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Chem. Pathol. Pharmacol. 9(4): 723-738, 1974. 

376. Vermande-van Eck, G. J. and J. W. Meigs. Changes in the 

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377. Kennedy, G. L., D. W. Arnold, and J. C. Calandra. 

Teratogenic evaluation of lead compounds in mice and 

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378. Hubermont, G., J. P. Buchet, H. A. Roels, and R. R. 

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pregnant rats. Toxicol. 5:379, 1976. 

379. Maisin, J. R., J. M . Jade, M . Lambiet-Collier. Progress report on morphological studies of the toxic effects of lead 

on the reproductive organs and the embryos. Economic 

Community of Europe Contract No. 080-74-7, Env. B. 

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380. Jacquet, P., A. Leonard, and G. B. Gerber. Progress report 

on studies into the toxic action of lead in biochemistry of 

the developing brain and on cytogenetics of post meiotic 

germ cells. Economic Community of Europe Contract No. 

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381. Cole, L.J. and L.J. Bachhuber. Effects of lead on the germ 

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382. Weller, C. V. The blastrophthoric effect of chronic lead 

poisoning. J. Med. Res. 55:271, 1915. 

383. Der, R., Z. Fahim, M. Yousef, and M. Fahim. Environmental interaction of lead and cadmium on reproduction 

and metabolism of male rats. Res. Comm. Chem. Pathol. 

Pharmacol. 74:689-713, 1976. 

384. Verma, M . M., Joshi, S. R., and A. O. Adeyemi. 

Mutagenicity and infertility following administration of 

lead sub-acetate to Swiss male mice. Experientia. 

50(5):486-487, 1974. 

385. McClain, R. M. and B. A. Becker. Teratogenicity, fetal 

toxicity, and placental transfer of lead nitrate in rats. Toxicol. Appl. Pharmacol. 5/:72-82, 1975. 

386. Ferm, V. H. and S. J. Carpenter. Developmental malformations resulting from the administration of lead salts. 

Exp. Mol . Pathol. 7:208-213, 1967. 

387. Ferm, V. H. and D. W. Ferm. The specificity of the 

teratogenic effects of lead in the golden hamster. Life Sci. 

70:35-39, 1967. 

388. Vallee, B. L. and D. D. Ulmer. Biochemical effects of mercury, cadmium and lead. Ann. Rev. Biochem. 47:91-128, 

1972. 

389. Ferm, V. H. The synteratogenic effect of lead and cadmium. Experientia. 25:56-57, 1969. 

390. Giliani, S. H. Congenital cardiac anomalies in lead 

poisoning. Pathol. Microbiol. (Basel). 59:85-90, 1973. 

391. Giliani, S. H. Congenital anomalies in lead poisoning. 

Obstet. Gynecol. 47:265-269, 1973. 

392. Millar, J. A „ V. Battistini, R. L. C. Cumming, F. Carswell, 

and A. Goldberg. Lead and 8-amino-levulinic acid 

dehydratase levels in mentally retarded children and in 

lead poisoned suckling rats. Lancet. 2:695, 1970. 

393. Porritt, N. Cumulative effects of infinitesimal doses of 

lead. Brit. Med. J, 2:92-94, 1931. 

394. Kremer, H. U. and M. N. Frank. Coexisting myxedema 

and chronic plumbism. Ann. Intern. Med. 42:1130-1 136, 

1955. 

395. Monaenkova, A. M. Functional state of the thyroid in 

chronic intoxication with some industrial poisons. Gig. 

Tr. Prof. Zabol. 7(2): 44-48, 1957. 

396. Zel'tser, M. E. The functional state of the thyroid gland in 

lead poisoning. Tr. Inst. Kraevoi. Patol. Akad., Nank, Kaz 

SSR. 70:116-120, 1962. 

397. Sandstead, H. H. and R. Galloway. Effect of chronic lead 

intoxication on in vivo I" 1 uptake by the rat thyroid. Proc. 

Fed. Soc. Exp. Biol. Med. /24:l8-20, 1967. 

398. Sandstead, H. H., E. G. Stant, A. B. Brill, L. 1. Arias, and 

R. T. Terry'. Lead intoxication and the thyroid. Arch. Int. 

Med. 725:632-635, 1969. 

399. Sandstead, H. H., D. N. Orth, K. Abe, and J. Stiel. Lead intoxication: Effect on pituitary and adrenal function in 

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400. Murashov, B. F. Functional state of the adrenal cortex in 

chronic poisoning with tetraethyl lead. Gig. Tr. Prof. 

Zabol. 70:46-47, 1966. 

401. Pines, A. G. Indexes of general reactivity in saturnine toxicity. Vroch. Delo. 5:93-96, 1965. 

402. Makotchenko, V. M. The functional condition of supra 

renal cortex in chronic poisoning with heavy metals (lead, 

mercury). Tr. Ukr. Nauch. Issled Inst. Eksp. Endoksinol. 

20:162-170, 1965. 

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403. Sandstead, H. H., A. M. Michelakis, and T. E. Temple. 

Lead intoxication. Its effects on the renin-aldosterase 

response to sodium deprivation. Arch. Environ. Health. 

20:356-363, 1970. 

404. Urbanowicz, H., J. Grabecki, and J. Kozielska. The urinary excretion of 5-hydroxyindoleacetic acid in industrial 

lead exposure. Med. Lav. 60:582-586, 1969. 

405. Schiele, R., K. H. Schalle, and H. Valentin. The influence 

of lead upon the tryptophan metabolism. Klin. Wschr. 

52:401-404, 1974. 

406. Cooper, W. C , I. R. Tabershaw, and K. W. Nelson. 

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517-529, 1973. 

407. Alvares, A. P., S. Leigh, J. Conn, and A. Kappas. Lead and 

methyl mercury: Effects of acute exposure on cytochrome 

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Exptl. Med. 755:1406-1409, 1972. 

408. Remmer, H., J. Schenkman, R. W. Estabrook, H. Sasame, 

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409. Scoppa, P., M. Roumengous, and W. Penning. Hepatic 

drug metabolizing activity in lead-poisoned rats. Experientia. 29:970-972, 1973. 

410. Alvares, A. P., S. Kapelner, S. Sassa, and A. Kappas. Drug 

metabolism in normal children, lead-poisoned children, 

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1975. 

411. Alvares, A. P., A. Fishbein, S. Sassa, K. E. Anderson, and 

A. Kappas. Lead intoxication: Effects on cytochrome 

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412. Tabershaw, I. R. and W. C. Cooper. Health Study of Lead 

Workers. A Report Prepared for the International Lead 

and Zinc Organization. 1974. 

413. Monaenkova, A. M. and K. V. Glotova. Cardiovascular 

changes in some chronic intoxications with industrial 

poisons (lead, carbon disulphide, benzene). Git. Tr. Prof. 

Zabol. 75(0:32-36, 1969. 

414. Vigdortchik, N. A. Lead intoxication in the etiology of hypertonia. J. Ind. Hyg. 77:1-6, 1935. 

415. Cramer, K. and L. Dahlberg. Incidence of hypertension 

among lead workers. Brit. J. Ind. Med. 25:101-104, 1966. 

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S. H. Webster, D. W. Armstrong, and R. R. Sayers. The 

control of lead hazard in the storage battery industry. 

Publ. Health. Bull. (Wash.) No. 262, 1941. 

417. Scroczynski, J., K. Zajusz, S. Kossmann, and A. Wegill. • 

Effect of experimental lead poisoning on the development 

of arteriosclerosis. Pol. Arch. Med. Wewn. 58:641-646, 

1967. 

418. Prerovska, J. Einfluss von Blei auf biochemische Veranderungen im Serum und Veranderungen in der Aderwant 

im Hinblick auf Atherosklerose. in: Proc. of the Int'l 

Symp: Environmental Health Aspects of Lead, Amsterdam, 2-6 October, 1972. Luxembourg, Commission of the 

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419. Myerson, R. M. and J. H. Eisenhauer. Atrioventricular 

conduction defects in lead poisoning. Am. J. Cardiol. 

77:409-412, 1963. 

420. Freeman, R reversible myocarditis due to chronic lead 

poisoning in childhood. Arch. Dis. Child. 40:389-393, 

1965. 

421. Silver, W. and R. Rodriguez-Torres. Electrocardiographic 

studies in children with lead poisoning. Pediatr. 

47:1124-1127, 1965. 

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423. Kosmider, S. and T. Petelnz. Zini ny elektrokardiograficzne u startazych osob prezeweleklym 

aawodowym zatrueiem olowiem. Pol. Arch. Med. Wewn. 

52:4.37-442, 1962. 

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Kaz. SSR. 25:11-13, 1972. 

425. Mambeeva, A. A. and I. D. Kobkova. The concentration 

of catecholamines in tissues of the cardiovascular system 

in experimental lead intoxication. Izv. Akad..Nauk 

Kazahst. SSR. Ser. Biol. 7:77-82, 1969. 

426. Hemphill, F., M. L. Kaerberle, and W. B. Buck. Lead suppression of mouse resistance to Salmonella typhimurium. 

Science. / 72:1031-1032, 1971. 

427. Selye, H., B. Tuckweber, and L. Bertok. Effect of lead acetate on the susceptibility of rats to bacterial endotoxins. J. 

Bacteriol. 97:884-890, 1966. 

428. Gainer, J. H. Activation of Rauscher leukemia virus by 

metals. J. Natl. Cancer Inst. 57:609-613, 1973. 

429. Gainer, J. H. Lead aggravates viral disease and represses 

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431. Koller, L. D. and S. Kovacic. Decreased antibody formation in mice exposed to lead. Nature. 250:148-150, 1974. 

432. Bingham, E., E. A. Pfitzer, W. Barkley, and E. P. Redford. 

Alveolar macrophages: Reduced number in rats after 

prolonged inhalation of lead sesquioxide. Science. 

762:1297-1299, 1968. 

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of the International Symposium: Environmental Health 

Aspects of Lead, Amsterdam, October 2-6, 1972. Luxembourg, Commission of the European Communities, p. 

221-230. 

434. Reigart, J. R. and C. D. Graber. Evaluation of the 

humoral immune response of children with low level exposure. Bull. Environ. Contam. and Toxicol. 16:1 12-117, 

1976. 

435. Hicks, R. M. Air-borne lead as an environmental toxin. 

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association with lead colic. Arch. Environ. Health. 

25:289-291, 1971. 

11-65 
P.10 

12. ASSESSMENT OF LEAD EXPOSURES AND ABSORPTION 

IN HUMAN POPULATIONS 

12 1 INTRODUCTION 

Although epidemiological studies provide the 

most directly relevant data for setting ambient air 

quality standards, such investigations are subject to 

methodological and practical difficulties. Of most 

interest are studies relating ambient air lead exposures directly to human health effects in various 

population groups. Unfortunately, few such studies 

exist. Standards setting, then, must rely on constructing (1) the linkage between exposures to environmental sources of lead and the incorporation of 

lead from those sources in various segments of the 

population as measured by blood lead levels and (2) 

the relationship between levels of lead in the blood 

and associated health effects. 

This chapter will examine the details of studying 

blood lead levels in human populations. Included 

will be an examination of the statistical considerations of such investigations as well as a discussion of 

the characteristics of the frequency distribution of 

blood lead values and of how these may be used as 

tools in setting environmental standards. In addition, the effects of geographic and demographic 

variables on lead burdens will be considered, 

Finally, the epidemiological and clinical studies on 

the relationships between environmental lead exposures and human absorption will be described, 

and, where available, quantitative estimates of those 

relationships will be presented. 

12.2 LEAD IN HUMAN POPULATIONS 

In this section, the statistical approaches for 

assessing blood lead levels in human populations 

will be discussed, as will their applications and implications. This discussion will be followed by a 

description of findings relating to the geographic 

and demographic distributions of blood lead levels. 

12.2.1 Statistical Descriptions and Implications 

Many surveys have described blood lead values in 

human populations. Not unexpectedly, the investigators' choices of statistics to describe central 

tendencies and dispersion patterns are not uniform. 

This lack of uniformity makes comparison of the 

various studies quite difficult. For example, central 

tendencies are expressed as either arithmetic or 

geometric means, and the measures of dispersion 

also vary. Often the arithmetic mean of the distribution is much larger than the geometric mean. 

12.2.1.1 FORM OF THE DISTRIBUTION OF 

BLOOD LEAD LEVELS 

Several authors have either suggested or implied 

that the distribution of blood lead levels for any 

relatively homogeneous population closely follows a 

lognormal distribution.13 Lognormality has also 

been noted for other metals, such as

 90Sr in bones of 

human populations.4 Snee has suggested that the 

Pearson system of curves provides a slightly better 

fit for the data of Azar et al. than the lognormal,5 

but the improvement derived from this system does 

not seem sufficient to warrant the use of this littleknown technique. Yankel et al.1

 and Tepper and 

Levin2 both found their lead data to be lognormally 

distributed. Further analysis of the Houston study of 

Johnson et al.,6 the Southern California study of 

Johnson et al.,7 and the study of Azar et al.3 also 

confirmed that a lognormal distribution provided a 

good fit to the data. For these reasons, much of what 

is presented in this chapter is based on the acceptance that homogeneous populations have a lognormal distribution of blood lead values. 

The lognormal distribution and its application to 

biological measurements are discussed by several 

authors.48-

9

 A variable is said to have a lognormal 

distribution if the logarithm of the variable-is normally distributed. Because of the skewed nature of 

the lognormal distribution, the median (50th percentile) is a more meaningful estimate of central tendency than the arithmetic mean. For the normal distribution, the best estimate of the median is X, the 

simple arithmetic mean. Forthe lognormal distribution, the best estimate of the median is the geometric 

mean (GM): 

12-1 
' *"*•*"" ' 

P.11 

GM = Exp[S (In(Xi))/n]. (12-1) 

i= 1 

The standard deviation of the logarithms is: 

S = [1 (ln(X;)- ln(GM))2/n-l]"2. (12-2) 

i= 1 

The geometric standard deviation, also known as the 

standard geometric deviation, is given by: 

GSD = Exp(S). 

If only the arithmetic mean, X, and arithmetic standard deviation, SD, are given, then the geometric 

mean and the geometric standard deviation can be 

estimated by:10 

GM = X/(l + SD2/X2)''2 (12-3) 

and 

GSD Exp[(ln(SD2

/X2 + l))'/2]. (12-4) 

The geometric standard deviation must be interpreted differently than the arithmetic standard 

deviation. Using the SD, approximately 68 percent 

of the population will fall between (mean - SD) and 

(mean + SD). These same limits for the lognormal 

distribution become GM/GSD and (GM)(GSD). 

For example, if a population has a geometric mean 

blood lead level of 20 with a GSD of 1.3, then 95 

percent of the population will have blood lead levels 

between 20/(1.3)'

 % and (20)(1.3)'-96

 or 11.96 and 

33.45. 

12.2.1.2 PERCENTILE ESTIMATES OF THE 

LOGNORMAL DISTRIBUTION 

From the GM and GSD, estimates of percentiles 

of the lognormal distribution can easily be obtained 

either numerically or graphically. Numerically, the 

pth percentile, X is estimated by 

X p = (GM)(GSD) ZP (12-5) 

where z is the z value from a standard normal table. 

The following values are often used: 

Percent Percent Percent 

1 

2.5 

5 

10 

p 

-2.326 

-1.960 

-1.645 

-1.282 

25 

50 

75 

90 

p 

-.674 

0.000 

0.674 

1.282 

95 

97.5 

99 

99.9 

p 

1.645 

1.960 

2.326 

3.090 

Another method of obtaining percentile estimates 

is a graphical one using lognormal probability 

paper. One point is placed where the geometric 

mean intersects the 50th percentile. A second point 

is placed where (GM) (GSD)2 326 intersects the 99th 

percentile. A line drawn through these two points 

gives the estimated cumulative frequency distribution. Figure 12-1, for example, is drawn with an 

assumed geometric standard deviation of 1.3. 

Q 20 — 

GM-GEOMETRIC MEAN 

GSD - GEOMETRIC STANDARD DEVIATION 

Illl l ! I 1 I I I I 

95 50 

PERCENT OF POPULATION WITH BLOOD.LEAD LEVELS 

EXCEEDING GIVEN VALUE 

Figure 12-1. Estimated cumulative distribution of blood lead 

levels lor populations in which the geometric mean level is 15, 

25, or 40 M9/dl. 

From this description of the distribution, estimates can be obtained of the percentage of blood 

lead values expected to exceed any given level for 

any given geometric mean blood lead level. For example, (Figure 12-1) in the populations with 

geometric mean blood lead levels of 15, 25, and 40 

Aig/dl whole blood, 0.1, 10, and 68 percent, respectively, will have blood lead levels exceeding 35 

Mg/dl. 

As stated above, Figure 12-1 was drawn with a 

GSD of 1.3. The effect of varying the geometric 

standard deviations on the percentage exceeding a 

specified blood lead value is shown in Figure 12-2 

because the value of the GSD has been shown to vary 

across studies (Table 12-1). A marked effect can be. 

noted. It is very important, therefore, to be sure of 

100 

80 ; I I 1 

1 Illl l 

^ 1 1 1 

1 1 1 1 1 1 1 1 1 1 1 1 I 1 1 IK -

GM = GEOMETRIC MEAN — 

GSD •= GEOMETRIC STANDARD DEVIATION — 

1 MINI -

O 10 

S 8 

PERCENT OF POPULATION WITH BLOOD-LEAD LEVELS 

EXCEEDING GIVEN VALUE 

Figure 12-2. Estimated cumulative distribution ol blood lead 

levels lor populations having a geometric mean blood lead 

level of 25 Mg/dl, but geometric standard deviations ol 1.2, 

1.3, or 1.5. 

12-2 
P.12 

the value used for the geometric standard deviation 

if the lognormal distribution is to be used in setting 

environmental standards. 

Because most blood lead data have been reported 

as arithmetic means and standard deviations, and 

because the raw data are not generally available, this 

chapter will use the term "mean" for arithmetic 

mean. The arithmetic standard deviations, when 

available, will be identified. If the geometric means 

are available, they will be reported as geometric 

means with the geometric standard deviation provided. 

TABLE 12-1. ANALYSIS OF VARIANCE FOR THE LOGARITHMS OF BLOOD LEAD VALUES FOR SELECTED STUDIES 

(Geometric standard deviations given in parentheses) 

Study 

Idaho' 

Seven City Study? 

Southern California-Males7 

Southern California-Females7 

Houston6 

Azar3 

Population 

size 

879 

1908 

64 

107 

189 

149 

Replicates 

per 

observation 

3 

1 

2 

2 

2 

2-8 

Number 

ol 

duplicates 

16b 

171 

64 

107 

189 

NAC 

Population 

variance3 

0.190 

(1.55) 

0.090 

(1.35) 

0.224 

(1.60) 

0.183 

(1.53) 

0.182 

(1.53) 

0.148 

(1.47) 

Within group 

variance3 

0.072 

(1.31) 

0.082 

(1.33) 

0.181 

(1.53) 

0.167 

(1.51) 

0.069 

(1.30) 

0.099 

(1.37) 

Measurement 

variance 

0.01-2" 

(1.12) 

0.063 

(1.28) 

0.216 

(1.59) 

0.141 

(1.45) 

0.094 

(1.36) 

0.049 

(1.25) 

a

 Includes measurement variation. 

D

 Based on a separate Center for Disease Control versus Idaho comparison of 16 samples of 1975 data, which are different from the 1974 data for the Idaho study.1 The 

estimates of population and within group variance come from the original study. 

c

 Not available. 

12.2.1.3 VARIATIO N IN BLOOD LEAD 

VALUES 

The total variation in blood lead values for any 

study is composed of three variance components: (1) 

between group, (2) within group or individual, and 

(3) method variation. The method variance results 

from both sampling and analytical measurement 

variations. The within group variance results from 

the difference in biological response among individuals with the same exposure as well as 

demographic differences in age, sex, race, 

socioeconomic status, and environmental background of the individuals in a group. The within 

group variance is a measure of the homogeneity of 

people in a group, but also includes method 

variance. The between group variance results from 

the differences in the composition of people in a 

group, such as police officers or housewives. In 

studying the effect of lead exposure on blood lead 

levels, it is necessary to separate these sources of 

variation to know whether the study results are 

meaningful. If the blood lead sampling and analysis 

errors are large, any effects of different lead exposure may not be seen. In a similar manner, if the 

group chosen for a study is not homogeneous, the 

within group variance may be so large that the 

differences in blood lead values cannot be interpreted as resulting from exposure. The sources of 

variation are estimated in Table 12-1 for several 

studies for which the raw data were available. The 

variation is expressed in terms of the natural 

logarithms of the blood lead values, and the calculations were made using standard analysis of 

variance techniques. The variances are converted to 

geometric standard deviations and these values are 

shown in parentheses. 

Table 12-1 shows that a large portion of the total 

variation is caused by measurement variation, except possibly for the Idaho1

 study. The measurement 

variation was unusually large for the Southern 

California study,7 suggesting that results from this 

study should be viewed with caution. Except for the 

Southern California study, the GSD for within group 

variation was consistently near 1.3. This number includes both biologic and measurement variation. It 

is possible for the measurement variation to exceed 

12-3 
P.13 

the within group variation if there is more than one 

reading per individual, however, as was the case in 

both the Southern California and Houston studies. 

12.2.1.4 PROBLEM OF FALSE EXCEEDENCES 

Lucas11 has described a problem that he terms 

"false exceedences." For example, a lognormal distribution with a geometric mean of 25 and a 

geometric standard deviation of 1.3 will have 3.7 

percent of the distribution above 40. As a hypothetical example, if half of the variation is caused by 

measurement variation, then the "true" distribution 

would have a geometric standard deviation of 1.2 

and would have only 0.6 percent of the distribution 

above 40. 

False exceedences become a real problem if a 

threshold value, such as 40, is determined from 

sources of data lacking a large measurement variation. In such cases, the estimated percentage of the 

distribution above a fixed level will be an overestimate as shown in the previous paragraph. It is extremely difficult to obtain more accurate estimates 

because the appropriate variance can only be estimated indirectly and only in cases where there are 

replicate measurements on the same individual. If, 

however, the threshold itself is estimated from data 

having this same measurement variation, then the 

problem is more difficult. In such cases, the observed variances including measurement variation 

may be more appropriate. As the technology of 

measurement improves, the problem will become 

much less significant. 

12.2.2 Geographic Variability in Human Blood 

Lead Levels 

Numerous studies have been conducted throughout the world establishing mean blood lead concentrations for various remote, rural, suburban, and 

urban populations. By examining the differences 

among the observed levels across these populations, 

inferences can be drawn concerning the ubiquity of 

lead exposures as well as their relative magnitudes. 

A word of caution, however, must be inserted here. 

Many of these data have been collected over a 

period of time in which measurement technology for 

blood lead determinations has changed and improved. Also, sometimes neither the methods of 

analysis nor the sampling scheme used have been reported. 

Studies of remote populations have been used to 

estimate the natural background blood lead level for 

humans.1215 Likewise, studies comparing either 

rural or suburban populations have been used to establish the effect of urban living on blood lead 

levels. All these studies, however, can be used to 

demonstrate the broad variety of populations in 

which lead from all environmental sources has been 

found in people. 

Only a few studies1215 have focused on remote 

populations. Goldwater and Hoover12 conducted an 

international study of urban and rural populations 

in which investigators from 14 countries participated; only non-occupationally exposed adults were 

studied. One laboratory did all the chemical 

analyses. Some of these populations — New Guinea 

aborigines, for example — were thought to be 

remote from the effects of industrialization. The 

mean and standard deviations of blood lead for the 

aborigines, however, were 22 and 5 /ug/dl, respectively. Examination of their living habits could shed 

no light on the sources of this lead. In contrast to 

this, urban residents from Peru in the same study had 

a mean of 7 /ig/dl and a standard deviation of 5 

Mg/dl. 

Stopps13-

14

 reported data on remote populations. 

Table 12-2 presents the blood lead means as ranging 

from 23 to 12/ug/100 g. 

In contrast to the findings of Goldwater and 

Hoover12 and Stopps,1314 Hecker et al.15 in a more 

recent study of Amazon River Basin Indians, using 

anodic stripping voltammetry, found a mean blood 

lead of 0.83 figldl with a standard deviation of 0.59 

in 90 subjects. The urinary levels were not quite as 

low as the blood leads (mean, 7.9 /ug/dl; SD, 5.7), 

but still are low in comparison with the values reported in Goldwater and Hoover.12 

TABLE 12-2. BLOOD LEAD LEVELS OF REMOTE 

POPULATIONS13-

14 

Populations 

Brazilian Indians 

Marshall Islanders 

Peruvian Indians 

Islanders off Australia 

Bushmen 

New Guinea natives 

East Africans 

Sample size 

11 

33 

39 

28 

68 

67 

63 

Blood lead. 

ug/100 g 

23 

23 

18 

17.5 

16 

13 

12 

A number of studies have specifically contrasted 

blood lead results between rural, suburban, and urban populations.21621

 Two of the methodologically 

better studies are those of Tepper and Levin,2 and 

Nordman.16 Tepper and Levin2 conducted a study of 

the blood lead levels of 11 groups of housewives 

from 8 U.S. metropolitan areas. Three of these, 

Chicago, New York, and Philadelphia, had urban12-4 
P.14 

suburan comparison groups. Table 12-3 displays the 

results of the contrasts between those groups as calculated by Hasselblad and Nelson.22

 In every case, a 

significant difference was obtained. 

TABLE 12-3. AGE AND SMOKING-ADJUSTED GEOMETRIC 

MEAN BLOOD LEADS IN URBAN VERSUS SUBURBAN 

AREAS OF THREE CITIES 

Cily 

Chicago, IL 

Philadelphia, PA 

New York. NY 

Three cities together 

Urban 

17.55 

20.12 

16.47 

18.05 

Blood Lead, ug % 

Suburban 

14.02 

17.88 

15.24 

15.71 

Urban excess 

3.53 

2.24 

1.23 

2.34 

Significant 

>0.01 

>0.01 

>0.01 

>0.01 

Nordman16 studied a series of populations in Finland including downtown urban, suburban, and 

rural populations. No statistically significant 

differences were observed between urban and rural 

or suburban residents. But, interestingly, none of the 

populations studied, which included traffic policemen, streetsweepers, downtown Helsinki residents, 

and rural controls, had a mean blood lead level that 

exceeded 13.5 figldl. 

Other studies permitting urban rural comparisons 

include those of Hofreuter et al.,17 Creason et al.,18 

Scanlon,19 Gershanik et al.,20 and Cohen et al.21 

Hofreuter et al.,17 in 1960, collected blood samples 

from about 120 people in each of 6 cities and from 

162 people in a rural area (central Ohio). Table 12-4 

displays the results of these comparisons. In all urban survey sites, the mean blood lead level was significantly higher than in the rural survey sites. 

TABLE 12-4. BLOOD LEAD CONCENTRATIONS IN SIX 

URBAN AND ONE RURAL POPULATION 

Survey site 

New Orleans, LA 

Chicago, IL 

New York, NY 

Cincinnati, OH 

Dallas, TX 

Denver, CO 

Rural 

No. ol 

samples 

130 

97 

112 

137 

128 

131 

162 

Mean 

blood lead. 

jjg/100g 

22 

20 

20 

20 

18 

19 

14 

Urban 

excess 

8 

6 

6 

6 

4 

5 

Creason et al.1-

8

 studied military recruits in the 

Chicago area at the time of their induction. By the 

very nature of the sample, only young male adults 

were included. Further, analysis was restricted to 

those having lived at the same home address for two 

or more years. The population was broken down by 

race and three residential locations, namely urban, 

suburban, and outstate. Median blood levels for 

whites were 22, 20, and 36 figldl for the urban, 

suburban, and outstate populations, respectively. 

Scanlon19 reported on umbilical cord blood lead 

levels for infants born to Boston area women. Mean 

blood lead levels for urban infants were 22.1 /ug/dl 

compared with 18.3 /ug/dl for the suburban 

newborn. This difference was not statistically significant. 

Gershanik et al.20 studying a larger sample of cord 

bloods in Shreveport, Louisiana, however, found a 

statistically significant difference between urban and 

suburban infant cord blood lead levels, 9.7 ± 3.9 

versus 8.3 ± 2.4 /xg/dl, respectively. 

Cohen et al.21 reported on a rural-urban comparison for children, aged 1 to 5 years, living in 2 

rural counties and in Hartford, Connecticut. 

Although the 2 samples were adequately matched on 

age, there was a major racial/ethnic difference — the 

urban population being either black or Puerto Rican 

and the rural primarily white. The mean and standard deviation of the blood lead concentrations 

were 32.7 ± 14.8 and 22.8 ± 11.0 for the urban and 

rural populations, respectively. 

Some of these same studies, as well as others, can 

be used to discern a wider picture of the variability 

of blood lead levels.121417 In the Goldwater and 

Hoover study,12 urban population mean blood lead 

levels were found to range from 7 to 25 figld\, 

whereas the mean for rural areas ranged from 9 to 

32 /xg/dl. The wide range of means in both population types suggests that lead can be found in many 

locations. 

Nordman16 reviewed the available literature on 

blood lead levels and concluded that "the Pb-B 

mean values for occupationally unexposed rural and 

urban populations range from 10 to 26 /ug/dl." Exceptions to this general range are found, however. 

Lower-than-usual blood lead levels have been reported from some parts of Sweden and Finland. 

There, levels in women were found to be 10 

/ug/dl.16-

23

 On the other hand, higher-than-usual 

blood lead values have been reported from sections 

of Italy and France.2427 Zurlo et al.,24 in particular, 

reported very high blood lead levels for adults in the 

Milan area, urban mean of 30 /xg/dl for males and 

23.7 figldl for females. 

Data obtained from adults within the United 

States follow a similar pattern. 2172 8 In data from 

Tepper and Levin,2 differences were noted in the 

geometric mean blood lead among the 11 populations of housewives studied. The lowest blood lead 

values were found in Houston, Texas, with a GM 

and a GSD of 12.5 and 1.31, respectively, whereas 

the highest were found in Rittenhouse, a section of 

12-5 
P.15 

Philadelphia —GM and GSD of 20.6 and 1.33, 

respectively. 

In the 1960 Hofreuter et al. study,17 blood samples were collected from people in six metropolitan 

areas and one rural control site. The mean blood 

lead values varied from 14 to 22 /ug/100 g. The maximum observed values ranged from 38 to 60 

Mg/100 g. 

Kubota et al.28 studied blood lead levels in male 

residents of 19 intermediate-sized cities across the 

United States. Mean blood levels were found to vary 

from 7.25 /ug/dl in Lafayette, Louisiana, to 20.34 

figldl in Jacksonville, Florida. The highest reported 

value, 109.27 /xg/dl, occurred in Fargo, North 

Dakota. A wide range in values was reported for 

each city, the largest being 5.91 to 109.27 /xg/dl in 

Fargo. Further, the authors report three cities with 

mean blood lead levels below 8.00 /ug/dl, namely 

Lubbock, Texas, 7.95; Geneva, New York, 7.65; 

and Lafayette, Louisiana, 7.25 /xg/dl. These low 

values approximate those found in parts of Scandinavia.16 

Workers at 23 DuPont Company plants were 

studied over a 5-year period, 1967 through 1971.29 

No time trend was noted for blood lead levels, and 

the samples were pooled per plant for the 5 years. 

The geometric mean values varied from a low of 

15.5 /ug/100 g for the Ashland, Wisconsin, plant to a 

high of 21.6 /ug/100g at the Los Angeles, California, 

plant. The overall geometric mean for the 23 locations was 18.2 /ug/100 g. 

Data addressing geographic variation of blood 

lead values in children are not as extensive. For the 

United States, Fine et al.,30 Baker et al.,31 and 

Joselow et al.32 provided the best available information. Fine et al.30

 studied 6151 children aged 1 to 

6 years in 14 intermediate-sized cities in Illinois in 

1971. Blood lead values (Table 12-5) were determined by an atomic absorption technique. Mean 

values for cities ranged from 19.8 to 32.9 figldl; the 

mean for all 14 cities was 25.5 /ug/dl. These values 

are indicative of sources of lead in the children's environment. 

Baker et al.31 determined blood lead values for 

1672 children aged 1 to 5 living in 19 towns containing smelters and 3 control towns. The smelter communities were selected for study because they had 

not previously been subject to thorough investigation. Blood lead values were determined by an 

atomic absorption technique. 

The mean blood lead levels for the lead and copper smelter towns did not differ from those control 

towns, as shown in Table 12-6. The children living 

TABLE 12-5. MEAN BLOOD LEAD VALUES FOR CHILDREN 

IN 14 INTERMEDIATE-SIZED CITIES IN ILLINOIS, 197130 

City 

Aurora 

Springfield 

Peoria 

East St. Louis 

Decatur 

Joliet 

Rock Island 

East Moline 

Harvey and Phoenix 

East Chicago Heights 

Chicago Heights 

Robbins 

Carbondale 

Rockford 

Total 

No. Ol 

children 

screened 

449 

670 

387 

376 

793 

383 

285 

298 

226 

172 

537 

103 

264 

1,208 

6,151 

% ol city's 

children 

ages 1-6 yr 

screened 

5.09 

7.28 

2.97 

4.09 

5.84 

4.54 

5.60 

12.32 

4.90 

17.13 

10.36 

6.78 

17.46 

7.31 

6.14 

Mean blood 

lead value, 

ug/dl 

28.2 

31.5 

32.9 

28.6 

21.5 

27.8 

25.0 

23.5 

22.6 

27.3 

25.2 

22.2 

28.5 

19.8 

25.5 

in zinc smelter towns, however, showed significantly 

higher blood lead values than the other three groups. 

The lowest mean blood lead value, 9.15 /ug/dl, was 

found in children for McGill, Nevada, whereas the 

highest mean value was found for Bartlesville, 

Oklahoma, with 28.60 /ug/dl. 

Joselow et al.32 compared the blood lead levels of 

children aged 3 to 5 years in Newark, New Jersey, 

and Honolulu, Hawaii, in 1973. The study included 

152 children who were matched for age and sex into 

2 groups of 76 from each city. The mean blood lead 

value for the Newark children was 28 /ug/dl, considerably higher than that found in Honolulu 

children, 17 /xg/dl. 

12.2.3 Demographic Variables and Human Blood 

Lead Levels 

Fewer data are available to evaluate the effects of 

age, sex, and race on blood lead levels. 

Children consistently develop higher blood lead 

levels than do adults in the same environmental setting. In El Paso, Texas,33

 in 1972, 70 percent of 

children 1 to 4 years old living near a primary lead, 

copper, and zinc smelter had blood lead levels >40 

/xg/dl, and 14 percent exceeded 60 /ug/dl. In 

children 5 to 9 years old, 45 percent exceeded 40 

figldl, as did 31 percent of measurements in individuals 10 to 19 years old and 16 percent of those 

over 19. 

In the vicinity of a primary lead smelter in Idaho 

in 1974, the geometric mean blood lead levels 

shown in Table 12-2 were obtained.1 As can be seen 

from Table 12-7, children under 10 years of age 

consistently had higher blood lead values than older 

children and adults within the same environment. 

12-6 
P.16 

TABLE 12-6. BLOOD LEAD LEVELS (WHOLE BLOOD) IN CHILDREN IN U.S. SMELTER AND COMPARISON TOWNS, 197531 

City 

No. ol 

samples Mean SEa GM GSD 

Percent 

exceeding 

35 ug/dl 

Comparison towns 

Albuquerque, NM 

Perryville, MO 

Safford, AZ 

Total 

Lead smelter towns 

Bixby, MO 

Glover, MO 

Herculaneum, MO 

Total 

Copper smelter towns 

Ajo. AZ 

Anaconda, MT 

Copper Hill, TN 

Douglas, AZ 

Hayden, AZ 

Hurley, MN 

McGill, NV 

Miami, AZ 

Morenci, AZ 

San Manuel, AZ 

White Pine. Ml 

Total 

Zinc smelter towns 

Amarillo. TX 

Bartlesville, OK 

Corpus Christi. TX 

Monaco, PA 

Palmerton, PA 

Total 

81 

85 

92 

258 

48 

23 

87 

158 

105 

64 

86 

97 

100 

42 

50 

94 

100 

101 

70 

909 

84 

87 

12 

62 

102 

347 

17.70 

16.88 

15.26 

16.56 

13.76 

12.05 

18.80 

16.34 

12.55 

13.38 

16.63 

20.47 

21.24 

14.33 

9.15 

17.00 

13.87 

18.01 

18.62 

16.36 

22.34 

28.60 

19.02 

14.84 

17.51 

21.04 

0.63 

0.74 

0.71 

0.41 

0.96 

1.19 

0.94 

0.66 

0.46 

0.95 

0.74 

0.86 

0.85 

1.23 

0.52 

0.74 

0.56 

0.55 

0.74 

0.25 

1.16 

1.91 

1.42 

0.82 

0.60 

0.66 

16.8 

15.8 

13.8 

15.4 

12.4 

11.1 

17.2 

14.6 

11.7 

11.6 

15.4 

18.9 

19.9 

12.8 

8.9 

15.5 

12.9 

17.2 

17.8 

14.8 

20.9 

23.6 

18.4 

13.7 

16.5 

18.6 

1.39 

1.42 

1.57 

1.57 

1.66 

1.58 

1.54 

1.64 

1.45 

1.77 

1.47 

1.49 

1.42 

1.60 

1.45 

1.59 

1.47 

1.37 

1.34 

1.58 

1.41 

1.92 

1.32 

1.49 

1.42 

1.63 

0.0 

2.4 

1.1 

1.2 

0.0 

0.0 

8.0 

4.4 

0.0 

1.6 

1.2 

3.1 

5.0 

4.8 

0.0 

3.2 

0.0 

1.0 

2.9 

2.0 

4.8 

31.0 

0.0 

1.6 

1.0 

9.5 

SE = standard error. 

TABLE 12-7. GEOMETRIC MEAN AND GEOMETRIC 

STANDARD DEVIATIONS (IN PARENTHESES) OF BLOOD 

LEAD LEVELS BY AGE AND STUDY SECTOR (-ug/dl) 

Study 

sector 

I 

II 

III 

<10 

66(1.33) 

47(1.30) 

34(1.26) 

Age. years 

10-19 

39(1.26) 

33(1.23) 

28(1.40) 

>20 

38(1.32) 

33(1.33) 

30(1.35) 

Likewise, a study of traffic exposure in Dallas, 

Texas,34 found mean blood lead concentrations of 

12 to 18 /xg/dl in children as contrasted with 9 to 14 

figldl in adults, when exposure levels are controlled. 

Simpson et al.35 summarized the results of 27 

neighborhood screening programs conducted 

throughout the United States in the spring and summer of 1971. They found that children less than 3 

years of age had a lower rate of elevated blood lead 

than children older than 3 years. Of those under 3 

years, 25.8 percent had values of 2 40.0 /xg/dl, 

whereas 31.4 percent of those 3 years of age or older 

had values240.0/xg/dl. 

Elam et al.36 studied pediatric patients in a 

Chicago outpatient service. The proportion of 

children (Table 12-8) with blood lead values 2 50 

figldl varied with age; the proportion over 50 figldl 

peaked at 18 to 30 months of age. 

TABLE 12-8. PROPORTION OF CHILDREN WITH BLOOD 

LEAD VALUES BETWEEN 50 AND 99 /xg/dl, BY AGE, 

CHICAG01971-197536 

Age. months 

% Blood lead 

50lo99/jg/dl 

6-17 

18-30 

31-42 

43-52 

55-66 

24 

40 

16 

12 

7 

A study of Philadelphia ghetto children37 conducted in 1972 through 1973 provides data relevant 

to the relationship between age and blood lead level. 

The study population consisted of 1559 black 

children aged 6 months to 18 years of age. Table 

12-9 presents the blood lead levels by age. In both 

12-7 
P.17 

G6PD normal and deficient children, the blood lead 

pattern of increase and decrease by advancing age 

pertains. The only increase, but a substantial one, is 

observed between children less than 1 year of age 

and those 1 to 3 years old. Blood lead levels 

decrease in all succeeding age groups. 

Billick et al,38 analyzed data from New York City 

lead screening programs from 1970 through 1976. 

The data include age in months, sex, race, residence 

expressed as health district, screening information, 

TABLE 12-9. MEAN BLOOD LEAD (/xg%) BY AGE, SEX, AND G6PD STATUS IN 1559 URBAN BLACK CHILDREN37 

Age, years Sex Number 

G6PD 

normal 

G6PD 

deficient 

<1 

1-3 

4-8 

9-13 

14-18 

Both 

Males 

Females 

Both 

Males 

Females 

Both 

Males 

Females 

Both 

Males 

Females 

Both 

Males 

Females 

61 

32 

29 

289 

133 

156 

404 

177 

227 

394 

189 

205 

242 

94 

148 

19.1 ± 

19.5 ± 

19.2 + 

29.1 ± 

30.5 ± 

28.8 ± 

25.0 ± 

24.6 ± 

25.1 ± 

21.3 ± 

20.4 ± 

21.7 ± 

18.7 ± 

18.5 ± 

18.8 ± 

9.5 

9.0 

9.2 

14.6 

15.1 

11.0 

12.6 

13.2 

11.1 

10.4 

10.9 

9.7 

9.7 

10.1 

8.9 

9 

6 

3 

40 

30 

10 

55 

38 

17 

44 

29 

15 

21 

13 

8 

18.3 ± 8.2 

18.8 ± 8.2 

17.3 ± 8.4 

33.2 ± 15.5 

33.1 ± 15.5 

33.6 ± 13.5 

25.7 ± 13.4 

25.2 ± 12.9 

26.1 ± 13.5 

23.0 ± 12.5 

22.1 ±11.8 

24.8 ± 13.9 

19.1 ± 9.9 

18.9 ± 9.3 

19.5 ± 10.1 

and blood lead values expressed in decades. Only 

the first screening data for individual children were 

included based on the analysis of venous blood. 

Only the data (178,588 values) clearly identified as 

coming from the first screening of a given child were 

used. All blood lead determinations were done by 

the same laboratory. The data presented are 

preliminary and an exhaustive analysis has not been 

completed. Table 12-10 presents the geometric 

means for the children's blood lead levels by age and 

TABLE 12-10. GEOMETRIC MEAN BLOOD LEAD LEVELS IN NEW YORK CITY LEAD SCREENING PROGRAM 

(Calculated on the basis of the Billick et al.38 data) 

Group and 

year 

Blacks 

1970 

1971 

1972 

1973 

1974 

1975 

1976 

Hispanic 

1970 

1971 

1972 

1973 

1974 

1975 

1976 

Whites 

1970 

1971 

1972 

1973 

1974 

1975 

1976 

1-12 

27.2 

25.2 

22.3 

22.6 

22.2 

20.5 

18.1 

21.5 

19.9 

18.7 

20.1 

19.7 

17.4 

17.9 

21.0 

19.9 

17.1 

20.3 

18.6 

19.1 

20.7 

13-24 

31.2 

29.7 

26.3 

26.9 

25.7 

22.9 

20.7 

24.9 

22.9 

20.6 

21.8 

21.4 

19.6 

18.6 

23.9 

22.8 

20.2 

21.5 

20.5 

20.0 

17.2 

25-36 

31.2 

30.4 

26.7 

26.3 

25.5 

22.9 

21.2 

25.5 

25.0 

22.1 

22.5 

23.0 

20.6 

19.2 

24.7 

22.9 

22.0 

21.9 

20.0 

19.0 

19.1 

Age. months 

37-48 

28.4 

29.8 

25.8 

25.6 

24.4 

22.3 

20.9 

23.9 

24.9 

22.6 

23.1 

22.6 

20.9 

19.3 

25.0 

23.0 

21.1 

22.1 

21.1 

18.2 

18.7 

49-60 

31.4 

28.7 

25.0 

24.5 

23.7 

21.7 

20.3 

24.1 

24.4 

22.1 

22.2 

22.1 

20.6 

19.2 

23.7 

23.9 

21.2 

20.6 

21.4 

19.8 

18.4 

61-72 

22.9 

27.7 

24.3 

24.1 

22.2 

21.8 

19.2 

24.5 

23.9 

22.0 

21.6 

20.1 

20.0 

18.2 

24.9 

21.9 

21.4 

21.6 

21.3 

18.0 

17.7 

73^ 

25.7 

27.0 

23.8 

23.1 

22.1 

19.6 

19.3 

24.0 

23.9 

21.3 

21.7 

20.3 

18.5 

18.4 

22.5 

21.7 

20.6 

21.1 

19.6 

17.3 

17.5 

12-8 
P.18 

race for the 7 years. It should be mentioned that the 

means presented were derived by EPA from the raw 

data provided by Billick et al.38 Because the blood 

lead levels were available to the nearest 10 /xg/dl, 

the midpoints of each interval were used to calculate 

the geometric means. These means were calculated 

for each 2-month interval for each age and ethnic 

group and were then combined across the six 2-

month intervals using an unweighted geometric 

mean so as to minimize any seasonal effects. 

It should be noted that all racial/ethnic groups 

show an increase in geometric mean levels from < 1 

to 1 to 2 years of age. Figure 12-3 shows the trends 

for 1970. Similar patterns hold for other years. The 

1 

i 

-

Illl l 

/ BLACK 

/ HISPANIC "*•— . . 

/ ^^ \ 

/ WHITE ^ v 

Illl l 

^ 

-

 T 

AGE, years 

Figure 12-3. Geometric means for blood lead values by race 

and age, New York City, 1971. 

differences in age-associated patterns for the three 

racial/ethnic groups may be influenced by the substantial differences in population sizes for the 

groups: whites were the smallest group, Hispanics 

were next, and blacks the largest. Table 12-11 shows 

the size of the groups for the 7 years. 

TABLE 12-11. NUMBER OF CHILDREN'S INITIAL SCREENS 

IN NEW YORK CITY PROGRAMS BY RACE/ETHNICITY AND 

YEAR, 1970-19773* 

Year White Black Hispanic 

1970 

1971 

1972 

1973 

1974 

1975 

1976 

1,282 

2,796 

1,350 

823 

601 

656 

491 

8,839 

23,174 

16,730 

9,722 

4,139 

4,585 

3,755 

8,251 

18,740 

10,153 

6,875 

2,498 

2,620 

2,178 

ages 8 days to 8 years showed increasing mean blood 

lead levels with age: 3.3 ± 2.6 figldl in the first year 

of life, increasing with each year to a mean of 11.5 ± 

4.9 figldl at age 6 to 8. 

In contrast to studies of children, most studies of 

adult populations do not show any marked effect of 

aging on blood lead levels.

 17

.

4

0-4' Nordman found 

that males and females over the age of 65 years had 

lower blood lead values than the rest of the adult 

population in his study.16 

Effects of sex on blood lead levels appear to be 

age dependent. Adult females are commonly found 

to have lower levels than males.2,16,17,23,24 Among 

children, however, sex does not appear to be a 

differentiating factor.4243 Tepper and Levin2 have 

suggested that the differences found in blood lead 

levels of adult men and women are not the result of 

either differences in lead intake from food or from 

differences in hematocrit levels between them. 

Data for the assessment of race as a factor in blood 

lead levels are relatively scarce. 18.25,38,44,45 The 

earlier studies1844 report only the number of cases 

above a specified blood lead level. One study18 

shows higher lead levels for blacks than Puerto 

Ricans, but the other44 reports that blacks had higher levels than nonblacks. 

In their study of military recruits, Creason et al.18 

compared white and black subjects. Data in Table 

12-12 show higher mean values for all black groups 

than for the whites. 

TABLE 12-12. BLOOD LEAD LEVELS (/ug/dl)18 IN MILITARY 

RECRUITS, BY RACE AND PLACE 

Place Number 

Urban 58 

Suburban 4 

Outstate 15 

Mean 

38 

80 

59 

90th 

percentile 

85 

124 

105 

Number 

203 

218 

406 

Mean 

31 

27 

39 

90th 

percentile 

69 

54 

71 

It is of interest to note that the age-associated pattern observed in the United States was not seen in a 

West German39 study. In that study, 363 children of 

The Billick et al.38 data show higher geometric 

mean blood lead values for blacks than for 

Hispanics or for whites. Table 12-13 presents these 

geometric means for the three racial/ethnic groups 

for 7 years. The consistency of the association is 

remarkable. 

Numerous data have been published showing the 

effect of various occupations on blood lead 

levels.16254046 In general, these data support the 

conclusion that workers exposed to automobile exhaust, lead fumes, or dust in manufacturing carry 

higher lead burdens than those who do not. 

12-9 
P.19 

TABLE 12-13. GEOMETRIC MEAN BLOOD LEAD LEVELS 

(Mg/dl) IN NEW YORK LEAD SCREENING PROGRAM, 

1970-1976, FOR CHILDREN UP TO 72 MONTHS OF AGE, BY 

RACE AND YEAR" 

Year 

1970 

1971 

1972 

1973 

1974 

1975 

1976 

Black 

28.6 

28.5 

25.0 

25.0 

23.9 

22.0 

20.0 

Hispanic 

24.0 

23.4 

21.3 

21.9 

21.6 

19.8 

18.7 

While 

23.8 

22.4 

20.4 

21.3 

20.8 

19.0 

18.6 

12.3 RELATIONSHIPS BETWEEN EXTERNAL EXPOSURES AND BLOOD LEAD 

LEVELS 

In previous chapters, it has been shown that lead: 

1. Is emitted from various sources, primarily 

automobiles and industrial operations. 

2. Is distributed across the environment. 

3. Is capable of being absorbed into the human 

body. 

This section will describe the relationships observed 

between the different environmental exposures and 

the resulting absorption as measured by blood lead 

levels. 

Lead that is emitted from mobile sources, e.g. automobile exhausts, and from stationary sources, e.g. 

industrial operations, either remains in the air or 

falls out, as discussed in Chapter 6. Studies have 

shown a buildup of lead in soil and dust as a result of 

emissions from these two sources. Further, the lead 

in soil and dust does not derive only from these 

sources but, in addition, from the deterioration and 

erosion of lead based paint. Therefore, although soil 

and dust are direct sources of human exposure to 

lead, they must also be viewed in terms of the primary mobile and stationary sources of the lead. 

Consequently, studies that examine only ambient air 

lead exposures may, in fact, underestimate the total 

contribution of airborne lead to the population's 

lead burden. 

Efforts to estimate experimentally the relative importance of combustion of leaded gasoline to total 

lead burden in humans have only recently been initiated. Manton has presented evidence from a 

preliminary study using lead isotope ratios.47 His 

findings suggest that automobiles supplied between 7 

± 3 and 41 ± 3 percent of the lead in blood of 

Dallas residents during 1972 to 1973. Garibaldi et 

al.,48 in a major study being conducted in Italy, are 

attempting such allocations on a much larger scale. 

It is hoped that these data will be available shortly. 

Because multiple sources of lead do exist and 

because each can contribute to the total lead burden 

of man, an important question to be addressed is the 

contribution of each source to the total body burden. 

In this section, individual studies examining the contribution from the major environmental sources of 

lead, that is, air, soil-dust, paint, food, and water, 

will be discussed. 

12.3.1 Air Exposures 

Studies of the relationship of air exposures to 

blood lead levels may be separated into two main 

categories: epidemiological and clinical. 

Epidemiological studies in turn may be grouped 

into three types: those pertaining to populations exposed to mobile sources of emission, those of 

populations exposed to stationary sources, and those 

in which only the amount of airborne lead is taken 

into account with no effort made to identify the 

source. 

Studies dealing with mobile sources of lead will be 

discussed first, followed by a presentation of stationary sources studies. Studies concerned with air lead 

levels regardless of sources will then follow, and 

clinical studies will complete the presentation. From 

this array, the studies that permit the calculation of 

the quantitative relationship between lead in air and 

lead in blood will be selectively analyzed and discussed. 

Clinical studies have the advantage of permitting 

precise control over the levels of exposure but have 

the disadvantages of studying people under somewhat artifical conditions and of dealing, by 

necessity, with very few subjects. All clinical studies 

to be presented were limited to adults. 

Epidemiological studies have the advantage of 

studying people in their natural state, but frequently 

have the disadvantage of rather imprecise estimates 

of the exposures encountered. These studies allow 

estimates of the relationship to be made for both 

adults and children. 

12.3.1.1 MOBILE SOURCE STUDIES 

12.3.1.1.1 Studies in the United States. A 1973 

Houston study examined the blood lead levels of 

parking garage attendants, traffic policemen, and 

adult females living near freeways.6 A control group 

for each of the three exposed populations was 

selected by matching for age, education, and race. 

Unfortunately, the matching was not altogether successful; traffic policemen had less education than 

their controls and the garage employees were 

younger than their controls. Females were matched 

12-10 
P.20 

adequately, however. The findings for the six groups 

studied are presented in Table 12-14. It should be 

noted that the mean blood lead values for traffic 

policemen and parking garage attendants, two 

groups regularly exposed to higher concentrations of 

automotive exhausts, were significantly higher than 

the means for their relevant control groups. 

Statistically significant differences in mean values 

were not found, however, between women living 

near a freeway and control women living at greater 

distances from the freeway. 

TABLE 12-14. MEAN BLOOD LEAD LEVELS FOR STUDY AND 

CONTROL GROUPS, HOUSTON^ 

Group 

Policemen 

Controls 

Garage attendants 

Controls 

Women living 

near freeway 

Controls 

Mean. 

jjg'd l 

23.1 

18.4 

28.3 

21.3 

12.9 

11.9 

SD 

9.21 

7.38 

10.33 

9.70 

4.47 

4.28 

Sample 

size 

141 

150 

119 

95 

120 

117 

P = 0.05 

P= 0.05 

P > 0.05 

A California study7-

49

 examined blood lead levels 

in relation to exposure from automotive lead in two 

communities, Los Angeles and Lancaster (a city 

representative of the high desert). Los Angeles residents studied were individuals living in the vicinity 

of heavily traveled freeways within the city. They included males and females, aged 1 through 16, 17 

through 34, and 35 and over. The persons selected 

from Lancaster represented similar age and sex distributions. On two consecutive days, blood, urine, 

and feces samples were collected. Air samples were 

collected from one Hi-Vol sampler in Los Angeles, 

located near a freeway, and two such samplers in 

Lancaster. The Los Angeles sampler collected for 7 

days; the 2 in Lancaster were utilized for 14 days. 

On the first day of air sampling, soil samples were 

collected in each area in the vicinity of study subjects. 

Lead in ambient air along the Los Angeles freeway averaged 6.3 ± 0.71 /xg/m3

, and in the Lancaster area the average was 0.6 ± 0.21 /ig/m3

. The 

mean soil lead in Los Angeles was 3633 figlg, 

whereas that found in Lancaster was 66.9 figlg. 

Higher concentrations of lead were found in the 

blood of children, as well as younger and older 

adults living near the freeway, than in individuals 

living in the control area. Table 12-15 shows the 

mean blood lead values for the six groups. 

Differences between Los Angeles and Lancaster 

groups were significant with the sole exception of the 

older males. 

TABLE 12-15. ARITHMETIC AND GEOMETRIC MEAN BLOOD LEAD LEVELS (Mg/dl) 

FOR LOS ANGELES AND LANCASTER, CA, BY SEX AND AGE7 

Groups by sex 

and age. years 

Total 

Males 

1-16 

17-34 

35-

Females 

1-16 

17-34 

35-

N 

126 

56 

20 

29 

7 

70 

18 

41 

11 

Los Angeles 

Mean 

16.4 

19.3 

23.5 

16.6 

18.5 

14.2 

16.7 

12.9 

14.7 

SEa 

0.7 

1.1 

2.5 

1.1 

2.0 

0.7 

1.8 

0.6 

1.5 

Geometric 

mean 

14.6 

17.2 

20.8 

15.1 

17.1 

12.8 

14.9 

11.8 

13.4 

N 

119 

50 

21 

18 

11 

69 

25 

16 

28 

Lancaster 

Mean 

10.5 

11.8 

11.1 

11.8 

13.0 

9.6 

10.2 

9.1 

9.3 

SE 

0.4 

0.6 

0.8 

0.9 

2.0 

0.4 

0.7 

1.2 

0.5 

Geometric 

mean 

9.6 

10.8 

10.4 

10.9 

11.1 

8.8 

9.6 

8.0 

8.7 

Significance 

of difference 

P b 

«.00 1 

«.00 1 

«00 1 

.003 

.09 

«00 1 

•C001 

<001 

<001 

a

 Standard error. 

b

 I test. 

It has been pointed out by Snee that, in the hightraffic-density area, the reported 29 percent of samples in children 1 through 16 years old exceeding 40 

figldl represented 5 individuals.50 For 3 of these a 

second blood sample showed approximately 20 

figldl; a second sample was not collected from the 

other 2. The disparity between blood samples taken 

on consecutive days from children in the study calls 

into question the validity of using these values to 

quantify the air lead to blood lead relationship. The 

differences between samples for adults, although 

somewhat larger than those found in other studies, 

appear acceptable for use in calculations, however. 

A study of the effects of lower-level urban traffic 

densities on blood lead levels was undertaken in 

Dallas, Tex., in 1976.34 The study consisted of two 

phases. One phase measured air-lead values for 

selected traffic densities and conditions, ranging 

12-11 
P.21 

from ^.1,000 to about 37,000 cars/day. The second 

phase consisted of an epidemiological study of 

traffic density and blood lead levels among residents. Figure 12-4 shows the relationship between 

arithmetic means of air lead and traffic density. As 

can be seen from the graph, a reasonable fit is shown. 

TABLE 12-17. SOIL LEAD LEVELS BY TRAFFIC DENSITY" 

-

-

o 

•r-" 

D 

I 

O 

I 

o 

I 

o 

1 

O 

! "1 

0 

o o^^^ ^ 

O 

O 

" " 

1 1 T 1 

0 

Y =• 0.6598 + 0.0263 X 

X = cars/day 

1 1 1 1 

-

-

_] 0 4,000 8.000 12.000 16.000 20.000 24.000 28.000 32.000 36,000 38.000 

TRAFFIC VOLUME, cars/day 

Figure 12-4. Arithmetic mean of air lead levels by traffic 

count, Dallas, 1976.3" 

In addition, during this phase, data for indooroutdoor comparisons of air lead levels were collected. In two areas, with traffic densities of 10,000 

and 20,000 cars/day, high volume samplers 

measured air lead outside of selected houses. At the 

same time, indoor air lead values for these houses 

were also collected. Table 12-16 shows the findings. 

Approximately a tenfold difference was found between indoor-outdoor values in both locations. It 

has been postulated that at least part of this 

difference is the result of using air conditioners. 

TABLE 12-16. MEAN AIR LEAD LEVELS (fj.g/m3) INDOORS 

AND OUTDOORS AT TWO TRAFFIC DENSITIES, DALLAS, 

TEX. 1976*" 

10.000 cars'day 20.000 cars day 

Outdoor Indoor Outdoor 

Mean 

N 

0.182 

9 

0.918 

9 

0.199 

5 

2.105 

5 

In addition, for all distances measured (5 to 100 ft 

from the road), air lead concentrations declined 

rapidly with distance from the street. At 50 ft concentrations were about 55 percent of the street concentration; at 100 ft concentrations were less than 40 

percent of the street concentrations. In air lead collections from 5 to 100 ft from the street, approximately 50 percent of the airborne lead was in the 

respirable range ( < 1 fim) and the proportions in 

each size class remained approximately the same as 

the distance from the street increased. 

Soil lead concentrations were higher in areas with 

greater traffic density (Table 12-17). The maximum 

soil level obtained was 730 figlg. 

Traffic density, 

vehicles/day 

Soil lead levels. 

II gig 

<1.000 

1,000-13,499 

13.500-19,499 

>19,500 

73.6 

92.2 

110.9 

105.9 

Dustfall samples for 28 days from 9 locations 

showed no relationship to traffic densities, but outdoor levels were at least 10 times the indoor concentration in nearby residences. 

In the second phase, three groups of subjects, 1 to 

6 years old, 18 to 49 years old, and 50 years and 

older, were selected in each of 4 study areas. Traffic 

densities selected were: < 1,000, 8,000 to 14,000, 

14,000 to 20,000, and 20,000 to 25,000 cars/day. 

The study groups averaged about 35 subjects, 

although the number varied from 21 to 50. The 

smallest groups were from the highest traffic density 

area. No relationship between traffic density and 

blood lead levels in any age groups was found 

(Figure 12-5). Blood lead levels were significantly 

higher in children, 12 to 18 figldl, than in adults, 9 

to 14 figldl. 

-

-

~ 

1 1 1 1 

A. 

f ' \ FEMALES < 9 

* / \ \ MALES < 9 

** -VfC—'" MALES >49 

°~~ ^ j ^ _Q _ FEMALES19-49 

ef " .Q_ 5 

FEMALES >4 9 

1 1 1 1 

< 1,000 1,000-13.500 13,500-

19,500 

19,500-

38.000 

TRAFFIC DENSITY, cars/day 

Figure 12-5. Blood lead concentration and traffic density by 

sex and age, Dallas, 1976.34 

Galke et al.43 studied blood lead levels in 187 

South Carolina children l to 5 years old in relation 

to lead in soil and to automobile traffic. The 

arithmetic mean blood lead level was related to both 

factors, as shown in Table 12-18. 

12-12 
P.22 

TABLE 12-18. BLOOD LEAD CONCENTRATIONS IN 

RELATION TO SOIL LEAD CONCENTRATIONS AND TRAFFIC 

DENSITY** 

(MQ/dl) 

Soil lead 

concentrations. 

uglg 

<585 

>585 

Total 

Low mean 

(951-1677 

cars/day) 

32 (7)a 

36(10) 

34(9) 

Automobile traffic density 

High mean 

(2446-9637 

cars/day) 

41(8) 

43(11) 

42(10) 

All densities 

35(8) 

41(11) 

38(10) 

a

 Standard deviation of a single observation. 

Caprio et al.51 compared blood lead levels and 

proximity to major traffic arteries in a study, reported in 1971, that included 5226 children in 

Newark, New Jersey. Over 57 percent of the 

children living within 100 ft of roadways had blood 

lead levels greater than 40 figldl. For those living 

between 100 and 200 ft from the roadways, more 

than 27 percent had such levels; and at distances 

greater than 200 ft, 31 percent exceeded 40 figldl. 

Table 12-19 indicates that the effect of automobile 

traffic was seen only in the group that lived within 

100 ft of the road. 

TABLE 12-19. BLOOD LEAD LEVELS IN CHILDREN AGED 1 

TO 5 IN NEWARK, NJ, IN RELATION TO DISTANCE OF 

RESIDENCE FROM A MAJOR ROADWAY, 1971" 

(M9/dl) 

Distance of residence 

from roadway, ft 

<100 

100-200 

>200 

number 

Percent blood lead levels 

<40 

42.6 

72.4 

68.4 

3401 

40-59 

49.3 

24.2 

26.9 

1562 

>60 

8.1 

3.4 

4.7 

263 

Number 

758 

507 

3961 

5226 

No other sources of lead were considered in this 

study. Data from other studies on mobile sources indicate, however, that it is unlikely that the blood 

lead levels observed in this study resulted entirely 

from automotive exhaust emissions. 

Daines et al. studied black women living near a 

heavily traveled highway in New Jersey.52 The subjects lived in houses on streets paralleling the highway at 3 distances, 3.7, 38.1, and 121.9 m. Air lead 

as well as levels for blood lead were measured. 

Mean annual air lead concentrations were 4.60, 

2.41, and 2.24 /ttg/m3, respectively, for the 3 distances. The mean air lead concentration for the area 

closest to the highway was significantly different 

from that in both the second and third, but the mean 

air lead concentration of the third area was not significantly different from that of the second. The 

results of the blood lead determinations paralleled 

those of the air lead. Mean blood lead levels of the 3 

groups of women, in order of increasing distance, 

were 23.1, 17.4, and 17.6 fig/100 g, respectively. 

Again, the first group showed a significantly higher 

mean that the other two, but the second and third 

groups' blood lead levels were similar to each other. 

Daines et al.,52 in the same publication, reported a 

second study in which the distances from the highway were 33.5 and 457 meters and where the subjects were white upper middle class women. 

Although the air lead levels were trivially different 

at these two distances, the blood lead levels did not 

differ. Because the residents nearest the road were 

already 33 m (+ 100 ft) from it and because other 

studies had shown an exponential decline in air lead 

levels with increasing distance from the road, reaching background air lead levels at 250 ft, the explanation may lie in the fact the air lead levels, although 

statistically different, were insufficient to be 

reflected in the blood lead levels. It is not possible to 

substantiate this possibility because the observed air 

lead values for the two distances were not reported. 

In 1964, Thomas et al.53 investigated blood lead 

levels in 50 adults who had lived for at least 3 years 

within 250 ft of a freeway (Los Angeles) and those of 

50 others who had lived for a like period near the 

ocean or at least 1 mile from a freeway. Mean blood 

lead levels for those near the freeway were 22.7 ± 

5.6 for men and 16.7 ± 7.0 figldl for women. These 

concentrations were higher than for control subjects 

living near the ocean: 16.0 ± 8.4 figldl for men and 

9.9 ± 4.9 figldl for women. The higher values, 

however, were similar to those of other Los Angeles 

populations. Measured mean air concentrations of 

lead in Los Angeles for October 1964 were 12.25 ± 

2.70 jag/m3 at a location 30 ft from the San Bernardino freeway; 13.25 ± 1.90 /u.g/m3

 at another location 40 ft from the same freeway; 6.40 ±2.1 5 /Lig/m3 

at a fourth floor location 300 ft from the freeway; 

and 4.60 ± 1.92 /u.g/m3 1 mile from the nearest freeway. The investigators concluded that the 

differences observed were consistent with coastal-inland atmospheric and blood lead gradients in the 

Los Angeles basin and that the effect of residential 

proximity to a freeway (25 to 250 ft) was not demonstrated. 

12.3.1.1.2 British studies. In a Birmingham, England, study, mean blood lead levels in 41 males and 

58 females living within 800 m of a highway interchange were 14.41 and 10.93 figldl, respectively, 

just prior to the opening of the interchange in May 

1972.54 prom October 1972 to February 1973 the 

respective values for the same individuals were 

18.95 and 14.93 fig/dl. In October 1973 they were 

12-13 
P.23 

23.73 and 19.21 figldl. The investigators noted 

difficulties in the blood collection method during 

the baseline period and changed from capillary to 

venous blood collection for the remaining two samples. To interpret the significance of the change in 

blood collection method, some individuals gave 

both capillary and venous blood at the second collection. The means for both capillary and venous 

bloods were calculated for the 18 males and 23 

females who gave both types of blood.55 The venous 

blood mean values for both these males and females 

were lower, 0.8 and 0.7 figldl, respectively. If these 

differences in means were applied to the means of 

the third series, the means for males would be 

reduced to 24.8 ,ug/dl and that for the females to 

18.7 figldl. These adjusted means still show an increase over the means obtained for the first series. 

On the other hand, discarding the means calculated 

for the first series and comparing only the means for 

venous bloods, namely series two and three, again 

shows an increase for both groups. The increase in 

blood lead values was larger than expected following the model of Knelson et al.56

 because air lead 

values near the road were approximately 1 ,u.g/m3. 

The investigators concluded that either the lead 

aerosol of very small particles behaved more like a 

gas so that considerably more than 37 percent of inhaled material was absorbed or that ingestion of 

lead-contaminated dust might be responsible. 

Studies of taxicab drivers have employed different 

variables to represent the drivers' lead exposure,5758 

one being night- versus day-shift drivers;51 the other, 

mileage driven.58 In neither case was any difference 

observed. 

The studies reviewed show that automobiles produce sufficient emissions to increase air and nearby 

soil concentrations of lead as well as increase blood 

lead concentrations in children and adults. The 

problem is of greater importance when houses are 

located within 100 ft (30 m) of the roadway. 

12.3.1.2 STATIONARY SOURCE STUDIES 

12.3.1.2.1 Primary smelters. Most studies of nonindustry-employed populations living in the vicinity of 

industrial sources of lead pollution were triggered 

because evidence of severe health impairment had 

been found. Subsequently, extremely high exposures 

and high blood lead concentrations were found. The 

following studies document the health problems that 

can develop as well as some of the relationships between environmental exposure and human response. 

12.3.1.2.1.1 El Paso, Texas. In 1972, the Center for 

Disease Control, formerly the Communicable Disease Center, studied the relationships between blood 

lead levels and environmental factors in the vicinity 

of a primary smelter emitting lead, copper, and zinc 

located in El Paso, Texas, that had been in operation 

since the late 1800's.33-

59

 Estimated lead emissions 

from this smelter were 297 metric tons in 1969, 519 

metric tons in 1970, and 317 metric tons in 1971,33 

These figures, however, include only stack emissions; the quantities in fugitive emissions via ventilation, windows, etc., are unknown. Daily highvolume samples collected on 86 days between 

February and June 1972 averaged 6.6 /ig/m3 of lead. 

Concentrations ranged from 0.49 to 75 /ig/m3. 

These air lead levels fell off rapidly with distance, 

reaching, as would be expected, background values 

approximately 5 km from the smelter. Levels were 

higher downwind, however. High concentrations of 

lead in soil and housedust were found, with the highest levels occurring near the smelter. The geometric 

means of 82 soil and 106 dust samples from the sector closest to the smelter were 1791 and 4022 figlg, 

respectively. Geometric means of both soil and dust 

lead levels near the smelter were significantly higher 

than those in study sectors 2 or 3 km farther away. 

Sixty-nine percent of children 1 to 4 years old living near the smelter had blood lead levels > 40 

/xg/dl, and 14 percent had blood lead levels that 

exceeded 60 figldl. Concentrations in older individuals were lower; nevertheless, 45 percent of the 

children 5 to 9 years old, 31 percent of the individuals 10 to 19 years old, and 16 percent of the 

individuals above 19 had blood lead levels all exceeding 40 figldl. The data presented preclude 

calculations of means and standard deviations. 

Data for people aged 1 to 19 years living near the 

smelter showed a relationship between blood lead 

levels and concentrations of lead in soil and dust. 

For individuals with blood lead levels >4 0 figldl, 

the geometric mean concentration of lead in soil at 

their homes was 2587 figlg, whereas for those with a 

blood lead concentration <40 figldl, home soils had 

a geometric mean of 1419 figlg. For housedust, the 

respective geometric means were 6447 and 2067 

Mg/gAnalysis found the effect of length of residence to 

be important only in the sector nearest the smelter. 

Forty-three percent of the 1- to 19-year-olds who 

had lived there 2 or more years had blood lead 

values 240 figldl, whereas only 18 percent of the 1-

to 19-year-olds who had lived there less than 2 years 

had similar levels. 

Additional sources of lead were also investigated. 

A relationship was found between blood lead con12-14 
centrations and lead release from pottery, but the 

number of individuals involved was very small. No 

relationships were found between blood lead levels 

and hours spent out of doors each day, school attendance, or employment of a parent at the smelter. The 

reported prevalence of pica also was minimal. 

It was concluded that the primary factor associated with elevated blood lead levels in the children 

was ingestion or inhalation of dust containing lead. 

Data on dietary intake of lead were not obtained 

because the climate and proximity to the smelter 

prevented any farming in the area. It was unlikely 

that the dietary lead intakes of the children from 

near the smelter and farther away were significantly 

different. 

12.3.1.2.1.2 Kellogg, Idaho. In 1970, EPA carried 

out a study of a lead smelter in Kellogg, Idaho.60-

61 

The study was part of a national effort to determine 

the effects of sulfur dioxide, total suspended particulate, and suspended sulfates, singly and in combination with other pollutants, on human health. It 

focused on mixtures of the sulfur compounds and 

metals. Although it was demonstrated that children 

had evidence of lead absorption, insufficient environmental data were reported to allow further 

quantitative analyses. 

In 1974, following the hospitalization of two 

children with suspected acute lead poisoning, CDC 

joined the State of Idaho in a comprehensive study of 

children in the area.'

 62

 The studies conducted in this 

area unfortunately used a bewildering array of 

designations in their reports, but all are related to 

the same industrial complex. 

The source of exposure was a*smelter whose 

records showed that emissions of lead into the atmosphere averaged 8.3 metric tons per month from 

1955 to 1964, 11.7 metric tons from 1965 to September 1973, and 35.3 metric tons from October 

1973 to September 1974.62 In September 1973, a fire 

destroyed the main filtration facility for the smelter. 

The study was initiated in September 1974, after two 

children were hospitalized with symptoms of lead 

poisoning. At that time, blood lead levels 240 figldl 

were found in 385 (41.9 percent) of 919 children less 

than 10 years old who were examined. About 99 percent of the 172 children living within 1.6 km of the 

smelter had blood lead values 240 figldl. The mean 

blood concentration declined with distance from the 

point of emission (Table 12-20). Blood lead levels 

were consistently higher in children 1 to 4 years old 

than in those 5 to 9 years old. In addition, higher 

levels in children were associated with reported active ingestion of lead-containing material (pica), 

with lower socioeconomic status, and with parental 

employment at the smelter or at a lead mine. A significant negative relationship between blood lead 

TABLE 12-20. GEOMETRIC MEAN BLOOD LEAD LEVELS BY AREA COMPARED WITH ESTIMATED AIR LEAD LEVELS FOR 1- TO 

9-YEAR-OLD CHILDREN LIVING NEAR IDAHO SMELTER (Geometric standard deviations, sample sizes, and distances from 

smelter are also given)" 

GM 

blood lead. 

ug/dl 

65.9 

47.7 

33.8 

32.2 

27.5 

21.2 

GSD 

1.30 

1.32 

1.25 

1.29 

1.30 

1.29 

Sample 

size 

170 

192 

174 

156 

188 

90 

Estimated 

air lead. 

/xg/mJ 

18.0 

14.0 

6.7 

3.1 

1.5 

1.2 

Distance from 

smelter. 

km 

0- 1.6 

•1.6- 4.0 

4.0-10.0 

10.0-24.0 

24.0-32.0 

about 75 

a

 EPA analysis of data from Yankel et al.1 

level and hematocrit value was found. Seven of 41 

children (17 percent) with blood lead levels 280 

figldl were diagnosed by the investigators as being 

anemic on the basis of hematocrit less than 33 percent, whereas only 16 of 1006 children (1.6 percent) 

with blood lead levels < 80 figldl were so diagnosed. 

Although no overt neurologic disease was observed in children with higher lead intake, 

differences were found in nerve conduction velocity. 

Details of this finding were discussed in a previous 

chapter. 

Beginning in 1971, ambient concentrations of lead 

in the vicinity of the smelter were determined from 

particulate matter collected in high-volume air 

samplers. Data indicated that monthly average 

levels measured in 1974 (Figure 12-6) were three to 

four times the levels measured in 1971.63 Individual 

exposures to lead were estimated by interpolation 

from these high-volume data, and a strong correlation was found between the estimates and the 

measured blood lead levels (r + 0.72). 

12-15 
P.25 

Figure 12-6. Monthly ambient air lead concentrations in 

Kellogg, Idaho, 1971 through 1975.63 

Subsequently, Yankel et al. published additional 

information concerning the 1974 study as well as the 

results of a follow-up study conducted in 1975.' The 

follow-up was undertaken to determine the effectiveness of control measures initiated after the 1974 

study. 

Between August 1974 and August 1975, the mean 

annual air lead levels decreased at all stations 

monitored (Figure 12-7). In order of increasing distance from the smelter, the concentrations in the two 

years were 18.0 to 10.3 /Ag/m3, 14.0 to 8.5 /ng/m3, 

6.7 to 4.9 jug/m3, and, finally, 3.1 to 2.5/ig/m3 at 10 

to 24 km. Similar reductions were noted in the 

housedust lead concentrations. 

In a separate report, von Lindern and Yankel described reductions in blood lead levels of children 

for whom determinations were made in both years.60 

It was pointed out that the children with the highest 

blood lead levels in 1974 had been relocated; their 

removal and subsequent relocation would complicate any analysis in which they were included. To 

compensate for this, the authors also presented separately the blood lead levels for those children living 

in the same home both years. This greatly reduced 

the number of observations reported. The results 

(Table 12-21) demonstrate that significant reductions in blood lead concentration can be effected, 

and that they were observed in each study area. In 

areas III, IV, and V, all mean blood lead levels were 

<40 figldl. 

The report of Yankel et al.1 showed that there 

I 1 AUG. 1974 

rrrr\ AUG. 1975 

CONTROL 

D_D_n 3 4 5 

BY AREA (SEE TEXT! 

Figure 12-7. Annual ambient air lead concentration, by area, 

before the August 1974 and August 1975 surveys.1 

were reductions in environmental lead contamination between 1974 and 1975, and that the correlations between blood lead levels and environmental 

or demographic factors were consistent from one 

year to the next. Five factors influenced, in a 

statistically significant manner, the probability of a 

child developing an excessive blood lead level: 

1. Concentrations of lead in ambient air 

(Mg/m3). 

2. Concentration of lead in soil (ppm). 

3. Age (years). 

4. Cleanliness of the home (subjective evaluation coded 0, 1, and 2, with 2 signifying 

dirtiest). 

5. General classification of the parents' occupation (dimensionless). 

Although the strongest correlation found was between blood lead level and air lead level, the 

authors concluded that it was unlikely that inhalation of contaminated air alone could explain the elevated blood lead levels observed. 

Yankel and von Lindern reasoned that even 

though air lead was the principal source, a major 

route of exposure was the ingestion of lead in soil 

and dust.1 They proposed that to protect the health 

12-16 
P.26 

TABLE 12-21. MEAN BLOOD LEAD LEVELS IN CHILDREN LIVING IN VICINITY OF A PRIMARY LEAD SMELTER, 1974 and 1975 

Group N H N 

II 

X 

Study area and data set 

III 

N •)( N 

IV 

X N 

V 

X 

Blood levels 

>80,ug/d|a 

in 1974 test 

Retested in 

1975 

Difference 

Blood levels 

>60 but <80 

/ug/dl in 1974 

test 

Retested in 

1975 

Difference 

Blood levels 

<60n.g/dl 

in 1974 test 

Retested in 

1975 

Difference 

90.2 

52.3 

-38.0 

64.5 — 

47.4 8 

-17.2 — 

52.3 — 

80.0 

61.0 

-19.0 

69.6 

50.3 

-19.3 

47.0 45.6 

37.4 23 36.0 20 39.8 

-14.9 — -11.0 — - 5.8 

14 

43.7 

37.4 

- 6.3 

61.0 

51.0 

-10.0 

43.4 

33.5 

- 9.9 

a

 Adapted from von Lindern and Yankel.63 

of the children in this area the regulation of environmental standards must take into account all of these 

routes of exposure. 

These investigators developed a mathematical 

model based on the 1974 data that included each of 

the five factors that had been shown to be correlated 

with increased blood lead levels. The model, shown 

below, can be used to estimate the effect of variations in the environmental factors on mean blood 

lead levels in children: 

1 n (Pb-B) =3.1 + 0.041 (Air) + 2.1 x 105 (Soil) + 

0.087 (Dust) + 0.018 (Age) + 0.024 (Occupation). 

(See above for definition of units). (12-6) 

12.3.1.2.1.3 CDC-EPA study. Baker et al.,31 in 

1975, surveyed 1774 children 1 to 5 years old, most 

of whom lived within 4 miles of 19 lead, copper, or 

zinc smelters located in various parts of the United 

States. Blood lead levels were modestly elevated 

near two of the 11 copper and two of the five zinc 

smelters. Although blood lead levels in children 

were not elevated in the vicinity of three lead 

smelters, their FEP levels were somewhat higher 

than those found in controls. Increased levels of lead 

and cadmium in hair samples were found near lead 

and zinc smelters; this was considered evidence of 

external exposure. No environmental determinations were made for this study. 

12.3.1.2.1.4 Meza Valley, Yugoslavia. A Yugoslavian study in the Meza Valley investigated exposures to lead from a mine and a smelter over a 

period of years.6469 The mine and smelter are located near a river flowing in the valley. The smelter 

produces about 23,000 metric tons annually. After 

control equipment was installed on 1 of 2 lead-emitting stacks, emissions were calculated to be 203.2 

metric tons/year. In 1967, 24-hr lead concentrations 

measured from 4 different days varied from 13 to 84 

/*g/m3 in the village nearest the smelter, and concentrations of up to 60 /ig/m3

 were found as far as 5 

km from the source. Mean particle size in 1968 was 

<0.8 /im. The lead levels were about 25,000 ppm in 

the most contaminated area. Analysis of some common foodstuffs showed concentrations that were 10 

to 100 times higher than corresponding foodstuff 

from the least exposed area (Mezica).64 

After January 1969 when partial control of emissions was established at the smelter, weighted 

average weekly exposure was calculated to be 27 

figlm* in the village near the smelter. In contrast to 

this, the city of Zagreb,65 which has no large station12-17 
P.27 

ary source of lead, had an average weekly air lead 

level of 1.1 figlm*. 

In 1968, the average concentration of ALA in 

urine samples from 912 inhabitants of six villages 

varied by village from 9.8 to 13 mg/liter. A control 

group had a mean ALA of 5.2 mg/liter. Data on lead 

in blood and the age and sex distribution of the 

villagers were not given.64 

Of the 912 examined, 559 had an ALA level > 10 

mg/liter of urine. In 1969, a more extensive study of 

286 individuals with ALA >10 mg/liter was undertaken.66

 ALA-U decreased significantly from the 

previous year. When the published data were examined closely, there appeared to be some discrepancies in interpretation. The exposure from dust 

and from food might have been affected by the control devices, but no data were collected to establish 

this. In one village, Zerjau, ALA-U dropped from 

21.7 to 9.4 mg/liter in children 2 to 7 years of age. 

Corresponding ALA-U values for 8- to 15-year-olds 

and for adult men and women were reduced from 

18.7 to 12.1, from 23.9 to 9.9, and from 18.5 to 9.0 

mg/liter, respectively. Because lead concentrations 

in air65 even after 1969 indicated an average exposure of 25 ^g/m3

, it is possible that some other explanation should be sought. The author indicated in 

the report that the decrease in ALA-U showed "the 

dependence on meteorologic, topographic, and technologic factors."66

 Lead in blood was determined, 

but according to the report "determination of lead in 

blood could not be used for exposure evaluation 

because all obtained values were in the normal 

limits" (under 80 figldl blood as defined by the 

author).fif> In light of current knowledge, this definition of normal levels is excessively high. 

The excretion of nonchelated lead in urine in 8.5 

percent of 209 individuals was above 0.1 mg/liter. 

The highest value recorded was 0.19 mg/liter. When 

treated with Ca EDTA, the mobilized lead in the 

urine of these individuals ranged from 0.5 to 4.2 

mg/liter, indicating the presence of total body burdens ranging from normal to ten times normal.6668 

Another finding of this project was a significant 

increase in reticulocytes, especially in children.66 

Forty-seven percent of exposed adults complained 

of pain in their bones compared with only 3 percent 

of the controls. 

Fugas et al.69 in a later report estimated the timeweighted average exposure of several populations 

studied during the course of this project. Stationary 

samplers as well as personal monitors were used to 

estimate the exposure to airborne lead for various 

parts of the day. These values were then coupled 

with estimated proportions of time at which these exposures held. In Table 12-22, the estimated timeweighted blood lead values as well as the observed 

mean blood lead levels for these studied populations 

are presented. An increase in blood lead values occurs with increasing air lead exposure. 

TABLE 12-22. MEAN BLOOD LEAD LEVELS IN SELECTED 

YUGOSLAVIAN POPULATIONS, BY ESTIMATED WEEKLY 

TIME-WEIGHTED AIR LEAD EXPOSURE69 

Population 

Rural I 

Rural II 

Rural III 

Postmen 

Customs officers 

Street car drivers 

Traffic policemen 

N 

49 

47 

45 

44 

75 

43 

27 

Timeweighted 

air lead 

Mg/m3 

0.079 

0.094 

0.146 

1.6 

1.8 

2.1 

3.0 

Mean blood 

lead level, 

jjg/dl 

7.9 

11.4 

10.5 

18.3 

10.4 

24.3 

12.2 

SD 

4.4 

4.8 

4.0 

9.3 

3.3 

10.5 

5.1 

12.3.1.2.1.5 East Helena, Montana. EPA in 1972 

investigated a lead-emitting smelter complex in East 

Helena, Montana.60 The quantities of lead emissions 

were not known. Air lead concentration, measured 

in 1969, yielded averages from several stations that 

varied from 0.4 to 4 /xg/m3; the maximum 24-hr 

value was found to be 15 figlm*. In the city of 

Helena, the average concentration was 0.1 jig/m3. 

Lead in soil was found to be 4000, 600, and 100 

figlg at distances of 1.6, 3.2, and 6.4 km (1, 2, and 4 

miles), respectively, from the smelting complex. Uncontaminated soil near the Helena Valley showed a 

mean of 16 figlg. Deposited lead (dustfall) was 

found to vary from 3 to 108 mg/m2-month in East 

Helena and from 1 to 7 mg/m^-month in Helena. 

Studies on humans by Hammer et al.61 were 

limited to children; lead values in hair and blood 

were found to be higher in East Helena than in 

Helena, the respective averages being 15.6 ± 5.1 

and 11.6 ± 4.0 figldl in blood and about 40 and 13 

ppm in hair. The hair values indicated differential 

exposure to lead. However, in the opinion of the investigators, although the blood lead values indicated 

an elevated exposure, it had not been excessive. No 

adverse health effects had been noted in these 

children. 

12.3.1.2.1.6 Other smelter studies. Other reports in 

the literature have also shown that people living 

near smelters have increased burdens of lead in their 

bodies.7072 It is clear, therefore, that emissions from 

primary lead smelters can cause elevated blood lead 

levels and other indicators of increased lead burdens 

in populations living near these stationary emission 

sources. 

12-18 
P.28 

The question of the accuracy of the reported 

analytic results in these studies is difficult to address 

because they spanned a period of time in which major strides were taken in improving analytical technology. Hence, the more recent studies are likely, 

but not necessarily, to provide more accurate information. 

Although many of the reports specified that the 

blood lead levels were done in duplicate, this unfortunately does not ensure their accuracy. This problem is discussed in more detail in Chapter 9. 

12.3.1.2.2 Other industrial sources. Exposures 

from both a primary and secondary smelter in the inner-city area of Omaha, Neb. have been reported by 

Angle et al. in a series of publications.7376 Studied 

from 1970 to 1977 were children from an urban 

school immediately adjacent to a small battery plant 

and downwind from two other lead emission 

sources, schools in a mixed commercial-residential 

area, and schools in a suburban setting. Children's 

blood lead levels were obtained by macro technique 

for 1970 and 1971, but Delves micro assay was used 

from 1972 on. The difference for the change in techniques was taken into account in the presentation of 

the data. Air lead values were obtained by Hi-Vol 

samplers, and dustfall values also were collected. 

Table 12-23 presents the authors' summary of all the 

data, showing that as air lead values decrease and 

then increase, dustfall and blood lead values follow. 

The authors used regression models, both log-linear 

and semilog, to calculate air lead/blood lead ratios 

and obtained values of 10.04 and 0.4, respectively. 

The 0.4 value is equivalent to a ratio of 10.4 at an air 

lead level of 1.0 pig/m3. 

TABLE 12-23. AIR, DUSTFALL, AND BLOOD LEAD CONCENTRATIONS IN OMAHA, NEB., STUDY, 1970-1977a'

75

-

76 

Group 

All urban children, site m: 

1970-71 

1972-73 

1974-75 

1976-77 

Children at school c. site c: 

1970-71 

1972-73 

1974-75 

1976-77 

All suburban children, site r: 

1970-71 

1972-73 

1974-75 

1976-77 

1.48 

0.43 

0.10 

0.52 

1.69 

0.63 

0.10 

0.60 

0.79 

0.29 

0.12 

M9 

± 

l+ 

± 

+ 

+ 

l+ 

+ 

+ 

l+ 

+ 

+ 

Air, 

m

3

 IN)b 

0.14(7:65) 

0.08(8;72) 

0.03(10:72) 

0.07(12:47) 

0.11(7:67) 

0.15(8:74) 

0.03(10:70) 

0.10(12:42) 

0.06(7:65) 

0.04(8:73) 

0.05(10:73) 

— 

Dustfall. 

ng m3 - mo IN)C 

— 

10.6 ± 0.3(6) 

6.0 ± 0.1(4) 

8.8 (7) 

— 

25.9 ± 2.4(5) 

14.3 + 4.1(4) 

33.9 (7) 

— 

4.6 ± 1.1(6) 

2.9 ± 0.9(4) 

— 

Blood. 

Mg'dl (N)d 

31.4 + 0.7(168) 

23.3 ± 0.3(211) 

20.4 ± 0.1(284) 

22.8 ± 0.7(38) 

34.6 ± 1.5(21) 

21.9 ± 0.6(54) 

19.2 + 0.9(17) 

22.8 ± 0.7(38) 

— 

19.6 ± 0.5(81) 

14.4 ± 0.6(31) 

18.2 ± 0.3(185) 

rPb-B» Pb-A= -0.95 (N = 10) 

Pb-B = 10.04 Pb-A + 17.06 

r

lnPb-B» Pb-A= 0.91 (N = 10) 

1n Pb-B = 0.4 Pb-A I 2.86 

Blood lead 1970-71 is by the macro technique, corrected for an established laboratory bias of 3 ng dl, macro-micro; all other values are by Delves micro assay. 

N = Number of months; number of 24-hour samples. 

N = Number of months. 

N = Number ot blood samples. 

Specific reports present various aspects of the 

work done. Black children in the two elementary 

schools closest to the battery plant had higher blood 

leads (34.1 figldl) than those in elementary and 

junior high schools farther away (26.3 /xg/dl). Best 

estimates of the air exposures were 1.65 and 1.48 

Mg/m3, respectively.73 The later study compared 

three populations: urban versus suburban high 

school students, ages 14 to 18; urban black children, 

ages 10 to 12, versus suburban whites, ages 10 to 12; 

blacks, ages 10 to 12, with blood lead over 20 fig 

percent versus schoolmates with blood lead levels 

below 20 fig percent.74 The urban versus suburban 

high school children did not differ significantly, 

22.3 ± 1.2 to 20.2 ± 7.0 figldl, respectively, with 

mean values of air lead concentrations of 0.43 and 

0.29 figlm3. For the 15 students who had environmental samples taken from their homes, correlation 

12-19 
coefficients between blood lead levels and soil and 

housedust lead levels were 0.31 and 0.29 respectively. 

Suburban 10-to-12-year-olds had lower blood 

lead levels than their urban counterparts, 17.1 ± 

0.7 and 21.7 ± 0.5 figldl, respectively.74 Air lead 

exposures were higher in the urban than in the 

suburban population, although the average exposure 

remained less than 1 /xg/m3. Dustfall lead measurements, however, were very much higher: 32.96 

mg/m2-month for urban 10-to-12-year-olds versus 

3.02 mg/m2-month for suburban ones. 

Soil lead and housedust lead exposure levels were 

significantly higher for the urban black high-lead 

group than for the urban low-lead group. A significant correlation (r = 0.49) between blood lead and 

soil lead levels was found. 

In a Dallas, Texas, study of two secondary lead 

smelters, the average blood lead levels of exposed 

children was found to be 30 figldl versus an average 

of 22 figldl in control children.77 For the two study 

populations, the air and soil lead levels were 3.5 and 

1.5 /xg/m3 and 727 and 255 ppm, respectively. 

Direct automobile traffic exposure was not considered. 

In Toronto, Canada, the effects of two secondary 

lead smelters on the blood and hair lead levels of 

nearby residents have been extensively studied.7879 

In a preliminary report, Roberts et al.78 stated that 

blood and hair lead levels were higher in children 

living near the two smelters than in children living in 

an urban control area. Biologic and environmental 

lead levels were reported to decrease with increasing 

distance from the smelter stacks. 

A later and more detailed report identified a high 

rate of lead fallout around the two secondary 

smelters.79 Fallout in the vicinity of the smelters was 

caused primarily by large particulate fugitive emissions rather than stack emissions. Lead emissions 

from the two smelters were estimated to be 15,000 

and 30,000 kg/yr. Lead concentrations in soil were 

as high as 40,000 and 16,000 ppm, respectively, 

close to the 2 smelters and dropped off exponentially with distance. They reached urban background levels of 100 to 500 ppm, 200 to 300 m from 

the smelter. Horn, in a later report, pointed out that 

the extremely high soil levels were the result of some 

samples containing scrap battery plate; in his report 

he states that the soil lead levels, excluding those 

contaminated samples, approached 8000 ppm in 

nonresidential areas and exceeded 4000 ppm in 

several residential yards.80 He also pointed out 

several other deficiencies in the data.80 A general 

criticism he leveled at the study's interpretation was 

that the authors concluded that soil lead was the 

main source of lead, a putative finding in Horn's 

view, especially considering that few soil samples 

were taken. 

Lead concentrations in dustfall were much higher 

at 1 of the 2 smelters, exceeding 1500 mg/cm2-

month. These concentrations also exhibited an exponential decrease with distance similar to that observed for soils. Because the lead fallout occurred 

over a small area and consisted primarily of large 

particles (in some cases the mass median diameter 

was as large as 4.6 ± 1.3 fim), it was believed that 

the emissions originated mainly from dust-producing operations at low height rather than from stack 

emissions.78 

Lead concentrations in air ranging from 1.0 to 5.3 

/xg/m3 were only twice those found at other Toronto 

urban sites away from the smelter (0.8 to 2.4 /xg/m3). 

The range of daily concentrations was much greater. 

At 60 m from the stack, lead in 96 air samples 

ranged from 0.5 to 725 /xg/m3, whereas at 220 m 94 

samples varied from <0.5 to 14 /ng/m3. Two groups 

of children living within 300 m of each of the 

smelters had geometric mean blood levels of 27 and 

28 /xg/dl, respectively; the geometric mean for 1231 

controls was 17 figldl. Twenty-eight percent of the 

sample children tested near one smelter during the 

summer and 13 percent of the sample children tested 

near the second smelter during the winter had blood 

lead levels >40 figldl. Only 1 percent of the controls had blood lead levels >40 /xg/dl. For children, 

blood lead concentrations increased with proximity 

to both smelters but this trend did not hold for 

adults generally. 

Lead levels in hair samples averaged 41 figlg in 

the smelter areas and 13 figlg in the control area.78 

Blood lead and hair lead levels were found to be related, thus indicating a fairly constant rate of absorption. The authors concluded that for children 

with excessive lead absorption the major route of 

lead intake was ingestion of contaminated dirt and 

dust.78-

79

 Increased excretion of 8-aminolevulinic 

acid and coproporphyrins was observed in most of 

these cases, and increased density of bone 

metaphyses was observed in four children. 

Blood lead levels in 293 Finnish individuals aged 

15 to 80 were significantly correlated with distance 

of habitation from a secondary lead smelter.81 The 

geometric mean blood lead concentration for 121 

males was 18.1 figldl; that for 172 females was 14.3 

figldl. In 59 subjects who spent their entire day at 

home, a positive correlation was found between 

12-20 
m. Only one of these 59 individuals had a blood lead 

> 4 0 figldl, and none exceeded 50 /xg/dl. 

A weaker correlation was obtained between 

ALAD activity and distance from the smelter, this 

being due almost entirely to the female subjects. Examination of ALAD activity for males showed it to 

be similar regardless of distance from the smelter. 

The authors speculate that this could be caused by 

other lead exposures in the male population. 

Two reports from the USSR describe effects of 

lead in an area near a smelter.8283 Average concentrations of lead in air were as high as 4.1 /xg/m3

 at 

a distance of 1500 m; peak exposures at this distance 

reached 9.7 /ng/m3. Neurological disturbances were 

noted in 50 percent of the subjects from the smelter 

area, compared with 6 percent in controls. No data 

were given on age, sex, and type of disturbances.82 In 

a later study, children from the area were found to 

excrete more coproporphyrin than controls and also 

more lead.83 The highest lead concentration in urine 

was reported to be 50 /xg/liter. 

Studies of the effects of storage battery plants have 

been reported from France and Italy.8485 The 

French study found that children from an industrialized area containing such a plant excreted 

more ALA than those living in a different area.84 Increased urinary excretion of lead and coproporphyria was found in children living up to 300 ft 

from a battery plant in Italy.85 Neither study gave 

data on plant emissions or lead in air. 

These studies demonstrate that stationary sources 

within urban areas do contribute to increases in air 

lead levels. They show not only that mean exposure 

levels are higher but that the range of exposures encountered in their vicinities is much larger for daily 

or longer averaging times than in the vicinity of 

mobile sources. Increases of 2 to 3 /xg/m3 in air lead 

concentrations have been associated with higher 

blood lead levels in exposed populations. 

Although the significantly higher air lead concentrations decrease rapidly with distance from the 

point of emission, they contribute, together with 

mobile emissions, to the generally higher air levels 

found in urban areas and thus to the higher blood 

lead levels found in urban populations. 

12.3.1.3 URBAN POPULATION STUDIES 

Another group of studies dealing with urban 

populations examined air lead and blood lead 

values without considering the specific sources of the 

lead in the air.2'

316

-

41'12

 Azar et al.3 obtained 24-hr 

air lead exposures for 150 males over a 2- to 4-week 

period using personal samplers. Study groups consisted of 30 men in each of 5 city-occupation categories. The subjects included cabdrivers, plant 

employees, and office workers. From two to eight 

blood samples were obtained from each subject during the air monitoring phase. Blood lead determinations were done in duplicate. Table 12-24 presents the geometric means for air lead and blood 

lead for the five groups. The geometric means were 

calculated by EPA from the raw data presented in 

the authors' report.3 

TABLE 12-24. GEOMETRIC MEAN AIR AND BLOOD LEAD 

LEVELS (/xg/100 g) FOR FIVE CITY-OCCUPATION GROUPS3 

(Data calculated by EPA) 

Group 

Plant employees 

Starke, FL 

Plant employees 

Barksdale, Wl 

Cabdrivers 

Philadelphia. PA 

Office workers 

Los Angeles. CA 

Cabdrivers 

Los Angeles. CA 

Geometric 

mean 

air lead. 

ng/m3 

0.59 

0.61 

2.59 

2.97 

6.02 

GSD 

2.04 

2.39 

1.16 

1.29 

1.18 

Geometric 

mean 

blood lead. 

ug/100 g 

15.4 

12.8 

22.1 

18.4 

24.2 

GSD 

1.41 

1.43 

1.16 

1.24 

1.20 

Sample 

size 

29 

30 

30 

30 

30 

Regression equations calculated by the authors for 

members of each of the individual study groups 

revealed no slopes significantly greater than zero. In 

view of the rather narrow range of lead exposures 

observed within the groups, this result is not surprising. Examination of the slopes for each study group 

showed they were homogeneous and thus could be 

combined. The specific method of combination can 

be argued, however. Azar et al. chose to use dummy 

variables to represent the differing intercepts of the 

study groups because the intercepts were not homogeneous. In effect, this means drawing a line with a 

pooled slope of 0.153 through the average blood 

lead concentration. 

The Tepper and Levin2 study, described in detail 

previously, included both air and blood lead 

measurements. Housewives were recruited from 

"locations in the vicinity of air monitors." Women 

included were > 19 and < 80 years of age, had no 

history of lead poisoning, and had not eaten wild 

game. Table 12-25 presents the geometric mean air 

and blood lead values obtained in the study, as 

calculated by EPA from the raw data. Geometric 

mean air lead values ranged from 0.17 to 3.39 

12-21 
P.31 

/xg/m3, and geometric mean blood lead values 

ranged from 12.5 (1.31) to 20.6 (1.33) /xg/dl. 

TABLE 12-25. GEOMETRIC MEAN AIR AND BLOOD LEAD 

VALUES FOR 11 STUDY POPULATIONS2 

(Data calculated by EPA) 

Community 

Los Alamos, NM 

Okeana.OH 

Houston, TX 

Port Washington, NY 

Ardmore, PA 

Lombard, IL 

Washington, DC 

Rittenhouse, PA 

Bridgeport, IL 

Greenwich Village. NY 

Pasadena, CA 

Geometric 

mean 

air lead. 

/ig 'm3 

0.17 

0.32 

0.85 

1.13 

1.15 

1.18 

1.19 

1.67 

1.76 

2.08 

3.39 

Blood lead./jg'dl 

GM 

14.9 

15.6 

12.5 

15.4 

18.0 

13.9 

19.2 

20.6 

17.6 

16.6 

17.5 

GSD 

1.28 

1.39 

1.31 

1.28 

1.38 

1.27 

1.26 

1.33 

1.27 

1.28 

1.31 

Sample 

size 

185 

156 

186 

196 

148 

146 

219 

136 

146 

139 

194 

Nordman reported a population study from Finland16

 in which data from five urban and two rural 

areas were compared. This study was described in 

detail above. Air lead data were collected by stationary samplers. All levels were comparatively low, 

particularly in the rural environment, where a concentration of 0.025 /xg/m3

 was seen. Urban-suburban levels ranged from 0.43 to 1.32 /ig/m3

. 

A study was undertaken by Tsuchiya et al.41 in 

Tokyo using male policemen who worked, but not 

necessarily lived, in the vicinity of air samplers. In 

this study, five zones were established, based on 

degree of urbanization, ranging from central city to 

suburban. Air monitors were established at various 

police stations within each zone. Air sampling was 

conducted from September 1971 to September 1972; 

blood and urine samples were obtained from 2283 

policemen in August and September 1971. Findings 

are presented in Table 12-26. A consistent correlation between air and blood lead means for the 

five zones is shown. 

TABLE 12-26. MEAN AIR AND BLOOD LEAD VALUES FOR 

FIVE ZONES IN TOKYO STUDY41 

Air lead, 

jig'm ^ 

Blood lead. 

ng 100 g 

0.024 

0.198 

0.444 

0.831 

1.157 

17.0 

17.1 

16.8 

18.0 

19.7 

Goldsmith42 obtained data for elementary school 

(9- and 10-year-olds) and high school students in 10 

California communities. Lowest air lead exposures 

were 0.28 /xg/m3 and highest were 3.4 /xg/m3. For 

boys in elementary school, blood lead levels ranged 

from 14.3 to 23.3 /xg/dl; those for girls ranged from 

13.8 to 204 figldl for the same range of air lead exposures. The high school student population was 

made up of only males from some of the 10 towns. 

The air lead range was 0.77 to 2.75 /xg/m3 and the 

blood lead range was from 9.0 to 12.1 /xg/dl. For the 

high school students the town with the highest air 

lead value did not have the highest blood lead level. 

A further comment on methodology pertains to the 

fact that a considerable lag time occurred between 

the collection and analysis of the blood samples. 

12.3.1.4 CLINICAL AND EXPERIMENTAL 

STUDIE S IN RELATIO N T O AI R 

LEAD/BLOOD LEAD RATIOS 

Griffin and his colleagues undertook two studies 

using volunteers exposed in a gas chamber to an artificially generated aerosol of submicron-sized particles of lead dioxide.86

 All volunteers were introduced into the chamber 2 weeks prior to the initiation of the exposure; the lead exposures were 

scheduled to last 16 weeks, although the volunteers 

could drop out whenever they wished. Twenty-four 

volunteers, including 6 controls, participated in the 

10.9 /xg/m3 exposure study. Twenty-one subjects, including 6 controls, participated in the 3.2 /xg/m3

 exposure study. Not all volunteers completed the exposure regimen. Blood lead levels were found to 

stabilize after approximately 12 weeks. Among II 

men exposed to 10.9 /xg/m3 for at least 60 days, a 

stabilized mean level of 34.5 ± 5.1 /xg/dl blood was 

obtained, as compared with an initial level of 19.4 

± 3.3 /xg/dl. AU but 2 of the 14 men exposed at 3.2 

/xg/m3 for at least 60 days showed increases and a 

stabilized level of 25.6 ± 3.9 figldl was found, compared with an initial level of 20.5 ± 4.4 /xg/dl. This 

represented an increase of about 40 percent above 

the base level. 

From the data Table 12-27 was constructed, 

which shows the time needed to reach specific blood 

lead levels at the two air lead concentrations. As can 

readily be seen even at the lower exposure, it takes 

only 7 weeks for the population mean blood level to 

increase by 5 /xg/dl. 

In the article, the authors described both the 

chemistry and particle size of the lead aerosols 

generated. In general, the aerosols used in this experiment were somewhat less complex chemically, 

as well as somewhat smaller, than those found in the 

ambient environment. Griffin et al.,86 however, 

point out that good agreement was achieved on the 

basis of the comparison of their observed blood lead 

12-22 
TABLE 12-27. LENGTH OF TIME NEEDED FOR MEAN BLOOD LEAD VALUES TO REACH SPECIFIED LEVELS AT TWO 

EXPOSURE LEVELS 

Exposure 

group 

1 

1 

1 

2 

2 

2 

Air lead 

level, jjg'm 

10.9 

10.9 

10.9 

3.2 

3.2 

3.2 

Avg. baseline 

blood lead 

level, (tig-'dl 

Target 

blood lead 

level, jjg/dl 

25 

30 

35 

25 

30 

35 

Time needed 

to reach 

target level, wk 

1 to 2 

4 

6 

7 

Not reached 

Not reached 

20.0 

20.0 

20.0 

20.8 

20.8 

20.8 

levels with those predicted by Goldsmith and Hexter's equation,87

 that is, log10 blood lead = 1.265 + 

0.2433 log 10 atmospheric exposure. 

In contrast to the study of Griffin et al. that 

approximates the exposure regimen of environmentally exposed persons, Kehoe studied long-term 

exposures under conditions approximating those of 

occupationally exposed individuals.88 Kehoe exposed a subject to an air lead as the sesquioxide first 

at 75 /xg/m3 then at 150 /xg/m3. Definite increases in 

urinary and blood lead levels emerged under each 

exposure. There appeared to be a plateau reached in 

the blood lead levels upon a steady state exposure. 

Gross compiled data from lead balance studies 

conducted by Kehoe between 1934 and 1972 and 

determined that increases of levels in blood, urine, 

and feces under controlled clinical exposure were 

0.38 /xg/dl, 0.88 /xg/day, and 2.50 /xg/day, respectively, for each increase of 1 /xg/m3

 in air lead 

levels.89 

The derivation of these estimates is currently unknown but was based on the results of ingestion and 

inhalation studies carried out on 16 individuals over 

21,000 person-days. During this period, there were 

102 study periods for the 16 subjects. None of the 

subjects experienced harmful effects as a result of 

the lead exposures, the highest of which were approximately 30 /xg/m3

 on a 24-hr basis (every other 

day to 6 days per week) for study periods up to 628 

days. With a single exception, in none of the subjects 

did the blood level exceed 40 /xg/dl. ' 

Rabinowitz and colleagues have conducted 

studies of lead metabolism by stable isotopes that 

permit the determination of blood/air lead relationships.9091

 In one study, a single volunteer was confined in a hospital's metabolic research ward for a 

period of 109 days for 23 hr a day.90 He was then 

removed into a "clean" room in which the air was 

filtered to remove the particulate lead. For the first 

15 days in the room, his daily lead intake was 

supplemented by lead additions to the diet to compensate for the loss of air lead intake. At the end of 

this 15-day period the dietary lead supplement was 

discontinued. He immediately showed a decliningblood lead level that eventually reached a 

minimum. He then left the "clean" room and his 

blood lead level went back up. Unfortunately, his 

blood lead did not stabilize after his exit from the 

"clean" room. 

A further report presents data, involving additional volunteers, from which a blood to air lead 

ratio can be derived.91 Subsequent to a stabilizing 

period in a metabolic ward, they entered the filtered 

air room and blood lead levels decreased. The blood 

lead levels did stabilize upon exit from the clean 

room. 

Chamberlain et al.92-

93

 reported on studies in 

which gasoline containing tetraethyl lead labeled 

with

 203Pb was burned in an internal combustion 

engine and the resulting tagged lead exhaust aerosol 

was inhaled by 6 volunteers. The lead concentration92

 was typically about 6 mg/m3 and the 

total particulate 30 mg/m3. The aggregates of particles about 0.6 fim in diameter were stable: those .5 

0.01 fim tended to coagulate. Exposures were for 30 

min or less, and the progress of the lead through the 

body was monitored. It was found that about 40 percent of the particles was retained, and that 60 percent was exhaled. The lung clearance rate for

 203Pb 

activity varied markedly, depending on whether the 

aerosol was irradiated. The transference of activity 

to the blood peaked at 50 hr after inhalation at 48 

percent of the initial lung burden. At 72 hr. about 

half of the lead had been removed to bone and other 

tissues and the other half had become attached to 

red cells. The amount of

 203Pb in the blood was 

found to decline with a biological half life of 16 

days. 

Chamberlain et al. then extrapolated these highlevel, short-term exposures to longer term ones. The 

following formula and data were used to calculate a 

blood-to-air level ratio: 

12-23 
P.33 

[T|/2 ] [%Deposition] [%Absorption] [Daily 

ventilation] 

[Blood volume] [0.693] 

where: a = blood to air lead ratio 

biological half life 

(12-7) 

1

 1/2 

Data used were: 

1. Airborne level = 1 /xg/m3 

2. Exposure = 24 hr/day 

3. Daily ventilation = 15m3/day 

4. % Deposition =40 * 

5. % Absorption = 50* 

6. Blood volume = 5400 ml 

'These values were determined experimentally in this study; all others are authors' 

assumptions. 

Using the above equation and values, Chamberlain et al.93

 obtained a ratio of 1.2, in contrast to 

a value of 1.1 reported in an earlier report,92 where 

slightly different assumptions were made. In this 

earlier report,92 data from Kehoe88 and Williams et 

al.94 were used in a similar manner to calculate 

ratios of 1.1 and 1.1, respectively. It is interesting to 

note the difference in the ratios calculated by 

Gross89 and Chamberlain et al.92 from the Kehoe 

data. However, the extrapolation of Chamberlain et 

al. of the short-term to long-term exposure is in 

close agreement with the results of Kehoe and of 

Williams et al., as Chamberlain et al. calculated 

them. 

Chamberlain's ratios have been recalculated by 

Bridbord95 on the basis of a more active person's 

daily ventilation of 20 m3. This, he states, would 

yield a ratio of 1.6 /xg/dl for each 1 /xg/m3 of air lead 

exposure. 

12.3.1.5 BLOOD/AIR LEAD RELATIONSHIPS 

Summarization of the relationship between lead in 

air and lead in blood requires the consideration of 

several distinct lines of evidence. These include: the 

minimal air lead concentration at which blood lead 

levels are first elevated, the form and magnitude of 

the relationship, the proportion of the population 

whose blood lead level exceeds any specific value at 

any given air lead concentration, and whether the 

form or magnitude of the relationship varies depending on whether the air lead exposure is increasing, remaining constant, or decreasing. 

On the first point, only a few studies have sufficiently precise estimates of air lead exposures to permit this calculation, namely Yankel et al.1

 and Azar 

et al.3 EPA used William's

 96

 test on the data from 

both these studies to determine the air lead levels at 

which blood lead levels were found to be significantly higher than the geometric mean blood lead 

levels of the groups exposed to the lowest air lead 

level, which thus served as controls. William's test is 

a multiple comparison test designed to make such 

comparisons. 

For data from the Yankel et al. study,1 EPA 

pooled the lowest two air lead exposure areas (V 

and VI) to form the control group. 

The test showed that area IV was the first, in the 

ordered data, that showed significant elevation of 

blood lead values. The corresponding air lead concentration for this area was 1.7 /xg/m3

. 

EPA, using this same test for the Azar et al. 

study,3 showed that blood lead values for the Philadelphia cabdrivers were significantly different from 

that for the pooled Starke and Barksdale plant 

employees that constituted the control population. 

Blood lead values for the Los Angeles office 

workers were also significantly higher than those of 

control populations. The corresponding air lead exposures were 2.6 and 3.1 /xg/m3

. respectively. 

The clinical study of Griffin et al.86 provides data 

that support the results of the EPA analysis of Azar 

et al.3 data. The data show that individuals exposed 

to 3.2 /xg/m3 had a definite increase in their blood 

leads as a result of this exposure. 

Thus, the available data are consistent as to the 

value of air lead concentration at which blood lead 

levels begin to increase. The Yankel et al. data1 

demonstrated this increase at 1.7 ,u.g/m3; the Azar et 

al. data,3 at 2.6 /xg/m3. These results are not inconsistent because the Azar et al. study did not have a 

population exposed to a level of air lead between 1 

and 2.6 /xg/m3. 

The derivation of the functional relationship between air lead exposure and blood lead levels has 

technical difficulties because the true form of this 

relationship is not linear. No matter what the 

difficulty in making this assessment is, the form of 

the relationship is extremely important because it is 

used to determine the effect of a change in the blood 

lead levels as a function of the air lead values. 

Some studies, by the very nature of their design, 

only permit calculating the ratio between a change in 

blood lead and associated change in the air lead concentration. For these situations, the calculated ratio 

can be considered as an estimate of the average ratio 

over the range of the air lead levels encountered. 

For those studies in which a functional relationship can be derived, this ratio can be estimated for a 

given air lead concentration by evaluating the 

derivative of the functional relationship at that 

12-24 
value. This ratio is subject to considerable change 

over the range of air lead levels encountered, depending on the form of the relationship that was fitted. We have chosen, wherever possible, to use the 

author's own model for the relationship. 

The earliest attempt to use epidemiological data 

to calculate a blood-to-air lead relationship was 

made by Goldsmith and Hexter.87 A linear regression equation of the logarithm of the blood lead 

level on the air lead level was performed on data 

from the Three-City Study.40 Data from Kehoe's observations on 4 individuals experimentally exposed 

to 10 and 150 /xg/m3 in a pattern equivalent to a normal work exposure were found to fit the equation. 

The slope of this line was not significant below 2 

figlm3 of air exposure, possibly because few observations were available in the Three-City Study below 

that level. The derived slope of the regression line 

suggests an increase of 1.3 /xg/dl for each microgram 

of air lead. 

Azar et al.3 used a log-log model to fit their data; 

the data, as well as the regression line, are presented 

in Figure 12-8. The slopes, that is, the ratios, were 

calculated from the equation, log Pb-B = 1.2557 + 

0.153 (log Pb-A), at the four air lead values shown 

in Table 12-28. These slopes ranged from 2.6 at an 

air lead of 1.0 /xg/m3 to 0.7 at an air lead of 5.0 

/xg/m3. It is important to note that all four air lead 

concentrations of interest are well within the range 

of the air levels observed. 

40 

20 

10 

-

1 

•' 

_—^—7~* 

*. 

• * • 

l 

1 

L-^-r~ 

• *.. 

9 

• 

1 

1 

•' 

" 

' 

» 

1 

1 1 1 

. ° 

. 

O LOS ANGELES OFFICE WORKERS 

A LOS ANGEt-ES CAB DRIVERS 

• BARKSDALE. WISCONSIN 

7STARKE, FLORIDA 

• PHILADELPHIA CAB DRIVERS 

1 1 1 

TOTAL AIR LEAD, ng/m 

Figure 12-8. Blood lead versus air lead for urban male 

workers.3 

TABLE 12-28. ESTIMATED BLOOD LEAD TO AIR LEAD RATIOS FOR FOUR AIR LEAD CONCENTRATIONS 

Study 

Epidemiological 

Azara 

Tepper-Levinb 

Nordmanb 

Nordman" 

Fugasb 

Johnsonb 

Johnson^ 

Tsuchiyab 

Goldsmithb 

Goldsmithb 

Yankel-von Linderna 

Chamberlains-Williams 

Dainesb 

Clinical 

Griffin" 

Griffin" 

Rabinowitz" 

Gross0 

Chamberlain0 

Chamberlainc-Kehoe 

Population 

Adult males 

Adult females 

Adult males 

Adult females 

Adults 

Adult males 

Adult females 

Adult males 

Children males 

Children females 

Children 

Adults 

Black females 

Adult males 

Adult males 

Adult males 

Adults 

Adults 

Adults 

Sample 

size 

149 

1908 

536 

478 

330 

64 

107 

591 

202 

203 

879 

482 

(unknown) 

11 @10.9 

14® 3.2 

2 

(21,000 person-days) 

7 

5 

1.0 

2.57 

0.87 

1.16 

Ratio at 

air lead concentrations, 

2.0 

1.43 

0.92 

1.21 

u. g/m' 

3.5 

0.89 

1.00 

(0.42)° 

(0.11) 

(2.64) 

(0.80) 

(0.60) 

(3.84) 

(2.30) 

(1.70) 

1.27 

(1.10) 

(2.30) 

(1.40) 

(1.65) 

(1.7,2.5) 

(0.38) 

(1.20) 

(1.10) 

5.0 

0.66 

1.08 

1.37 

a

 Authors' regression equation evaluated at specific air lead. 

b

 EPA calculation. 

c

 Authors' calculations. 

d

 Ratios presented in parentheses are not calculated from any regression equation. 

12-25 
P.35 

One of the authors, Snee,50 has since reanalyzed 

the data using a more complicated model for the 

relationship. His newer model attributes less of the 

increase in blood lead to air lead exposures and 

more to geographic area differences. The improvement in fit by use of this newer model is insignificant. 

Furthermore, in the new model, the area differences 

are correlated with the air lead differences. For 

these reasons, the original model is believed to be 

more appropriate for estimating the total effect of 

air lead. 

Yankel et al.1 used a log-linear model (Equation 

12-6) to fit their data. The slopes of the four air lead 

values shown in Table 12-28 were calculated from 

this equation. These ranged from 1.2 at an air lead 

level of 1.0 /xg/m3 to 1.4 at an air lead of 5.0 yxg/m3. 

Again, all air lead concentrations were within the 

range of the data. 

One assumption inherent in the calculation of the 

regression of blood lead on air lead using standard 

least squares is that the air lead values have been 

measured with no error. Unfortunately, this assumption is not correct. Obviously, the monitored air lead 

values are not the exact values inhaled by the subjects in the exposure area. The effect of measurement 

error in the independent variable is discussed by 

Kendall and Stuart.97 In general, the calculation 

regression coefficients are underestimates of the true 

values. If either the error in the dependent variable, 

or the error in the independent variable, or the ratio 

of the two errors were known, then improved estimates could be calculated. 

The Yankel et al. study1 gives sufficient information to estimate the effect of this problem. The 

authors assigned 1 of 33 different estimated exposure levels to each individual in the study. If the 

within level variances of blood lead values are 

pooled for these 33 levels, the result is a pooled 

GSD of 1.28. Using the value of 1.28 for the error in 

the dependent variable, the regression coefficient of 

0.041 reported by Yankel and von Lindern becomes 

0.052. This adjustment increases the estimated 

blood lead to air lead ratio from 1.21 to 1.44 at 2 

figlm3 and from 1.37 to 1.69 at 5 Mg/m3-

This problem may exist in some of the other 

studies, but it is not a serious problem in two of the 

other more important studies. In the Azar study,3 

personal samplers were used, so that individual exposures were measured more accurately than in any 

other epidemiologic study. In the Griffin study the 

air lead levels were controlled extremely closely, so 

that there was almost no variation in the exposure 

value. 

The reanalysis of the Tepper-Levin study2 as reported by Hasselblad and Nelson22

 was used to estimate the relationship of air lead to blood lead levels. 

A log-linear model was used that allowed for age 

and smoking differences, as well as the air lead exposure. This form of the model was chosen because it 

gave a better fit to the data than did the log-log 

model. The slopes were calculated from the loglinear model at the four air lead values shown in Table 12-28. These slopes ranged from 0.9 at an air 

lead of 1.0 figlm3 to 1.1 at an air lead of 5.0 /xg/m3. 

The air lead values only ranged from 0.2 to 3.4 

/u.g/m3, however, 

Daines et al. reported two studies examining 

variations in blood lead ratios with distance from 

busy highways.52 The studies were conducted in 

Camden, New Jersey, and involved black females. 

Only one of these studies can be used to determine 

the blood lead/air lead ratio because no air lead data 

were reported for the other study. In this study, 

blood lead ievels of black females living in residences that were 3.7,38.1, and 121.9m distant from 

the highway were determined. Yearly mean air and 

blood lead levels for these three groups are presented in Table 12-29. From these values a ratio 

may be calculated as follows: 

23.1-17.6 ratio = A ,,, ~ ~A = 2.3 for the total population. 4.60-2.24 

Using a similar calculation, housewives were found 

to have a ratio of 3. 

TABLE 12-29. YEARLY MEAN AIR AND BLOOD LEAD LEVELS 

OF BLACK FEMALES IN RELATION TO DISTANCE OF 

RESIDENCE FROM A BUSY HIGHWAY 

Study 

area 

Area A 

AreaB 

Area C 

In Yugoslavia, Fugas et al. in the study described 

earlier,69 estimated the weekly time-weighted air 

lead exposures of eight population groups. The estimates were based on air lead values monitored at 

various locations and estimated proportions of time 

the individuals spent at those locations. The timeweighted exposure estimates, sample sizes, and 

blood lead levels for this study were presented 

earlier (Table 12-22). A weighted regression 

analysis was chosen for these data because the sample sizes of the customs officers and policemen 

varied from those for the other groups. The range of 

air leads was from 0.079 to 3.0 ,ug/m3. The resulting 

slope is 2.64, and is presented in Table 12-28. 

Distance from 

highway, m 

3.7 

38.1 

121.9 

Air lead. 

Mg/m' 

4.60 

2.41 

2.24 

Blood lead 

jjg/l00g 

23.1 

17.4 

17.6 

12-26 
P.36 

Snee50 has criticized the inclusion of the streetcar 

drivers because of differences in social status and 

habits from the other groups. The effect of removing 

these subjects would be to reduce the calculated 

slope. This group was not removed because the air 

lead exposure was more precisely estimated than in 

other studies. 

Data on Tokyo policemen reported by Tsuchiya et 

al.41 and discussed in detail previously in this 

chapter may also be used to calculate a slope. Unfortunately, the slope that is derived can only be looked 

upon as confirmatory evidence and not as additional 

evidence because of the time difference between 

sampling the air and sampling the blood. Another 

possible complicating factor is the rural-urban gradient that parallels the air lead concentrations. 

Weighted regression analysis was used on the blood 

and air lead data reported in Table 12-26. The estimated slope is 3.8 and is recorded in Table 12-28. 

The observed range in air lead concentrations was 

0.024 to 1.157 Mg/m3. 

From the Johnson et al. study in California,6 estimates of the ratio between blood and air lead levels 

can be derived. Because of analysis problems encountered in the blood lead determinations of 

children, it was decided that a valid estimate could 

not be derived. Therefore, only data for adults will 

be treated here. It was decided to pool the data for 

adults and present separate ratios for males and 

females aged 17 and above. Geometric mean blood 

lead levels were used in the calculation because the 

blood lead data were found to follow a log-normal 

distribution. 

For males, the pooled geometric means were 15.5 

and 11.0 figldl for Los Angeles and Lancaster, 

respectively. For females, the corresponding values 

are 12.1 and 8.4 figldl. The ratio was calculated as 

follows for males: ratio = (15.5-11.0)/(6.3-0.6) = 

0.8. The ratio for females was 0.6. These values are 

tabulated in Table 12-28. 

Nordman in his doctoral dissertation16 reported 

on blood and air lead levels for several populations 

in Finland (Table 12-30). Because of the large variation in the sample sizes for these populations, EPA 

calculated a weighted regression equation. The slope 

of the equation was estimated for both males and 

females separately and is 0.4 and 0.1, respectively, 

as presented in Table 12-28. It should be noted that 

the range of air lead concentrations covered by this 

study was 0.025 and 1.32 Mg/m3. 

Data from Goldsmith42 on elementary and high 

school children in a number of California towns can 

also be used in the calculation of the slopes. EPA has 

TABLE 12-30. BLOOD AND AIR LEAD LEVELS BY SEX IN 

FINNISH POPULATION STUDYTM 

Group 

Pertummaa 

Pyhajarui 

Suburban 

Downtown 

Policemen 

Street sweepers 

Air lead, 

Mg/m3 

0.025 

0.025 

0.74 

0.90 

1.32 

1.32 

Male blood lead, 

N 

243 

— 

37 

142 

28 

86 

ixg/dl 

Avg 

12.1 

— 

10.6 

11.4 

13.5 

13.3 

SD 

4.5 

— 

2.8 

3.3 

2.8 

4.1 

Female blood lead, 

N 

256 

93 

81 

37 

— 

11 

/jg/di 

Avg 

9.6 

8.6 

9.7 

8.5 

— 

10.4 

SD 

3.5 

2.5 

2.6 

2.0 

— 

3.0 

separately analyzed the raw data from this study for 

elementary school males and females. The results of 

these analyses show ratios of 2.30 and 1.70, respectively (Table 12-28). 

Chamberlain et al.92 analyzed the data of 

Williams et al.96 on occupationally exposed persons 

using personal monitors. Chamberlain adjusted the 

occupational exposures to 24-hr exposures by 

calculating the elevation in blood lead from a nonexposed population. He calculated a slope of 1.1. 

Clinical studies also provide data useful in quantitating the relationship between blood and air lead. 

Griffin et al.,86 in their clinical study of the largest 

number of subjects to date, exposed individuals to 2 

levels of air lead concentrations, 10.9 and 3.2 

Mg/m3. The study design, it was believed, precludes 

fitting an overall equation to these data, and a separate calculation of a ratio is presented for the two experiments. In both experiments, the background air 

lead levels were estimated to be 0.15 Mg/m3- 1°

 tn e 

3.2 Mg/m3 air lead exposure, the men increased their 

mean blood lead levels from 20.5 to 25.6 figldl. 

This yields a ratio of 1.65 (25.6-20.5)/(3.2-0.15). 

The 10.9 Mg/m3 air lead exposure resulted in an increase of blood lead levels from 19.4 to 34.5 figldl. 

This gives a ratio of 1.40 (34.5-19.4)/( 10.9-0.15). 

These values are shown in Table 12-28. 

Chamberlain et al.92 reanalyzed the Kehoe results 

by adjusting the 37.5-hr exposures per week to a 24-

hr equivalent. They used data from 5 subjects whose 

24-hr equivalent exposures ranged from 0.6 to 73.5 

Mg/m3. The calculated ratios ranged from 0.6 to 2.0, 

with an overall mean of 1.1 for the data. 

In contrast to the analysis of Kehoe's work by 

Chamberlain in which a 1.1 ratio was calculated, 

Gross89 reports a ratio of 0.38 for these data. At this 

time, no details are available concerning his 

methods. Therefore, the apparent discrepancy between these two analyses cannot be evaluated. 

Chamberlain et al.,92*

93

 as discussed earlier, 

calculated ratios of 1.1 and 1.2 based on the ex12-27 
P.37 

trapolation of a short-term exposure to a long-term 

one. The calculation involves a number of experimentally determined as well as assumed numbers. 

As described previously, Rabinowitz et al.91 

studied three individuals for metabolic changes in 

blood lead as a function of changes in the air lead 

concentration. In contrast to the other clinical 

studies described wherein air lead levels were increased, in this study the subjects were placed in a 

"clean room" in which the air was filtered. This 

study, therefore, pertains to the situation in which 

the air lead concentration has decreased. The blood 

lead levels were determined from the stabilized 

mean both when the subject was breathing normal as 

well as filtered air. One of the men did not have a 

stabilized blood lead after returning to breathing 

normal air; therefore, he could not be used in determining the ratio. The relevant data for calculating 

the ratio are included in Table 12-31. 

TABLE 12-31. BLOOD AND AIR LEAD DATA 

FROM CLINICAL STUDY91 

Subject 

D 

E 

Estimated 

Normal air, 

JJ g/m3 

0.91 

0.91 

air lead 

Filtered air, 

li g/m3 

0.072 

0.072 

Blood lead 

Normal air, 

/»g/l00g 

20.2 

16.3 

Filtered air, 

Mg/100 g 

18.8 

14.2 

The calculation for subject D was done as follows: 

ratio = (20.2-18.8)/(0.91-0.072) = 1.7. The 

calculation for subject E results in a ratio of 2.5. 

Only one data set (Azar et al.3) is available on 

which to estimate a dose-response relationship, that 

is, the proportion of a population exceeding a 

specified blood lead level for any specific exposure. 

The reasons for the paucity of data are twofold: (1) 

access is needed to the raw data and (2) the exposure 

data should be relatively precise. 

The regression equation for the Azar study3 has 

already been discussed. The mean square error 

(MSE) about this equation was calculated for all five 

areas combined. From the MSE, estimates of the 

percentage of the population exceeding a given 

blood lead level for a given air lead level are given 

by: 

Percent = 

Plog,0 (blood lead) - 1.2257-0.1531 log|0 (air lead)1 

100 f rl( HMSE"2 ]} 

where: N(x) is the cumulative normal integral of a 

standard normal variable up to the point x. These 

percentages are given in Table 12-32 for a range of 

air lead values. 

These tabulated percentages may not be representative of the general population, since they are based 

on a single study of 149 subjects. They are presented 

because they are the best estimates available of a 

dose-response relationship. 

TABLE 12-32. ESTIMATED PERCENTAGE OF POPULATION 

EXCEEDING A SPECIFIC BLOOD LEAD LEVEL IN RELATION 

TO AMBIENT AIR LEAD EXPOSURE* 

Percent exceeding blood lead level ol: 

r lead, 

ig/m3 

0.5 

1.0 

1.5 

2.0 

2.5 

3.0 

3.5 

4.0 

4.5 

5.0 

6.0 

7.0 

8.0 

20.0 

ug/dl 

15.22 

26.20 

34.12 

40.23 

45.15 

49.23 

52.69 

55.67 

58.27 

60.57 

64.45 

67.63 

70.28 

30.0 

f<g/di 

0.59 

1.67 

2.88 

4.12 

5.35 

6.57 

7.75 

8.90 

10.01 

11.09 

13.16 

15.10 

16.92 

40.0 

Mg/dl 

0.02 

0.07 

0.16 

0.26 

0.38 

0.51 

0.66 

0.81 

0.97 

1.14 

1.48 

1.83 

2.20 

a

 Data derived Irom the equation ol Azar et al.3 

The last element in defining the relationship between lead in blood and lead in air is a discussion of 

the effect that varying the concentration of lead in 

air has on the blood lead levels. Most of the data 

previously presented have dealt with steady state or 

increasing air lead concentrations. This section will 

summarize the results of studies showing the effect of 

decreasing the concentration of lead in air on the 

blood lead levels of human populations. 

Rabinowitz et al.'s study

 9I

 provides estimated 

ratios for two subjects under carefully controlled 

conditions who experienced a decrease in their air 

lead concentrations. For the two subjects, a 1 Mg/m3 

decrease in air lead levels resulted in a 2 figllOO g 

decrease in blood lead levels. 

Baker98 presented data to the EPA Science Advisory Board showing decreases in blood lead levels 

in the vicinity of an Idaho smelter between 1974 and 

1975 (fable 12-33). Information from all study 

areas combined indicated that blood lead levels had 

decreased by 2.3 figldl for each 1 Mg/m3 reduction 

in air lead. This same investigator provided additional information in a separate communication to 

EPA showing that, when analyses were limited to 

children of nonsmelter workers, blood lead levels 

decreased 2.0 figldl in all study areas for each 

decrease of 1 figlm3 of air lead. If the analyses included only those children of nonsmelter workers 

exposed to air lead levels ranging from 0.5 to 10 

12-28 
Mg/m3

, blood lead levels decreased 1.3 figldl for 

each unit decrease in air lead and also showed a 

higher ratio at greater air lead concentrations. From 

these analyses, it seems apparent that a single ratio 

cannot describe the data from this study. 

TABLE 12-33. COMPARISON OF BLOOD LEAD LEVELS IN 

CHILDREN WITH AIR LEAD LEVELS FOR 1974 AND 1975 

(EPA analyses) 

Study 

area 

1 

2 

3 

4 

Blood lead levels, 

1974 

69 

49 

36 

33 

II g/dl 

1975 

46 

38 

32 

27 

Diff. 

23 

11 

4 

5 

Ai 

1974 

18 

14 

6.7 

3.1 

lead levels, 

Ii g/m3 

1975 

10.3 

8.6 

4.9 

2.5 

Diff. 

7.7 

5.4 

1.8 

0.6 

Pb-B diff./ 

Pb-A diff. 

3.0 

2.0 

2.2 

8.0 

Data from Angle and Mclntire's studies7376 in 

Omaha also provide data in this regard. They found 

blood lead levels of urban children, aged 6 to 18, to 

consistently decrease during the years 1970 to 1973. 

This decrease was almost 10 figldl across all study 

groups. Furthermore, this decrease has been found 

to be closely correlated with a decrease in air lead 

from about 1.5 to less than 0.5 Mg/m3. In a reanalysis 

of the full data base, Angle has calculated an overall 

equation of Pb-B = 10.04 (Pb-A) + 17.06, r = 

0.95. 

Data from New York City analyzed by HUD3 8 

and described in detail in the demographic 

variability section of this chapter may also provide 

supportive data for the notion that a decrease in 

blood lead level is associated with decreased air lead 

exposure. In the New York lead screening program 

geometric mean blood lead values have been noted 

as decreasing consistently from 1970 to 1976. During this time, some changes occurred in the number 

of children sampled, so that the more recent years 

have far fewer data points than the earlier years. No 

significant break in the trend was observed as the 

change in sample size was noted. Data from one HiVol air station provided continuous air lead values 

over this period in New York City. The air lead 

values measured there, not really representative of 

the exposure of the children being studied, have 

been following a similar pattern. It is also interesting 

to note that lead in gasoline in New York City was 

also being reduced during this period. 

The quantitative estimates provided from the 

three studies discussed show decreasing air lead concentrations vary from a minimum of 1.3 to 8 or 10 

figldl. These data suggest that a greater ratio may 

hold for decreases in air lead than for steady state or 

increasing exposures. 

In summary, in all quantitative studies presented, 

a positive relationship between blood lead and air 

lead has been found. The form and magnitude of the 

relationship, however, has not been found to be constant but varies in the studies reviewed. Table 12-28 

summarizes the quantitative estimates derived from 

the review and analysis of the literature. 

In general, the data show that the blood lead to air 

lead ratio is not constant over the range of air exposure encountered (it varies in most studies between 1 and 2), that males appear to have higher 

ratios than females, and that children have a slightly 

higher ratio than adults. Also, the data suggest that 

more attention should be given to studies of decreasing air lead concentrations in that the ratios derived 

from such studies appear higher than those of steady 

state or increasing exposures. 

12.3.2 Soil and Dust Exposures 

The relationship of exposure to lead contained in 

soil and housedust and the quantity of lead in 

humans, particularly in children, has been the subject of scientific investigation for some time. 7 8 "- 1 0 5 

Duggan and Williams105 have recently published an 

assessment of the risk of increased blood lead resulting from the ingestion of lead in dust. Some of these 

studies have been concerned with the effects of such 

exposures:7899102 others have concentrated on the 

means by which the lead in soil and dust becomes 

available to the body.I03104 

In one of the earliest investigations, Fairey and 

Gray conducted a retrospective study of lead 

poisoning cases in Charleston, South Carolina.99 

Two-inch core soil samples were collected from 170 

randomly selected sites in the city and were compared with soil samples taken from the yards of 

homes where 37 cases of lead poisoning had occurred. The soil lead values obtained had a wide range, 

from 1 to 12,000 ppm, with 75 percent of the samples containing less than 500 ppm. A significant 

relationship between soil lead levels and lead 

poisoning cases was established; 500 ppm was used 

as the cutpoint in the chi-square contingency 

analysis. This study was the first to examine this 

complex problem and, although data support the 

soil lead hypothesis, they were not such as to allow 

for quantification of the relationship between soil 

lead and blood lead levels. Furthermore, because no 

other source of lead was measured, the association 

found might have been caused by confounding additional sources of lead, such as paint or air. 

12-29 
P.39 

A later study by Galke et al., also in Charleston, 

used a house-to-house survey to recruit 194 black 

preschool children.43 Soil lead, paint lead, and air 

lead exposures as measured by traffic density were 

established for each child. When the population was 

divided into 2 groups based on the median soil lead 

value (585 figlg), a 5-Mg/dl difference in blood lead 

levels was obtained. Soil lead exposure for this 

population ranged from 9 to 7890 figlg. A multiple 

regression analysis of the data showed that vehicle 

traffic pattern, when defined by area of recruitment 

(i.e., high or low); lead level in exterior siding paint; 

and lead in soil were all independently and significantly related to blood lead levels. 

Barltrop et al.100 described two studies in England 

investigating the soil lead to blood lead relationship. 

In the first study, children aged 2 and 3 and their 

mothers from two towns chosen for their soil lead 

content each had their blood lead level determined 

from a capillary sample. Hair samples were also collected and analyzed for lead. Lead content of the 

suspended particulate matter and soil was measured. 

Soil samples for each home were a composite of 

several 2-in. core samples taken from the yard of 

each home. Chemical analysis of the lead content of 

soil in the two towns showed a two- to threefold 

difference, with the values in the control town being 

about 200 to 300 ppm compared with about 700 to 

1000 ppm in the exposed town. A difference was also 

noted in the mean air lead content of the two towns, 

0.69 Mg/m3 compared with 0.29 Mg/m3. respectively. 

Although this difference existed, both air lead 

values were thought low enough not to affect the 

blood level values differentially. Mean surface soil 

lead concentrations for the two communities were 

statistically different, the means for the high and low 

community being 909 and 398 ppm, respectively. 

Despite this difference, no statistically significant 

differences in mothers' blood lead levels or 

children's blood or hair levels of lead were noted. 

There was, however, suggestive evidence of a 

difference in hair lead levels for children. Further 

statistical analysis of the data, using correlational 

analysis on either raw or log-transformed blood lead 

data, likewise failed to show a statistical relationship 

of soil lead with either blood lead or hair lead. 

The second study was reported in both preliminary and final form.100101

 In the more detailed 

report,101 children's homes were classified by their 

soil lead content into three groups, namely < 1,000, 

1000 to 10,000, and > 10,000 ppm. As shown in Table 12-34, children's mean blood lead levels increased correspondingly from 20.7 to 29.0 figldl. 

Mean soil lead levels for the low and high soil exposure groups were 420 and 13,969 ppm, respectively. Mothers' blood levels, however, did not 

reflect this trend; nor were the children's fecal lead 

levels different across the soil exposure areas. 

TABLE 12-34. MEAN BLOOD AND SOIL LEAD 

CONCENTRATIONS IN ENGLISH STUDY101 

Category 

of soil lead, 

ppm 

<1000 

1000-10000 

>10000 

Sample 

size 

29 

43 

10 

Children's 

blood lead, 

n g/dl 

20.7 

23.8 

29.0 

Soil lead 

PPm 

420 

3390 

13969 

Other studies have investigated the relationship of 

dust lead to absorption.3378102106 Some of these also 

included measurements of soil lead. 

Lepow et al.,106 for example, studied the lead content of air, housedust, and dirt, as well as the lead 

content of dirt on hands, food, and water, to determine the cause of chronically elevated blood lead 

levels in ten 2- to 6-year-old children in Hartford, 

Connecticut. Lead based paints had been eliminated 

as a significant source of lead for these children. 

Ambient air lead concentrations varied from 1.7 to 

7.0 Mg/m3. The mean lead concentration in dirt was 

1,200 figlg and in dust, 11,000 figlg. The mean concentration of lead in dirt on children's hands was 

2,400 ppm. The mean weight of samples of dirt from 

hands was 11 mg, which represented only a small 

fraction of the total dirt on hands. Observation of 

the mouthing behavior in these young children lead 

to the conclusion that the hands-in-mouth exposure 

route was the principal cause of excessive lead 

accumulation in these children. 

Angle et al.,74 studying children in Omaha, 

Nebraska, found several interesting associations between soil or housedust lead concentrations and 

blood lead levels. In this report, three groups of 

children were compared: (1) suburban versus urban 

high school, (2) suburban versus urban 10- to 12-

year-olds, and (3) black elementary school children 

with blood lead < 20 versus > 20. Air lead levels, 

all of which were less than 1 Mg/m3, were not shown 

to be related to blood lead levels. Soil and housedust 

were associated, although not always statistically 

significantly. 

Creason et al.,102 studying hair metal levels in the 

New York metropolitan area, used both dustfall and 

housedust as their exposure variables. Three 

geographic areas in metropolitan New York were 

chosen to represent an exposure gradient. Limited 

dustfall and housedust samples were taken to verify 

12-30 
the gradient and to estimate its magnitude. Hair 

samples were collected from residents in locations 

enrolled in other air pollution studies. Mean total 

environmental and hair lead levels were then compared. Hair lead levels ranged from 12 figlg in the 

low area to 17 figlg in the high. Mean dustfall and 

housedust lead levels ranged from 2 to 16 mg/m2-

month, and from 279 to 766 figlg. respectively. 

Hair lead levels in both children and adults were 

found to be significantly related to both dustfall and 

housedust lead. No attempt was made to determine 

the original source of these dusts. Further, the study 

design did not permit the establishment of which of 

the two dust types or both were the actual contributors to the hair lead levels. The investigators concluded that the primary cause of elevated blood lead 

levels in children was ingestion or inhalation of dust 

containing lead. 

Two other studies, which were described in more 

detail in Section 12.3, can be used to examine the 

relationship of lead in soil and dust with lead in 

blood.1-

34

 Yankel et al. showed that lead in both soil 

and dust was independently related to blood lead 

levels. In their opinion, 1000 ppm soil lead exposure 

was cause for concern. Reanalysis of the Dallas 

traffic study showed a significant slope of blood lead 

levels in relation to soil lead levels (/3 = 0.0662).34 

Lastly, Shellshear's case report from New Zealand 

ascribes a medically diagnosed case of lead poisoning to high soil lead content in the child's home 

environment.107 

Two studies have investigated the mechanism by 

which lead from soil and dust gets into the 

body.103104 Sayre et al. in Rochester, New York, 

demonstrated the feasibility of housedust being a 

source of lead for children.103 Two groups of houses, 

one inner-city and the other suburban, were chosen 

for the study. Lead-free sanitary paper towels were 

used to collect dust samples from house surfaces and 

the hands of children.108 The medians for the hand 

and household samples were used as the cutpoints in 

the chi-square contingency analysis. A statistically 

significant difference between the urban and suburban homes for dust levels was noted, as was a 

relationship between household dust levels and hand 

dust levels.106 

Ter Haar and Aronow104 investigated lead 

absorption in children that can be attributed to ingestion of dust and dirt. They reasoned that because 

the proportion of the naturally occurring isotope 

210Pb varies for paint chips, airborne particulates, 

fallout dust, housedust, yard dirt, and street dirt, it 

would be possible to identify the sources of ingested 

lead. They collected 24-hr excreta from 8 hospitalized children for the first day of hospitalization. 

These children, 1 to 3 years old, were suspected of 

having elevated body burdens of lead, and one criterion for the suspicion was a history of pica. Ten 

children of the same age level, who lived in good 

housing in Detroit and the suburbs, were selected as 

controls and 24-hr excreta were collected for them. 

The excreta were dried and stable lead as well as 

210Pb content was determined. For seven hospitalized children, the stable lead mean value was 

22.43 figlg dry excreta, and the eighth child had a 

value of 1640 figlg. The controls' mean for stable 

lead was 4.1 figlg dry excreta. However, the respective means for

 210Pb expressed as pCi/g dry matter 

were 0.044 and 0.040. The authors concluded that 

because there is no significant difference between 

these means for

 210Pb, the hypothesis that young 

children with pica eat dust is not supported. 

However, all that the data, in fact, do show is that 

both groups of children were comparable as to the 

amounts of

 210Pb and vastly different in respect to 

stable lead per gram of dry excreta. The hospitalized 

children ingested larger amounts of material containing stable lead. Granting that the hospitalized 

children ingested leaded paint chips and the controls 

did not. does not permit the conclusion that all the 

210Pb found in all the children originated in food 

and that no dirt and dust was ingested by control 

children whereas hospitalized children ate only 

paint chips. 

The data from all these studies can be summarized 

fairly succinctly. There is evidence that children can 

pick up lead from their environment by getting it on 

their hands. Duggan and Williams105 have summarized the literature on the amounts of lead ingested by ingestion of dust. In their opinion, a quantity of 50 Mg of lead is ingested daily by children by 

means of street dust. As yet there are no solid data 

directly demonstrating the next link, that is, transfer 

of dust and soil from hand to mouth. A clinical case 

report has indicated, however, that soil lead levels 

can lead to excessively elevated blood lead levels. 

Also, the data of Barltrop101 and Galke et al.43 indicate that soil lead exposures, often found in urban 

settings, can contribute between 5 and 8 figldl to the 

blood's lead burden.33101 

The consensus appears to be that observable in-, 

creases in blood lead levels occur at soil or dust lead 

exposures of 500 to 1000 ppm. From the data available in the literature, a summary table (Table 

12-35) was constructed by EPA. A regression 

analysis was used to relate the logarithm of the 

12-31 
P.41 

blood lead to the logarithm of the soil lead. From 

the regression, a coefficient, b, the mean percent age 

increase in blood lead for a two fold increase in soil 

TABLE 12-35. SUMMARY OF SOIL LEAD/BLOOD LEAD RELATIONSHIPS 

lead, can be calculated: 

% increase = 100 [exp(b/log (2))] (12-7) 

Study 

Age, 

years 

Regression 

coefficient, 

log-log 

Geom. mean 

blood lead, 

ug/dl 

Geom. mean 

soil level. 

»g/g 

Mean % increase 

in Pb-B for 2 x soil 

level 

Charleston.SC43 

Kellogg, ID1 

Dallas, TX34 

England101 

1-5 

1-9 

1-5 

2-3 

0.0432 

0.0528 

0.0662 

0.0840 

36.4 

37.5 

11.4 

23.2 

451.6 

1518.1 

91.6 

1849.1 

3.0 

3.7 

4.7 

6.0 

Table 12-35 shows a surprising consistency in the 

percentage increase in mean blood lead levels for a 

twofold increase in soil lead levels (3 to 6 percent), 

given the wide diversity in populations studied and 

soil levels encountered. The Charleston study involved black preschool children living in the inner 

city with several additional known environmental 

sources of lead. The Idaho study was of a smelter site 

in a rural setting. Barltrop's data from England 

showed virtually no environmental source other 

than that from soil. The Dallas study was of a community that was relatively lead free. It is interesting 

to note that the larger estimates of the percentage increase in blood lead occurred in the children with 

the lowest blood lead levels. 

12.3.3 Food and Water Exposures 

In typical urban settings, food probably constitutes the body's largest direct source of lead 

because almost every item in the diet contains some 

measurable amount of the metal. 

Three approaches have been used to estimate dietary intake of lead: duplicate meals, market basket 

surveys, and fecal lead determinations. The estimated dietary lead intake of Americans has 

decreased markedly since the presentation of 

Kehoe's data in the 1940's, which indicated, based 

on fecal lead determinations, that the daily intake 

was between 100 and 350 fig/day.88 Most of the 

more recent comparable data2109110 have reduced 

that estimate to between 50 and 150 Mg/day. The 

California study of Johnson et al.7 points to a daily 

intake of about 100 to 150 Mg. such intake being 

similar for both rural and urban populations. Also, 

Chisholm and Harrison,109 in a study of children 

aged 12 to 35 months, found a mean fecal excretion 

rate of 132 Mg/day, and Barltrop and Killola a value 

of 130Mg-110 

Much recent work has been concerned with the 

lead content of the market basket or total diet in 

which the content of foods meeting typical nutritional needs is analyzed. The foodstuffs are assembled in accordance with national food sample surveys. One such study111112

 has indicated that the 

lead content of the diet of young adults averages 150 

to 200 Mg/day, and another113 cites a figure of 254 

Mg/day for 15- to 20-year-old males. At least 30 percent of this amount in the latter study was attributed 

to the consumption of canned foods. Kolbye111 and 

Mahaffey et al.112 have suggested an average foodbased intake of 80 to 100 Mg of lead for children 12 

to 35 months old. Additional studies in this field 

have been reviewed by Mahaffey.112 

Despite the above estimates of dietary lead content, the quantitative relationship between dietary 

intake and blood lead levels is not well established; 

the bulk of the studies described in Chapter 10 that 

address this relationship, however, point to a sustained value of 6 figldl for 100 Mg of dietary lead intake. 

Water, itself, can also be a source of significant 

quantities of lead with the metal present in the supply itself. More frequent, however, is an increase in 

the quantity of particulate or dissolved lead as water 

is delivered from the treatment plant to the user 

through the lead pipes often found in older housing. 

Most natural waters contain only from 10 to 20 

Mg/liter of lead and most problems occur when lead 

piping is used in areas in which the drinking water is 

lead solvent; that is, it is soft and has a low pH. 

Although the use of lead piping has been largely 

prohibited in recent construction, occasional 

episodes of poisoning from this lead source still occur. These cases most frequently involve isolated 

farms or houses in rural areas, but a surprising situation was revealed in 1972 when Beattie et al.114

-

115 

showed the seriousness of the situation in Glasgow, 

Scotland, which had very pure but soft drinking 

water as its source. They demonstrated a clear association between blood lead levels and inhibition of 

the enzyme ALAD in children living in houses with 

(1) lead water pipes and lead water tanks, (2) no 

12-32 
lead water tank but with more than 60 ft of lead piping, and (3) less than 60 ft of lead piping. The mean 

lead content of the water as supplied by the reservoir 

was 17.9 figlliler; that taken from the faucets of 

groups 1, 2, and 3 was 934, 239, and 108 Mg/l'ter, 

respectively. 

Another English study1 1 6 showed a clear 

difference between the bone lead content of the 

populations of Glasgow and London, the latter having a hard, relatively nonsolvent water supply.-

In a study of 1200 blood donors in Belgium,117 

persons from homes with lead piping and supplied 

with corrosive water had significantly higher blood 

lead levels. 

In Boston, Mass., an investigation was made of 

water distributed via lead pipes. In addition to the 

data on lead in water, account was taken of 

socioeconomic and demographic factors as well as 

other sources of lead in the environment.118119 Participants, 771 persons from 383 households, were 

classified into age groups of <6, 6 to 20, and >20 

years of age for analysis.118 A clear association between water lead and blood lead was apparent (Table 12-36). For children under 6 years of age, 34.6 

percent of those consuming water with lead above 

the U.S. standard of 50 Mg/'iter had a blood lead 

value 2 35 figldl. whereas only 17.4 percent of those 

consuming water within the standard had blood lead 

valuesof235 figldl. 

TABLE 12-36. BLOOD LEAD LEVELS OF 771 PERSONS IN 

RELATION TO LEAD CONTENT OF DRINKING WATER, 

BOSTON, MASS.118 

Persons consuming water (standing grab samples) 

Blood lead 

levels, /jg/dl 

<50iig Pb/liler f5G>gPb/liter 

No. Percent Percent Total 

<35 

>35 

Total 

622 

61 

683 

91 

9 

100 

68 

20 

88 

77.3 

22.7 

100.0 

690 

81 

771 

x = 14.35; dl = 1. 

P <0.01. 

Greathouse et al. have published an extensive 

regression analysis of these data.119 Blood lead 

levels were found to be significantly related to age, 

education of head of household, sex, and water lead 

exposure. Of the two types of water samples taken, 

standing grab and running grab, the former was 

shown to be more closely related to blood lead 

levels than the latter. 

As noted in Chapter 10 of this document, roughly 

10 percent of lead in solid foodstuffs is absorbed by 

adults; the corresponding value for liquids is about 

50 percent. The relative risk for exposure to waterborne lead is, therefore, considerably greater. 

12.3.4 Effects of Lead in the Housing Environment: Lead in Paint 

A major source of environmental lead exposure 

for the general population comes from lead contained in both interior and exterior paint on dwellings. The amount of lead present, as well as its accessibility, depends upon the age of the residence 

(because older buildings are painted with paint 

manufactured before lead content was regulated) 

and the physical condition of the paint. It is 

generally accepted by the public and by health professionals that lead based paint is the major source of 

pediatric lead poisoning with clinical symptoms in 

the United States.120 

The level and distribution of lead paint in a dwelling is a complex function of history, geography, economics, and the decorating habits of its residents. 

Lead pigments were the first pigments produced on a 

large commercial scale when the paint industry 

began its growth in the early 1900's. In the 1930's 

lead pigments were gradually replaced with zinc and 

other opacifiers. By the 1940's, titanium dioxide 

became available and has now become the most 

commonly used pigment for residential coatings. 

There was no regulation of the use of lead in house 

paints until 1955, when the paint industry adopted a 

voluntary standard that limited the lead content in 

paint, for interior uses, to no more than 1 percent by 

weight of the nonvolatile solids. At about the same 

time, local jurisdictions began adopting codes and 

regulations that prohibited the sale and use of interior paints containing more than 1 percent lead.121 

In spite of the change in paint technology and 

local regulations governing its use, and contrary to 

popular belief, interior paint with significant 

amounts of lead was still available in the 1970's. A 

1971 study in New York City found that 8 of 76 

paints tested had a lead content ranging from 2.6 to 

10.8 percent, well above the city's legally permissible 1 percent level.122

 Later studies by the National 

Bureau of Standards123 and by the Consumer Product Safety Commission124

 showed a continuing 

decrease in the number of interior paints with lead 

levels greater than 1 percent. By 1974, only 2 percent of the interior paints sampled were found to 

have greater than 1 percent lead in the dried film.124 

The level of lead in paint in a residence that 

should be considered a hazard remains in doubt. Not 

only is the total amount of lead in paint important, 

but also the accessibility by a child of the painted 

12-33 
P.43 

surface as well as the frequency of ingestion. Attempts to set an acceptable lead level, in situ, have 

been unsuccessful and preventive control of lead 

paint hazards has been concerned with levels of lead 

in paint currently manufactured. In one of its 

reviews, NAS concluded: '"Since control of the lead 

paint hazard is difficult to accomplish once multiple 

layers have been applied in homes over two to three 

decades, and since control is more easily regulated 

at the time of manufacture, we recommend that the 

lead content of paints be set and enforced at time of 

manufacture."125 

Legal control of lead paint hazards is being attempted by local communities through health or 

housing codes and regulations. At the Federal level, 

the Department of Housing and Urban Development has issued regulations for lead hazard abatement in housing units assisted or supported by its 

programs. Generally, the lead level considered 

hazardous ranges from 0.5 to 2.5 mg/cm2, but the 

level of lead content selected appears to be dependent more on the sensitivity of field measurement by 

different regulatory bodies (using X-ray fluorescent 

lead detectors) than on direct biological doseresponse relationships. Regulations also require 

lead hazard abatement when the paint is loose, flaking, peeling, or broken, or in some cases when it is on 

surfaces within reach of a child's mouth. 

Some studies have been carried out to determine 

the distribution of lead levels in paint in residences. 

A survey of lead levels in 2370 randomly selected 

dwellings in Pittsburgh provides some indication of 

the lead levels to be found.126 Figure 12-9 shows the 

distribution curves for the highest lead level found 

in dwellings for three age groupings. The curves bear 

out the statement often made that paint with high 

levels of lead is most frequently found in pre 1940 

residences. One cannot assume, however, that high 

level lead paint is absent in dwellings built after 

1940. In the case of the houses surveyed in Pittsburgh, about 20 percent of the residences built after 

1960 have at least one surface with more than 1.5 

mg/cm2 lead. 

The distribution of lead within an individual 

dwelling varies considerably. Figure 12-10 presents 

the distribution of the highest paint lead measurements on walls, doors, and windows for all the 

buildings sampled. These data show that the lead is 

not uniformly distributed throughout the units. Lead 

paint is most frequently found on doors and windows where lead levels greater than 1.5 mg/cm2

 were 

found on 2 percent of the surfaces surveyed, whereas 

Al 

LEAD LEVEL (X). mg/cm 

Figure 12-9. Cumulative distribution of lead levels in dwelling 

units:*" 

only about l percent of the walls had lead levels 

greater than 1.5 mg/cm2.

126 

The literature120 generally accepts the premise 

that the presence of lead in paint is a necessary but 

not sufficient condition for a hazard to be present. 

Accessibility in terms of peeling, flaking, or loose 

paint is also a necessary condition for the presence of 

a hazard. Figure 12-11 shows the distribution of 

lead levels and nonintact conditions for dwellings 

and surfaces for the Pittsburgh sample. Of the total 

samples surveyed, about 14 percent of the residences 

would have accessible paint with a lead content 

greater than 1.5 mg/cm2. 

It is not possible to extrapolate the results of the 

Pittsburgh survey nationally; however, additional 

data from a pilot study of 115 residences in Washington. D.C. showed similar results.127 

An attempt was made in the Pittsburgh study to 

obtain information about the correlation between 

12-34 
Al 

10

 r—i—,— 

0.9 

0.8 

0.7 

0.6 

0.5 

0.4 

0.3 

0.2 

0.1 

1 

1 

i 

1'. 

y, 

\\\ 

IM 

M 

" * \ 

1 M 

1 M 

" 1 \\ 

1 *K 1 M - 1 \\ 

I VjW-DOORS 

r- \ A \ U 

\ n 

\ \ 

" i 

i i i 

I i """?"" 

-

_ 

-

-

LEAD LEVEL (X), mg/cm 

Figure 12-10. Cumulative distribution ol lead levels by location in dwelling, all ages.126 

the quantity and condition of lead paint in buildings 

and the blood lead of children who resided there.128 

Blood lead analyses and socioeconomic data for 456 

children were obtained along with the information 

about lead levels in the dwelling. Figure 12-12 

shows-the cumulative distribution of the blood lead 

levels for this group. Figure 12-13 is a plot of the 

blood lead levels versus the fraction of surfaces 

within a dwelling with lead levels of at least 2 

mg/cm2. Analysis of the data shows a low correlation 

between the blood lead levels of the children and 

fraction of surfaces with lead levels above 2 mg/cm2, 

but a stronger correlation between the blood lead 

levels and condition of the painted surfaces in the 

dwelling in which children reside. This latter correlation appeared to be independent of the lead 

levels in the dwellings. 

Two other studies have attempted to relate blood 

lead levels and paint lead as determined by X-ray 

fluorescence. Reece et al. in Cincinnati studied 81 

LEAD LEVEL (XI. mg/cm* 

Figure 12-11. Cumulative distribution of lead levels in dwelling units with unsound paint conditions.126 

children from two lower socioeconomic communities.129

 Blood leads were analyzed by the 

dithizone method. There was considerable lead in 

the home environment, but it was not reflected in the 

children's blood lead. Analytic procedures used to 

test the hypothesis were not described; neither were 

the raw data presented. 

Galke et al. in their study of inner-city black 

children measured the paint lead, both interior and 

exterior, as well as soil and traffic exposure.43 In a 

multiple regression analysis, exterior siding paint 

lead was found to be significantly related to blood 

lead levels. 

Although most of the evidence indicates that the 

source of exposure in childhood lead poisoning is 

almost invariably peeling lead paint and broken 

lead-impregnated plaster found in poorly main12-35 
P.45 

5 ioo 

5 80 

"TT" ~n—r—i—i i i i i i i—i—i— i i i i i i -| 

STD. DEV. = 1.39 

MEDIAN =20.7wg/dl 

\ I I I I I I I I I 1 I I I I I 

Figure 12-12. Cumulative frequency distribution of blood lead 

levels found in Pittsburgh housing survey.126 

The findings are presented in order to place in 

proper perspective both the concept of total lead exposure and the concept that lead paint is one source 

of lead that contributes to the total body load. The 

background contribution of lead from other sources 

is still not known even for those children for whom a 

potential lead-paint hazard has been identified; nor 

is it known what proportion of lead came from which 

source. 

TABLE 12-37. RESULTS OF SCREENING AND HOUSING 

INSPECTION IN CHILDHOOD LEAD POISONING CONTROL 

PROJECT BY FISCAL YEAR"1.

1

" 

z > 

UJ LJJ 

Q 20 

O 

o 

I I I I I I I I 

SURFACES IN BAD CONDITION, i.e., PEELING 

_ CHALKING, OR POOR SUBSTRATE 

ALL SURFACES 

* • 

I I I I 

• 

'I I I 

o 

I I 

-

— —• — 

I 

Fiscal year8 

Results 1976'" 197513' 1974"' 

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0 

FRACTIONS OF SURFACES WITH LEAD > 2 mg/cm2 

Figure 12-13. Correlation of children's blood lead levels with 

fractions of surfaces within a dwelling having lead concentrations 22 mg Pb/cm2

. 

tained houses, there are also reports of exposure 

cases that cannot be equated with the presence of 

lead paint. Further, the analysis of paint in homes of 

children with lead poisoning has not consistently 

revealed a hazardous lead content.120 For example, 

one paper reported 5466 samples of paint obtained 

from the home environment of lead poisoning cases 

in Philadelphia between 1964 and 1968. Among 

these 5466 samples of paint, 67 percent yielded positive findings defined as paint with more than 1 percent lead.130 

Data published or made available by the Center 

for Disease Control, Department of Health, Education, and Welfare, also show that a significant number of children with undue lead absorption occupy 

buildings that were inspected for lead-based paint 

hazards, but in which no hazard could be demonstrated.131132

 Table 12-37 summarizes the data obtained from the HEW funded lead-based paint 

poisoning control projects for fiscal years 1974, 

1975, and 1976, plus the transition quarter July 1, 

1976 to September 30, 1976. These data show that in 

about 40 to 45 percent of confirmed cases of elevated blood lead levels, a possible source of lead 

paint hazard could not be located. The implications 

of these findings are not clear. They should not, 

however, weaken the role of lead-based paint as a 

major environmental source of lead for children. 

No. children 

screened 

No. children 

with elevated 

lead exposure 

No. dwellings 

inspected 

No. dwellings 

with lead 

hazard 

500,463 440,650 371,955 

69,131" 28,5971= 16,228<= 

50,276 30,227 23,096 

28,333 17,609 13,742 

a

 Fiscal year 1976 includes transition quarter. 

bCDC Classes ll-IV. 

0

 Confirmed blood lead level if"40 ug/dl. 

12.3.5 Secondary Exposure of Children from 

Parents' Occupational Exposure 

Excessive intake and absorption of lead for 

children can result when a parent who works in a 

dusty environment with a high lead content brings 

dust home on his clothes, shoes, or even his automobile. Once home, this dust is then available to his 

children. 

Excessive intake and absorption also can occur 

when children voluntarily ingest nonfood items, 

such as clay, plaster, or paint chips. This is the classical pica, which refers to the intentional ingestion of 

nonfood material rather than to the passive, nonintentional ingestion of dust from a dirty finger or 

piece of candy that has been dropped and thus contaiminated. 

Landrigan et al.62 reported that the 174 children 

of smelter workers who lived within 24 km of the 

smelter had significantly higher blood lead levels, a 

mean of 55.1 figldl, than the 511 children of persons 

in other occupations who lived in the same areas 

whose mean blood lead level was 43.7 figldl. 

Analyses by EPA staff of the data collected in 

Idaho showed that employment of the father at the 

lead smelter, at a zinc smelter, or in the lead mine 

12-36 
resulted in higher blood lead levels in the children 

living in the same house with such fathers than 

children whose fathers were employed in different 

locations (Table 12-38). 

TABLE 12-38. GEOMETRIC MEAN BLOOD LEAD LEVELS 

(Mg/dl) OF CHILDREN BY PARENTAL EMPLOYMENT 

(EPA analysis of 1974 data) 

Age and 

study 

area 

1 to 3 

years 

1 

2 

3 

4 

5 

6 

4 to 9 

years 

1 

2 

3 

4 

5 

6 

Lead smelter 

worker 

77.1(12)=* 

56.8(11) 

33.7(6) 

29.6(4) 

— 

— 

73.6(32) 

49.6(21) 

33.3(21) 

30.9(4) 

24.5(2) 

— 

Lead/zinc 

mine worker 

65.7(25) 

53.5(21) 

54.5(15) 

36.0(16) 

31.8(29) 

— 

65.8(28) 

43.8(32) 

35.5(39) 

33.0(53) 

27.1(79) 

— 

Zinc smelter 

worker 

66.3(11) 

55.1(6) 

32.3(2) 

41.7(4) 

— 

— 

59.3(16) 

51.9(4) 

35.2(7) 

35.6(5) 

— 

— 

Other 

occupation 

65.9(13) 

48.5(30) 

34.8(26) 

31.5(22) 

27.2(16) 

22.4(34) 

59.2(33) 

44.9(67) 

32.1(58) 

29.1(44) 

26.4(60) 

20.5(56) 

a

 Sample sizes in parentheses. 

The effect associated with parental employment 

appears to be much more prominent in the most contaminated study areas nearest to the smelter. This 

may be the effect of an intervening socioeconomic 

variable: the lowest paid workers, employed in the 

highest exposure areas within the industry, might be 

expected to live in the most undesirable locations, 

which are closest to the smelter. 

The importance of the infiltration by lead dusts 

into clothing, particularly the undergarments, of 

lead workers has been demonstrated in a number of 

studies of the effects of smelters.133 It was noted in 

the United Kingdom that elevated blood lead levels 

were found in the wives and children of workers 

even when they resided some considerable distance 

from the facility. It was most prominent in the 

families of workers who themselves had elevated 

blood lead levels. Quantities of lead dust were found 

in workers' cars and homes. It apparently is not 

sufficient for a factory merely to provide outer protective clothing and shower facilities for lead 

workers. In another study in Bristol, from 650 to 

1400 ppm of lead was found in the undergarments of 

workers as compared with 3 to 13 ppm in undergarments of control subjects. Lead dust will remain on 

the clothing even after laundering: up to 500 mg of 

lead has been found to remain on an overall garment 

after washing.134 

Baker et al.135 found blood lead levels >30 figldl 

in 38 of 91 children whose fathers were employed at 

a secondary lead smelter in Memphis, Tenn. Housedust, the only source of lead in the homes of these 

children, contained a mean of 2687 figlg compared 

with 404 figlg in the homes of a group of matched 

controls. Mean blood lead levels in the workers' 

children were significantly higher than those for 

controls and were closely correlated with the lead 

content of household dust. In homes with lead in 

dust < 1000 figlg, 18 children had a mean blood 

lead level of 21.8 ± 7.8 figldl, whereas in homes 

where lead in dust was >7000 figlg, 6 children had 

a mean blood lead level of 78.3 ± 34.0 figldl. 

Landrigan et al.62 also reported a positive history 

of pica for 192 of the 919 children studied in Idaho. 

This history was obtained by physician and nurse interviews of parents. Pica was most common among 

2-year-old children and only 13 percent of those 

with pica were above age 6. Higher blood lead levels 

were observed in children with pica than in those 

without pica. Table 12-39 shows the mean blood 

lead levels in children as they were affected by pica, 

occupation of the father, and distance of residence 

from the smelter. It is interesting that, among the 

TABLE 12-39. GEOMETRIC MEAN BLOOD LEAD LEVELS FOR CHILDREN BASED ON REPORTED OCCUPATION OF FATHER, 

HISTORY OF PICA, AND DISTANCE OF RESIDENCE FROM SMELTER" 

Area 

1 

2 

3 

4 

5 

6 

Distance 

Irom 

smeller, km 

1.6 

1.6 to 4.0 

4.0 to 10.0 

10.0 to 24.0 

24.0 to 32.0 

75. 

Pica 

78.7 

50.2 

33.5 

— 

— 

— 

Lead 

smelter 

worker 

No 

pica 

74.2 

52.2 

33.3 

30.3 

24.5 

— 

Lead/zinc mine 

Pica 

75.3 

57.1 

36.7 

38.0 

31.8 

— 

worker 

No 

pica 

63.9 

46.9 

33.5 

32.5 

27.4 

— 

Zinc smelter 

Pica 

69.7 

62.7 

36.0 

40.9 

— 

— 

worker 

No 

pica 

59.1 

50.3 

39.6 

36.9 

— 

— 

Other 

occupations 

No 

Pica pica 

70.8 59.9 

37.2 46.3 

33.3 32.6 

— 39.4 

28.0 26.4 

17.3 21.4 

12-37 
P.47 

populations living nearest to the smelter, environmental exposure appears to be sufficient at times to 

more than overshadow the effects of pica, but this 

finding may also be caused by inadequacies inherent 

in collecting data on pica. 

These data indicate that in a heavily contaminated 

area, blood lead levels in children may be significantly increased by the intentional ingestion of nonfood materials having a high lead content. 

Data on the parents' occupations are, however, 

more reliable. It must be remembered also that the 

stud y area s wer e no t homogeneou s 

socioeconomically. In addition, the type of work an 

individual does in an industry is probably much 

more important than simply being employed in a 

particular industry. The presence in the home of an 

industrial employee exposed occupationally to lead 

may produce increases in the blood lead levels ranging from 10 to 30 percent. 

12.3.6 Miscellaneous Sources of Lead 

Although no studies are available, it is conceivable that destruction of lead-containing plastics (to 

recover copper), which has caused cattle poisoning, 

also could become a source of lead for humans. A 

more general problem is waste disposal, because 

lead-containing materials may be incinerated and 

may thus contribute to increased air lead levels. This 

source of lead has not been studied in detail. 

The consumption of illicitly distilled liquor has 

been shown to produce clinical cases of lead poisoning. Domestic and imported earthenware with improperly fired glazes have also been related to clinical lead poisoning. This source becomes important 

when foods or beverages high in acid are stored in 

containers made from these materials because the 

acid releases lead from the walls of the containers. 

Particular cosmetics popular among some Oriental and Indian ethnic groups contain high percentages of lead that sometimes are absorbed by users in 

quantities sufficient to be toxic. 

12.4 SUMMARY 

Blood lead levels in homogeneous human populations have almost invariably been found to be lognormal. A number of such data sets were examined 

and they displayed a geometric standard deviation 

(GSD) ranging from 1.3 to 1.5. 

From the lognormal distribution, given a mean 

blood lead level and an estimated geometric standard deviation, it is possible to predict the percentages of a population whose blood lead levels exceed 

a specified value. It is also possible to estimate the 

likely increase in mean blood lead levels for a 

population exposed to specific increases in environmental lead. Coupling these two procedures provides a method by which standards may be chosen to 

protect the health of the population. 

Blood lead levels have been found to exhibit considerable geographic variability. Generally they are 

lowest in rural settings, higher in suburban areas, 

and highest in inner-city areas. These values follow 

the presumed lead exposure gradient. Blood lead 

values were also found to vary by age, sex, and race, 

although in a somewhat more complex fashion. 

Generally, young children have the highest levels, 

with little difference between sexes. In older segments of the population, after eliminating occupational exposure in lead workers, males have a higher 

blood lead than females. The published data comparing the blood lead levels of various racial and 

ethnic groups of the population suggest that blacks 

have higher blood lead levels than whites, with 

Puerto Ricans sometimes at an intermediate level. 

Results of the numerous studies of environmental 

exposures of man have indicated strongly that man 

does indeed take up lead from each source to which 

he is exposed. Equally important, these studies have 

shown that the blood lead level is the summation of 

the absorption from each of these sources. 

Data for the two most widespread environmental 

sources other than food permit summary statements 

concerning their quantitative relationship with 

blood lead levels: ratios between blood lead levels 

and air lead exposures were shown to range 

generally from 1:1 to 2:1. These were not, however, 

constant over the range of air lead concentrations 

encountered. There are suggestive data indicating 

that the ratios for children are in the upper end of 

the range and may even be slightly above it. There is 

also some slight suggestion that the ratios for males 

are higher than those for females. 

For soil lead exposures, a consistent association 

with blood lead levels has been established. 

Children exposed to higher soil and housedust lead 

concentrations have been shown to have elevated 

concentrations of lead on their hands, but an association of elevated blood lead levels with elevated 

hand lead levels has not yet been established. Quantitatively, blood lead levels have been shown to increase 3 to 6 percent when the soil or dust lead content is doubled. 

Significant water lead exposures in this country 

have occurred only in places using leaded pipes 

coupled with a soft water supply. Such exposures 

have been shown to be associated with significant 

12-38 
elevations of blood lead. They have also been linked 

to cases of mental retardation. 

Exposure to leaded paint still comprises a very 

serious problem for American children in urban settings. Although new regulations governing the lead 

content of paint should alleviate the problem in new 

housing, the poorly enforced regulation and lack of 

regulation of the past have left a heavy burden of 

lead exposures from paint. Most of the studies on 

lead poisoning in children have assumed an association with leaded paint, but very rarely have these 

studies measured the amount of exposure. There is, 

nevertheless, strong suggestive evidence that the 

contribution from this source can be very significant. 

Lead exposure via food is thought to be the source 

of a significant portion of blood lead. Direct quantitative equations describing the relationship of 

blood to food lead levels have not been published, 

but studies described in Chapter 10 do address this 

relationship. 

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86. Griffin, T. B., F. Coulston. H. Wills, J. C. Russell, and J. 

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88. Kehoe, R. A. The metabolism of lead in man in health and 

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90. Rabinowitz, M. B. Lead contamination of the biosphere 

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Kinetic analysis of lead metabolism in healthy humans. J. 

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94. Williams, M. K., E. King, and J. Walford. An investigation 

of lead absorption in an electric accumulator factory with 

the use of personal samplers. Brit. J. Indus. Med. 

26:202-216, 1969. 

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means when several dose levels are compared with a zero 

dose control. Biometrics. 27:103-117. March 1971. 

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Board's Subcommittee on Scientific Criteria for Environmental Lead. Washington, D. C. January 31, 1977. 

99. Fairey, F. S. and J. W. Gray III. Soil lead and pediatric 

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Significance of high soil lead concentrations for childhood 

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12-42 
128. Urban, W. D. Statistical Analysis of Blood Lead Levels of 

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lead levels and the in situ analysis of wall paint by X-ray 

fluorescence. Amer. J. Dis. Child. 724:500-502, 1972. 

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Med. 296:260-261, 1977. 

12-43 
P.53 

13. EVALUATION OF HUMAN HEALTH RISKS 

1

 FROM EXPOSURE TO LEAD AND ITS COMPOUNDS 

13.1 INTRODUCTION 

The preceding chapters of this document have described lead production, the eonomics of lead 

utilization, the dispersion of lead in the environment — particularly in air, dust, and soil —and, 

finally, have reviewed the effects of lead on the 

health of man. Although attempting to relate these 

various issues to one another, this chapter 

specifically will attempt to assess and to quantitate 

the health effects that arise from exposure of man to 

lead in the environment and, more precisely, from 

exposure to lead in air. Six central questions to be 

addressed are as follows: 

1. What are the sources of lead in the environment? (Sections 13.2 and 13.3) 

2. What are the routes and mechanisms by 

which lead from these sources enters the 

body? (Sections 13.2 and 13.3) 

3. What part do averaging times for these exposures play? (Section 13.4) 

4. How does the body respond to the entrance 

of lead? (Section 13.5) 

5. Are there groups within populations which 

are particularly vulnerable to lead? (Section 

13.6) 

6. What is the magnitude of the risk exposures 

in terms of the number of persons exposed in 

various subgroups of populations? (Section 

13.7) 

Each of the above questions is addressed separately 

as a subsection of this chapter, and the relevant section is noted beside each question. 

Now that the questions to be addressed in this 

treatment of risk assessment have been outlined, it is 

necessary to define the terms which will be 

employed. These include: 

1. Dose is the amount or concentration of a 

chemical that is presented over time to an 

organism, organ, cell, or subcellular component. Ideally, dose should be defined as the 

amount or concentration of the chemical at a 

specific intracellular site of effect. 

2. External dose is the amount of the contaminant in the external environment (air, water, 

food, etc.) to which humans are exposed. 

3. Effective dose or internal dose is the amount 

of the contaminant absorbed by the body. 

4. Effect is a biologic change which results from 

exposure to a chemical. 

5. Dose-effect relationship is a quantitative 

relationship between the dose and the 

specific effect that is established after gradations in the severity of an effect have been 

measured. 

6. Critical effect is the first adverse functional 

change, reversible or irreversible, to be 

caused by exposure to a particular chemical. 

7. Subcritical effect is a change that is 

demonstrable by biochemical or other test, 

but which does not appear to impair function; some such changes may be adaptive in 

nature. 

8. Critical dose or critical concentration is the 

level of a chemical at which the critical effect 

appears. 

9. Critical organ is the organ which manifests 

the critical effect; it need not be the organ 

with the highest concentration of the chemical nor that which ultimately suffers the most 

serious injury. 

Dose-effect relationships will vary among the 

members of a population. Response is the proportion of the population that manifests a particular 

effect at a particular dose level.1 This is a more 

restrictive definition of response than that used in 

bioassay as described by Finney.2 The relationship 

between dose and the proportion responding is the 

dose-response relation, which will most commonly 

be expressed by a sigmoid-shaped curve. 

13.2 SOURCES, ROUTES, AND MECHANISMS OF ENTRY 

13.2.1 Sources 

Of the estimated 161,225 metric tons of lead emit13-1 
P.54 

ted into the atmosphere in 1975, the combustion of 

gasoline additives and waste oil accounted for 95 

percent of total inventoried emissions. Each of the 

remaining emission sources accounts for only a 

small part of the total quantity of lead, but has the 

potential of creating localized situations of high air 

lead concentrations, e.g., primary lead smelters. 

Once lead is introduced into the air it undergoes a 

variety of processes including dry deposition, precipitation, and resuspension. These processes result 

in a variable proportion of lead being retained in the 

air and then being distributed over a wide area. 

Other portions are deposited on land, in dust, and on 

water, resulting in increased lead concentrations in 

each. 

Other uses of lead result in additional human exposure. The addition of lead to paint makes lead 

directly available by ingestion of paint chips and 

paint-saturated plaster. In addition it becomes indirectly available through dust contaminated with 

lead freed by the weathering process of paint. This 

primary source is currently under regulation, but a 

vast stock of housing painted with high-lead-content 

paint still exists. 

Lead's malleability and ductility have resulted in 

the use of this metal in pipes for carrying drinking 

water. When such pipes are used in areas with soft 

water of low pH, a potential exists for heavy lead 

contamination of drinking water. It is difficult to 

estimate the overall magnitude of this danger, but 

there have been specific localized examples in the 

United States. 

A final quantitatively significant source of lead is 

the human diet. Lead present in foodstuffs is the sum 

of the amount present in the raw foodstock and of 

lead introduced via processing and packaging. Canned products such as vegetables and milk have been 

shown to contain higher quantities of lead than the 

same products packaged differently. This is due, in 

part, to the presence of lead solder in the seams of 

cans. Baby foods have also been shown to have higher lead contents because of the preservatives used. 

The origin of lead in raw food stocks is still a matter 

of some controversy, although part of it is likely to 

be the consequence of man's activities which result in 

making lead available for uptake by animals and 

plants. Such redistribution and subsequent uptake of 

lead by plants is well illustrated by fivefold increases 

in the amount of lead present in tree rings over a 50-

year period. 

It is important to realize that human exposure and 

intake are not limited to the primary sources of lead 

in the environment but, rather, to the sum of primary, secondary, and tertiary sources. Table 13-1 displays these sources. 

TABLE 13-1. SOURCES OF LEAD FOR HUMAN EXPOSURES 

Primary 

exposure 

source 

Air 

Paint 

Water from 

leaded pipes 

Food 

aReentrainment 

Secondary 

exposure 

source 

Dust and 

soil 

Water 

Dust and 

soil 

Tertiary 

exposure 

source 

Food 

Runoff water 

Aira 

Runoff water 

Aira 

13.2.2 Routes and Mechanisms of Entry 

Chapter 10 presents data on the entry of lead into 

the human body. Two routes of entry are of principal 

importance, inhalation and ingestion. Intake of airborne lead is governed by the physical and chemical 

state of inhaled lead, particle size retention in the 

lung, and absorption from the lung into the red 

blood cells. 

The second major route of entry is ingestion, both 

of food and of nonfood material. Uptake is controlled by the nutrient balance of the food ingested, 

particularly that of iron, by the physical nature of 

the lead-bearing material ingested, and by the 

chemical composition of the substance. Here, too, 

the lead is absorbed by circulating red blood cells. 

The total internal dose of lead which confronts the 

organ systems of the body is the sum of the lead intake by both routes of entry: inhalation and ingestion. Thus the total internal dose represents the summation of all external sources to which the body is 

exposed. Some of these exposures may be of 

different relative significance in diverse population 

groups due to variances in metabolism or behavior 

among different segments of the population. 

13.3 EVIDENCE OF INCREASED BLOOD 

LEAD LEVELS IN HUMANS EXPOSED TO 

ENVIRONMENTAL LEAD 

13.3.1 Relationships Between Blood Lead Levels 

and Single-Source Exposures 

Research has been conducted on all six major exposure sources — air, dust, soil, water, paint, and 

food. Chapter 12 provided the detailed description, 

evaluation, and findings of those studies. Not all 

sources have been studied with the same intensity, 

13-2 
P.55 

and food has been studied least. In addition, food as 

a tertiary exposure source is difficult to evaluate. 

Lead content in food due to packaging and processing has been studied more thoroughly than contribution from that lead present at the point of origin. 

Single-source studies of air have included both 

epidemiological and clinical investigations. Clinical 

data uniformly demonstrate the actual uptake of airborne lead into blood, and epidemiologic data also 

generally support such a relationship. 

Studies concerned with dust and soil lead exposures will be considered together since in many 

studies the investigators did not attempt to deal with 

these sources separately. Considerable evidence exists that these exposures can be significant determinants of blood lead levels. Furthermore, investigations of children exposed to lead-contaminated dust 

have demonstrated more lead on the children's 

hands, thus documenting a plausible route of entry 

which is due to normal oral behavior in young 

children. It may be worth reiterating here that the 

dose of lead ingested from dust and soil appears to 

be additive to that inhaled from air. 

The popular assumption that lead-based paint is 

the single causative agent of elevated blood lead 

levels in children has resulted in limiting the definition of high-risk children to those residing in older 

housing. As a result, lead screening programs have 

been established with the sole purpose of identifying 

children with elevated lead levels among those living in old housing. Abatement efforts have frequently been unable to find lead paint sources for 

children with high blood levels found by such 

screening programs. The possible contributory role 

of airborne lead to the lead burden of urban 

children has until recently received little attention. 

Finally, studies from Glasgow and Boston have 

shown elevated blood lead levels in conjunction 

with elevated levels of lead in the drinking water. 

Secondary effects of occupational exposure have 

been examined in children whose parents work in 

lead industries. It has been found that parents carry 

home lead-contaminated dust. Significant relationships between house dust levels and blood lead 

levels have invariably been established in these 

studies. 

13.3.2 Multiple-Source Exposures 

Studies measuring the quantity of lead in multiple 

sources, around primary lead smelters or in urban 

settings, have consistently demonstrated an additive 

relationship between blood lead levels and exposure 

to the several sources studied. 

13.3.3 Effect of Host Factors on Blood Lead 

Levels 

Host characteristics that mediate the relationship 

between exposure to lead and blood lead level have 

been examined in several studies. In particular, age 

has been shown to be a significant factor in determining blood lead levels; this relationship is discussed below in more detail in the section (13.6) on 

populations at greatest risk. 

Sex differences have been found to be age related. 

Particularly among preschool boys and girls, virtually no difference has been established. In the 

adult population, however, males generally exhibit 

higher levels than females. 

Data on the racial/ethnic factor are sparse. One 

study has reported.that black children have higher 

lead levels than do white children. Although the significance of the racial/ethnic factor cannot be established at this time, it seems reasonable to assume that 

it is the socioeconomic rather than the genetic 

dimension of this variable that may prove to be relevant. 

Socioeconomic variables such as income and 

education have not been examined adequately as independent factors. Associated characteristics such as 

residence in old housing, or proximity to high-density traffic arteries or to stationary sources such as 

smelters, have been shown to be directly relevant. 

In epidemiological studies the health status as a 

variable has not been examined. Conditions such as 

iron deficiency anemia, other states of malnutrition, 

sickle cell anemia, and lactose intolerance as host 

factors in lead intake and determinants of 

physiological and pathological changes have only 

recently come under study. No findings are available 

as yet. 

13.3.4 Summary of the Quantitative Relationship 

Statistical evaluation of the data collected from 

population and clinical studies has been presented in 

the previous chapter. There it was noted that the 

weight of the evidence indicates that blood lead 

levels follow a lognormal distribution in exposed 

populations with a geometric standard deviation of 

1.3 to 1.5. It was also seen that the lognormal distribution has properties that make it amenable to use in 

the standard-setting process, since it permits an estimate of the proportion of the population whose 

blood lead levels exceed any specified level. 

Detailed examination of the clinical and 

epidemiological studies relating air lead levels to 

blood lead levels is presented in Chapter 12. Evidence indicates that a positive relationship exists be13-3 
P.56 

tween blood and air lead levels, although the exact 

functional relationship has not yet been clarified. 

Available data indicate that in the range of air lead 

exposures generally encountered by the population, 

the ratio of the increase in blood lead per unit of air 

lead is from 1 to 2. It appears that the ratio for 

children is in the upper end of the range and that 

ratios for males may be higher than those for 

females. 

Quantitative relationships can also be established 

between blood lead levels and exposure to lead in 

soil. There is general agreement that blood lead 

levels begin to increase at soil lead levels of from 

500 to 1000 ppm. Mean percent increases in blood 

lead levels, given a twofold increase in soil lead 

levels, ranged from 3 to 6. This is a remarkable consistency, given the divergence of the populations 

studied. 

13.4 AVERAGING-TIME CONSIDERATIONS 

One of the major areas of concern in dealing with 

quantitation of the relationship between a health 

effect and an external dose of some environmental 

pollutant is the determination of how long an exposure must occur before there is an effect. 

Evidence presented in Chapter 12 indicates that a 

5 figldl increase in blood lead can result from an air 

lead exposure of 3.2 /ug/m3 for a period of 7 weeks. 

Furthermore, FEP levels have been shown to increase within 2 weeks of an increase of blood lead 

levels. Therefore, an air lead exposure of 3.2 figlm3 

lasting about 1 to 2 months can definitely increase 

the blood lead level. 

13.5 BIOLOGICAL AND ADVERSE HEALTH 

EFFECTS OF LEAD IN MAN 

Lead does not presently have associated with it 

any biological effect in man which can be considered 

beneficial; therefore, any consideration of the health 

effects of lead in man must be done from a point of 

view that acknowledges the absence of any health 

benefit/health cost ratio. 

An additional and extremely important aspect of 

lead's effect on health impairment that must be considered in risk assessment is the question of whether 

these effects are reversible once present. 

Physiological damage to central nervous system 

tissue is presently widely accepted as being irreversible; thus prevention of lead exposure is most urgent 

when one considers severe neurological effects. 

Irreversibility is also accepted in the case of renal 

tissue damage resulting from chronic lead exposure, 

particularly in cases where these effects are 

manifested morphologically. 

We speak of physiological irreversibility in the 

cases of neurological or renal tissues, but the concept of irreversibility of an effect being likely or 

assured by nonbiological factors such as continuing, 

long-term exposure to airborne lead must also be 

considered. Hematological effects are of relevance 

here. Although a number of these hematological 

effects may be biochemically reversible, if the probability of the person being removed from the exposure setting inducing these effects is slight or nonexistent, for whatever reason, then defacto irreversibility exists. 

This section summarizes the biological effects of 

lead on man with particular reference to significance 

of these effects for human health. Much of the attention in this section will be directed to those biological effects which may collectively be termed 

"subclinical." By definition, subclinical effects are 

disruptions in function, which may be demonstrated 

by special testing but not by the classic techniques of 

physical examination; using the term "subclinical" 

in no way implies that those effects are without consequences to human health. 

13.5.1 Assessment of Hematological Effects of 

Lead 

A multiplicity of effects of lead on the 

hematopoietic system exists. These effects were discussed in detail in Chapter 11, Section 3, and are 

briefly summarized here. 

13.5.1.1 ANEMIA 

Anemia is a classic manifestation of clinical lead 

intoxication, often occurring prior to neurological 

and other system impairment. The mechanism of 

anemia in lead exposure apparently involves both 

decreased production of hemoglobin and enhanced 

destruction of erythrocytes. Reports on children indicate that statistically significant decreases in 

hemoglobin levels begin to appear at a blood lead 

level of 40 figldl or somewhat below. In adults a significant decrease in hemoglobin level appears to 

become evident at a blood lead level of 50 figldl. 

13.5.1.2 LEAD EFFECTS ON HEME SYNTHESIS 

A large number of studies have been done on the 

effects of lead on heme synthesis in humans. Lead 

interferes with heme synthesis at several points along 

the heme-biosynthetic pathway. The two most important points of interference are: (1) the condensation of two units of 8-aminolevulinic acid 

dehydratase to form porphobilinogen and (2) the in13-4 
sertion of iron into protoporphyrin IX which is 

catalyzed by the enzyme ferrochelatase. 

13.5.1.3 EFFECT OF LEAD ON 8-AMINOLEVULINATE DEHYDRATASE (8-ALAD) 

AND 8-AMINOLEVULINIC ACID (8-ALA) EXCRETION 

A number of studies have shown the high sensitivity of 8-ALAD to lead and the negative correlation between blood lead and the logarithm of 8-

ALAD activity. These studies are described in Section 11.3. It appears that this relationship holds true 

for industrial workers, the general population, and 

children. 

The dose-response relationship between blood 

lead and the logarithm of ALAD activity appears to 

be linear coefficient of correlation (r) = 0.84. 

ALAD inhibition is first noted at whole blood levels 

of 10 to 20 figldl (Chapter 11). This high degree of 

sensitivity makes application and interpretation of 

the test difficult. ALAD inhibition is virtually complete at blood lead levels of 70 to 90 figldl. 

Data summarized by Hernberg3 suggest that heme 

biosynthesis is not decreased by ALAD inhibition 

until activity of the enzyme has fallen to less than 20 

to 30 percent of normal. In addition to its effect on 

red blood cell ALAD, lead appears to inhibit 

ALAD activity in liver. It has also been suggested 

that in young children lead may inhibit activity of 

ALAD in brain. 

13.5.1.4 EFFECT OF LEAD ON IRON INSERTION INTO PROTOPORPHYRIN 

Accumulation of protoporphyrin in erythrocytes 

in lead exposure is the result of lead-induced inhibition of the intramitochondrial enzyme, ferrochelatase. The inhibitory effect of lead on ferrochelatase may either be direct or may be mediated 

by a disruption in the function of mitochondrial 

membranes. 

The effect of lead on the formation of heme is not 

limited to the hematopoietic system. Experimental 

animal studies have shown a lead effect on the hemerequiring protein, cytochrome P-450, an integral 

part of the hepatic mixed-function oxidase (Chapter 

11), the systemic function of which is detoxification 

of exogenous substances. Heme synthesis inhibition 

also takes place in neural tissue. 

The elevation of free erythrocyte protoporphyrin 

(FEP) has been shown by a large number of studies 

to be exponentially correlated with blood lead level 

in children and adults. 

Present information shows that at relatively fixed 

blood lead values children and probably women 

have higher protoporphyrin levels in their blood 

than adult males. The exact reason for this is not 

known, but it may be of endocrinological origin. 

Elevation in protoporphyrin is considered not 

only to be a biological indicator of impaired 

mitochondrial function of erythroid tissue but also 

an indicator of accumulation of substrate for the 

enzyme ferrochelatase. It therefore has the same 

pathophysiological meaning as increased urinary 8-

ALA (vide supra). For these reasons accumulation of 

protoporphyrin has been taken to indicate 

physiological impairment in humans, and this clinical concensus is expressed in the 1975 Statement of 

the Center for Disease Control (CDC), USPHS. The 

criterion used by CDC to indicate an effect of lead 

on heme function is an FEP level of 60 /xg/dl in the 

presence of a blood lead level above 30 figldl whole 

blood. 

More recent information relating to threshold of 

lead effects indicates that FEP levels begin to increase at a blood lead value of 15 to 20 fig Pb/dl 

blood in children and women and, at a somewhat 

higher value, 20 to 25 fig Pb/d 1 blood, in adult men. 

13.5.1.5 OTHER EFFECTS ON HEME SYNTHESIS 

There are other abnormalities of heme synthesis 

that are a result of lead exposure. For example, it is 

well known that an increased urinary coproporphyrin level is found in lead poisoned children 

and lead workers. It is not known whether this effect 

results from specific enzyme inhibition, from 

upstream accumulation of substrate secondary to the 

inhibition of iron insertion into protoporphyrin, or 

from a disturbance of coproporphyrin transport 

through the mitochondrial membrane. 

An increased activity of 8-ALA synthetase is seen 

in lead intoxication, but this change probably arises 

as a negative feedback control to 8-ALA response to 

inhibition upstream in the heme-biosynthetic pathway. Few data exist to quantitate the health significance of this effect. 

13.5.1.6 EFFECTS OF LEAD ON GLOBIN SYN^ 

THESES 

Hemoglobin synthesis may also be impaired by the 

inhibition by lead of globin biosynthesis. Globin is 

the protein moiety of hemoglobin. One recent study 

shows an effect on globin synthesis in vitro on human 

reticulocytes at lead concentrations corresponding 

to a blood lead level of 20 figldl. 

13-5 
P.58 

13.5.2 Assessment of Neurobehavioral Effects of 

Lead 

As reviewed in Chapter 11, an extensive literature 

documents the adverse effects of lead on the central 

and peripheral nervous systems of many human and 

nonhuman mammalian species. Only limited doseresponse data exist that might allow external lead 

exposure parameters to be linked directly to the occurrence of particular neurobehavioral effects. In 

contrast, more data exist relating blood lead levels 

to neurobehavioral deficits; major emphasis here is 

therefore focused on the concise summarization of 

relationships between human blood lead levels and 

neurobehavioral effects. 

13.5.2.1 CENTRAL NERVOUS SYSTEM 

EFFECTS 

Among the most profoundly deleterious effects of 

lead poisoning are those associated with severe CNS 

damage that occur at toxic high exposure levels. The 

acute overt manifestations of neural damage at high 

lead exposure levels include such symptoms as irritability, stupor, convulsions, and/or coma, which 

characterize the well-known encephalopathy syndrome. Such symptoms at times occur abruptly during the course of much milder symptomatology or 

even in apparently asymptomatic lead poisoned individuals and may progress to death within 48 hr. 

Even in the absence of death or prolonged unconsciousness, it is now widely accepted that irreversible neural damage typically occurs as one of the sequelae of nonfatal lead encephalopathy episodes. 

Such permanent neural damage is reflected by signs 

of continuing CNS impairment ranging from subtle 

neurobehavioral deficits to severe mental retardation or continuing mental incompetence. What is not 

yet universally agreed upon, however, are the lead 

levels sufficient to produce lead encephalopathy and 

its sequelae. 

In regard to the issue of threshold levels for lead 

encephalopathy, blood lead levels of 120 figldl or 

more are currently widely accepted as necessary to 

produce encephalopathy symptoms in adults. The 

published evidence bearing on this point, however, is 

very limited. Included among such evidence are a 

few scattered reports suggesting that acute encephalopathy or death may occur in adults at blood 

lead levels under 100 figldl (from 80 to 100 figldl), 

but the rarity of such cases and ambiguities in the reported data render it difficult to accept those reports 

as evidence for encephalopathy in adults at blood 

lead levels below 120 figldl. 

Much better evidence exists for the occurrence of 

lead encephalopathy in children at blood lead levels 

below 120 figldl or even 100/xg/dl. That is, it is well 

documented that such symptoms occur for some 

children beginning at the 100 figldl level; also, 

several scattered reports suggest that somewhat 

lower threshold levels may obtain, i.e., in the 80 to 

100 figldl range, although such reports must be 

viewed with caution as in the case for analogous 

results for adults. 

As indicated earlier, the issue of whether apparently asymptomatic children experience subtle 

neurobehavioral deficits at low-to-moderate blood 

lead levels in the 40 to 80 /xg/dl range remains a subject of much controversy. A thorough, critical 

review of the relevant literature presented in 

Chapter 11, nevertheless, leads to the conclusion 

that blood lead levels of 50 to 60 figldl are likely 

sufficient to cause significant neurobehavioral impairments for at least some apparently asymptomatic 

children. The impairments consist mainly of cognitive or sensory-motor integration deficits, but do 

not appear to include the occurrence of hyperactivity; that latter effect seems to be much better established as one of the neurological sequelae following encephalopathy at higher lead levels. 

13.5.2.2 PERIPHERAL NEUROPATHY 

EFFECTS 

In addition to the above CNS effects, peripheral 

nervous system damage also results from exposures 

to lead. Such effects have been best documented as 

occurring after long, chronic, high-level exposures 

in adults exhibiting other symptoms of lead intoxication. Recent studies of apparently asymptomatic 

adults, usually occupationally exposed to lead, 

however, present reasonably strong evidence for peripheral neuropathy at more moderate lead exposure levels, i.e., at blood lead levels in the range 

of 50 to 70 figldl. Peripheral neuropathy effects are 

typically associated with adult exposures, having 

been reported much less frequently for children. A 

few reports of lead-induced peripheral neuropathies 

in children, however, contain evidence for the occurrence, in some rare instances, at blood lead levels 

as low as 50 to 60 figldl. 

13.5.2.3 RESULTS OF ANIMAL STUDIES AS 

SUPPORTIVE EVIDENCE 

Review of the literature on the neurobehavioral 

effects of lead in animals provides evidence supportive of the above conclusions from human studies. 

That is, there appears to be a differential sensitivity 

of newborn or young animals of many species to the 

neurobehavioral effects of lead. This applies both to 

13-6 
P.59 

the induction of lead encephalopathy at high exposure levels and more subtle neurobehavioral 

deficits at lower, more moderate exposure levels. In 

regard to specific types of subtle neurobehavioral 

effects, hyperactivity appears to occur mainly at 

blood lead levels in excess of 70 to 80 figldl and, 

therefore, probably most closely parallels the post 

encephalopathic hyperactivity well demonstrated as 

one of the sequelae of lead encephalopathy in 

humans. Other behavioral changes, interpreted as 

indicative of cognitive impairments resulting from 

CNS effects, appear to occur in animals at blood 

lead levels below those associated with acute encephalopathic effects, i.e., in the 30 to 80 /xg/dl 

blood lead level range. This parallels rather closely 

the effects observed for humans, especially children, 

except that cognitive deficits have not been very well 

documented in the children at levels below 50 to 60 

figldl. The external lead exposures yielding the 

above results for animals, however, typically appear 

to be much higher than those producing comparable 

effects in humans; the comparability of animal 

studies and human studies is therefore often questioned. If one focuses on the resulting blood lead 

levels achieved, regardless of associated external 

dose, however, the results of the animal studies 

parallel those of the human studies remarkably well. 

In discussing the neurobehavioral effects of lead, 

above in the present section and in Chapter 11, a distinction has repeatedly been made between threshold levels yielding severe symptoms of lead 

encephalopathy seen at high exposure levels and 

more subtle neurobehavioral deficits observed at 

lower exposure levels. This approach may inappropriately convey an impression of such effects occurring in a discrete, step-like fashion as particular 

threshold blood lead levels are reached. It is important to note that this may occur insofar as shifting 

from apparent no-effect levels to levels at which 

fairly well substantiated neurobehavioral effects 

have been found to occur, i.e., around 50 to 60 

figldl; beyond that point, however, further increases 

in relative levels of neural damage, as indicated by 

increasingly severe neurological or behavioral 

deficits, occur in a more or less smoothly ascending 

fashion in relation to increasing blood lead levels. 

These relationships are presented later in an 

approximate manner in Table 13-2. Due to 

differences in individual susceptibility, it should be 

emphasized that the upper end of the range of blood 

lead levels at which subtle neurobehavioral effects 

have been reported to occur for some individuals 

merges or overlaps substantially with the lower end 

of the range at which much more severe encephalopathic symptoms have been observed, and 

that the shift from subtle to severe neural symptoms 

may be quite abrupt. 

13.5.3 Effects of Lead on Reproduction and 

Development 

Although the effects of lead exposure in humans 

have usually been associated with the hematopoietic, 

neural, and renal systems, concern needs to be 

equally directed to the entire area of reproduction 

and development, with special emphasis on the 

vulnerability of pregnant women or, more accurately, the vulnerability of the fetus. 

Attention in this area is focused on two aspects of 

reproduction: (1) the gametotoxic effects of lead, 

i.e., lead effects on spermatogenesis and ovarian 

function, and (2) postconception events through 

delivery. 

13.5.3.1 HUMAN GAMETOTOXICITY 

Some data involving effects of lead exposure on 

the fertility of males exist, and these have been observed at blood lead levels of 50 to 80 /xg/dl under 

conditions of occupational exposure. With regard to 

women, one study on lead effects (see Reproduction 

and Development section, Chapter 11) raises the 

possibility that the ovarian cycle may be disturbed in 

the age range of 20 to 25 years with air lead levels 

around 7 /xg/m3. 

13.5.3.2 POSTCONCEPTION LEAD EFFECTS 

Both early literature and more current studies 

conclusively show that lead crosses the placental 

barrier. Such fetal exposure therefore commences at 

about the end of the first trimester (12 weeks) and 

continues throughout fetal development. As has 

already been pointed out, the distribution of lead 

within the fetus at different stages of development is 

probably more important than the total amount present at birth. 

Tissue analysis also demonstrates that, in Americans from newborns through persons aged 19 years, 

brain lead levels appear to be most elevated at birth 

and then diminish with development. 

A number of studies show passage of lead through 

the placental barrier by comparing cord blood lead 

and maternal blood lead levels. These studies 

further serve to shed some light on the effect of 

various factors in infant blood lead values. 

In a group of cord blood/maternal blood matchings, infant blood levels were highly correlated with 

those of their mothers. A second study showed that 

13-7 
P.60 

blood values for infants whose mothers were urban 

residents were significantly higher than those of 

rural infants. 

A study done in a lead-belt area of the United 

States raises the possibility that lead may affect the 

course of normal delivery of children since there 

were more incidents of preterm delivery and premature membrane rupture in pregnant women in this 

region compared to a group from a relatively unexposed area. 

13.5.4 Other Health Effects 

13.5.4.1 RENAL EFFECTS 

Nephropathy is a condition usually considered in 

its chronic form and that can best be related to 

prolonged exposure to lead with a corresponding 

blood lead level of about 70 figldl. Because chronic 

lead nephropathy results only after prolonged or 

repeated exposures, it is impossible to recapitulate 

accurately the exposure history; therefore, determination of an exposure threshold for this condition 

is impossible. 

13.5.4.2 EFFECTS OF LEAD ON THE ENDOCRINOLOGICAL, HEPATIC, CARDIOVASCULAR, AND IMMUNOLOGICAL 

SYSTEMS 

Although some studies have been done in 

reference to each of the systems in this subsection, 

there exists too little quantitative information relating blood lead levels to the endocrinological, 

hepatic, and cardiovascular systems. 

13.5.5 Does-Effect/Response Relationships 

In any discussion of the risk assessment directed 

toward a particular agent, such as lead, two questions arise: 

1. What are the lowest levels of the internal 

dose (blood lead level) that give rise to any 

biological effect? 

2. What dose-response relationships are obtained that define a proportion of a population manifesting a given biological effect at 

a particular internal dose? 

Information summarized in the preceding section 

dealt with relationships between blood lead levels 

and various biological effects of lead. Many of the 

data discussed above concerned threshold levels at 

which health effects of lead are first observed in 

different population groups. Table 13-2 summarizes 

the threshold levels at which various specific 

hematological and neurobehavioral effects have 

been observed for particular subpopulations. 

A number of investigators have attempted to 

quantitate more precisely lead's dose-response 

relationship, i.e., the proportion of a population exhibiting health effects at a given blood lead level. 

TABLE 13-2. SUMMARY OF LOWEST OBSERVED EFFECT LEVELS 

Lowest observed 

effect level Population group 

10 

15-20 

25-30 

40 

40 

40 

50 

50-60 

50-60 

80-100 

100-120 

ALAD inhibition 

Erythrocyte protoporphyrin elevation 

Erythrocyte protoporphyrin elevation 

Increased urinary ALA excretion 

Anemia 

Coproporphyrin elevation 

Anemia 

Cognitive (CNS) deficits 

Peripheral neuropathies 

Encephalopathy symptoms 

Encephalopathy symptoms 

Children and adults 

Women and children 

Adult males 

Children and adults 

Children 

Adults and children 

Adults 

Children 

Adults and children 

Children 

Adults 

Due to the limited availability of data, most such attempts have been restricted to effects on the 

hematologic system, in particular the elevation of 

FEP, the inhibition of ALAD activity, and the excretion of ALA in the urine. 

In regard to defining dose-response relationships 

for hematological effects, three different assessments 

of such relationships have been carried out46 and 

published. For example, in the approach of 

Zielhuis,4 dose-response relationships were 

developed for ALAD, ALA-U, and FEP as obtained for adults, male and female, and children. In 

Figure 13-1 are presented the dose-response data for 

children and adults for ALAD at inhibition levels of 

40 and 70 percent. In Figure 13-2, a corresponding 

relationship for urinary ALA is given for adult 

males, and Figure 13-3 presents the corresponding 

13-8 
P.61 

data for FEP in adult males, adult females, and 

children. 

z 

O S« 80 

I- Q 

< UJ 

_l H 

= 2 

SS 60 

">• A 

u. . 

O I ; 40 — 

_ 

— 

1 1 

x J / / 

/ / / 

/ 

/ 

/ 

/ 

/ 

/ 

/ y 

l - V 

/ / 

1 

—(^40 % 

70% / / / / / / / 

/ / 

1 1 

"P 

1 

* - 1 

>40 % 

>70 % 

ADULTS 

CHILDREN 

1 

—. 

_ 

-

If < 

O I 20 

0 10 30 50 70 

BLOOD LEAD LEVEL, ug Pb/dl 

Figure 13-1. Dose-response curve for percent ALAD inhibition for adults and children as a function of blood lead 

level. 

°- < 60 

O w 

uu A 

> 5 mg/liter 

mg/liter 

30 50 

BLOOD LEAD LEVEL, ug Pb/dl 

Figure 13-2. Dose-response curve for ALA in urine (ALA-U) 

as a function of blood lead level.4 

As can be seen from Figure 13-1, there appears to 

be a marked difference at 40 percent inhibition of 

ALAD activity between children and adults, such a 

difference decreasing as one goes to 70 percent inhibition. For example, at 20 /xg/dl blood lead, approximately 10 percent of adults show 40 percent 

enzyme inhibition, whereas the corresponding value 

for children is somewhat above 80 percent. It should 

also be noted that there is apparently a steep rise in 

the linear portion of these sigmoid relationships, 

e.g., 20 percent of adults show a 40 percent inhibition in ALAD at 20 figldl blood lead, whereas virtually all of the adult population shows 40 percent 

inhibition at 40 figldl. A similar steepness in the 

curve is seen in regard to children. 

Figure 13-2 presents dose-response data for ALA 

in urine exceeding two discrete levels, >5 and >10 

mg/liter, with increasing blood lead. It may be seen 

that the response in the linear portion of the curve is 

much less steep than for ALAD. For example, for 

approximately 5 percent of adults, the no-response 

level for ALA >5 mg/liter is about 30 figldl blood 

lead. At 60 figldl blood lead, the corresponding percentage of the population showing this response is in 

excess of 80 percent. The corresponding plot for 

ALA > 10 mg/liter shows a less steep slope than the 

former case. At 60 figldl blood lead, the corresponding percentage of the adult population is approximately 40. 

The composite dose-response plot presented in 

Figure 13-3 shows an increased response in FEP in 

adult females compared to adult males. Children 

show a greater response than adult males only up to 

blood lead levels of about 45 /ug/dl. The data of 

Zielhuis are extracted from a number of reports. In 

Figure 13-4, interestingly, wherein are contained the 

o A 

< » 

100 

80 

60 

40 

20 

-

-

1 1 1 1 

ADULT FEMALES /* " 

1 /l*""' l 1 

1 1 1 

/ADUL T MALES 

1 / CHILDREN 

1 1 1 

-

-

-

-

-

30 50 

BLOOD LEAD LEVEL, ug Pb/dl 

Figure 13-3. Dose-response curve for FEP as a function of 

blood lead level.4 

Q 

UJ 

K < 

(/> 

A 

ADULT MALES 

20 30 

BLOOD LEAD LEVEL, ug Pb/dl 

Figure 13-4. Dose-response curve for FEP as a function of 

blood lead level.5 

13-9 
.P.62_ 

dose-response data of Roels et al.5 for FEP in adult 

males, adult females, and children, it appears that 

children show the most heightened response, 

followed by adult females, and the least response in 

adult males. The slope for the linear portion of the 

response curve is quite steep in the case of children; 

20 percent of the children show elevated response 

(82 /xg/dl rbc) at 20 /ug/dl blood lead, whereas virtually all the children exceed this value at 35 /ug/dl 

blood lead. 

The dose-response data of Piomelli6 are presented 

in Figure 13-5 and consist of composite plots for 

mean plus 1 standard deviation (33 figldl whole 

blood) and the mean plus 2 standard deviations (51 

fig FEP/dl whole blood). In the data presented in 

Figure 13-5. blood lead levels in excess of 28 figldl 

whole blood were not used in tne calculations. It appears from the above that there exists a threshold at 

about 15 figldl whole blood. 

> 98 — 

Q 95 — 

98 

95 

90 

75 

50 

25 

5 

2 

1 

1 

NOTE 

1 

1 1 1 1 1 1 1 

POINTS OUTSIDE THE RANGE OF THE SOLID LINES 

WERE NOT USED IN CALCULATIONS 

0 

r> 

-

s * — 

FEP > MEAN + 1 S.D. (33 ug/dl) ' 

j* y 

Jg rf FEP>MEAN + 2 S.D. 

_ tmJT j f (51 ug/di) ? y* 

S QV J C (NATURAL FREQUENCY) — 

o ° /f^ ^ 

1 " 1 I I I I 1 

? 25 -

° ,„_ = 

< 5 -

0 10 20 30 40 

BLOOD LEAD LEVEL, ug Pb/dl 

Figure 13-5. Dose-response curve for FEP as a function of 

blood lead level.6 

EPA has carried out analyses of the data from the 

Azar et al. study7 and calculated a dose-response 

curve for urinary ALA (Figure 13-6). These doseresponse curves were plotted for two different cutoff points. These points were the mean values for 

blood lead levels less than 13 figl 100 g, plus 1 standard deviation and plus 2 standard deviations, 

respectively. From the mean plus 2 standard deviations curve, it is readily apparent that the linear portion of the curve is quite steep. At a blood lead level 

of 20 figldl, only 6 percent of the population exceed 

the mean plus 2 standard deviations value of the 

control population, whereas at a blood lead level of 

50, 50 percent of the population exceeds that value. 

Furthermore, when one examines the figure at 40 

figldl, the value at which ALA in urine is taken to 

suggest health impairment, the Azar et al. data show 

that about 30 percent of the population shows an 

elevation in this parameter. 

4 80 

< 

<so 

s 

Z 50 

o 

MEAN+ 1 S.D. 

MEAN + 2 S.D. 

MEAN ALA-U » 0.32 FOR BLOOD 

LEAD < 13 ug/dl 

J I I I I I 

BLOOD LEAD LEVEL, ug Pb/dl 

Figure 13-6. EPA calculated dose-response curve for ALA-U 

(from Azar et al.7). 

In Table l 3-3 are tabulated proportions of the 

study populations in the Zielhuis and Azar reports 

showing elevated urinary ALA versus blood lead 

level. The data for Zielhuis are as cited in Figure 

13-2, the percentage of subjects with ALA-U greater 

than 5 mg/liter being used. The Azar data in Table 

13-3 refer to the mean plus two standard deviations 

data set. For purposes of comparison of doseresponse data for FEP, the studies of Zielhuis,4 

Roels,5 and Piomelli6 are tabulated in Table 13-4. 

As in the case for the table of ALA-U data, it should 

be kept in mind that differences exist in cut-off 

points for FEP response to lead in the various 

studies. 

TABLE 13-3. ESTIMATED PERCENTAGE OF SUBJECTS 

WITH ALA-U EXCEEDING S mg/liter FOR VARIOUS BLOOD 

LEAD LEVELS 

Blood lead levels. 

ijg'dl 

10 

20 

30 

40 

50 

60 

70 

4 

Zielhuis. 

% 

0 

0 

6 

24 

48 

76 

96 

Azar et at.. 

% 

2 

6 

16 

31 

50 

69 

84 

13-10 
TABLE 13-4. ESTIMATED PERCENTAGE OF CHILDREN 

WITH EP EXCEEDING CUT-OFF POINTS FOR VARIOUS 

BLOOD LEAD LEVELS 

Blood lead 

level, ug/dl 

10 

20 

30 

40 

50 

60 

70 

80 

Zielhuisa% 

0 

6 

22 

37 

49 

— 

— 

— ' 

Roels et al,.b% 

3 

27 

73 

100 

— 

— 

— 

— 

Piomelli.c% 

9 

11 

48 

80 

— 

— 

— 

— 

aEP > EP of children with Pb-B < 20 iig/dl. 

bEP >82 ugd l cells. 

CEP >EPo l 33ug'dl. 

13.6 POPULATIONS AT RISK 

Population at risk is a segment of a defined 

population exhibiting characteristics associated with 

significantly higher probability of developing a condition, illness, or other abnormal status. This high 

risk may result from either greater inherent susceptibility or from exposure situations peculiar to that 

group. What is meant by inherent susceptibility is a 

host characteristic or status that predisposes the host 

to a greater risk of heightened response to an external stimulus or agent. 

In regard to lead, two such populations are 

definable. They are preschool age children, 

especially those living in urban settings, and pregnant women, the latter group owing mainly to the 

risk to the conceptus. Children are such a population 

for both of the reasons above, whereas pregnant 

women are at risk primarily due to the inherent 

susceptibility of the conceptus. 

13.6.1 Children as a Population at Risk 

Children are developing and growing organisms 

exhibiting certain differences from adults in terms of 

basic physiologic mechanisms, capability of coping 

with physiologic stress, and their relative metabolism of lead. Also, the behavior of children frequently places them in different relationship to 

sources of lead in the environment, thereby enhancing the opportunity for them to absorb lead. 

Furthermore, the occurrence of excessive exposure 

often is not realized until serious harm is done. 

Young children do not readily communicate a medical history of lead exposure, the early signs of such 

being common to so many other disease states that 

lead is frequently not recognized early as a possible 

etiological factor contributing to the manifestation 

of other symptoms. 

13.6.1.1 INHERENT SUSCEPTIBILITY OF 

THE YOUNG 

Discussion of the physiological vulnerability of 

the young must address two discrete areas. Not only 

should the basic physiological differences be considered that one would expect to predispose children 

to a heightened vulnerability to lead, but also the actual clinical evidence must be considered that shows 

such vulnerabilty does indeed exist. 

In Chapter 10, Section 10.6 was devoted to the 

metabolic considerations in identifying susceptible 

subgroups. Factors discussed in that section included: (1) greater lead intake of infants on a per 

unit body weight basis, which is probably related to 

greater caloric and water requirement; (2) greater 

intake as well as net. absorption (see GI section), 

greater net respiratory intake as well as greater net 

absorption and retention from the GI tract; (3) rapid 

growth rate may reduce the margin of safety against 

a variety of stresses including iron, calcium, and 

vitamin deficiency; (4) dietary habits of children are 

quite different from adults; normal hand-to-mouth 

activity probably results in the transfer of lead-contaminated dust and dirt via thumb sucking or in 

retrieval of dirt-contaminated foodstuffs; (5) the 

metabolic requirements for protein, calcium, and 

iron are so great relative to intake that a negative 

balance in these factors may exist; (6) in very young 

children metabolic pathways and factors such as the 

blood-brain barrier are known to be incompletely 

developed; and (7) partitioning of lead in the bones 

of children is different from that of adults. Only 60 

to 65 percent of the lead body burden is in the bones 

of children, and this fraction may be more labile. 

Hematologic and neurologic effects in children 

have been shown to have lower thresholds per unit of 

blood lead than in adults. In particular, the lowest 

observed effect levels for FEP and anemia are lower 

for children than adults. With reference to 

neurologic effects, the onset of encephalopathy and 

other injury to the nervous system appears to vary 

both regarding likely lower thresholds in children 

for some effects and in. the typical pattern of 

neurologic effects presented, e.g., in encephalopathy 

or other CNS deficits being more common in 

children versus peripheral neuropathy being more 

often seen in adults. Not only are the effects more 

acute in children than in adults, but also the 

neurologic sequelae are usually much more severe in 

children. 

Upon careful examination of the data, it should be 

noted that certain geographic or socioeconomic fac13-11 
P.64 

tors appear to emerge as important factors determining the differential susceptibility of some groups 

of children for lead-induced neurologic damage. 

That is, there seems to be distinct variation in effects 

or a lack thereof as reported for children in different 

studies depending upon the geographic areas from 

which the study populations were drawn. For example, the few credible reports of lead encephalopathy 

in children at blood lead levels less than 100 ug/dl 

all concern children from inner-city areas. 

Similarly, statistically significant effects or borderline effects indicative of more subtle neurobehavioral deficits in lead-exposed children at 

moderately elevated blood lead levels have been reported for groups of children drawn from inner-city 

populations of urban centers. In contrast, only a few 

statistically significant neurobehavioral effects have 

yet been reported for populations of children experiencing similar elevations in blood lead levels, 

but residing near primary smelter facilities in semirural areas. 

One cannot determine with any certainty the 

specific factors that might contribute to the apparent 

differential sensitivity of inner-city children to the 

neurobehaviora l effects of lead. Several 

possibilities, however, might be reasonably considered, including the following: 

1. Parameters of lead exposure probably 

differed substantially for the populations 

under study; the smelter area children, for 

example, may have experienced much more 

gradual accumulations of lead during the 

course of long-term, low-level exposures 

versus probable repeated brief episodes of 

somewhat higher level exposures being 

superimposed on any long-term, low-level 

exposures for the inner-city children. 

2. The exposures of the smelter children likely 

included significantly higher levels of other 

metallic species, e.g., zinc, that are known to 

reduce the pathological impact of lead on 

many organ systems. 

3. Differences in nutritional status likely existed between the smelter and inner-city 

children, with the latter probably having a 

higher incidence of iron, calcium, and 

vitamin deficiency; or other differences in 

dietary content and habits might be invoked 

as an explanation. 

4. Interactions between lead exposures and 

other factors associated with the stresses of 

urban versus nonurban living may also contribute to the apparent differential susceptibility of inner-city chilren. 

13.6.1.2 EXPOSURE CONSIDERATIONS 

Children's dietary habits as well as the diets themselves differ markedly from adults and, as a result, 

place children in a different relationship to several 

sources of lead. The dominance of canned milk and 

processed baby food in the diet of many young 

children is an important factor is assessing their exposure to lead since both those foodstuffs have been 

shown to contain higher amounts of lead than components of the adult diet. The importance of these 

lead sources is not their relationship to airborne lead 

directly but, rather, their role in providing a higher 

baseline lead burden to which the airborne contribution is added 

Children ordinarily undergo a stage of development in which they exhibit mouthing behavior, for 

example, thumbsucking. At this time they are at risk 

of picking up lead-contaminated soil and dust on 

their hands and hence into their mouths where it can 

be absorbed. Scientific evidence documenting at 

least the first part of the chain is available. 

There is, however, an abnormal extension of the 

mouthing behavior, called pica, which occurs in 

some children. Although diagnosis of this is 

difficult, children who exhibit this trait have been 

shown to purposefully eat nonfood items. Much of 

the lead-based paint problem is known to occur 

because children actually ingest chips of leaded 

paint. 

13.6.2 Pregnant Women and the Conceptus as a 

Population at Risk 

There are some rather inconclusive data indicating that women may in general be at somewhat higher risk to lead than men. However, pregnant women 

and their concepti as a subgroup are demonstrably at 

higher risk. It should be pointed out that, in fact, it 

really is not the pregnant woman per se who is at 

greatest risk but, rather, the unborn child she is 

carrying. Because of obstetric complications, however, the mother herself can also be at somewhat 

greater risk. This section will first describe the 

general evidence for all women and then the evidence that pertains to pregnant women exclusively. 

Studies have demonstrated that women, like 

children, in general tend to show a heightened 

response of erythrocyte protoporphyrin levels upon 

exposure to lead. The exact reason for this 

heightened response is not known but may relate to 

endocrine differences between men and women. In 

13-12 
P.65 

particular, the levels of testosterone may play a role 

in this response. 

As stated above, the primary reason pregnant 

women are a high-risk group is because of the fetus 

each is carrying. In addition, there is some suggestive evidence that lead exposures may affect maternal complications of delivery. 

With reference to maternal complications at 

delivery, information in the literature suggests the 

incidence of preterm delivery and premature membrane rupture relates to maternal blood lead level. 

Further study of this relationship as well as studies 

relating to discrete health effects in the newborn are 

required. 

Vulnerability of the developing fetus to lead exposure arising from transplacental transfer of 

mother's blood lead content was discussed in Section 

11.6. This process starts at the end of the first trimester. Cord blood studies involving mother-infant 

pairs repeatedly have shown a correlation between 

maternal and fetal blood lead levels. Furthermore, 

the observed positive correlation of urinary ALA 

levels with blood lead levels in newborns indicates 

that some heme-biosynthetic derangement is apparent at birth and must therefore have commenced 

in utero. 

Further suggestive evidence, cited in Chapter 11, 

has been advanced for prenatal lead exposures of 

fetuses possibly leading to later higher instances of 

postnatal mental retardation among the affected offspring. The available data are insufficient to state 

with any certainty that such effects occur or to determine with any precision what levels of lead exposure 

might be required prior to or during pregnancy in 

order to produce such effects. 

13 7 DESCRIPTION OF U.S. POPULATION IN 

RELATION TO PROBABLE LEAD EXPOSURES 

In this section estimates are provided of the number of individuals potentially at risk to lead exposures. Unfortunately the latest census data are 

only from 1970,8 although some estimates are available from the National Center for Health Statistics 

for 1975.9 This is unfortunate since some significant 

changes are thought to have occurred in the population structure since the 1970 census. 

Because most lead exposures, excepting areas with 

primary lead smelters, occur in what the Bureau of 

the Census calls urban areas, an estimate of the potential risk of airborne lead exposure can be made 

from the total urban population of the United States. 

That this may be an acceptable first approximation 

can be gleaned by comparing the frequency distribution of air lead concentrations for urban and rural 

National Air Sampling Network stations in Chapter 

7. This comparison readily shows a distinct 

difference in exposure between the two types of stations. Based on examination of the urban stations as 

well as of literature data on both air lead and soil 

and dust lead values, a strong case can be made to 

support the assumption that the area which the 

Bureau of the Census calls the central city of the urban areas is at even higher risk of lead exposure. 

Therefore, in regard to exposures other than 

localized point stationary sources of lead, the 

population at risk is the urban one and, in particular, 

the central city residents. For the United States in 

1970, these values were 149 and 64 million people, 

respectively8 (Table 13-5). From the table it can 

TABLE 13-5. POPULATION AND PERCENT DISTRIBUTION, URBAN AND RURAL, BY RACE 1970 CENSUS4 

inn (10°) 

Urban 

Inside urbanized areas 

Central cities 

Urban fringes 

Outside urbanized areas 

Rural 

Total. United States 

128.773(72.4) 

100.952(56.8) 

49.547 (27.9) 

51.405(28.9) 

27.822(15.7) 

48.976 (27.6) 

177.773 

20,552 (80.7) 

17,495 (68.7) 

14,375 (56.5) 

3,120 (12.3) 

3,057 (12.0) 

4,911 (19.3) 

25.463 

149.325(73.5) 

118.447(58.3) 

63.922(31.5) 

54.525 (26.8) 

30.878(15.2) 

53.887 (26.5) 

203,212 

readily be seen that a higher proportion of the nonwhite population lives in urban areas than whites 

(80.7 versus 72.4 percent) and is possibly subject to 

greater exposure to airborne lead. Furthermore, this 

disparity is even greater when one considers the 

central city population only, which may be subject to 

even higher levels of lead pollution from a multitude 

of sources. 

From the previous discussion of populations at 

risk, however, two subgroups of this total population 

were defined as being at even higher risk — 

children, especially those under 5, and pregnant 

13-13 
TABLE 13-6. NUMBER OF BIRTHS BY RACE AND SIZE OF POPULATION8 

P.66 

Urban areas of given 

size from 1970 census 

Births 

White 

772.230 

286.706 

600.166 

1.432.162 

3.091.264 

Black 

321.412 

37.024 

65.790 

148.136 

572.362 

Births 

Others 

24.394 

4.182 

10.394 

28.790 

67.760 

Total 

1.118.036 

327.912 

676.350 

1,609.088 

3.731,386 

> 100,000 

50-99,999 

10-49,999 

59,999 

Total 

Urban areas of given 

Size from 1975 census White Black Others Total 

> 100,000 

50-99,999 

10-49,999 

59,999 

571.478 

222.735 

478.382 

1.279.401 

276.387 

37.885 

64.481 

132.828 

26.332 

5.921 

13.039 

35.329 

874,197 

266.541 

555.902 

1,447.558 

Total 2.551.996 511.581 80.621 3.144,198 

women. There is insufficient evidence at this time to 

determine whether any racial or ethnic group suffers 

an innate susceptibility to lead. 

In the United States in 1970 about 12 million 

children under 5 years of age lived in urban areas. 

Approximately 5 million of these children lived in 

central city areas.8 Since between-census population 

estimates are not available for urban-rural comparisons, the only way to use the 1975 population 

estimates is to assume that the percent distribution 

obtained in 1970 still holds true. If in fact that is the 

case, the more recent estimates would be about 11 

million children, in urbanized areas and 4.6 million 

in the central city. An estimate made by the National 

Bureau of Standards of the total child population 

with blood lead values equal to or greater than 40 

figldl in a recent year was 600,000.10 This total is 

clearly a cause for concern in view of the health data 

presented in Section 13.4 above. Of course, the use 

of this figure, based on the many lead-screening programs conducted in this country, is not meant to imply that all of these values resulted from airborne 

lead. They probably do not, since paint lead exposures are an additional important source. But, on 

the other hand, the addition of an airborne component of lead exposure on top of these levels would 

adversely affect the public health. If airborne lead 

were the only contribution to these children's lead 

values, the potential health effects ascribable to that 

exposure could be significant. 

The difficulty in estimating the number of pregnant women exposed to air lead is even greater; this 

is because the number of. pregnant women is not 

tabulated on an urban-rural basis. Therefore, for 

this document, the number of pregnant women will 

be estimated from the number of live births (Table 

13-6).8 Unfortunately these data also are not tabulated on an urban-rural basis but, rather, on a 

population size of place of residence. It can readily 

be seen that the total number of births has declined 

in the time 1970 to 1975. If one assumes only the 

highest population size category to be at risk of lead 

exposure, there are still almost 900,000 newborns at 

risk of lead absorption from their mothers. 

13.8 REFERENCES FOR CHAPTER 13 

1. Nordman, C. H. Environmental lead exposure in Finland. 

A study on selected population groups. Dissertation. 

University of Helsinki, Helsinki. 1975. 

2. Finney, D. J. Statistieal method in biological assay. 

Charles Griffin and Co., London. 1971. p. 5. 

3. Hernberg, S. Biochemical. Subclinical and Clinical 

Responses to Lead and Their Relation to Different Exposure Levels, as Indicated by the Concentration of Lead 

in Blood. In: Effects and Dose-Response Relationships of 

Toxic Metals. G. F. Nordberg (ed.). Elsevier Scientific 

Publishing Co.. Amsterdam. 1976. Part BIS. 

4. Zielhuis, R. L. Dose-response relationships for inorganic 

lead: I. Biochemical and hematological responses. Int. 

Arch. Occup. Hlth. 55:1-18. 1975. 

5. Roels, H., Buchet, J. P., R. Lawrie, and G. Hubermont. 

Impact of air pollution by lead on the heme biosynthetic 

pathway in school-age children. Arch. Environ. Hlth. 

J/:3 10-316, 1976. 

6. Piomelli. S. Reanalysis of data from S. Piomelli. C. Seaman, D. Zullow. A. Curran, and B. Danidow. Metabolic 

evidence of lead toxicity in "normal" urban children. 

Clin. Res. 25.-495A. 1977. Presented to Environmental 

Protection Agency staff and consultants. Research 

Triangle Park. N.C. September 28, 1977. 

13-14 
7. Azar, A.. R. D. Snee. and K. Habibi. An epidemiological 9. U. S. National Center for Health Statistics, Vital Statistics 

approach to community air lead exposure using personal of the U. S.. 1975, Data for 1975 Births. Unpublished -

air samplers. Environ. Qual. Saf.Suppl. 11:254-290. 1975. provided by NCHS. 

8. U. S. Bureau of the Census, Statistical Abstracts of the 10. National Bureau of Standards. Survey Manual for 

United States. 1976 (97th Ed.). Washington, D.C. 1976. p. Estimating the Incidence of Lead Paint in Housing. NBS 

18, Table 19. ' Technical Note 921, September 1976. 

13-1 5 
APPENDIX A 

GLOSSARY* 

Absorption (of lead): Transfer of lead into an organism via intestinal wall, alveolar surface, or skin. 

Accumulation (of lead): Net positive difference between intake and output of lead over an extended 

period. 

Acetyl coenzyme A (CoA): Coenzyme, derived principally from the metabolism of glucose and fatty 

acids, that takes part in many biological acetylation reactions; oxidized in the Krebs cycle. 

Acetylcholine: Compound released from certain 

autonomic nerve endings; acts in the transmission 

of nerve impulses to excitable membranes. 

Acetylcholinesterase : Enzyme in excitabl e 

membranes that inactivates acetylcholine. 

/3-Acetyl glucosaminadase: Enzyme that hydrolyzes 

the terminal glucosaminidic bonds of odd-numbered oligosaccharides to yield N-acetylglucosamine and the next lower even-numbered 

oligosaccharide. 

Acid-fast: Describes a cell or bacterium that retains 

a dye that has a negatively charged molecule. 

Acid phosphatase: Enzyme that hydrolyzes, in an 

acid medium, monophosphoric esters, with 

liberation of inorganic phosphate. 

Adenocarcinoma: Carcinoma derived from glandular tissue or in which the tumor cells form recognizable glandular structures. 

Adenoma: Benign epithelial tumor in which the cells 

form recognizable glandular structures or in 

which the cells are clearly derived from glandular 

epithelium. 

Adenosine diphosphate (ADP): Coenzyme composed of adenosine and two molecules of 

phosphoric acid; important in intermediate cellular metabolism; a product of the hydrolysis of 

adenosine triphosphate (ATP). 

Adenosine triphosphate (ATP): Nucleotide occurring in all cells, where it serves in the storage of 

energy and in the transfer of energy in metabolic 

processes; composed of adenosine and three 

molecules of phosphoric acid. 

"Compiled from standard reference works and, to a lesser extent, from information 

furnished by experts in the respective disciplines. 

Adenosine triphosphatase (ATPase): Enzyme that 

mediates the removal of water from ATP: ATP + 

H2 0 — ADP + orthophosphate. 

Adenyl cyclase: Enzyme that catalyzes the formation of cyclic adenosine-3', 5'-monophosphate 

(cyclic AMP). 

Adenylic acid: (1) Generic name for a group of 

isomeric nucleotides; (2) Phosphoric acid ester of 

adenosine ; also known as adenosin e 

monophosphate (AMP). 

Adrenaline: See Epinephrine. 

Adrenergic: Describes the chemical activity of 

epinephrine or epinephrine-like substances. 

Adrenergi c synapse : Synaps e at which 

norepinephrine is liberated when a nerve impulse 

passes. 

Advection: Process of transport of an atmospheric 

property, or substance within the atmosphere, 

solely by the mass motion of the atmosphere. 

Aerodynamic diameter: Expression of aerodynamic 

behavior of an irregularly shaped particle in 

terms of the diameter of an idealized particle; that 

is, aerodynamic diameter is the diameter of a 

sphere of unit density that has aerodynamic 

behavior identical to that of the particle in question. Thus, particles having the same aerodynamic diameter may have different dimensions 

and shapes. 

Aerodynamic drag: Aerodynamic resistance; retarding force that acts upon a body moving through a 

gaseous fluid and that is parallel with the direction of motion of the body. 

Aerodynamic particle size: Sphere of unit density 

that has aerodynamic behavior identical to that of 

the particle in question. 

Aerosol: System in which the dispersion medium is a 

gas and the dispersed phase—composed of solid 

particles or liquid droplets—does not settle out 

under the influence of gravity. 

Aerosol particles: Solid particles 10 l 2 t o 10 ' fim in 

diameter, dispersed in a gas. 
P.69 

Agglomeration: Process by which precipitation particles grow by collision with an assimilation of 

cloud particles or other precipitation particles. 

Aitken dust counter: Instrument for determining 

dust content of the atmosphere; a sample of air is 

mixed, in an expandable chamber, with a large 

volume of dust-free air containing water vapor. 

Upon sudden expansion, the chamber cools 

adiabatically below its dewpoint, and droplets 

form with the dust particles as nuclei and are 

counted by means of a grid under a microscope. 

Aitken nuclei: Microscopic particles in the atmosphere that serve as condensation nuclei for 

droplet growth during the rapid adiabatic expansion produced by an Aitken dust counter (see 

above). 

Aldolase: Enzyme that acts on a ketose-1-phosphate 

to yield dihydroxy-acetone phosphate plus an 

aldehyde; e.g., fructose-1, 6-diphosphate = 

dihydroxyaceton e phosphat e + D -

glyceraldehyde-3-phosphate. 

Alkaline phosphatase: Enzyme that hydrolyzes, in 

alkaline medium, monophosphoric esters, with 

liberation of inorganic phosphate; found in 

plasma and serum, bone, etc. 

Alkalinity: Excess of hydroxyl ions over hydrogen 

ions, generally expressed as milliequivalents per 

liter. 

Alveola r macrophages: Rounde d granula r 

phagocytic cells, within the alveoli of the lungs, 

that ingest inhaled material. 

Ambient air: The surrounding, well-mixed air. 

Aminoacyl synthetase: Enzyme that catalyzes the 

coupled reactions of amino acid activation in 

which an amino acid is first attached to adenosine 

monophosphate and then to a transfer-RNA 

molecule. 

e-Amino group of lysine: The amino group, NH2, attached to e, or 5th, carbon atom from the carboxyl carbon in the amino acid, lysine: H2N-CH2-

CH 2-CH 2-CH 2-CH (NH 2)-COOH. 

8-Aminolevulinic acid (ALA, or 8-ALA): COOHCH2-CH2-CO-CH2-NH2; intermediate in the biosynthesis of heme-containing compounds; formed 

from succinyl-coenzyme A and glycine. 

8-Aminolevulinic acid dehydratase (ALAD): 

Enzyme in heme biosynthetic pathway that mediates formation of porphobilinogen from 8-

aminolevulinic acid. 

8-Aminolevulinic acid synthetase (ALAS): Enzyme 

in heme biosynthetic pathway that mediates the 

formation of 8-aminolevulinic acid from succinyl-CoA via 2-amino-3-ketoadipate. 

Amphetamine: a-Methylphenethylamine. Drug 

used to stimulate the central nervous system, increase blood pressure, reduce appetite, and 

reduce nasal congestion. Abuse may lead to dependence, characterized by strong psychic dependence associated with an increase in REM (rapideye-movement) sleep, hunger, apathy, and 

depression. 

Anamnestic response: Rapidly increased antibody 

level following renewed contact with a specific 

antigen, even after several years. 

Anodic stripping voltammetry: An electrochemical 

method of analysis. 

Anophthalmia: Developmental defect characterized 

by complete absence of the eyes or by the presence 

of vestigial eyes. 

Anorexia: Loss of appetite. 

Anoxia: Relative lack of oxygen; caused by inadequate perfusion of tissues by blood carrying normal amounts of oxygen or by normal perfusion of 

blood carrying reduced amounts of oxygen. 

Antipyrine (C,,H12ON2): Compound used as an antipyretic, analgesic, and antirheumatic drug. 

Area source: Consists of a number of point sources 

arranged in a two-dimensional array. 

Astrocytic proliferation (astrocytosis): Proliferation 

of astrocytes owing to the destruction of nearby 

neurons during a hypoxic or hypoglycemic 

episode. 

Ataxia: Failure of muscular coordination. 

Atmospheric turbulence: Motion of the air (or other 

fluids) in which local velocities and pressures 

fluctuate irregularly in a random manner. 

Avoidance task: Behavioral testing procedure used 

to measure an animal's avoidance and escape performance. In a one-way task only one response is 

appropriate, whereas in a two-way task either of 

two responses is appropriate, depending on the 

existing test conditions. 

Axonal degeneration: Degeneration of axons, the 

processes or nerve fibers that carry the unidirectional nerve impulse away from the nerve cell 

body. 

Balance experiments: Experiments on man or other 

animals that involve quantitative measurements 

of intake (via respiration and ingestion) and loss 

(via exhalation and excretion) of a specific element or substance. A positive balance means that 

more is taken in than is lost over a specific time. 

Basophilic stippling: Spotted appearance of 

relatively immature red blood cells that contain 

cytoplasmic material that stains deeply with basic 

dyes. 

A-2 
P.70 

Biosphere: The part of the earth's crust, waters, and 

atmosphere where living organisms can subsist. 

Blood-brain barrier: The barrier created by semipermeable cell walls and membranes to passage 

of some molecules from the blood to the cells of 

the central nervous system. 

Body burden: The total amount of a specific substance (for example, lead) in an organism, including the amount stored, the amount that is mobile, 

and the amount absorbed. 

Bond energy: The enthalpy change that accompanies 

the breaking of a chemical bond between two 

atoms. The total bond energy of a molecule gives 

a measure of its thermodynamic stability. 

Boundary layer: Layer of fluid in the immediate 

vicinity of a bounding surface; refers ambiguously 

to the (1) laminar, (2) turbulent, (3) planetary, or 

(4) surface boundary layers. 

Brainstem: Stemlike portion of the brain connecting 

the cerebral hemispheres with the spinal cord: 

Bremsstrahlung: Radiation that is emitted by an 

electron accelerated in its collision with the 

nucleus of an atom. 

Brownian movement: Random movements of dispersed small particles suspended in a fluid; 

results from random collisions between the 

molecules of the dispersing medium and the particles of the dispersed phase. 

CaEDTA: Edathamil calcium disodium, which is 

the calcium disodium salt of ethylene -

diaminetetraacetate, a chelating agent. CaEDTA 

is used in the study, diagnosis, and treatment of 

poisoning by various heavy metals, including 

lead. 

CaEDTA mobilization test: Test in which a known 

quantity of CaEDTA is injected parenterally and 

the amount of lead excreted in urine during a 

known period beginning immediately thereafter is 

measured. This procedure is used both clinically 

and experimentally and is thought to provide an 

index of the mobile fraction of the total body 

burden of lead. 

Carcinogenesis: Development of carcinoma; or, in 

more recent usage, producing any kind of malignancy. 

Carcinoma: Malignant new growth made up of 

epithelial cells tending to infiltrate the surrounding tissues and give rise to metastases. 

Cascade impactors: Low-speed impaction device for 

use in sampling both solid and liquid atmospheric 

suspensoids; consists of four pairs of jets (each of 

progressively smaller size) and sampling plates 

working in series and designed so that each plate 

collects particles of one size range. 

Catalase: Enzyme that catalyzes the decomposition 

of hydrogen peroxide; contains four hematin 

groups per molecule; found in liver and red blood 

cells. 

Catecholamines: Group of sympathomimetic amines 

containing a catechol moiety; especially 

epinephrine, norepinephrine, and dopamine. 

Catenation: Property of an element that enables it to 

link to itself to form chains, e.g., carbon. 

Cerebellum: Large dorsally projecting part of the 

brain having the special function of muscle coordination and maintenance of equilibrium. 

Cerebral anoxia: Relative lack of oxygen in the 

brain. 

Cerebral cortex: Thin layer of gray matter on the 

surface of the cerebral hemisphere, folded into 

gyri, with about two-thirds of its area buried in 

the depths of the fissures. 

Chelate: Chemical compound in which a metallic 

ion is sequestered and bound into a ring by 

covalent bonds to two or more nonmetallic atoms 

in the same molecule. 

Chelant: Chemical compound that will react with 

metals to form chelates; a chelating agent. 

Cholinergic: Stimulated, activated, or transmitted 

by acetylcholine; applied to those nerve fibers 

that liberate acetylcholine at a synapse when a 

nerve impulse passes. 

Cholinesterase: Enzyme that catalyzes the hydrolysis of acylcholine to choline and an anion. 

Chemical energy: Energy produced or absorbed in 

the process of a chemical reaction. 

Chi-square test: Test of statistical significance based 

on frequency of occurrence; used to test probabilities or probability distributions (goodness 

of fit), statistical dependence or independence 

(association), and common populatio n 

(homogeneity). 

Chlorinity: Measure of chloride content, by mass 

(g/kg), of water; sometimes determined to permit 

calculation of salinity. 

Choroid plexus: Any of the highly vascular, folded 

processes that project into the third, fourth, and 

lateral ventricles of the brain. 

Chromatid: One of the pair of stands, formed by 

longitudinal splitting of a chromosome, that are 

joined by a single centromere in somatic cells 

during mitosis; one of a tetrad of strands formed 

by lengthwise splitting of paired chromosomes 

during the diplotene stage of meiosis. 

A-3 
P.71 

Chromophore: Any chemical group whose presence 

gives a decided color to a compound and that 

united with certain other groups to form dyes. 

Chromosomes: Threadlike structures in animal or 

plant nuclei, seen during karyokinesis (nuclear 

division characteristic of mitosis), that carry the 

linearly arranged genetic material. 

Chronic nephritis: Chronic inflammation of the kidneys. 

Coagulation: Process that converts numerous 

droplets into a smaller number of larger precipitation particles. 

Coalescence: Merging of two liquid drops into a 

single larger drop. 

Colic: Paroxysmal pain in the abdomen, caused by 

spasm, distention, or obstruction of any one of the 

hollow viscera. 

Colloidal materials: See Colloidal system. 

Colloidal system: An intimate mixture of two substances, one of which, called the dispersed phase 

(or colloid), is uniformly distributed in a finely 

divided state through the second substance (dispersion medium); the dispersion medium may be 

a gas, liquid, or solid. 

Combustion nucleus: Condensation nucleus formed 

as a result of industrial or natural combustion 

processes. 

Complement: Complex proteins in normal serum 

that interact to combine with antigen-antibody 

complex, producing lysis when the antigen is in an 

intact cell; important in host defense mechanism 

against invading microorganisms. 

Complex: Chemical compound in which a part of the 

molecular bonding is of the coordinate type. 

Complexing: Formation of a complex compound; 

see Complex. 

Condensation: Physical process by which a vapor 

becomes a liquid or solid; opposite of evaporation. In meteorology, the term is limited to 

transformation of vapor to a liquid. 

Condensation nucleus: Particle, either liquid or 

solid, upon which condensation of water vapor 

begins in the atmosphere. 

Condensation particles: See Aitken nuclei. 

Confidence interval: A range of values (a, <a <a2) 

determined from a sample by definite rules so 

chosen that, in repeated random samples from the 

hypothesized population, an arbitarily fixed proportion (1-e) of that range will include the true 

value, x, of an estimated parameter. 

The limits, a, and a2, are called confidence limits; 

the relative frequency (1-e) with which these 

limits include a is called the confidence coefficient; and the complementary probability, e, is 

called the confidence level. As with significance 

levels, confidence levels are commonly chosen as 

.05 or .01, the corresponding confidence coefficients being .95, .99. 

Confidence intervals should not be interpreted as 

implying that the parameter itself has a range of 

values; it has only one value, a. On the other 

hand, the confidence limits (ap a2), being derived 

from a sample, are random variables the values of 

which on a particular sample either do or do not 

include the true value a of the parameter. 

However, in repeated samples, a certain proportion (namely 1-e) of these intervals will include 

a, provided that the actual population satisfied 

the initial hypothesis. 

Contamination: Contact with an admixture of an unnatural agent, with the implication that the 

amount is measurable. 

Convection: Atmospheric motions that are predominantly vertical, resulting in vertical transport and 

mixing of atmospheric properties. 

Convulsions: Violent, involuntary contraction or 

series of contractions of the voluntary muscles. 

Coprogen III: Coproporphyrinogen III, an intermediary metabolite in heme biosynthesis. It is a 

natural precursor of heme. 

Coprogenase: Coproporphyrinogenase, the enzyme 

that converts coproporphyrinogen III to protoporphyrin IX. 

Coproporphyrin: Urinary pigment derived from 

coproporphyrinogen, an intermediate in the biosynthesis of heme. 

Coproporphyrinogen (syn. coprogen): A fully 

reduced colorless tetracarboxylic tetrapyrrole. 

Isomers I and III are found in biologic systems. 

Cortex: See Cerebral cortex. 

Corpus callosum: Band of nerve tissue connecting 

the cerebral hemispheres in man and higher mammals. 

Corpus striatum: A subcortical mass of gray and 

white substance in each cerebral hemisphere, containing the caudate nucleus and the lentiform 

nucleus. 

Cortical atrophy: Wasting away of the outer layer(s), 

e.g., of the brain or kidney. 

Creatinine: C4H2ON3; compound formed by 

dehydration of creatine; found in urine, blood, 

and muscle. 

Cristae: Inner membranes of mitochondria, the surfaces of which are studded with roughly spherical 

particles attached to the cristae by stalks. 

A-4 
P.72 

Cumulative frequency distribution: Proportion of a 

distribution that lies below a given value. 

Curie: Unit of radioactivity; quantity of radionuclide that has 3.7 x IO10

 disintegrations per 

minute (dpm). 

Cysteine: Amino acid that occurs as a constituent of 

glutatione and of cystine. 

Cytochrome c: Small heme protein containing one 

atom of iron per molecule; its principal biologic 

function is in electron transport. See 

Cytochromes. 

Cytochrome c oxidase (cyt. a3): Enzyme that 

catalyzes the oxidation of cytochrome c: 4 

reduced cytochrome c + 0 2 = 4 oxidized 

cytochrome c + 2H2 0. 

Cytochrome c reductase: Enzyme that catalyzes the 

reduction of oxidized cytochrome c: NADH2 + 

oxidized cytochrome c = NAD + reduced 

cytochrome c. 

Cytochrome P-450: a fc-type cytochrome, one of the 

mixed-function oxidases in the microsomal 

system responsible for the oxidation of steroids 

and drugs and other foreign compounds. 

Cytochromes: Complex protein/heme respiratory 

pigments occurring in plant and animal cells, 

usually in mitochondria, that function as electron 

carriers in biological oxidation. 

Demyelination: Destruction of the myelin, a fatlike 

substance forming a sheath around the nerve 

fibers. 

Density: Ratio of mass of a substance to the volume 

occupied by it (usually expressed in g/cm3). 

Dentine: Also dentin; chief substance or tissue of the 

teeth, that surrounds the tooth pulp and is 

covered by enamel on the crown and by cementum on the roots of the teeth. 

Denver Development Screening Test: Rating scales 

employed to assess four areas of child development: (1) gross motor, (2) fine motor-adaptive, 

(3) personal-social, and (4) language. 

Deoxyribonucleic acid (DNA): A nucleic acid in the 

form of a doublestranded helix of a linear 

polymer; made up of repeating units of 2-deoxyribose, phosphate, and a purine or a pyrimidine; 

carrier of genetic information coded in the sequence of purines or pyrimidines (organic bases). 

Deposition: (1) Deposit of particles from the ambient air or atmosphere onto a surface; (2) 

removal of particles from inhaled air by the 

respiratory tract. 

Detection limit: A limit below which an element or 

compound can not be detected by the method or 

instrument being used for analysis. 

Dichotomous sampler: Air-sampling device that 

separates particulates into two fractions on the 

basis of diameter; the cutpoint varies with the size 

of the aperture. 

Diffusion: In meteorology, the exchange of fluid 

parcels between regions in space in apparently 

random small-scale motions. 

p-Dimethylaminobenzaldehyde: Ehrlich's reagent; 

(CH3 ) 2N.C6H4 .CHO. 

Diphenylthiocarbazone: See Dithizone. 

Dispersion: Distribution of finely divided particles 

in a medium. 

Dithizone: Diphenylthiocarbazone; C6H5N:N-CSNH»NH-C6H5; reagent used in the analysis of 

lead. 

Dithizone methods: Colorimetric methods of 

analysis for lead that involve the reaction of lead 

with dithizone to form lead dithizonate, which is 

measured spectrophotometrically at 510 nm. 

Dopamine: Hydroxytyramine, produced by the 

decarboxylatio n of dop a (dihydroxy -

phenylalanine), which is an intermediate product 

in the synthesis of norepinephrine. 

Dorsal root ganglion: Group of sensory nerve cell 

bodies located on the posterior root of each spinal 

nerve; joins peripherally with ventral, or motor, 

root to form the nerve before it passes outside the 

vertebral column. 

Downwind: In the same direction that the wind is 

blowing; on or toward the lee side. 

Dry deposition: The deposit of particles on a surface 

in the absence of precipitation. 

Dust: Solid materials suspended in the atmosphere 

in the form of small irregular particles, many of 

which are microscopic in size. 

Dustfall: Dry deposition of airborne dust particles. 

Dysoria: Any abnormality of vascular permeability. 

E. coli: Short, gram-negative, rod-shaped, enteric 

bacterium. 

Edema: Presence of abnormally large amounts of 

fluid in the intercellular tissue spaces of the body; 

usually applied to the demonstrable accumulation of excessive fluid in the subcutaneous tissues. 

Electromyographic: Pertaining to electromyography, the recording and study of the intrinsic 

electrical properties of skeletal muscle. 

A-5 
P.73 

Electron microprobe: X-ray method in which 

electrons from a hot-filament source are accelerated electrostatically, then focused to an extremely small point on the surface of a specimen 

by an electromagnetic lens; method for nondestructive analysis of chemical composition by 

measurement of resulting backscatter or other 

phenomena. 

Electronegativity: Electro-affinity. 

Encephalitis: Inflammation of the brain. 

Encephalopathy: Any degenerative disease of the 

brain. 

Epidemiology: Study of the distribution and determinants of disease in human population groups. 

Epinephrine: Hormone secreted by adrenal medulla 

that acts to increase blood pressure by means of 

stimulation of heart action and constriction of peripheral blood vessels. 

Episodal: Adjective in current usage that denotes an 

air pollution episode; that is the occurrence of 

short-term, peak air pollutant concentrations of 

crisis proportions. 

Epithelial: Pertaining to or composed of epithelium; 

that is, covering of external or internal body surfaces, including linings of vessels and other small 

cavities, composed of cells joined together with 

cementing substances. 

Equilibrium vapor pressure: Vapor pressure of a 

system in which two or more phases of a substance 

coexist in equilibrium. 

Erosion: Movement of soil or rock from one point to 

another by the action of the sea, running water, 

moving ice, precipitation, or wind. 

Erythrocyte porphyrin: See Free erythrocyte protoporphyrin. 

Erythrocyte protoporphyrin: See Free Erythrocyte 

portoporphyrin. 

Erythrocytes: Red blood cells. 

Erythropoiesis: Formation of red blood cells. 

Ethylenediaminetetraacetic acid (EDTA): Used in 

the form of calcium-disodium salt as a chelating 

agent to complex with lead and other metals and 

remove them from the body by urinary excretion. 

Evaporation: Physical process by which a liquid or 

solid is transformed to the gaseous state; opposite 

of condensation. 

Evoked-response technique: A technique widely 

used in electrophysiology in which a stimulus 

(e.g., electric shock, light flash, click) is applied 

peripherally to the electrode used to detect the 

response. 

Exencephaly: A developmental anomaly characterized by an imperfect cranium, the brain lying 

outside the skull. 

Exposure level: Concentration of a contaminant to 

which the population in question is exposed. 

Exudate: Material, such as fluid, cells, or cellular 

debris, that has escaped from blood vessels and 

has been deposited in tissues or on tissue surfaces, 

usually as a result of inflammation; contains high 

content of protein, cells, or solid materials 

derived from cells. 

Fallout: In air pollution, particulate matter that falls 

to the surface of the earth through the action of 

gravity; a passive phenomenon unrelated to atr 

mospheric or mechanical motion. 

Fanconi syndrome: In this document, the triad of 

glycosuria, hyperaminoaciduria, and hyr 

pophosphatemi a in the presenc e of hy7 

perphosphaturia that is associated with injury to 

proximal renal tubular cells. 

Flinch/jump thresholds: Behavioral testing procedure used to measure pain threshold by measuring sensitivity to shock. The shock intensity at 

which animals first flinch and first jump in 

response to foot shock is recorded. 

Flux: Rate of flow of some quantity, often used in 

reference to some form of energy; also called 

transport. 

Fornix: General term for an archlike structure or the 

vaultlike space created by such a structure; fornix 

of cerebrum—efferent pathway of the hippocarrij 

pus. 

Free erythrocyte porphyrin (FED): See Free 

erythrocyte protoporphyrin. 

Free erythrocyte protoporphyrin (FEP): Intermeditate in the biosynthesis of heme; specifically, the 

immediate precursor to heme synthesis in which 

one atom of iron is inserted into the protoporphyrin nucleus to form heme. Used interchangeably with erythrocyte protoporphyrin 

and erythrocyte porphyrin. 

Fugitive dust: Dust that escapes from industrial pro* 

cesses, soil surfaces, roadways, etc.; dust that cannot be contained by air pollution control practices. 

/3-Galactosidase: Enzyme that hydrolyzes galacr 

tosides (compounds containing a sugar and a nonsugar component) to produce D-galactose. 

Galena: Lead sulfide ore. 

Ganglia: Plural of ganglion, a general term for a 

group of nerve cell bodies located outside the 

central nervous system; basal ganglia—masses of 

gray matter in the cerebral hemisphere. 

A-6 
Gastrointestinal mucosa: Mucous membrane of the 

stomach and intestine. 

Geometric mean: An estimate of the median of a lognormal distribution, calculated as the antilogarithm of the mean of the logarithms of the observations. 

Geometric standard deviation: A measure of dispersion for a lognormal distribution; it is the antilogarithm of the standard deviation of the 

logarithms of the observations. (Also known as 

standard geometric deviation.) 

Glacier: Mass of land ice flowing slowly (at present 

or in the past) from an accumulation area to an 

area of ablation. 

Glacier ice: Any ice that is or once was part of a 

glacier. 

Glomerular filtration: Filtration of plasma by the 

glomeruli of the kidney that removes fluids, 

electrolytes; glucose, amino acids, and other 

small molecules; 80 to 85 percent of water and 

virtually all of the other substances are reabsorbed by the proximal tubules. 

Glomerulus: Anatomical term designating a tuft or 

cluster of blood vessels or nerves; often used 

alone to designate renal glomeruli, which are 

coils of blood vessels, one projecting into the expanded end or capsule of each of the uriniferous 

tubules of the kidney. 

Glucose-6-phosphate dehydrogenase: Enzyme important in maintenance of adequate concentrations of reduced glutathione in red blood cells. 

Deficiency of this enzyme is inherited as a sexlinked trait; it mediates the reaction, Dglucose-6-phosphate + NADP = D-glucono-8-

lactone 6-phosphate + NADPH2. 

/3-Glucuronidase: Enzyme that mediates the hydrolysis of natural and synthetic glucuronides; 

yields /3-D-glucuronate as a product. 

Glutamate dehydrogenase: Enzyme that mediates 

the removal of hydrogen atom(s) from glutamate, 

the salt or ester of glutamic acid, which is a dicarboxylic amino acid. 

Glutathione: Tripeptide that serves as a coenzyme 

and acts as a respiratory carrier of oxygen. 

Reduced glutathione (GSH) is present in red cells 

and is associated with glucose-6-phosphate 

dehydrogenase and reduced nicotinamide 

adenine dinucleotide phosphate in maintenance 

of red cell integrity. 

Glycosuria: Presence in the urine of glucose, a simple sugar formed from more complex sugars and 

normally retained in the body as a source of 

energy. 

Grignard process: A relatively common synthetic 

procedure for the preparation of organometallic 

compounds from an organomaghesium precursor. 

Groundwater: All subsurface water, especially that 

part that is in the zone of saturation. 

Half-life: Time required for a system decaying at an 

exponential rate (such as an element in radioactive disintegration) to be reduced to one-half its 

initial size, intensity, or numerical amount. 

Haze: Fine dust or salt particles dispersed through a 

portion of the atmosphere; the particles are so 

small they cannot be felt or individually seen with 

the naked eye, but they diminish horizontal 

visibility and give the atmosphere a characteristic 

opalescent appearance that subdues all colors. 

Hematofluorometer: Commercially available portable spectrofluorometer used to measure 

erythrocyte protoporphyrin (porphyrin) directly; 

in wide use in lead screening programs. 

Hematopoiesis: Formation and development of 

blood cells. 

Hematopoietic system: System of cells in bone marrow, spleen, and lymph nodes concerned with formation of cellular elements of the blood. 

Hemin : Crystallin e chlorid e of heme , 

C34H33N404FeCl. 

Heparin: Mucopolysaccharide acid occurring 

naturally in various tissues, especially the liver 

and lungs; sodium heparin, a mixture obtained 

from animal tissues, is an anticoagulant used in 

vivo and in vitro. 

High-volume sampler: Device for taking a large 

sample of air in a minimal span of time, routinely 

about 2000 m3/24 hr (1.38 m3/min), or even as 

high as 2880 m3/24 hr (2 m3/min). 

Hippocampus: Curved elevation in the inferior horn 

of the lateral ventricle of the brain; important 

functional component of the limbic system, the 

system controlling autonomic functions and certain aspects of emotion and behavior. 

Histidine residue: One of the naturally occurring 

peptide linkages in a protein, containing the 

chemical group, imidazole: 

HC = CI I 

N NH V 

C 

H 

A-7 
P.75 

Homovanillic acid: A methylated metabolite of hydroxytyramine: 

CH3 0 

HO CH2-COOH 

Hydrocephalus: Condition characterized by abnormal accumulation of fluid in the cranial vault, accompanied by enlargement of the head, prominence of the forehead, atrophy of the brain, mental deterioration, and convulsions. 

Hyperactivity: Abnormally increased activity. 

Developmental hyperactivity of children is 

characterized by constant motion—exploring, experimenting, etc.—and is usually accompanied by 

distractibility and low tolerance for frustration. It 

usually abates during adolescence. May result 

from brain damage or psychoses. 

Hyperkinesia: Abnormally increased motor function 

or activity; see Hyperactivity. 

Hyperkinetic: Characterized by abnormally increased muscular movement. 

Hyperkinetic-aggressive behavior disorder: A disorder characterized by overactivity, restlessness, 

distractibility, and short attention span. 

Hyperphosphaturia: Above-normal amounts of 

phosphate compounds in the urine. 

Hyperuricemia: Abnormal amounts of uric acid in 

the blood. 

Hypochromic anemia: A condition characterized by 

a disproportionate reduction of red cell 

hemoglobin, compared with the volume of 

packed cells. 

Hypophosphatemia: Abnormally decreased amount 

of phosphates in the blood. 

Hypothalamus: Portion of the diencephalon that 

forms the floor and part of the lateral wall of the 

third ventricle of the brain. 

Imidazole group: See Histidine residue. 

Impactor: General term for instruments that sample 

atmospheric particles by impaction; such devices 

consist of a housing that constrains the air flow 

past a sensitized sampling plate. 

Impinger: Device used to sample dust or other particles in the air; draws in a measured volume of air 

and directs it through a jet to impact on a wetted 

surface. 

In situ: In the original location. 

Interstitial fibrosis: A progressive formation of 

fibrous tissue in the interstices in any structure; in 

the lungs, it reduces aeration of the blood. 

In vitro: Outside the living organism. 

In vivo: Within the living organism. 

Iron deficiency: A deficiency of iron-containing 

foods in the diet such that not enough iron is 

available for incorporation into newly formed 

hemoglobin; iron deficiency within the body may 

also result from poor intestinal absorption of iron 

in spite of a dietary sufficiency. 

Ischemia: Deficiency of blood in a part, caused by 

functional constriction or actual obstruction of a 

blood vessel. 

Ischemic: Pertaining to, or affected with, ischemia. 

Isocortex: Neopallium; that portion of the cerebral 

cortex showing stratification and organization 

characteristic of the most highly evolved type of 

cerebral tissue. 

Isokinetic sampling: Taking a sample of air without 

changing the speed or direction of the air as it enters the sampler. 

Jiggle platform: Apparatus used in behavioral testing to measure an animal's activity. Generally 

consists of a spring-loaded platform equipped 

with a detector for measuring movement. 

a-Ketoglutarate: Salt of a-ketoglutaric acid, a 

dibasic keto acid occurring as an intermediate in 

carbohydrate (Krebs cycle) and protein metabolism. 

Kilocalorie: Unit of heat energy equal to 1000 calories; also known as large calorie. 

Lactic acid dehydrogenase (LDH): Catalyzes reduction of pyruvic acid by reduced nicotinamide 

adenine dinucleotide; prevents buildup of pyruvate in anaerobic glycolysis. 

Leached: Subjected to the action of percolating 

water or other liquid that removes the soluble 

substances. 

Lead particles: Lead-containing particles. 

Lead poisoning (syn. lead intoxication, plumbism, 

saturnism): A disease condition reflecting the adverse effects of the absorption of lead into the 

system. 

Lead subacetate (syn. lead monosubacetate, 

monobasic lead acetate): Pb(C2H3 02 ) 2 «2Pb 

(OH)2. 

Learning paradigm: A particular set of experimental 

conditions used to study learning. 

Ligand: A molecule, ion, or atom that is attached to 

the central atom of a coordination compound, a 

chelate, or other complex. 

Line source: Consists of a number of point sources 

arranged in a straight line, usually across wind 

(see Point source). 

A-8 
P.76 

Lipoamide dehydrogenase: Trivial name for 

lipoamide oxidoreductase; enzyme catalyzing the 

reaction, NAD + dihydro-lipoamide = NADH2 

+ oxidized lipoamide. 

Lithosphere: The rigid outer crust of rock on the 

earth, about 80 km deep; more recently, with 

development of plate tectonics theory, the outer 

100 km of the earth's surface. 

Lognormal distribution: A variable whose 

logarithms follow a normal distributirin. 

Lumen: The cavity or channel within a tubular 

organ; in this document, intestinal. 

Lymphocyte: Mononuclear leukocyte (a white blood 

cell) with a deeply staining nucleus containing 

dense chromatin; chiefly a product of lymphoid 

tissue, it participates in humoral and cell-mediated immunity. 

Lysosome: Submicroscopic organelle, found by 

electron microscope in many types of cells, that 

contains various hydrolytic enzymes and is normally involved in localized intracellular digestion. 

a-Mannosidase: Enzyme that catalyzes the hydrolysis of a-D-mannoside to an aocohol and Dmannose, a simple sugar. 

Mass median diameter (MMD): Geometric median 

size of a distribution of particles, based on weight. 

Mass median equivalent diameter (MMED): Convenient parameter for characterizing airborne particulates; divides the total mass of aerosol particles into two equal parts: half the mass resides in a 

relatively smaller number of particles larger than 

this median size and half resides in a relatively 

larger number of particles having diameters 

below this median size. 

Maze: System of intersecting paths used in tests of 

intelligence and learning in experimental 

animals. 

McCarthy Scales of Intelligence: A standardized intellectual assessment instrument (appropriate for 

ages 2.5 to 8.5 yr), consisting of five subtests 

yielding individual scores in (1) verbal, (2) perceptual-performance, (3) quantitative, (4) memory, and (5) motor, as well as yielding a general 

cognitive index comparable to an intellectual 

quotient (I.Q.) score. 

Mean: Used synonymously with the arithmetic 

mean; that is, the sum of the observations divided 

by the sample size. 

Meninges: Three membranes that envelope the brain 

and spinal cord; the dura mater, pia mater, and 

arachnoid. 

Messenger RNA (mRNA): Linear polymer of 

nucleotides that is transcribed from and complementary to a single strand of DNA; carries information for protein synthesis to the ribosomes. 

Metabolites: End products of metabolic processes 

that transform one compound into another in living cells. 

Microcytic anemia: Condition in which the majority 

of the red cells are smaller than normal. 

Micromelia: Developmental anomaly characterized 

by abnormal smallness or shortness of the limbs. 

Microsome: One of the finer granular elements of 

protoplasm; part of the endoplasmic reticulum, 

site of various metabolic and synthetic processes 

including incorporation of amino acids into proteins. 

Mist: Microscopic and more or less hygroscopic 

water droplets suspended in the atmosphere. 

Relative humidity when mist is present is often 

less than 95 percent. 

Mitochondria: Small organelles found in the 

cytoplasm of cells; principal sites of generation of 

energy, they contain enzymes of the Krebs and 

fatty acid cycles and the respiratory pathway. 

Mobilizable lead: The fraction of the total lead content of the body that can be removed by chelating 

agents. 

Molal: Containing one mole or one gram molecular 

weight in 1000 grams (1 kg) of solute. 

Molar: Containing one mole or one gram molecular 

weight of solute in 1000 ml (1 liter) of solution. 

Mole: That amount of chemical compound whose 

mass in grams is equivalent to its formula mass, 

i.e., mass numerically equal to the molecular 

weight and most frequently expressed as the gram 

molecular weight (the weight of one mole expressed in grams). 

Midbrain: Mesencephalon; portions of the adult 

brain derived from the embryonic midbrain. 

Miniature end-plate potentials (MEPP's): Small potential changes in the neighborhood of the end 

plate representing the response of the membrane 

to release of acetylcholine in quantities insufficient to depolarize the membrane to threshold 

levels. 

Monoamine: Organic compound to which an amine 

(-NH2group) is attached; e.g., serotonin. 

Monamine oxidase: Flavoprotein that catalyzes the 

aerobic oxidation of physiological amines to the 

corresponding aldehydes and ammonia; acts upon 

serotonin, a nervous system regulator, to yield 5-

hydroxy-indolealdehyde. 

A-9 
P.77 

Monominergic: Stimulated, activated, or transmitted by monoamines; applied to nerve fibers that 

liberate monoamines at a synapse when a nerve 

impulse passes. 

Motor skills: Skilled movements that depend on the 

integrity of the nervous system for control. 

Mutagenicity: Property of being able to induce 

genetic mutation, i.e., a permanent, transmissable 

change in the genetic material. 

Myelopathy: Pathology of the muscle fibers. 

Myxedema: Nonpitting edema characterized by dry, 

waxy type of swelling, with abnormal deposits of 

mucin in the skin and other tissues; associated 

with hypothyroidism. 

Nasopharynx: The part of the pharynx that lies 

above the level of the soft palate; the pharynx 

being the muscular, membranous sac between the 

mouth, the nares, and the esophagus. 

National Air Surveillance Networks (NASN): Networks of monitoring stations for sampling air to 

determine extent of pollution. Established jointly 

by Federal and state governments. 

Neoplasm: An aberrant new growth of abnormal 

cells or tissue in which the growth is uncontrollable and progressive. 

Nephritis: Inflammation of the kidney. 

Nephropathy: Disease of the kidneys. 

Nerve conduction: Passage of a nerve impulse 

manifested by an electric impulse that travels 

along the nerve. 

Neuropathy: Functional disturbances and/or 

pathological changes in the peripheral nervous 

system; affects the neurons (nerve cells, including 

cell body, axon, and dendrites). 

Neuropil: Dense feltwork of interwoven cytoplasmic 

processes of nerve cells and of neuroglial cells in 

the central nervous system and in some parts of 

the peripheral nervous system. 

Nictitating membrane: Thin membrane, or inner or 

third eyelid, present in many animals; capable of 

being drawn across the eyeball, as for protection. 

Norepinephrine: Hormone secreted by neurons; acts 

as a transmitter substance at the peripheral sympathetic nerve endings and probably in certain 

synapses in the central nervous system. 

Normal distribution (Gaussian distribution): Fundamental frequency distribution of statistical 

analysis. A continuous variate, x , is said to have 

a normal distribution or to be normally distributed if it possesses a density function, f(x), 

that satisfied the equation: 

f (x) =_U-( X- ^ W (-oo< X <oc), 

cr27r ' 

where fi is the arithmetic mean (or first moment) 

and o- is the standard deviation. About two-thirds 

of the total area under the curve is included between x = fi-a and x = fi + o\ 

Normal population: Collection of quantities having 

a normal distribution. 

Normoblast: Nucleated percursor cell intermediate 

in the formation of erythrocytes. 

Nuclear inclusion bodies: Round, oval, or irregularly shaped bodies appearing in the nuclei of 

cells. 

Nucleus: Small mass of differentiated protoplasm 

rich in nucleoproteins and surrounded by a 

membrane; found in most animal and plant cells; 

contains chromosomes and functions in metabolism, growth, and reproduction. 

One-way avoidance tasks: See Avoidance task. 

Optical emission spectrography: Analytical method 

in which the sample is vaporized and decomposed, and the constituent elements excited by an 

electrical arc or a high voltage spark. The light 

emitted as a consequence of the excitation passes 

through a spectrograph and the resulting 

spectrum is recorded photographically. 

Paraplegia: Paralysis of the legs and lower part of 

the body. 

Parenchyma: General term to designate functional 

elements of an organ as distinguished from its 

framework, or stroma. 

Particle eddy diffusivity: The diffusion of particles 

by eddies in a turbulent flow. 

D-penicillamine: Product of penicillin; whitish 

crystalline powder used as a metal complexing 

agent to remove excess metals from the body. 

Peptidergic: Stimulated, activated, or transmitted by 

peptides; applied to those nerve fibers that liberate peptides at a synapse when a nerve impulse 

passes. 

Photolysis: Chemical decomposition by the action of 

light. 

Phrenic nerve: Arising from the third, fourth, and 

fifth cervical segments of the spinal cord, the 

nerve that innervates the diaphragm. 

Pica: Habitual ingestion of nonfood items. 

Pinna: Projecting part of the ear lying outside the 

head. 

Plumbism: Lead poisoning; saturnism. 

A-10 
Point source: A single isolated stationary source of 

pollution. 

Polarography: An electroanalytical technique in 

which the current through an electrolysis cell is 

measured as a function of the applied potential. 

Polyneuropathy: Disease that involves several 

nerves. 

Polysomes: Complex of ribosomes bound together 

by a single messenger ribonucleic acid (mRNA) 

molecule. Also known as polyribosome. 

Porphobilinogen (PBG): Intermediate in the biosynthesis of heme that does not accumulate under 

normal circumstances. 

Porphyrin: Any one of a group of iron-free or magnesium-free cyclic tetrapyrrole derivatives that 

occur universally in protoplasm. They form the 

basis of the respiratory pigments, such as 

cytochromes and chlorophyll, of animals and 

plants. 

Precipitation: Any or all forms of water particles, 

liquid or solid, that fall from the atmosphere and 

reach the ground. 

Prevailing wind direction: Wind direction most frequently observed during a given period. 

Primary smelting: Extraction of metal from ore. 

Promotional energy: Energy required to promote an 

electron from its free atom ground state to the hybridization state required for bonding. 

Protoporphyrin (PP): Porphyrin that is the proteinfree precursor to hemoglobin, myoglobin, 

catalase, and certain respiratory pigments. 

Protoporphyrin IX: An isomer of protoporphyrin. 

Proximal convoluted tubules: Convoluted portion 

of the vertebrate nephron (functional unit of the 

kidney) lying between Bowman's capsule and the 

loop of Henle; functions in resorption of sugar, 

Na

 + ,C1 , and water. 

Psychomotor: Pertaining to motor effects of cerebral 

or psychic activity. 

Pyrimidine-5'-nucleotidase: Enzyme that mediates 

hydrolysis of pyrimidine-5'-phosphate to yeild inorganic phosphorus and the corresponding 

pyrimidine nucleoside. 

Pyrrole: Heterocyclic ring compound, consisting of 

four carbon atoms, one nitrogen atom, and five 

hydrogen atoms, that is a component of 

chlorophyll, hemin, and many other important 

naturally occurring substances. 

Pyruvate: Salt of pyruvic acid, an important intermediate in carbohydrate (Krebs cycle) and protein metabolism. 

Reentrainment: Resuspension of particulate matter, 

especially dust, in the ambient air; see text dicussion of resuspension. 

Reference method: In this document, the official, accepted method for sampling and analysis of an 

element or compound; method to which other 

methods are compared for accuracy and precision, and/or for reporting of data. 

Relative humidity: Dimensionless ratio of actual 

vapor pressure of the air to the saturation vapor 

pressure; usually expressed as percent. 

Renal insufficiency: State in which the kidneys are 

unable to remove a sufficient proportion of the 

effete, or spent, matter of the blood. 

Reticulocytosis: Increase in the number of 

reticulocytes (young red blood cells showing 

basophilic network under vital staining) in the peripheral blood. 

Ribonucleic acid (RNA): Nucleic acid in the form of 

a linear polymer, usually a single strand, composed of repeating units of nucleotides (the 

organic bases; adenine, cytosine, guanine, and 

uracil) conjugated to ribose and kept in sequence 

by phosphodieste r bonds. Involved intracellularly in protein synthesis. 

Ribosomes: Complex small particles in the living 

cell, composed of various proteins and three 

molecules.of RNA; site of synthesis of proteins. 

Sampling error: Difference between a measured 

value and the true value that results from sampling techniques and procedures. 

Sampling train: Pollutant collecting device consisting of a series of components through which an air 

stream passes. Components usually include 

prefitter; pipes or ducts; means for measuring air 

flow; an air pump; and a detector or sensor that 

gives an immediate reading or a collector in 

which the pollutant is subsequently measured. 

Saturnism: Lead poisoning. 

Schwann cell: One of the large nucleated masses of 

protoplasm lining the inner surface of the 

neurilemma, a membrane wrapping the nerve 

fiber. 

Secondary smelting: Extraction of metal from scrap 

and salvage. 

Sedimentation: The act or process of deposition of 

sediment; can refer (1) to the deposition of airborne particulate matter on a surface or (2) to the 

deposition and accumulation of solid matter on 

the bed of a body of water. 

Seizure: Sudden onset or recurrence of a disease or 

an attack; specifically, an epileptic attack, or convulsion. 

A-ll 
P.79 

Septum-frontal forebrain: Describes anatomical 

connections in the brain between the septal area 

and the forebrain. 

Sequela: Any lesion or affection that follows or is 

caused by an attack of disease. 

Serotonin: A vasoconstrictor, 5-hydroxytryptamine, 

found in serum and many body tissues, including 

the intestinal mucosa, pineal body, and central 

nervous system, especially the hypothalamus, 

midbrain, basal ganglia, and spinal cord; believed 

to be a neurotransmitter that plays a regulatory 

role in the central nervous system. 

Serum glutamic-oxaloacetic transaminase (SGOT): 

Enzyme that transfers an amino group from Lglutamic acid to oxaloacetic acid, forming 8-

ketoglutaric acid plus L-aspartic acid. Oxaloacetic and 8-ketoglutaric acids are both major 

intermediates in the citric acid cycle (Krebs cycle), the energy-generating cycle. 

Serum glutamic-pyruvic transaminase (SGPT): 

Enzyme that transfers an amino group from Lglutamic acid to pyruvic acid, forming 8-

ketoglutaric acid plus L-alanine. 8-Ketoglutaric 

acid is a major intermediate in the Krebs cycle, 

and pyruvic acid is the immediate precursor of 

acetylcoenzyme A, which combines with oxaloacetic acid to form citric acid in the citric acid 

cycle (Krebs cycle). 

Shuttle box: Two-compartment chamber used in 

animal behavior; the movement from one compartment to the other is the behavior that is 

studied. 

Soret band: Band in the violet end of the spectrum of 

hemoglobin. 

Spina bifida: Developmental anomaly characterized 

by defective closure of the bony encasement of the 

spinal cord. 

Stabilimeter: Device used to measure an animal's activity by measuring vertical movement of the 

floor. 

Stack emissions: Effluents released into the atmosphere from the exhaust flue of a building; 

usually refers to pollutants but can refer to steam 

or other nonpolluting effluents. 

Standard deviation: A measure of dispersion or 

variation, usually taken as the square root of the 

variance. 

Standard geometric deviation: Measure of dispersion of values about a geometric mean; the portion of the frequency distribution that is one standard geometric deviation to either side of the 

geometric mean accounts for 68 percent of the 

total samples. 

Standard normal deviation: Measure of dispersion 

of values about a mean value; the positive square 

root of the average of the squares of the individual deviations from the mean. 

Stanford-Binet I.Q. Test: A standardized intellectual assessment instrument (appropriate for ages 

2 yr to adult), yielding a general intelligence quotient (I.Q.) score. 

Steady state exposure: Exposure to an environmental pollutant whose concentration remains constant for a period of time. 

Stoichiometry: Numerical relationship of elements 

and compounds as reactants and products in 

chemical reactions. 

Stratosphere: Atmospheric shell about 55 km deep 

that begins where the troposphere ends, at 10 to 

20 km from the earth's surface. 

Striatum: Corpus striatum; subcortical mass of gray 

and white substance in front of and lateral to the 

thalamus in each cerebral hemisphere. 

Stroma: Supporting tissue or matrix of an organ, as 

distinquished from its functional element, or 

parenchyma. 

Subclinical lead poisoning: Toxic effects of lead that 

do not produce clinically discernible signs. 

Succinate: Salt of succinic acid, important intermediate in carbohydrate (Krebs cycle) and protein metabolism. 

Succinoxidase: Complex enzyme system, containing 

succinic dehydrogenase and cytochromes, that 

catalyzes the conversion of succinate and molecular oxygen to fumarate ( a Krebs cycle intermediate). 

Succinyl coenzyme A: COOH(CH2)2COOH-S-CoA; 

compound formed from succinic acid and 

coenzyme A in the citric acid cycle (Krebs cycle). 

It provides free energy for the synthesis of a 

molecule of ATP and can participate in acylating 

reactions for the introduction of a succinyl group; 

it also participates in other metabolic reactions, 

such as the synthesis of porphyrins. 

Sulfhydryl group: The -SH group occurring in 

reduced glutatione and in cysteine. 

Superior cervical ganglion: A group of nerve cell 

bodies located outside the central nervous system, 

situated near the cervix. 

Surface water: All bodies of water on the surface of 

the earth. 

Synapse: Region of contact between processes of two 

adjacent neurons. 

Synaptic uptake: Movement of a chemical into the 

neuron in the area of the synapse. 

A-12 
P.80 

Synaptosomal transport: Uptake of a chemical into 

isolated synapses. 

Synergetic: Working together; an agent that works 

synergistically with one or more other agents. 

Synergistic effects: Joint effects of two or more 

agents, such as drugs that increase each other's 

effectiveness when taken together. 

Telencephalon: Paired cerebral vesicles, from which 

the cerebral hemispheres are derived. 

Teratology: Science that deals with abnormal 

development of the fetus and congenital malformations. 

Teratospermia: Presence of malformed spermatozoa 

in the semen. 

Temperature inversion: Layer of air in which temperature increases with altitude; very little turbulent exchange occurs within it. 

Terminal velocity: See Terminal fall velocity. 

Terminal fall velocity (terminal velocity): Particular falling speed, for any given object moving 

through a fluid medium of specified physical 

properties, at which the drag forces and buoyant 

forces exerted by the fluid on the object just equal 

the gravitational force acting on the object, after 

which it falls at constant speed unless it moves 

into air layers of different physical properties. In 

the atmosphere, the latter effect is so gradual that 

objects such as raindrops, which attain terminal 

velocity at great heights above the surface, may be 

regarded as continuously adjusting their speeds to 

remain at all times essentially in the terminal fall 

condition. 

Topography: (1) General configuration of a surface, 

including its relief; may be a land or water-bottom surface; (2) natural surface features of a 

region, treated collectively as to form. 

Transaminases: Enzymes that catalyze the transfer 

of an amino group of an amino acid to a keto acid 

to form another amino acid; also known as 

aminotransferases. 

Transfer RNA (tRNA): Smallest ribonucleic acid 

molecule found in cells; its structure is complementary to messenger RNA and it functions in 

transferring amino acids from their free state to a 

growing polypeptide chain. 

Transformation: In this document, changes in physical or chemical form of lead-containing particles 

or compounds that occur with time and space 

during atmospheric and environmental residence 

and/or transport. 

Translocation: Transfer of metabolites, nutritive 

materials, or other substances from one part of a 

plant to another. 

Transport: In this document, movement of lead and 

its compounds from one place to another in the 

environment. 

Transudation: Passage of serum or other body fluid 

through a membrane or tissue surface; may or 

may not be the result of inflammation. 

Troposphere: The atmospheric shell extending 

about 10 to 20 km from the earth's surface. 

Trypan Blue: An acid, azo dye used in vital staining; 

under normal conditions, it does not enter most 

areas of the brain from the blood. 

Tumor: Any abnormal mass of cells resulting from 

excessive cellular multiplication. 

Turbulence: State of fluid flow in which instantaneous velocities exhibit irregular and apparently random fluctuations so that, in practice, 

only statistical properties can be recognized and 

analyzed; turbulence can transport suspended 

matter at rates far in excess of rates of transport 

by diffusion and conduction in a laminar flow. 

Two-way aviodance tasks: See Avoidance task. 

Tyrosine: Amino acid (p-hydroxyphenylalanine, 

CgHnOjN) found in most proteins and synthesized metabolically from phenylalanine. It is a 

precursor of dopamine and of the hormones, 

epinephrine , norepinephrine , an d 

triiodothyronine. 

Ultradian rhythms: Biological rhythm with a frequency higher than circadian (24 hr). 

Uncertainty: Standard deviation of a sufficiently 

large number of measurements of the same quantity by the same instrument or methods; the noncorrectable inaccuracy of the instrument. 

Upwind: Toward the direction from which the wind 

is flowing; counter to the wind. 

Urobilinogen: Colorless compound formed in the intestine by the reduction of bilirubin (a bile pigment that is a breakdown product of heme); some 

is excreted in the feces where it is oxidized to 

urobilin; some is reabsorbed and reexcreted in the 

bile (as bilirubin) or in the urine. 

Uroporphyrin: Any of several isomeric, metal-free 

porphyrins, occurring in small quantities in normal urine and feces. 

Vacuolization: Formation of vacuoles, any small 

spaces or cavities formed in the protoplasm of a 

cell. 

A-13 
P.81 

Vacutainers: Registered trademark of sealed ampules, maintained under a slight vacuum and containing an anticoagulant, into which blood samples may be drawn directly. 

Vanillyl mandelic acid (vanilmandelic acid): A major metabolite of the catechloamines; used to 

assess quantitatively the endogenous production 

of catecholamines. 

Variance: A measure of dispersion or variation of a 

sample from its expected value. It is usually 

calculated as a sum of squared deviations about a 

mean divided by the sample size. 

Wechsler Intelligence Test (WISC): A standardized 

intellectual assessment instrument (appropriate 

for ages 6 yr to 16 yr 11 mo), consisting of 12 subtests designed to yield verbal and performance intellectual scores. 

Wet deposition: Removal of particles from the atmosphere via precipitation; rainout. 

Wind: Air motion relative to the surface of the earth. 

Vertical components are relatively small, 

especially near the surface of the earth; hence, the 

term denotes almost exclusively the horizontal 

component. 

WPPSI Test: A version of the WISC test, but consisting of 10 subtests representing a downward extension of the WISC appropriate for younger 

children (ages 4 to 6.5 yr). 

Xenobiotics: Chemicals foreign to biologic systems. 

X-ray diffraction analysis: Analysis of the crystal 

structure of materials by passing Xrays through 

them and registering the diffraction (scattering) 

image of the rays. 

X-ray powder diffraction techniques: Analytical 

techniques in which an X-ray beam of known 

wavelength strikes a finely ground powder sample; the crystal planes of the powder diffract the 

beam and these diffraction lines are recorded on 

photographic film. 

X-ray spectrography: Analytical method employing 

an X-ray spectrometer (instrument for producing 

the X-ray spectrum of a material and measuring 

the wavelengths of components) that is equipped 

with photographic or other recording apparatus. 

Zinc erythrocyte porphyrin: The biochemically correct form for the erythrocyte protoporthyrin or 

porphyrin that is elevated in lead exposure or 

iron deficiency anemia. Used interchangeably in 

this document with erythrocyte porphyrin, 

erythrocyte protoporthyrin, and free erythrocyte 

porphyrin or protoporthyrin. 

A-14 
P.82 

APPENDIX B 

PHYSICAL/CHEMICAL DATA FOR LEAD COMPOUNDS 

B.l DATA TABLES 

TABLE B-1, PHYSICAL PROPERTIES OF INORGANIC LEAD COMPOUNDS' 

Compound 

Lead 

Acetate 

Azide 

Bromate 

Bromide 

Carbonate 

Carbonate, 

basic 

Chloride 

Chlorobromide 

Chromate 

Chromate, 

basic 

Cyamide 

Fluoride 

Fluorochloride 

Formate 

Hydride 

Hydroxide 

lodate 

Iodide 

Nitrate 

Nitrate, basic 

Oxalate 

Oxide 

di Oxide 

Oxide (red) 

Phosphate 

Sulfate 

Sulfide 

Sulfite 

Thiocyanate 

Abbreviations: 

a - acid 

al - alcohol 

alk - alkali 

d - decomposes 

expl - explodes 

Formula 

Pb 

Pb(C2H302)2 

Pb(N3)2 

Pb(Br03)2-H20 

PbBr2 

PbC03 

2PbC03-Pb(OH)2 

PbCI2 

PbCIBr 

PbCr04 

PbCr04-PbO 

Pb(CN)2 

PbF2 

PbFCI 

Pb(CHO)2 

PbH2 

Pb(OH)2 

Pb(l03)2 

Pbl2 

Pb(N03)2 

Pb(OH)(N03) 

PbC204 

PbO 

Pb02 

Pb304 

Pb3(P04)2 

PbS04 

PbS 

PbS03 

Pb(SCN)2 

glyc - glycol 

i - insoluble 

s - soluble 

M.W. - molecular weight 

S.G. - specific gravity 

MP. - melting point 

M.W. 

207.19 

325.28 

291.23 

481.02 

367.01 

267.20 

775.60 

278.10 

322.56 

323.18 

546.37 

259.23 

245.19 

261.64 

297.23 

209.21 

241.20 

557.00 

461.00 

331.20 

286.20 

295.21 

223.19 

239.19 

685.57 

811.51 

303.25 

239.25 

287.25 

323.35 

S.G. 

11.35 

3.25 

— 

5.53 

6.66 

6.6 

6.14 

5.85 

— 

6.12 

6.63 

— 

8.24 

7.05 

4.63 

— 

— 

6.155 

6.16 

4.53 

5.93 

5.28 

9.53 

9.375 

9.1 

7 

6.2 

7.5 

— 

3.82 

M.P. 

327.5 

280 

expl. 

d180 

373 

d315 

d400 

501 

— 

844 

— 

— 

855 

601 

d190 

d 

d145 

d300 

402 

d470 

d180 

d300 

888 

d290 

d500 

1014 

1170 

1114 

d 

d190 

Solubility, g/100 

Cold 

water 

i 

44.3 

0.023 

1.38 

0.8441 

0.00011 

i 

0.99 

— 

6x10-6 

i 

si s 

0.064 

0.037 

1.6 

— 

0.0155 

0.0012 

0.063 

37.65 

19.4 

0.00016 

0.0017 

i 

i 

1.4x10-5 

0.00425 

8.6x10-5 

i 

0.05 

Hot 

water 

i 

22150 

0.0970 

Si s 

4.71100 

d 

i 

3.34100 

— 

i 

i 

s 

— 

0.1081 

20 

— 

si s 

0.003 

0.41 

127 

s 

— 

— 

0.0056 

— 

i 

0.2 

ml 

Other 

solvents 

sa 

sglyc 

— 

— 

sa 

sa.alk 

sHN03 

ial 

— 

sa.alk 

sa.alk 

sKCN 

sHN03 

— 

ial 

— 

sa.alk 

sHN03 

s.alk 

s.alk 

sa 

sa 

s.alk 

sa 

sa . 

s.alk 

— 

sa 

sa 

s.alk 

B-l 
P.83 

TABLE B-2. TEMPERATURE VARIATION OF THE VAPOR PRESSURES OF COMMON LEAD COMPOUNDS* 

Name 

Lead 

Lead bromide 

Lead chloride 

Leadflouride 

Lead iodide 

Lead oxide 

Lead sulfide 

Formula 

Pb 

PbBr2 

PbCI2 

PbF2 

Pbl2 

PbO 

PbS 

MP. 

327.4 

373 

501 

855 

402 

890 

1114 

1 mm 

973 

513 

547 

solid 

479 

943 

852 

(solid) 

10mm 

1162 

610 

648 

904 

571 

1085 

975 

(solid) 

Temperature "C 

40mm 

1309 

686 

725 

1003 

644 

1189 . 

1048 

(solid) 

100mm 

1421 

745 

784 

1080 

701 

1265 

1108 

(solid) 

400mm 

1630 

856 

893 

1219 

807 

1402 

1221 

760mm 

1744 

914 

954 

1293 

872 

1472 

1281 

B.2. THE CHELATE EFFECT 

The stability constants of chelated complexes are 

normally several orders of magnitude higher than 

those of comparable monodentate complexes; this 

effect is called the chelate effect and is very readily 

explained in terms of kinetic considerations. A comparison of the binding of a single bidentate ligand 

with that of two molecules of a chemically similar 

monodentate ligand shows that, for the monodentate 

case, the process can be represented by the equations: 

M + BF=^M- B (B-l) 

M-B + Br=^MB 2 (B-2) 

k

d 

The related expressions for the bidentate case are: 

The overall equilibrium constants, therefore, are: 

K

'-k b k d

; K 2 - k2k4 

For a given metal, M, and two ligands, B and B-B, 

which are chemically similar, it is established that k, 

and ka have values similar to each other, as do k2 

and kb, k4 and kd; each of these pairs of terms represents chemically similar processes. The origin of the 

chelate effect lies in the very large value of k3 relative to that of kc. This comes about because k3 represents a unimolecular process, whereas kc is a 

bimolecular rate constant. Consequently, K2 »K, . 

This concept can, of course, be extended to'polydentate ligands; in general, the more extensive the 

chelation, the more stable the metal complex. 

Hence, one would anticipate, correctly, that polydentate chelating agents such as penicillamine or 

EDTA can form extremely stable complexes with 

metal ions. 

M + B-BF=^M-B- B (B-3) B.3 REFERENCES FOR APPENDIX B 

M-B-B =*rvK ) 

L B y 

1. Handbook of Chemistry and Physics. 56th Ed. R.C. Weast 

(ed.). Cleveland, The Chemical Rubber Co. 1975. 

(B-4) 2. Stu.ll. D.R. Vapor pressure of pure substances: Organic compounds. Ind. Eng. Chem. J9(4):5 1 7-540. 1947. 

B-2 
APPENDIX C 

ADDITIONAL STUDIES OF ENVIRONMENTAL 

CONCENTRATIONS OF LEAD 

This collection of studies is intended to extend 

and detail the general picture of lead concentrations 

in the environment and in proximity to identified 

major sources as portrayed in Chapter 7. The list is 

by no means all-inclusive, but is intended to be 

representative and to supplement the data cited in 

Chapter 7. 

C.l GENERA L 

CENTRATIONS 

AMBIEN T AIR CONC.l.1 Seven-City Study 

A special lead study (Seven-City Study) was conducted for 12-month periods between 1968 and 

1971 in Cincinnati, Los Angeles, Philadelphia, 

Houston, New York City, Washington, D.C, and 

Chicago. Samples of ambient air were analyzed by 

atomic absorption spectroscopy. The monthly 

average lead concentrations obtained are summarized in Table C-1. 

This study, specifically designed to measure ambient lead concentrations at a variety of sites within 

each of the cities, incorporated techniques that 

would provide the most precise measure of ambient 

lead concentrations available. A membrane filter 

was used instead of a glass filter, and the samples 

were collected continuously over 2 to 3 days rather 

than collected in biweekly 24-hr periods as in the 

NASN. The high annual average lead concentrations 

found in the Los Angeles area are largely attributable to heavy automotive emissions. 

C.l.2 Birmingham, Alabama 

During 1964 and 1965, seasonal levels of trace 

metals were determined from suspended particulate 

samples collected at 10 area sampling sites at Birmingham, Alabama, as a part of the Alabama 

Respiratory Disease and Air Pollution Study initiated in 1962. This monitoring study produced data 

representative of area source industrial pollution. 

Samples from each of the 10 sites were composited 

on a seasonal basis to give a total of 40 pooled samples. The lead data are summarized in Table C-2. 

The maximum seasonal lead concentration (3.5 

/ug/m3) occurred at Birmingham site 4 during the 

winter. Only 2 sites showed average concentrations 

> 2 figlm3 for the year, Birmingham site 4 (3.0 

figlm3) and Tarrant (2.3 /Ag/m3). These results are 

typical for a medium-sized industrialized urban 

area. 

C. 1.3 Kanawha Valley, West Virginia3 

A comprehensive air pollution study was conducted in the Kanawha River Valley in the vicinity 

of Charleston, West Virginia (Figure C-1), during 

1964 and 1965. Twenty-four-hour samples of suspended particulate matter were collected at 14 

strategically located sites. Samples from selected 

sites were composited on a seasonal basis (fall 1964, 

winter 1964 and 1965, and summer 1965) and the 

composites were analyzed for trace-metal content by 

the NASN emission spectrographic procedure. The 

data for lead are presented in Table C-3. Highest 

concentrations of suspended lead were found during 

the fall of 1964 at the St. Albans, Kanawha City, and 

Charleston sites. 

Lead in dustfall measurements (settled particulates) for the same stations are also presented in 

Table C-3. The dustfall was collected by exposing 

wide-mouth jars for a period of 1 month; then composite samples were analyzed. The highest average 

concentrations of settled lead occurred at the 

Smithers site (11.2 mg/m2-mo), and at the South 

Charleston-East site (11.6 mg/m2-mo). 

The combustion of solid .fuels (coal and coke) is 

the primary source of lead emissions in the Kanawha 

Valley. Additional sources are metallurgical operations, asphalt hot-mix production, and other industrial processes. In most cases, these sources have 

inadequate air pollution control equipment. The 

lead concentrations found are somewhat low when 

C-1 
P.85 

TABLE C-1. SUMMARY OF MONTHLY AVERAGE LEAD 

CONCENTRATIONS FOUND IN SEVEN-CITY STUDY' 

City 

LOS Angeles 

Philadelphia 

Cincinnati 

Los Alamos 

Houston 

Chicago 

Washington, D.C. 

New York 

a

 C - commercial; I - industrial; R 

Site 

type8 

C 

C 

R 

R 

R 

R 

I 

C 

M 

C 

C 

I 

R 

M 

R 

R 

R 

R 

C 

R ' 

I 

P 

F 

F 

R 

C 

R 

C 

C 

C 

M 

R 

R 

R 

M 

R 

M 

C 

R 

R 

M 

R 

R 

C 

C 

R 

R 

F 

R 

R 

M 

M 

R 

R 

M 

R 

R 

R 

R 

Months 

of data 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

12 

7 

12 

12 

12 

7 

12 

12 

12 

12 

12 

12 

11 

12 

12 

12 

12 

12 

12 

12 

12 

Monthly concentration, 

Min. 

2.4 

2.6 

2.1 

2.7 

2.1 

1.4 

1.7 

2.5 

1.3 

1.2 

2.6 

1.5 

0.9 

0.6 

0.6 

1.1 

0.8 

0.7 

1.3 

0.8 

1.2 

0.5 

0.1 

0.2 

0.1 

Q1 

0.7 

0.7 

1.2 

1.5 

1.0 

0.6 

0.6 

1.0 

1.1 

1.0 

1.3 

1.4 

1.2 

0.9 

1.1 

1.2 

0.7 

1.2 

1.6 

1.4 

1.0 

0.9 

1.8 

0.8 

1.1 

1.4 

1.4 

1.3 

1.2 

6.8 

0.9 

0.9 

0.8 

(i g/m3 

Max. 

5.8 

6.8 

5.0 

5.4 

4.4 

3.9 

7.0 

7.6 

2.7 

2.6 

5.1 

3.0 

2.0 

1.7 

1.5 

2.6 

1.7 

1.6 

3.1 

2.6 

2.8 

1.2 

0.5 

0.5 

0.3 

0.3 

2.7 

1.9 

3.2 

4.1 

2.2 

1.4 

1.2 

1.7 

1.7 

2.1 

2.2 

2.3 

2.2 

2.7 

2.1 

3.5 

1.6 

2.2 

3.9 

2.8 

1.7 

1.6 

3.5 

1.8 

2.9 

2.6 

2.1 

2.2 

2.7 

1.9 

1.6 

1.4 

1.4 

Avg. 

4.2 

4.5 

3.6 

3.8 

3.1 

2.5 

3.7 

4.8 

1.9 

1.8 

3.8 

2.2 

1.4 

1.1 

1.1 

1.7 

1.3 

1.0 

2.0 

1.5 

2.2 

0.9 

0.3 

0.3 

0.2 

0.2 

1.2 

1.1 

2.2 

2.4 

1.3 

0.9 

0.8 

1.3 

1.4 

1.6 

1.8 

1.9 

1.6 

1.3 

1.6 

2.0 

1.1 

1.7 

2.3 

1.8 

1.2 

1.1 

2.4 

1.1 

1.7 

2.1 

1.7 

1.7 

2.1 

1.4 

1.2 

1.2 

1.1 

- residential; M - mixed; F - farm; and P - park. 

TABLE C-2. SEASONAL LEAD CONCENTRATIONS IN 

BIRMINGHAM, ALABAMA, AREA, 1964-1965 

(/xg/m') 

Place 

Bessemer 

Birmingham 

Birmingham 

Birmingham 

Birmingham 

Fairfield 

Irondale 

Mt. Brook 

Tarrant 

Vestavia 

Site 

1 

3 

4 

5 

7 

1 

1 

1 

1 

1 

Seasonal average 

Spring 

0.9 

0.7 

3.2 

1.2 

1.2 

0.6 

0.6 

0.5 

1.1 

0.8 

Summer 

0.7 

1.4 

2.8 

1.6 

1.4 

0.5 

0.4 

0.6 

1.8 

0.8 

concentrations 

Fall 

1.1 

1.7 

2.3 

1.8 

1.3 

0.6 

0.9 

1.0 

3.0 

0.5 

Winter 

0.6 

1.4 

3.5 

0.8 

1.8 

0.3 

0.6 

0.5 

3.4 

0.7 

Study period 

average 

concentration 

0.8 

1.3 

3.0 

1.4 

1.4 

0.5 

0.6 

0.6 

2.3 

0.7 

one considers the diversity of industrial activity and 

the meteorological and topographic characteristics 

prevailing. The highest values found were associated 

with sampling sites adjacent to major traffic arteries, 

which demonstrates the contribution from mobile 

sources. 

C. 1.4 Study of Lead Deposition in 77 Cities4 

Settled particulates were collected in 77 midwestern cities from September through December 

1968. Within each city, sites were chosen to represent residential, commercial, and industrial areas. 

The lead content of the settled particulates was 

determined by atomic absorption spectrophotometry, and the depositions were expressed as mg/m2

-

mo. The highest amounts found in residential, commercial, and industrial areas were in South Bend, 

Indiana (80 mg/m2-mo in November); Nashville, 

Tennessee (346 mg/m2-mo in October); and Omaha, 

Nebraska (137 mg/m2-mo in November); respectively. Maximum readings by month occurred in 

Muncie, Indiana (industrial) (105 mg/m2-mo in September); Nashville, Tennessee (commercial) (346 

mg/m2-mo in October); Omaha, Nebraska (industrial) (137 mg/m2

-mo in November); and 

Waterloo, Iowa (industrial) (94 mg/m2-mo in , 

December). The data are summarized in Table C-4. 

C.2 SOURCE-ORIENTED AMBIENT AIR 

CONCENTRATIONS 

C.2.1 Southern Solano County, California3 

The State of California Air Resources Board 

coordinated a joint study, conducted by several state 

agencies between March 1970 and November 1971, 

to determine the cause of death of a number of 

horses in the Benicia area from 1968 to 1970. Figure 

C-2 is a map of this area showing sampling site locations. The evidence strongly suggested that the 

C-2 
TABLE C-3. LEAD DATA FROM KANAWHA VALLEY STUDY' 

Sampling sites. 

location and no. 

Falls View (1) 

Smithers (5) 

Montgomery (6) 

Cedar Grove (7) 

Marmet(11) 

Kanawha City (13) 

Charleston (15) 

West Charleston (17) 

North Charleston-W (19) 

South Charleston-E (20) 

Dunbar (22) 

St. Albans (24) 

Nitro (25) 

Nitro-West (27) 

Fall 

1964 

— 

0.4 

— 

0.5 

— 

2.1 

— 

— 

— 

2.7 

— 

1.3 

1.0 

— 

Winter 

1964-1965 

0.2 

0.3 

0.6 

0.4 

0.5 

0.8 

0.9 

0.7 

0.7 

0.6 

0.4 

0.9 

1.4 

0.1 

Spring 

1965 

— 

0.3 

— 

0.2 

— 

0.6 

— 

— 

— 

0.6 

— 

0.3 

0.2 

— 

Summer 

1965 

0.0 

— 

0.4 

— 

0.5 

— 

— 

— 

1.0 

— 

0.4 

0.3 

— 

Study period 

average 

— 

0.2 

— 

0.4 

— 

1.0 

— 

— 

— 

1.2 

— 

0.7 

0.7 

— 

Lead in settled particulates, 

mg/m^/mo. 

study period 

average 

11.2 

6.7 

4.8 

3.8 

2.8 

— 

8.6 

11.6 

3.0 

3.4 

— 

EASTCHARLESTON 

CHARLESTON 

CREDE 

WEST CHARLESTON 

NORTH CHARLESTON, EAST 

NORTH CHARLESTON. WEST 

SOUTH CHARLESTON. EAST 

SOUTH CHARLESTON, WEST 

DUNBAR 

INSTITUTE 

ST.ALBANS 

NITRO 

WEST OF ST. ALBANS 

WEST QF NITRO 

Figure C-1. Locations of fixed sampling stations in Kanawha 

River Valley.3 

TABLE C-4. DATA ON LEAD DEPOSITION IN 77 

MIDWESTERN CITIES4 

(mg/m2/mo) 

Lead deposition Lead deposition 

Area 

Residential 

Commercial 

Industrial 

Concentration, 

geometric 

5.24 

9.80 

12.78 

mean Month 

September 

October 

November 

December 

Concentration. 

geometric mean 

9.11 

8.71 

9.15 

8.06 

horses died of lead poisoning that was caused by ingestion of lead deposited on pasture grass from a 

smelter plant at Selby, California. The ambient air 

concentrations of particulate lead were typical of 

those found in urban and suburban areas. It was concluded that horses in this area should not be allowed 

to subsist on pasture grass alone, but should receive 

supplemental feed. Tables C-5 and C-6 contain the 

data on suspended and deposited lead obtained during the study. Note that the fallout rates are on a 

daily basis. 

Figure C-2. Air sampling sites for Southern Solano County, 

California, study.5 

C.2.2 Omaha, Nebraska6 

In April and May of 1968, a study of settled lead 

by the EPA Division of Health Effects Research 

showed central Omaha, Nebraska, to have the highest concentrations of deposited lead of 22 midwestern cities. Because automobile emissions should 

reflect the relatively low population density, the 

possibility of a significant contribution to air lead 

C-3 
P.87 

TABLE C-5. LEAD CONCENTRATIONS IN AIR DETERMINED 

BY ANALYSIS OF SUSPENDED PARTICULATE, SOUTHERN 

SOLANO COUNTY, CALIFORNIA, MARCH-MAY 1970s 

Site 

Carquinez Bridge 

Elliot Cove 

Babson house 

Braitodump 

Walsh house 

Braito TV transmitter 

site 

Wesner pasture 

Wesner pasture 

Wesner pasture 

Gomez pasture 

Wesner house 

San Francisco" 

Fremont0 

San Rafael" 

Distance 

from 

Selby,a 

km 

1.9 

3.0 

3.7 

5.6 

57 

7.7 

7.8 

8.0 

8.3 

10.0 

10.2 

22.0 

20.0 

19.2 

Lead concentration! 

High 

8.45 

0.93 

0.82 

0.69 

0.62 

1.07 

0.56 

0.66 

0.51 

0.28 

0.22 

3.50 

2.24 

2.04 

Low 

0.35 

0.27 

0.58 

0.07 

0.14 

0.25 

0.40 

0.11 

0.03 

0.03 

0.02 

1.15 

0.59 

0.41 

,/xg/m3 

Mean 

3.49 

0.52 

0.70 

0.64 

0.40 

0.59 

0.42 

0.38 

0.27 

0.11 

0.14 

2.12 

1.04 

1.14 

a

 Location of suspected lead emissions source. See text. 

D

 1969 data provided by Bay Area Air Pollution Control District. 

TABLE C-6. TOTAL LEAD AND LEAD FALLOUT 

DETERMINED BY ANALYSIS OF DUSTFALL SAMPLES, 

SOUTHERN SOLANO COUNTY, CALIFORNIA, 

JUNE-SEPTEMBER 1970* 

Site 

Distance 

from 

Selby.a 

km 

Sample 

period, 

days 

Total 

solids. 

mg 

Total 

lead, 

n9 

Lead 

fallout. 

mg/m2-day 

Carquinez 

Bridge 

Braito dump 

Braito TV transmitter site 

Wesner 

pasture 

Wesner 

pasture 

Wesner 

pasture 

Wesner 

pasture 

Wesner 

pasture 

Wesner 

pasture 

Wesner 

pasture 

Wesner 

pasture 

Gomez 

pasture 

Drachman 

pasture 

1.9 30 49.2 

5.6 30 58.7 

7.7 60 101.7 

8.0 31 370 

8.0 31 162 

8.0 31 171.4 

8.0 31 109.8 

8.0 31 351.7 

8.0 31 220.2 

8.0 30 83.5 

8.3 30 163.6 

10.0 32 45.0 

13.4 30 26.5 

1435 

195 

2.78 

0.38 

520 

185 

155 

195 

255 

210 

4535 

430 

705 

150 

75 

0.50 

0.35 

0.29 

0.37 

0.48 

0.39 

8.51 

0.83 

1.37 

0.27 

0.15 

from other sources (two battery plants, one refinery) 

in the central city area was considered. Consequently, from May to November 1970, monitoring 

of air lead in Omaha was conducted at five sites: one 

industrial (I), one commercial (C), one mixed (M), 

and two residential (R). All samples were taken at 

15-ft elevation, and all data were reported as the 

composited averages of 24-hr samples collected 3 

times weekly. The monthly composite average of air 

lead concentrations at the sampling sites is shown in 

Figure C-3. Air lead levels in central Omaha at sites 

C and I were not only comparable with those of similar sites in Chicago, New York City, and Houston 

from the same months, as reported by EPA, but the 

maximum monthly mean at the industrial site (in 

July) exceeded the maximum monthly mean of all 

sites in these other cities. 

ATMOSPHERIC LEAD - OMAHA 

MONTHLY COMPOSITE 

MAY - NOVEMBER 1970 

RESIDENTIAL 

a

 Location of suspected lead emissions source. See text. 

MAY JUN JUL AUG SEP OCT NOV 

TIME, months 

Figure C-3. Omaha, Nebraska study: mean monthly composite atmospheric lead at Industrial, commercial, mixed, 

and two residential sites. Mean is that of representative 24-

hour samples collected three times weekly. The autumnal 

peak at all but the industrial site parallels the usual Omqha 

pattern for particulates.6 

C.2.3 El Paso, Texas7'

8 

The El Paso, Texas, study was initiated in 1971 as 

a result of the discovery of increased lead deposition 

in the vicinity of a local smelter whose emissions 

C-4 
rose from 256 MT in 1969 to 463 MT in 1970. The 

El Paso City-County Health Department then began 

special ambient air and soil sampling in addition to 

routine operation of their nine-station particulate 

sampling network. Particulate' samples were collected with high-volume samplers over 24-hr 

periods and were then analyzed for lead by atomic 

absorption spectroscopy. The results for 1971 from 

the nine-station network are given in Table C-7. 

Daily sampling at 6 selected sites in Smeltertown 

was continued beginning in February 1972. Daily 

lead concentrations at four ground level sites ranged 

from 0.49 to 75 figlm3 and averaged 6.6 jixg/m3 over 

86 days. Average concentrations of 3.6 and 6.5 

/ug/m3 were found at 2 rooftop sites. 

TABLE C-7. LEAD CONCENTRATIONS IN SUSPENDED 

PARTICULATE AIR SAMPLES FROM EL PASO, TEXAS, 197V 

Location 

Airport 

Northeast 

Canutillo 

Shorty Way 

Tillman 

Ysleta 

Coronado 

Kern 

Executive 

Distance 

from 

km 

12.8 E 

16 NE 

15.2 NW 

8NW 

4.8 SE 

21.6 SE 

4.8 N 

2.4E 

1.6 NE 

samples 

84 

73 

45 

75 

70 

71 

94 

26 

65 

Suspended atmospheric 

lead concentration 

Range 

0.38 to 5.82 

0.12 to 3.68 

0.10 to 1.50 

0.18 to 4.51 

0.02 to 22.16 

0.18 to 4.81 

0.08 to 8.62 

0.12 to 7.28 

0.26 to 6.67 

./jg/m3 

Average 

0.96 

0.76 

0.46 

1.03 

2.69 

1.39 

0.83 

2.72 

1.16 

C.2.4 Helena Valley, Montana9 

During the summer and fall of 1969, a sourceoriented study of the Helena Valley, Montana, area 

(Figure C-4) was undertaken using dustfall bucket 

and high-volume sampling techniques. During this 

period, Helena residents were exposed to an average 

daily lead concentration of 0.1 figlm3, with maximum concentrations of up to 0.7 /ug/m3

. The residents of the East Helena area were exposed to an 

average daily concentration of 0.4 to 4.0 /ug/m3, depending upon proximity to the source, with maximum daily exposures of up to 15 figlm3

. Within a 1-

mile radius of the East Helena smelter, settled particulate lead values ranged from 30 to 108 mg/m2

/ 

mo. Table C-8 summarizes the dustfall and suspended particulate data acquired during this study, 

and Figure C-4 shows the deposition of lead 

(dustfall) in the area. 

SCALC. kitamM*? 

L 

HTTLIAUI 

••ARTICULATC Lf AD. 

g^>10TO<3 0 

1)111 >JO TO < MO 

Figure C-4. Settleable particulate lead radial distribution 

from Helena Valley environmental pollution study.9 

C.2.5 Southeast Missouri10 

Studies were carried out in 1971 in the Viburnum' 

Trend or New Lead Belt in southeast Missouri to 

determine the magnitude and distribution of atmospheric pollutants from lead mining and smelting 

operations. This industrial district has become one 

of the world's largest lead-producing areas by mining more than 392,277 MT of lead, or 75 percent of 

the entire U.S. lead production, during 1970. Settleable particulates were collected monthly at 10 

locations in western Iron County shown in Figure 

C-5. Annual averages for each site are included in 

the figure; monthly maximum values are listed in 

Table C-9. Annual averages for suspended lead collected in Glover, Mo. (Site 43, southeastern Iron 

County), by high-volume sampler were 3.4 /ng/m3 

(20 samples) in 1970, 5.3 /xg/m3 (32 samples) in 

1971, and 5.6 Mg/m3 (28 samples) in 1972. 

TABLE C-8. PARTICULATE DATA SUMMARY FROM HELENA VALLEY, MONT., ENVIRONMENTAL POLLUTION STUDY" 

Settleable particulate lead. mg/m2/mo 

Suspended particulate lead 

in glass fiber filter sample, iig/rrfl 

Station 

1 

2 

3 

4 

6 

Location3 

0.8 mi; 34° 

2.5 mi; 105° 

0.4 mi; 112° 

4.5 mi; 274° 

0.5 mi; 2° 

Jun. 

3 

1 

54 

1 

— 

Jul. 

19 

4 

106 

4 

— 

Aug. 

10 

3 

5 

3 

— 

Sept. 

19 

9 

63 

7 

27 

Oct. 

40 

10 

108 

7 

60 

No. samples 

76 

87 

85 

82 

34 

Max. 

5.3 

2.5 

16.0 

7.0 

15.0 

Min. 

< md° 

< md 

< md 

< md 

0.2 

Average 

0.45 

0.24 

1.25 

0.10 

3.89 

a

 Distance and compass direction from smelter stack, 

b Minimum detectable. 

C-5 
BUICK TOWtR # 0«3 

Figure C-5. Annual average of settleable particulate lead at 

sites near Missouri lead mine and smelter, g/mJ/Tno.10 

C.2.6 Helsinki, Finland" 

Investigators for the Agricultural Research 

Center in Tikkurila, Finland, an industrial and residential area near Helsinki, found high lead levels in 

soil. To clarify the origin of this excess lead, the Institute of Occupational Health conducted a dustfall 

lead survey in the area. Eighty collectors were located over a 40-km2

 area for a period of 1 month, 

October 6 to November 7, 1970. Individual ashed 

samples were analyzed by emission spectrography 

and the water-soluble fractions were analyzed by 

atomic absorption spectroscopy. 

The highest lead deposition values in Helsinki 

were observed in areas with heavy traffic and ranged 

from 10 to 20 mg/m2/mo as compared to 0 to 4 

mg/m2/mo in predominantly housing and residential 

areas. 

In the Tikkurila area, industrial contributions increased deposited lead values fortyfold in some 

areas. The deposited lead values ranged from background in outlying areas to as high as 200 mg/m2

/mo 

near a lead smelter, with most of the values below 

100mg/m2/mo. 

C.2.7 Meza River Valley, Yugoslavia12 

In 1967, work was initiated in the community of 

Zerjav, situated in the Slovenian Alps on the Meza 

TABLE C-9. PEAK DEPOSITION RATES OF LEAD MEASURED IN SOUTHEAST MISSOURITM 

1971 

Station 

no. 

Wind 

direction Distance, m 

Lead deposition rate, 

mg/m^/mo 

Wind frequency, % 

prevailing direction 

May-June 

July 

August 

September 

October 

November 

6 

7 

10 

7 

7 

3 

E 

SSE 

NE 

SSE 

SSE 

WNW 

81 

91 

633 

91 

91 

61 

5.88 

5.54 

4.57 

7.76 

5.10 

2.01 

18(S). 12(WNW) 

14(SSE), 13(S). 10(SSW) 

14ISSE). 1KS). 10ISSW) 

22IS). 12ISSE). 121SSW) 

10(N). 10(W). 10ISE). 11 (ESE) 

26(S). 12ISSW). 10(WSW).8(SSE) 

River, to investigate contamination by lead of the 

air, water, snow, soil, vegetation, and animal life, as 

well as the human population. The smelter in this 

community produces about 19,954 MT of lead annually; until 1969 the stack emitted lead oxides 

without control by filters or other devices. Five sampling sites with high-volume samplers operating on a 

24-hr basis were established in the four principal settlements within the Meza River Valley (Figure C-6): 

(1) Zerjav, in the center, the site of the smelter, 

housing 1503 inhabitants; (2) Rudarjevo, about 2 

km to the south of Zerjav with a population of 100; 

(3) Crna, some 5 km to the southwest, population 

2198, where there are two sites (Crna-SE and CrnaW); and (4) Mezica, a village about 10 km to the 

northwest of the smelter with 2515 inhabitants. The 

data in Table C-10 are sufficient to depict general 

environmental contamination of striking proportions. 

C.2.8 Ontario,Canada1* 

Studies of lead concentrations in soils, vegetation, 

and the ambient air were conducted in the vicinity of 

a secondary smelter and a battery manufacturing 

plant in a large urban area in southern Ontario. For 

comparative purposes, data were also collected in a 

similar control neighborhood that had no such industrial sources. Emissions of lead from the smelter 

were estimated to be 17 tons per year; from the battery plant, 6 tons per year. Averages and ranges of 

C-6 
flIVERS 

rrfflflp SETTLEMENTS 

Figure C-6. Schematic plan of lead mine and smelter from 

Meza Valley, Yugoslavia, study.12 

TABLE C-10. ATMOSPHERIC LEAD CONCENTRATIONS (24-

hr) IN THE MEZA VALLEY, YUGOSLAVIA, NOVEMBER 1971 

TO AUGUST 197212 

Site 

Mezica 

Zerjav 

Rudarjevo 

CrnaSE 

CrnaW 

Minimum 

0.1 

0.3 

0.5 

0.1 

0.1 

Pb concentration jjg/m^ 

Maximum 

236.0 

216.5 

328.0 

258.5 

222.0 

Average 

24.2 

29.5 

38.4 

33.7 

28.4 

lead concentrations are summarized in Table C-11. 

Both soil and foliage samples showed definite trends 

toward reduced concentrations with increasing distance from the industrial sources. 

C.3 CONCENTRATIONS OF LEAD IN SOILS 

AND URBAN DUSTS 

As mentioned in Chapter 5, surficial materials in 

the continental United States contain an average of 

about 15 ppm of lead; 94 percent of the measurements showed 30 ppm or less. Higher concentrations 

are encountered in the vicinity of lead ore deposits 

and, of course, in the proximity of human activities 

involving lead. Soils apparently receive lead in the 

amounts of about 1 figlcm2/yr from precipitation 

and 0.2 /ig/cm2/yr from dustfall14 in areas remote 

from intensive human activity. These small additions to the lead content of the soil are not detectable 

by ordinary means because they add only about 0.2 

percent to the total lead in the top 6 in of the soil. 

Lead levels are higher in surface soils than in deeper 

layers. Swain and Mitchell15 studied lead profiles in 

8 soil types in Scotland and showed that the lead 

content at 115 cm (45 in) averaged one-half that at 

the surface. The reduction of concentration with 

depth is also substantiated by the findings of others. 

Goldschmidt16 proposed the theory that lead is concentrated in the humus or organic fraction of soils in 

forests because it is taken up slowly by tree roots and 

transported to the leaves, which fall and decay. 

Tyler17 points out that a passive ion exchange favors 

an accumulation of lead and other heavy metals in 

dead organic matter, litter, and humus. He also 

states that most plant material subjected to decomposition usually shows an increase in the concentration of lead, cadmium, nickel, iron, copper, etc., 

calculated on dry weight. 

The use of leaded gasolines has produced elevated 

soil lead levels adjacent to most streets and roadways. This phenomenon was first observed as early 

as 1933 in England,18 and has been intensively 

TABLE C-11. COMPARISON OF LEAD LEVELS IN THE SURROUNDINGS OF TWO 

LEAD INDUSTRY FACILITIES AND AN URBAN CONTROL AREA" 

Industry or 

area 

Secondary smelter 

Mean 

Range 

Battery plant 

Mean 

Range 

Urban control area 

Mean 

Range 

Soil, ppm 

(0.5 cm depth! 

2.615 

133 to 21.200 

1.996 

95 to 17.300 

482 

18 to 1.450 

Tree foliage ppm 

Unwashed 

250 

38 to 3.530 

149 

34 to 459 

73 

15 to 253 

Washed 

187 

27 to 2.740 

76 

16 to 387 

43 

10»o124 

Air, /ig/m^ 

(24-hour samples) 

3.87* 

Max1 74.4 

2.21° 

Max-31.0. 

1.02c 

Max: 4.0 

aApril 1973 to May 1974. 

bNovember 1973 to May 1974. 

c

January 1974 to April 1974. 

C-7 
P.91 

studied in recent years.19 An example of this 

phenomenon is taken from a study of the Saline 

Branch watershed, which includes Champaign, Illinois. One facet of this comprehensive study20

 consisted of analyses for lead in soil at increasing distances from a low-traffic-volume street (400 vehicles/day) and a high-traffic-volume street (14,000 

vehicles/day). As shown on curve A in Figure C-7, 

lead concentrations stabilized at about 20 ppm 

beyond 15 meters from the low-volume street and 

rose slightly near the house. Unfortunately, the exterior construction of the house is not described. As 

curve B in Figure C-7 shows, lead concentrations of 

about 1800 ppm in the soil adjacent to the highvolume street are 9 times higher than in soil adjacent 

to the low-volume street; the concentration drops 

rapidly to a minimum of 30 ppm a little more than 

20 m from the street and then rises again abruptly 

near the house to 90 ppm. This house is described as 

brick and unguttered. Although some leaching of 

lead from painted trim may be involved, the increase 

near the house is believed attributable chiefly to lead 

particles in traffic dust washed from the unguttered 

roof by rain and deposited in the soil next to the 

house. 

E 1000 — 

a 

o. 

_• 20 0 

DISTANCE FROM STREET, meters 

Figure C-7. Soil transects by two streets: Curve A = lowtraffic-volume (400 veh/day); Curve B = high-traffic-volume 

(14,000 veh/day).20 

Soil lead levels in the vicinity of stationary sources 

of lead emissions are often very high, and. unlike the 

rapid drop-off near highways, very extensive. This is 

particularly true for old installations. Figure C-8 

shows levels recently found near an old smelter in El 

Paso, Texas.21 Similar data, compiled from a 3-yearold Russian lead smelter, 2 2

 are shown in 

Table C-12. The concentration decrease with both 

depth and distance is also apparent here. Information on soluble lead levels in soil near a similar complex in Great Britian is presented in a report by Little and Martin.23

 Barltrop reported values up to 

30,000 ,u.g/g in villages in the eastern half of Derbyshire County, England.24

 In this instance, the soil 

included lead contamination from old mine tailings 

and possible natural mineralization, i.e., the concentrations were not exclusively atmospheric in 

origin. 

DON * ANACOUN 

UMTE D STATU! 

Figure C-8. Surface soil levels (ppm) of lead in El Paso, 

Texas, and Dona Ana County, New Mexico, 1972.21 

TABLE C-12. LEAD CONTENT OF SOIL NEAR 3-YEAR-OLD 

RUSSIAN SMELTER, E. KAZAKHSTAN 

(mg/100 g air-dried soil)a 

Distance trom Surface Soil depth 

source, m 

500 

1.000 

2.000 

3.000 

5.000 

16.000 

layer 

23.9711 

9.0163 

1.4207 

1.2192 

0.1031 

0.0943 

25 cm 

4.1747 

1.8368 

0.7432 

0.5991 

0.0649 

0.0778 

75 to 100 cm 

0.0748 

— 

0.0545 

0.0474 

0.0233 

0.0292 

Multiplying by 10 yields ppm. 

Table C-13, derived from studies done in 1959 

and I960,25 gives lead levels of soil adjacent to 

another Russian lead smelter. The plant is located in 

a valley surrounded by mountains that hinder 

natural ventilation. In addition, plant emissions are 

inadequately controlled. Methods of sample preparation and analysis of the soil samples are not 

given, however; nor is it stated whether the soil 

weights used were for dried or undried material. 

Paluch and Karweta26 reported observations on 

soil lead near a new lead-zinc primary smelter in Poland. Soil analyses were made in several areas prior 

to operation of the factory and after 1 year of operation. Samples were extracted with hot concentrated 

hydrochloric acid and analyzed for lead content by 

the dithizone method. Levels found are given in 

milligrams of lead per kilogram of dried soil. Values 

C-8 
TABLE C-13. LEAD CONTENT OF SOIL IN VICINITY OF RUSSIAN LEAD PLANT IN KAZAKHSTAN'S 

from 

km 

On grounds 

0.5 

1.0 

1.5 

2.0 

3.0 

5.0 

40.0 

Number 

of 

samples 

12 

10 

20 

6 

6 

4 

4 

4 

Maximum 

11.170.0 

2.420.0 

1:170.0 

720.0 

1.070.0 

340.0 

97.0 

3.0 

0 to 1 cm depth 

Minimum 

1.300.0 

470.0 

130.0 

170.0 

250.0 

130.0 

80.0 

2.5 

Lead content ot soi 

Average 

5.546.0 

1.156.0 

613.0 

369.0 

530.0 

235.0 

88.5 

2.7 

, mg/100 g a 

Maximum 

6.800.0 

650.0 

990.0 

720.0 

610.0 

260.0 

46.0 

Trace 

25 cm depth 

Minimum 

510.0 

130.0 

200.0 

70:0 

70.0 

100.0 

40.0 

Trace 

Average 

3.143.0 

458.0 

430.0 

340.0 

260.0 

180.0 

43.0 

Trace 

Multiplying by 10 yields ppm. 

given are the average of three samples. Two sites are 

of particular interest, a woods of young pines 2 km 

from the smelter and a tree nursery at 3 km. Before 

and after lead levels in the top 5 cm of soil at these 

locations were 39 and 89 mg/kg for the former, and 

54 and 81 mg/kg for the latter. At other sampling 

sites the data were quite variable, but these were 

agricultural lands subject to cultivation, to fertilization, or to both. The wooded sites were not disturbed 

in this manner. 

C.4 REFERENCES FOR APPENDIX C 

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Contract No. PH-22-68-28. U. S. Environmental Protection Agency. Washington, D.C. Publication No. EPARI-73-005. 1973. 

2. Hauser, T. R., J. J. Henderson, and F. B. Benson. The 

polynuclear hydrocarbon and metal concentration of the air 

over the Greater Birmingham Area. Human Studies 

Laboratory, U. S. Environmental Protection Agency. 

Research Triangle Park, N.C. Unpublished Report. 

3. Kanawha Valley Air Pollution Study. U.S. Environmental 

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study in trace element pollution of air in 77 midwestern 

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P. Hemphill (ed.). Columbia, University of Missouri Press. 

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5. Maga. J.A.. F.B. Hodges, C.B. Christenson, and D.J. 

Callaghan. A Joint Study of Lead Contamination Relative to 

Horse Deaths in Southern Solano County. Los Angeles. 

State of California Air Resources Board. September 1972. 

178 p. 

6. Mclntire, M. S. and C. R. Angle. Air lead: Relation to lead 

in blood of black school children deficient in glucose-6-

phosphate dehydrogenase. Science. / 77.520-522, August 

1972. 

7. Henderson, J. J. and P. A. Hudson. Unpublished trip report 

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(ASARCO), Cause No. 70-1701. Air Quality Enforcement 

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Study. U.S. Environmental Protection Agency. Research 

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Lead Smelter Industry. Rolla. University of Missouri Press. 

1972. 13 p. 

11. Laamanen, A. and A. Ryhanen. Aerial distribution of 

dustfall lead in the neighborhood of some lead emitters. 

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Biological Significance of Some Metals as Air Pollutants. 

Final Report. Part I: Lead. U. S. Department of Health, 

Education, and Welfare, Consumer Protection and Environmental Health Service. Washington, D.C. January 1974. 

Linzon, S. N., B. L. Chai, P. J. Temple, R. G. Pearson, and 

M. L. Smith. Lead contamination of urban soils and vegetation by emissions from secondary lead industries. J. Air 

Pollut. Control Assoc. 26(7): 650-654, 1976. 

Lead: Airborne Lead in Perspective. Washington, D.C,National Academy of Sciences. 1972. p. 28. 

15. Swaine, D. J. and R. L. Mitchell. Trace element distribution 

in soil profiles. J. Soil Sci. //(2):347-368, 1960. 

Goldschmidt, V. M. The principles of distribution of chemical elements in minerals and rocks. J. Chem. Soc. (London.) 

655-673. 1937. 

13 

14. 

16 

I 7. Tyler. G. Heavy metals pollute nature, may reduce productivity. Ambio. /(2):52-59, 1972. 

18. Dunn, J. T. and H. C. L. Bloxam. The occurrence of lead, 

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20. Rolfe, G. L. and A. Haney. An Ecosystem Analysis of Environmental Contamination by Lead. Institute for Environmental Studies, University of Illinois at Urbana-Champaign. 

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Health, Education, and Welfare. Atlanta, Georgia. Morbidity and Mortality Weekly Report. 22(49):405-407, 1973. 

C-9 
P.93 

22. Pakhotina, N.S. Sanitary hygienic evaluation of industrial 

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Literature on Air Pollution and Related Occupational Diseases. U. S. Public Health Service. Washington, D.C. 

J.-93-97, I960. 

23. Little, P. and M. H. Martin. A survey of zinc, lead and cadmium in soil and natural vegetation around a smelting complex. Environ. Pollut. 5:241-254, July 1972. 

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26 

dusts for human populations. Arh. Hig. Rada Toksikol. 

(Yugoslavia.) 26:81-93, 1975. 

Smokotnina, T. N. Hygienic evaluation of air pollution with 

wastes from a lead plant. Hig. Sanit. (USSR). 27(6):87-90, 

1962. 

Paluch; J. and S. Karweta. The accumulation of zinc and 

lead in soil and plants. In: Lectures of 6th Int'l Congress of 

Forestry Specialists for Smoke Damage. Katowice. (Poland.) 

1968. p. 127-138. 

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APPENDIX D 

UNITS AND METRIC CONVERSION FACTORS 

In each of the disciplines dealing with lead in a 

sector of the environment, conventions for units 

have evolved that are convenient to each but not always familiarly translatable from one to the other, 

even when expressed in metric units. There are also 

two distinct categories of measurements: concentrations and transfer rates. Within each category of 

measurements, straightforward conversion factors 

translate the quantitites from one system of units to 

another. Connections between the two categories are 

bridged only by mathematical models of varying 

complexity that account for all significant transfer 

rates, both into and out of a given context, as well as 

measure that context's capacity to distribute and 

equilibrate any net change that will add to or 

substract from its initial concentration. 

D.l CONCENTRATIONS 

Airborne lead concentrations are customarily reported in units of mass per volume: micrograms of 

lead per cubic meter of air (fig/m3). Concentrations 

of lead in soils and dusts are reported in units of 

mass per mass: micrograms of lead per gram of the 

parent material (figlg), or as parts per million 

(ppm). When ppm refers to mass, the expression is 

interchangeable with figlg. 

Concentrations of lead in water (dissolved or suspended) may be reported in parts per billion (ppb) 

or micrograms per liter (/xg/liter). For our purposes, 

a liter of water can be equated with lOOOg, and units 

of jag/liter can be interchanged with ppb or 

nanograms per gram (ng/g). 

Concentrations of lead in food are usually given in 

parts per million (ppm), micrograms per gram 

(figlg). or milligrams per kilogram (mg/kg), all of 

which are interchangeable. 

Concentrations of lead in blood may be reported 

in micrograms per deciliter (figldl) or in 

micrograms per 100 grams (figll00 g). These are not 

equivalent since 1 dl of blood weighs between 105 

and 106 g. 

D.2 TRANSFER RATES 

In general, transfer rates describe the movement 

of material from one medium or context to another 

in units of mass per time or mass per quantity (mass 

or volume) of a parent material. Some rates include 

a linear or area dimension to express the transfer per 

unit of interface between media. 

The lead in ores that is transfered to smelters and 

hence to manufactured products is described by production figures and reported in tons (short) per year 

(tons/yr) or tonnes (metric) per year (MT/yr). The 

attendant dispersal of some of that lead into the air, 

water, and soil is described by emission factors: tons 

per year (tons/yr), kilograms per day (kg/day), 

pounds per ton of raw material or product (lb/ton), 

pounds per thousand gallons (lb/103 gal), grams per 

kilometer (g/km), etc. 

The most familiar transfer rate between media is 

perhaps the dustfall or deposition rate, reported in 

tons per square mile per year (tons/mi2/yr), 

milligrams per square meter per month (mg/m2/mo), 

etc. 

The culminating concern is with transfer rates, involving the human body, through inhalation and ingestion followed by retention and absorption into 

fluids and tissues, and, finally, excretion, all of 

which are commonly expressed in micrograms per 

day, micrograms per kilogram of body weight per 

day, or, even, as micrograms per square meter of 

body surface. 

D-l 
P.95 

D.3 UNITS D.4 CONCENTRATION CONVERSION 

FACTORS 

1 m = lOVm = 102cm = 10"3km = 3.281 ft = 

39.37 j n 1 PPb (mass) = 1 ng/g = Ifiglkg 

1 ppm (mass) = 1 figlg = 1 mg/kg 

1 m2= 104cm2= 10-6km2= 10.76 ft2 = ] mg/liter (water) » 1 ppm » I figlg 

1550 in2 1 Mg/liter (water) *£* 1 ppb 

lm3 = 106cm3 = 999.97 liters = 35.31 ft3 = ' ^8 / d l (blood) « 0.95 fig/l00 g (blood) 

6.1 x 104 in3 = 264.2 gal D.5 TRANSFER RATE CONVERSION 

l g = 10* ug= 103mg= 103kg= 0.035 oz = FACTORS 

0 0022 1b 1 mg/m2/mo= 2.85x10-3 tons (short)/mr2/mo 

1 tonne/yr - 2.74 kg/day = 

1 tonne (metric) = 1000 kg = 106g= 1.1023 tons (short )/yr 

1.1023 tons (short) 1 fig/day = 3.53 x 108oz (av.)/day 

D-2 
P.96 

APPENDIX E 

ABSTRACT OF A REVIEW OF THREE STUDIES 

ON THE EFFECTS OF LEAD SMELTER 

EMISSIONS IN EL PASO, TEXAS 

Presented by Warren R. IVluir 

Council on Environmental Quality 

Washington, D.C. 

At the International Conference on Heavy 

Metals in the Environment 

Toronto, Ontario, Canada 

October 1975 

The committee reviewed two independent studies conducted in 1973 by Dr. Landrigan (CDC) and Dr. 

McNeil (ILZRO) to determine the effects of community lead exposures near the ASARCO smelter in El 

Paso, Texas. The CDC study used a random sample approach to group participating children, and in the 

ILZRO study match paired groups were selected on the basis of residence. In both studies the criteria for 

subclassification with regard to lead exposure were blood lead levels. Neuropsychological dysfunction was 

evaluated by several tests including WISC, WPPSI, and McCarthy scales. Statistical differences in test results 

could not be directly correlated to blood lead levels. 

The opinion of the committee was that no firm conclusions could be drawn from the studies as to whether or 

not there are subclinical effects of lead on children in El Paso and that the reports and data made available 

have not clearly demonstrated any psychologic or neurologic effects in the children under study. It noted the 

absence of major chronic clinical effects, and concluded that these studies therefore do not bear upon the conclusions of other investigations under different conditions and those in which clinical effects have been confirmed. However, because of inherent problems of study design and the limitations in the tests used, this finding should not lead to a conclusion that low levels of lead have no effects on neuropsychological performance. 

Ellen Silbergeld, Ph.D., NIH, Eileen Higham, Ph.D., and Mr. Russell Jobaris, Johns Hopkins University, 

Department of Medical Psychology, served as special consultants. 

The committee decided to limit its focus to a review of the three studies, and to attempt to account for and 

interpret the differences between the studies. Thus, aspects not related to differences were not emphasized. 

The committee limited its consideration to the following materials: (1) reports of the three studies under 

consideration; (2) other materials provided by the authors of the studies; (3) background information and 

documents collected by Dr. Muir in El Paso. This presentation today consists of excerpts from a draft committee report. 

E l HISTORY 

El Paso is situated on the Mexican border in the western part of Texas. A lead smelter owned by American 

Smelting and Refining Company (ASARCO) has been located on the southwestern border of the city, on the 

Rio Grande River, since 1887. The area most conspicuously involved in the studies, Smeltertown, was a 2 x 6 

block area located between the plant and the river. Smeltertown is no longer in existence, having been 

destroyed in December 1972. About 2 km south of Smeltertown is Old Fort Bliss, a considerably smaller 

community, whose inhabitants were considered in some, but not all, of the studies. 

The ASARCO smelter produces lead, zinc, copper, and cadmium. Particulate matter is removed from airborne wastes in a series of baghouses; remaining emissions contain approximately 40 lb of lead per day. 

The El Paso City County Health Department began an investigation of the ASARCO smelter in early 1970, 

in preparation for an air pollution suit filed by the city in April 1970. As part of this investigation, Dr. 

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P.97 

Bertram Carnow was hired by the city as a consultant. At his suggestion, the city began to sample the blood 

lead levels of El Paso children to determine whether any had been over-exposed to lead. This included a large 

number of Smeltertown children. Based upon early results in 1971, Dr. Carnow visited El Paso, and saw a 

selected group of children with high blood lead levels. He interviewed the children, and reviewed their medical records. The information contained in the medical histories, and Dr. Carnow's interviews, constitute the 

observations reported by Dr. Carnow in the paper presented to the American Pollution Control Association 

(APCA). The clinical observations were in a paragraph of a paper otherwise devoted to a consideration of the 

effects of the smelter on the environment as a whole, and the extent of its emissions. This report contains no 

details on the age, exposures, individual signs and symptoms, or diagnostic criteria used in the ten cases reported. Our committee focused its attention, therefore, upon the two full-scale follow-up epidemiological 

studies conducted by Dr. Landrigan (CDC) and Dr. McNeil (ILZRO). 

In 1973 ASARCO began a separate investigation of the population of Smeltertown, and asked Dr. James 

McNeil of the International Lead Zinc Research Organization (ILZRO) for his assistance in the examination 

and possible treatment of children with elevated blood levels greater than 60 mg/100 ml. 

As a result of public concern over widespread lead poisoning throughout the city of El Paso, the mayor requested aid from the Federal Government. A separate protocol for a Center for Disease Control (CDC) study 

was submitted to and approved by the Public Health Board in 1973 with the understanding that the two 

studies would proceed independently, with those children in the ILZRO sponsored study being excluded 

from the CDC study. 

In the summer of 1973, CDC and ILZRO proceeded independently to collect data for their respective 

studies. CDC's examinations were done in two weeks in June 1973, while McNeil's were carried out over the 

course of the summer with the aid of the El Paso public school system. 

The CDC group supplied to the Committee data in detail, which were sufficient to allow the committee to 

conduct statistical tests and analyze characteristics of groups. For the ILZRO study, this committee requested 

data sufficient to carry out similar in-depth analyses. All of the requested data were supplied; however, they 

were not in such a form as to allow recalculation of most of the statistical findings of the study or to allow 

comparison with the CDC findings. 

E.2 STUDY DESIGN 

The environmental sampling that was performed was common for both of these studies. In the selection of 

study and control populations, the Landrigan CDC study used a classical approach of a random sample 

survey to determine the prevalence of abnormal blood lead values. The 13 census tracts most adjacent to the 

smelter were divided into three areas. The sampling frame was designed to obtain about 100 study subjects 

from each area for various age groups. Of 833 occupied residences, interviews were obtained from 758 study 

subjects in the 1-19 age group. The participating children were divided into a lead-absorption group (40-80 

figllOO ml) of 46 and a control group (< 40 /xg/100 ml) of 78. There is no detailed description as to how the 

children were chosen. 

CDC used these same children as the basis for the later study of neuropsychological dysfunction. All but 3 

children chosen for study came from the 1972 prevalence survey; 5 children with known preexisting defects 

such as with a history of symptoms compatible with acute lead poisoning or acute lead encephalopathy and 

those who had received chelation therapy were excluded. 

While it is understood that a number of Smeltertown children with blood lead levels over 40 /i.g/100 ml 

were eventually involved in litigation, most of them took part in the studies. However, on the recommendation of the lawyers representing the children, at least one group of 18 did not participate in the ILZRO study. 

In the absence of identification by names of the individuals in the three studies, it has been impossible to 

evaluate the effects of non-participation. 

The ILZRO study was very different; 138 children from Smeltertown agreed to participate in a study. Residence, not blood lead, was the selection criterion. Two control groups were chosen, and were reported to have 

been matched on age, sex, ethnic background, and income, with one set chosen from El Paso and another set 

for those 8 years of age or under from a rural area about 12 miles from the smelter. This classification had the 

effect of grouping together children who, under the CDC criteria, would have been in "lead" and "control" 

groups. 

E-2 
The criteria used for subclassification of children with regard to lead exposure were based in both studies 

on the blood lead level. Whereas the CDC study utilized blood lead values obtained at only two points in 

time, ILZRO, which was faced with the problem that many children had repeated blood lead measurements 

with marked variations over a period of 18 months (the levels being generally lower after exposure was discontinued), classified children on the basis of the average of the "two highest" recorded values. 

This criterion results in a substantial increase in the number of children in the apparently higher blood lead 

category and a corresponding decrease in the number of those in the apparently lower blood lead level 

category. 

Although it is understandable that this type of selection was used to avoid underestimating the problem of 

lead intoxication in the population examined, it ultimately resulted in muddling of the separation between 

groups (and possibly obscuring eventual differences). For example, the selection for analysis of children from 

the same geographical area, subclassified according to blood lead level, in the ILZRO study, may give the impression that the effects of lead itself are being studied in a homogeneous population. However, since exposure was geographically the same, other factors inherent to each individual child may be responsible for the 

difference in blood lead level observed. 

An additional method of classification could have been the use of free erythrocytic protoporphyrin 

measurements (FEP) which have been shown to provide an indication of metabolic effects of lead absorption 

on metabolism, particularly useful in blood lead level ranges (40-60 figllOO ml) where analytical and 

biological fluctuation may result in uncertain classification. (The ILZRO study included this test but did not 

include it as a basis for data analysis.) Absence of elevation of free erythrocytic protoporphyrin may indicate 

those instances where high blood lead levels were spurious. 

The following psychometric tests were employed by the two studies: 

1. Wechsler Intelligence Scale for Children, WISC (CDC, ILZRO) 

2. McCarthy Scales of Children's Abilities (ILZRO) 

3. Wechsler Preschool and Primary Scale of Intelligence, WPPSI (CDC) 

4. Lincoln-Oseretsky Motor Development Scale (ILZRO) 

5. California Test of Personality Adjustment (ILZRO) 

6. Frosting Perceptual Quotient (ILZRO) 

7. Bender Visual-Motor Gestalt Test (CDC, ILZRO) 

8. Peabody 

9. WRAT 

10. Wepman 

11. Draw-a-person 

All of the tests selected by both studies were appropriate for the ages of the children to whom they were administered. Since the common ground for these studies is the WISC test, with the WPPSI used by CDC and the 

McCarthy Scales by ILZRO for the younger children in their studies, the Committee concentrated on these 

three tests and the results obtained for them. 

E.3 RESULTS 

The study by CDC reports results for 27 children given the WPPSI (12 with blood lead levels 40-80 figllOO 

ml and 15 with blood lead levels less than 40 figllOO ml) and for 97 children tested with the WISC (34 in the 

"lead group" and 63 in the "control group"). Statistical analyses were performed on grouped data with onetailed tests. Significant differences between lead and control groups are reported in this study for the performance IQ's of the WICS and WPPSI. In subtest scores, significant differences were found in Coding on the 

WISC and Geometric Design on the WPPSI. When data from both tests are combined, a significant difference 

between lead and control groups on performance IQ is found. No differences were found between groups in 

verbal IQ's or full-scale IW's of the WISC or WPPSI. 

The ILZRO study based on match pairing solely by residences reports no significant differences in scores 

on the WISC or McCarthy scales between groups with increased lead absorption and pair-matched controls. 

Statistical analysis was by means of two-way analysis of variance by age and blood lead levels. 

The two studies base much of their conclusions upon psychometric and neurological testing of children 

from El Paso and Smeltertown. The reported significant differences and psychometric and neuromotor functions in the CDC study were clouded by potentially important methodological difficulties. These included 

E-3 
P.99 

age differences between case and control groups, limited statistical treatment of the psychometric data collected, and, in the ILZRO study, the use of an average of the two highest blood lead levels to categorize lead 

exposure. 

In addition, both the studies shared the following inherent problems: 

1. Non-random exclusion of large groups of children 

2. Uncertainties as to the selection of control groups 

3. Reliance upon blood lead as the indicator of lead exposure and intoxication in analyses of data 

4. Measurement of a limited aspect of psychological behavior 

5. Lack of consideration of the potentially disruptive influences on test taking of the razing of Smeltertown, closing of its school, resettlement, litigation, and public controversy 

6. Inability to rule out possible preexisting conditions 

The Committee stressed the last issue, noting the likelihood that any behavioral or genetic factors that predispose an individual child to ingest or absorb more lead than another child equally exposed may itself be 

correlated to he result of psychometric testing. In other words an increased blood lead level may reflect, 

rather than cause, a preexisting difference in intelligence or behavior, an issue inherent in virtually all 

retrospective studies of the effects of low level blood lead. 

The opinion of the committee was that no firm conclusions could be drawn from the studies as to whether or 

not there are subclinical effects of lead on children in El Paso and that the reports and data made available 

have not clearly demonstrated any psychologic or neurologic effects in the children under study. It noted the 

absence of major chronic clinical effects, and concluded that these studies therefore do not bear upon the conclusions of other investigations under different conditions and those in which clinical effects have been confirmed. However, because of inherent problems of study design and the limitations in the tests used, this finding should not lead to a conclusion that low levels of lead have no effects on neuropsychological performance. 

£ -4 * US- GOVERNMENT PRINTING OFFICE; 1978— 757-140/668 1