occupational lead exposure and women

PREVENTIVE MEDICINE 7, 31 l- 321 (1978)

Occupational Lead Exposure and Women

KENNETH BRIDBORD

Nationul Institute for Occuputionul Safety und Heulth. Center for Diseuse Control, U.S. Public Health Service, U.S. Depurtment of He&h, Educution, und Wevure,

5600 Fishers Lune, Rockville. Murylund 20857

The toxicity of lead has been known for approximately 2000 years, but the issue of women exposed to lead in the workplace has received relatively little attention until recent years. The major thesis of this paper is that the fetus represents an organism which is sensitive to lead and that the fetus is exposed to lead through the mother by the fact that lead crosses the placental barrier. Fetal exposure to lead is, in the author’s opinion, the critical issue involved in assessing occupational exposure to lead among women of childbearing age. Multiple studies have demonstrated that concentrations of lead in the mother’s blood are comparable to concentrations of lead in umbilical cord blood at birth. Many investigators consider the demonstrated effects of lead upon the hematopoietic system to be the earliest effect associated with lead exposure. Control strategies which prevent significant alterations in the heme synthetic pathway of the mother should prevent such changes in the fetus and thus protect against the more serious adverse effects of fetal lead exposure.

I. INTRODUCTION The toxicity of lead has been known for approximately 2000 years, but the issue

of women exposed to lead in the workplace has received relatively little attention until recent years. This paper reviews the literature in this area and the conclusions represent the personal opinions of the author. In the space allotted, however, it has not been possible to present a critical review of all the evidence.

The major thesis of this paper is that the fetus represents an organism which is sensitive to lead and that the fetus is exposed to lead through the mother by the fact that lead crosses the placental barrier. Fetal exposure to lead is, in the author’s opinion, the critical issue involved in assessing occupational exposure of women to lead. The best available information on potential fetal effects from lead comes from studies of young children exposed to lead. The results of these studies in children are helpful in defining lead exposures to women of childbearing age which represent a potential hazard to the fetus.

II. ADULT EXPOSURE TO LEAD

Lead may enter the body from a number of sources. For the general urban population with no unusual source of lead exposure, lead absorbed into the body comes primarily from the diet and from the ambient air. In urban areas, approximately one-third of the lead absorbed into the body of an adult comes from inhalation of air contaminated with lead, derived primarily from motor vehicle emissions (47-49).

For persons exposed to lead on the job, the occupational exposure must be added to that from general environmental sources, which in certain instances may already be excessive. The most important source of lead intake for exposed workers is inhalation. In addition, workers may also ingest significant quantities of

311 0091-7435/78/0073 -03 11$02.00/0 Copyright Q 1978 by Academic Press. Inc.

All rights of reproduction in any form reserved.

312 KENNETH BRIDBORD

lead-contaminated dusts on fingers, lips, cigarettes, etc. When work clothing contaminated by lead dust is brought home, this has caused elevated blood lead levels in children of workers (5).

A number of studies help to quantitate the contribution of airborne lead to lead absorption in adults. The evidence comes from two types of studies: epidemiolog- ic studies measuring blood lead levels and employing personal and stationary air monitors; and clinical studies including those using lead isotopes.

Table 1 summarizes those studies in which a quantitative assessment of airborne contribution to blood lead levels is possible (9). The blood lead increment is ex- pressed as the increment in blood lead assuming air lead exnosures over an 8-hr work day for a 40-hr work week. Considering the wide variations in study design, it is surprising how close many of the measured or estimated blood lead increments are. In assessing these increments, it has been assumed that the relationship between air lead and blood lead is approximately linear over the narrow range of air lead exposures which have been measured. This, of course, may not be true, particularly at higher levels of air lead exposure in which blood lead may not increase as much for a given increment of air lead as at the lower levels of exposure. The dose- response relationships described in Table 1 were derived primarily from observa- tions in males and are valid for blood lead levels up to about 40 E.Lg/lOO g. The increments in blood lead per unit of 40-hr average air lead exposure tend to average about 0.5 pg/lOO ml/pg/m3 in male workers with some higher and some lower values being reported. As noted below, the increment for women may be somewhat smaller. It is unlikely, however, that this increment would continue for air lead exposures much above 50 pg/m3, 40-hr week average exposure. Above 50 pg/m3, the increment in blood lead for each increment in air lead would be lower, perhaps in the range of 0.2 to 0.4 pug/100 g/pg/m3. One study, for example, observed blood lead increments of about 0.2 pg/ 100 ml for each pg/m3 of air lead exposure among men exposed to air lead levels in the range of 50 to 200 pLLg/rn3 (64). Consequently, if the blood lead level of a male worker is between 10 and 20 pug/100 g from general environmental exposure before beginning work with lead, the blood lead level would rise to between 35 and 45 pg/lOO g following a 40-hr average air lead exposure of about 50 &m3.

The data suggesting a smaller increment in blood lead in women than in men are summarized in Table 2. These data depict a consistent increase in male compared with female blood lead levels of about 30%. Data from the National Institute for Occupa- tional Safety and Health (NIOSH), however, suggest that there may not be a difference in blood lead between men and women occupationally exposed to presumably equivalent quantities of lead, but with blood lead levels generally above 40 pg/lOO g (57). Without precise measures of exposure, it is difficult to make absolute conclusions as to the absorbability of lead in men or women. This 30% increase in male blood lead levels probably does not hold for blood lead levels above 40 pug/100 g. This may be because women tend to be exposed to less lead from the general envi- ronment than men and thus would enter the workplace with a lower blood lead level than men. As exposure to lead for both men and women in the workplace increases, with the workplace becoming the predominant source of exposure, the difference in blood lead levels between men and women occupationally exposed to lead would tend to decrease. If the blood lead differences in Table 2 represent primarily a dif-

FORUM: WOMEN’S OCCUPATIONAL HEALTH 313

ference in general environmental lead exposure between men and women, and not a biologic difference, then blood lead levels of women entering the workplace would be about 5 pg/lOO g lower than those of men entering the workplace.

III. FETAL EXPOSURE TO LEAD

Multiple studies have established the fact that lead crosses the placenta of pregnant women and enters the fetal tissues with lead levels in the mother’s blood comparable to concentrations of lead in umbilical cord blood at birth (7,21,24,27, 28, 38, 65). Correlation coefficients between lead in umbilical cord blood and blood lead in the mother have been reported as high as 0.84 (7). The fact that the blood-brain barrier in the newborn is relatively immature raises additional con- cern as to the presence of lead in fetal tissues. The central nervous system does most of its growing during fetal life and during the year or two following birth.

IV. EFFECTS OF LEAD ON THE HEMATOPOIETIC SYSTEM

The earliest demonstrated effect of lead involves its ability to inhibit the heme biosynthetic pathway. A number of indicators of such effects have been studied including the enzyme aminolevulinic acid dehydrase (ALAD), aminolevulinic acid (ALA) in urine, and erythrocyte protoporphyrin activity. Effects of lead on ALAD are first measurable at blood lead levels in the range of 10 to 20 pg/lOO ml (29, 59). ALA in the urine begins to appear at blood lead levels in the range of 30 to 50 pg/ 100 ml (23, 51, 60). Increased erythrocyte protoporphyrins also occur at blood lead levels above about 30 pug/100 ml (11, 15,50,61). The Center for Disease Con- trol (CDC) considers blood lead levels of 30 pg/lOO ml in children, accompanied by increased erythrocyte protoporhyrins, to be evidence of lead poisoning (11). In this regard, studies have shown a correlation between ALAD activity in human mothers and fetuses (27, 39). Most recently, an inhibition of erythrocyte ALAD activity related to lead in both the pregnant woman and the fetus has been observed (34).

The fact that ALAD is inhibited in both mother and fetus exposed to lead indi- cates the need to keep fetal lead exposure no higher than a level associated with significant impairment to the ALAD system in the mother. Such impairment occurs as blood lead levels rise above 30 pg/lOO ml, corresponding to increased ALA in the urine and/or increased erythrocyte protoporphyrins. Since blood lead levels in the fetus are comparable to those in the mother, as a first approximation, to keep blood lead levels in the fetus below 30 &lo0 ml, blood lead levels in the mother must also be kept under 30 pg/lOO ml.

V. EFFECTS OF LEAD ON THE NERVOUS SYSTEM Lead is capable of damaging both the central and the peripheral nervous system.

If exposure is sufficient, the central nervous system may be severely damaged, resulting in coma, convulsions, and even death. This condition, referred to as acute encephalopathy, has often been observed in young children. Studies in children have shown that, once acute encephalopathy has occurred, there is a high probability of permanent, irreversible damage to the nervous system (10, 14, 54).

A number of studies suggest that permanent damage to the nervous system may have occurred in children only moderately exposed and in whom no overt symptoms of toxicity had appeared. These effects include behavioral problems such as

TABL

E 1

EVID

ENCE

FO

R A

CONT

RIBU

TION

O

F AI

RBOR

NE

LEAD

TO

LE

AD

ABSO

RPTI

ON

IN

HUM

.4NS-

QUAN

TITA

TIVE

AS

SESS

MEN

T (9

) CA

.2

Bloo

d le

ad i

ncre

men

t fo

r a

40-h

r wo

rk

week

Type

of

stud

y

Epid

emio

logi

c

Res

ults

Male

Lo

s An

gele

s ta

xi

driv

ers

expo

sed

to

wee

kly

aver

age

air

lead

le

vels

of

6.10

&m

3 ha

d av

erag

e bl

ood

lead

le

vels

of

24.

6 g/

100

g co

mpa

red

with

of

lice

work

ers

expo

sed

to a

n ai

r le

ad

of

3.06

&m

3 wi

th

aver

age

bloo

d le

ads

of 1

9.9

&IO

0 g

(4).

Clin

ical

Clin

ical

Epid

emio

logi

c

Air

lead

ex

posu

res

of

2 kg

/m3

in

adul

t m

ales

co

ntrib

uted

30

-40%

to

le

ad

ab-

sorb

ed

into

th

e bo

dy

(lead

iso

tope

te

ch-

niqu

es

used

). Ai

r le

ad

expo

sure

of

2 +

gIrn

3 ca

used

an

inc

rem

ent

in b

lood

le

ad

of a

bout

7

/.&lo

o g

(47-

49).

Bloo

d le

ad

leve

ls

of m

en

expo

sed

to

arti-

fic

ial

lead

ae

roso

l of

3.2

pg/

rn’

incr

ease

d an

av

erag

e of

8 &

IO0

ml.

For

men

exp

osed

to

ai

r le

ads

of

10.9

&m

3 th

e av

erag

e bl

ood

lead

inc

reas

e wa

s ab

out

18 @

g/10

0 m

l (2

6).

Bloo

d le

ad

leve

ls

of w

omen

liv

ing

near

a

road

way

aver

aged

23

.1

pg/lO

O

ml

com

- pa

red

with

17

.5 &

lOO

m

l am

ong

resid

ents

gr

eate

r di

stan

ces

away

. Ai

r le

ad l

evel

s we

re

mea

sure

d on

fro

nt

porc

h an

d in

ho

mes

of

in

divid

ual

subj

ects

and

blo

od

lead

inc

rem

ents

ca

n be

cal

cula

ted

by a

ssum

ing

8-hr

exp

osur

e to

fro

nt

porc

h le

vels

an

d 16

-hr

expo

sure

to

in

door

le

vels

(16

).

(per

&m

3 of

air

lead

exp

osur

e)

0.37

/&

loo

g

Com

men

ts

Die

tary

le

ad

cont

ribut

ions

no

t ad

e-

quat

ely

cons

ider

ed

but

com

parin

g pe

ople

fro

m

sam

e m

etro

polita

n ar

ea

tend

s to

m

inim

ize

thes

e di

ffere

nces

. Pe

rson

al

air

mon

itors

gr

eatly

im

- pr

ove

accu

racy

of

air

lead

ex

posu

re

mea

sure

men

ts.

0.85

/&l

o0

g

0.40

-0.6

0 &I

O0

ml

1.02

&IO

0 g

Onl

y th

ree

subj

ects

we

re

exam

ined

bu

t sim

ilar

resu

lts

were

de

taile

d by

fo

ur

diffe

rent

ap

proa

ches

, in

cludi

ng

E fil

tratio

n of

th

e ai

r wh

ich

was

%

brea

thed

. D

ieta

ry

lead

wa

s ca

refu

lly

1 co

ntro

lled.

z

Nat

ure

of t

he

aero

sol

gene

rate

d di

f- E

fere

d fro

m

that

in

the

am

bien

t ai

r in

z

such

a w

ay

to p

ossi

bly

incr

ease

le

ad

Fi

abso

rptio

n th

roug

h th

e lu

ngs;

co

n-

$ ve

rsel

y th

e se

dent

ary

stat

e of

the

su

bjec

ts

mig

ht

have

te

nded

to

de

- cr

ease

ab

sorp

tion.

D

ieta

ry

lead

re

- m

aine

d re

ason

ably

cons

tant

an

d ea

ch m

an s

erve

d as

his

own

co

ntro

l.

Age

and

socio

econ

omic

stat

us

may

ha

ve

been

im

porta

nt

conf

ound

ing

varia

bles

. N

o m

easu

re

was

mad

e of

di

etar

y le

ad

sour

ces.

Ai

r le

ad

leve

ls

were

m

easu

red

in

the

hom

es

of

stud

y su

bjec

ts,

prov

idin

g a

bette

r ex

posu

re

asse

ssm

ent

than

th

at

with

m

onito

rs

loca

ted

farth

er

away

.

Clin

ical

Epid

emio

logi

c

Epid

emio

logi

c

Epid

emio

logi

c

Lead

iso

tope

s sh

owed

a

40%

re

tent

ion

in

the

lung

s of

inh

aled

le

ad

aero

sol

gene

rate

d in

an

inte

rnal

co

mbu

stio

n en

gine

(6

&m

3).

Theo

retic

al

calcu

latio

ns

show

an

in

cre-

m

ent

in b

lood

of

adu

lts

betw

een

1.2

and

1.6

pg/lO

O

ml

for

each

@

m3

of 2

4-hr

ai

r le

ad

expo

sure

de

pend

ing

upon

wh

ethe

r 15

or

20 m

3 is

ass

umed

to

be

in

hale

d ea

ch

day

(1.3

.

High

er

bloo

d le

ads

obse

rved

in

ad

ults

re

- sid

ing

in

prox

imity

to

a

heav

ily

trave

led

freew

ay

com

pare

d wi

th

subu

rban

co

ntro

ls.

Bloo

d le

ad

incr

emen

ts

can

be c

alcu

late

d by

as

sum

ing

8-hr

ex

posu

re

to

ambi

ent

leve

ls

and

16-h

r ex

posu

re

to

half-

ambi

ent

leve

ls

while

in

door

s (3

1).

Polic

emen

in

H

oust

on

have

bl

ood

lead

le

vels

ab

out

4.7

~g/lO

O

g hi

gher

th

an

amon

g co

ntro

ls

(non

polic

emen

) in

th

e sa

me

city

. Po

licem

en

are

expo

sed

to

airb

orne

le

ad

leve

ls

of

abou

t 10

pg/

m3

durin

g wo

rkin

g ho

urs

com

pare

d wi

th

cont

rols

wh

o pr

esum

- ab

ly

would

be

exp

osed

to

air

lead

of

abo

ut

1 kg

/m3

durin

g wo

rk

(30)

.

Men

ex

pose

d to

ou

tdoo

r wo

rk

in

Stoc

k-

holm

ha

d av

erag

e bl

ood

lead

le

vels

6.

9 kg

/ 10

0 m

l hi

gher

th

an

men

wi

th

indo

or

work

. Ai

r le

ad

in

the

brea

thin

g zo

ne

of

traffi

c po

licem

en

aver

aged

9.

9 fig

/m3

(25)

.

0.40

-0.5

3 pg

/lOO

ml

0.34

(m

ale)

an

d 0.

30 (

fem

ale)

p&

100

ml

0.52

/&l

oo

g

0.78

&lo

0 m

l

Sede

ntar

y ha

bits

of

su

bjec

ts

may

ha

ve

caus

ed

decr

ease

d re

tent

ion

of

inha

led

lead

. Th

eore

tical

ca

lcula

tions

as

sum

ed

only

sh

ort-t

erm

tra

nsfe

r of

le

ad f

rom

th

e lu

ngs

to t

he b

lood

. U

se

of a

n in

tern

al

com

bust

ion

engi

ne

pro-

vi

des

a m

ore

real

istic

le

ad a

eros

ol.

Expo

sed

and

cont

rol

grou

ps

reas

on-

ably

m

atch

ed

for

perti

nent

co

- va

riate

s.

Die

tary

le

ad

cons

ider

ed

in

the

anal

ysis

.

Air

lead

ex

posu

res

were

no

t di

rect

ly

mea

sure

d am

ong

stud

y su

bjec

ts;

the

bloo

d le

ad

incr

emen

ts

depe

nd

upon

es

timat

es

of

expo

sure

fro

m

othe

r st

udie

s.

Cal

cula

tion

ussu

mes

no

di

f- fe

renc

es

in

air

lead

ex

posu

re

be-

twee

n ex

pose

d an

d co

ntro

l gr

oups

wh

ile

off t

he jo

b.

Cal

cula

tion

assu

mes

an

in

crem

enta

l ai

r le

ad

expo

sure

of

abo

ut

9 &m

3,

40 h

r pe

r we

ek

amon

g ou

tdoo

r co

m-

pare

d wi

th

indo

or

wor

kers

. It

is a

lso

assu

med

th

at

no

diffe

renc

e ex

ists

in

le

ad

expo

sure

be

twee

n gr

oups

wh

ile

off

the

job.


TABLE 2 BLOOD LEAD LEVELS IN ADULT MEN JND WOMEN

Increase in male Blood lead level compared with female

w 100 k!) blood lead level

Male Female (%) Reference

17.2

19.9

24.0 19.0

16.6

14.9

12.4

18.0 15.0

16.6 18.5 11.8 13.0

10.6

12.9 14.7 9.1 9.3

14.4 10.9 19.0 14.9 23.7 19.2

I5 (56) 60 (30)

33 (62) 27

57 (25) 29 (31) 26 30 40

24 (63 28 23

22.7 16.7 36 (58) 16.0 9.9 62

17.0 12.7 34 (55) 20.6 12.7 62 40.9 30.4 35

hyperactivity, difficulty in task performance, deficiency in IQ, and nerve conduction deficits.

Psychological tests, medical examinations, nerve conduction studies, and school records were used to evaluate possible effects of childhood lead exposure below overt toxicity. Adverse effects were seen in children with blood lead levels in excess of 60 pug/100 g (1). Children with blood leads over 50 pg/lOO ml exhibited mild CNS symptoms including behavioral and school difficulties (46).

Behavioral disturbances in children, such as hyperactivity, have been associated with blood lead levels between 25 and 55 pg/lOO ml (17). Treatment of hyper- kinetic children with chelating agents has produced clinical improvements, suggesting lead as an etiologic agent (18). In this regard, mice exposed to high levels of lead from birth developed hyperactivity which, as in children with this disorder, responded atypically to CNS stimulants and depressants (53).

A particularly important group of studies on lead toxicity involved a prospective evaluation of children in Virginia. In the initial investigation, exposed children were more likely to exhibit abnormal or suspect behavior and fine motor disabili- ties than children not so exposed (19). Subjects in this investigation were followed prospectively. The lead-exposed group had a mean blood lead of 58 pg/lOO g, (range: 40- 100 pg/lOO g) but blood leads were not measured in the controls. Lead intake differences between exposed and control groups were established based on measures of urinary coproporphyrins.

In a 3-year follow-up investigation, the results of the earlier study were con- firmed with the lead-exposed children showing deficits in global IQ and associated


abilities, in visual and fine motor coordination, and in behavior (20). School failure as a result of learning and behavioral problems was found more frequently in the lead-exposed, compared with the control, group. Of note is the fact that tooth lead levels in the lead-exposed group were significantly greater than in the controls. These data are consistent with neurobehavioral deficits observed in children with blood lead levels ranging from 40 to 70 pg/lOO ml (45).

In other studies, asymptomatic children with increased lead absorption were compared with a matched control group (6). A significantly increased incidence of hyperactivity was observed in the exposed children compared with controls but no significant differences were observed in other tests, including IQ and fine motor function. The exposed group had a previous history of two blood lead levels greater than 50 &IO0 ml compared with the control group with blood lead levels under 30 cl.g/lOO ml. Children exposed to lead emissions from a primary lead smelter were not found to show overt neurologic toxicity, although a negative correlation was noted between blood lead level and motor nerve conduction velocity (35). Earlier studies had noted that children with elevated blood lead levels above 40 pg/lOO g or with other evidence of lead poisoning had reduced mean motor nerve conduction velocities compared with normal children (22). Of note is the fact that slowing of the maximal motor conduction velocities of the median and ulnar nerves has been observed among lead workers who had never had a blood lead level above 70 /.&lo0 ml (52). More recently, motor nerve conduction velocities in lead workers were found to be significantly delayed in the blood lead range between 30 and 70 cl.g/lOO g (3).

Particularly relevant to this paper are studies of exposure to lead from water during the first year of life and to the mother during pregnancy in England (8). The probability of mental retardation was significantly increased when lead in the water exceeded 800 ~.~g/1000 ml. Elevated blood lead levels were also found in the retarded group (25.4 pg/lOO ml) compared with the control group (17.8 pg/lOO ml). In a follow-up study, blood lead concentrations were examined retrospectively from blood on cards used for the testing of phenylketonuria during the first 2 weeks of life (41). There appeared to be a significant relationship between blood lead concentration and mental retardation. Water lead concentrations in the maternal home during pregnancy also correlated with the blood leads from the mentally retarded children. Mean blood lead levels in the mentally retarded group were 25.5 compared with 20.9 pg/lOO ml in the controls. Perhaps more important was the fact that blood leads over 30 &lOO ml at birth were observed in one-third of the mentally retarded children, compared with 12.5% of the controls.

Not all studies of lead in children have shown positive relationships between low to medium level exposure and the development of subtle neurologic effects. Neurologic and motor development in a group of children with a mean blood lead level of 81 &lo0 ml was compared with a control group with a mean blood lead of 38 pug/100 g, and no difference was found between the two (32). In a subsequent study, children with blood lead levels ranging from 6 1 to 200 kg/ 100 ml were compared with a control group with blood lead levels under 40 /.&lo0 ml, and no significant differences between the groups were found based on tests of cognitive and sensory function (33). No relationship between blood lead level and mental func- tioning was found in a group of children exposed to industrial lead emissions (37).


Another study failed to observe adverse neurologic effects in a group of children exposed to lead emissions near a smelter in El Paso, Texas (40); those results are in conflict with reports of neurologic deficits in the same children (36).

VI. EFFECTS OF LEAD UPON THE REPRODUCTIVE PROCESS

Of particular importance in any discussion of reproductive effects and lead is the reported association between lead exposure to the mother and subsequent miscarriages and/or stillbirths. Historical data document the effect of lead in de- creasing fertility and increasing abortion rate. Exposure to lead in these early studies, however, was in all likelihood considerably higher than in modern times. For example, reproductive effects were associated with exposure of either the father or the mother to lead including either miscarriage, stillbirth, or prematurity (43). Studies suggest that there is a definite fetal risk, maximum in the first trimester, from intrauterine exposure to high concentrations of lead in maternal blood (2). Exposure to lead during the first trimester of pregnancy may cause fetal injury (44). Studies of lead in maternal and fetal blood suggest that lead might increase the incidence of early membrane rupture and premature deliveries (21).

VII. CONCLUSIONS Many investigators consider the demonstrated effects of lead upon the hema-

topoietic system to be the earliest effect associated with lead exposure. Control strategies which prevent significant alterations in the heme synthetic pathway should protect against the more serious adverse effects associated with lead (11, 13, 42). It is noteworthy that available data indicate significant alterations in heme synthesis at blood lead levels of 30 pg/lOO ml and above in children. Fur- ther, a number of studies suggest adverse effects on the neurologic system in children at blood lead levels above 30 to 40 &lOO ml. Accordingly, it would seem prudent to keep blood lead levels of newborn infants, and thus blood lead levels of their mothers, below 30 &lo0 ml.

Assuming, based upon the above discussion, that blood lead levels of 30 pg/lOO ml and above in the mother pose a risk to the developing fetus, how can this be translated into limits of exposure to airborne lead in the workplace?

As discussed above, an air lead exposure of about 50 pg/m3 for a male entering the work force with a preemployment blood lead in the range of 10 to 20 t&100 g would eventually cause an increase in blood lead levels in the range of 35 to 45 kg/100 g. If one assumes that in this blood lead range males have a blood lead about 30% greater than females, than an air lead exposure of about 50 pg/m3 should keep blood lead levels in female workers in the range of 25 to 35 ~@I00 g. Alternatively, if one assumes that women entering the work force have blood lead levels about 5 &lo0 g lower than men due to differences in general environmental exposure, an air lead exposure of about 50 pg/m3 in the workplace would result in blood lead levels in female workers in the range of 30 to 40 pg/lOO g. On this basis, it is concluded that, to keep blood lead levels of women workers below 30 &lOO g, 40-hr time-weighted average, weekly air lead exposures would have to be no higher than 50 pg/m3.


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