Declaration of Maridee Ann Gregory, M.D.

    SENT BY:NHeLP died LEE WE he Aa 6240075:416 

DANIEL E. LUNGREN, Attorney General 
of the State of Califorma 

CHARLTON G. HOLLAND, III 
Assistant Attorney General 

STEPHANIE WALD 
Supervising Deputy Attorney General 

LAN E. VAN 
Deputy Attorney General 

2101 Webster Street, 12th Floor 
Oakland, California 94612-3049 
Telephone: (413) 464-1173 

Attorneys for Defendant 

UNITED STATES DISTRICT COURT 

NORTHERN DISTRICT OF CALIFORNIA 

No. C 90 3620 EFL 

DECLARATION OF MARIDEE 
ANN GREGORY, M.D. 

ERIKA MATTHEWS AND JALISA 
MATTHEWS, by their guardian ad litem Lisa 
Matthews, and PEOPLE UNITED FOR A 
BETTER OAKLAND, On Behalf of 
Themselves and All Others Similarly Situated, 

) 
) 
) 
) 
) 

Plaintiffs, | 

Vv. ) 

) 
) 
) 
) 
) 
) 

MOLLY COYE, M.D., Director, California 
Department of Health Services, 

Defendant. 

  

    
I, MARIDEE ANN GREGORY, declare: 

L I am a Doctor of Medicine and a Board Certified Pediatrician. I have 

spent my entire professional career since 1965 in the area of maternal and child health. 

I was first employed by the State Department of Health Services in 1981 as Chief of 

Maternal and Child Health. Since 1987 I have served as chief of the California 

Childrens Services Branch within the Department. [ also serve as medical consultant to 

the Child Health and Disability Prevention Branch of the Department and have been 

the medical consultant in the drafting of program letters regarding lead screening and 

1, 

  

 



   

SENT BY +NHelLP : “id oH ¥ 11 Hy a 5240075: 817 

v
o
 

0
0
 

~
~
 

O
v
 

b
n
 

p
A
 

W
L
 

of
 
S
E
R
 

BE
E 

S
E
 

S
E
 

S
E
 

RR
R 

S
E
 

TE
E 

C
E
 

TT
 

C
S
 

S
E
 
R
e
 

El
 

M
E
 

R
E
 

=
F
 

o
h
 

A
h
 
p
W
 

D
e
 

S
Y
 

f
e
d
 

O
y
 

W
A
 
E
W
 

R
Y
 
e
T
 

    

testing matters within the last four or five years. 

2 The matters stated below are personally known to me and if called as a 

witness I could and would testify competently concerning the same. 

3. The Department of Health Services does not dispute the seriousness of 

the problem of lead poisoning in children. In fact, as recently as March 12, 1991, the 

Department's former Director, Dr. Kenneth Kizer stated that: "Lead poisoning is the 

most significant environmental health problem facing California children today, and 

insufficient consideration is being given to this potential problem during routine child 

health evaluations." What the Department does dispute is whether either the law or 

good medical practice requires the actual testing of children’s blood for the presence of 

lead in all cases, and particularly very young children in the Early and Periodic 

Screening, Diagnostic and Treatment ("EPSDT") Program of the Federal Medicaid 

Program (known as the Medi-Cal program in California, and administered by the 

Department of Health Services). 

4, The Department believes that neither applicable laws nor good medical 

practice requires that all EPSDT children receive blood lead tests as a part of the 

mandatory screening process. Rather, it is the Department's position that young (i.e., 

under 6 years old) EPDST children should first be screened by their treating physicians 

for both the presence of objective medical indications and/or environmental factors 

which might indicate the possibility of lead toxicity. If either or both are presenti then 

a blood test would be indicated. 

3 A blood test is an intrusive procedure which causes some degree of 

discomfort, and in the vast majority of cases is simply unnecessary to determine 

whether a child is at risk of lead poisoning. Further, there is a significant cost factor 

involved in completing a blood test which must be considered in an age of limited 

  

1. CDHP Provider Information Notice #91-6, included as Exhibit C in the 

Exhibits In Support Of Plaintiffs’ Motion For Partial Summary Judgment. 

2 

  

 



3 
' 

  

    

SENT BY :NHeLP io @® Ty eln a a Ha 62400751418 

v
v
 

0
 

9
 

Oo
 

i
n
 

p
p
 

W
W
 
N
O
 

o
S
 

LF 
E
E
 

i 
e
e
l
 

a
d
 

e
l
 

e
T
 

e
T
 

= 
SE
E 

= 
SE
 

S
S
R
 

St
 

=
 

C
y
 

W
D
 

0
0
 

3
 

O
h
 

L
h
 

RB
 
U
D
 

O
S
 

    

resources, although the Department has been absolutely clear in its communications 

with physician/providers that the cost of a blood test for lead is a covered cost in the 

Child Health and Disability Prevention Program (see the penultimate paragraph of 

CHDP Provider Information Notice #91-6). The message the Department sends to 

physicians is that blood lead tests should be given to young EPSDT children whenever 

and wherever medically indicated and that cost is not a factor -- good medical 

judgment is. 

6. While it is recognized that certain pediatricians advocate universal blood 

lead testing for young children, that position is not universally shared. On March 3, 

1987, the American Academy of Pediatrics published its Statement On Childhood Lead 

Poisoning in its journal Pediatrics? While recognizing as an ideal the concept of 

  

universal blood lead testing, the Statement recognized that ". . . the incidence of lead 

may be so low in certain areas that pediatricians may prudently consider their patients 

to be at little risk of lead toxicity . . "/ and set out priority guidelines to assist 

pediatricians in deciding whether the need for a blood lead test was indicated. 

7. On June 4, 1991, I spoke by telephone with Raymond J. Koteras, M.H.A,, 

Director of the Division of Technical Committees, of the Department of Maternal, 

Child and Adolescent Health of the American Academy of Pediatrics. Mr. Koteras 

confirmed to me that, while the matter of child blood lead testing is currently under 

review by several Academy committees, the aforementioned Statepgent is and remains 

the position of the Academy. 

8. The Department believes that its position is consistent with the 

requirements of the Health Care Financing Administration's ("HCFA") State Medicaid 

Manual (included as Plaintiffs’ Exhibit N) wherein it is stated that a blood lead level 

  

2. A copy of this Statement is attached hereto as Exhibit A. 

3. Op. cit, at p. 463. 

  

 



Y      

SENT BY NHeLP : ® Fann Ei: B240075: 419 

I
 

ww
 

o
o
 

~
3
 

O
n
 

b
h
 

Ln
 
W
o
 

N
O
R
N
R
N
N
O
R
E
R
 

F
 

 
d
 

p
d
 

e
l
 

p
e
d
 

p
e
d
 

p
e
d
 

e
d
 

pe
d 

“t
h 

b
h
 

W
W
 
N
=
 

O
O
 

W
V
 
O
C
 
N
h
 

A
W
 
N
R
O
 

t
a
 

BD
 

-1
 

C
n
     

assessment is mandatory where age and risk factors so indicate. (Ex. N, at p. 5-14) 

The Manual goes on to specifically require that all Medicaid eligibie children ages 1-3 

be screened for lead poisoning. However, the Manual section wherein the requirement 

to screen is contained also contains several significant caveats concerning testing: 

"Physicians providing screening/assessment services under the EPSDT program use their 

medical judgment in determining the applicability of the laboratory tests or analysis to 

be performed. +. « As appropriate, conduct the following laboratory tests: . . . 1 In 

general, use the EP test as the primary screening test." (Ex. N, at p. 5-14 through 3- 

15) Clearly, the ultimate decision as to whether a blood lead test should be given has 

been left to the determination of the physician. 

9. It is the present belief of the Department that universal blood lead: 

testing of young EPSDT children is not medically indicated, legally required nor fiscally 

prudent. 

I declare under penalty of perjury that the foregoing is true and correct. 

Executed at Sacramento, California this 6th day of June, 1991. 

M hod A ant, 

     



   

  

SENT BY:NHelLP ® 32.07 da 02400755820 

EXHIBIT A 
 



  
  

S
L
E
 

A
E
E
 

ER
SE
 

A 
e
i
 

i
n
i
a
d
d
 

CA
TT

 
UN

EY
 

N
E
S
T
 

A
R
E
 

i 
. 

. 

a
 

RR 
N
E
T
,
 

SE
 

a 
E
L
S
E
S
 

EP 

i
F
L
t
 

    4 

L
E
 

i
 

   

   

  

4 
oy
 

L
E
S
S
 

wr
 

do
 

r
e
y
.
 

E
E
E
 

w
R
 
S
p
 
A
t
 

HR
) 

S
N
 

R
r
 A 

S
m
 

a
i
n
 

S
i
n
d
e
n
 

H
E
A
R
 

    

B
a
k
 

ad
hd

 
P
H
 

R
r
 
B
i
n
i
 

O
r
 

2 
2 E
W
 

  

  

SENT BY:NHeLP Pa . 1p: 
oN 

dy 

Committee on Environmental Hazards 

Committee on Accident and Poison Prevention 

Statement on Childhood Lead ‘Poisoning 

  

1 

Lead remains a significant hazard to the health 

of American children.’® Virtually all children in 
the United States are exposed to lead that has been 
dispersed in air, dust, and soil by the combustion 
of leaded gasoline, Several hundred thousand chil- 
dren, most of them living in older houses, are at 
risk of ingesting lead-based paint as well as lead- 
bearing soil and house dust contaminated by the 
deterioration of lead-based paint. Although the in- 
cidence of symptomatic lead poisoning and of lead- 
related mortality has declined dramatically,’ data 
from targeted screening programs’ and from a ne- 
  

tional survey” show that there are many asympto- 
“matic children with increased absorption of lead in 
  

  

  

all regions of the United States. It is particularly 
prevalent in areas of urban poverty. 

hildhood lead poisoning can readily be detected 
by_gimple. and_inexpensiy ¢ screening’ technigues; 
however, screening is sporadic and in some areas 
not available. 

Despite wide recognition of the importance of 
preventing children’s exposure to lead, state and 
federal funding for the screening of children and 
for the removal of environmental lead hazards has 
diminished in recent years. Thus, pediatricians at- 
tempting to address the problem of childhood lead 
exposure face serious economic and administrative 
obstacles to effective intervention, 

This statement reviews current approaches to the 
diagnosis, treatment, and prevention of lead poi- 
soning, and it recommends steps to reduce the 
pervasive impact of lead on children’s health. Some 
of these recommendations are addressed to practi- 
tioners and others to agencies of state and federal 
government. It is important to recognize that vir- 
tually all of these preventive steps are after the 
fact, Ideally, in keeping with the precepts of pri- 

mary prevention, lead should have been prohibited 

from ever having become dispersed in the modern 
environment. 

  

PEDIATRICS (ISSN 0031 4005). Copyright © 1887 by the 

American Academy of Pediatrics. 

has been shown conc 

BACKGROUND AND DEFINITIONS 

Lead has no biologic value. Thus, the ideal whole 
blood lead level is 0 ug/dl.. According to the Second 
National Health and Nutrition Examination Sur- 
vey (NHANES II); conducted from 1876 to 1980,° 
the mean blood lead level in American preschool 
children was approximately 16 ug/dL. Substantially 
lower lead levels are seen in persons remote from 
modern industrialized civilization® and in the re- 
mains of prehistoric man. 

Until recently, whole blood lead levels as high as 
30 ug/dL were considered acceptable. However, dis- 
turbances in biochemical function are demonstrable 
at concentrations well below that figure. For ex- 
ample, inhibition of 3-aminolevulinic acid dehy- 
drase, an enzyme important to the synthesis of 
heme, occurs at whole blood lead levels below 10 
pg/dL."® Also, the enzyme ferrochelatase, which 
converts protoporphyriti to heme, iz inhibited in 
children at a blood lead concentration of approxi: 
mately 16 pg/dL; thus, elevations in erythrocyte 
protoporphyrin above normal background become 
evident at blood lead levels above 16 ug/dL.? In 
addition, depression of circulating levels of 1,25- 
dihydroxyvitamin D (the active form of vitamin D) 
is seen at blood lead levels well below 25 g/dL, 2% 
Neuropsychologic dysfunction, characterized by 

reduction in intellizence and ‘alteration in | a Behiavio or, 
usively to occur in agympto- 

matic children w Sn Rs Tead levels at 
The results of clinical and epidéiislogic ‘studies 
conducted in the United States,” Germany,” and 
England" indicate clearly that blood lead levels 
below 50 ug/dl. cause neuropsychologic deficits in | 
asymptomatic children. Recent clinical and exper: 
imental studies suggest that neuropsychologic dam- 
age may be produced in children with blood lead 
levels below 35 pg/dL.}® 

Short stature, decreased weight, and diminished 
chest circumferanre have recently been found in 

analyses of dite From the NHANES II survey to be 
significantly associated with blood lead levels in 
American children younger. than 7 years of age, 

  

  

  

62400757821 

 



    { 

SENT BY: NHeLP ® 3 12:08 

after controlling for age, race, sex, and nutritional 

status. Although the effects are small, the results 
are statistically robust,’ 

In light of these data, an expert Advisory Com- 
mittee to the Centers for Disease Control (CDC) 

has determined that a blood lead level of 25 ug/dL 
or above indicates excessive lead absorption in chil- 
dren and constitutes grounds for intervention.’ 

Increased lead absorption was previously defined 
by & blood lead level of 30 ug/dL. Furthermore, the 
CDC committee has now defined childhood lead 
poisoning as a blood lead level of 25 ug/dL in 
association with an erythrocyte protoporphyrin 
leval of 85 ug/dL or more.’ The Academy concurs 
in these definitions. Also, the Academy anticipates 
that as evidence of the low-dose toxicity of lead 
continues to develop, these definitions will be low- 
ered still further. 

PREVALENCE OF LEAD POISONING 

Data from NHANES II® indicate that between 
1876 and 1980 the national prevalence of blood lead 
levels of 30 pg/dL or higher was 4% among Amer- 
ican children 6 months to 5 years of age. Applying 
this rate to US census data, it may be estimated 

that, between 1976 and 1980, 780,000 American 
preschool children had excess levels of lead in their 
blood. In the NHANES II data, there was wide 

disparity in the prevalence of elevated blood lead 
levels between black children (12%) and white chil- 
dren (2.0%) irrespective of social class or place of 
residence. A similar disparity was noted in mean 
blood lead levels, which were 21 xg/dL in black 
preschool-aged children and 15 pg/dL in white chil- 
dren of the same age. Prevalence rates for elevated 
blood lead levels were highest among families in 

densely populated urban areas and in those with 
incomes of less than $15,000 per year. However, it 
should be noted that cases of lead poisonings were 
found also in families of higher income and in rural 
settings. 

Between 1976 and 1980, the average blood lead 
level in Americans of all ages decreased from 15.8 
to 10.0 ug/dL according to the NHANES I1.* This 
decrease coincided with a reduction in the use of 
lead additives in gasoline. Additional factors in this 

_ reduction may have included a simultaneous reduc- 
tion in the lead content of foodstuffs, the impact of 
targeted screening programs in high-risk areas, and 
an increase in public awareness of the hazards of 
lead. 

SOURCES OF LEAD 

Environmental Sources 

Lead is ubiquitous. A natural constituent of the 

ey 

earth’s crust, lead may be found in drinking water, 
soil, and vegetation. Its low melting point, mallea- 
bility, and high density, as well as its ability to form 
alloys, have made lead useful for myriad purposes, 

--Many of these uses (eg, rediation shields, storage i 

batteries) are not intrinsically dangerous, However, 
when lead is used for purposes other than intended ~3§ 
(eg, burning of storage battery casings), when it is 
incorrectly applied or removed (eg, improper use of 
lead ceramic glazes, burning and sanding of old 
leaded paint), when it is disseminated rather than 
reused (combustion of lead additives in automotive 
fuels), or when it ie improperly discarded, lead 
‘enters the human environment in potentially haz- # 
ardous form. 

For purposes of estimating risk to children, pad 
sources may be categorized as low, intermediate, 
and high dose (Table 1). 
Low-Dose Sources. These sources of lead inclide 

air, food, and drinking water, Together, these 
sources, which have accounted for an average esti- 
mated blood lead concentration of approximately 
10 ug/dL in the recent past, probably now account “3 
for a blood level concentration of about 6 ug/dL. 
Mean ambient air lead concertrations currently ki: 
average less than 1 ug/m® of air, although in areas ps 
near lead smelters, concentrations may be she, 
tially higher, 

Average dietary intake of lead increases fc 20 Ee 
#g/d during early infancy to 60 to 80 pg/d by & to 
8 years of age.’ Except in isolated areas, it would. : 

yy 
i Aa : 

6240075422 

      

appear that the majority of public drinking water ¢% 5 
supplies in the United States have a lead concen-. 
tration of less than 20 pg/dL. However, these data 
may be misleading if, as iz generally the case, the 
water samples have been obtained from the distri- 
bution plant prior to the distribution of water 
through a plumbing system that contains lead 4 
pipes. The lead solvency of drinking water can be 
reduced by reducing acidity of water supplies and 
by abandoning the use of lead-based solder at pipe 
joints in new and replacement plumbing, Commu. 
nities with excessive lead in water have successfully 
used each of these remedial approaches. i 

  

TABLE 1. Common Sources of Lead 

Low dose 
Food 
Ambient air 
Drinking water 

Intermediate dose 
Dust (housshold) 
Interior paint removal 
Soil contaminated by automobile accident 
Industrial sources 
Imprope® temoval of exterior paint 

High dose 
Interior and exterior pat 
  

PF) : 

    

   
   

   

     
   

   

  

    
   

  

   

      

   

  

   

        

  

 



(
 

=
r
)
 

  

f 

SENT BY :NHelLP 
4 wu!       

      

   

nN . 

" Intermediate-Dose Sources. These sources in- 

£5 clude dust and soil in children’s play areas. Dust 

BY: ond soil are contaminated principally by automo- 

IB tive exhaust and by the weathering and deteriora- 

gi tion of old lead paint (both interior and exterior). 

Bi Although background soil lead contaminants in 

BF rural areas are generally less than 200 ppm, concen- 

£ trations of lead in urban soil can exceed 3,000 ppm. 

BF: In industrial areas where lead smelters have been 

3 situated (eg, El Paso, TX; Kellogg, ID), the lead 

“content of dust can, however, exceed 100,000 ppm,*® 

.- thus producing significant elevations in children’s 

© blood lead levels. Each increase of 100 ppm in the 

lead content of surface soil above a level of 300 ppm 

SY is associated with a mean increase in children's 

3 whole blood lead levels of 1 to 2 pg/dL. When dust 

. and soil are the only sources of exposure to lead, 

fk symptoms are rarely encountered, although lead 

{38 toxicity may occur. Soil lead may, however, be 

E. extremely difficult to abate, and chronic low-grade 

[3 

| 
| 

-
—
—
—
—
 

E
T
C
 

S
a
 

n 

pl 
- 

L
a
n
n
y
 

: 

oF 
H
y
e
 

ingestion may continue undetected even after a 

child has come to medical attention. The proper 

site for disposal of lsad waste, such as lead-contam- 

&. inated soll, is a hazardous waste facility that has 

38. been approved by the US Environmental Protec- 

tion Agency. | 
= High-Dose Sources. These sources are those in   which the concentrations of lead are sufficient to 

produce acute and potentially fatal illness, Lead- 

based paint on both the interior and exterior sur- 

E
R
s
 

Pl
 

So
 
i
 

O   

A
 

t
n
 

r
o
n
 

- 
1
 

$1 
7 

oe
 

2 
o
t
 

2 
t
n
 

faces of housing remains the most common high. 

dose source of lead for preschool-aged children. It 

continues to be the experience of most pediatricians 

that virtually all cases of symptomatic lead poison- 

ing and blood lead levels greater than 70 ug/dL 

result from the ingestion of lead paint chips. 

Lead-based paint is still widespread. A 1878 US 

census survey found that 8 million of the 27 million 

occupied dwellings in the United States, which had 

t been built prior to 1940 when use of lead-based 

pain: was common,” were deteriorated or dilapi- 

dated. An additional 22 million dwellings were built 

between 1940 and 1960, and 75% of these units are 

estimated to contain lead-based paint. Nationally, 

according to the 1978 census survey of housing, 8% 

of rental units have peeling paint. 

Although the use and manufacture of interior 

lead-based paint declined dramatically during the 

1950s, exterior lead-based paint continued to be 

available until the mid-1970s and is still available 

for maritime use, farm and outdoor equipment, road 

stripes, and other special purposes. Thus, potential 

for domestic misuse of lead-based paint continues 

to exist. Manufacturers could voluntarily decrease 

the lead content of interior paint until 1877, when 

the US Consumer Product Safety Commission en- 

RE 
eh 

ual
ly 

In
ss
uh
 
W
O
A
-
 

Ut 
* P

o% 
SY
P 

& 
+ 

- 
T
E
T
Y
T
T
Y
Y
R
I
Y
 ET
 

- 
F
m
 

= 

    
| 

i 

; on
 

@® a 62400757823 hi Li 

acted regulations banning the sale in interstate 

commerce of paints for exposed interior and exte- 
rior residential surfaces containing more than 
0.06% lead by weight in final, dry solid form. 

A previously unforeseen, but increasingly recog- 
nized, danger is that of improper removal of lead- 

based paint from older houses during renovation 
or, ironically, during cleaning to protect children. 
Torches, heat guns, and sanding machines are par- 
ticularly dangerous because they can create a lead 
fume.? Sanding not only distributes lead as & fine 
dust throughout the house but also creates small 
particles that are more readily absorbed than paint 

chips. The greatest hazard in paint removal appears 
to be to the person doing the “deleading” and to 
the youngest children in the dwelling. There mdy 
be significant morbidity. Persons who perform this 
work should comply with the standards for occu- 
peational exposure to lead which have been devel 
oped by the US Occupational Safety and Health 
Administration. Pregnant women, infants, and 

children should be removed from the house until 

deleading is completed and cleanup accomplished. 

Proper cleaning of the dust and chips produced in 
deleading must include complete removal of all 
chipping and peeling paint and vacuuming and 
thorough wet mopping, preferably with high-phos- 
phate detergents. This waste must be discarded in 
& secure site, 

Another previously unrecognized hazard lies in 
sandblasting. This technique is commonly used to 

remove lead from exterior surfaces, There are no 

standardized safeguards. Recent case reports of lead 
poisoning among sandblasters underscore the haz- 

ard. ® Sandblasting creates large amounts of lead- 
laden dust and debris which, if improperly disposed 
or not properly removed, redouble the hazard, 

Uncommon Sources (Table 2) 

Additional lead sources include hobbies such as 
artwork with stained glass and ceramics, particu- 

larly when conducted in the home. Folk medicines 

TABLE 2. Uncommon Sources of Lead 

Metallic objects (shot, fishing weight) 
Lead glazed ceramics 
Qld toys and furniture 
Storage battery casings 
(Gasoline sniffing 
Lead plumbing 
Exposed lead solder in cans 
Imported canned foods and toys 
Folk medicines (eg, azarcon, Greta) - 
Legged glass artwork 
Cosmetics 
Antique pewter 
Farm equipment Na 

  

  

 



  

SENT BY:NHelLP ® piel 

used to treat gastrointestinal ailments may contain 
lead and mercuric or arsenical salts. Recent reports 
have noted lead poisoning from use of azarcon (lead 
tetroxide)* and Greta (lead monoxide) among Mez- 
ican-Americans and from use of Pay-loc-ah, a 
Chinese folk remedy,” among Hmong refugee chil- 
dren. Cosmetics (ceruse, surma, or kohl), particu- 
larly those from Asia, may contain white lead or 
lead sulfide®” and have caused severe lead poison- 
ing. Another source of lead is improperly soldered 
cans, particularly those containing acidic food- 
stuffs. Food should not be heated in such cans, as 
heating increases the dissolution of lead. Pediatri- 
cians should realize as a practical matter that the 
lead content of imported earthenware toys, medi- 

cines, or canned foods cannot readily be regulated, 
In addition, antique toys, cribs, and utensils may 
have a significant lead’ content. ; 

Lead-glazed pottery is a. potential source of Toad 
in food and drink. If not fired at high temperatures, 
lead may be released from the glaze in large 
amounts when such pottery is used for cooking or 
for storage of acidic foodstuffs. Also, if pottery 
vessels are washed frequently, even & properly fired 
glaze can deteriorate, releasing unsafe levels of pre- 
viously adherent lead.” Sporadic cases of f plumbism 
have been traced to lead-glazed pottery.” : 
Among the oldest sources of lead in America is 

antique pewter. Food should not be cooked or stored 
in antique pewter vessels or dishes. Although un- 
common, many of the above sources have been 
essociated with severe, symptomatic, and even fatal 
lead poisoning. 

Finally, a number of cases of lead poisoning have 
been reported among the children of workers in 
smelters, foundries, battery factories, and other 
lead-related industries. ®®¥ These workers can bring 
home highly concentrated lead dust on their skin, 
shoes, clothing, and automobiles. This source of 

exposure can be avoided by providing showers at 
work, by providing workers with a change of cloth- 
ing, and by having clothing laundered at the work- 
place. 

In summary, it can be inferred from the 
NHANES II data that most children in the United 
States with increased lead absorption have been 
exposed to low-dose or to intermediate-dose lead 
sources. Four percent of children have blood lead 
levels in excess of 30 pg/dL, but only 0.1% have 
levels exceeding 50 pg/dL.? 

ROUTES OF ABSORPTION 

Ingestion is the principal route of lead absorption 
in children. Because of the high density of lear 
ingestion of surprisingly small quantities may pro- 
duce toxic effects. A lead paint chip weighing only 

‘480 EADY POIGSOINIMM 

TY 

1 g (approximately 1 em’ in surface area) and 
containing 5% lead by weight will deliver a potential 
dose of 50 mg (50,000 ug); by comparison, the safe 
upper limit for daily intake of lead by children is 5 
g/kg of body weight. Because ingestion of such 
chips ie not uncommon, it might be expected that 

large numbers of children would have symptomatic 
lead poisoning. However, most ingested chips are 
swallowed whole or in large pieces, rendering much 

"of the lead contained in them unavailable for ab- 
sorption. 

Several recent studies have reported the effec- 
tiveness of normal hand-to-mouth activity ass e 
means for the transfer of lead-laden dust from the 
environment into children ®* True pica (the in- 
discriminate ingestion of nonfood substances), al. 
though still an important risk factor,* need not/be 
present. 

Inhalation is the second major route of lead ab. 
. sorption for children. Lead absorbed by way of the 

lungs contributes in additive fashion to the total 
body lead burden. The efficiency of respiratory 
absorption depends on the diameter of airborne 
lead particles, For most common lead aerosols of 
mixed particle size, it has been estimated thet be. - 
tween 30% and 50% of total inhaled lead is con- 
tained in particles of sufficiently small diameter 

02400757824 

(lesz than 6 um) to be retained in the lungs and 
absorbed. Larger particles deposit in the nose, 
throat, and upper airways where they are cleated 
by ciliary action and then are either expectorated 
or swallowed. 

PREDISPOSING FACTORS 

Factors known to increase susceptibility to lead 
toxicity include nutritional deficiencies and age- 
related oral behavior (with or without pica) (Table 
3). 

Animas] and humen studies” have shown that 
deficiencies of iron, calcium, and zinc all resultiin 3 
increased gastrointestinal absorption of lead. of fo og 
particular concern is the effect of lack of iron,” ; 
because the prevalence of iron deficiency in infancy . 
is at least 156% and may be higher. % Iron deficiency, } 
even in the absence of anemia, appears to be the’ 
single most important predisposing factor for in- 
creased absorption of lead, Conspicuous examples : 
of nutritional iron deficiency include-breest<fed in-: 
fants and “milk babies” who may receive little food ; 

TABLE 3. Predisposing Factors for Lead Poisoning | 

Nutritional deficiency of iron, calcium, TINE | 
Sickle cell digease 

  

Young age 

Hand-to-mouth activity, including pica hy : 
Metabolic disease \ a 
  

“- 

      Erte
 

kL
 
TT
 

pe
 
—
—
 

  

  
x . 

     
   

| t
c
 
t
r
 
2
 

r
r
 

h
s
 

—
—
 

— 
— 

  

  

  

 



4 
2
 
th

 
rn
 

-
—
 

  
  

  

t 

SENT BY :NHeLP 
pg 

. - 

-
 

o
t
o
.
 

oy
 

«h
p 

Tm
 

+ 

WA
LZ
 
T
I
R
E
 S

T 
kn 

esd
 

ir 

v 
fe. 

1 
On - BY 

ERE | = 

n a = 

. TIE 
a 

at 
a 

  

     

    

‘ 
* 

% 

level, erythrocyte protoporphyrin level, or both. 

  

   woh . 

    E other than milk until 12 to 18 months of age. In 

k the presence of iron deficiency insufficient to pro- 
duce anemisa, gastrointestinal absorption of lead is 

increased severalfold. 

SCREENING 

Screening for lead poisoning is sporadic. Methods 
used have included determination of blood lead 

8 cell for 
Hs in high- 

0 guide the interpretation of screening re- 
«sults, the CDC has developed a series of guidelines 

(Tables 4 and 5). 
The erythrocyte protoporphyrin determination 

provides a sensitive and inexpensive screen for both 
increased lead absorption and iron deficiency, two 
of the most common preventable health problems 
in childhood; elevation in the erythrocyte proto- 
porphyrin level can reflect iron deficiency before 
anemia becomes clinically evident. There is increas- 
ing interest, therefore, in adopting the erythrocyte 
protoporphyrin determination as a screening tool 
for both problems, particularly because it is more 
sensitive to iron deficiency than the hematocrit.™ 

Both capillary tubes and filter paper have been 
"used for obtaining screening samples. Capillary 

tubes are cumbersome but have the advantage of 
providing sufficient blood for concomitant lead de- 

TABLE 4. Zinc Protoporphytin by Hematofluorometer: 
Risk Classification of Asymptomatic Children for Prior- 
ity Medical Evaluation® 
  

  

  

Blood Lead E 
{ug/dL) Protoporphyrin 

(ug/dL) 

35 36-74 75-174 >176 

Not done 1 t + t 
<24 I Ia Ia t 
25-48 Ib II III ITI 
50-69 § III II Iv 
=70 § 5 IV IV 
  

* Diagnostic evaluation is more urgent than the classifi- 
cation indicates for (1) children with any symptoms 
compatible with lead toxicity, (2) children younger than 

+ disposition reshona more complete medical and labora- 

"86 months of age, (3) children whose blobd lead and 
ervthrocyteprotoporphyrin levels place them in the upper 
part of a particular-class, (4) children whose siblings are 
in a higher class. These guidelines refer to the interpre- 
tation of screening results, but the final] diagnosis and 

tory ¢ ofthe child, 
t Blood leadtest-needed to estimate risk. i 
+ Ervthropoietic. protoporphyria. Iron deficiency may 
cause elevated erythrocyte protoporphyrifidevels up to 
300 ug/dL, but this is rare. a 
§ In practicgzthis:;combination of results is not generally 
observed: if3¥- is observed, immediately retest with whole 
blood. 

® F32+12 Th Ll 

TABLE 6. Erythrocyte Protoporphyrin (EP) by Extrac- 
tion: Risk Classification of Asymptomatic Children for - 

  

  

  

Priority Medical Evaluation® 

Blood Lead EP (ug/dL) 

(ug/dL) <B% 35-109 110-248 >250 

Not done 1 t t + 
<24 1 Ia Ia 1 
25-48 Ih II II III 
50-69 § 111 I IV 
=70 § 4 IV IV 
  

* Diagnostic evaluation is more urgent than the classifi- 
cation indicates for (1) children with any symptoms 
compatible with lead toxicity, (2) children younger than 
86 months of age, (8) children whoae blood lead and EP 
lavels place them in the upper part of & particular class, 
(4) children whose siblings are in a higher class, These 
guidelines refer to the interpretation of screening results, 
but the final disgnosis and disposition rest on a more 
complete medical and laboratory examination of the 
child. Screening tests are not diagnostic. Therefore, every 
child with a positive screening test result should be 
referred to a physician for evaluation, with the degree of 
urgency indicated by the risk classification. At the first 
diagnostic evaluation, if the screening test was done on 
capillary blood, & venous blood léad level should be de- 
tarmined in a laboratory that participates in the Centers 
for Disease Control's blood lead proficiency-tasting pro- 
gram. Even when tests are done by experienced person- 
nel, blood lsad levels may vary 10% to 15%, depending 
on the level being testad. Tests for the same child may 
vary a8 much 8s £5 ug/dL in a 24-hour period. Thus, 
direction should not necessarily be Interpreted as indie- 
ative of actual changss in the child's lead absorption or 
excretion. 
t Blood lead test needed to estimate risk. 
1 Erythropoistic protoporphyria. Iron deficiency may 
cause elevated EP levels up to 300 pg/dL, but thie i rare, 
§ In practice, this combination of results is not generally 
shaeed; if it is observed, immediately retest with whole 
blo 

  

termination if the erythrocyte protoporphyrin level 
is elevated. Filter paper sampling provides ease of 
collection and transport, but the accuracy of anal 
yaes based on filter paper samples is not yet estab- 
lished. Determination of the blood lead level by 
fingerstick sampling is subject to contamination by 
lead on the skin, whether collection is by capillary 
tube or filter paper. Such contemination does not 
affect the determination of the erythrocyte proto- 
porphyrin level, 5 : 

Two analytical techniques are available for de- 
termination of erythrocyte protoporphyrin: (1) ex- 
traction of protoporphyrin from erythrocytes and 
subsequent measurement in a fluorimeter and (2) 
direct fluorimetry of a thin layer of RBCs (heme- 
tofluorometer). Because values derived from these 
two methods may differ (Tables 4 and §), a pedia- 
trician should be aware of which is in use. When in 
doubt, the extraction method is preferred, because: 
of its greater reprodudibility, particularly at lower 
concentrations of erythrocyte protoporphyrin. 

 



   
5 

SENT BY:NHeLP 

  

PA 5-10-91 5 12:13 

It is most important to note that screening tests 
are not diagnostic. Every child with a positive 
screening test result should be referred to & pedia- 

trician for further evaluation, with the urgency of 
referral indicated by the risk classification (Tables 
4 and b). At the first diagnostic evaluation, if the 
seresxing 18st. was performed on capillary blood, & 
venous blood lead level should be determined in 8 

~lahgratory that participates in an eceredited blood 
lead proficiency-testing program. To reduce the 
likelihood of false-positive results, lead-free sy- 
ringes, needles, and tubes must be used in obtaining 
venous blood samples for lead analysis, 

The developmentally disabled who reside in 
“halfway houses” or community residences or who 
attend school in older buildings deserve special 
attention in lead-screening programs. Because this 
population may be older than preschool age, pro- 
tective statutes may not recognize their high-risk 
status, particularly with respect to pica behaviors. 
Physicians caring for developmentally disabled pa- 
tients should be aware that their risk of lead inges- 
tion may continue long beyond the age of 6 years. 

INTERVENTION 

Once a diagnosis of increased lead absorption has 
been confirmed by venous blood lead determina- 
tion, the sine qua non of intervention is the prompt 
and complete termination of any further exposure 
to lead.*® This intervention requires accurate iden- 
tification of the source of lead and either its removal 
or removal of the child from the unsafe environ- 
ment, Some states (eg, Massachusetts) have passed 
stringent legislation requiring prompt removal of 
lead hazards in cases of lead poisoning, and there 
are strong penalties for failure to comply. At all 
costs, a child should not be permitted to enter or to 
be present in o leaded environment during deleading 
until the deleading, subsequent cleanup, and rein. 
spection have been satisfactorily completed, Al- 
though some regulations call only for removal of 
leaded paint from “chewable” surfaces (eg, window 
sills and door frames) or up to & height of 1.2 m (4 
ft), all chipping and peeling paint should be re- 
moved from all surfaces, particularly from ceilings. 

After deleading, the house must be thoroughly 
cleaned and reinspected to assure compliance with 

  

  

safety regulations. Indeed, repeated thorough clean- __1s unproven: but, in children who have blood lead 
ing 1s advisable, especially in the case of deterio- 
rated or dilapidated housing, High-phosphate de- 
tergents are particularly useful in removing lead 
dust. Children should not return home until ¢lean- 
ing is completed. 

Medical intervention should begin with thro- 
rough clinicel evaluation in®4ding diagnostic stud- 
ies of lead toxicity and, when indicated, & lead 
mobilization test.*® Diagnostic studies should in- 

-482 LEAD POUSARNING 

ol ak 

clude a blood cell count with RBC indices, a retic- 
uloeyte count, and, if indicated and available, tests 
of serum iron and iron-binding capacity, and a 
serum ferritin assay. Routine urinalysis might be 
considered. Because chelating agents are poten- 
tially nephrotoxic, BUN and/or serum creatinine 
velues should be determined before chelation to 
rule out occult renal disease either secondary to 
plumbism or preexisting.“ Roentgenographic stud- 
ies to be considered include a film of the abdomen 
to detect radiopaque paint chips or other leaded 
materials in the gastrointestinal tract and s film of 
the metaphyseal plate of a growing “long” bone, 
usually the proximal fibula, to detect interference 
with calcium deposition, the so-called “Jead line.” 
Because this phenomenon is usually seen only after 
several weeks of increased lead absorption in chil- 
dren whose blood lead levels may exceed 50 ug/dL, 
its presence or absence may help to determine the 
duration of increased lead exposure. 

Once a diagnosis of plumbism has been made, a 
child's condition and the effect of intervention 
should be monitored by serial venous determina- 
tions of the blood lead and, if available, erythrocyte 
protoporphyrin levels. If iron deficiency is present, 
iron studies should also be repeated periodically to 
monitor compliance with iron replacernent therapy. 

The lead mobilization test may be used to assess 
the “mobilizable” pool of lead in a child for whom 
chelation therapy is contemplated. Lead mobiliza- 
tion is determined by measuring lead diuresis in = 
timed urine collection following a single dose of 
chelating agent.®# This test is most helpful in 
determining which children with blood lead concen- 
trations in the range of 25 to 55 ug/dL will require 
a full course of chelation therapy and also in deter- 
mining the advisability of further chelation in a 
child already receiving therapy. It should be noted 
that the erythrocyte protoporphyrin level is not a 
useful predictor of the amount of chelatable lead 
and may, in fact, be misleading in this regard. 

Therapeutic modalities include removing the -.. 
child from lead exposure, improving nutrition, 
administration of iron supplements, and chelation 
therapy. *#~4" In children with mild increased lead 

  

gbsorption, the efficacy of chelation therapy to _ : 
modify neurobehayioral outcomes of-lead. toxicity 

levels between 25 and 65 pg/dL and & positive lead 
mobilization test, it is highly desirable to rapidly 
decrease the readily mobile, potentially most toxic 
fraction of body lead stores by three to five days of = 
CaNas-ethylenediaminetetraacetic acid (calcium 
disodium EDTA) therapy. 

Long-term follow-up is indicated in all cases of . 
lead exposure. Children near or at school age who 
have a history of plumbism should have a neuro. ¥ 

M
E
E
 

1 

y 

Fl 

’ 

6240075:82¢ 

fa
ia
r.
. 

E
n
e
 

75
4 

5 
Tr
y,
 

7} 
s;
 

F
O
E
 

0 L
A
N
E
 

LI 
0) 

T
e
)
 

ee
 

oy
 

IJ 
f
a
d
 

S
p
t
 

- 
S
i
n
 

fo T
L
L
 
I
E
 

EL T
a
e
 

s 
TIU

RS 
OP 

Ee 
4s

 
ni
 
S
T
 p

e 
Ai
 

ap
t 

ih 
d
i
y
,
 

hl
   

~ 

EAE A 
DES 

fy n 

- A 

SELEY, 

by { Pons 
4 

iy        

     
 



~
~
 
l
m
 

on 
n
h
 

0 
e
e
 

35
 
n
n
 

m
m
o
 

a
o
 

  

    

a
 

  

L
E
R
 

P
L
A
S
 
w
a
 
a
p
 
w
e
 

saad 
wo 

2 
-y 

s
e
i
 

~ 
ll 

a 

-
—
.
 

a 
F
Y
e
T
E
F
F
U
T
T
T
I
Y
Y
Y
 

  

h 

3 BY :NHel 

E- ' sure; and 
+ lead, even in asymptomatic children, are largely 
irreversible. Guided by these premises, the goal of 
our recommendations is to prevent lead absorption. 

Ir
is
 

% 

Oi 

  

P | — 

ing handicaps, and school authorities should be 
Br . encouraged to offer appropriate guidance. 

x. RECOMMENDATIONS 

Qur recommendations rest on three premises: (1) 
that exposure to lead is widespread; (2) that lead 

causes neuropsychologic and other serious impair- 
ments in children at relatively low levels of expo- 

(3) that the neuropsychologic effects of 

Pediatricians must play a central role in this 
prevention. Although our recommendations are di- 
vided into two categories—those directed princi- 
pally to practitioners and those directed to govern- 
ment agencies—the distinction is somewhat artifi- 
cial. Throughout the past five decades, pediatri- 
cians, acting individually, as well as collectively 
through the Academy, have been prime movers in 
stimulating the agencies of government to protect 
the children of the United States against exposure 

to lead. It is important that this tradition of public 
involvement continue and that pediatricians con- 
tinue to act publicly as advocates for the health of 
children. 

Recommendations for Practitioners 

1. The Academy recommends that the erythro- 
cyte protoporphyrin test be used for screening chil- 
dren for lead toxicity, when that test is available. 

Additionally, the erythrocyte protoporphyrin test 
is a sensitive indicator of subclinical iron deficiency 
and may add complementary information to the 
determination of hematocrit values. It will not, 
however, identify children with anemia due to acute 
blood loss or hemoglobin C, 88, 8C, or E disease, 
The Academy encourages clinical and hospital lab- 
oratories to make the erythrocyte protoporphyrin 
test widely and economically available, 

_2. Upon consideration of recent CDC recommen- 
dations, the Academy recommends that, iaeally, all 
preschool children should be screened for ead ab- 
80 sarption. by. mean. of the srvihroeyta profeodt 

er. it is. recognized that the in- 
cidence of oh exposure may be so low ip certain 
areas that pediatricians may prudently consider 
their patients. to. be at little risk of TJead “toxicity; 
therefore, the, following priority y guidelines I ranked 
from highest to lowest are offered to assist t pedia- 
tricians in 1 deciding which children _ to. ‘screen. (a) 

children, 19 121 to, 38 ‘months of age, who | live ir in or are 

  

  

  

  
  

  
  

phy Te 
  

(highest); (b)_children,.8 8 “months to 6 years c of “age, 
and play- who are ‘siblings, housemates, . visitors, 

    

   

  

d toxicity; (c) 
der housing where 
  

    i der, dilapidate 9 
he rah sana be me] 
lead smelters and processin & par- 

«ents or.other honseho isle ey ate in & 
lead-related occupation or hobby. Frequency of 

screening should be flexible but should be guided 
by consideration of a child's age, nutrition and iron 
status, and housing age, housing condition, and 
population density. The first erythrocyte protopor- 
phyrin test should generally occur at the same time 
as the determination of the hematocrit, which typ- 
ically is performed between 9 and 15 months of age. 
Because the prevalence of lead poisoning increases 
sharply at 18 to 24 months of age, any child judged 
to be at elevated risk of plumbism should have a 
second erythrocyte protoporphyrin test performed 
at or about 18 months of age and at frequent 
intervals (3 to 6 months) thereafter appropriate to 
the degree of risk. Surveillance should continue 
routinely up to age 6 years and, if appropriate, 
longer. 

3. The Academy sitommends that any child, in 
whom increased lead absorption or lead poisoning 
has been confirmed by venous blood lead determi. 
nation, be followed closely by means of repeat ve- 
nous tests. For such children, ‘abatement of envi- 
ronmental sources of lead is essential. 

4. The Academy notes that some predisposing 

factors for lead poisoning, iron deficiency in partic- 

ular, are preventable. Pediatricians should make 

vigorous efforts to identify and correct iron defi. 
ciency, calcium deficiency, and other nutritional 
deficiencies, particularly in children from areas of 
high lead exposure. 

5. The Academy recommends that pediatricians 
attempt vigorously to educate parents, particularly 
parents of children in high-risk populations, about 
the hazards of lead, its sources and routes of ab- 
sorption, and safe approaches to the prevention of 
exposure. 

   
     

Recommendations for Public Agencles 

1. The Academy recommends that reporting of 
cases of lead poisoning to state health departments 
be mandatory in all states. 

2. The Academy notes that, in the present ap- 
proach to screening for lead, inspection of a child's 
environment is generally undertaken only when an 
elevated blood lead level is found. In effect, children 
are used as biologic monitors for environmental 
lead. The Academy recommends that this sequence 
be reversed. A national program for systematic 
screening of lead hazards in housing is overdue. 
The enormity of the task favors a stepwise ap- 

 



{ 

  

  

IT 

    - 
SENT BY: NHeLP 

proach, Suggested approaches might include: 
screening of oldest housing, followed by newer 
housing; screening of housing in inner cities, then 
in less densely populated areas; and targeted 
screening of housing with small children. 

8. The Academy supports the prompt, vigorous, 
and safe abatement of all environmental lead haz- 
ards. The US Department of Housing and Urban 
Development, state health departments, and local 
health departments should require that all hazard. 
ous lead-based paint (exterior and interior) be re- 
moved from all housing. Development of methods 
of abatement, which are safer and more effective 
than those currently in use (torches, heat guns, and 
sanders) must be given high priority to prevent the 
further endangering of lead-poisoning victims. The 
US Environmental Protection Agency is urged to 
persist in its laudable plan to promptly and finally 
remove all lead from gasoline. 

4. The Academy urges the US Congress and the 
US Department of Health and Human Services to 
become fully cognizant of the high prevalence of 
childhood lead poisoning in the United States, its 
irreversible consequences, and its great human and 
fiscal costs. Restoration of funding is urgently 
needed for screening, hazard identification, and 
hazard abatement. 

5. The Academy recommends that state health 
departments and Academy chapters exert their 
maximum influence to assure that state licensing 
agencies permit laboratories to perforz blood lead 
and erythrocyte protoporphyrin tests only if those 
laboratories consistently meet criteria for accuracy 
and repeatability as determined by their perform- 
ance in interlaboratory proficiency-testing pro- 
grams. 

SUMMARY 

Patterns of childhood lead poisoning have 
changed substantially in the United States. The 
mean blood lead level has declined, and acute in- 
toxication with encephalopathy has become uncom- 
mon. Nonetheless, between 1976 and 1880, 780,000 
children, 1 to 6 years of age, had blood lead concen- 
trations of 30 ug/L or above. These levels of ab- 
sorption, previously thought to be safe, are now 
known to cause loss of neurologic and intellectual 
function, even in asymptomatic children. Because 
this loss is largely irreversible and cannot fully be 
restored by medical treatment, pediatricians’ ef- 
forts must be directed toward prevention. Preven- 
tion js achieved by reducing children’s exposure to 
lead and by early detection of increased absorption, 

Childhoa# lead poisoning is now defined by the 
Academy as a whole blood lead concentration of 25 
£g/L or more, together with an erythrocyte proto- 

484 1 FAD DAIQARIIR IS 

porphyrin level of 85 ug/dL or above. This defini- 
tion does not require the presence of symptoms. Jt 
is identical with the new definition of the US Public 
Health Service. Lead poisoning in children previ- 
ously was defined by a blood lead concentration of © 
30 pg/dL with an erythrocyte protoporphyrin level 
of 50 ug/dL. 

To prevent lead exposure in children, the Acad. 
emy urges public agencies to develop safe and effec- 
tive methods for the removal and proper disposal 
of all lead-based paint from public and private 
housing, Also, the Academy urges the rapid and 
complete removal of all lead from gasoline. 

To achieve early detection of lead poisoning, the 
Academy ends hildren in the 
United States at risk of exposure to lead be screened 
for ead abaotpiion at approximately 12 months of 
  

ry dl 

age by means of the erythroc nn 
uh when that test is available, Furthermore, the 
Academy recommends follow-up erythrocyte pro- 
toporphyrin testing of children judged to be at high 
risk of lead absorption. Repor+ing of lead poisoning 
should be mandatory in all states, 

- ACKNOWLEDGMENT 

We are grateful for the assistance of J, Julian Chisolm, 
Jr, MD, Jane L. Lin-Fu, MD, Vernon Houk, MD, John ib 
Stevenson, MD, and John F. Rosen, MD. 

COMMITTEE ON ENVIRONMENTAL 
HAZARDS, 1984-1986 

Philip J. Landrigan, MD, Chairman 
John H. DiLiberti, MD 
Stephen H. Gehlbach, MD 
John W. Graef, MD 
James W. Hanson, MD 
Richard J, Jackson, MD 

Gerald Nathenson, MD 

Liaison Representatives 
Henry Falk, MD 
Robert W, Miller, MD 

Walter Rogan, MD 
Diane Rowley, MD 

COMMITTEE ON ACCIDENT AND POISON i 
PREVENTION, 1984-1988 

Joseph Greensher, MD, Chairman 
Regine Aronow, MD 

Joel L., Bass, MD 

William E. Boyle, Jr, MD 

Leonard Krassner, MD 
Ronald B, Mack, MD 
Sylvia Mieik, MD 
Mark David Widome, MD 

Liaison Representatives 
Andre I'Archeveque, MD 

i. 
. 

a 

  

3 
L
E
E
 

is
 

re
gi
 

Sh
in
 

en.
 

P
i
p
e
t
t
e
s
 

oa
 

1 

  

- 

wg 

H 

Ek] 
td, 

ad 
5 

+ 

+ - q- 

  

     
     
 



  

          

  

h |
 

OO
 

—
—
—
 

—
—
 

i
e
 

—
—
—
—
—
 

—
—
 
"
n
s
 

-—
— 

          

=
 

——
 

A 
x 
. 

ve 

$ ue 
T 

i 

J 
v 

A
A
 

S
R
 

ER
 
a
e
 

S 

4 

SENT BY :NHeLP oo 
Ta ee, 

a 

CF 8 

     

   

    

Gerald M. Breitzer, DO 
Chuck Williams, MD 

AAP Section Liaison 
Jerry Foster, MD 
Joyce A. Schild, MD 

REFERENCES 
1. Centers for Disease Control: Surveillance of childhood lead 

poisoning— United States, MMWR 1882;31:132-134 
E _ 2. Mahaffey KR, Annest JL, Roberta J, et al: National esti. 

mates of blood lead levels: United States 1978-1980: Asso- 
ciated with selectsd demographic and socioeconomic factors. 
N Engl J Med 1082;807:673-678 

8 Klein R: Lead poisoning, Adv Pediatr 1877;24:108-132 
® 4. Annest JL, Pitkle JL, Makue D, et al Chronological trend 

in blood lead levels between 1976 and 1980, N Engl J Med 
1883;308:1873-1877 

5. Plomelli 8, Corash L, Corash MB, et zl: Blood jead concen- 
trations in a remote Himalayan population. Sciance 1980; 
210:1136-1137 

8. Grandjean P, Fjerdingetad E, Nielsen OV: Lead concentra- 
tion in mummified nubian brains. Presented at the Inter- 
national Conference on Heavy Metals in the Environment, 
Toronto, Canada, Oct 27-31, 1975 

7. Hernbarg 8: Biochemical and clinieal effects and TESpOnEES 
az indicated by blood concentration, in Singhal RL, Thomas 
J8 (eds): Lead Toxicity, Baltimore, Urban & Schwarzenberg, 
Inc, 1880 

8. Berlin A, Schaller KH, Grimes H, ot al: Environmental 
exposure to lead: Analytical and epidemiological investiga. 

. tions using the Eurcpean standardized method for blood 
delta-aminolevulinic acid dehydratase activity determina. 
tion. Int Arch Occup Environ Health 1877;38:135~141 

f. Piomelll 8, Seaman C, Zullow D, at al: Threshold for lead 
damage to heme synthesis in urban children, Proc Natl Acad 
Sei USA 1682;79:3335-3338 

EO 10. Mahaffey XR, Rosen JF, Chesney RW, at al: Association 
batwean age, blood lead concentration, and serum 1,25- 
dinydrozyealciferol levels in children, Am J Cla Nutr 
1982:35:1327-1331 

11, Ross JF, Chesney RW, Hamstru A, et al; Reduction in 
1.95-dihydroxyvitamin D io children with increased lead 
absorption. N Engl J Med 1880;302:1126-1131 

12. Needleman H, Gunnoe C, Leviton A, st al: Deficits in 
psychologic and classroom performance of children with 
elevated dentine lead levels, N Engl J Med 1878;30:685- 
695 

18. Winneke G, Kramer G, Brockhaus A, et al: Neuropsycho- 
logical studies in children with elevated tooth lead concen- 
tration. Int Arch Occup Environ Health 198%:51:169-183 

14. Yuls W, Lansdowne R, Millar IE, et al: The relationship 
between blood lead concentrations, intelligence and attain- 
ment in a school population: A pilot study. Dev Med Child 
Neurol 1681;23:6687-578 

15, Rutter M: Low levsl lead exposure: Sources, effects, and 
implications, in Rutter M, Jones RR, (ads): Lead ve. Health, 
New York; John Wiley & Sons, 1883, pp 333-370 

16. Schwartz J, Angle C, Pitcher H: Relationship batween child- 
hood blood ead levels and stature. Pediatrics 1986;77:281- 
288 

12._Centers for Nissese Control: Preventing lead poisoning in 
_young children. MMWR 1885,84:67-68 

18. Landrigan PJ, Gehlbach SI Resmi BF, et al: Epidemic 
lead absorption near an ore smelter: The role of particulata 
lead N Engl J Med 1875; 1282:128-123 

18. Assessment of the Safety of Lead and Lead Salts in Food: A 
Report of the Nutrition Foundation’s Expert Advisory Com. 
Bttee, Washington, DC, The Nutrition Foundation, 1982 

20. Bureau of the Census. Statistical Abstracts of the Unitad 
Statas, 1880, ed 101. Washington, DC, US Pearimens of 
Commerce, 1980 

Es #29 
  

) ee HY ay it 

21. Bureau of the Census: Annual Housing Surpey, 1878, Cur- 
rent Housing reports series H-150-T8. Washington DC, US - 
Department of Commerce, 1979 

22. Fischbein A, Anderson KE, Sassa 8, et al: Lead poisoning 
from “do-it-yourself” heat guns for removing lead.based 
paint: Report of two cases, Environ Res 1981;24:425431 

23. Landrigan PJ, Baker EL, Himmelstein JS, ot al: Exposure 
to lsad from the Mystic Hver bridge: The dilemma of de- 
leading, N Engl J Med 1882;306:873.876 

24. Bose A, Vashistha K, O'Loughlin BJ: Azareén por Evie. 
cho—Another cause of lead toxicity, Pediatrics 1883,72:106~ 
108 

25. Centers for Disease Control: Folk ramedy-aasociated dad 
poisoning in Hmong ¢hildren—Minnesota. MMWR 1088; 
32:656-666 

26. Ali AR, Smalls ORC, Aslam M: Surma and lead poisoning, 
Br Med J 1978;3:815-816 

27. Shaltout A, Yaish 8A, Fernando N: Lead encephalopathy in 
infants in Kuwait. Ann Trop Poediatr 1981:1:208-215 

28. Miller C: The pottery and plumbiam puzzle, Med J Austr 
1682:30:442-443 

28, Ostarud HT, Tufts E, Holmes M8: Plumbism at the Green 
Parrot goat farm. Clin Toxicol 1978:6:1-7 

30, Baker EL Jr, Folland DE, Taylor TA, et al: Lead poisoning 
in lead workers and their children: Home contamination 
with industrial dust. N Engl J Med 1877:296:260-261 

81. Chisolm JJ Jr: Fouling one's own nest. Pediatrics 
1878;62:614-617 

32. Ziegler EE, Edwards BB, Jansen RL, ot al: Absorption and 
retention of lead by infants. Pediatr Res 1878;12:26-34 

33. Roels HA, Buchet JP, Lauwerys RR, ot al: Exposure to lead 
+ by the oral and the pulmonary routes of children living in 
the vicinity of a primary lead amelter. Environ Res 
1980;22:81-94 

8. Rayre JW, Charney E, Vostal J, ot al: House and hand dust 
as a potential source of childhood lead exposure. Am J Dis 
Child 1974;127:1687-171 

35. Charney E, Kessler B, Farfel M, ot al: Childhood I "i 
poisoning: A controlied trial of the effect of dust-con 
atau on blood lead levels, N Engl J Med 1883;308: J085- 
109 

36. Baritrop D: The prevalence of pica. Am J Dis Chiid 
1966;112:116-123 

37. Mahaffey KR: Nutritional factors in lead poisoning. Nutr 
Rev 1981:39:353-362 

38. Nathen D, Oski F: Hematology of Infancy and Childhood, ed 
2. Philadelphia, WE Saundars Co, 1881 

38. Yip R, Schwartz §, Deinard AS: Screening for iron defl- 
clency with the erythrocyte protoporphyrin test. Pediatrics 
1983;72:214-219 

40. Piomelli 8, Rosen JF, Chisolm JJ Jr, et al: Management of 
childhood lead poisoning. J Padiatr 1884;108:525-582 

41. Preventing Lead Poisoning in Young Children, publication 
No. 00-2629. Atlante, Centers for Disease Control, April 
1678 

42. Blickman JH, Wilinson R, Graef J: The lead line revisited 
AJR 1086;74:88-63 

43. Markowitz ME, Rosen JF; Assessment of lead sons; in 
children: Validation of 8-hour CaNa*EDTA provocative tést. 
J Pediatr 1984;104:337-341 

44. Teisinger J, 8rbova J: The value of mobilization of lead by 
calcium sthylene diaminetetrancetate in the diagnosis of 
lead poisoning. Br J Ind Med 1858;16:148-153 

45. Chisolm JJ Jz, Barltrop D: Recognition and management of 
childesn with increased lead absorption. Arch Dis Child 
1879:54:249-262 

46. Graef JW: Clinical outpetiont management of childhood 
lead poisoning, in Chisolm JJ Jr, O'Hara D (eds): Lead 
Absorption in Children. Baltimore, Urban & Schwarzenberg,” 
1882, pp 153-164 

47. Chisolm JJ Jr: Management of increased lead absorphiod® 
Ttlustrative cases, in Chisolm JJ Jr, O'Hara D (eds): Lead 
Absorption in Children. Baltimore, Urban & Schwarzenberg, 
1882, pp 172-182 a 

SE al 
RY 

RE i 
rt 

 



    
SENT BY :NHeLP ® y 12217 2 a 6240075,830 

aliN-PG—-'91 THU 11:4F TTORNEY BEN: WHF ICE EL NUL? Va els roe   ——— 

DANIEL E. LUNGREN, Attorney General 
of the State of California 

CHARLTON G. HOLLAND, II 
Assistant BEL et General 

Ee Depry Attorney Cored 
Deputy A General 

2101 Webster Street, 12th Floor 
Oakland, California 94612-3049 
Telephone: (415) 464-1173 

Attorneys for Defendant 

UNITED STATES DISTRICT COURT 

NORTHERN DISTRICT OF CALIFORNIA G
G
 

0
 

=~
 

Ah
 

W
r
 

He
 

LB
 

N
N
 

ee
 

No. C 90 3620 EFL 

DECLARATION OF RUTH 8S. 12 | Matthews, and PROPLE UNITED FOR A 
RANGE, MPH. PHN, BETTER OAKLAND, On Behalf of 

13 || Themselves and All Others Similarly Stinated, 

) 

) 

14 Plaintifts, 

15 Ya | 

) 
) 

16 | MOLLY Cav pe w Director, California 
Department of Ith Services, 

Defendant. 
  

5 

20 § I, RUTH S. RANGE, declare: 

21 I hold an M.S. degree in Nursing. I have spent my endre professionai 

23 | carcer since 1958 in the area of public health, I have been employed by the Stato 

23 | Department of Health Services since 1977 as Chief of the Regional Operations Section 

24 | of the Child Health and Disability Prevention Branch of the Departinent. As such I 

25 { have been significantly involved in lead screening and testing matters within the last 

26 | decade. 

27 5 The matters stated below are personally known to me and if called as a 

L     DECLARATION OF AUTH 8. RANGE, M.S. PHN 

 



   

  

5 

SENT BY:NHeLP gl 0-10-91 3 12:18 21374809 1- 62400757431 
2a e166 PEs igs ie ee JUN=@E~"51 THU 11:4€ ATTORNEY GEN: OFFICE TEL NO:415~ 

Ww
 

0
 
«
h
n
 

a
 

L
a
 
N
e
 

10 

R
E
E
 

E
S
R
 

‘   

witness 1 could and would testify competently concerning the sare. 

3. The Department of Health Services does not dispute the seriousness of 

the problem of lead poisoning in children. In fact, as recently as March 12, 199], the 

Department's former Director, Dr, Kenneth Kizer stated that: "Lead poisoning is the 

most significant environmental health problem facing California children today, and 

insufficient consideration is being given to this potential problem during routine child 

health evaluations." What the Department docs dispute is whether either the law or 

good medical practice requires the actual testing of children’s blood far the presence of 

lead in all cases, and particularly very young children in the Early and Periodic 

Screening, Diagnostic and Treatment ("EPSDT") Program of the Federal Medicaid 

Program (known as the Medi-Cal program in California, and administered by the 

Department of Health Services). 

4, The Department belicves that neither applicable laws nor good medical 

practice requires that all EPSDT children receive biood lead tests as a part of the 

mandatory screening process. Rather, it is the Department's position that young (ic. 

vnder 6 years old) EPSDT children should first be screensd by their treating physicians 

for bath the presence of objective medical indications and/or environmental factors 

which might indicate the possibility of lead toxicity. If cither or both are present then 
it a blood test would be indicated. While the State Medicaid Manual (Plaintiffs' Exhibit 

N) recommends the erythrocyte protoparphyrin ("EP") test as the "primary screening 

test” (Ex. N, at p. 5-15), this test is falling into disfevar due to its relative wreliability 

vis-a-vis a blood lead test. (The former is a "pinprick” test while the latter draws a 

sample of venous blood.) 

5. A blood test is an intrusive procedure which causes some degree of 

discomfort, and in the vast majority of cases is simply unnecessary to determine 

  

1. CDHP Provider Informadon Notice #91.6, inchudad as Exhibit C in the 
Exhibits In Support Of Plaintiffs’ Motion For Partial Summary Judgment, 

2. 

DECLARATION OF RUTH 8 RANGE, M8, F.H.N. 

  

   



   
+NHelLP 
mead LIN— 

V
G
 

~~
 

O
h
 

km
 

B
e
 

WW
 

BN
 

ee
 

et
 

eh
 

hd
 

ph
 

fb
 

pe
 

h
 

L
h
 

H
B
 

W
O
 

NN
 
=
D
 

17   
  

=10-81 ; 12:18 4 91- 62400751832 
Ile Ho4 -41 ir) 1114. : FIURNEY BENT FELICE TEL MUS415 fai} 

whether a child is at risk of lead poisoning, Further, there is a significant cost factor 

invalved in completing a blood test which must be considered In an age Of lunited 

resources. In Fiscal Year 1989-90 Department records indicate that therc were 539,576 

children under the age of six in the Medi-Cal program. The cost of an EP test is 

$7.50, so the total cost of providing each of these children with such & test would be 

$4,046,820. The cost of the more reliable blood lead test is $22.50, so the total cost of 

providing each of these children with such a test would be $12,140,460, 

6. It ig the present belief of the Department that univarsal blood lead 

testing of young EPSDT children is not medically indicated, legally required nor fiscally 

prudent, 

I declare under penalty of perjury that the foregoing is true and correct. 

Executed at Sacramento, Cabiformda this 7th day of June, 1991 

  
DECLARATION CF AUTH 9. RANGE, M.A, PHN,