- Email: [email protected]
When to order a lead level?
When to Order a Lead Level? ELSEVIER
Karen R. Judy, MD RUSH PRESBYTERIAN ST. LUKE'S MEDICAL CENTER, CHICAGO, ILLINOIS, USA
Emergenc!i Medicine Update Abstract Elevated lead levels are a common problem in adults and especially children in the United States today. Lead is absorbed usually through the gastrointestinal tract after ingestion of leaded paint or dust contaminated with lead. Another route of ex-
posure is inhalation from polluted air particularly in the vicinity of smelters or battery manufacturing
plants. Children are especially at risk of lead toxicity because they absorb lead much more easily than adults. The pathogenesis of lead toxicity is not known. Patients can easily be screened for risk of lead toxicity with a simple series of questions. Awareness of the possibility of lead poisoning in children as well as adults is important in detection of this often subtle condition that
usually causes subtle but irreversible neuropsyehologic findings. Elevated lead levels can result in loss of intelligence as measured by iq points, as well as neurobehavioral sequelae including hyperactivity and antisocial behavior. In adults lead toxicity can manifest as memory loss or mood disturbances. Treatment of lead toxicity involves removal of the source of exposure and then chelation therapy. © 1996 K. R. Judy. MEDICAL UPDATE FOR PSYCHIATRISTS 1;5:146-148, 1996.
© 199G K. R. ludu ISSN IQ82-75"7919G/$15.QQ PII b'1082-75"7919G)QQQG3-5
Lead is a ubiquitous neurotoxin that has poisoned man for more than 5000 },ears. The hazards of lead were recognized in the U.S. in the 1970's and since that time the mean blood lead levels have declined from 15.9 mcg/dl in 1976 to approximately 6 meg/dl in 1990 in pediatric patients ( 1 ). Lead poisoning now most fiequently occurs as au asymptomatic condition with possible neurobehavioral consequences. It continues to be prevalent as demonstrated by a stu@ in 1994 in which it was estimated that 1.7 million children between the ages of 1 to 5 have blood lead levels at or above 10 mcg/dl (2). The overall prevalence rate for the U.S. population of blood lead levels greater than 10 mcg/dl is estimated to be 4.5%. For all children 1 to 5 years of age, the prevalence rate is 8.9%; in low income households it is 16.3%. For African American children in low income households the prevalence is "28.4% (3). There is no such thing as a "normal" lead level, only that level which we are wilhng to tolerate. Sources of Lead Most of childhood exposure to lead occurs through lead paint ingestion and air pollution. Lead paint was banned in 1977 but many inner city children live in old housing, especially pre-1960 housing with old peeling paint present. It is estimated that 74% of all homes built in the U.S. prior to 1978 have leadbased paint in them (3). Lead-contaminated dust and soil can be found in many areas especially during remodeling projects placing non-poor children also at risk. Contamination of drinking water through improperly soldered pipe joints or lead plumbing is another source of lead. hnported canned foods, Southern Asia or Hispanic folk reme-
Address reprint requests to: Karen R. Judy', MD Associate Director Pediatric Emergeney Room, Rush Presb}~erian St. Luke's Medical Center, 17'25 W. Harrison St., Chicago, IL. 60612-38`24.
dies, and poorly glazed ceramic dishes can contain lead. Mrborne lead is produced by smelters, refineries and combustion of leaded gasoline (which was outlawed in 1973). Children whose parents work in lead smelters or battery manufacturing plants are also at risk. Adults are exposed to lead through various occupations and hobbies as listed on Table 1.
Absorption and Distribution Lead freely crosses the placenta and accumulates in the developing fetus so that infants of mothers with elevated lead levels are often born with potentially toxie lead burdens. Maternal eord blood lead levels of 10 to 15 meg/dl appear to be assoeiated with reduced gestational age and reduced birth weight (3). Recent studies indicate that there is little transfer of lead to the infant in breast milk when the mother has a blood lead level less than 40 meg/dl (3). Most absorption for children occurs through ingestion and gastrointestinal absorption. Young ehildren are more likely to ingest or inhale lead beeause of their proximity to the floor and frequent hand to mouth behaviors and pica. The percentage of ingested lead that is absorbed is four to five times greater in children than adults (4). Mso, lead absorption is enhanced by iron deftPlenty, which is frequently found in preschool and inner eity etfildren. Because children have a higher mineral turnover in bone, more lead is stored and released in kids placing them at higher risk (5). Lead is carried by red blood cells through the bodv and deposited in soft tissue and bone. The half-life of lead in bone is measured in years; possibly up to 20 years (5). Chelation mobilizes lead from blood and soft tissues but not from bone. There is significant re-equilibration of lead stores so that lead stored in bone can later eanse toxicity once these shifts oecur. Thus children who have been identified with elevated lead levels in the past or who have undergone treatment for lead
When to Order a Lead Level?
MEDICAL UPDATE FOR PSYCHIATRISTS
Table !. Possible Methods of Exposure Oeeupations
Auto repairers Battery manufacturers or repairers
Brass/copper foundry Bridge reconstruction
Hobbies
Environmental
Other
Car or boat repair Casting lead figures (toy soldiers, etc.)
Ceramic ware/Pottery Lead eustal
Furniture refinishing Home remodeling
Lead paint (especially maritime paint) Lead painted homes
Jewehy making Lead soldering (electronics) Painting Preparing lead shot, fishing sinkers, bullets Reloading cartridges Stained glass making Target shooting at firing ranges
Lead soldered cans (imported) Proximity to lead related industries
Asian cosmetics Folk remedies (greta, azareon, pay-loo-ah, ghasard, Hai ge fen, Bali Goli, Kandu, Kohl, X-yoo-Fa, Mai ge fen and poying tan) Gasoline sniffing (organic lead)
workers
Chemical manufacturers Gas station attendants Glass manufacturers Industrial machinery equipment operators Lead smelters and refineries Lead miner Migrant farm worker
Renovating/remodeling older homes Soil/dust near industries, roadways Use of water form leaded pipes
Plastics manufacturers Plumbers, pipe fitters Police officers Printers Radiator repair Rubber products manufacturers Steel welders and cutters
elevation must receive careful lougitudinal follow-up. Toxicity is usually caused by chronic ingestion of small amounts rather than a single acute ingestion. Pathogenesis
The exact mechanism by which lead affects children's health is not known. Lead binds to sulfhydryl groups on enzymes and alters their activity; among the enzymes affected are delta-aminolevulinie acid (ALA) dehydrase, 1,25 Vitamin D hydroxylase, brain eytoehrome, and brain adenylate cyclase (6). Lead alters cellular calcium metabolism; it competes with calcium, sodimn, and magnesium in neurotransmission. More recently, lead has been shown to interfere with the development of the endogenous opioid system of the brain. All of these are possible mechanisms for observed effects, but none have been demonstrated to occur in association with a given outcome. Neuropsuchologic Sequelae
It has been recognized for decades that high dose exposure to lead in eMdren
place them at risk for acute eneephalopa@ and chronic, persistent neuropsyehologic sequelae, such as mental retardation, seizures, and behavioral dysfunction. Much of the damage to the brain is irreversible. It is believed that even low levels of lead exposure also place children at risk for neurobehavioral dysfunction. Reduced reaction times, poorer ratings on classroom behavior, and reduced intelligence have all been documented in low level lead exposure. A recent study showed that I.Q. was decreased by 6 points for ever}, 10 meg/dl increase in lead level (7). In 1979 Needleman did a study that showed a dose response between lead and negative ratings of children's behaviors (distractible, aggressive, disorganized, hyperactive) by teachers (5). Several other studies have documented that children with elevated lead levels are more hyperactive and aggressive. A study in 1996 showed that children with elevated lead levels are at increased risk for antisocial and delinquent behavior and the effect followed a developmental course (8). Other effects of lead include sensorineural hear147
ing loss, chronic nephropathy, hypertension, decreased stature.
W h e n to Order a Lead Level
A lead level should be emergently obtained in any patient with eneephalopathy, seizures and focal neurologie findings. Other signs and symptoms compatible with lead poisoning are: loss of appetite, abdominal cramps, constipation, anemia, apathy, lethargy or periodic vomiting (3). Children with a hearing impairment or developmental delay are also at risk for elevated lead. Behavioral problems such as hyperactivity, aggressive behavior or antisocial behavior can be manifestations of lead poisoning as can learning disabilities and decreased school performance. Any of these complaints or problems need to be correlated with the patients risk for lead exposure as determined by several questions including: Does the patient live in a high risk area (i.e. urban, near lead producing industries such as smelters or battery recycling plants ) ?
g. n. Judy
Does he live in or regularly visit a home built before 19607 Are any home renovations being performed? Does a sibling or playmate have an elevated lead level? Does the patient hve with a person whose occupation or hobby involves exposure to lead? Does the patient receive any herbal or home remedies? Has the child visited Mexico or Central America or South America? Are ceramic dishes or pottery used at home? Adults with lead poisoning often present with weakness and focal palsies (i.e., wrist drop). If an adult reports a decrease in memory, attention, concentration particularly if they work in a lead industry or are involved in hobbies that expose them to lead, a lead level should be documented. Baker et al. found that foundry workers had an increased rate of depression, confusion, anger, fatigue and tension with blood lead levels greater than 40 mcg/dl (9). This study reports the necessity of specific inquiries that should be made of individuals with affectual complaints to clarify the nature of their work and workplace exposure to lead.
Avoiding Lead Hazards Children with elevated lead levels should receive an iron and calcium rich diet. A low fat diet has also been found to decrease lead absorption (10). Environments with high lead concentrations should be cleaned thoroughly with wet mopping using phosphate detergents particularly around window sills and stairwells. Children's hands should be washed frequently, especially prior to meals. Cribs and playpens should be moved away from surfaces containing lead paint.
Treatment Lead levels greater than 10 mcg/dl are now considered noteworthy. At this
MEDICAL UPDATE FOR PSYCHIATRISTS
level, risk factors should be reviewed and nutritional status assessed (paying particular attention to iron and calcium status). Follow-up should be obtained in 3 - 6 months. At levels greater than 20, the child should receive a complete medical evaluation and referral to other practitioners experienced in the treatment of lead poisoned children. Environmental inspection and lead abatement should be performed by trained professionals. Abatement involves evacuating the entire family from the residence during the abatement procedure to decrease risk of exposure ( 11 ). Other siblings should be screened and iron replacement considered. Close follow-up is needed at monthly intervals. At levels greater than 45 mcg/dl, chelation with oral succimer or iv Calcium EDTA should be started. Oral succimer enhances excretion of lead; it is used for a 20-day course with close follow-up for rebound lead levels. Symptoms of lead poisoning in a child with a lead level of 50 mcg/di or greater is considered a medical emergency. Blood lead levels greater than 70 mcg/ dl require acute hospitalization for intramuscular BAL (dimercaprol) as well as iv Calcium EDTA therapy over a 5 day course. BAL chelates lead and is excreted in bile and urine. Close monitoring of hydration status and kidney function is necessary with these agents (12). Seizures are controlled with diazepam or paraldehyde. Management of increased intracranial pressure and cerebral edema should be conducted in a pediatric intensive care setting. For lead levels of 10-19 mcg/dl, use nutritional counseling, cleaning house, close follow-up; for 20-45 mcg/dl use pediatric referral, environmental inspection, considering iron replacement therapy; and for >45 mcg/dl, refer for treatment by chelation. Lead toxicity is a common occurrence in today's population. Many of the adults and children that psychiatrists examine and treat are at risk for lead toxicity due to exposure from multiple sources. Lead can have an irreversible neuropsychologic
impact that can prevent the patient from obtaining his or her fidl potential. Patients can easily be screened by asking a series of questions to determine the patients risk of lead exposure and then obtaining a venous sample if indicated. The earlier elevated lead levels are recognized, the sooner they can be addressed with minimal neuropsychological impact. This will benefit the patient and society as well.
References 1. Graef J, Clinical Toxicology Review, Massachusetts Poison Control System. May 1992; 14 (8). 2. Brady D, Pirkle J, Kramer R, et al. Blood Llead levels in the U.S. population. JAMA 1994;272:277-283. 3. Illinois Department of Public Health. Guidelines for Detection and Management of Lead Poisoning for Physicians and Healthcare Providers. Jan 1996. 4. Weitzman M, Glotzer D. Lead Poisoning. Pediatr Rev 1992; 13(12) :461-468. 5. Puente AE, Reynolds CR, eds. Neuropsychological Toxicology: 2nd ed. Plenum Press, New York, 1995. 6. Needleman HL. The current status of childhood lead toxici~. Adv Pediatr 1993; 49:125-137. 7. Bellinger DC, Stiles KM, Needleman HL. Low-level lead exposure, intelligence, and academic achievement longterm follow-up study. Pediatrics 1992; 90:855-861. 8. Needleman HL, Riess JA, Tobin MJ, Biesecker GE, Greenhouse JB. Bone lead levels and delinquent behavior. JAMA 1996;275:363-369. 9. Baker EL, Feldman RG, White RF, Harley JP. The role of occupational lead exposure in the genesis of psychiatric and behavioral disturbances. Acta Psychiatrica Scandinavica Suppl 1983;303: 38-48. 10. Lucas SR, Sexton M, Langenberg P. Relationship between blood lead and nutritional factors in preschool children: a cross-sectional study. Pediatrics 1996; 97:74-78. 11. Chisolm JJ, Farfel M. Environmental. control and deleading. Pediatr Ann 1994;23:627-633. 12. Berlin C, German R, et al. Treatment guidelines for lead exposure in children. Pediatrics 1995;96:155-159.
Karen R. Judy, MD RUSH PRESBYTERIAN ST. LUKE'S MEDICAL CENTER, CHICAGO, ILLINOIS, USA
Emergenc!i Medicine Update Abstract Elevated lead levels are a common problem in adults and especially children in the United States today. Lead is absorbed usually through the gastrointestinal tract after ingestion of leaded paint or dust contaminated with lead. Another route of ex-
posure is inhalation from polluted air particularly in the vicinity of smelters or battery manufacturing
plants. Children are especially at risk of lead toxicity because they absorb lead much more easily than adults. The pathogenesis of lead toxicity is not known. Patients can easily be screened for risk of lead toxicity with a simple series of questions. Awareness of the possibility of lead poisoning in children as well as adults is important in detection of this often subtle condition that
usually causes subtle but irreversible neuropsyehologic findings. Elevated lead levels can result in loss of intelligence as measured by iq points, as well as neurobehavioral sequelae including hyperactivity and antisocial behavior. In adults lead toxicity can manifest as memory loss or mood disturbances. Treatment of lead toxicity involves removal of the source of exposure and then chelation therapy. © 1996 K. R. Judy. MEDICAL UPDATE FOR PSYCHIATRISTS 1;5:146-148, 1996.
© 199G K. R. ludu ISSN IQ82-75"7919G/$15.QQ PII b'1082-75"7919G)QQQG3-5
Lead is a ubiquitous neurotoxin that has poisoned man for more than 5000 },ears. The hazards of lead were recognized in the U.S. in the 1970's and since that time the mean blood lead levels have declined from 15.9 mcg/dl in 1976 to approximately 6 meg/dl in 1990 in pediatric patients ( 1 ). Lead poisoning now most fiequently occurs as au asymptomatic condition with possible neurobehavioral consequences. It continues to be prevalent as demonstrated by a stu@ in 1994 in which it was estimated that 1.7 million children between the ages of 1 to 5 have blood lead levels at or above 10 mcg/dl (2). The overall prevalence rate for the U.S. population of blood lead levels greater than 10 mcg/dl is estimated to be 4.5%. For all children 1 to 5 years of age, the prevalence rate is 8.9%; in low income households it is 16.3%. For African American children in low income households the prevalence is "28.4% (3). There is no such thing as a "normal" lead level, only that level which we are wilhng to tolerate. Sources of Lead Most of childhood exposure to lead occurs through lead paint ingestion and air pollution. Lead paint was banned in 1977 but many inner city children live in old housing, especially pre-1960 housing with old peeling paint present. It is estimated that 74% of all homes built in the U.S. prior to 1978 have leadbased paint in them (3). Lead-contaminated dust and soil can be found in many areas especially during remodeling projects placing non-poor children also at risk. Contamination of drinking water through improperly soldered pipe joints or lead plumbing is another source of lead. hnported canned foods, Southern Asia or Hispanic folk reme-
Address reprint requests to: Karen R. Judy', MD Associate Director Pediatric Emergeney Room, Rush Presb}~erian St. Luke's Medical Center, 17'25 W. Harrison St., Chicago, IL. 60612-38`24.
dies, and poorly glazed ceramic dishes can contain lead. Mrborne lead is produced by smelters, refineries and combustion of leaded gasoline (which was outlawed in 1973). Children whose parents work in lead smelters or battery manufacturing plants are also at risk. Adults are exposed to lead through various occupations and hobbies as listed on Table 1.
Absorption and Distribution Lead freely crosses the placenta and accumulates in the developing fetus so that infants of mothers with elevated lead levels are often born with potentially toxie lead burdens. Maternal eord blood lead levels of 10 to 15 meg/dl appear to be assoeiated with reduced gestational age and reduced birth weight (3). Recent studies indicate that there is little transfer of lead to the infant in breast milk when the mother has a blood lead level less than 40 meg/dl (3). Most absorption for children occurs through ingestion and gastrointestinal absorption. Young ehildren are more likely to ingest or inhale lead beeause of their proximity to the floor and frequent hand to mouth behaviors and pica. The percentage of ingested lead that is absorbed is four to five times greater in children than adults (4). Mso, lead absorption is enhanced by iron deftPlenty, which is frequently found in preschool and inner eity etfildren. Because children have a higher mineral turnover in bone, more lead is stored and released in kids placing them at higher risk (5). Lead is carried by red blood cells through the bodv and deposited in soft tissue and bone. The half-life of lead in bone is measured in years; possibly up to 20 years (5). Chelation mobilizes lead from blood and soft tissues but not from bone. There is significant re-equilibration of lead stores so that lead stored in bone can later eanse toxicity once these shifts oecur. Thus children who have been identified with elevated lead levels in the past or who have undergone treatment for lead
When to Order a Lead Level?
MEDICAL UPDATE FOR PSYCHIATRISTS
Table !. Possible Methods of Exposure Oeeupations
Auto repairers Battery manufacturers or repairers
Brass/copper foundry Bridge reconstruction
Hobbies
Environmental
Other
Car or boat repair Casting lead figures (toy soldiers, etc.)
Ceramic ware/Pottery Lead eustal
Furniture refinishing Home remodeling
Lead paint (especially maritime paint) Lead painted homes
Jewehy making Lead soldering (electronics) Painting Preparing lead shot, fishing sinkers, bullets Reloading cartridges Stained glass making Target shooting at firing ranges
Lead soldered cans (imported) Proximity to lead related industries
Asian cosmetics Folk remedies (greta, azareon, pay-loo-ah, ghasard, Hai ge fen, Bali Goli, Kandu, Kohl, X-yoo-Fa, Mai ge fen and poying tan) Gasoline sniffing (organic lead)
workers
Chemical manufacturers Gas station attendants Glass manufacturers Industrial machinery equipment operators Lead smelters and refineries Lead miner Migrant farm worker
Renovating/remodeling older homes Soil/dust near industries, roadways Use of water form leaded pipes
Plastics manufacturers Plumbers, pipe fitters Police officers Printers Radiator repair Rubber products manufacturers Steel welders and cutters
elevation must receive careful lougitudinal follow-up. Toxicity is usually caused by chronic ingestion of small amounts rather than a single acute ingestion. Pathogenesis
The exact mechanism by which lead affects children's health is not known. Lead binds to sulfhydryl groups on enzymes and alters their activity; among the enzymes affected are delta-aminolevulinie acid (ALA) dehydrase, 1,25 Vitamin D hydroxylase, brain eytoehrome, and brain adenylate cyclase (6). Lead alters cellular calcium metabolism; it competes with calcium, sodimn, and magnesium in neurotransmission. More recently, lead has been shown to interfere with the development of the endogenous opioid system of the brain. All of these are possible mechanisms for observed effects, but none have been demonstrated to occur in association with a given outcome. Neuropsuchologic Sequelae
It has been recognized for decades that high dose exposure to lead in eMdren
place them at risk for acute eneephalopa@ and chronic, persistent neuropsyehologic sequelae, such as mental retardation, seizures, and behavioral dysfunction. Much of the damage to the brain is irreversible. It is believed that even low levels of lead exposure also place children at risk for neurobehavioral dysfunction. Reduced reaction times, poorer ratings on classroom behavior, and reduced intelligence have all been documented in low level lead exposure. A recent study showed that I.Q. was decreased by 6 points for ever}, 10 meg/dl increase in lead level (7). In 1979 Needleman did a study that showed a dose response between lead and negative ratings of children's behaviors (distractible, aggressive, disorganized, hyperactive) by teachers (5). Several other studies have documented that children with elevated lead levels are more hyperactive and aggressive. A study in 1996 showed that children with elevated lead levels are at increased risk for antisocial and delinquent behavior and the effect followed a developmental course (8). Other effects of lead include sensorineural hear147
ing loss, chronic nephropathy, hypertension, decreased stature.
W h e n to Order a Lead Level
A lead level should be emergently obtained in any patient with eneephalopathy, seizures and focal neurologie findings. Other signs and symptoms compatible with lead poisoning are: loss of appetite, abdominal cramps, constipation, anemia, apathy, lethargy or periodic vomiting (3). Children with a hearing impairment or developmental delay are also at risk for elevated lead. Behavioral problems such as hyperactivity, aggressive behavior or antisocial behavior can be manifestations of lead poisoning as can learning disabilities and decreased school performance. Any of these complaints or problems need to be correlated with the patients risk for lead exposure as determined by several questions including: Does the patient live in a high risk area (i.e. urban, near lead producing industries such as smelters or battery recycling plants ) ?
g. n. Judy
Does he live in or regularly visit a home built before 19607 Are any home renovations being performed? Does a sibling or playmate have an elevated lead level? Does the patient hve with a person whose occupation or hobby involves exposure to lead? Does the patient receive any herbal or home remedies? Has the child visited Mexico or Central America or South America? Are ceramic dishes or pottery used at home? Adults with lead poisoning often present with weakness and focal palsies (i.e., wrist drop). If an adult reports a decrease in memory, attention, concentration particularly if they work in a lead industry or are involved in hobbies that expose them to lead, a lead level should be documented. Baker et al. found that foundry workers had an increased rate of depression, confusion, anger, fatigue and tension with blood lead levels greater than 40 mcg/dl (9). This study reports the necessity of specific inquiries that should be made of individuals with affectual complaints to clarify the nature of their work and workplace exposure to lead.
Avoiding Lead Hazards Children with elevated lead levels should receive an iron and calcium rich diet. A low fat diet has also been found to decrease lead absorption (10). Environments with high lead concentrations should be cleaned thoroughly with wet mopping using phosphate detergents particularly around window sills and stairwells. Children's hands should be washed frequently, especially prior to meals. Cribs and playpens should be moved away from surfaces containing lead paint.
Treatment Lead levels greater than 10 mcg/dl are now considered noteworthy. At this
MEDICAL UPDATE FOR PSYCHIATRISTS
level, risk factors should be reviewed and nutritional status assessed (paying particular attention to iron and calcium status). Follow-up should be obtained in 3 - 6 months. At levels greater than 20, the child should receive a complete medical evaluation and referral to other practitioners experienced in the treatment of lead poisoned children. Environmental inspection and lead abatement should be performed by trained professionals. Abatement involves evacuating the entire family from the residence during the abatement procedure to decrease risk of exposure ( 11 ). Other siblings should be screened and iron replacement considered. Close follow-up is needed at monthly intervals. At levels greater than 45 mcg/dl, chelation with oral succimer or iv Calcium EDTA should be started. Oral succimer enhances excretion of lead; it is used for a 20-day course with close follow-up for rebound lead levels. Symptoms of lead poisoning in a child with a lead level of 50 mcg/di or greater is considered a medical emergency. Blood lead levels greater than 70 mcg/ dl require acute hospitalization for intramuscular BAL (dimercaprol) as well as iv Calcium EDTA therapy over a 5 day course. BAL chelates lead and is excreted in bile and urine. Close monitoring of hydration status and kidney function is necessary with these agents (12). Seizures are controlled with diazepam or paraldehyde. Management of increased intracranial pressure and cerebral edema should be conducted in a pediatric intensive care setting. For lead levels of 10-19 mcg/dl, use nutritional counseling, cleaning house, close follow-up; for 20-45 mcg/dl use pediatric referral, environmental inspection, considering iron replacement therapy; and for >45 mcg/dl, refer for treatment by chelation. Lead toxicity is a common occurrence in today's population. Many of the adults and children that psychiatrists examine and treat are at risk for lead toxicity due to exposure from multiple sources. Lead can have an irreversible neuropsychologic
impact that can prevent the patient from obtaining his or her fidl potential. Patients can easily be screened by asking a series of questions to determine the patients risk of lead exposure and then obtaining a venous sample if indicated. The earlier elevated lead levels are recognized, the sooner they can be addressed with minimal neuropsychological impact. This will benefit the patient and society as well.
References 1. Graef J, Clinical Toxicology Review, Massachusetts Poison Control System. May 1992; 14 (8). 2. Brady D, Pirkle J, Kramer R, et al. Blood Llead levels in the U.S. population. JAMA 1994;272:277-283. 3. Illinois Department of Public Health. Guidelines for Detection and Management of Lead Poisoning for Physicians and Healthcare Providers. Jan 1996. 4. Weitzman M, Glotzer D. Lead Poisoning. Pediatr Rev 1992; 13(12) :461-468. 5. Puente AE, Reynolds CR, eds. Neuropsychological Toxicology: 2nd ed. Plenum Press, New York, 1995. 6. Needleman HL. The current status of childhood lead toxici~. Adv Pediatr 1993; 49:125-137. 7. Bellinger DC, Stiles KM, Needleman HL. Low-level lead exposure, intelligence, and academic achievement longterm follow-up study. Pediatrics 1992; 90:855-861. 8. Needleman HL, Riess JA, Tobin MJ, Biesecker GE, Greenhouse JB. Bone lead levels and delinquent behavior. JAMA 1996;275:363-369. 9. Baker EL, Feldman RG, White RF, Harley JP. The role of occupational lead exposure in the genesis of psychiatric and behavioral disturbances. Acta Psychiatrica Scandinavica Suppl 1983;303: 38-48. 10. Lucas SR, Sexton M, Langenberg P. Relationship between blood lead and nutritional factors in preschool children: a cross-sectional study. Pediatrics 1996; 97:74-78. 11. Chisolm JJ, Farfel M. Environmental. control and deleading. Pediatr Ann 1994;23:627-633. 12. Berlin C, German R, et al. Treatment guidelines for lead exposure in children. Pediatrics 1995;96:155-159.