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 All

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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: epidemiologic 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 expressed 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 doseresponse relationships described in Table 1 were derived primarily from observations in males and are valid for blood lead levels up to about 40 E.Lg/lOOg. 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 Occupational 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 environment 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-

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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 concern 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 Control (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 indicates 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

TABLE

Blood lead levels ficial lead aerosol average of 8 &IO0 air leads of 10.9 lead increase was

Blood lead levels of women living near a roadway averaged 23.1 pg/lOO ml compared with 17.5 &lOO ml among residents greater distances away. Air lead levels were measured on front porch and in homes of individual subjects and blood lead increments can be calculated by assuming 8-hr exposure to front porch levels and 16-hr exposure to indoor levels (16).

Clinical

Epidemiologic

of men exposed to artiof 3.2 pg/rn’ increased an ml. For men exposed to &m3 the average blood about 18 @g/100 ml (26).

Air lead exposures of 2 kg/m3 in adult males contributed 30-40% to lead absorbed into the body (lead isotope techniques used). Air lead exposure of 2 +gIrn3 caused an increment in blood lead of about 7 /.&loo g (47-49).

Clinical

1 ABSORPTION

IN HUM.4NS-QUANTITATIVE

&IO0

1.02 &IO0

0.40-0.60

0.85 /&lo0

g

g

g

ml

of air lead exposure)

0.37 /&loo

(per &m3

Blood lead increment for a 40-hr work week

TO LEAD

Male Los Angeles taxi drivers exposed to weekly average air lead levels of 6.10 &m3 had average blood lead levels of 24.6 g/100 g compared with oflice workers exposed to an air lead of 3.06 &m3 with average blood leads of 19.9 &IO0 g (4).

LEAD

Epidemiologic

OF AIRBORNE

Results

FOR A CONTRIBUTION

Type of study

EVIDENCE

(9)

Age and socioeconomic status may have been important confounding variables. No measure was made of dietary lead sources. Air lead levels were measured in the homes of study subjects, providing a better exposure assessment than that with monitors located farther away.

Nature of the aerosol generated differed from that in the ambient air in such a way to possibly increase lead absorption through the lungs; conversely the sedentary state of the subjects might have tended to decrease absorption. Dietary lead remained reasonably constant and each man served as his own control.

Only three subjects were examined but similar results were detailed by four different approaches, including filtration of the air which was breathed. Dietary lead was carefully controlled.

Dietary lead contributions not adequately considered but comparing people from same metropolitan area tends to minimize these differences. Personal air monitors greatly improve accuracy of air lead exposure measurements.

Comments

ASSESSMENT

E z Fi $

E % 1 z

CA.2

Higher blood leads observed in adults residing in proximity to a heavily traveled freeway compared with suburban controls. Blood lead increments can be calculated by assuming 8-hr exposure to ambient levels and 16-hr exposure to half-ambient levels while indoors (31).

Policemen in Houston have blood lead levels about 4.7 ~g/lOO g higher than among controls (nonpolicemen) in the same city. Policemen are exposed to airborne lead levels of about 10 pg/m3 during working hours compared with controls who presumably would be exposed to air lead of about 1 kg/m3 during work (30).

Men exposed to outdoor work in Stockholm had average blood lead levels 6.9 kg/ 100 ml higher than men with indoor work. Air lead in the breathing zone of traffic policemen averaged 9.9 fig/m3 (25).

Epidemiologic

Epidemiologic

(1.3.

Lead isotopes showed a 40% retention in the lungs of inhaled lead aerosol generated in an internal combustion engine (6 &m3). Theoretical calculations show an increment in blood of adults between 1.2 and 1.6 pg/lOO ml for each @m3 of 24-hr air lead exposure depending upon whether 15 or 20 m3 is assumed to be inhaled each day

Epidemiologic

Clinical

pg/lOO ml

0.78 &lo0

0.52 /&loo

ml

g

0.34 (male) and 0.30 (female) p&100 ml

0.40-0.53

Calculation assumes an incremental air lead exposure of about 9 &m3, 40 hr per week among outdoor compared with indoor workers. It is also assumed that no difference exists in lead exposure between groups while off the job.

Air lead exposures were not directly measured among study subjects; the blood lead increments depend upon estimates of exposure from other studies. Calculation ussumes no differences in air lead exposure between exposed and control groups while off the job.

Exposed and control groups reasonably matched for pertinent covariates. Dietary lead considered in the analysis.

Sedentary habits of subjects may have caused decreased retention of inhaled lead. Theoretical calculations assumed only short-term transfer of lead from the lungs to the blood. Use of an internal combustion engine provides a more realistic lead aerosol.

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KENNETH

BRIDBORD

TABLE BLOOD

Blood w

LEAD

LEVELS

IN ADULT

2 MEN JND

WOMEN

Increase in male compared with female blood lead level

lead level 100 k!)

Reference

Male

Female

(%)

17.2

14.9

I5

(56)

19.9

12.4

60

(30)

24.0 19.0

18.0 15.0

33 27

(62)

16.6

10.6

57

(25)

16.6 18.5 11.8 13.0

12.9 14.7 9.1 9.3

29 26 30 40

(31)

14.4 19.0 23.7

10.9 14.9 19.2

24 28 23

(63

22.7 16.0

16.7 9.9

36 62

(58)

17.0 20.6 40.9

12.7 12.7 30.4

34 62 35

(55)

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 hyperkinetic 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 disabilities 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 confirmed with the lead-exposed children showing deficits in global IQ and associated

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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 functioning was found in a group of children exposed to industrial lead emissions (37).

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BRIDBORD

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 decreasing 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 hematopoietic 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. Further, 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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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 Heult...
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