/
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-233]**PEER REVIEWED**

Blood lead level was determined in forty-five traffic controllers working on Alexandria road intersections. Central nervous system dysfunction in the subjects /was studied/ by means of performance tests. Biochemical indicators related to lead exposure such as delta-aminolevulinic acid dehydratase and hemoglobin in their blood were also determined. Results indicated that most of the subjects studied have a comparably high blood lead level. They also showed significantly poorer performance scores than that obtained in a previous study with a group of textile workers of the same age and educational levels. The mean of the blood lead level in the traffic controllers was found to be 68.28 + or - 13.22 ug/dl. This is a very high level compared to an acceptable level of 30.00 ug/dl. All neurobehavioral symptoms demonstrated in the traffic controllers could be attributed to a high level of lead exposure. /Inorganic lead/
[Ahmed NS et al; Arch Environ Health 42 (2): 92 (1987)]**PEER REVIEWED**

Three epidemiological studies of workers exposed to lead & lead compounds were reviewed previously. ... A study on battery workers in the UK is now avail, & studies of a USA lead smelter & of a Swedish copper smelter have also been reported. ... The excess of resp cancer in these studies were relatively small, showed no clear-cut trend with length or degree of exposure, & could have been confounded by factors such as smoking or exposure to arsenic. ... /Lead and lead compounds/
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. S7 230 (1987)]**PEER REVIEWED**

Short-term (acute): Exposure to inorganic lead can cause decreased appetite, insomnia, headache, muscle and joint pain, colic, and constipation. /Inorganic lead/
[Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. DHHS(NIOSH) Publication No. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981., p. ]**PEER REVIEWED**

Long-term (chronic): Exposure to inorganic lead can cause weakness, weight loss, nausea, vomiting, constipation, blue or blue-black dot-like pigmentation on the gums (lead line), severe headache and abdominal cramps, delirium, convulsions, and coma. /Inorganic lead/
[Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. DHHS(NIOSH) Publication No. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981., p. ]**PEER REVIEWED**

Health effects from lead, inorganic fumes and dusts (as Pb) /are/ cumulative blood and neurologic effects/reproductive hazard. /Lead, inorganic fumes and dusts (as Pb); from table/
[Cralley, L.J., L.V. Cralley (eds.). Patty's Industrial Hygiene and Toxicology. Volume III: Theory and Rationale of Industrial Hygiene Practice. 2nd ed., 3A: The Work Environment. New York, NY: John Wiley Sons, 1985., p. V3A 172]**PEER REVIEWED**

Following ingestion of a large amount of any soluble lead salt ... the initial signs and symptoms are due largely to local irritation of the alimentary tract, ... pain, leg cramps, muscle weakness, paresthesias, ... coma, and death may follow within 1 or 2 days. /Lead/
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-138]**PEER REVIEWED**

Intoxication from multiple exposures ... represents a response to the accumulative retention of lead from repeated small intakes. Chronic plumbism expresses itself in many diverse ways, but three major clinical syndromes are recognized. The alimentary type ... the neuromuscular type ... /and/ ... the cerebral type ... In any type of chronic plumbism, the patient may show facial pallor, a gingival lead line, mild jaundice, anemia, basophilic stippling of the red blood cells, albuminuria, cylindruria, porphyrinuria, and excessive urinary and blood concentrations of lead. /Lead/
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-138]**PEER REVIEWED**

One of the characteristic cellular metabolic reactions in lead intoxication is the formation of intranuclear inclusion bodies, a discrete, dense-staining mass found in the liver parenchyma and in the tubular lining cells of the kidney in man and animal. Consisting of a dense, central core and outer fibrillary zone, they can be identified and distinguished from those from bismuth intoxication or from those of viral origin by special stains (mercury bromophenol blue and basic fuchsin). Lead has been identified by direct chemical analysis to be in the form of a lead-protein complex to the extent of about 50 ug lead/mg protein. The included lead is 60 to 100 times more concentrated than whole kidney lead. /Lead/
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 2073]**PEER REVIEWED**

Lead toxicity in adults results primarily from workplace exposure via inhalation. Lead exposure can occur by ingestion as a result of the lack of proper hygiene in lead contaminated environments (eg, eating or smoking in areas of lead work). /Lead/
[Ellenhorn, M.J. and D.G. Barceloux. Medical Toxicology - Diagnosis and Treatment of Human Poisoning. New York, NY: Elsevier Science Publishing Co., Inc. 1988., p. 1030]**PEER REVIEWED**

IN THE LEAD OXIDE EXPOSED WORKERS IN THE STATE OF NUEVO LENO, MEXICO, SIGNIFICANT INCR IN CHROMOSOME DAMAGE, BLOOD LEAD LEVELS AND URINARY DELTA-AMINOLEVULINIC ACID LEVELS WERE SEEN IN COMPARISON TO CONTROLS. AS FOR GENETIC MARKER FREQUENCIES, SIGNIFICANT DIFFERENCES BETWEEN THE WORKERS & CONTROLS WERE SEEN ONLY IN THE RH BLOOD GROUP. NO SIGNIFICANT ASSOCIATION WAS FOUND BETWEEN GENETIC MARKERS & CHROMOSOME DAMAGE. /LEAD OXIDE/
[GARZA-CHAPA R ET AL; ARCH INVEST MED 11 (4): 547 (1980)]**PEER REVIEWED**

Colic is seen in children and US EPA concluded that the lowest-observed-adverse-effect level was in the range of 2.88-4.80 umol/L (60-100 ug/dl). /Inorganic Lead/
[WHO; Environ Health Criteria #165: Inorganic Lead p.203 (1995)]**PEER REVIEWED**

Reproductive effects /of men/ from occupational exposure to lead include asthenospermia, hypospermia, teratospermia and hypogonadism. In men, effects on sperm or the testes may result from chronic exposure to lead at blood levels of the order of 1.92-2.4 umol/liter (40-50 ug/dl). /Inorganic lead/
[WHO; Environ Health Criteria #165: Inorganic Lead p.205 (1995)]**PEER REVIEWED**

... The mortality was examined for the total 34 yr period 1947-1980. Elevated standardized mortality ratios for malignant neoplasms have been found in both battery and production workers, the excess deaths being predominantly from gastrointestinal tract cancer and lung cancer. In the battery workers, there were 34 deaths from stomach cancer with 20.2 expected and 109 deaths from lung cancer with 87.8 expected, both standardized mortality ratios being significantly raise. /Lead/
[Friberg, L., Nordberg, G.F., Kessler, E. and Vouk, V.B. (eds). Handbook of the Toxicology of Metals. 2nd ed. Vols I, II.: Amsterdam: Elsevier Science Publishers B.V., 1986., p. V1 373]**PEER REVIEWED**

... It has been possible to develop dose-effect relationships for lead exposure and anemia. However, since so many other factors may influence the degree of anemia, it has been more common to define a level of hemoglobin concentration and then to develop a dose-response relationship for the percent of the population with that or a lower concentration of hemoglobin. /Lead cmpd/
[Friberg, L., Nordberg, G.F., Kessler, E. and Vouk, V.B. (eds). Handbook of the Toxicology of Metals. 2nd ed. Vols I, II.: Amsterdam: Elsevier Science Publishers B.V., 1986., p. V1 152]**PEER REVIEWED**

Suggestive evidence of a lead-related decrease in hearing acuity in children has been reported. Hearing thresholds at 2000 Hertz increased linearly with maximum blood lead levels, indicating that lead adversely affects auditory function. The blood lead levels in 75 asymptomatic black children, 3-7 years old, ranged from 6 to 59 ug/dL (mean = 26.7 ug/dL). The children were healthy and did not have middle ear infections at the time of testing. /Lead compound/
[Robinson GS et al; World Health Organization Regional Office for Europe, 177-82 (1985) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.46 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

The most extensive was a series of a large number of workers at 6 domestic lead production plants (smelters and recycling plants) and 10 battery plants. Increased incidences of total malignant neoplasms were observed for both categories of lead workers, but the increase was statistically significant only for lead production workers. The increase in total malignancies appeared to be due to small, statistically nonsignificant increases in digestive and respiratory tract tumors (evident in both the lead production and battery workers) and urinary tract tumors (in production workers). /Lead cmpd/
[Cooper WC; Ann NY Acad Sci 271:250-59 (1976) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.56 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

/It was/ reported that lead had no cancer-inducing properties, although standard mortality ratios of 125-149% for total malignant neoplasms, 172% for respiratory cancer, and 229% for cancers of other sites were reported in battery workers. In a recent evaluation of a more select subset from the original study, ... increased standard mortality ratios for total malignancies in both groups of workers (statistically significant only in the battery workers) attributed to digestive and respiratory cancers were reported. These small excesses of cancer death could not be correlated with onset, duration, or level of exposure. /Lead compound/
[Cooper WC; New York, NY: Academic Press, 111-43 (1981) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.56 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

In a study of lead workers, 15 who were identified had no other risk factors for renal disease and who had previously unsuspected lead nephropathy (detected as reduced glomerular filtration rates). Only 3 of the 15 men had experienced symptoms of lead poisoning. Blood lead levels were as follows: >80 ug/dL in 1 subject, 40-80 ug/dL in 11 subjects, and <40 ug/dL in 3 subjects. Examination of renal biopsies from 12 of these men revealed focal interstitial nephritis in 6, in addition to nonspecific changes, including deformed mitochondria, in proximal tubules. /Lead compound/
[Wedeen RP et al; Arch Intern Med 139: 53-7 (1979) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.29 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

Significantly increased central and peripheral nervous system and gastrointestinal symptoms were reported among 25 lead workers with maximum blood lead levels of 50-69 ug/dL and significantly increased central nervous system symptoms among 20 lead workers with maximum blood lead levels <50 ug/dL. /Lead compound/
[Haenninen H et al Neurotoxicology 1: 333-47 (1979) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.37 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

288 lead exposed workers (current or historical blood lead level of >35 ug/dL) at three battery plants with 181 unexposed workers (current blood lead level of less than or equal to 35 ug/dL) at a truck frame plant reported a few differences in neurobehavioral or psychosocial indices. Because the lead exposed workers were younger, less educated, employed for fewer years, and earned less income than the unexposed workers, the analysis adjusted for age , education, and income. Exposed workers had mean current, time weighted average and peak blood lead levels of 40.0, 48.8, and 78.8 ug/dL, respectively. /Lead compound/
[Parkinson DK et al; Am J Epidemiol 123: 261-9 (1986) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.37-8 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

Twenty unexposed men (mean blood lead level = 20.4 ug/dL; range = 11.1-27.1 ug/dL), 20 men exposed to low lead levels (mean blood lead level = 31.7 ug/dL; range = 26-35 ug/dL), and 20 men exposed to high lead levels (mean blood lead level = 52.5 ug/dL; range = 45-60 ug/dL) at an electric storage battery plant were studied. Significant dose-response trends were observed in symptoms such as loss of appetite, paresthesia in lower limbs, weakness of upper limbs, and dropping of objects, with the most marked increases in neurological symptoms in the high-lead group. The high-lead workers performed significantly less well on neurobehavioral tests, with general performance on cognitive and visual motor coordination tasks and verbal reasoning ability most markedly impaired. /Lead compound/
[Campara et al; Int Arch Occup Environ Health 53: 233-46 (1984) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.38 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

Blood lead levels were reported on school children residing near a battery plant in Shanghai, China. A significant dose-effect relationship was found between children's blood lead levels and their neuropsychological performance without any obvious signs of lead poisoning. The blood levels in these children (6-14 years old) ranged from 10 to >30 ug/dL; IQ decreased as blood lead level increased. This dose-response existed after confounding variables were controlled. However, no non-lead-exposed group was used. The study estimated that an increase of 10 ug/dL of blood would result in a lowering of verbal IQ of 8 points, performance IQ of 7 points, and full-scale IQ of 9 points. /Lead compound/
[Wang L et al; Biomed Environ Sci 2: 325-30 (1989) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.44-5 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

In a cross-sectional study of 236 mothers and their infants in Glasgow, Scotland, reductions were demonstrated in gestational age with increasing cord or maternal blood lead levels. In the 11 cases of premature birth (gestational age <38 weeks), maternal blood lead levels averaged approximately 21 ug/dL, and cord blood lead levels averaged approximately 17 ug/dL at delivery. The overall geometric mean blood lead levels at delivery were 14 ug/dL (maternal) and 12 ug/dL (cord). Statistical analyses showed significant negative coefficients for length of gestation against log-transformed maternal or cord blood levels. Birth weight was not associated with blood lead levels. /Lead compound/
[Moore MR et al; Scott Med J 27: 113-22 (1982) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.48 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

Eighteen separate measures were made on a total of 201 boys and girls aged 5.5 years to assess a variety of cognitive, performance, neuropsychological, and behavioral end points. The children were randomly selected from birth records from inner city area of Birmingham, United Kingdom. The selection criteria were quite stringent to control for confounding factors in neuropsychological development. There were no significant correlations between blood lead and any of the three IQ measures. Birth order and mother's IQ were good predictors of IQ. The Factual Performance Test time decreased with increasing blood levels (an improvement in performance), but results of the star copying test were poorer as lead levels increased. /It was/ concluded that the effects of lead found in this inner urban area (mean blood lead = 13.05 ug/dL) in the United Kingdom are small and generally not significant. /Lead compound/
[Harvey PG et al; Br J Dev Psychol 6: 145:56 (1988) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.45 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

One hundred and four children of lower socioeconomic status were evaluated on the Bayley Mental Development Index (MDI) or Stanford-Binet IQ Scale at ages 10 months to 6.5 years by Schroeder. Hierarchical backward stepwise regression analyses indicated that blood lead levels (range: 6-59 ug/dL) were a significant source of the variance in IQ and MDI scores after controlling for socioeconomic status and other factors. Fifty of the children were examined again 5 years later at which time blood lead levels were less than or equal to 30 ug/dL. The 5 years follow-up IQ scores were inversely correlated with contemporary and initial blood lead levels, but the effect of lead was not significant after covariates, especially socioeconomic status, were including in the analysis. /Lead compound/
[Schroeder SR et al; Environ Res 38: 144-154 (1985) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.44 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

Neurobehavioral function was measured in 59 lead workers and 59 controls matched for age, type of job, time on the job, education level, smoking history and alcohol assumption. Statistically significant decreases in the lead-exposed workers were seen for critical flicker fusion reaction, simple reaction time , tracking speeds, hand steadiness tests, and sensory store memory. Sensory store memory speed showed a low but statistically significant correlation with blood lead concentrations. Measurement of neurobehavioral function seemed well chosen, and repeated measures with associated appropriate statistics were used. The performance of the lead-exposed workers was significantly impaired. /Lead compound/
[Williamson AM, RKC Teo; Br J Ind Med 43:374-380 (1986) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.39 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

Autopsies of occupational workers showed that the lead content in lungs was elevated compared to control levels. Autopsies of nonoccupational subjects revealed that males had a higher lead content in tissues compared to females; however, sex differences in lead levels were not observed in tissues of children. In most soft tissues (including brain), lead does not appear to accumulate as a function of age in humans over 20 years old, but these data are based on limited sample size. /Lead compound/
[Barry PSI; Br J Ind Med 32: 119-39 (1975) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.103 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

Dose-response information on a pediatric population relating blood lead levels with the occurrence of acute encephalopathy and death was compiled ... The range of blood levels associated with encephalopathy was approximately 90-800 ug/dL (mean ~330 ug/dL), and the range associated with death was approximately 125-750 ug/dL (mean = 327 ug/dL). All but 1 of the 98 cases of fatal encephalopathy had blood levels 150 ug/dL. /Lead compound/
[Chisolm JJ Jr; J Pediatr 60: 1-17 (1962) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.20 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

High levels of lead have been suggested as a causative agent in Sudden Infant Death Syndrome (SIDS). Blood lead levels in 41 victims of Sudden Infant Death Syndrome (3.9 + or - 1.8 ug/dL) were compared to those of 77 living control babies (3.5 + or - 1.2 ug/dL) and 5 babies of the same ages who died from traumatic causes (3.5 + or - 2.1 ug/dL). The authors controlled for several factors that may influence blood lead levels, including post-mortem shifts in blood water, age, sex, social class, nutrition, fever prior to death or sampling, birth weight, complications at birth, premature birth, and pregnancy history of the mothers. None of these factors differed significantly between the Sudden Infant Death Syndrome babies and the control babies. The post-mortem shift in blood water was accounted for by calculation of the lead concentration in blood dry weight. ... a significantly greater number of the highest lead concentrations in dry blood were found in the Sudden Infant Death Syndrome group than in the control babies (p <0.01) as determined by chi-square analysis. Based on these results, there may be an association between higher body burdens of lead and Sudden Infant Death Syndrome, but the mechanism behind this association cannot be determined at this time. Possibilities include an effect of lead on prenatal and/or postnatal neurological development. /Lead compound/
[Drasch et al; Eur J Pediatr 147: 79-84 (1988) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.20 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

Construction workers (race not specified) using oxyacetylene torches to cut a metal bridge that had been painted with lead-based paint were reported to exhibit increases in heart rate and blood pressure after 4 wk of exposure. Steep increases in blood lead levels were observed only 2 wk after work began. Peak blood lead levels ranged from 48-120 ug/dL. Personal breathing zone exposure to airborne lead ranged from 600-4,000 ug/cu m. /Lead compound/
[Marino et al; Arch Environ Health 44: 140-145 (1989) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.21 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

An increased risk of death due to cerebrovascular disease was observed in a cohort of 1,261 white male newspaper printers (typesetters). /Lead compound/
[Michaels D et al; Int J Epidemiol 20: 970-983 (1991) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.21 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

In adults, a study of 75 autopsies of persons who had resided in a soft-water, leached soil region of North Carolina found a positive correlation between lead level in the aorta and death from heart-related disease. The association persisted after adjustment for the effect of age. /Lead compound/
[Voors AW et al; Arch Environ Health 37: 98-102 (1982) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.25 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

In a study of 102 cases of occupational lead poisoning, 17 cases of clinically verified chronic nephropathy were found. Endogenous creatinine clearance was <80 ug/dL. The mean blood lead level for the entire study population was 80 ug/dL (range = 42-141 ug/dL). Nephropathy was more common among those exposed to lead for more than 10 years than among those exposed for less than 10 years. /Lead compound/
[Lilis R et al; Br J Ind Med 25: 196-202 (1968) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.29 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

Excessive lead exposure has been implicated as a causative agent in kidney disease associated with gout. A correlation was found between the amount of mobilizable lead and the degree of renal impairment in 44 veterans with gout. The 44 gout patients were similar with respect to age, duration of gout, hypertension, history of lead exposure, serum uric acid concentration, blood lead and kidney function was assessed by measuring serum creatinine concentration, creatinine clearance, and 24-hr urinary protein excretion. The results of the 3-day EDTA lead mobilization test were significantly different for the gout patients with renal impairment than for the gout patients without renal impairment. The gout patients with renal impairment excreted 806 + or - 90 ug lead over the 3 days compared to 470 + or - 52 ug lead per three days in patients with gout but no renal impairment. The upper limit of normal in this test is 600 ug lead excreted over 3 days. To rule out the possibility that the renal impairment itself was the cause of excessive mobilizable lead in patients with gout, 10 patients with renal disease but no gout were used as controls for the EDTA lead mobilization test. These controls excreted approximately the same amount of lead over the 3 days as the gout patient 424 + or - 72 ug lead). In addition, the severity of renal impairment (as determined by the serum creatinine concentration) was directly correlated with the amount of mobilizable lead measured in the EDTA test. It is important to note that the gout patients with high mobilizable lead and renal impairment had blood lead levels and ZPP concentrations that were no different from the rest of the group, indicating that there was no indication of lead overexposure in these individuals until the EDTA lead mobilization test was administered. Based on these results, it may be concluded that excessive lead absorption may somehow be involved in the renal impairment associated with some forms of gout. /Lead compound/
[Batuman V et al; N Engl J Med 304: 520-23 (1981) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.31 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

... The Fanconi syndrome is estimated to occur in approximately one out of three children with encephalopathy and blood lead levels of approximately 150 ug/dL. /Lead compound/
[National Academy of Sciences; Lead: Airborne lead in perspective: Biologic effects of atmospheric pollutants. 71-177, 281-313 (1972) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.32 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

In a preliminary report of a cohort study of Danish children of homogeneous social/ethnic background joining the first grade in 1982-1983, tooth lead was significantly associated with height after controlling for other variables (e.g., child's medical history, dietary history, behavior, tobacco smoking of parent, and sociodemographic factors). Exposed children had tooth lead levels of greater than 18.7 ug/g, while controls had tooth lead levels less than 5 ug/g. The average blood lead level in the exposed cohort was <60 ug/dL. The investigators concluded that early lead absorption was a risk factor for impaired growth in children. /Lead compound/
[Lyngbye T et al; International Conference on Heavy Metals in the Environment: The influence of environmental factors on physical growth in school age: A study of low level lead exposure p.210-12 (1987) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.35 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

Disturbances in reaction time, visual motor performance, hand dexterity, IQ test and cognitive performance, nervousness, mood or coping ability were observed in lead workers with blood lead levels of 50-80 ug/dL. /Lead compound/
[Arnvig E et al; Toxicol Lett 5: 399-404 (1980) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.38 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

... Observed hyperactivity and a decrement of approximately 16 IQ points on the McCarthy General Cognitive Index (GCI) among children who had previously had encephalopathy and whose average maximum blood lead levels at the time of encephalopathy were 88 ug/dL (average blood lead level = 59-64 ug/dL). Asymptomatic children with long-term lead exposures and average maximum blood lead levels of 68 ug/dL (average blood lead level = 51-56 ug/dL vs. 21 ug/dL in controls) had an average decrement of 5 IQ points on the McCarthy GCI. ... Children with short-term exposure and average maximum blood lead levels of 61 ug/dL (average blood lead level = 46-50 ug/dL) did not differ from controls. /Lead compound/
[Rummo JH et al; Arch Environ Health 34: 120-5 (1979) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.42 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

In comparison with children having low dentin lead levels (<10 ppm), children having high dentin lead levels (>20 ppm) had significantly lower full-scale WISC-Revised scores; IQ deficits of approximately 4 points; and significantly poorer scores on tests of auditory and verbal processing, on a test of attentional performance as measured by reaction time under conditions of varying delay, and on a teachers' behavioral rating. The frequency of non-adaptive classroom behavior as rated by teachers increased in a dose-related fashion to dentin lead levels. /Lead compound/
[Needleman HL et al; N Engl J Med 300: 689-95 (1979) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.42 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

... A cohort of children studied as primary school students was reexamined as young adults (mean age = 18.4 yr). Neurobehavioral functioning had been found to be inversely related to dentin lead levels at the earlier examination. When the 132 were reexamined 11 yr. later, impairment of neurobehavioral function was still found to be related to the lead content of teeth shed at the ages of 6 and 7 years. In this study, higher lead levels in childhood were significantly associated with lower class standing in high school, increased absenteeism, lower grammatical-reasoning scores, lower vocabulary, poorer hand-eye coordination, longer reaction times, and slower finger tapping. /Lead compound/
[Needleman HL et al; N Engl J Med 322: 83-8 (1990) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.43 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

Maternal and infant hair lead levels, determined from hair samples taken at birth, were found to be correlated inversely with results on neurobehavioral tests (McCarthy Scales of Children's Abilities) when the children were tested at 6 yr of age. /Lead compound/
[Bonithon-Kopp C et al; Neurobehav Toxicol Teratol 8: 307-310 (1986) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.52 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

A group of 150 workmen with long-term lead exposure were categorized by clinical and toxicological data into four groups: lead-poisoned (mean blood lead level = 74.5 ug/dL), and moderately (mean = 52.8 ug/dL), slightly (mean = 41 ug/dL), or physiologically (mean = 23 ug/dL) exposed to lead. The lead-poisoned group and moderately exposed group had decreases in fertility, as measured by asthenospermia, hypospermia, and teratospermia. The effect of lead was thought to be directly on the testes because tests for changes in gonadotropin secretion were negative. /Lead compound/
[Lancranjan I et al; Arch Environ Health 30: 396-401 (1975) as cited in U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) p.54 (1993) ATSDR/TP-92/12]**PEER REVIEWED**

Food and Environmental Agents: Effect on Breast-Feeding: Reported Sign or Symptom in Infant or Effect on Lactation: Lead: Possible neurotoxicity. /From Table 7/
[Report of the American Academy of Pediatrics Committee on Drugs in Pediatrics 93 (1): 142 (1994)]**PEER REVIEWED**

Bone may be affected adversely by lead but also serves as the body's major storage site. /Inorganic lead/
[WHO; Environ Health Criteria: Lead p.110 (1995)]**PEER REVIEWED**

One of the characteristic cellular metabolic reaction in lead intoxication is the formation of intranuclear inclusion bodies, a descrete, dense-staining mass found in the liver parenchyma and in the tubular lining cells of the kidney in man and animal. /Lead/
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 1711]**PEER REVIEWED**

Inorganic lead causes contraction of the peripheral vascular system and affects the blood and blood forming tissues (bone marrow). The "normal" cases of lead poisoning in industry always include hemopoietic effects; These occur very early, before the appearance of /other/ symptoms or signs and, therefore, are important for diagnosis. Lead shortens the life of erythrocytes and impairs hemoglobin synthesis. /Lead cmpd/
[International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983., p. 1201]**PEER REVIEWED**

Chronic exposure to lead has been found to produce infertility, germinal epithelium damage, oligospermia and testicular degeneration, decreased sperm motility, and prostatic hyperplasia. /Lead/
[Thomas, J.A., K.S. Korach, J.A. McLachlan. Endocrine Toxicology. New York, NY: Raven Press, Ltd., 1985., p. 167]**PEER REVIEWED**

There is convincing evidence that lead is transferred to neonates via maternal milk. It appears that maternal milk might be a source of lead for the neonates, particularly when metal levels are elevated in the mother. /Lead/
[Thomas, J.A., K.S. Korach, J.A. McLachlan. Endocrine Toxicology. New York, NY: Raven Press, Ltd., 1985., p. 168]**PEER REVIEWED**

Arthralgia, often associated with muscle aches and pain, is a frequent symptom in lead poisoning. Although generally thought to appear mainly in chronic poisoning, joint pain is often reported even by persons exposed briefly (weeks) who have relatively low blood lead concentrations. It is a symptom that ... frequently indicates that the blood lead concentration is on the rise. /Lead/
[Rom, W.N. (ed.). Environmental and Occupational Medicine. 2nd ed. Boston, MA: Little, Brown and Company, 1992., p. 744]**PEER REVIEWED**

The earliest subjective symptoms /of lead poisoning in working adults/ are diffuse and include weariness at the end of the day. The patient is moody and irritable and may fall asleep watching television. Often he loses his interest in leisure-time activities. Such mild symptoms frequently occur with blood-lead levels below 80 ug/100 ml. /Lead and compounds/
[Zenz, C., O.B. Dickerson, E.P. Horvath. Occupational Medicine. 3rd ed. St. Louis, MO., 1994, p. 518]**PEER REVIEWED**

... /Researchers/ found impaired performances on tests of verbal concept formation, perceptual performance, and memory in a lead-exposed group with present lead concentrations between 40 and 60 ug/100 ml. /Lead/
[Zenz, C., O.B. Dickerson, E.P. Horvath. Occupational Medicine. 3rd ed. St. Louis, MO., 1994, p. 782]**PEER REVIEWED**

A study of 260 infants prospectively followed from birth suggests that the expected stature of a child born to a mother with a prenatal blood lead concentration over 7.7 ug/dL is about 2 cm shorter at 15 mos of age if, potentially, the infant also incurred a 10 ug/dL blood level increase during the 3- to 15-month interval of life. /Lead/
[Ellenhorn, M.J., S. Schonwald, G. Ordog, J. Wasserberger. Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins, 1997., p. 1565]**PEER REVIEWED**

Moderate effects on follicle stimulating hormone and luteinizing hormone have been correlated with lead levels over about 50 ug/dL. /Lead/
[Ellenhorn, M.J., S. Schonwald, G. Ordog, J. Wasserberger. Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins, 1997., p. 1565]**PEER REVIEWED**

The relative risk of preterm delivery at exposure levels of 14 ug/dL or greater was 8.7 times the risk at levels of up to 8 ug/dL in one prospective study. A Cincinnati study noted a half-week's reduction in gestation for every 10 ug/dL increment in blood lead. /Lead/
[Ellenhorn, M.J., S. Schonwald, G. Ordog, J. Wasserberger. Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins, 1997., p. 1565]**PEER REVIEWED**

Lead has an adverse effect on fetuses, particularly in the later stages of development. Distribution of lead in fetal tissues was examined in a case in which a woman was exposed during pregnancy. The female worker was exposed to lead dust for 8 hr daily when conception occurred. ... Measurements of lead content were started after the end of the exposure and continued for 6 months until normal values were obtained. Because of half-life of nearly 20 days for lead elimination from blood, the estimated body burden at the end of exposure was about 1200 ppb. The fetal tissue samples contained between 0.4 (brain) and 7.9 (liver) ug Pb/g dry weight. The fetal lead was stored mainly in bone, blood, and liver. /Lead/
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 2073]**PEER REVIEWED**

Small increases in blood pressure have been related to adults with PbB levels down to 7 ug/dl. /Lead/
[American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 849]**PEER REVIEWED**

... PbB concentrations in excess of 60 ug/100 g ... have been associated with peripheral neuropathy, gastrointestinal disturbances and anemia. ... Nerve conduction velocities ... /decreases/ in workers with maximal blood leads between 50 and 70 ug/100 g. /Lead/
[American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 849]**PEER REVIEWED**