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Increased lead absorption in children with accidental ingestions
Increased Lead Absorption in Children with Accidental Ingestions LAWRENCE
Children with accidental ingestions exhibit excessive hand-tomouth behavior. In a lead-burdened environment, hand-to-mouth behavior contributes to increased lead absorption. To test the hypothesis that accidental-ingestion patients experience greater lead absorption than other urban children, 95 children under 6 years of age with recent ingestlons of nonlead-containing materials and a matched control group were compared. lngestors had higher mean blood lead levels than controls (25.0 pg/dl versus 22.2 pg/dl, P = 0.036) and higher mean etythrocyte protoporphyrinlevels (40.6 pg/dl versus 28.6 pg/dl, P = 0.006). Ingestion victims were more than three times as likely as controls to be classified as having increased lead absorption. Thumbsucking was twice as common among ingestors as controls (37% versus 19%). These findings indicate that children with accidental ingestions are at greater risk of increased lead absorption than other urban children. (Am J Emerg Med 1985;3:301-304)
The identification of asymptomatic children with increased lead absorption should be a priority in urban and other lead-contaminated areas. Data from the recent National Health and Nutrition Examination Survey II (1976- 1980)’ indicate a 4% prevalence of elevated blood lead levels (330 pg/dl) among children aged 6 months through 5 years in the continental United States. The prevalence of elevated blood lead (PbB) among black children in that age group is 12.2%, and black children from low-income families living in central cities experience the greatest degree of lead absorption. Young children are exposed to lead via lead paint, soil, air, housedust, food, and water.* Lead-based paint remains the most significant source of lead exposure for children. 2,3 Children living near heavy in-
From the Division of General Pediatrics, University of Pennsylvania, and the Children’s Hospital of Philadelphia, Philadelphia. Dr. Hammer was a Robert Wood Johnson Fellow in General Academic Pediatrics when this study was performed. Presented in part at the Ambulatory Meeting, Washington, D.C., May 12-15.
Pediatric 1982.
Association
Manuscript received August 23, 1984; revision received vember 7,, 1984; revision accepted November 14, 1984.
No-
Address reprint requests to Dr. Hammer: Department of Pediatrics, Children’s Hospital at Stanford, Stanford University School of Medicine, 520 Willow Road, Palo Alto, CA 94304. Key Words:
Accidental
poisoning,
lead poisoning.
D. HAMMER,
MD, STEPHEN LUDWIG, MD, FRED HENRETIG, MD
dustry, automobile traffic, and ore smelters are also exposed to high levels of airborne lead3v4; yet, Roels et at5 have suggested that transfer of lead-contaminated dust and dirt from hand to mouth may be an important source of lead exposure, even in areas of high air-lead contamination. Children with excessive lead absorption have been shown to have higher concentrations of lead on their hands and in and around their homes.6,7 Pica for paint and dirt contributes to lead exposure.* The relationship between less severe forms of handto-mouth behavior, such as finger sucking and mouthing of non-food objects, and increased lead absorption has been suggested by several authors, but remains controversial.5-7 As children who have had episodes of accidental poisoning are known to exhibit excessive mouthing behavior and thumbsucking,g-‘3 we hypothesized that children with recent histories of accidental ingestion would have a higher prevalence of increased lead absorption than non-ingestion patients from the same geographical area. METHODS The hypothesis was tested in a prospective study conducted from January 1981 through March 1982. Children under 6 years of age who were treated in the emergency department of an urban children’s hospital for an episode of accidental poisoning (with nonleadcontaining substance) had blood drawn for blood lead and erythrocyte protoporphyrin (EP) levels at the time of their emergency visit. Children under 6 years of age, who were having blood drawn for lead screening during visits to the pediatric clinic of the same hospital, served as controls. Children with prior histories of accidental poisoning were excluded from the control group. Controls were matched with ingestors as follows: for each ingestor we selected a control of the same sex, race, and age (within three months if under 4 years old and within six months if 4 years old or older) who had blood drawn for lead screening within a month of the ingestor’s episode of accidental poisoning.14 If more than one child could be matched as a control by these criteria, the child whose lead screening occurred nearest in time to the episode of poisoning was used as a control. One white child in the ingestion group was matched with a black child in 301
AMERICAN
TABLE 1.
JOURNAL
OF EMERGENCY
Characteristics
of Patients
MEDICINE
Studied
No. Male Female Age (range) Age (mean f SD) Race % Black % White Home painted in past 10 years (%) Peeling paint in the home (%) Move within past year (%) History of thumbsucking (%) Reported mouthing of nonfood items (%) Receive regular primary care from any source l
Mean ages compared
n Volume 3, Number 4 n July 1985
using two-tailed
matched
(%)
Controls
P Value*
95 51 44 lo-67 months 28.7 2 13 months
95 51 44 lo-61 months 27.4 2 13 months
NS NS NS
RESULTS Demographic characteristics of the two groups are shown in Table 1. The groups did not differ significantly with respect to any of the demographic variables, including age and geographical location of their
NS
95 5 29 56 33 19 90 100
94 6 17 47 42 37 85 98
t-test. Other comparisons
the control group who otherwise met the selection criteria described above. All matching was done by one author who was blind to the results of the serum lead and EP determinations. Blood was drawn by standard venipuncture technique into lead-free collection tubes. Serum lead determinations were performed by atomic absorption l5 The EP levels were determined spectrophotometry. by the extraction method of Piomelli,i6 in the laboratory of the City Health Department of Philadelphia, which participates in regular interlaboratory proficiency testing with the Centers for Disease Control, Atlanta, Georgia, and the Department of Health, Commonwealth of Pennsylvania (R. Churi, personal communication, 1982). Parents of all participants in the study completed a questionnaire regarding their housing (age, location, presence of lead paint, or prior history of lead paint), the child’s prior history of thumb-sucking and mouthing behavior, accidental ingestions, and usual source of health care. Source of payment for medical care was used as a reflection of socioeconomic status. Increased lead absorption was defined as the presence of PbB greater than or equal to 30 kg/d1 with EP greater than or equal to 50 pg/dl.17 The chi-square test was used to compare the numbers of children with increased lead absorption in the two groups. Mean PbB and EP levels were compared using matched t-tests. Informed consent was obtained from participants under guidelines approved by the Committee for Protection of Human Subjects.
302
lngestors
made using the x2 statistic
NS NS NS NS co.01 NS NS with d.f. =
1,
homes, condition of the paint in the homes, recent move to a new location, or source of payment for care (over 90% of each group were receiving medical assistance from the Commonwealth of Pennsylvania). Almost all ingestors and controls received regular primary care from either the Children’s Hospital of Philadelphia or one of the local Health Department clinics. Significantly more ingestors than controls had a history of thumbsucking (37% versus 19%; P s 0.01 by x2 test). Mouthing of non-food objects was reported in 85% of ingestors and 90% of controls. Results of the PbB and EP measurements are shown in Table 2. Children with ingestions had significantly higher mean PbB and EP values than controls. The ingestion group contained ten children with increased lead absorption, whereas the control group contained only three (P c 0.05by x2 test, d.f. = 1) (Table 3); relative risk of increased lead absorption in the ingestion group versus the control group was 3.33. Sixteen ingestors and 15 controls had PbB levels greater than 30 p.g/dl with EP levels less than 50 pg/dl. Four children had levels of PbB greater than 50 p&d]. Of these, three were in the ingestion group, and one was in the control group. None had been screened previously. DISCUSSION Recent data from the second National Health and Nutrition Examination Survey (NHANES II) have highlighted the persistent prevalence of increased lead absorption among pre-school children in the United States, particularly among black children from lowincome families living in urban areas.’ In NHANES II, the mean blood lead levels (+ SEM) for black children 6 months to 5 years of age from families with annual incomes of less than $6,000 was 22.9 2 0.9 kg/ dl. Likewise, the mean PbB (? SEM) for pre-school black children living in urban areas of greater than l,OOO,OOOpopulation was 22.2 4 0.8 p,g/dl. These
HAMMER
means are similar to the mean PbB (+ SEM) found among the children in our control group (22.2 + 0.8 (*g/dl), which was also composed predominantly of black inner-city children from low-income families. Our data demonstrated a further increased lead absorption in the children who presented with accidental ingestions. There were no significant differences between the ingestion and control groups regarding age, sex, race, age and geographical distribution of housing, condition of house paint, and month of entry into the study. Although socioeconomic status was not measured directly, both groups had equivalent numbers of subjects who relied on medical assistance for payment of services (over 90% in each group). Furthermore, both groups were composed of children from the geographical area around the hospital, which is predominantly one of low socioeconomic status. No measurements of lead in the homes and neighborhoods of these children was attempted. Participants in both groups generally lived in homes more than 25 years old. Very few homes had been recently painted, and none had been recently de-leaded. Thus, the environmental exposure to lead was similar for both groups of participants. The ingested materials did not contain lead, and none of the study’s participants had a prior history of lead intoxication. Children in both groups received regular primary care, often including lead screening; yet, these data show that screening in the emergency department setting is also of value. The increased lead absorption found in children in the ingestion group may be a result of their hand-tomouth behavior.5 Charney, et a16 have shown that children with increased lead absorption have more lead on their hands than other children and that their homes are more lead-contaminated. Similar to the results of study by Turbeville and Fearnow,13 the ingestion group in this study had a higher rate of thumbsucking than the control group, and this is a direct source of exposure to hand-surface lead. Craig,9 Baltimore and Meyer,“) Shaw,” and Sibertr2 have all described higher rates of hand-to-mouth behavior in children with ingestions than in other children. These findings have clinical significance with regard to the management of children in the emergency department or outpatient clinical setting in areas of the TABLE 2.
Blood
Lead and EP* Test Results (Mean
* SD)
lngestors (n = 95)
Controls (n = 95)
P Value+
Blood lead (pg/dl)
25.0 * 10.5
22.2 * 7.7
0.036
EP (kg/d1 whole blood)
40.6 2 39.0
26.6 2 14.0
0.006
* Erythrocyte protoporphyrin. t By two-tailed matched t-test.
ET AL n LEAD ABSORPTION
TABLE3. Lead Absorption
of Patients lngestor
IN CHILDREN
Studied Control
(no.)
(no.) Increased’ Not increased l
PbB z 30 pgldl
10 a5
3 92
and EP z= 50 Fg/dl.
U.S. where lead absorption remains a problem. Children in this study with accidental ingestions were three times as likely as controls to have increased lead absorption (as defined by PbB 230 kg/d1 and EP ~50 t&dl). Ten children with ingestions and three controls required further medical attention as a result of the results of this screening process for increased lead absorption. Though the mean PbB in the ingestion group was only 2.8 Fg/dl greater than that of the control group, ingestors were more likely to have higher PbB and EP levels than controls. Three ingestors and one control had PbB levels 350 pg/dl. The likelihood that an ingestor would have increased lead absorption was 10.5% in this study. At this prevalence rate, screening for increased lead absorption can be cost effective using EP determinations alone.” Children participating in this study were not all screened for iron deficiency; therefore, it is not possible to determine the extent to which iron deficiency may have contributed to the elevation in EP seen in the ingestion group. Some investigators think that iron deficiency may be associated with pica. l9 It is possible that iron deficiency in some of the subjects in this study may have contributed to pica and an increased tendency toward accidental ingestion. In any case, the finding of an elevated EP along with elevated PbB should lead the physician to suspect iron deficiency in addition to increased lead absorption. A note of caution is in order in generalizing these results. This study was carried out in an urban environment that is still heavily contaminated with lead. Lead exposure resulting from mouthing behavior is most significant in such an environment. The levels of PbB and EP found in the control group indicate that children in this environment are still being exposed to significant amounts of lead. Children with ingestions were three times as likely as controls in a similar environment to have elevated PbB and EP. We recommend that children who reside in lead-contaminated geographical areas, and who have had acidental ingestions, should be tested for evidence of increased lead absorption. REFERENCES 1. Mahaffey KR, Annest JL, Roberts J, et al. National of blood lead levels: United States, 1976-1980. Med 1982:307:573-579.
estimate N Engl J
303
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
n Volume 3, Number 4 n July 1985
2. Chisholm JJ, Barltrop D. Recognition and management of children with increased lead absorption. Arch Dis Child 1979;54:249-282. 3. Centers for Disease Control. Increased lead absorption and lead poisoning in young children. J Pediatr 1975;87:824830. 4. Landrigan PJ, Gahlback SH, Rosenblum BF, et al. Epidemic lead absorption near an ore smelter. N Engl J Med 1975;292:123-129. 5. R+s HA, Bucket J-P, Lauwerys RR. et al. Exposure to lead by the oral and the pulmonary routes of children living in the vicinity of a primary lead smelter. Environ Res 1980;22:81-94. 8. Charney E, Sayre J, Coulter M. Increased lead absorption in inner city children: Where does it come from? Pediatrics 1980;85:226-231. 7. Baltrop D, Strehlow CD, Thornton I, et al. Absorption of lead from dust and soil. Postgrad Med J 1975;51:801-804. 8. Griggs RC, Sunshine I, Newill VA, et al. Environmental factors in childhood lead poisoning. JAMA 1964;187:703707. 9. Craig JO. Oral factors in accidental poisoning. Arch Dis Child 1955;30:419-423. 10. Baltimore CL, Meyer RJ. A study of storage, child behavior
384
11. 12. 13.
14.
15. 16. 17.
traits, and mothers’ knowledge of toxicology in 52 poisoned families and 52 comparison families. Pediatrics 1968;42:312-317. Shaw MTM. Accidental poisoning in children: A psychosocial study. N Z Med J 1977;85:269-272. Sibert JR, Newcombe RG. Accidental ingestion of poisons and child personality. Postgrad Med J 1977;53:254-256. Tuberville DF, Fearnow RF. Is it possible to identify the child who is a “high risk” candidate for the accidental ingestion of a poison? Clin Pediatr 1976;15:918-919. Hunter JM. The summer disease: An integrative model of the seasonality aspects of childhood lead poisoning. Sot Sci Med 1977;11:691-703. Hessel DW. Simple and rapid determination of lead in blood. Atomic Absorption Newsletter 1968;7:3. Piomelli S. A micromethod for free erythrocyte protoporphyrin-The FEP. J L Clin Med 1973;81:932-940. Centers for Disease Control. Preventing lead poisoning in young children. US. Department of Health, Education,
and Welfare Public Health Service, Atlanta, Georgia. April, 1978. 18. Berwick IM, Komaroff AL. Cost effectiveness of lead screening. N Engl J Med 1982;306:1392-1398. 19. Crosby WH. Pica. JAMA 1976;235:2765.
Children with accidental ingestions exhibit excessive hand-tomouth behavior. In a lead-burdened environment, hand-to-mouth behavior contributes to increased lead absorption. To test the hypothesis that accidental-ingestion patients experience greater lead absorption than other urban children, 95 children under 6 years of age with recent ingestlons of nonlead-containing materials and a matched control group were compared. lngestors had higher mean blood lead levels than controls (25.0 pg/dl versus 22.2 pg/dl, P = 0.036) and higher mean etythrocyte protoporphyrinlevels (40.6 pg/dl versus 28.6 pg/dl, P = 0.006). Ingestion victims were more than three times as likely as controls to be classified as having increased lead absorption. Thumbsucking was twice as common among ingestors as controls (37% versus 19%). These findings indicate that children with accidental ingestions are at greater risk of increased lead absorption than other urban children. (Am J Emerg Med 1985;3:301-304)
The identification of asymptomatic children with increased lead absorption should be a priority in urban and other lead-contaminated areas. Data from the recent National Health and Nutrition Examination Survey II (1976- 1980)’ indicate a 4% prevalence of elevated blood lead levels (330 pg/dl) among children aged 6 months through 5 years in the continental United States. The prevalence of elevated blood lead (PbB) among black children in that age group is 12.2%, and black children from low-income families living in central cities experience the greatest degree of lead absorption. Young children are exposed to lead via lead paint, soil, air, housedust, food, and water.* Lead-based paint remains the most significant source of lead exposure for children. 2,3 Children living near heavy in-
From the Division of General Pediatrics, University of Pennsylvania, and the Children’s Hospital of Philadelphia, Philadelphia. Dr. Hammer was a Robert Wood Johnson Fellow in General Academic Pediatrics when this study was performed. Presented in part at the Ambulatory Meeting, Washington, D.C., May 12-15.
Pediatric 1982.
Association
Manuscript received August 23, 1984; revision received vember 7,, 1984; revision accepted November 14, 1984.
No-
Address reprint requests to Dr. Hammer: Department of Pediatrics, Children’s Hospital at Stanford, Stanford University School of Medicine, 520 Willow Road, Palo Alto, CA 94304. Key Words:
Accidental
poisoning,
lead poisoning.
D. HAMMER,
MD, STEPHEN LUDWIG, MD, FRED HENRETIG, MD
dustry, automobile traffic, and ore smelters are also exposed to high levels of airborne lead3v4; yet, Roels et at5 have suggested that transfer of lead-contaminated dust and dirt from hand to mouth may be an important source of lead exposure, even in areas of high air-lead contamination. Children with excessive lead absorption have been shown to have higher concentrations of lead on their hands and in and around their homes.6,7 Pica for paint and dirt contributes to lead exposure.* The relationship between less severe forms of handto-mouth behavior, such as finger sucking and mouthing of non-food objects, and increased lead absorption has been suggested by several authors, but remains controversial.5-7 As children who have had episodes of accidental poisoning are known to exhibit excessive mouthing behavior and thumbsucking,g-‘3 we hypothesized that children with recent histories of accidental ingestion would have a higher prevalence of increased lead absorption than non-ingestion patients from the same geographical area. METHODS The hypothesis was tested in a prospective study conducted from January 1981 through March 1982. Children under 6 years of age who were treated in the emergency department of an urban children’s hospital for an episode of accidental poisoning (with nonleadcontaining substance) had blood drawn for blood lead and erythrocyte protoporphyrin (EP) levels at the time of their emergency visit. Children under 6 years of age, who were having blood drawn for lead screening during visits to the pediatric clinic of the same hospital, served as controls. Children with prior histories of accidental poisoning were excluded from the control group. Controls were matched with ingestors as follows: for each ingestor we selected a control of the same sex, race, and age (within three months if under 4 years old and within six months if 4 years old or older) who had blood drawn for lead screening within a month of the ingestor’s episode of accidental poisoning.14 If more than one child could be matched as a control by these criteria, the child whose lead screening occurred nearest in time to the episode of poisoning was used as a control. One white child in the ingestion group was matched with a black child in 301
AMERICAN
TABLE 1.
JOURNAL
OF EMERGENCY
Characteristics
of Patients
MEDICINE
Studied
No. Male Female Age (range) Age (mean f SD) Race % Black % White Home painted in past 10 years (%) Peeling paint in the home (%) Move within past year (%) History of thumbsucking (%) Reported mouthing of nonfood items (%) Receive regular primary care from any source l
Mean ages compared
n Volume 3, Number 4 n July 1985
using two-tailed
matched
(%)
Controls
P Value*
95 51 44 lo-67 months 28.7 2 13 months
95 51 44 lo-61 months 27.4 2 13 months
NS NS NS
RESULTS Demographic characteristics of the two groups are shown in Table 1. The groups did not differ significantly with respect to any of the demographic variables, including age and geographical location of their
NS
95 5 29 56 33 19 90 100
94 6 17 47 42 37 85 98
t-test. Other comparisons
the control group who otherwise met the selection criteria described above. All matching was done by one author who was blind to the results of the serum lead and EP determinations. Blood was drawn by standard venipuncture technique into lead-free collection tubes. Serum lead determinations were performed by atomic absorption l5 The EP levels were determined spectrophotometry. by the extraction method of Piomelli,i6 in the laboratory of the City Health Department of Philadelphia, which participates in regular interlaboratory proficiency testing with the Centers for Disease Control, Atlanta, Georgia, and the Department of Health, Commonwealth of Pennsylvania (R. Churi, personal communication, 1982). Parents of all participants in the study completed a questionnaire regarding their housing (age, location, presence of lead paint, or prior history of lead paint), the child’s prior history of thumb-sucking and mouthing behavior, accidental ingestions, and usual source of health care. Source of payment for medical care was used as a reflection of socioeconomic status. Increased lead absorption was defined as the presence of PbB greater than or equal to 30 kg/d1 with EP greater than or equal to 50 pg/dl.17 The chi-square test was used to compare the numbers of children with increased lead absorption in the two groups. Mean PbB and EP levels were compared using matched t-tests. Informed consent was obtained from participants under guidelines approved by the Committee for Protection of Human Subjects.
302
lngestors
made using the x2 statistic
NS NS NS NS co.01 NS NS with d.f. =
1,
homes, condition of the paint in the homes, recent move to a new location, or source of payment for care (over 90% of each group were receiving medical assistance from the Commonwealth of Pennsylvania). Almost all ingestors and controls received regular primary care from either the Children’s Hospital of Philadelphia or one of the local Health Department clinics. Significantly more ingestors than controls had a history of thumbsucking (37% versus 19%; P s 0.01 by x2 test). Mouthing of non-food objects was reported in 85% of ingestors and 90% of controls. Results of the PbB and EP measurements are shown in Table 2. Children with ingestions had significantly higher mean PbB and EP values than controls. The ingestion group contained ten children with increased lead absorption, whereas the control group contained only three (P c 0.05by x2 test, d.f. = 1) (Table 3); relative risk of increased lead absorption in the ingestion group versus the control group was 3.33. Sixteen ingestors and 15 controls had PbB levels greater than 30 p.g/dl with EP levels less than 50 pg/dl. Four children had levels of PbB greater than 50 p&d]. Of these, three were in the ingestion group, and one was in the control group. None had been screened previously. DISCUSSION Recent data from the second National Health and Nutrition Examination Survey (NHANES II) have highlighted the persistent prevalence of increased lead absorption among pre-school children in the United States, particularly among black children from lowincome families living in urban areas.’ In NHANES II, the mean blood lead levels (+ SEM) for black children 6 months to 5 years of age from families with annual incomes of less than $6,000 was 22.9 2 0.9 kg/ dl. Likewise, the mean PbB (? SEM) for pre-school black children living in urban areas of greater than l,OOO,OOOpopulation was 22.2 4 0.8 p,g/dl. These
HAMMER
means are similar to the mean PbB (+ SEM) found among the children in our control group (22.2 + 0.8 (*g/dl), which was also composed predominantly of black inner-city children from low-income families. Our data demonstrated a further increased lead absorption in the children who presented with accidental ingestions. There were no significant differences between the ingestion and control groups regarding age, sex, race, age and geographical distribution of housing, condition of house paint, and month of entry into the study. Although socioeconomic status was not measured directly, both groups had equivalent numbers of subjects who relied on medical assistance for payment of services (over 90% in each group). Furthermore, both groups were composed of children from the geographical area around the hospital, which is predominantly one of low socioeconomic status. No measurements of lead in the homes and neighborhoods of these children was attempted. Participants in both groups generally lived in homes more than 25 years old. Very few homes had been recently painted, and none had been recently de-leaded. Thus, the environmental exposure to lead was similar for both groups of participants. The ingested materials did not contain lead, and none of the study’s participants had a prior history of lead intoxication. Children in both groups received regular primary care, often including lead screening; yet, these data show that screening in the emergency department setting is also of value. The increased lead absorption found in children in the ingestion group may be a result of their hand-tomouth behavior.5 Charney, et a16 have shown that children with increased lead absorption have more lead on their hands than other children and that their homes are more lead-contaminated. Similar to the results of study by Turbeville and Fearnow,13 the ingestion group in this study had a higher rate of thumbsucking than the control group, and this is a direct source of exposure to hand-surface lead. Craig,9 Baltimore and Meyer,“) Shaw,” and Sibertr2 have all described higher rates of hand-to-mouth behavior in children with ingestions than in other children. These findings have clinical significance with regard to the management of children in the emergency department or outpatient clinical setting in areas of the TABLE 2.
Blood
Lead and EP* Test Results (Mean
* SD)
lngestors (n = 95)
Controls (n = 95)
P Value+
Blood lead (pg/dl)
25.0 * 10.5
22.2 * 7.7
0.036
EP (kg/d1 whole blood)
40.6 2 39.0
26.6 2 14.0
0.006
* Erythrocyte protoporphyrin. t By two-tailed matched t-test.
ET AL n LEAD ABSORPTION
TABLE3. Lead Absorption
of Patients lngestor
IN CHILDREN
Studied Control
(no.)
(no.) Increased’ Not increased l
PbB z 30 pgldl
10 a5
3 92
and EP z= 50 Fg/dl.
U.S. where lead absorption remains a problem. Children in this study with accidental ingestions were three times as likely as controls to have increased lead absorption (as defined by PbB 230 kg/d1 and EP ~50 t&dl). Ten children with ingestions and three controls required further medical attention as a result of the results of this screening process for increased lead absorption. Though the mean PbB in the ingestion group was only 2.8 Fg/dl greater than that of the control group, ingestors were more likely to have higher PbB and EP levels than controls. Three ingestors and one control had PbB levels 350 pg/dl. The likelihood that an ingestor would have increased lead absorption was 10.5% in this study. At this prevalence rate, screening for increased lead absorption can be cost effective using EP determinations alone.” Children participating in this study were not all screened for iron deficiency; therefore, it is not possible to determine the extent to which iron deficiency may have contributed to the elevation in EP seen in the ingestion group. Some investigators think that iron deficiency may be associated with pica. l9 It is possible that iron deficiency in some of the subjects in this study may have contributed to pica and an increased tendency toward accidental ingestion. In any case, the finding of an elevated EP along with elevated PbB should lead the physician to suspect iron deficiency in addition to increased lead absorption. A note of caution is in order in generalizing these results. This study was carried out in an urban environment that is still heavily contaminated with lead. Lead exposure resulting from mouthing behavior is most significant in such an environment. The levels of PbB and EP found in the control group indicate that children in this environment are still being exposed to significant amounts of lead. Children with ingestions were three times as likely as controls in a similar environment to have elevated PbB and EP. We recommend that children who reside in lead-contaminated geographical areas, and who have had acidental ingestions, should be tested for evidence of increased lead absorption. REFERENCES 1. Mahaffey KR, Annest JL, Roberts J, et al. National of blood lead levels: United States, 1976-1980. Med 1982:307:573-579.
estimate N Engl J
303
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
n Volume 3, Number 4 n July 1985
2. Chisholm JJ, Barltrop D. Recognition and management of children with increased lead absorption. Arch Dis Child 1979;54:249-282. 3. Centers for Disease Control. Increased lead absorption and lead poisoning in young children. J Pediatr 1975;87:824830. 4. Landrigan PJ, Gahlback SH, Rosenblum BF, et al. Epidemic lead absorption near an ore smelter. N Engl J Med 1975;292:123-129. 5. R+s HA, Bucket J-P, Lauwerys RR. et al. Exposure to lead by the oral and the pulmonary routes of children living in the vicinity of a primary lead smelter. Environ Res 1980;22:81-94. 8. Charney E, Sayre J, Coulter M. Increased lead absorption in inner city children: Where does it come from? Pediatrics 1980;85:226-231. 7. Baltrop D, Strehlow CD, Thornton I, et al. Absorption of lead from dust and soil. Postgrad Med J 1975;51:801-804. 8. Griggs RC, Sunshine I, Newill VA, et al. Environmental factors in childhood lead poisoning. JAMA 1964;187:703707. 9. Craig JO. Oral factors in accidental poisoning. Arch Dis Child 1955;30:419-423. 10. Baltimore CL, Meyer RJ. A study of storage, child behavior
384
11. 12. 13.
14.
15. 16. 17.
traits, and mothers’ knowledge of toxicology in 52 poisoned families and 52 comparison families. Pediatrics 1968;42:312-317. Shaw MTM. Accidental poisoning in children: A psychosocial study. N Z Med J 1977;85:269-272. Sibert JR, Newcombe RG. Accidental ingestion of poisons and child personality. Postgrad Med J 1977;53:254-256. Tuberville DF, Fearnow RF. Is it possible to identify the child who is a “high risk” candidate for the accidental ingestion of a poison? Clin Pediatr 1976;15:918-919. Hunter JM. The summer disease: An integrative model of the seasonality aspects of childhood lead poisoning. Sot Sci Med 1977;11:691-703. Hessel DW. Simple and rapid determination of lead in blood. Atomic Absorption Newsletter 1968;7:3. Piomelli S. A micromethod for free erythrocyte protoporphyrin-The FEP. J L Clin Med 1973;81:932-940. Centers for Disease Control. Preventing lead poisoning in young children. US. Department of Health, Education,
and Welfare Public Health Service, Atlanta, Georgia. April, 1978. 18. Berwick IM, Komaroff AL. Cost effectiveness of lead screening. N Engl J Med 1982;306:1392-1398. 19. Crosby WH. Pica. JAMA 1976;235:2765.