Document pmm0XqbxY5RLZrKyyjzVxgp4k
ETIIYL CORPORATION
iNTr.n-ori'ici-;
To Mr. H. E. Hesselberg
Fu o m
Sue A. Gendernalik
Su h j e c t Lead Poisoning in Child run
Anna iss
Ad d h k s s
Da t e
May 14, 1971
Attached is a memorandum on this subject based on a review of the literature. While no attempt has been made at an exhaustive literature search, the literature reviewed does represent a fairly good survey of the more recent information and presumably reflects the thinking of some of the medical authorities in the field.
There are indications that EPA may take the position that present levels of lead in the air are harmful because they can be sufficient to push a child, already exposed to abnormally high levels of lead from ingestion, over the threshold into overt poisoning. While this seems a little like a 300 -lb lady claiming it was the last ounce that made her obese, I have some thoughts that may help in disputing such a position.
1. There are some rather strong statements by medical authorities that implicate ingested lead as the cause of lead poisoning in children. The following statement by Jacobziner is fairly typical, others are included in the attached memorandum:
"While inhalation of lead fumes and absorption through the skin may also cause lead poisoning, all cases in children reported in New York City in the past decade have occurred as a result of ingestion. "
The literature reviewed in preparing the attached memorandum contains accounts of only a few instances of lead poisoning caused by inhalation. In all cases it was associated with expsoure to abnormally high concen trations due to such things as burning old storage battery casings for fuel, living near a smelter or, in one instance, living in a foundry.
2, It has been suggested that lead from automobile exhaust settling near the curbs or in the streets creates a source high in lead easily accessible to children.
It is well established that lead poisoning is almost always found in children aged 1 to 5 and is especially prevalent among children between 1 and 3. It seems unlikely that children in this age group would play at the curb or in the street even in slum areas. They would probably be traffic statistics before they were poisoned by lead from eating street sweepings.
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In this regard the literature reviewed did not report street sweepings as a source* of lead in any of the eases studied. When dirt was found to be the source, it was always dirt containing paint chips that had either been scraped or had peeled from the exterior of a dwelling. One investigation in Minneapolis reported using dilapidated dwellings with badly peeling exterior paint surrounded by areas immediately adjacent to the house where there was no vegetation as a means of finding children with lead poisoning. They found that 9 out of 24 children living in 14 such homes had abnormally high Levels of lead in urine.
It is generally accepted that sources containing less than 1% lead are not potentially hazardous with regard to exposure to lead. There is little data in the literature, but street sweepings would seem to fall in this category. Samples collected in New York City in 1924 averaged 1190 ppm while samples collected in 1934 contained 1760 ppm on the average.
The report of the Swiss Leaded Gasoline Commission values for the percent of lead in settled dust in streets in Zurich for the period 1948 to 1 955 ranged from 0.01 to 0.2% Pb.
Dr. Vaun Newill recently reported that street sweepings in New York City containerl 2650 pg Pb/g. He also reports a concentration of 4.8 mg Pb/ft2 measured by Dr. Edward Ferrand in fifteen street samplings in New York OCitv in June 1969. This is combined with an average dustfall of 10 g/nr/mo found in industrial sections of 77 midv/estern cities to obtain the 5160 pg Pb/g.
Chisolm says it is easy for a child to get 50 to 100 mg of lead from the ingestion of a single small paint chip. Thus this exposure would appear to be more severe than would be expected from street sweepings.
3. The pronounced seasonal distribution of lead poisoning may be used to support the argument that children are exposed to lead from automobile exhaust when playing outside in the summer months. Chisolm and others estimate that 3 to 6 months of exposure to lead precedes overt lead poisoning. This being so, it is difficult to support a case for outside sources of lead as tlie cause for lead poisoning in the early part of the summer. The attached memorandum indicates that there are other factors that may explain this seasonal variation.
SAC :c l Att.
Sue A. Gendcrnalik
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LEAD POISONING IN CHILDREN
'
Lead poisoning continues to be a major public health problem among
children in urban areas of the United States. The cause is well understood
and the means of prevention is known. However, prevention is a formidable
problem because it entails renovation and reconstruction of housing in large
areas.
The children most often affected are between one and five years of age
with the highest incidence occurring in the eighteen month to two year age group. Jacob/.iner^ reported that 82. 5% of the cases studied in New York
City were, among children 1 to 3 years old. There appears to be no significant difference in incidence between sexes but the incidence among siblings is observed frequently. The children arc usually from families in the low socioeconomic levels who live in houses built prior to World War II when interior house paints were formulated with lead pigments comprising 30 to
(2) 70% of the total solids of the paint.
Lead paint on interior surfaces has been identified by numerous investigators as the most frequent source of lead in childhood poisoning. Jacobzincr^ states: "In nearly 90% of the reported cases, a careful history
revealed that affected children ingested flakes of plaster or paint peelings (2)
for several months prior to diagnosis. " Chisolm and Harrison reported
that indoor paint was responsible for 83% of the cases they studied and that
windowsills and frames were the source of the paint in 64% of the cases. (3)
Cohen of Children's Hospital, Washington, D. C. said, "As far as we
are concerned, lead poisoning (in children) is due to ingestion of lead - contamm
substances, primarily lead-containing paints."
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N 814.01
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Investigators frequently report that in the homes visited, crumbling, painted plaster and loose paint chips from walls, ceilings, door frames and windowsills are readily accessible to children. Outdoor sources of paint are to be found on porches, fences and particularly in the dirt near the foundation of houses where paint flakes either scraped or peeled from the exterior of the house become mixed with the dirt. This was found to be tire area in which children frequently played.
The painted surfaces are frequently comprised of multiple layers. Even in homes where the more recent coats are newer paints containing
(4, 5, 6) less than 1% lead, paint flakes have been found to contain up to 50% lead because, of the peeling of multiple layers.
(2, 7) Chisolm ' has emphasized the. severity of the exposure to lead associated with the ingestion of paint chips or painted plaster. He found the mean daily fecal output of lead by lead-poisoned children was 44 mg Pb per day. This amount of lead would be provided by the ingestion of 0. 88 g paint chips containing 5% Pb. Obviously, paint chips containing higher percentages of lead would provide this exposure in lesser amounts of paint chips. Chisolm points out that the daily fecal output of these lead-poisoned children was six times that of severely exposed industrial workers and eleven times that of workers in various trades with less severe exposure. He also suggested that 'The more frequent occurrence of encephalopathy in children as compared with adults may depend in part upon the more intense exposure rather than upon any inherent biologic differences between child and adult. "
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The relationship between childhood lead poisoning and old, poorly
maintained housing is clearly pointed out by a study conducted in Cleveland
(g)
during the summer months of 1959 and I960.
Four census tracts within the
area known as the "lead belt" were chosen for the study. Based on I960
census data, the population of all four areas was similar with respect to
racial, educational, financial backgrounds and family size. In three of the
areas, 98% of the houses were constructed prior to 1939 while in the fourth
area all dwellings, represented by a housing project, had been constructed
since 1950. A door-to-door survey was conducted to obtain the study sample
which included all the children in preselected age groups in each of the four
areas. During the two-year period, 994 children between 1 and 5 years of
age were admitted to the program. Only 3% of the urine samples obtained
from the children in area 4 were abnormal (0.08 mg/liter or higher while
25% to 37% of the samples from the other three areas were abnormal. No
abnormal urine samples were found among children 12 to 23 months old in
area 4 while 22% to 27% were abnormal from the other three areas. A history
of pica was found in 22 to 50% of the children from the three areas containing
the old housing whereas only 5% was reported in the fourth area.
Pica (9)
According to Barltrop the term pica relates to the magpie (Pica pica),
a bird known for its capricious and voracious appetite. Pica is the ingestion
of substances not normally regarded as food. While the tendency for hand-to-
mouth activity is quite normal in children through the first year, if continued
beyond this it often becomes pica. Pica usually stops at about 3 years of age,
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but it has been known to continue up to 14 years and even beyond. (3)
Lourie reported that 50 to 60% of Negro clinic patients aged 1 to 2 years treated at Children's Hospital in Washington, D. C. had pica. Surprisingly, he also found that 28% of white private patients in the same age group had pica. In children admitted for poisonings of all kinds, 67% of those in the early age group had pica. He points out that what is usually regarded as "accidental" poisoning isn't accidental at all.
Pica is frequently associated with lead poisoning in children and most frequently involves paint chips, painted plaster and dirt containing paint chips. Other items ingested include clay, laundry starch, ashes, putty, string, crayons, matches, cigarette butts and newspaper. Persons with pica usually specialize in one or two specific items.
Two major factors are involved with pica in young children. One is an unusual interest in oral activity and the other is emotional difficulties associated by immature mothers or mothers who are absent when the child is in critical training stages. The child may be born with a large amount of oral interests or "mouthing" or it can be encouraged by the mother's handling of the child. Oral interest is encouraged by mothers who, when a baby is upset, put a bottle in its mouth, give it a pacifier, or stuff its mouth with cookies. Cases are even reported of mothers giving the child the thing that gives her comfort --even to clay and laundry starch. A significant number of children with pica are weaned from the bottle at a very late age and some use pacifiers at 3 and 4 years of age.
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Lourie reported that 63% of the mothers of children with pica had pica themselves.
Children with pica in low socioeconomic groups are often from families where fathers are absent or unavailable. This fosters maternal dependency and the mothers frequently are passive and inactive and often have a life history of despair. They arc often overcome with feelings of helplessness and hopelessness and even when they know what has to be done cannot mobilize
e
themselves. In some cases the mothers too are absent from the family, and the children are left in the care of older children or other emotionally immature adults for long periods of time.
Lourie reported that in some instances pica is culturally determined. This is particularly true in persons with associations to areas of the Southeast where dirt eating is fairly common and clay-eating parties and picnics are held. Pica was a problem on Southern plantations among the slaves. They found that eating dirt made them incapacitated and unable to work. Mouthlocks were used to prevent some slaves from using this as a means of suicide.
With such an emotional and cultural environment and with sources of lead readily accessible, the association of pica and lead poisoning in children is obvious.
Nutritional deficiency has been suggested as a possible cause of pica. However, the work of Gulelius et al^ ^ appears to dispute this.
Seasonal Distribution There is a marked seasonal distribution associated with lead poisoning
and particularly with lead encephalopathy. The Baltimore City Health
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Department^**' *^ investigated 720 cases of lead poisoning in children
between 1931 and 1958. Of these, about two-thirds occurred during the
summer months --June through September. The same seasonal distribution
was observed in each of the years studied. A similar seasonal pattern is shown by 1529 cases reported in New York Cily from 1954 through 1963^ ^ and f,or 11G977n0. (!3) Stud..ies m qS, t. TLou. is, (12) Philadel.phia, (14) am, Chi. cago (12)
have also exhibited the same seasonal distribution.
Several factors have been suggested to explain the high incidence of
lead poisoning among children in the summer. Some have been partially
substantiated by studies in animals. However, the responsible agent or
agents in children has not been fully identified. The absorption of calcium
is known to be enhanced by vitamin D and since lead, like calcium, is a
bivalent metal, it has been suggested that lead may be metabolized similarly.
(15)
Shelling and Hooper
proposed that vitamin D increased the absorption
of lead from the intestines if the diet was high in calcium and low in phosphorus.
This theory has been partially borne out by Rapaport and Rubin in studies on rat
Animals who were fed a diet containing lead and either exposed to the sun or
fed supplementary vitamin D, lost weight, became ill and died. Those who
were fed a diet containing lead while kept in the dark and were not given
supplementary vitamin D, showed only retardation of growth.
This theory depends on the diet being high in calcium and low in phosphorus Sobel and his cowoekers^ ^ showed that vitamin D had no pronounced effect
on the concentration of lead in blood if the diet was low in calcium and high in phosphorus. With the fortified vitamin D mill; used as a major food source
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for children in low income families, many authorities feel that while increased
ultraviolet radiation may play a role in the seasonal distribution of childhood
lead poisoning, it is probably not the only factor involved.
Another explanation offered for the high incidence of lead poisoning in the
summer months is the increase in environmental temperature. Investigators
have reported increased susceptibility in animals to some drugs and chemicals
with exposure to high ambient temperatures or with increase in body tempera-
(17 18)
ture. '
The animal work relating to the effect of increased temperature
on lead absorption indicates that the effect is related to the extent of the
exposure to high temperature. Blackman (19) showed that rabbits injected subcutaneously with lead for
seven weeks died within 102 hours when subjected to a temperature of 99F,
whereas those similarly injected but kept at room temperature survived, as did the control sample at 99 "F. Germuth et al^ ^ reported a seasonal
variation in the susceptibility of rabbits to subcutaneous injections of lead.
The average survival time was shorter in summer than in winter.
(12)
Experiments
were conducted in which mice were injected with lead
acetate or lead nitrate, either intravenously or intraperitoneally, and
exposed continuously to temperatures of 72F or 95F. The mice were
injected with a single dose of lead sufficient to cause death in 20 to 40% of
the animals when maintained at the lower temperatures. The experiment
was repeated several times and the data were combined for statistical
treatment. The exposure of.the mice to the higher temperature after injection
resulted in significantly higher mortality, hastened the onset of death and
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accelerated the rate of dying. The effects were more pronounced when
injected intravenously than when injected intrapcritoncally which seems to
rule out increased absorption of lead from the peritoneal cavity.
(12)
Baetjer
reported that mice exposed to 95 F for only eight hours
a day showed less effect of the high temperature than when exposed
continuously.
(14)
Rapaport and Rubin
reported no apparent affect on rats fed a high
lead diet and exposed to 104 F for four hours each day.
Since children exposed to high temperature tend to sweat and can thus
be dehydrated, tests were conducted in which mire were restricted in water
intake sufficient to cause a 12% loss in body weight over a 3-day period.
The mire were then injected with lead and maintained at 72 F or 95 F.
Dehydration significantly increased mortality at both temperatures and
hastened the onset of death at the higher temperature when the lead was
injected intraperitoneally. It has been suggested that a 12% loss of body
weight in three days represents rather severe dehydration. (3)
Lourie suggests that the increase in intestinal infections among
children in the summer may cause dehydration and acidosis which may
result in mobilization of lead stored in the bones and increased circulation
of lead through the tissues.
While these studies leave many questions unanswered and appear to be
conflicting in sonic respects, they do indicate that the body stresses brought
on by high temperatures associated with the .summer months may be a factor
in the seasonal distribution of lend poisoning in children.
LIA-76513
Still another factor in the increase in lead poisoning in warm weather is the increased expsoure to lead-containing paint used on exterior surfaces and especially to flakes of this material mixed with the dirt in tire yards in which children play.
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REFERENCES
1. Jacobz.inc r, Harold, "Lead Poisoning in Childhood: Epidemiology, Manifestations, and Prevention, " Clinical Pediatrics, 5, 277-282, May 19 6.
2. Chisolm, J. J. , Jr. and Harrison, Id. E. , "The-Exposure of Children to Lead, " Pediatrics, 18, 943,-957, Dec. 1956.
3. Cohen, G. J. , Lourie, R. S. and Abernathy, W. , "Grand Rounds: Pica and Lead Poisoning. " CHnical Proceedings, 21, 193-204, JulyAug. 1965.
4. Patton, J. L. , "Lead Poisoning --Five Casel, " Nursing Times, 64, 284, March 1968.
5. Kopito, L. , Briley, A. M. and Shwachman, Id. , "Chronic Plumbism in Children. Diagnosis by Hair Analysis, " J. Amer. Med. Assoc. , 209, 243 -8, July 1969.
6. Barltrop, D. and KillaJa, N. J. P. , "Factors Influencing Exposure of Children to Lead, " Arch. Diseases in Childhood, 44, 476-9, August 1969.
7. Chisolm, J. J. , Jr. , "Childhood Lead Intoxication, " Medical Times, 98, 92-106, Sept. 1970.
8. Griggs, R. C., Sunshine, I., Newill, V. A., Newton, B. W. , Buchanan, S. and Rasch, C. A., "Environmental Factors in Childhood Lead Poisoning, " J. Amer. Mod. Assoc. , 187, 703-707, March 7, 1964.
9. Barltrop, D. , "Lead JJoisoning in Childhood, " Post Grad. Med. J. , 44, 537-48, July 1968.
10. Gutclius, M. F. , Millican, F. K. , Layman, E. M. , Cohen, G. J. and Dublin, C. C. , "Nutritional Studies of Children with Pica. 1. Controlled Study Evaluating Nutritional Status, " Pediatrics, 29, 1012 (1962).
11. Williams, H. , Kaplan, E. , Couchman, C. E. and Sayers, R. R. , "Lead Poisoning in Young Children, " Public Health Reports, 67, 230-236, (March 1952).
12. Baetjer, A. M. , "Effects of Season and Temperature on Childhood Plumbism, " Industrial Medicine; and Surgery, 28, 137-143 (March 1959).
13. Chisolm, J. J. , Jr., "Lead Poisoning," Sci. Amer, , 224, 15-23 (Feb. 1971).
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14. Rapaport, M. and Rubin, M. I., "Lead Poisoning--A Clinical and Experimental Study of the Factors Influencing the Seasonal Incidence in Children, " Amcr. .T. of Diseases in Children, 6 1, 245-255 (1941).
15. Shelling, D. II. and Hooper, K. B. , "Calcium and Phosphorus Studies, " Bull. Johns Hopkins Hospital, 58, 137 (1936).
16. Sobcl, A. E. , "The Biochemical Behavior of Lead. Influence of Calcium, Phosphorus and Vitamin D on Lead in Blood and Bone, " J, Biological Chcm. , 132, 239 (1940).
17. Fuhrman, F. A. , "The Effect of Body Temperature on Drug Action, " Physiological Review, 26, 247 (1946).
18. Baetjer, A. M. and Smith, R. , "Effect of Environmental Temperature on Reaction of Mice to Parathion, An Anticholinesterase Agent, " Amer. J. Physiology, 186, 3 9 (1956).
19. Blackman, S. S. , "The Lesions of Lead Encephalitis in Children, " Bull, Johns Hopkins Hospital, 6_1_, 1 (1937).
20. Germuth, F. G. and Eagle, H. , "The Efficacy of BAL (2, 3-Dimercapto propanol) in the Treatment of Experimental Lead Poisoning in Rabbits, " J. Pharm, and Exp, Thcrap. , 92, 397 (1948).
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