United States
Environmental Protection
Agency
Health Effects Research
Laboratory
Cincinnati OH 45268
EPA 600/1-78-067
November 1978
Research and Development
Study of Children's
Blood-Lead Levels
Within Families
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RESEARCH REPORTING SERIES
Research reports of the Office of Research and Development, U.S. Environmental
Protection Agency, have been grouped into nine series. These nine broad cate-
gories were established to facilitate further development and application of en-
vironmental technology. Elimination of traditional grouping was consciously
planned to foster technology transfer and a maximum interface in related fields.
The nine series are:
1. Environmental Health Effects Research
2. Environmental Protection Technology
3. Ecological Research
4. Environmental Monitoring
5. Socioeconomic Environmental Studies
6. Scientific and Technical Assessment Reports (STAR)
7. Interagency Energy-Environment Research and Development
8. "Special" Reports
9. Miscellaneous Reports
This report has been assigned to the ENVIRONMENTAL HEALTH EFFECTS RE-
SEARCH series. This series describes projects and studies relating to the toler-
ances of man for unhealthful substances or conditions. This work is generally
assessed from a medical viewpoint, including physiological or psychological
studies. In addition to toxicology and other medical specialities, study areas in-
clude biomedical instrumentation and health research techniques utilizing ani-
mals — but always '"- :~i—'-•"' ':—*;— *~ ^..^«.^ t-^oit
This document is available to the public through the National Technical Informa-
tion Service, Springfield, Virginia 22161.
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EPA-600/1-78-067
November 1978
STUDY OF CHILDREN'S BLOOD-LEAD
LEVELS WITHIN FAMILIES
by
Danica Prpic-Majjic
Institute for Medical Research
and Occupational Health
Zagreb, Yugoslavia
Special Foreign Currency Program
JF-3-570-2
Project Officer
Robert J.M. Horton
Health Effects Research Laboratory
Research Triangle Park, N.C. 27711
U.S. ENVIRONMENTAL PROTECTION AGENCY
OFFICE OF RESEARCH AND DEVELOPMENT
HEALTH EFFECTS RESEARCH LABORATORY
RESEARCH TRIANGLE PARK, N.C. 27711
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DISCLAIMER
This report has been reviewed by the Health Effects Research
Laboratory, U.S. Environmental Protection Agency, and approved
for publication. Approval does not signify that the contents
necessarily reflect the views and policies of the U.S. Environmental
Protection Agency, nor does mention of trade names or commercial
products constitute endorsement or recommendation for use.
ii
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FOREWORD
The many benefits of our modern, developing, industrial society are
accompanied by certain hazards. Careful assessment of the relative risk
of existing and new man-made environmental hazards is necessary for the
establishment of sound regulatory policy. These regulations serve to
enhance the quality of our environment in order to promote the public
health and welfare and the productive capacity of our Nation's population.
The Health Effects Research Laboratory, Research Triangle Park,
conducts a coordinated environmental health research program in toxicology,
epidemiology, and clinical studies using human volunteer subjects.
These studies address problems in air pollution, non-ionizing
radiation, environmental carcinogenesis and the toxicology of pesticides
as well as other chemical pollutants. The Laboratory participates in
the development and revision of air quality criteria documents on
pollutants for which national ambient air quality standards exist or
are proposed, provides the data for registration of new pesticides or
proposed suspension of those already in use, conducts research on
hazardous and toxic materials, and is primarily responsible for providing
the health basis for non-ionizing radiation standards. Direct support
to the regulatory function of the Agency is provided in the form of
expert testimony and preparation of affidavits as well as expert advice
to the Administrator to assure the adequacy of health care and surveillance
of persons having suffered imminent and substantial endangerment of
their health.
Some information is available indicating that children respond
differently to environmental lead exposure in terms of intake, absorption
and blood lead level. However, few studies have been undertaken to
compare different age groups in the same setting. In this investigation
comparisons are made of lead exposure and its effects on parents and
children in selected households in the presence of high and low atmospheric
lead exposures.
F. G. Hueter, Ph. D.
Acting Director,
Health Effects Research Laboratory
iii
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ABSTRACT
The comparative studies of the biological indices of elevated exposure to
lead in children and adults were conducted with the intention of reaching a
better understanding of lead absorption in children. Three family groups were
examined. Group 1 consisted of families who lived in the vicinity of a lead
smelter and whose fathers were occupationally highly exposed to lead. Group
2 consisted of families settled in the same area, but whose fathers had no
supplemental occupational exposure to lead. The third was the control group
consisting of families who lived in an area with very low exposure and whose
fathers were not occupationally exposed to lead. Families were selected with
one child under 4 years and, if possible, another child of school age. In the
environmental survey air, dustfall lead, household-dust lead, and drinking-
water lead were analyzed.
It was found that the population living near a lead smelter, except for
the fathers occupationally exposed to lead, had biological findings at the
level of a "slightly elevated" exposure. The fathers occupationally exposed
to lead could be classified as a group with "excessive" exposure.
Three biological parameters—erythrocyte 6-aminolevulinic dehydratase
activity, erythrocyte protoporphyrin, and blood lead—are the most sensitive
indices of increased lead absorption, regardless of age or sex. They are
good parameters to establish the difference in lead absorption from the en-
vironment. On the basis of these parameters the following sequence of lead
absorption was established in family members living in an area with elevated
lead exposure: fathers > school-age children = children up to 4 years >
mothers. Children with fathers occupationally exposed to lead had a slight
additional lead exposure in comparison with children whose fathers had no
supplemental occupational exposure to lead.
The increased lead absorption from the environment in the area inves-
tigated near a lead smelter had no effect on hemoglobin decrease in the pop-
ulation.
There are some indications that children absorb and retain through in-
halation about twice as much lead as adults.
This report was submitted in fulfillment of a Special Foreign Currency
Program (JF-2-570-2) by the Institute for Medical Research and Occupational
Health (Zagreb, Yugoslavia) under the sponsorship of the U.S. Environmental
Protection Agency. The report covers a period of 2% years (February 24, 1975
to August 23, 1977).
IV
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CONTENTS
Abstract IV
Figures VI
Tables XII
Acknowledgments XV
1. Introduction 1
2. Conclusions 2
3. Recommendations 3
4. Study of children's blood-lead levels within families ... 4
Material and methods 4
Results and discussion 9
References 122
Appendix 126
V
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FIGURES
Number Page
1 Scheme of the lead-contaminated area 18
2 Frequency distribution of hemoglobin (Hb) in lead-exposed
groups 1 and 2 . 19
3 Frequency distribution of hematocrit (Hct) in lead-exposed
groups 1 and 2 20
4 Frequency distribution of basophilic stippled cells (BpE)
in lead-exposed groups 1 and 2 21
5 Frequency distribution of reticulocytes (Rtc) in lead-
exposed groups 1 and 2 22
6 Frequency distributions of erythrocyte protoporphyrin (EP)
in lead-exposed groups 1 and 2 23
7 Frequency distribution of 6-aminolevulinic acid dehydratase
activity (ALAD) in lead-exposed groups 1 and 2 24
8 Frequency distribution of lead in blood (Pb-B) in lead-
exposed groups 1 and 2 25
9 Frequency distribution of 6-aminolevulinic acid in urine
(ALA-U mg/100 ml) in lead-exposed groups 1 and 2 26
10 Frequency distribution of 6-aminolevulinic acid in urine
(ALA-U mg/24 h) in lead-exposed groups 1 and 2 27
11 Frequency distribution of coproporphyrin in urine
(CP-U yg/100 ml) in lead-exposed groups 1 and 2 28
12 Frequency distribution of coproporphyrin in urine
(CP-U yg/24 h) in lead-exposed groups 1 and 2 29
13 Frequency distribution of hemoglobin (Hb) in
control group 30
14 Frequency distribution of hematocrit (Hct) in
control group 31
VI
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FIGURES (continued)
Number Page
15 Frequency distribution of basophilic stippled cells (BpE)
in control group 32
16 Frequency distribution of reticulocytes (Rtc) in
control group „ 33
17 Frequency distribution of erythrocyte protoporphyrin
(EP) in control group 34
18 Frequency distribution of 6-aminolevulinic acid
dehydratase activity (ALAD) in control group 35
19 Frequency distribution of lead in blood (Pb-B)
in control group 36
20 Frequency distribution of 6-aminolevulinic acid in urine
(ALA-U mg/100 ml) in control group 37
21 Frequency distribution of 6-aminolevulinic acid in urine
(ALA-U mg/24 h) in control group 38
22 Frequency distribution of coproporphyrin in urine
(CP-U yg/100 ml) in control group 39
23 Frequency distribution of coproporphyrin in urine
(CP-U yg/24 h) in control group 40
24 Percentile distribution of Pb-B (yg/100 ml) in
control group 41
25 Semilogarithmic correlation in a total study population
between 6-aminolevulinic acid dehydratase activity and
lead in blood (log ALAD/lin Pb-B) 42
26 Semilogarithmic correlation in a total study population
between erythrocyte protoporphyrin and lead in blood
(log EP/lin Pb-B) 43
27 Semilogarithmic correlation in a total study population
between 6-aminolevulinic acid in urine and lead in blood
(log ALA-U mg/100 ml/lin Pb-B) 44
28 Semilogarithmic correlation in a total study population
between 6-aminolevulinic acid in urine and lead in blood
(log ALA-U mg/ 24 h/lin Pb-B) 45
VII
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FIGURES (continued)
Number
29 Semilogarithmic correlation in a total study population
between coproporphyrin in urine and lead in blood
(log CP-U yg/100 ml/lin Pb-B) ................. 46
30 Semilogarithmic correlation in a total study population
between coproporphyrin in urine and lead in blood
(log CP-U yg/24 h/lin Pb-B) .................. 47
31 Semilogarithmic correlation in fathers of a total study
polulation between 6-aminolevulinic acid dehydratase
activity and lead in blood (log ALAD/lin Pb-B) .........
32 Semilogarithmic correlation in fathers of a total study
population between erythrocyte protoporphyrin and lead
in blood (log EP/lin Pb-B) ................... 49
33 Semilogarithmic correlation in fathers of a total study
population between 6-aminolevulinic acid in urine and
lead in blood (log ALA-U mg/100 ml/lin Pb-B) .......... 50
34 Semilogarithmic correlation in fathers of a total study
population between 6-aminolevulinic acid in urine and
lead in blood (log ALA-U mg/24 h/lin Pb-B) ........... 51
35 Semilogarithmic correlation in fathers of a total study
population between coproporphyrin in urine and lead in
blood (log CP-U yg/100 ml/lin Pb-B) .............. 52
36 Semilogarithmic correlation in fathers of a total study
population between coproporphyrin in urine and lead in
blood (log CP-U yg/24 h/lin Pb-B) ............... 53
37 Semilogarithmic correlation in mothers of a total study
population between 6-aminolevulinic acid dehydratase
activity and lead in blood (log ALAD/lin Pb-B) ......... 54
38 Semilogarithmic correlation in mothers of a total study
population between erythrocyte protoporphyrin and
lead in blood (log EP/lin Pb-B) ................ 55
39 Semilogarithmic correlation in mothers of a total study
population between 6-aminolevulinic in urine and lead
in blood (log ALA-U mg/100 ml/lin Pb-B) ............ 56
VIII
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FIGURES (continued)
Number Page
40 Semilogarithmic correlation in mothers of a total study
population between 6-aminolevulinic acid in urine and
lead in blood (log ALA-U mg/24 h/lin Pb-B) 57
41 Semilogarithmic correlation in mothers of a total study
population between coproporphyrin in urine and lead in
blood (log CP-U ug/100 ml/lin Pb-B) 58
42 Semilogarithmic correlation in mothers of a total study
population between coproporphyrin in urine and lead in
blood (log CP-U Ug/24 h/lin Pb-B) 59
43 Semilogarithmic correlation in children of school age
of a total study population between 6-aminolevulinic
acid activity and lead in blood (log ALAD/lin Pb-B) 60
44 Semilogarithmic correlation in children of school age
of a total study population between erythrocyte proto-
porphyrin and lead in blood (log EP/lin Pb-B) 61
45 Semilogarithmic correlation in children of school age
of a total study population between 6-aminolevulinic acid
in urine and lead in blood (log ALA-U mg/100 ml/lin Pb-B) ... 62
46 Semilogarithmic correlation in children of school age
of a total study population between 6-aminolevulinic acid
in urine and lead in blood (log ALA-U mg/24 h/lin Pb-B) .... 63
47 Semilogarithmic correlation in children of school age
of a total study population between coproporphyrin in urine
and lead in blood (log CP-U yg/100 ml/lin Pb-B) 64
48 Semilogarithmic correlation in children of school age
of a total study population between coproporphyrin in urine
and lead in blood (log CP-U yg/24 h/lin Pb-B) 65
49 Semilogarithmic correlation in children up to 4 years of a
total study population between 6-aminolevulinic acid
dehydratase activity and lead in blood (log ALAD/lin Pb-B) ... 66
50 Semiligarithmic correlation in children up to 4 years of a
total study population between erythrocyte protoporphyrin
and lead in blood (log EP/lin Pb-B) 67
IX
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FIGURES (continued)
Number Page
51 Semilogarithmic correlation in children up to 4 years of a
total study population between 6-aminolevulinic acid in
urine and lead in blood (log ALA-U mg/100 ml/lin Pb-B) ..... 68
52 Semilogarithmic correlation in children up to 4 years of a
total study population between 6-aminolevulinic acid in
urine and lead in blood (log ALA-U mg/24 h/lin Pb-B) ...... 69
53 Semilogarithmic correlation in children up to 4 years of a
total study population between coproporphyrin in urine and
lead in blood (log CP-U yg/100 ml/lin Pb-B) .......... 70
54 Semilogarithmic correlation in children up to 4 years of a
total study population between coproporphyrin in urine and
lead in blood (log CP-U yg/24 h/lin Pb-B) ........... 71
55 Semilogarithmic correlation in fathers of a total study
population between hemoglobin and lead in blood
(log Hb/lin Pb-B) ....................... 72
56 Correlation in fathers of a total study population between
hemoglobin and lead in blood (lin Hb/lin Pb-B) ......... 72
57 Semilogarithmic correlation in mothers of a total study
population between hemoglobin and lead in blood
(log Hb/lin Pb-B) ....................... 74
58 Correlation in mothers of a total study population between
hemoglobin and lead in blood (lin Hb/lin Pb-B) ......... 75
59 Semilogarithmic correlation in children of school age of a
total study population between hemoglobin and lead in blood
(log Hb/lin Pb-B) ....................... 76
60 Correlation in children of school age of a total study
population between hemoglobin and lead in blood
(lin Hb/lin Pb-B) ....................... 77
61 Semilogarithmic correlation in children up to 4 years of a
total study population between hemoglobin and lead in blood
(log Hb/lin Pb-B) ....................... 78
62 Correlation in children up to 4 years of a total study
population between hemoglobin and lead in blood
(lin Hb/lin Pb-B) ....................... 79
X
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FIGURES (continued)
Number Page
63 Semilogarithmic correlation in fathers of a total study
population between hemoglobin and 6-aminolevulinic acid
dehydratase activity (lin Hb/log ALAD) 80
64 Semilogarithmic correlation in mothers of a total study
population between hemoglobin and 6-aminolevulinic acid
dehydratase activity (lin Hb/log ALAD) 81
65 Semilogarithmic correlation in children of school age of
a total study population between hemoglobin and
6-aminolevulinic acid dehydratase activity (lin
Hb/log ALAD) 82
66 Semilogarithmic correlation in children up to 4 years of
a total study population between hemoglobin and
6-aminolevulinic acid dehydratase activity (lin
Hb/log ALAD) 83
67 Semilogarithmic correlation in fathers of a total
study population between hemoglobin and erythrocyte
protoporphyrin (lin Hb/log EP) 84
68 Semilogarithmic correlation in mothers of a total study
population between hemoglobin and erythrocyte proto-
porphyrin (lin Hb/log EP) 85
69 Semilogarithmic correlation in children of school age of
a total study population between hemoglobin and
erythrocyte protoporphyrin (lin Hb/log EP) 86
70 Semilogarithmic correlation in children up to 4 years of
a total study population between hemoglobin and erythrocyte
protoporphyrin (lin Hb/log EP) 87
71 Yearly cycles of mean monthly air lead concentrations in
lead smelter area (averages of five sampling sites) 88
72 Median erythrocyte protoporphyrin (EP) in fathers and mothers
according to median residential distance from lead
smelter 89
73 Median erythrocyte protoporphyrin (EP) in children of school
age and in children up to 4 years according to median
residential distance from lead smelter 90
XI
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TABLES
Number £§.
1 The number of families in the examined groups 91
2 The number of family members within examined groups 91
3 Age distribution in parents 92
4 Age distribution in children 93
5 Habitation distribution by distance from lead smelter
in lead-exposed group 1 94
6 Habitation distribution by distance from lead smelter
in lead-exposed group 2 94
7 Statistical parameters of biological data in lead-exposed
group 1 (fathers occupationally exposed to lead) 95
8 Statistical parameters of biological data in lead-exposed
group 2 (fathers not occupationally exposed to lead) 96
9 Statistical parameters of biological data in control
group 97
10 Statistical significance of the difference within lead-
exposed group 1 (fathers occupationally exposed to
lead) 98
11 Statistical significance of the difference within lead-
exposed group 2 (fathers not occupationally exposed
to lead) 100
12 Statistical significance of the difference within
control group 102
13 Statistical significance of the difference between
lead-exposed group 1 (fathers occupationally exposed
to lead) and lead-exposed group 2 (fathers not
occupationally exposed to lead) 104
XII
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TABLES (continued)
Number Page
14 Statistical significance of the difference between lead-
exposed group 1 (fathers occupationally exposed to lead)
and control group 105
15 Statistical significance of the difference between lead-
exposed group 2 (fathers not occupationally exposed to
lead) and control group 106
16 Statistical significance of the difference between lead-
exposed group 1 (fathers occupationally exposed to lead),
lead-exposed group 2 (fathers not occupationally exposed
to lead) , and control group 106
17 Air-lead concentration (yg/m3) at five sites in lead
smelter area 108
18 Statistical parameters of air-lead concentration (yg/m3)
at five sites in lead smelter area (December 1973-
October 1976) 109
19 Statistical parameters of annual air-lead concentration
(yg/m3) at five sites in lead smelter area (December 1973-
October 1976) 109
20 Statistical significance of the difference between air-lead
concentration (yg/m3) at five sites in lead smelter area
(December 1973-October 1976) 110
21 Air-lead concentration (yg/m3) at one site in control
area 110
22 Statistical parameters of air-lead concentration (yg/m3)
at one site in control area (November 1974-October 1975) ... Ill
23 Lead amount in dustfall (mg/m2/month) at four sites in
lead smelter area Ill
24 Statistical parameters of lead amount in dustfall
(mg/m2/month) at four sites in lead smelter area
(November 1975-October 1976) 112
25 Lead amount to dustfall (mg/m2/month) at one site
in control area 112
26 Statistical parameters of lead amount in dustfall
(mg/m2/month) at one site in control area
(November 1975-October 1976 113
XIII
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TABLES (continued)
Number Page
27 Lead content of household dust (yg/g) in lead smelter
area (December 1976) 113
28 Statistical parameters of lead content in household
dust (yg/g) in lead smelter area (December 1976) 114
29 Lead content of household dust (yg/g) in control
area (October 1975)
30 Statistical parameters of lead content in household
dust (yg/g) in control area (October 1975) .......... 115
31 Water-lead concentration (yg/1) in lead smelter
area (December 1976) .....................
32 Water-lead concentration (yg/1) in control area
(October 1975) ........................ 116
33 Ratio content in various environmental media between
the exposed and the control area ............... 116
34 Estimated lead absorption (yg/Pb/day/kg) from lead-
exposed and control area ................... 117
35 Biological indices of lead absorption in comparison
with median residential distance of fathers (group 2)
from lead smelter .... ................... 118
36 Biological indices of lead absorption in comparison
with median residential distance of mothers (group 1
and group 2) from lead smelter ................ 119
37 Biological indices of lead absorption in comparison
with median residential distance of school age
children (group 1 and group 2) from lead smelter ....... 120
38 Biological indices of lead absorption in comparison
with median residential distance of children up to
4 years (group 1 and group 2) from lead smelter ........ 121
A-l Lead-exposed group 1 ...................... 126
A-2 Lead-exposed group 2 ...................... 129
A-3 Control group .......................... 134
XIV
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ACKNOWLEDGMENTS
The work presented in this report was performed by the following staff
of the Institute for Medical Research and Occupational Health (Zagreb)
Research advisors: M. Fugas (M.Sc., Chemical Engineering) and A.
Markicevic (M.D., Specialist in Occupational Health)
Research assistants: V. Karacic (Chemist), E. Kersanc (Biologist),
R. Paukovic (M.Sc., Chemical Engineering), J. Pongracic (Chemist),
S. Telisman (M.Sc., Chemist), A. Vukovic (Chemist), B. Wilder
(Physicist)
Technicians: M. Erceg, B. Matijevic, M. Milas, A. Sirec
Consultants: T. Beritic (M.D., Specialist in Internal Medicine and
Occupational Health, professor), M. Seric, (M.D., Ph.D., Epidemiol-
ogist, professor)
From other institutions the following coworkers also participated in
the work:
B. Cretnik (M.D., Specialist in Pediatrics), Health Center, Ravne na
KoroSkem
J. Susnik (M.D., Specialist in Occupational Health), Health Center,
Ravne na Koroskem
Z. Skuric (Ph.D., Chemical Engineering, assistant professor), School of
Public Health "Andrija Stampar", Zagreb
F. Valic (Ph.D., Chemical Engineering, Industrial Toxicologist, profes-
sor), School of Public Health "Andrija Stampar, Zagreb (as a consultant)
XV
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SECTION 1
INTRODUCTION
There is general agreement about the fact that data on lead absorption
and toxicity in children are still quite scarce. The nature and extent of
lead toxicity cannot be predicted on the basis of information obtained in
adults. Comparative studies of the biological changes indicative of ele-
vated exposure to lead in children and adults are therefore very useful.
This aspect of lead toxicology is the basis of this report, the results of
which have been obtained over a period of 2% years by the team of workers
listed in the acknowledgments.
The report is divided into sections. Sections 2 and 3 contain the main
conclusions and recommendations for further studies. Section 4 reports on
the results of research concerning biological indices of lead absorption,
environmental survey, and residential distance from lead-emitting sources.
The results obtained are presented in 38 tables and 73 diagrams. The Refer-
ence Section gives a list of publications pertinent to the subject of this
report. The three tables in the appendix present the individual biological
indices of lead absorption.
The situation in regard to lead exposure is somewhat unusual in Yugosla-
via, where this study was done. In the smaller communities it has long been
the custom that most household containers are made by local potters. These
are usually lead glazed and fired at low temperatures. Acid foods and bever-
ages can leach lead from such glazes, particularly during prolonged contact.
The principal beverage is wine, which is somewhat acid. Persistent education-
al efforts by health authorities have reduced this problem considerably, but
it is still present in rural areas in some parts of the country. This causes
blood-lead levels in rural areas without industrial exposure to be higher
than in such areas in other parts of Europe.
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SECTION 2
CONCLUSIONS
The results of simultaneous studies of children and adults in three
family groups comparable in their socioeconomic status, but differing in lead
exposure, have shown that three biological parameters—erythrocyte 6-
aminolevulinic dehydratase activity, erythrocyte protoporphyrin, and blood
lead—were the most sensitive indices of increased lead absorption, regard-
less of age or sex. They are good parameters to establish the differences
in lead absorption from the environment.
Families who lived in the vicinity of a lead smelter showed the following
sequence of lead absoprtion: fathers > school-age children = children up to
4 years > mothers.
Children from lead-exposed areas with fathers occupationally exposed to
lead showed a slight additional lead exposure in comparison with children
settled in the same area, but whose fathers had no supplemental occupational
exposure to lead.
The increased lead absorption from the environment in the investigated
area near a lead smelter had no effect on Hb decrease in the population.
When the four environmental media in the exposed and in the control area
were compared, the lead content in the specimens examined from the exposed
area had decreased according to the following sequence: air > dustfall > house-
hold dust > water.
The estimated air-lead absorption expressed on the basis of body weight
was about twice as high in children as in adults. This finding is very im-
portant in the assessment of the permissible levels of lead exposure in child-
ren living near a lead smelter.
Erythrocyte protoporphyrin is the best biological index in the evaluation
of body-response normalization with regard to increasing residential distance
from the lead-emitting source.
Relationship analysis between biological parameters indicate that blood
lead is not the best parameter to which other parameters'should be related.
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SECTION 3
RECOMMENDATIONS
In children with slightly elevated lead exposure from the environment,
the most important recommendation is to control 6-aminolevulinic acid dehy-
dratase activity, erythrocyte protoporphyrin, and blood-lead concentrations.
The other biological indices of increased lead absorption are less significant
Erythrocyte protoporphyrin concentration seems to be the most representative
indicator of long-term lead absorption, while blood lead and to a lesser ex-
tent erythrocyte 6-aminolevulinic acid dehydratase activity reflect more
actual exposure and day-to-day variability.
In the assessment of permissible levels of lead exposure from the envi-
ronment, special care should be devoted to children because they absorb and
retain a larger portion of inhaled and dietary lead than adults.
In the vicinity of a lead smelter where the combined exposure to lead
and other metals accompanying lead ores takes place, effects of some other
metals on hemoglobin synthesis could not be excluded. There were some indi-
cations that simultaneous exposure to other metals along with lead could have
a moderating effect against increased lead absorption, but supporting data
is needed. Therefore a further study which would take into account the simul-
taneous absorption of lead, zinc, iron, and copper is recommended.
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SECTION 4
STUDY OF CHILDREN'S BLOOD-LEAD LEVELS WITHIN FAMILIES
The nature and extent of lead toxicity in children cannot be predicted
on the basis of information on adults, because "the child is not just a little
man"; the differences are anatomic, physiologic, pathologic, and immunolog-
ic (1).
The infant is more susceptible to lead than the adult. Balance studies
showed that children absorb much more dietary lead than adults, approximately
50% in children (2) and 10% in adults (3) . Comparative data on airborne lead
absorption in children and adults are not available.
At present no evidence is known to exist to show whether neurochemical
or neurophysiological changes precede changes in the hematopoietic system.
Several biochemical tests demonstrate early effects of lead on the hemato-
poietic system. In contrast with these tests there are no comparable neuro-
chemical tests for the measuring of early metabolic changes in the nervous
system. The hematopoietic system is currently considered to be the site where
the first measurable adverse effect ("critical effect") occurs (4-6) . The
quantitative determinations of characteristic indicators showing lead effect
on the hemoglobin synthesis are the most common parameters in the assessment
of elevated lead exposure.
A lead smelter area is a particularly good location in which to study
lead absorption, both in adults and children. Chronic inhalation and inges-
tion of lead by contaminated air, food, and water are common characteristics
of a population living in the vicinity of a lead smelter. It is in such an
area, therefore, that comparative studies can be carried out most effective-
ly.
The three aforementioned aspects—the deficiency of information on lead
absorption and toxicity in children, the opportunity to measure the adverse
effect of lead on hemoglobin synthesis by means of characteristic parameters
in blood and urine, and an available location for conducting comparative
studies in adults and children—constituted the basis of this project.
MATERIAL AND METHODS
Three family groups, comparable in their socioeconomic status but differ-
ing in lead exposure, have been investigated. Group 1 consisted of families
who lived in the vicinity of a lead smelter and whose fathers were occupation-
ally highly exposed to lead. Group 2 consisted of families resident in the
same area with a high nonoccupational lead exposure, but whose fathers had no
-------
supplemental occupational exposure to lead. The third was the control group,
consisting of families who lived in an area with a low lead exposure and whose
fathers were not occupationally exposed to lead. Families were selected with
one child under 4 years and, if possible, another child of school age.
It had been planned to examine 20 families in each group. Although
efforts were made to complete this number, in the first lead-exposed group
and in the control group fewer families were examined. The explanation for
this was the relatively small number of families with a small child and the
negative attitude of parents to blood tests in small children. In the second
lead-exposed group one additional family was included in the study. Table 1
presents the number of families in the groups examined and Table 2 the number
of family members within the groups examined. The total number of subjects
was 181.
The age of the fathers was 23 to 46 years, of the mothers 21 to 44 years,
of the children of school age 5 to 16 years, and of the small children 11
months to 4 years. The age distribution for parents is presented in Table 3,
and for both groups of children in Table 4.
The subjects in both lead-exposed groups lived in a river valley close to
a lead smelter (Figure 1). Several settlements (A, BI, B2, GI, €2, GS, D) are
located at various distances from the smelter. Table 5 and Table 6 show the
residential distance distribution from the lead smelter for both groups. The
majority of families lived in settlement D, vhich was most distant from the
emitting source.
The valley was about 500 m above sea level. Winds blew either from the
southwest, bringing humid air and rain, or from the northeast, bringing dry,
cold air and fair weather. The mean monthly temperatures Varied from 3 to
17.5°C with a maximum of about 30°C and a minimum of about -16°C. Snow, which
usually falls in the second half of November, remains on the ground for 100
to 210 days, approximately.
The subjects in the control group were matched to the exposed families
with regard to the socioeconomic status and nutritional condition. They
lived in several settlements (E, F, G, H, I) about 400 m above sea level in
a climate very similar to that of the lead-exposed area.
In the subjects examined, the following biological indicators of ele-
vated lead exposure were determined: hemoglobin (Hb), hematocrit (Htc),
basophilic stipple cells (BpE) count, reticulocyte (Rtc) count, erythrocyte
protoporphyrin (EP), 6-aminolevulinic acid in urine (ALA-U), and total
coproporphyrin in urine (CP-U).
Hb was determined spectrophotometrically by the cyanmethemoglobin meth-
od (7). Hematocrit was determined by the standard method according to
Wintrobe (8). BpE were fixed and stained according to the method of Hamel (9),
using Loffler's methylene blue solution. In each blood film a total of 1000
red blood cells was counted. Rtc were vitally stained with 1% Brilliant-
Cresyl-blue solution in ethanol, and a total of 1000 red blood cells was
counted in the film.
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The concentration of EP was determined according to the method of Riming-
ton as modified by Cripps and Peters (10). In this assay 5 to 10 ml of blood
with heparin as anticoagulant were used. The packed red cell volume (V) was
calculated from the hematocrit. Red cells were separated from plasma and were
treated with 50 ml of an ethyl acetate: acetic acid (4:1 ratio) mixture and
allowed to stand overnight in the dark at 4°C. On the following day the
erythrocyte extract was filtered and washed with the ethyl acetate and acetic
acid mixture until the filtrate containing hematin and porphyrins (uroporphyrin,
coproporphyrin,, and protoporphyrin) became colorless. In this filtrate uro-
porphyrin was discarded with a saturated sodium acetate solution. Any re-
maining coproporphyrin and protoporphyrin in sodium acetate washings were re-
extracted with fresh ethyl acetate. Protoporphyrin and coproporphyrin were
separated from hematin by extraction with 3 N NCI until the successive acid
extracts no longer showed any fluorescence under the Hg-lamp (366 nm) - The
acid extract of porphyrin was neutralized with solid sodium acetate to pH 3.2
and then shaken with 50 ml portions of ether. From the ether extract copro-
porphyrin was extracted with successive 2- to 3-ml portions of 0.1 N HC1 until
all coproporphyrin was removed, which was confirmed by examination of the
extracts for red fluorescence under the Hg-lamp (366 nm) . Protoporphyrin was
then extracted in the same way, using 1.5 N HCl, and the total volume (v)
recorded. The absorption of the acid protoporphyrin solution was measured
against water in a 1-cm cell at 380 nm (A38o)» 430 nm (Ai+so) and at the maxi-
mum absorption in the Soret region (Amax) using a Beckman DB-G spectrophoto-
meter. The EP concentration expressed as yg EP/100 mlE was calculated accord-
ing to the formula suggested by Rimington (10). In this formula [2Amax- (Ai^o
± A38o)] .C. YJ tne symbol A is related to the corresponding absorptions, CT is
the correction constant with value of 1.226, v is the total volume of 1.5
N HCl protoporphyrin extract, and V is the volume of the packed red cells which
was used in the analysis. The precision of the method expressed as a relative
standard deviation was 4.0% (X = 207.9 ug EP/100 mlE; N = 8).
ALAD activity was determined according to the modified method of Bonsi-
gnore et al. (11). Modification of the original method was applied in the
lower pH value of the ALA substrate (pH=6.8) by the use of a sodium phosphate
buffer instead of a carbonate buffer and in the volume of reagents, which was
increased to twice the original volume. First, 0.4 ml of whole blood was
hemolyzed in 2.6 ml of distilled water, and then to this hemolyzate 2 ml of
freshly prepared 0.01 M 6-aminolevulinic acid were added. From this solution
2-ml aliquots were distributed in two centrifuge tubes. In tube 1 ("blank")
2 ml of mercury (II) chloride-trichloroacetic acid solution were added. Both
tubes were incubated in a 37± 0.2°C water bath for 1 hour, following which the
porphobilinogen reaction in tube 2 was stopped by the addition of 2 ml of
mercury (II) chloride-trichloroacetic acid solution. Both deproteinized sam-
ples were then centrifuged at 2500 rpm. The porphobilinogen formed was deter-
mined by the Ehrlich reaction: 2 ml of the supernatant was added to 2 ml of
modified Ehrlich reagents, and after 10 minutes absorption was measured on the
Beckman DB-G spectrophotometer against water at 555 nm in a 1-cm cell. The
supernatant of the blank tube was treated in the same way. The enzyme activity
was expressed in units, one unit being defined as the difference in absorption
in matched 1-cm cells between the specimen in which reaction had taken place
and the blank tube, corrected for the sample dilution and the percent of
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hematocrit. The relative standard deviation for this method was 0.8%
(X = 201.6 units/mlE; N=6) .
Lead in blood was analysed by flameless atomic absorption spectrophotom-
etry (12) using Perkin-Elmer HGA-72. The original method was slightly mod-
ified (13) with regard to the volume of the injected sample and the tempera-
ture program. To 2 ml of 0.1% Triton X - 100, 0.5 ml of whole blood and 0.1
ml of 0.5 % nitric acid were added. From this diluted sample 0.02 ml was in-
jected directly into the graphite tube, and the absorption was measured at
283.3 nm. The follwoing temperature program was experimentally selected as
optimum: drying at 100°C for 40 s, ashing at 100-450°C ("ramp" program),
and atomization at 2045°C for 10 s. The calculation was made according to
the addition method, using freshly prepared standard solutions of 1 yg Pb/ml
and 5 yg Pb/ml in_0.5% nitric acid. The relative standard deviation for this
method was 2.4% (X = 17.5 yg Pb/100 ml; N-ll) and 4.9% (X = 48.8 yg/100 ml;
ALA-U was determined by the Davis-Andelman (14) modification of the
Mauzerall-Grannick method. The separation and isolation of ALA from a urine
sample (1 ml of a 24-hour specimen*) was carried out by disposable plastic
chromatography columns (Bio-Rad Laboratories) . From the cationic (hydrogen)
column ALA was eluted with 7.0 ml acetate buffer (pH 4.6), and this eluate was
collected in a 10-ml volumetric flask. After the addition of 0.2 ml of ace-
tylacetone and acetate buffer to the mark, the sample was allowed to stand
in a boiling water bath for 10 minutes. The porphobilinogen formed was deter-
mined by the modified Ehrlich's reagent: a 2-ml aliquot was mixed with 2 ml
of modified Ehrlich reagent and after 15 minutes absorption was measured on
a Beckman DB-G spectrophotometer against water at 555 nm in a 1-cm cell. A
blank with water was prepared in the same way. The calculation was made
according to the regression line obtained by known ALA concentrations (3 to
52 yg ALA/ml urine) . The relative standard deviation for this method is
3.5% (X - 0.475 mg/100 ml; N=6) .
CP-U concentration was measured fluorometrically by the method of
Schwartz et al. (15). The urine sample (5 ml of 24-hour specimen*) was acid-
ified by buffered acetic acid. Porphyrins were extracted with ethyl acetate
and the extract washed with a sodium acetate solution to remove uroporphyrins .
Coproporphyrin precursors were oxidized with iodine. Total coproporphyrins
(I + III) were extracted with several portions of 1.5 N hydrochloric acid.
The combined extract was made up to 25 ml with 1.5 N hydrochloric acid. The
fluorescence was measured by means of the spectrofluorimeter Perkin-Elmer
MPF-2A. A standard curve was made by the known coproporphyrin concentrations.
The sensitivity of the method is 1 yg/100 ml urine.
Families from the smelter area were examined in May/ June 6f 1976, and
those in the control area in October of 1975. The results obtained were
statistically evaluated and compared. Analysis of variance, Student's t-test,
correlation, and frequency distribution analyses were carried out. In cases
* It was impossible to obtain a 24-hour sample from children up to 4 years
of age.
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where the F-test values showed that both standard deviations did not belong
to the same population the significance of the difference between the two
groups examined was determined by the method of Cochran and Cox (16), instead
of using the standard t-test (results marked with an asterisk in the tables)-
In the environmental survey air lead, dustfall lead, household-dust lead,
and drinking-water lead were analysed.
Air-lead concentration in the exposed area was measured for 3 consecu-
tive years (1974 to 1976) at five sites in settlements 4.0 and 0.5 km N.
(Figure 1, sites 1 and 2), 1.5 and 2.0 km SSW. (Figure 1, sites 3 and 4), and
2.5 km SW. (Figure 1, site 5) from the lead smelter. Weekly samples from
about 14 m3 of air were collected on the membrane filters of 1-inch diameter
filtration surface by means of diaphragm pumps. The exact volume of the air
samples was recorded by a gas meter. The filters with the samples were dis-
solved in nitric acid solution, evaporated to dryness, and redissolved in
EDTA solution (to prevent loss of lead due to absorption) . The final solu-
tion, after being made up to a certain volume (2, 5, 10 ml or more) should
have 1% EDTA and pH 8. The samples were analysed using a Unlearn SP 90
atomic absorption spectrophotometer under the following conditions : current
6 mA, acetylene flow 1000 ml/min, airflow 5000 ml/ min, burner height 0.8 cm,
and slit width 0.2 mm. A blank and a set of standards were run with each set
of samples. The concentration of lead in the final solution (yg/ml) was read
from a calibration curve and converted into the concentration of lead in air
(yg/m3). The sensitivity of the method was 2 yg Pb per 1 ml of the final :
solution.
In the control area over a 1-year period (November 1, 1974 to October 30,
1975) air-lead concentration was measured at one site. Daily samples from
about 200 m of air were collected on the membrane filters of a 4-inch diam-
eter filtration surface by means of a high-volume sampler. The samples were
analysed in the same way as the samples from the lead-contaminated area.
Lead content of dustfall was measured simultaneously at four sites in the
exposed area (Figure 1, sites 1, 2, 3, and 5), and at one site in the control
area, for a period of 1 year (November 1, 1975 to October 31, 1976). Monthly
samples of deposited lead were collected in plastic containers of 1.5-liter
volume with a 10-cm diameter opening, evaporated to dryness, dissolved in
nitric acid, evaporated again, redissolved in 1% EDTA, and analysed by atomic
absorption spectrophotometry.
Samples of household dust were collected in 26 homes, 14 from the exposed
area and 12 from the control area. Household dust was sampled by a pump with
a special adapter supplied with a screen at its opening to prevent coarse
particles and small objects from being collected on the membrane filter, which
served as a sampling surface. The total weight of dust was determined, and
subsequently the sample was analysed for lead by the same procedure as the
samples of airborne lead.
Samples of water were collected from five sites in both the exposed and
the control area. In both areas only part of the homes were supplied from
the public water supply. Many homes had a well of .their own or an individual
running water system. In some cases water was used from a fresh-water spring.
8
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All kinds of water, therefore, were included in the lead analyses. Water
samples were collected in 5-liter plastic containers with 0.2 ml HN03 to pre-
vent absorption of Pb on the walls of the containers. One liter aliquot of
the sample was neutralized by ammonia and separated by anion exchange from in-
terfering ions. The eluate was evaporated to dryness, dissolved in 1% EDTA
solution (pH=8) , and analysed by atomic absorption spectrophotometry.
RESULTS AND DISCUSSION
Biological Indices of Lead Absorption
The individual laboratory findings of the lead-exposed groups, 1 and 2,
and of the control group are presented in the Appendix (Tables A-l, A-2, and
A-3). Figures 2 to 23 show the frequency distribution for each parameter in
the groups examined. In the two lead-exposed groups the obtained results for
the mothers and for both groups of children were pooled. As visible from the
diagrams the distributions do not follow an ideal pattern of normal or skewed
distribution. The small number of the subjects examined might be an explan-
ation of this variation. Differences in nutritional habits, alcohol consump-
tion, and environmental circumstances in the house or working place might be
additional reasons.
The results obtained are summarized in subgroups—fathers, mothers, child-
ren of school age,_and children up to 4 years—and presented separately as
arithmetic means (X) with standard deviations (SD) and standard errors (SE)
for each group in Tables 7, 8, and 9. The fathers in group 1, occupationally
exposed to lead, showed findings in accordance with their exposure which were
significantly different from all other subjects examined. These findings can
be classified as "excessive" exposure. The fathers in group 2 have findings
at the level of a "slightly elevated" exposure. The mothers, school-age child-
ren, and small children in both exposed groups could be classified in the same
category. Blood-lead concentrations obtained in the control group were a
little higher than expected. Percentile distribution (Figure 24) differed
from that proposed by Zielhuis (17), but was very close to the results of
Secchi et al. (18). The environmental survey did not show any specific fea-
tures for the group under investigation. It has been assumed, therefore, that
the other factors, due to nutritional habits and lead-contaminated alcohol
consumption, might be the source of individual "abnormal1! blood-lead concen-
trations. This finding should not have any bearing on the final conclusion,
because the control group was matched to the exposed groups with regard to
the socioeconomic status and nutritional condition. Thus the expected differ-
ences reflect the actual values.
The significance of the differences in arithmetic means was tested among
the fathers, mothers, school-age children, and small children within each
group examined.
Within the lead-exposed group 1 (Table 10) there was a statistically sig-
nificant difference in the majority of findings between fathers and mothers,
and fathers and both groups of children. Mothers and children did not differ
very much. Between the mothers and both groups of children the difference was
-------
significant for ALAD activity (lower in children), Rtc number (higher in
mothers), and ALA-U expressed in 24-hour diuresis (higher in mothers). In
addition, mothers had significantly higher Hb, Hct, and CP-U expressed in 24-
hour diuresis than small children. Between school-age children and small
children the only significant difference was in ALA-U, expressed in 24-hour
diuresis.
In the second lead-exposed group (Table 11) the fathers had significantly
lower ALAD values than the mothers. Statistically significant differences in
the same direction were found between fathers and school age children for Hb,
Hct, Pb-B, and ALA-U, expressed in 24-hour diuresis, and between fathers and
children up to 4 years for Hb, Hct, Pb-B, and ALA-U. Higher lead absorption
in fathers could be attributed to the fact that the fathers possibly spent
more time in areas with higher contamination levels. Alcohol consumption
could be an additional factor. Between the mothers and both groups of child-
ren the difference was significant for Pb-B and EP concentration (both higher
in children), and for ALA-U and CP-U, expressed in 24-hour diuresis (both
higher in mothers)- In addition, small children had significantly lower ALAD
activity, Hb, and Hct values than the mothers. Between school-age children
and small children the difference was significant for Hb, Hct, ALA-U, and
CP-U, expressed in 24-hour diuresis (higher in school-age children) .
In both lead-exposed groups the difference in Hb and Hct between the sub-
jects may be attributed to the difference in sex and age. The higher Rtc fig-
ures in mothers than in both groups of children was probably caused by the
regular menstrual bleeding, which stimulated the release of reticulicytes from
the bone marrow to the peripheral blood.
Comparing three very important parameters, Pb-B, ALAD, and EP, first as
a measure of the dynamic body-lead pool (19) , second as the most sensitive
index for an early response to the slightest lead exposure (20) , and third as
the best indicator of total lead body burden (21) , one may conclude that the
following was the sequence of lead absorption in family members of both groups:
fathers > school-age children = children up to 4 years > mothers. The popula-
tion of mothers was the least-exposed group, which may be explained by the fact
that mothers spend more time at home and in places which are less contaminated
by lead.
In the control group (Table 12) there was a significant difference in Hb
and Hct among family members too. With reference to the other findings the
fathers showed significantly higher Pb-concentration and lower ALAD activity
than all the other subjects. This could be associated with lead-contaminated
alcohol consumption. The difference between adults and children for ALA-U and
CP-U, both expressed in 24-hour diuresis, and between school-age and small
children for CP-U, expressed in 24-hour diuresis, should be taken with cau-
tion, because urine samples for analysis in children were not always collected
over a period of 24 hours.
The significance of the difference in arithmetic means between exposed
groups 1 and 2, and between each exposed group and the control group, of
fathers, mothers, and both groups of children has been presented separately
in Tables 13, 14, and 15.
10
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In the lead-exposed groups (Table 13) the fathers of group 1 had signifi-
cantly higher EP concentration, ALA-U excretion, and lower ALAD activity than
the fathers in group 2. A small difference was established in Hct values,
while the other parameters did not differ significantly- The only difference
in the mothers was a higher Pb-B concentration in group 1 than in group 2.
Children too had one different parameter, ALAD activity, which was lower in
group 1 than in group 2. The results call attention to the difference in the
mothers and in both groups of children because the difference in the fathers
was expected. It may be assumed that mothers and children in group 1, whose
husbands and fathers were occupationally exposed to lead, had a slight addi-
tional lead exposure. There are two possible explanations: first, the resi-
dential distribution in regard to distance from the lead smelter may have
been different in group 1 than in group 2, and second, fathers who were
occupationally exposed to lead may have contaminated the environment of the
house by bringing home dust in their clothes and hair. Tables 5 and 6 show
that the residential distribution in regard to distance from the lead smelter
was not the same in both groups. Another point, however, was that the number
of families living close to the lead-emitting source in locations A, B] , and
B2 were almost the same (33% in group 1 and 28% in group 2). The environment-
al survey showed that the average concentration of lead in household dust in
group 1 was higher than in group 2 (see p. 14), but the difference was not
statistically significant. It is not possible to verify which factor pre-
vailed in the observed difference.
A comparative analysis of subjects in lead-exposed group 1 and in the
control group (Table 14) demonstrated that all parameters except one (Hct)
differed more or less significantly in fathers, which was compatible with
their occupational exposure to lead in group 1. In the mothers and both
groups of children the differences were highly significant in ALAD activity
and in EP concentration in small children. Significant differences were found
in Pb-B of mothers and small children, in EP of mothers and school children,
and less significant differences in ALA-U and CP-U of mothers. Other param-
eters did not differ significantly, although in some of them (e.g. Pb-B and
ALA-U/100 ml in school children) the difference was almost significant.
A comparative analysis of subjects in lead-exposed group 2 and in the
control group (Table 15) showed that in each subgroup the difference between
groups was very significant with regard to EP concentration and ALAD activity.
The same level of significancy was found in Pb-B concentration except in
mothers, whose difference was not significant (P<0.10). As mentioned pre-
viously, mothers of both lead-exposed groups were the least exposed to lead.
Less significant differences were found in the BpE number in fathers, in ALA-U
expressed per 100 ml of urine in school-age children, and in CP-U expressed
in 24-hour diuresis in mothers. The other parameters did not differ signifi-
cantly.
The statistical significance of the difference between the three examined
groups was established by analysis of variance. Three parameters, ALAD, EP,
and Pb-B, are the most sensitive indices of increased lead absorption, regard-
less of sex or age (Table 16). They are good parameters to establish the
difference in lead absorption from the environment. ALA-U and CP-U were found
to be good indicators in fathers and mothers but not in children. This may be
11
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explained by the fact that urine samples in children were not always collect-
ed over a period of 24 hours. The mean diuresis in fathers was 822 ± 333.4 ml,
in mothers 796 ± 294.9 ml, in school-age children 467 ± 275.5 ml, and in small
children 146 ± 150.6 ml. A statistically significant difference in Rtc and
BpE number in fathers should be attributed to their occupational exposure to
lead. This was an indirect indication that both parameters were useful in the
control of workers occupationally exposed to lead.
Hb concentration in four subgroups did not differ significantly between
three examined groups (Table 16). On the other hand, a significant difference
in Hb (t=2.235; P<0.05) between the fathers in lead-exposed group 1 and those
in the control group (Table 14) was found by analysis of Student's t-test.
This discrepancy may be explained by the fact that the level of the observed
significance was at the upper limit (P<0.05) of significancy- The increased
lead absorption from the environment in the investigated area close to the
lead smelter had no effect on Hb decrease in the population. This is a very
important conclusion of this report.
The fact that Hb was not significantly decreased, although lead absorption
was significantly increased, can be attributed to the presence of zinc and
other metals which accompany lead ores. In the animal studies zinc showed a
moderating effect on ALAD inhibition (22-23). Lead-induced anemia in rats
was completely prevented when optimal levels of copper and iron were supple-
mented in the diet (24) . It is reasonable to assume that the findings in
animals might be related to human beings, but this should be the subject of
a separate study.
The ALAD activity, EP, ALA-U, and CP-U concentrations were compared with
Pb-concentration in the total study population and in subgroups. Semiloga-
rithmic relationship was found to be better than linear relationship. Figures
25-30 present such a relationship in a total study population. There is a
highly significant (P<0.001) correlation between ALAD and Pb-B, EP and Pb-B,
ALA-U and Pb-B, and significant (P<0.01) correlation between CP-U and Pb-B.
In the subgroups of fathers (Figures 31-36) the results were almost the same.
In mothers (Figures 37-42) correlation was significant for EP-Pb-B (P<0.001)
and ALAD-Pb-B (P<0.05) but not for urine parameters with Pb-B. In children
of school age (Figures 43-48) and in small children (Figures 49-54) highly
significant relationship (P<0.001) was found between ALAD-Pb-B and EP-Pb-B.
Furthermore, children of school age showed a significant relationship (P<0.05)
between ALA-U expressed per 100 ml of urine and Pb-B. There is no plausible
explanation for the negative correlation between CP-U expressed in 24-hour
diuresis and Pb-B in small children.
The relationship between Hb and Pb-B was established in subgroups only.
Both semilogarithmic and linear relationships were carried out. In fathers
the correlation was negative but not significant (Figures 55 and 56) . In
mothers the correlation was unexpectedly positive, but significant (P<0.05)
only for the relationship lin Hb/lin Pb-B (Figures 57 and 58) . The findings
in both groups of children were even more surprising. The correlation between
Hb and Pb was positive and significant (P<0.02) for each group of children and
for semilogarithmic and linear relationship (Figures 59-62). This is contra-
dictory to the findings of Landrigan et al. (25), who found a significant
12
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negative relationship between blood-lead level and hematocrit values in a study
of 1047 children living near a lead smelter. In the present study a relative-
ly small number of subjects were studied in each subgroup (less than 50). In
a small group of subjects with slightly elevated lead exposure from the envi-
ronment, there is more chance of a "false" direction of statistical assessment
than in a large group with the same exposure, or in a small group with more
marked excessive lead exposure, such as fathers occupationally exposed to lead.
An additional explanation of the results obtained in mothers and children could
be the simultaneous exposure to lead and other metals, such as zinc, copper,
and iron, which have a "protective" effect against increased lead absorption
(22-24). "Pure" and "mixed" lead exposure should not be identical, and we
cannot exclude the possibility that lead alone may affect the Hb-concentration,
but not in conjunction with other metals.
The results obtained are not unique. Wibowo et al. (26) found in males
(N=57), not occupationally exposed to lead, a positive significant (P<0.05)
correlation between mean corpuscular hemoglobin concentration (MCHC) and Pb-B.
At the same time the correlation between Hb and Pb-B was positive too (r=0.20)
but not significant. A positive significant correlation between MCHC and Pb-B
was explained by the acknowledged fact that most of the lead in blood was in
the erythrocytes and bound by hemoglobin (27-28).
Blood lead, owing to the dynamic interchange of the body-lead pool, is
probably not the best parameter to which other parameters should be correlated.
In order to check this assumption Hb was related with ALAD and EP for each
subgroup. Lin Hb and log ALAD or Hb relationship was chosen for the following
reasons: 1) in the present study lin Hb values correlated with lin Pb-B
yielded better correlation coefficients than log Hb values for most relation-
ships (Figures 55-62). The best fit for the regression line for ALAD or EP and
Pb-B was found to be with log ALAD activity or log EP concentration and lin
Pb-B level (21, 29-31). The results obtained for each subgroup have been pre-
sented graphically in Figures 63-66 for the relationship between lin Hb and log
ALAD, and in Figures 67-70 for the relationship between lin Hb and log EP. Only
in fathers was the correlation significant, e.g. positive (P<0.001) for the re-
lationship Hb and ALAD, and negative (P<0.01) for the relationship Hb and EP
(Figure 67). In the other subgroups no significant relationship was found.
These findings have proved to be more convincing than those with Pb-B, which may
be an indirect confirmation that Pb-B is not an adequate comparable parameter.
Environmental Survey
The concentration of airborne lead, measured at five sites, 1-5, in a
lead-exposed area for a period of 3 consecutive years (December 1973 to
October 1976) are presented jln Table 17. The data are summarized and pre-
sented as arithmetic means (X) with standard deviations (SD) and standard
errors (SE) for 3 consecutive years together (Table 18) and for each year
separately (Table 19). As shown in Table 19, the average concentrations of
air lead in the exposed area did not vary too much over the 3 years of mea-
surements. The highest average concentration was found at site 3, which was
1.5 km SSW. from the smelter. The concentration at site 1, which was the most
distant from the emitting source, was consistently the lowest and differed
significantly from that at sites 2, 3, 4, and 5 (Table 20). The differences
13
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between sites 2, 3, 4, and 5 were not significant (Table 20). The actual
exposure may have been less different than shown by fixed stations, since the
population moved within the valley during the course of the day. Yearly cycles
of mean monthly air-lead concentration (average of five sampling sites) have
been presented in Figure 71. All yearly cycles showed a winter maximum, which
was influenced by meteorological factors. The extremely high concentration
in December 1975 was, however, partly caused by deficiency of filter opera-
tion. The mean of air-lead averages at five sampling sites for 3 consecutive
years (16.73 ug/m3) was about twice as high as the annual mean found by
Landrigan et al. (32) near an ore smelter. The lowest value at site 1 (4.0
km N. from the smelter) was about twice as high as the level found by Landri-
gan et al. (25) at the same distance from the smelting plant.
The concentration of airborne lead measured at one side (community G)
in the control area for a 1-year period (November 1974 to October 1975) is
presented in Table 21. Summarized data are shown in Table 22. Comparing
the results in the control area with those in the lead-exposed area, one may
see that the lowest air-lead concentration in the lead-exposed area (Table 18,
sampling site 1) was still about 100 times higher than that of the control
area. The mean of five sampling sites for 3 consecutive years (16.73 Ug/m )
was as much as 178 times higher than air lead in the control area.
The lead amount in dustfall, measured simultaneously at four sites in the
exposed area, over a period of 1 year (November 1975 to October 1976) is pre-
sented as monthly means in Table 23. The summarized results are shown in Table
24. Dustfall lead increased on approaching the lead smelter. The highest
average amount of lead was found at site 3 (1.5 km SSW. from the smelter), and
the lowest was found at site 1 (4.0 km N. from the smelter), identical to the
case of air-lead concentration. The largest quantities of dustfall lead were
collected in November and December, although there is no distinct yearly cycle.
The results are comparable with those obtained by Nordman et al. (33).
The lead amount in dustfall measured at one site in the control area for
a period of 1 year (November 1975 to October 1976) has been shown as monthly
means in Table 25. The summarized results have been shown in Table 26. The
average annual means at four sites in the lead-exposed area (173.75 mg/m3)
was 77-times higher than the average annual mean in the control area (2.252
mg/m2).
The lead content of household dust in the lead smelter area collected in
December 1976 simultaneously in seven homes where the father was occupationally
exposed to lead (group 1), and in seven homes with the father not occupation-
ally exposed (group 2), is shown in Table 27. The summarized data for each
group are presented in Table 28. Household dust in group 1 contained more
lead than the dust of group 2, although this difference was not significant
(t = 0.670; P>0.5). In each group there was a negative trend in the lead
content of household dust with regard to the residential distance from the
smelter.
The lead content of household dust in the control area collected in
October 1975 in 12 homes is presented in Table 29. The summarized data are
shown in Table 30. Homes in the lead-exposed area (groups 1 and 2) contained
about 21 times more lead in household dust than homes in the control area.
14
-------
Concentrations of lead in water samples from the exposed area (December
1976) and the control area (October 1975) are presented in Tables 31 and 32.
Though the lead content in the water was about six times higher in the ex-
posed area than in the control area, drinking water did not represent a seri-
ous source of lead intake, as all levels were below 50 yg/1, the recommended
safe upper limit for lead in drinking water (34).
When the four environmental media in the exposed and control areas are
compared, the lead content in the specimens examined from the exposed area
decreased according to the following sequence: air > dustfall > household
dust > water (Table 33).
If one uses the data obtained on air lead (the average of 16.73 yg/m3)
and assumes that on the average 15 m3 of air was inhaled by adults per day,
that 95% of the particles were respirable, that 50% of what is inhaled was
retained and completely absorbed (35), that men spent on the average 4 hours
and women 2 hours per day outdoors, and that the indoor lead level was on the
average 60% of the outdoor level (36), then the estimated air contribution to
daily absorption was 79.47 yg for men and 75.49 yg for women. Comparative
estimated values in the control area (air-lead average 0.09 yg/m3) were 0.43
yg for men and 0.41 yg Pb/day for women. For children the actual percentage
retention of inhaled lead is not known. Therefore the same percentage re-
tention was used as that determined for adults. Adjustment was made for the
smaller respiratory volume (12 m3/day for school children and 6 m3/day for
small children) . Assuming that school age children spent on the average 5
hours per day outdoors, the corresponding estimated values were 65.64 yg for
the exposed area and 0.35 yg/day for the control area. On the assumption that
small children spent on the average 2 hours per day outdoors, values of 30.20
yg for the exposed area and 0.18 yg/day for the control area were obtained.
From the results obtained it became evident that with regard to absolute values
the fathers had the highest and the small children the lowest lead absorption
from the air. If, however, the daily lead absorption from the air has been
expressed on the basis of body weight (the average for men 75, for women 70,
for school-age children 29 and for all small children 13 kg), then the child-
ren's body burden from the air was twice that of the adults (Table 34). This
finding is very important in the assessment of permissible levels of lead
exposure in children living near a lead smelter. This explains why children
from the lead-exposed area showed a higher response to lead than the mothers.
In the exposed area and the control area the air contribution to lead
absorption was practically the same in fathers and mothers (Table 34). On the
other hand the biological indices of lead absorption showed that in each ex-
amined group the fathers had higher lead exposures than the mothers. If the
group of subjects occupationally highly exposed to lead were not taken into
account, the logical assumption was that the fathers had an additional lead
exposure, probably through consumption of lead-contaminated alcohol.
The dustfall polluted by lead in lead-exposed areas is another important
source of increased lead absorption in children. It is a well known fact that
children play with sand and earth and that they usually like to chew non-food
substances (pica). Moreover they have higher metabolic rates, and their lead
absorption from the gastrointestinal tract is significantly higher than in
15
-------
adults. Alexander et al. (2) found an absorption of up to 53% in eight child-
ren aged from 3 months to 8 years. Recently Mahaffey (37) estimated lead
exposure for normal children on the basis of 40% absorption. Generally one
may assume that children absorb 3 to 10 times the amount of lead that adults
absorb.
Household dust in lead-exposed group 1 had more lead than the household
dust in lead-exposed group 2, although the difference was not significant. In
agreement with this finding ALAD activity in children of both ages was signif-
icantly lower (P<0.02 in school-age children and P<0.05 in children up to 4
years) in group 1 than in group 2. Sayre et al. (38) found that if dirt or
dust in the child's environment contained a high concentration of lead, more
lead was present on the hands or on objects that were handled and was avail-
able for ingestion via normal mouthing activities. This could explain the
results obtained.
Lead contribution from water in the present study has been estimated as
the lowest. Estimates of water intake have ranged from 300 ml/day for child-
ran to as much as 2 liters/day for adults (39) - Taking into account these
data and the average lead concentration of 10.22 yg/l.in the exposed area, the
estimated daily intake for children was 3.07 yg Pb and for adults 20.44 yg Pb/
day, which corresponded to absorption of 1.54 yg Pb/day in children (on the
basis of 50% absorption) and 2.0 yg Pb/day in adults (on the basis of 10%
absorption).
Biological Indices of Lead Absorption and Residential Distance
from the Lead Smelter
Owing to the small number of families living in different settlements
and/or asymmetric distribution, the comparison between biological indices of
lead absorption and the residential distance from the lead smelter has been
made by means of median values. In subgroup "Fathers" only nonoccupationally
exposed subjects were included, while in other subgroups subjects from groups
1 and 2 were pooled. Tables 35-38 present, separately for each family sub-
group, the studied biological indices in comparison with the residential dis-
tance to the lead smelter.
There was practically no alteration in Hb, Htc, BpE, and Rtc with prox-
imity to the smelter in any of the subgroups. On the other hand there was a
trend towards normal values with the distance from the lead smelter in EP con-
centration and ALAD activity. This was especially evident for EP concentration,
which followed a curvilinear relationship (Figures 72 and 73). There was an
exception in the case of small children living very close to the lead smelter
in settlement A (median distance 500 m); these children had lower EP concentra-
tions than children living in settlements BI and B2 (median distance 1900 m).
ALAD activity was also inverse to the expected findings; higher activity was
found in children of settlement A than in children of settlement B! and B2.
One of the possible reasons could be that parents, aware of the environmental
contamination by lead in settlement A, were more concerned about their child-
ren than parents in other places more distant from the lead smelter. Another
reason could be the difference in nutritional habits and the source of food
(lead-contaminated milk or milk commercially produced and packed elsewhere).
Neither of these aspects has been studied, and it is not possible to draw
any conclusions.
16
-------
Although the concentration of Pb-B was not uniform, it did not show the
expected trend towards normalization with residential distance from the emit-
ting source. Actually the highest median value in each subgroup, apart from
the mothers, was found in subjects living very close to the smelter (150-800 m),
Thereafter the concentration did not decrease gradually with regard to residen-
tial distance. In the studies of Nordman et al. (33), who found a negative
correlation between Pb-B and the residential distance from the emitting source,
a total of 293 adult inhibitants were examined. Landrigan et al. (32) inves-
tigated 758 children from 1 to 19 years of age and found significant differ-
ences between Pb-B means and residential distance. In both studies a large
group of subjects were analyzed. The small number of subjects in the present
study did not allow us to compare the results obtained with those obtained in
large groups. However, by dealing with our data exclusively, the conclusion
may be drawn that Pb-B is a less valid parameter than ALAD, particularly if
compared with EP in the assessment of body response normalization, with regard
to increasing residential distance from the lead smelter.
Concentrations of ALA-U and CP-U showed a somewhat decreasing trend with
regard to the distance in fathers only, while in other subgroups the proximity
to the smelter had no effect. Our impression is that the scattering in results
of normal range could be attributed more to natural variations and/or to in-
adequate urine sampling than to the residential distance from the smalter.
17
-------
o
RIVERS
SETTLEMENTS
SMELTING PLANT
AIR-LEAD SAMPLING
SITES
1 : 50,000
Figure 1. Scheme of the lead-contaminaied area.
18
-------
15-
10-
5-
0
N= 12
15-
5-
n -
N = 20
r
— i
FREQUENCY
15 -
10-
5 —
0_
15 -
10-
15-
5-
N = 33
ra
N = 29 CH
rrrrs//',
•HMI
9 F£
H F^
1
If
|#*V*3 M<
rxx/i Ch
N = 30 (Q
I^QO^l Ch
T'TWI 'G
65$4
fl
66&
&W
>wS
:-l_
THERS (Group 1)
THERS(Group2)
|^
DTHERS (Group 1 + Group 2)
1ILDREN -SCHOOL AGE
roup 1 + Group 2)
1ILDREN - UP TO 4 YEARS
roup 1 + Group 2)
0 I I II
10 12 14 16 13
Hbg/ 100ml
Figure 2. Frequency distribution of hemoglobin (Hb) in lead-exposed groups 1 and 2.
19
-------
15
10 -
5 —
0
N = 12
LLi
a
15 —
10 —
5 —
n —
N = 20
I
15
10
5
0
15
10
5
0
15
10
5
0
N = 33
N = 29
FATHERS (Group I)
FATHERS (Group 2)
MOTHERS 'Group 1 + Group 2)
CHILDREN - SCHOOL AGE
(Group 1 + Group 2)
CHILDREN - UP TO 4 YEARS
(Group 1 + Group 2)
35 39
47
51
Hct %
Figure 3. Frequency distribution of hematocrit (Hct) in lead-exposed groups 1 and 2.
20
-------
FREQUENCY
30 -
20 -
10 -
0 -
30 -
20 -
10 -
0 -
30 -
20 -
10 —
0 -•
30 -
20 -
10 -
0 -
30-
20-
10-
0-
N-12
gjffiijjjpgj
N = 20
N = :
!3
mia FATHERS (Group 1)
N = '.
30
H
Y//
1 1 FATHERS (Group 2)
w:-,::-x:l MOTHERS (Group 1+2)
\SS'S'\ CHILDREN - SCHOOL AGE
N = 30 (Group 1 + Group 2)
WA CHILDREN - UP TO 4 YEARS
^vw
xxgs
?cw
(Group 1 + Group 2)
1 i I 1 I
2000
4000
6000
8000
10000
Bp E/106 £
Figure 4. Frequency distribution of basophilic stippled cells (BpE) in lead-exposed groups
1 and 2.
21
-------
15
10 —
5 —
0
N = 12
>
CJ
a
LLI
oc
15 —
n
N = 20
15 H
10 H
N = 33
15
10
N = 30
FATHERS (Group 1)
FATHERS (Group 2}
N = 30
£2323 MOTHERS (Group 1 +2)
//'/A CHILDREN-SCHOOL AGE
(Group 1 +2)
IV.-VJ CHILDREN - UP TO 4 YEARS
(Group 1 + 2)
Rtc %
Figure 5. Frequency distribution of reticulocytes (Rtc) in lead-exposed groups 1 and 2.
22
-------
30
20 —
10 —
0
N = 12
30
20 —
10 —
0
N = 20
u
z
UJ
O
OJ
CE
30 —
20 —
10 —
n —
N =
33
::;X::;:;:l.:.x.!:!;!:l
30
20
10-
0
30
20
= 29
= 29
FATHERS (Group 1)
FATHERS (Group 2)
CHILDREN - SCHOOL AGE
(Group 1 + Group 2;
IVxV^ CHILDREN - UP TO 4 YEARS
(Group 1 + Group 2)
ii
/^^^vlwupv^i ff^fy^^
I i
0 200 400 600
EP,ug/ 100ml £
1 i
800 1000
Figure 6. Frequency distribution of erythrocyte protoporphyrin (EP) in lead-exposed groups
1 and 2.
23
-------
;_J N = 12
15
10
5
0
N = 20
1 1
01
_J N = 33
>
o
u 10 —
a
a 5 —
LL
15 —
o
15 —
5 —
N =
N =
29
f^
V//S
v-rr-X///.
30
^
^^
%
///
'///*
'//,'
%$$
*£$
////.
///A
$£&
gg
$$£
SS59 FATHERS (Group 1)
f I FATHERS (Group 2)
"7yyy/yA/'//'x
W^\ MOTHERS (Group 1 + Group 2)
r/yyj CHILDREN -SCHOOL AGE
(Group 1 + Group 2)
l*AM CHILDREN - UP TO 4 YEARS
(Group 1 + Group 2)
^88^^^
Til!
40 80 120 160
ALAD units /ml E
200
220
Figure 7. Frequency distribution of 5-aminolevulinic acid dehydratase activity (ALAD) in lead-
exposed groups 1 and 2.
24
-------
10 H
N = 12
5H
0 —
5,
n —
N = 20
l~
I
1 1 1
> 10
CJ
p»
LU
Z>
O ,-
LJJ 3
N = 33
I-.',
FATHERS (Group 1)
FATHERS (Group 2)
_| N = 30
t'-ij:!-h.!:l MOTHERS (Group 1 + Group 2)
i/y/,j CHILDREN - SCHOOL AGE
(Group 1 + Group 2)
KJWU CHILDREN - UP TO 4 YEARS
(Group 1 + Group 2)
50 70 90
Pb - B,ug / 100 ml
130
Figure 8. Frequency distribution of lead in blood 'Pb—B) in lead-exposed groups 1 and 2.
25
-------
20 -H
N = 12
20-
10-
FREQUENCY
— * ho
=> 0 O C
N = 20
N = 31
20 J N=30
10 H
FATHERS (Group 1)
FATHERS (Group 2)
WMi t > n
MOTHERS (Group 1 + Group 2)
20 -
g
N = ;
13
i
1
l///x1 CHILDREN -SCHOC
(Group 1 •+• Group 2)
IJWVI CHILDREN -UP TO
( Group 1 + Group 2)
)L AGE
4 YEARS
I I I I I
0.80 1.60 2.40 3.20
ALA- U mg/100ml
4.00
4.80
Figure 9. Frequency distribution of 5-aminolevulinic acid in urine (ALA—U mg/100 ml) in
lead-exposed groups 1 and 2.
26
-------
30 H
N = 12
15 H
30 H
N = 20
15 H
> 30 H
ui
a
•jj
cc
LL
Ol
I
N = 31
FATHERS (Group 1)
30 -
15 —
n —
I i rn i ncno luroup £.>
%
///
^//
W'
> > > ,\
MOTHERS (Group 1-r Group 2)
30 —
15 -
N = 11 (Group 1
+ Group 2)
^
-------
30 —
N = 12
15 -
30
15 —
N = 31
> 30
o
s
tu
C 15
UJ
S.
u.
30 —
15 -
30 -
15 —
N = 11
FATHERS (Group 1)
FATHERS (Group 2)
!:•••:•:•:::•::] MOTHERS (Group 1 + Group 2)
'f//A CHILDREN-SCHOOL AGE
(Group 1 + Group 2)
CHILDREN - UP TO 4 YEARS
(Group 1 + Group 2)
I
40
120
I
200
I
280
I
360
CP- U jug/100 ml)
Figure 11. Frequency distribution of coproporphyrin in urine (CP-U ^g/100 ml) in lead-exposed
groups 1 and 2.
28
-------
30 —
15 —
N = 12
>
u
a
LU
30 -
15 -
0 -
N = 19
j
j
30-
N = 31
30 —
15 —
N = 30
1440
1600
FATHERS (Group 1)
FATHERS (Group 2)
KvXvXi MOTHERS (Group 1 + Group 2)
30 —
15 —
\/ / / /\ LiHILUH
N = 10 (Group 1
= l\i — SLMt-'UL AljL
+ 2}
ixKXXl CHILDREN -UP TO 4 YEARS
(Group 1
H
0 111
0 160 320 480
+ Group 2)
I I
640 800
I
960
Figure 12. Frequency distribution of coproporphyrm in urine (CP—U M9/24 h) in lead-exposed
groups 1 and 2.
29
-------
8 —
6 —
O j_i.
8 —
6 —
4 —
u 0 —
LJJ
D
C
N = 16
N = 16
p^,
!
...
|
j
• — I
_ N = 7
6 —
4 —
n — i
y^
m
^ Y77*
_ N = 17
10
FATHERS
!•:•:•:•:•:•:•:< MOTHERS
V//A CHILDREN - SCHOOL AGE
CHILDREN - UP TO 4 YEARS
14 16 18
Hb g/ 100ml
T~
20
T
22
Figure 13. Frequency distribution of hemoglobin (Hb) in control group.
30
-------
8 —
6 —
4 —
n —
N = 16
I
I 1
o
UJ
3
O
4 -H
2H
N = 16
ill
_J N = 7
6 —
4 —
0
n —
%
I
I
8
6 —
4 —
2 —
0
FATHERS
MOTHERS
'///A CHILDREN - ',
CHILDREN -UP TO 4 YEARS
I
43
47
Hct %
I
51
I
55
I
59
Figure 14. Frequency distribution of hematocrit iHct) in control group.
31
-------
10 —
5 —
15 -
10 —
5 -
" n
FREQUEIV
01 c
10 -
5-
Q
15 -
10 —
0 — '
N =
16
N = 16
in ii in.
N = 7
^
%'
7771
N = 17
I
Hi
V^
•xvv*
^.Xvi
1 I FATHERS
!:*:•:•:•:•:•! MOTHERS
/7771 CHILDREM -SCHOOL AGE
!xV-^^ CHILDREN - UP TO 4 YEARS
AVx KS
-------
3 !
6 —
4 —
2 -
0
6 —
4 —
2 -
>
Z 0
UJ
3
LU
LL
8 —
6 —
4 -
8 — i
S —
4 —
2 — !
N = 16
N = 15
N = 7
ISI = 17
I
0
"!?X?v
P
jp£
g££<
H
1§
1
w
!t-'-:i:x:
^
H..A/ '
^
^Wj
S
$H
3
rn
IPil Jiil
V7Z\
I 1 FATHERS
://VJ CHILDREN -SCHOOL AGE
XX:<'<1 CHILDREN - UP TO 4 YEARS
m
\\i\\
20 30 40 50 60
Rtc %
Figure 16. Frecuency distribution of rsticulocytes (Rtcj in control group.
33
-------
15 H
N = 16
10H
15 H
•10 H
>
o
N = 16
o
LU
cc
15 H
10 H
N = 7
15 H
10 H
N = 16
I FATHERS
t:-:W:WI MOTHERS
CHILDREN - SCHOOL AGE
CHILDREN - UP TO 4 YEARS
20
I
40
I
60
EP/jg/ 100ml E
I
SO
100
120
Figure 17. Frequency distribution of erythrocyte protoporphyrin (EP) in control group.
34
-------
8 -
6 -
4 —
2
0
3 -
6 —
4 -
2 —
> .
CJ n
2 U
LU
a
LJ
U_
8 —
6 —
4 —
2 _
8 —
6 ~"
4 —
2 -J
N = 16
r~
N = 16
N = 7
iM = 17
I
p&
>c\XH
>Cv<<
^§
^
<5vv<
vvv
wC*
w.
I I FATHERS
i V.\V.m MOTHERS
>c£j£ rv/yj CHILDREN -SCHOOL AGE
&5£ 1>WV! CHILDREN - UP TO 4 YEARS
sH
£§§§^$S3
PIII
90 130 170 210 250
ALAD units / ml E
290
330
-igure 18. Frequency distribution of ;-ammolevulinic acid dehydratase activity (ALAD) in
co 'trol qrouo.
35
-------
6 —
8 —
6 —
j. «
2 —
> n
LJ
a
X
"• 8-
6 —
A —
2 -
8 —
6 —
4 —
2 —
N =
N =
N =7
N =
16
16
17
r^X
C
F^
i
?^
Rvvsd
b^
R^^
R/v<>
b^5
vvv<
^
-------
15 —
10-
5 -
M = 16
15-
10 —
5 —
N = 15
C
LU
FT 15-i
10 —
5 —
N = 7
15-
10 -
5 -
E^M-
tel
N = 16
! 1 FATHERS
fc<%
£
-------
15 -
10 —
5 -
15 -
10 -
5 —
o
UJ
O
EL 15 -
10 -
5 -
g
15 -
10 -
5 —
0
N = 16
j
IN = 15
N = 7
•
N = 16
H
1
I
^^—
T--?ri
1 1 FATHERS
v::;:::::;:::l MOTHERS
\///A CHILDREN -SCHOOL AGE
PWV-J CHILDREN -UP TO 4 YEARS
1 1 1
8 12 16
ALA - U mg / 24 h
20
24
Figure 21. Frequency distribution of .5-aminolevulinic acid in urine (ALA-U mg/24 h) in
control grouo.
38
-------
UJ
a
LU
8 -
4 —
2 —
0
6 —
4 -
2
g
3 —
6 —
6 —
4
2 —
N = 16
N = 5
:•:•:•:•:•
N = 7
^
%
^
777\
N = 13
I H FATHERS
m
^
•$&$
w
WCx
VS?8<
>WV<
xyq&.
KXXX
>§OC
«cc<
r:-:-:-:'^ MOTHERS
fxVA) CHILDREN - SCHOOL AGE
^^<5J CHILDREN - UP TO 4 YEARS
1 III
0 20 40 30 80 100 120
CP - U.ag ' 100 ml
Figure 22. Frequency distribution of coproporphyrin in urine (CP-U M3/100 ml) in control group.
39
-------
o
O
8 -
6 —
n _
N =
16
N = 15
6 -
4 -
n —
^
I
FATHERS
MOTHERS
CHILDREN-SCHOOL AGE
KXXX1 CHILDREN - UP TO 4 YEARS
160
240
320
400
480
CP - U ing / 24 h
Figure 23. Frequency distribution of coproporphyrin in u'ine (CP-U ^g/24 h) in control group.
40
-------
70
60
GO
40
30
FATHERS
MOTHERS
CHILDREN SCHOOL AGE (2 no. 5 f.)
CHILDREN UP TO 4 YEARS (7 m. 10 f.)
ALL MEMBERS OF FAMILY
THE PROPOSED GUIDE (Zielhuis, Ref. 17}
THE RESULTS OF SECCHI ET AL. (Ref. 18)
10
40
50
PERCENT
GO
70
80
90
100
Fiyuie 24. Percenlile dibtribulion of Pb-B (pg/100 ml) in control group.
41
-------
1000
500
100 |—
50
<
_1
<
10
5 —
1 —
N = 180
r = 0.677, P < 0.001
Log ALAD = 2.364 - 0.011 Pb - B
£> Control group
• Lead—exposed group 1
0 Lead—exposed group 2
20 40 60 80 100
Pb-B tig/ 100ml
120
140
Figure 25. Semilogarithmic correlation in a total study population between 5-aminolevulinic
acid dehydratase activity and lead in blood (log ALAD/lin Pb-S).
42
-------
N = 179
r = 0.659, P < 0.001
Log EP= 1.042 +0.015 Pb-B
1000
500 -
TOO -
c 50 -
o
o
Control group
• Lead—exposed group 1
O Lead—exposed group 2
20 40 60 80 100
Pb - B,ug/ 100ml
120
140
Figure 26. Semilogarithmic correlation in a total study population between erythrocyte proto-
porphyrin and lead in blood (log EP'lin Pb-B).
43
-------
10.00
5.00
IM = 169
r = 0.386, P < 0.001
Log ALA - U100m| = -0.606 + 0.004 Pb- B
1.00 r-
0.50 I-
0.10
0.05 —
0.01
L
& Control group
• Lead—exposed group 1
O Lead—exposed group 2
I
20 40 60 80
Pb - B,ug / 100 ml
100
120
140
Figure 27. Semilogarithmic correlation in a total study population between '-aminolevulinic
acid in urine and lead in blood (log ALA—U mg/100 ml/lin Pb—B).
44
-------
100
10
1.0
<
_j
<
0.1
0.01
N = 157
r = 0.339, P < 0.001
Log ALA24h = 0.031 + 0.006 Pb - B
*0
A Control group
• Lead-exposed group 1
O Lead-exposed group 2
I
I
20 40 60 80
Lead M9/ 100ml blood
100
120
140
Figure 28. Semilogarithmic correlation in a total study population between 5-aminoievulinic
acid in urine and lead in blood (log ALA-U mg/24 h/lin Pb—8).
45
-------
1000
100
Q.
CJ
10
1 r-
N = 153
r = 0.289, P < 0.01
Log CP - U100m| = 0.852 + 0.003 Pb - B
• •
*
& Control group
• Lead-exposed group 1
O Lead-exposed group 2
_L
20 40 60 80 100
Pb - B,ug / 100ml
120
140
Figure 29. Semilogarithmic correlation in a total study population between coproporphyrin
in urine and lead in blood (log CP-U ag/100 ml/lin Pb-B).
46
-------
1000
N = 152
r = 0.249, P < 0.01
Log CP - U24h = 1.523 + Pb - B
100 I—
e.
o
10 \—
A ontrol group
| • Lead—exposed group 1
| o Lead—exposed group 2
<10 60 80 100
Pb - Btigf 100 ml
120
140
Figure 30. Semilogarithmic correlation in a total study population between coproporphyrin in
urine and lead in blood flog CP-U ^ig/24 h/!in Pb-B).
47
-------
1000
500 -
r = 0.701, P< 0.001
Log ALAD = 2.429 - 0.012 Pb - B
1 i—
& Control
« Lead—exposed group 1
O Lead—exposed group 2
I
20 40 60 80 100
Pb-B/jg/IOOml
120
140
Figure 31. Semilogarithmic correlation in fathers of a total study population between 5-amino-
levulinic acid dehydratase activity and lead in blood (log ALAD/lin Pb—B).
48
-------
1000
500
I
100 r
- 50 -
o
o
IM = 48
r = 0.772, P< 0.001
Log EP = 0.772 + 0.017 Pb - B
A Control group
• Lead—exposed group 1
O lead-exposed group 2
20 40 60 80
Pb- Bug/ 100ml
100
120
140
Figure 32, Semilogarithmic correlation in fathers of a total study population between erythro-
cyte protoporphyrin and lead in blood (log EP/lin Pb—31.
49
-------
N = 48
r =0.513, P < 0.001
Log ALA - U100m| = 0.612 + 0.005 Pb -B
10.00 !—
5.00
0.01 i—
A Control
* Lead—exposed group 1
O Lead—exposed group 2
I
20
40
60
80
/ 100ml
100
120
140
Figure 33. Semilogarithmic correlation in fathers of a total study population between 5-amino-
levulinic acid in urine and lead in blood (log ALA—U mg/100 ml'lin Pb—B),
50
-------
100 -
10.0 -
f 1.0
CM
<
_J
<
0.1
0.01
L
N =48
r =0.470, P<0.001
Log ALA24h = 0.277 + 0.005 Pb - B
• O
00
A Control group
• Lead-exposed group 1
O Lead-exposed group 2
I
20 40 60 80
Pb-Bfjg/ 100ml
100
120
140
Figure 34. Semilogarithmic correlation in fathers of a total study population between <5-amino-
levulinic acid in urine and lead in blood (log ALA—U mg/24 h/lin Pb—8).
51
-------
1000
N = 47
r = 0.377, P> 0.01 P< 0.01
Log CP - U100m| = 0.843 + 0.005 Pb - B
o
o
—I
Control
Lead—exposed group 1
Lead—exposed group 2
I
20 40 60 80
Pb -Bug/ 100ml
100
120
140
Figure 35. Semilogarithmic correlation in fathers of a total study population between copro-
porphyrin in urine and lead in blood (log CP-U Mg/100 ml/lin Pb-B).
52
-------
1000
100
a.
D
a.
o
N = 47
r = 0.366. P < 0.02
Log CP - U24n = 1.723 * 0.005 PB Pb - B
& Control
• Lead—exposed group 1
O Lead—exposed group 2
*
•
I
20 40 60 30 100
Pb-B ug/ 100ml
120
Figure 36. Semilogarithmic correlation in fathers of a total study population between copro-
norphyrin in urine and lead in blood (log CP-U ^g/24 h/lin Pb-B).
53
-------
1000
N = 49
r = 0.331, P< 0.05
Log ALAD = 2.220 - 0.006 Pb - B
500 1-
100
LU
1 so
3
Q
10 —
£, Control group
• Lead—exposed group 1
O Lead—exposed group 2
1
20 40 60 80 100
Pb - B/ug/ 100ml
120
140
Figure 37. Semilogarithmic correlation in mothers of a total study population between 6-amino-
levulinic acid dehydratase activity and lead in blood (log ALAD/lin Pb-B).
54
-------
1000
500
100
UJ
•5 50
o
o
C-
LU
10
N =49
r = 0.476, P < 0.001
Log EP = 1.001 + 0.016 Pb - B
^ Control group
• Lead—exposed group 1
O Lead—exposed group 2
I
20 40 60 80
Pb-B/jg/ 100ml
100
120
140
Figure 38. Semilogarithmic correlation in mothers of a total study population between erythro-
cyte protoporphyrin and lead in blood (log EP'lin Pb—8).
55
-------
10.00
1.00
0.10 -
N = 46
r = 0.159, P> 0.10
o •
CD
o.oi ;—
^ Control group
• Lead—exposed group 1
O Lead—exposed group 2
I
20 40 60 80 100
Ph -Bug/ 100ml
120
140
Figure 39. Semilogarithmic correlation in mothers of a total study population between 5-amino-
levulinic acid in urine and lead in blood (log ALA-U mg/100 ml/lin Pb-B).
56
-------
10.0 r-
1.0
0.1 -
N = 46
r = 0.234, P> 0.10
0.01 j—
I A Control group
j • Lead—exposed group 1
O Lead—exposed group 2
I I I
20 40 60
I
80
I I I
100 120 140
Pb -Bfjg/ 100ml
Figure 40. Semilogarithmic correlation in mothers of a total study population between 5-amino-
levulinic acid in urine and lead in blood (log ALA-U mg/24 h/lin Pb-B).
57
-------
1000
N = 46
r = 0.258, P > 0.05
TOO —
c
o
o
10 -
1 —
a AO
A Control group
• Lead—exposed group 1
O Lead—exposed group 2
20
40
60
80 100
/ 100ml
120
140
Figure 41. Semilogarithmic correlation in mothers of a total study population between copro-
porphyrin in urine and lead in blood (log CP - U ^ig/100 ml/lin Pb-B).
58
-------
1000
N = 46
r =-0.100, P> 0.10
100
a.
(J
10
o o
00
o • •
1 '
A Control group
• Lead - exposed group 1
O Lead - exposed group 2
I
20 40 60 80
Pb • B M9 / 100 ml
100
120
140
Figure 42. Semilogarithmic correlation in mothers of a total study population between copro-
porphyrin in urine and lead in blood (log CP-U jjg/24 h/lin Pb-B).
59
-------
1000
500 j—
N = 36
r = 0.626, P < 0.001
Log ALAD = 2.194 - 0.008 Pb - 8
A Control group
• Lead-exposed group 1
O Lead-exposed group 2
20 40 60 80 100
Pb-BMg/ 100ml
120
140
Figure 43. Semilogarithmic correlation in children of school age of a total study population
between ^-aminolevulinic acid dehydratase activity and lead in blood (log ALAD/
tin Pb-B).
60
-------
5000
1000
100
o
o
Cl
a.
n.
10
N =36
r = 0.634, P < 0.001
Log EP = 1.209 +0.013 Pb-B
-------
10.0 i—
N = 36
r =0.275, P> 0.10
1.0
c
3
<
_j
<
0,1
• AOO O°«
'o o *c o°
o
o
0.01 —
A Control group
• Lead-exposed group 1
O Lead-exposed group 2
20 40 60 80 100
Pb - B^g / 100ml
120
140
Figure 45. Semiiogarithmic correlation in children of school age of a total study population
between o-aminolevulinic acid in urine and lead in blood (log ALA-U mg/100ml/
tin Pb-B).
62
-------
10.0
1.0
X
Tt
<
_l
<
0.1 —
0.01 -
IM = 36
r = 0.352, P< 0.05
Log ALA-U24h = - 0.001 + 0.004 Pb - 3
& Control group
• Lead-exposed group 1
O Lead-exposed group 2
20 40 60 80
Pb- BMS/ 100ml
100
120
140
Figure 46. Semilogarithmic correlation in children of school age of a total study population
between o-aminolevulinic acid in urine and lead in blood (log ALA—U mg/24h/lin
Pb-B).
63
-------
1000
r =0.167, P> 0.10
100
o
o
• •
10
• 00
• o
1 ,-
£ Control group
» Lead-exposed group 1
O Lead-exposed group 2
20
40
60
80
/ 100ml
100
120
140
Figure 47. Semilogarithmic correlation in children of school age of a total study population
between coproporphyrin in urine and lead in blood (log CP-U ng/100 ml/lin Pb—B).
64
-------
1000 L_
IM = 36
r 0.238, P> 0.10
100 -
10
o
o oo
'00 • 0
o
o
a Control group
• Lead-exposed group 1
O Lead-exposed group 2
I
20 40 60 80 100
Pb-B/ig/ 100ml
120
140
Figure 48. Semilogarithmic correlation in children of school age of a total study population
between coproporphyrin in urine and lead in blood (log CP—U jug/24 h/lin Pn—b).
65
-------
1000
500
100 -
= 50 r-
3
Q
N = 47
r = 0.525, P < 0.001
Log ALAD = 2.354 - 0.010 Pb - B
a Control group
• Lead-exposed group 1
O Lead-exposed group 2
20 40 60 30 100
Pb - Bf:g/ 100ml
120
140
Figure 49. Semilogarithmic correlation in children up to 4 years of a total study population
between S-aminolevulinic acid dehydratase activity and lead in blood (log ALAD/
lin Pb-B).
66
-------
1000
500
i\l = 46
r =0.608, P< 0.001
Log EP = 0.913 + 0.019 Pb - B
100 -
- 50 -
a.
a.
LU
10
Control group
Lead-exposed group 1
Lead-exposed group 2
20
40
60
Pb-
80
/ 100ml
100
120
140
Figure 50. Semilogarithmic correlation in children up to 4 years of a total study population
between erythrocyte protoporphyrin and lead in blood (log EP/lin Pb—B).
67
-------
10.0
IM = 39
r - -0.105, P> 0.10
1.0 r-
0.1
0.01 ':—
| A Control group
I • Lead-exposed group 1
I o Lead-exposed group 2
20 40 60 80 100
Pb-B tig I 100ml
120
140
Figure 51. Semilogarithmic correlation in children up to 4 years of a total study population
between o-aminolevulinic acid in urine and lead in blood (log ALA—U mg/100 ml/lin
Pb-B).
68
-------
10.0
N = 27
r = 0.129, P> 0,10
<
_i
<
1.0 :—
»r-
• •
0.01
A Control group
* Lead-exposed group 1
O Lead-exposed group 2
_L
20 40 60 80 100
Pb - B fig I 100 ml
120
140
rigure 52. Semilogarithmic correlation in children up to 4 years of a total study population
between 5-aminolevulinic acid in urine and lead in blood (log ALA—U mg/24 h/lin
Pb-B).
69
-------
1000
N = 23
r =0.351, P> 0.05
100
10
•o
•
A Control group
• Lead-exposed group 1
O Lead-exposed group 2
I
I
20 40 60 80 100
Pb -B ug/ 100ml
120
140
Figure 53. Semilogarithmic correlation in children up to 4 years of a total study population
between coprcporphyrin in urine and lead in blood (log CP—U ^g/100 ml/lin Pb—B).
70
-------
1000
100
Q.
o
10
N = 23
r = 0.538, P < 0.01
Log CP - U24 h - 1.587 - 0.009 Pb - B
1 i—
a Control group
• Lead-exposed group 1
O Lead-exposed group 2
20 40 60 80 100
Pb- B jig/ 100ml
120
140
Figure 54. Semilogarithrnic correlation in children up to 4 years of a total study population
between coproporphyrin in urine and lead in blood (log CP—U yg/24 h/lin Pb—SI.
71
-------
N =48
r =0.100, P> 0.10
100 i—
o
o
10
o »o
o o
1 —
a Control group
• Lead-exposed group 1
O Lead-exposed group 2
20 40 60 80 100
Pb-B fig/ 100ml
120
140
F'qure 55. Similogarithmic correlation in fathers of a total study population between hemo-
globin and lead in blood (log Hb/lin Pb—B).
72
-------
o
o
20
16
12
4 r—
N = 48
r =0.103, P>0.10
Control group
Lead-exposed group 1
Lead-exposed group 2
o o
o o° «>
o o *
•
•
I
20 40 60 80 100
Pb-B,ug/100ml
120
140
Figure 56. Correlation in fathers of a total study population between hemoglobin and lead
in blood din Hb/lin Pb-B).
73
-------
N = 49
r =0.239, P> 0.10
100
a
o
-0
10
Cft
1 r
£ Control group
• Lead-exposed group 1
O Lead-exposed group 2
20 40 60 80
Pb - B fig I 100 mi
100
120
140
Figure 57. Semilogarithmic correlation in mothers of a total study population between hemo-
globin and lead in blood (log Hb/lin Pb—B).
74
-------
N=49
r =0.313, P<0.05
Hb= 13.780 +0.027 Pb-B
16
12
A Control group
• Lead-exposed group 1
O Lead-exposed group 2
i
20 40 60 80 100
Pb - Bjug ' 100 ml
120
140
Figure 58. Correlation in mothers of a total study population between hemoglobin and lead
in blood din Hb/lin Pb-B).
75
-------
N = 36
r = 0.402, P < 0.02
Log Hb = 1.1351 + 0.0005 Pb - B
ICO
si
.3
10
1!-
& Control group
• Lead-exposed group 1
O Lead-exposed group 2
20 40 60 80
Pb - B^ig / 100 ml
100
120
140
Figure 59. Semilogarithmic correlation in children of school age of a total study population
between hemoglobin and lead in blood (leg Hb/lin Pb—8).
76
-------
N = 36
r = 0.392, P < 0.02
Hb = 13.682 +0.016 Pb-B
o
o
18 'r-
A Control group
• Lead-exposed group 1
O Lead-exposed group 2
I
J
I
20 40 60 80 100
Pb- 3,L!g/100ml
120
140
Figure 60. Correlation in children of school age of a total study population between hemo-
globin and lead in blood din Hb/lin Pb—B).
77
-------
N = 47
r =0.353, P<0.02
Log Hb = 1.0978 + 0.0008 Pb - B
100 -
10
£ Control group
• Lead-exposed group 1
O Lead-exposed group 2
I I !
III!
20
40
60
80
/ 100ml
100
120
140
:igure 61. Semilogarithmic correlation in children up to 4 years of a total study population
between hemoglobin and lead in blood (log Hb/lin Pb—8).
78
-------
N = 47
r = 0.364, P < 0.02
Hb = 12.534 +0.024 Pb-B
o
o
.3
I
A .
I
A Control group
• Lead-exposed group "!
O Lead-exposed group 2
i
20
i I
40 60
!
80
I !
100 120
I
140
Pb -B.ug/ 100ml
Figure 62. Correlation in children up to 4 years of a total study population between hemo-
globin and lead in blood (lin Hb/lin Pb—B).
79
-------
o
o
N = 48
r = 0.509, P < 0.001
Hb = 14.584 + 1.267 log ALAD
20 —
16
12 —
j & Control group
j • Lead-exposed group 1
j O Laad-exposed group 2
1
I
1
10 100
ALAD units / ml E
1000
Figure 63. Semilogarithmic correlation in fathers of a total study population between hemo-
globin and 5-aminolevulinic acid dehydratase activity (lin Hb/log ALAD).
80
-------
N =49
r =0.084, P> 0.10
o
o
20
16
12 '-
r
Control group
Lead-exposed group 1
i O Lead-exposed group 2
4 f
r
10 100
ALAD units / ml £
1000
Figure 64. Semilogarithmic correlation in mothers of a total study population between hemo-
globin and 5-aminolevulinic acid dahydratase activity din Hb/log ALAD).
81
-------
N = 36
r =0.104, P> 0.10
o
o
20
16 r
r
o
80 • „
9
°
12
A Control group
• Lead-exposed group 1
O Lead-exposed group 2
10 100
ALAD units / ml E
1000
Figure 65. Semilogarithmic correlation in children of school age of a total study population
between hemoglobin and 6-aminolevulinic acid dehydratase activity (lin Hb/log
ALAD).
82
-------
N=47
r =0.194, P> 0.10
- 20
16
12
r
° of°*°
2 o
o
o
oo
3 i-
A Control group
• Lead-exposed group 1
O Lead-exposed group 2
I
10 100
ALAD units / ml E
1000
Figure 66. Semilogar'thmic correlation in children up to 4 years of a total study population
between hemoglobin and 5-aminolevulinic acid dehydratase activity (lin Hb/log
ALAD).
83
-------
IM = 48
r = 0.383, P < 0.01
Hb = 18.084 - 0.775 Log EP
o
o
4 i-
A Control group
• Lead-exposed group 1
O Lead-exposed group 2
10
100
1000
EPfig/ 100ml
Figure 67. Semiloganthmic correlation in fathers of a total study population between hemo-
globin and erythrocyte protopo'rphyrin (lin Hb/log EP).
84
-------
N =49
r = -0.156, P> 0.10
o
o
20
16
12 —
•v9 •
o o
8 I-
4 i—
& Control group
• Lead-exposed group 1
O Lead-exposed group 2
10
100
100ml E
1000
Figure 68. Semilogarithmic correlation in mothers of a total study population between hemo-
globin and erythrocyte protoporphyrin (lin Hb/'log EP),
85
-------
N = 36
r =0.144, P> 0.10
o
o
20
16
• •
o •-
H
12 i—
& Control group
* Lead-exposed group 1
O Lead-exposed group 2
r
_L
10
100
100ml E
1000
Figure 69. Semilogarithmic correlation in children of a school age of a total study population
between hemoglobin and erythrocyta protoporphyrin (lin Hb/log EP).
86
-------
N =46
r = 0.025, P> 0.10
o
o
- 20
16
12
8 >-
4
a Control group
• Lead-exposed group 1
O Lead-exposed group 2
•
• o o
•
oo
I
10 100
EPjug/ 100ml E
1000
Figure 70. Semilogarithmic correlation in children up to 4 years of a total study population
between hemoglobin and erythrocyte protoporphyrin (lin Hb/log EP).
87
-------
40 -
30 -
a.
Q
<
UJ
_i
DC
20 -
10 -
1976
Figure 71. Yearly cycles of mean monthly air lead concentrations in lead smelter area
(Averages of five sampling sites).
88
-------
200
160 —
"H 120
a
o
a.
c.
80
40 —
A FATHERS (Group 1)
O MOTHERS (Group 1 + Group 2}
_L
2000 4000
DISTANCE (m) FROM LEAD SMELTER
6000
Figure 7?. Median erythrocyte protoporphyrin (EP) in fathers and mothers according to
median residential distance from lead smelter.
89
-------
200 —
160
120
30
40
1
CHILDREN - SCHOOL-AGE (Group 1 + Group 2)
CHILDREN UP TO 4 YEARS ( Group 1 -^ Group 2)
2000 4000
DISTANCE (m) FROM LEAD SMELTER
6000
Figure 73. Median erythrocyte protoporphyrin (EP) in children of school age and in children
up to 4 years according to median residential distance from lead smelter.
90
-------
TABLE 1. THE NUMBER OF FAMILIES IN THE EXAMINED GROUPS
Group N
Lead-exposed group 1 12
Lead-exposed group 2 21
Control group 16
TABLE
2. THE NUMBER OF FAMILY MEMBERS
WITHIN EXAMINED GROUPS
Family
relationship
Father
Mother
Child -
school age
Child -
up to 4 years
Lead-exposed groups
Group 1 Group 2
12 20
12 21
9 21
(6 m 3 f) (12 m 9 f)
11 19
(6 m 5 f) (8m 11 f)
Control group Total
16 48
16 49
7 37
(2 m 5 f)
17 47
(7 m 10 f)*
m Male
f Female
* Two daughters were twins.
91
-------
TABLE 3. AGE DISTRIBUTION IN PARENTS
Fathers' age
20-25
26-30
31-35
36-40
41-45
46-50
Lead-exposed
Group 1
N %
2
3
3
3
1
—
16.7
25.0
25.0
25.0
8.3
—
groups
Group
N
_
4
9
5
2
—
2
%
_
20.0
45.0
25.0
10.0
—
Control group
N %
2 12.5
2 12.5
3 18.8
5 31.2
2 12.5
2 12.5
Mothers' age
Lead-exposed
Group 1
20-25
26-30
31-35
36-40
41-45
46-50
N
5
3
3
1
-
-
%
41.7
25.0
25.0
8.3
-
-
groups
Group
N
2
7
8
3
1
_
2
%
9.5
33.3
38.1
14.3
4.8
_
Control group
N %
3 18.8
2 12.5
4 25.0
4 25.0
3 18.8
_ _
92
-------
TABLE 4. AGE DISTRIBUTION IN CHILDREN
School
children' s
age
5-7
8-10
11-13
14-16
Lead-exposed groups
Group 1 Group 2
N
5
2
2
—
%
55.
22.
22.
~
6
2
2
N
9
7
4
1
%
42
33
19
4
.9
.3
.0
.8
Control group
N
2
4
—
1
%
28.
57.
_
14.
6
1
3
Small Lead-exposed groups
children's Group 1 Group 2
age N % N %
Control group
N %
up to 11
1-2
3-4
9.1
72.7
18.2
1
17
1
5.3
89.4
5.3
1
11
5
5.9
64.7
29.4
93
-------
TABLE 5. HABITATION DISTRIBUTION BY DISTANCE FROM LEAD SMELTER IN LEAD-EXPOSED GROUP 1
Habitation
A
BI, B2
Cj , C2 , C3
D
Distance (m)
from lead
smelter
150 - 800
1900
3000-3400
4200-6500
Family
number
3
1
3
5
Fathers
3
1
3
5
Family
Mothers
2
2
3
5
members examined
Children
school age up
3
1
2
3
Children
to 4 years
2
1
3
5
TABLE
6. HABITATION
DISTRIBUTION
BY DISTANCE FROM
LEAD SMELTER
IN LEAD-EXPOSED GROUP 2
Habitation
A
B1 , B2
Cj , C2 > L.J
D
Distance (m)
from lead
smelter
150 - 800
1900
3000-3400
4200-6500
Family
number
2
4
3
12
Fathers
2
4
3
11
Family
Mothers
2
4
3
12
members examined
Children
school age up
2
4
3
12
Children
to 4 years
2
4
3
10
-------
TABLE 7. STATISTICAL PARAMETERS OF BIOLOGICAL DATA IN LEAD-EXPOSED GROUP 1
(FATHERS OCCUPATIONALLY EXPOSED TO LEAD)
Ul
BLOOD
Statis-
tical
param-
eter
N
X
SD
SE
N
X
SD
SE
N
X
SD
SE
Hb
g/
100 ml
12
15.76
1.811
0.523
12
15.24
1.063
0.307
8
14.23
1.194
0.422
Hot
%
12
42.38
2.144
0.619
12
41.17
1.193
0.345
8
40.78
1.778
0.629
BPE/
106E
12
1341.7
1940.22
560.09
12
608.3
675.57
281.62
9
211.1
437.16
145.72
Rtc
%o
12
17.1
7.49
2.16
12
15.6
6.84
1.98
C
9
10.7
3.43
1.14
EP
yg/ioo
ml E
F A T H E
12
552.42
266.409
76.906
M 0 T H E
12
96.80
93.944
27.119
H I L D R
8
142.24
111.328
39.360
C H I L D R E
N
X
SD
SE
11
13.97
1.085
0.327
11
39.18
1.454
0.438
11
436.4
657.68
198.30
11
10.7
3.61
1.09
11
144.32
72.597
21.889
ALAD
units/
ml E
R S
12
13.48
11.694
3.376
R S
12
71.49
29.226
8.437
Pb
yg/
100 ml
12
91.42
31.577
9.115
12
46.66
17.939
5.179
ALA
mg/
100 ml
12
1.613
0.8279
0.2390
11
0.596
0.3274
0.0987
URINE
mg/
24 h
12
11.238
5.7235
1.6522
11
3.958
2.2661
0.6833
CP
yg/
100 ml
12
44.1
29.46
8.50
11
9.0
3.31
1.00
yg/
24 h
12
315.8
211.93
61.18
11
65.6
34.61
10.43
E N (school age)
8
41.84
15.606
5.518
N (up
11
49.09
17.719
5.342
8
61.50
39.902
14.107
to 4 years)
11
53.22
20.632
6.221
9
0.502
0.2696
0.0899
9
0.403
0.2173
0.0724
9
1.696
1.0780
0.3593
7
0.723
0.4136
0.1563
9
10.2
5.76
1.92
6
7.9
2.48
1.01
9
39.4
32.25
10.75
6
18.5
16.28
6.65
-------
TABLE 8. STATISTICAL PARAMETERS OF BIOLOGICAL DATA IN LEAD-EXPOSED GROUP 2
(FATHERS NOT OCCUPATIONALLY EXPOSED TO LEAD)
Statis-
tical
param-
eter
N
X
SD
SE
N
X
SD
SE
N
X
SD
SE
N
X
SD
SE
Hb
g/
100 ml
20
16.83
0.962
0.215
21
14.41
1.230
0.268
21
14.73
0.850
0.186
19
13.43
1.271
0.292
Hct
%
20
44.02
1.235
0.276
21
40.45
1.923
0.420
21
40.28
1.724
0.376
19
38.92
1.564
0.359
B L 0 0
BpE/
10SE
20
605.0
900.57
201.37
21
200.0
524.40
114.43
21
300.0
1166.19
254.48
19
610.5
1393.99
319.80
D
Rtc
%o
20
12.4
4.64
1.04
21
13.7
6.42
1.40
C H
21
10.5
4.08
0.89
C H
19
12.7
5.45
1.25
URINE
EP
yg/ioo
ml E
F A T H
20
129.41
115.858
25.907
MOTH
21
69.76
44.322
9.672
I L D R
21
139.96
106.154
23.165
I L D R
18
138.99
112.896
26.610
ALAD
units/
ml E
E R S
20
50.47
35.591
7.958
E R S
21
95.38
44.829
9.782
Pb
MS/
100 ml
20
70.19
24.806
5.547
21
32.93
9.648
2.105
ALA
mg/
100 ml
20
0.476
0.2166
0.0484
20
0.344
0.1128
0.0252
mg/
24 h
20
3.861
2.0415
0.4565
20
2.690
0.9142
0.2044
CP
yg/
100 ml
19
20.2
46.05
10.57
20
8.8
4.06
9.08
yg/
24 h
19
157.4
321.47
73.75
20
70.0
34.52
7.72
E N (school age)
21
64.17
31.136
6.794
E N (up to
19
71.63
30.714
7.046
21
50.39
15.887
3.467
4 years)
19
45.19
12.436
2.853
21
0.465
0.2569
0.0561
14
0.286
0.1643
0.0439
21
2.091
0.9343
0.2039
4
0.588
0.7559
0.3780
21
8.5
4.72
1.03
5
9.7
3.29
1/47
21
42.4
25.19
5.50
4
16.3
8.10
4.05
-------
TABLE 9. STATISTICAL PARAMETERS OF BIOLOGICAL DATA IN CONTROL GROUP
Statis-
tical
param-
eter
N
X
SD
SE
N
X
SD
SE
N
X
SD
SE
N
X
SD
SE
Hb
g/
100 ml
16
17.09
1.134
0.284
16
14.74
1.087
0.272
7
13.99
1.075
0.406
17
13.36
0.714
0.173
Hct
%
16
44.16
2.700
0.675
16
41.47
1.737
0.434
7
39.43
1.134
0.429
17
38.38
2.198
0.533
B L 0 0
BpE/
106E
16
50.0
200.0
50.0
16
50.0
200.0
50.0
7
85.7
226.78
85.71
17
400.0
1104.54
267.89
D
Rtc
%o
16
10.
3.
0.
16
11.
7.
1.
7
11.
6.
2.
C H
17
10.
3.
0.
EP
yg/ioo
ml E
PATH
16
4 13.00
71 3.335
93 0.834
MOTH
16
9 17.36
08 16.728
77 4.182
CHILD
7
4 10.71
45 3.836
44 1.450
I L D R E
17
6 13.79
10 4.538
77 1.101
ALAD
units/
ml E
E R S
16
151.19
29.461
7.365
E R S
16
177.74
22.347
5.587
Pb
Ug/
100 ml
16
37.65
9.278
2.319
16
28.23
7.615
1.904
ALA
mg/
100 ml
16
0.374
0.1605
0.0401
15
0.355
0.1043
0.0269
U
mg/
24 h
16
2.878
1.0801
0.2700
15
2.922
1.5239
0.3935
R I N E
yg/
100 ml
16
11.3
5.74
1.43
15
12.5
4.66
1.20
CP
yg/
24 h
16
84.7
38.76
9.69
15
102.2
51.72
13.35
REN (School age)
7
176.31
12.422
4.695
N (up to
17
188.62
20.494
4.971
7
29.37
4.936
1.866
7
0.283
0.1125
0.0425
7
1.410
1.5062
0.5693
7
11.4
4.96
1.88
7
44.1
22.60
8.54
4 years)
17
30.05
6.056
1.469
16
0.334
0.0958
0.0239
16
0.626
0.4025
0.1006
13
10.6
3.73
1.03
13
23.2
12.92
3.58
-------
TABLE 10. STATISTICAL SIGNIFICANCE OF THE DIFFERENCE WITHIN LEAD-EXPOSED GROUP 1
(FATHERS OCCUPATIONALLY EXPOSED TO LEAD)
00
Statis-
tical
param-
eter
Hb
g/
100 ml
Hct
%
BpE/
10 6E
BLOOD
Rtc
%o
URINE
EP
yg/ioo
ml E
F A T H E
t
P
t
P
0.857
> 0.10 >
2.277
< 0.05 >
1.707
0.10
1.813
0.05
1.170
> 0.10
1.954
> 0.05
0.512
> 0.50 <
FAT
2.620*
< 0.05 <
5.587*
0.001 <
HERS
4.748*
0.001 <
FATHERS &
t
P
t
P
2.902
< 0.01 <
1.935
>0.05 >
4.220
0.001
0.544
0.50
1.524
> 0.10
1.253
> 0.10
2.645*
< 0.05 <
MOT
2.145
< 0.05 >
5 . 104*
0.001 <
HERS
0.951
0.10 <
ALAD
units /
ml E
R S &
6.384*
0.001
& C H
4.384
0.001
C H I L
5.635
0.001
& C H
2.941
0.01
Pb
yg/
100 ml
MOTH
4.650
< 0.001
I L D R E
1.781
> 0.05
D R E N
3.462
< 0.01
I L D R E
0.988
> 0.10
ALA
mg/
100 ml
E R S
3.933*
< 0.01 <
N (school
4.351*
< 0.01 <
mg/
24 h
4.072*
0.01
age)
5.643*
0.001
yg/
100 ml
4.102*
< 0.01
3.890*
< 0.01
CP
yg/
24h
4.031*
< 0.01
4.450*
< 0.01
(up to 4 years)
4.845*
< 0.001 <
N (school
0.704
>0.10 <
6.336*
0.001
age)
2.930*
0.02
4.233*
< 0.01
0.559
> 0.50
4.831*
< 0.01
1.749
> 0.05
(continued)
-------
TABLE 10. (continued)
Statis-
tical
param-
eter
t
P
t
P
Hb Hct
g/ %
100 ml
2.831 3.569
=0.01 <0.01
C
0.487 2.087
>0.50 >0.05
BpE/
106E
0.499
>0.50
H I L D
0.916
>0.10
B L 0 0
Rtc
%o
M 0
2.168
<0.05
D
URINE
EP
ALAD
yg/100 units/
ml
T H
1.
>0.
E
E R S
364 2
10 <0
REN (school age)
0.000
»0.50
0.
»0.
046 0
50 >0
ml E
& C H
.243
.05
& C H
.944
.10
Pb
yg/
100 ml
I L D R E
0.810
>0.10
I L D R E
0.537
>0.50
mg/
ALA
mg/ yg/
100 ml 24 h 100 ml
N (up
1.577
>0.10
N (up
0.858
>0.10
to 4
4.
<0.
to 4
2.
<0.
years)
615* 0.731
01 >0.10
years)
483* 1.037
05 >0.10
CP
yg/
24 h
3.808
<0.01
1.653
>0.10
* The significance of the difference between two groups examined was
determined by method of Cochran and Cox (Ref. 16).
-------
TABLE 11. STATISTICAL SIGNIFICANCE OF THE DIFFERENCE WITHIN LEAD-EXPOSED GROUP 2
(FATHERS NOT OCCUPATIONALLY EXPOSED TO LEAD)
o
o
Statis-
tical Hb
param- g/
eter 100 ml
Hct
%
BpE/
106E
B L 0 0
Rtc
%0
D
EP
yg/ioo
ml E
FATHERS
t
P
t
P
t
P
t
P
7.043
< 0.001
7.387
< 0.001
9.376
< 0.001
0.981
> 0.10
7.103
< 0.001
8.018
<0.001
1.749
>0.05
0.940
>0.10
11.262 0.015
<0.001»0.50
0.302
>0.50
0.358
>0.50
0.745
> 0.10
F A T H
1.388
> 0.10
F A T H E
0.184
»0.50
MOTH
1.929
>0.05
2.157*
<0.05
E R S &
0.293
>0.50
R S &
0.258
>0.50
E R S
2.796*
>0.01
URINE
ALAD
units/
ml E
& M 0
3.561
< 0.001
C H I L
1.309
> 0.10
C H I L
1.991
> 0.05
& CHI
2.621
< 0.02
Pb
yg/
100 ml
T H E R S
6.280*
< 0.001
ALA
mg/
100 ml
2.419*
<0.05
mg/
24 h
2.341*
< 0.05
yg/
100 ml
1.077
> 0.10
CP
yg/
24 h
1.179
> 0.10
D R E N (school age)
3.027
< 0.01
0.149
>0.50
D R E N (up to 4
4.008*
< 0.001
L D R E N
4.305*
< 0..001
2.908
<0.01
3.540*
< 0.01
years)
5.522
< 0.001
1.105
> 0.10
0.982
> 0.10
1.555
> 0.10
1.910
> 0.05
(school age)
1.968
>0.05
2.075
< 0..05
0.226
> 0.50
2.912
< 0.01
(continued)
-------
TABLE 11. (continued)
Statis-
tical
param-
eter
t
P
t
P
Hb Hct
g/ %
100 ml
2.473 2.769
<0.02 <0.01
3.755 2.616
<0.001 <0.02
B
BpE/
LOO
Rtc
10 6E %o
1.
<0.
C H
0.
>0.
M 0
209
10
I L D
760
10
THE
0.533
>0.50
REN
1.434
>0.10
D
EP
yg/ioo
ml E
R S &
2.445
<0.05
(school
0.027
»0.50
ALAD
units/
ml E
CHILD
1.970
>0.05
age) & C
0.762
>0.10
Pb
yg/
100 ml
R E N (up
3.458
<0.01
mg/
ALA
mg/
100 ml 24 h
to 4
1.146
>0.10
H I L D R E N
1.158
>0.10
2.513
<0.02
years)
4.892
<0.001
(up to 4
3.500
<0.01
URINE
yg/
100 ml
0.544
>0.50
years)
0.696
>0.10
CP
yg/
24 h
6.160
<0.001
3.821
<0.001
* The significance of the difference between two groups examined was determined by
method of Cochran and Cox (Ref. 16).
-------
TABLE 12. STATISTICAL SIGNIFICANCE OF THE DIFFERENCE WITHIN CONTROL GROUP
o
NJ
BLOOD
Statis-
tical Hb Hct
param- g/ %
eter 100 ml
t
P
t
P
t
P
t
P
5.976
<0.01
6.257
<0.01
11.217
<0.01
1.535
>0.10
F
3.352
<0.01
F
5.914*
<0.01
F
6.720
<0.01
M
3.343
<0.01
BpE/
10 6E
A T H E
0.000
>0.50
A T H E
0.360
>0.50
A T H E
1.284
>0.10
0 T H E
0.360
>0.50
Rtc
%o
R S &
0.750
>0.10
R S &
0.383
>0.50
R S &
0.166
>0.50
R S &
0.166
>0.50
EP
yg/ioo
ml E
MOTH
1.022
>0.10
C H I L
1.369
>0.10
C H I L
0.572
>0.50
C H I L
1.502
>0.10
ALAD
units/
ml E
E R S
2.872
<0.01
D R E N
2.876*
<0.01
D R E N
4.212
<0.01
D R E N
0.196
>0.50
Pb
U.R I N E
ALA
yg/ mg/
100 ml 100 ml
3.139
<0.01
0.393
>0.50
mg/
24 h
0.092
>0.50
yg/
100 ml
0.643
>0.50
CP
yg/
24 h
1.061
>0.50
(school age)
2.782* 1.557
<0.02 >0.10
(up to 4
2.769
<0.01
years)
0.857
>0.10
2.330
<0.05
7.816
<0.01
0.042
>0.50
0.397
>0.50
3.143
<0.01
5.953
<0.01
(school age)
0.428
>0.50
1.431
>0.10
2.185
<0.05
0.493
>0.50
3.666*
<0.01
(continued)
-------
TABLE 12. (continued)
BLOOD
Statis-
tical
param-
eter
t
P
t
P
Hb Hct
g/ %
100 ml
4.281 4.496
<0.01 <0.01
C H
1.428 1.535
>0.10 >0.10
BpE/
10 6E
MOTH
1.284
>0.10
I L D R
1.117
>0.10
Rtc
%o
E R S
0.673
>0.50
EP
yg/ioo
ml E
& CHI
0.826
>0. 10
E N (school age)
0.313
>0.50
1.692
>0. 10
ALAD
units/
ml E
LORE
1.455
>0.10
& C H
1.800
>0.05
Pb
yg/
100 ml
N (up to
0.757
>0.10
I L D R E
0.286
>0.50
U
R I N E
ALA
mg/
100 ml
4 years)
0.584
>0.50
N (up to
1.046
>0.10
mg/
24 h
5.653
<0.01
4 years)
1.356
>0.10
yg/
100 ml
1.201
>0.10
0.373
>0.50
CP
yg/
24 h
5.716
<0.01
2.257
<0.05
x The significance of the difference between two groups examined by the method
Cochran and Cox (Ref. 16).
-------
TABLE 13. STATISTICAL SIGNIFICANCE OF THE DIFFERENCE BETWEEN LEAD-EXPOSED GROUP 1
(FATHERS OCCUPATIONALLY EXPOSED TO LEAD) AND LEAD-EXPOSED GROUP 2 (FATHERS
NOT OCCUPATIONALLY EXPOSED TO LEAD)
o
•e-
BLOOD
Statis-
tical
param-
eter
t
P
t
P
t
P
t
P
Hb Hct
g/
100 ml
1.892 2
>0.05 <0
2.037 1
>0.05 >0
1.084 0
>0.10 >0
1.232 0
>0.10 >0
%
.420
.05
.325
.10
.682
.50
.459
.50
BpE/
10 SE
1.238
>0.10
1.343
X).10
0.303
>0.50
C
0.463
>0.50
Rtc
%o
1.961
>0.05
0.784
>0.10
C H I L
0.138
>0.50
H I L D
1.206
>0.10
EP
yg/100
ml E
PATH
5.213*
<0.001
MOTH
0.937
>0.10
ALAD
units/
ml E
E R S
4.279*
<0.001
E R S
1.849
>0.05
Pb
yg/
100 ml
1.990
>0.05
2.456*
<0.05
rag/
100 ml
4.663*
<0.001
1.787
>0.05
URINE
ALA
mg/
24 h
4.304*
<0.01
1.778
>0.05
yg/
100 ml
1.762
>0.05
0.148
>0.05
CP
yg/
24 h
1.647
>0.10
0.339
>0.05
D R E N (school age)
0.050
>0.50
R E N (up
0.155
>0.50
2.551*
<0.02
0.765
>0.10
0.349
>0.50
0.956
>0.10
0.789
>0.10
0.248
>0.50
to 4 years)
2.549*
<0.05
1.173
>0.10
1.382
>0.10
0.330
>0.50
0.997
>0.10
0.283
>0.50
* The significance of the difference between two groups examined was determined by method of
Cochran and Cox (Ref. 16).
-------
TABLE 14. STATISTICAL SIGNIFICANCE OF THE DIFFERENCE BETWEEN LEAD-EXPOSED GROUP 1
(FATHERS OCCUPATIONALLY EXPOSED TO LEAD) AND CONTROL GROUP
Statis-
tical
param-
eter
t
P
5 t
Ul
P
t
P
t
P
Hb
g/
100 ml
2.235
<0.05
1.219
>0.10
0.410
>0.50
1.649
>0.10
Hot
%
1.943
>0.05
0.541
>0.50
1.773
>0.05
1.160
>0.10
B
BpE/
106E
2.294*
<0.05
1.952
>0.05
0.742
>0.10
0.109
>0.50
L 0 0 D
Rtc
%o
2.849*
<0.02
1.393
>0.10
0.260
>0.50
0.075
>0.50
EP
yg/ioo
ml E
F A
7.014*
<0.001
M 0
2.895*
<0.02
C H I L
3.339*
<0.02
C H I L
5.956*
<0.001
ALAD
units/
ml E
T H E R
Pb
yg/
100 ml
S
ALA
mg/
100 ml
18.232* 5.717* 5.113*
< 0.001 <0.001 <0.001
T H E R
10.500
< 0.001
D R E N
4.758
< 0.001
D R E N
19.121
< 0.001
S
3.340*
<0.01
2.356*
<0.05
URINE
mg/
24 h
4.994*
<0.001
1.314
>0.10
yg/
100 ml
3.150*
<0.01
2.241
<0.05
CP
yg/
24 h
4.595*
<0.001
2.160
<0.05
(school age)
2.258*
>0.05
(up to 4
3.625*
<0.01
2.202
>0.05
years)
0.905
>0.10
0.425
>0.50
0.522
>0.50
0.447
>0.50
1.872
>0.05
0.342
>0.50
0.622
>0.50
*. The significance of the difference between two groups examined was determined by method of
Cochran and Cox (Ref. 16).
-------
TABLE 15. STATISTICAL SIGNIFICANCE OF THE DIFFERENCE BETWEEN LEAD-EXPOSED GROUP 2
(FATHERS NOT OCCUPATIONALLY EXPOSED TO LEAD) AND CONTROL GROUP
BLOOD
Statis-
tical
param-
eter
t
P
t
P
t
P
t
P
Hb Hct
g/ %
100 ml
0.674
>0.50
0.864
>0.10
1.657
>0.10
0.206
>0.50
0.192
>0.50
1.689
>0.05
1.490
>0.10
0.840
>0.10
BpE
106E
2.675*
<0.02
1.201
>0.10
0.798
>0.10
0.505
>0.50
Rtc
%o
1.433
>0.10
0.798
>0.10
0.346
>0.50
1.430
>0.10
EP
yg/ioo
ml E
F A
4.491*
<0.001
M 0
4.973*
>0.001
C H I L
5.569*
<0.001
CHILD
4.701*
<0.001
ALAD
units/
ml E
T H E R
9.289
< 0.001
T H E R
7.311*
< 0.001
D R E N
13.579*
< 0.001
Pb
yg/
100 ml
S
5.412*
<0.001
S
1.656
<0.10
(school
5.339*
<0.001
REN (up to 4
13.567
< 0.001
4.718*
<0.001
ALA
mg/
100 ml
1.623
>0.10
0.298
>0.50
age)
2.586*
<0.02
years)
0.960
>0.10
URINE
mg/
24 h
1.853
>0.05
0.523
>0.50
1.126
>0.10
0.097
>0.50
yg/
100 ml
0.834
>0.10
0.404
>0.50
1.353
>0.10
0.501
>0.50
CP
Ug/
24 h
0.977
>0.10
2.094
<0.05
0.167
>0.50
1.276
>oao
* The significance of the difference between two groups was determined by method of Cochran and Cox
(Ref. 16).
-------
TABLE 16. STATISTICAL SIGNIFICANCE OF THE DIFFERENCE BETWEEN LEAD-EXPOSED GROUP 1
1 (FATHERS OCCUPATIONALLY EXPOSED TO LEAD), LEAD-EXPOSED GROUP 2 (FATHERS
' NOT OCCUPATIONALLY EXPOSED TO LEAD), AND CONTROL GROUP
o
-vl
BLOOD
Statis-
tical
param-
eter
F.
P
F
P
F
P
Hb
g/
100 ml
1.195
>0.20
2.023
>0.05
1.883
<0.20
Hct
%
3.138
>0.05
1.717
<0.20
1.279
>0.20
BpE/
106E
4.483
<0.02
3.036
>0.05
0.146
>0.20
Rtc
%o
5.721
<0.01
1.008
>0.20
C
0.120
>0.20
EP
yg/ioo
ml E
FAT
46.674
< 0.001
MOT
7.743
< 0.005
H I L D
4.999
< 0.02
ALAD
units/
ml E
HERS
87.654
< 0.001
HERS
37.747
< 0.001
Pb
yg/
100 ml
19.326
< 0.001
8.997
< 0.001
ALA
mg/
100 ml
25.584
< 0.001
7.553
< 0.005
mg/
24 h
27.479
< 0.001
2.546
< 0.10
URINE
Ug/
100 ml
3.499
<0.05
4.119
<0.02
CP
Ug/
24 h
3.464
<0.05
3.483
<0.05
REN (school age)
61.306
< 0.001
CHILDREN (up
F
P
1.262
>0.20
0.744
>0.20
0.166
>0.20
1.336
>0.20
13.843
< 0.001
142.638
< 0.001
4.025
< 0.05
1.894
< 0.20
1.175
> 0.20
1.048
X).20
0.067
X).20
to 4 years)
11.489
< 0.001
1.583
> 0.20
0.139
> 0.20
1.303
>0.20
0.543
X).20
-------
TABLE 17. AIR-LEAD CONCENTRATION (ug/m3) AT
FIVE SITES IN LEAD SMELTER AREA
Sampling sites
Date
Month Year
XII 1973
I 1974
II
III
IV
V
VI
VII
VIII
IX
X
XI
XII
I 1975
II
III
IV
V
VI
VII
VIII
IX
X
XI
XII
I 1976
II
III
IV
V
VI
VII
VIII
IX
X
1.
(4.0 km N)*
24.21
14.69
17.09
21.94
12.69
22.80
16.86
12.82
6.76
2.07
3.03
5.39
5.90
5.00
4.10
2.90
3.90
3.30
3.80
4.40
6.30
3.30
4.70
9.00
23.30
16.20
9.40
11.40
11.00
6.60
14.50
13.90
13.30
14.40
13.90
2.
(0.5 km N)*
15.53
11.61
9.31
13.19
8.54
13.97
17.45
8.93
10.91
7.68
31.99
30.64
21.00
19.20
22.20
21.30
25.00
11.50
22.00
6.90
5.40
32.30
22.90
35.80
35.10
24.40
16.30
19.30
13.80
14.30
6.70
6.60
17.30
15.90
16.80
3.
(1.5 km SSW)*
Pb pg/m3
39.69
48.11
25.83
25.89
8.71
9.50
13.38
7.14
12.55
19.81
24.07
34.05
18.60
16.20
26.90
17.80
12.50
10.00
17.30
5.70
4.80
33.30
22.70
44.50
59.50
28.50
37.10
25.80
9.10
6.70
8.00
18.30
15.60
13.60
35.30
4.
(2.0 km SSW)*
13.39
16.43
9.06
9.48
16.92
18.26
16.81
8.87
16.46
13.47
19.25
26.36
16.00
15.60
19.50
11.60
8.80
13.50
18.50
5.20
5.00
22.40
23.00
31.70
54.20
25.30
32.80
11.70
4.80
7.30
8.40
22.80
11.10
13.20
31.90
5.
(2.5 km SW)*
45.11
44.95
22.61
20.03
6.79
31.19
10.04
5.35
11.19
11.30
13.83
22.80
13.80
12.00
17.60
14.50
7.60
9.60
12.90
4.20
3.10
21.10
9.40
14.20
55.10
17.70
36.30
14.80
5.00
11.50
5.50
14.00
10.90
8.10
27.00
Relative position of sampling sites (1-5) to the smelter.
108
-------
TABLE 18. STATISTICAL PARAMETERS OF AIR-LEAD CONCENTRATION
(yg/m3) AT FIVE SITES IN LEAD SMELTER AREA
(DECEMBER 1973-OCTOBER 1976)
Statis-
tical
param-
eter
N
X
SD
SE
Sampling sites
1.
(4.0 km N)*
35
10.41
6.551
1.107
2.
(0.5 km N)*
35
17.48
8.480
1.433
3.
(1.5 km SSW)*
Pb yg/m3
35
21.62
13.306
2.249
4
(2.0 km SSW)*
35
17.12
9.915
1.676
5
(2.5 km SW)*
35
16.89
12.383
2.093
* Relative position of sampling sites (1-5) to the smelter.
TABLE 19. STATISTICAL PARAMETERS OF ANNUAL AIR-LEAD CONCEN-
TRATION (yg/m3) AT FIVE SITES IN LEAD AREA (DECEM-
BER 1973-OCTOBER 1976)
Statis-
tical
param-
eter
N
X
SD
SE
N
X
SD
SE
N
X
SD
SE
Sampling sites
1.
(4.0 km N)*
12
13.36
7.689
2.220
12
4.69
1.721
0.497
11
13.44
4.226
1.274
2.
(0.5 km N)* (1
DECEMBER
12
14.97
8.188
2.364
DECEMBER
12
20.46
9.050
2.613
DECEMBER
11
16.95
7.882
2.370
3. 4.
.5 km SSW)* (2.0 km SSW)*
Pb yg/m3
1973-NOVEMBER
12
22.39
13.123
7.788
Pb yg/m3
1974-NOVEMBER
12
19.19
11.459
3.308
Pb yg/m3
19 75- OCTOBER
11
23.41
16.024
4.831
1974
12
15.40
5.002
1.444
1975
12
15.90
7.805
2.253
1976
11
20.32
14.937
4.504
5.
(2.5 km SW)*
12
20.43
13.719
3.960
12
11.67
5.222
1.507
11
18.72
15.261
4.601
* Relative position of sampling sites (1-5) to the smelter.
109
-------
TABLE 20. STATISTICAL SIGNIFICANCE OF THE DIFFERENCE BETWEEN
AIR-LEAD CONCENTRATION (yg/m3) AT FIVE SITES IN
LEAD SMELTER AREA (DECEMBER 1973-OCTOBER 1976)
Comparable
Statistical parameter
sampling —
sites
1
1
1
1
2
2
2
3
3
4
- 2
- 3
- 4
- 5
- 3
- 4
- 5
- 4
- 5
- 5
t
3.904
4.472
3.341
2.737
1.552
0.163
0.233
1.604
1.540
0.086
P
<0.001
<0.001
<0.01
<0.01
>0.1
>0.5
>0.5
>0.1
>0.1
>0.5
TABLE 21. AIR-LEAD CONCENTRATION (yg/m3)
AT ONE SITE IN CONTROL AREA
Date
Month Year
XI 1974
XII
I 1975
II
III
IV
V
VI
VII
VIII
IX
X
Sampling site in community G
Pb yg/m3
0.09
0.11
0.10
0.19
0.05
0.13
0.11
0.08
0.03
0.04
0.08
0.12
110
-------
TABLE 22. STATISTICAL PARAMETERS OF AIR-LEAD CONCENTRATION
(yg/m3) AT ONE SITE IN CONTROL AREA (NOVEMBER 1974-
OCTOBER 1975)
Statis-
tical
param-
eter
N
1C
SD
SE
Sampling site in community G
Pb yg/m3
12
0.09
0.044
0.013
TABLE 23. LEAD AMOUNT IN DUSTFALL (mg/m2/month) AT FOUR
SITES IN LEAD SMELTER AREA
Sampling sites
Date
1.
(4.0 km N)*
2.
(0.5 km N)*
3.
(1.5 km SSW)*
4.
(2.5 km SW)*
Month Year
Pb mg An2 /month
XI 1975
XII
I 1976
II
III
IV
V
VI
VII
VIII
IX
X
126
94
104
-
110
70
26
5
59
184
58
21
419
248
333
225
58
218
61
15
257
201
108
147
612
437
312
287
268
137
57
7
316
91
120
486
401
331
203
253
119
129
50
30
185
104
46
135
Relative position of sampling sites (1, 2, 3, 5) to the smelter.
Ill
-------
TABLE 24. STATISTICAL PARAMETERS OF LEAD AMOUNT IN DUSTFALL
(mg/m2/month) AT FOUR SITES IN LEAD SMELTER AREA
(NOVEMBER 1975-OCTOBER 1976)
Statis-
tical
param-
eter
N
~K
SD
SE
1. 2.
Sampling sites
3.
(4.0 km N)* (0.5 km N)* (1.5 km SSW)*
11 12
77.9 190.
52.54 119.
15.84 34.
Pb mg/m2/ month
12
8 260.8
14 186.22
39 53.76
4.
(2.5 km SW)*
12
165.5
115.40
33.31
Relative position of sampling sites (1, 2, 3, 5) to the smelter.
TABLE 25. LEAD AMOUNT IN DUSTFALL (mg/m2/month) AT
ONE SITE IN CONTROL AREA
Date Sampling site in community G
Month Year Pb mg/m2/month
XI 1975
XII
I 1976
II
III
IV
V
VI
VII
VIII
IX
X
0.30
-
0.30
1.10
1.80
7.53
0.90
2.73
3.17
3.17
2.40
1.37
112
-------
TABLE 26. STATISTICAL PARAMETERS OF LEAD AMOUNT IN DUSTFALL
(mg/m2/month) AT ONE SITE IN CONTROL AREA (NOVEM-
BER 1975-OCTOBER 1976)
Statistical
parameter
Sampling site in community G
_, . , .
Pb mg/rn^ /month
N
X
SD
SE
11
2.25
2.038
0.615
TABLE 27- LEAD CONTENT OF HOUSEHOLD DUST (yg/g) IN LEAD
SMELTER AREA (DECEMBER 1976)
Home
(father's
initials)
K.N.
V.F.
J.K.
K.S.
NX
S-.B.
H.A.
V
S.L.
T.M.
J.J.
P.H.
P.J.
C.F.
B.D.
P.D.
Community
A
A
A
Bi
Ci
C3
D
A
BI
B2
B2
D
D
D
Group 1
6300
5100
5100
4000
3000
1400
1300
Group 2
Pb yg/g
6700
6800
2000
1000
1700
1200
1000
113
-------
TABLE 28. STATISTICAL PARAMETERS OF LEAD CONTENT IN
HOUSEHOLD DUST (yg /g) IN LEAD SMELTER AREA
(DECEMBER 1976)
Statistical
parameter
N
X
SD
SE
Group 1
Pb Ug/g
7
3742.8
1927.74
728.62
Group
7
2914
2646
1000
2.
.3
.02
.10
TABLE 29. LEAD CONTENT OF HOUSEHOLD DUST
CONTROL AREA (OCTOBER 1975)
(yg/g) IN
Home
(father's
initials)
V.S.
V.F.
V.I.
M.F.
J.F.
N.I.
J.A.
O.D.
A.I.
A.G.
P.J.
J.F.
Community
F
F
F
G
G
G
E
E
E
H
H
H
Pb ug/g
200
160
160
250
310
200
130
80
120
110
120
50
114
-------
TABLE 30. STATISTICAL PARAMETERS OF LEAD CONTENT IN HOUSEHOLD
DUST (yg/g) IN CONTROL AREA (OCTOBER 1975)
Statistical
parameter
Pb yg/g
N
X
SD
SE
12
157.5
73.13
21.11
TABLE 31. WATER-LEAD CONCENTRATION (yg/1) IN
LEAD SMELTER AREA (DECEMBER 1976)
Home
(father's
initials)
Z.H.
G.E.
P.J.
O.S.
P.J.
Community
B2
B2
B2
Ci
C3
Type
Domestic
Domestic
of water supply
running water system
running water system
Public water supply
Well
Well
Pb yg/1
12.9
11.1
10.0
7.4
9.7
115
-------
TABLE 32. WATER-LEAD CONCENTRATION (yg/1)
IN CONTROL AREA (OCTOBER 1975)
Home
(father's Community Type of water supply
initials)
J.A. E Well
O.D. E Well
V.I. F Well
V.S. F Well
M.F. G Public water supply
Pb yg/1
2.4
2.6
2.5
1.5
0.3
TABLE 33. RATIO CONTENT IN VARIOUS ENVIRONMENTAL MEDIA
BETWEEN THE EXPOSED AND THE CONTROL AREA
Medium Ratio in lead content
Air 178 : 1
Dustfall 77 : 1
Household dust 21 : 1
Water 6 : 1
116
-------
TABLE 34. ESTIMATED LEAD ABSORPTION (yg Pb/day/kg)
FROM THE AIR IN POPULATION FROM LEAD-
EXPOSED AND CONTROL AREA*
Family Lead-exposed area Control area
relationship ——
group yg Pb/day/kg
Fathers 1.060 0.006
Mothers 1.079 0.006
Children
(school age) 2.264 0.012
Children
(up to 4 years) 2.323 0.014
x Calculated on basis of the average air-lead concentration of 16.73 yg/m3
in the exposed area and 0.09 yg/m3 in the control area, and under the
assumptions described on page 15.
117
-------
TABLE 35. BIOLOGICAL INDICES OF LEAD ABSORPTION IN COMPARISON WITH MEDIAN
RESIDENTIAL DISTANCE OF FATHERS (GROUP 2) FROM LEAD SMELTER
Biological inde}
Hb g/100 ml
Hct %
BpE/106E
Rtc %o
EP yg/100 ml E
ALAD units/ml E
Pb-B yg/100 ml
ALA-U mg/100 ml
ALA-U mg/24 h
CP-U Ug/100 ml
CP-U yg/24 h
Distance (m) of habitation from lead smelter
500
150 - 800
16.6 (2)
16.6 - 16.6
44.5 (2)
44.0 - 45.0
100 (2)
0 - 200
9.5 (2)
9-10
198.5 (2)
115.1 - 282.0
19.1 (2)
7.1 - 31.1
105.8 (2)
87.9 - 123.7
0.64 (2)
0.62 - 0.66
5.61 (2)
4.96 - 6.27
11.5 (2)
10.5 - 12.5
101.0 (2)
84 - 119
1900
1900 - 1900
16.1 (4)
15.0 - 17.0
43.5. (4)
42.0 - 44.5
750 (4)
0 - 3200
15.0 (4)
6-22
118.6 (4)
36.2 - 371.7
33.0 (4)
5.9 - 52.5
52.5 (4)
35.0 - 79.4
0.40 (4)
0.25 - 1.00
3.06 (4)
1.90 - 7.00
10.7 (4)
5.0 - 210.0
108.4 (4)
25 - 1470
3150
3000 - 3400
17.5 (3)
16.7 - 17.8
45.5 (3)
44.0 - 45.7
0 (3)
0 - 1600
12.0 (3)
5-17
91.8 (3)
69.2 - 410.9
59.6 (3)
13.1 - 68.1
101.6 (3)
69.8 - 110.1
0.32 (3)
0.15 - 0.72
3.60 (3)
1.05 - 4.48
8.5 (2)
6.5 - 10.5
96.5 (2)
46 - 147
4500
4200 - 6500
17.3 (11)
15.6 - 18.5
44.0 (11)
41.0 - 46.0
500 (11)
0 - 2400
12.0 (11)
8-20
69.7 (11)
47.7 - 294.2
57.9 (11)
16.6 - 145.5
59.7 (11)
35.0 - 95.8
0.43 (11)
0.22 - 0.79
4.08 (11)
0.94 - 7.11
10.0 (11)
4.5 - 15.5
69.0 (11)
20 - 217
All values are expressed in median/range.
( ) Number of subjects.
118
-------
TABLE 36. BIOLOGICAL INDICES OF LEAD ABSORPTION IN COMPARISON WITH MEDIAN
RESIDENTIAL DISTANCE OF MOTHERS (GROUP 1 AND GROUP 2) FROM LEAD
SMELTER
Distance (m) of habitation from lead smelter
Biological index
Hb g/100 ml
Hct %
BpE/105 E
Rtc %o
EP lJg/100 ml E
ALAD units/ml E
Pb-B yg/100 ml
ALA-U mg/100 ml
ALA-U mg/24 h
CP-U yg/100 ml
CP-U yg/24 h
500
150 - 800
14.7 (4)
13.8 - 17.1
40.7 (4)
40.0 - 41.0
0 (4)
0 - 900
13.0 (4)
8-31
161.5 (4)
117.3 - 205.1
55.5 (4)
19.4 - 124.1
37.1 (4)
27.6 - 68.8
0.36 (4)
0.22 - 0.38
2.78 (4)
2.20 - 3.04
7.7 (4)
4.5 - 12.5
69.0 (4)
34 - 100
1900
1900
14.4 (6)
13.8 - 15.6
40.2 (6)
39.5 - 42.5
200 (6)
0 - 2100
14.5 (6)
9-16
84.4 (6)
31.9 - 297.6
55.1 (6)
23.4 - 91.0
37.2 (6)
21.4 - 70.0
0.33 (5)
0.20 - 0.83
3.00 (5)
2.31 - 9.13
9.5 (5)
2.0 - 15.0
114.0 (5)
14 - 150
3150
3000 - 3400
15.7 (6)
14.0 - 16.7
40.2 (6)
41.0 - 43.0
0 (6)
0-0
18.5 (6)
8-25
59.0 (6)
23.6 - 142.7
96.9 (6)
55.0 - 131.4
47.0 (6)
29.3 - 71.1
0.31 (6)
0.16 - 0.79
2.53 (6)
1.56 - 4.74
7.7 (6)
6.0 - 13.5
69.0 (6)
42 - 105
4500
4200 - 6500
14.5 (17)
11.0 - 16.2
40.0 (17)
35.5 - 44.5
0 (17)
0 - 3200
11.0 (17)
5-30
45.0 (17)
8.7 - 113.8
95.8 (17)
52.7 - 221.8
32.4 (17)
17.2 - 47.2
0.38 (16)
0.29 - 1.37
2.82 (16)
0.66 - 5.48
8.7 (16)
3.5 - 21.6
55.5 (16)
14 - 108
All values are exposed in median/range.
( ) Number of subjects.
119
-------
TABLE 37. BIOLOGICAL INDICES OF LEAD ABSORPTION IN COMPARISON WITH MEDIAN
RESIDENTIAL DISTANCE OF SCHOOL AGE CHILDREN (GROUP 1 AND GROUP
2) FROM LEAD SMELTER
Distance (m) of habitation from lead smelter
Biological index
Hb g/100 ml
Hct %
BpE/106 E
Rtc %o
Ep Ug/100 ml
ALAD units /ml E
Pb-B Ug/100 ml
ALA-U mg/100 ml
ALA-U mg/24 h
CP-U lag/ 100 ml
CP-U yg/24 h
500
150 - 800
14.5 (5)
13.6 - 15.5
40.0 (5)
38.5 - 42.0
0 (5)
0 - 1200
9.0 (5)
6-15
214.4 (5)
121.0 - 442.0
22.7 (5)
16.2 - 59.2
73.0 (5)
39.0 - 127.3
0.45 (5)
0.36 - 1.29
1.80 (5)
1.08 - 4.10
16.0 (5)
10.5 - 22.5
34.0 (5)
22 - 105
1900
1900 - 1900
14.5 (4)
14.1 - 15.3
40.0 (4)
40.0 - 40.5
0 (5)
0 - 5300
12.0 (5)
7-15
120.6 (4)
61.3 - 305.0
35.1 (4)
21.7 - 48.7
42.8 (4)
37.2 - 65.3
0.45 (5)
0.16 - 0.54
2.25 (5)
1.15 - 2.63
10.0 (5)
6.5 - 15.5
63.0 (5)
35 - 98
3150
3000 - 3400
14.4 (5)
13.0 - 15.3
39.5 (5)
38.7 - 42.5
0 (5)
0 - 700
13.0 (5)
7-24
87.1 (5)
65.9 - 320.3
54.4 (5)
27.2 - 100.3
55.1 (5)
25.7 - 78.8
0.41 (5)
0.15 - 0.78
1.92 (5)
0.93 - 2.05
4.5 (5)
3.5 - 8.5
23.0 (5)
9-34
4500
4200 - 6500
15.0 (15)
12.6 - 16.3
41.7 (15)
37.0 - 43.2
0 (15)
0 - 1000
9.0 (15)
6-15
76.0 (15)
29.8 - 246.5
66.9 (15)
37.7 - 123.6
44.0 (15)
17.6 - 64.8
0.40 (15)
0.24 - 0.93
2.00 (15)
0.38 - 4.62
7.0 (15)
3.0 - 13.5
35.0 (15)
5-74
All values are expressed in median/range.
( ) Number of subjects.
120
-------
TABLE 38. BIOLOGICAL INDICES OF LEAD ABSORPTION IN COMPARISON WITH MEDIAN
RESIDENTIAL DISTANCE OF CHILDREN UP TO 4 YEARS (GROUP 1 AND
GROUP 2) FROM LEAD SMELTER
Distance (m) of habitation from lead smelter
Biological index
Hb g/100 ml
Hct %
BpE/106 E
Rtc %o
Ep vtg/100 ml E
ALAD units /ml E
Pb-B yg/100 ml
ALA-U mg/100 ml
500
150 - 800
14.5 (4)
13.2 - 14.9
39.7 (4)
38.0 - 41.0
0 (4)
0 - 800
7.0 (4)
7-14
160.1 (4)
90.3 - 206.0
57.6 (4)
43.9 - 72.1
52.1 (4)
38.6 - 70.8
0.25 (4)
0.09 - 0.40
1900
1900 - 1900
13.8
10.4 -
40.0
36.5 -
0 -
0 -
13.0
7 -
178.5
99.0 -
34.2
24.6 -
39.7
32.2 -
0.13
0.03
(5)
14.9
(5)
41.0
(5)
1700
(5)
16
(4)
• 532.0
(5)
73.7
(5)
68.5
(4)
- 0.40
3150
3000 - 3400
13.4 (6)
11.8 - 14.9
39.2 (6)
36.0 - 40.0
0 (6)
0 - 1200
9.5 (6)
5-15
95.2 (6)
60.1 - 317.4
65.2 (6)
22.5 - 109.1
44.9 (6)
22.9 - 91.8
0.40 (3)
0.19 - 0.43
4500
4200 - 6500
13.6 (15)
11.8 - 15.8
38.0 (15)
37.0 - 42.5
0 (15)
0 - 5100
11.0 (15)
7-24
86.7 (15)
43.3 - 188.5
63.8 (15)
29.6 - 114.6
47.6 (15)
28.4 - 78.3
0.46 (12)
0.13 - 0.71
ALA-U mg/24 h
0.36 (1)
1.33 (3) 0.28 (7)
0.32 - 1.72 0.17 - 1.10
CP-U yg/100 ml
CP-U yg/24 h
12.5 (1)
25.0 (1)
6.5 (3)
6.0 - 7.0
24.0 (3)
6-46
9.0 (7)
6.0 - 13.5
10.0 (6)
3-23
All values are expressed in median/range.
( ) Number of subjects.
121
-------
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10. Cripps, D.J., and H.A. Peters. Fluorescing Erythrocytes and Porphyrin
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12. Fernandez, T.T. Mlcromethod for Lead Determination in Whole Blood by
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Orenstein, J.A. Mather, A.J. Yankel, and J.H. von Lindern. Increased
Lead Absorption With Anemia and Slowed Nerve Conduction in Children
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26. Wibowo, A.E.E., P. Del Castilho, R.F.M. Herber, and R.L. Zielhuis. Blood
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with Constituents of Erythrocytes. Health Phys., 25:37-42, 1973.
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31. Piomelli, S. A Micromethod for Free Erythrocyte Porphyrins: The FEP
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38. Sayre, J.W., E. Charney, J. Vostal, and I.E. Pless. House and Hand Dust
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170, 1974.
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125
-------
TABLE A-l. LEAD-EXPOSED GROUP 1
NJ
ON
Subject
and
Family re-
community
V.F.
V.V.
V.B.
V.A.
Z.M.
V
Z.B.
Z.N.
Z.B.
O.P.
O.M.
O.P.
J.K.
J.A.
J.A.
J.R.
S.B.
S.B.
S.K.
A
A
A
A
D
D
D
D
D
D
D
A
A
A
A
Ci
Ci
lationship Age
f.
m.
s.
s.
f .
m.
d.
s.
f .
m.
d.
f .
m.
s.
s.
f .
m.
d.
37 yr
38 yr
12 yr
1 yr
28 yr
25 yr
6 yr
2 yr
23 yr
22 yr
1 yr
42 yr
34 yr
6 yr
1 yr
29 yr
24 yr
2 yr
Hb
g/
100 ml
14.7
14.9
15.5
14.2
14.9
14.5
12.6
13.8
18.2
15.6
15.8
16.7
17.1
14.5
14.9
16.9
16.7
14.1
Hct
42.0
41.0
42.0
41.0
41.0
42.0
43.0
40.5
45.0
41.5
40.0
43.5
40.5
39.0
38.5
43.0
42.0
40.0
B
BpE/
106E
7100
900
1200
0
900
3200
0
300
1200
700
0
800
0
0
0
900
0
0
L 0
Rtc
%o
33
16
15
7
16
23
10
9
17
13
9
12
11
9
8
14
8
9
0 D
EP
yg/ioo
ml E
966.9
153.5
212.4
206.0
804.2
36.2
76.0
85.6
670.1
25.7
151.2
479.7
169.5
121.0
134.4
406.9
142.7
317.4
ALAD
units/
ml E
8.6
59.0
22.6
49.4
1.5
82.4
42.1
37.3
10.0
75.9
43.8
16.4
124.1
59.2
72.1
15.6
55.0
22.5
Pb
yg/
100 ml
118.7
68.8
115.3
70.8
92.0
17.2
17.6
36.1
57.9
42.7
78.3
85.1
42.7
52.7
50.7
125.1
71.1
91.8
U R I
N E
ALA Coproporphyrin
mg/
100 ml
1.90
0.38
1.08
0.09
2.73
0.69
0.38
0.71
1.39
0.61
0.57
1.29
0.34
0.45
0.40
1.08
0.47
0.40
mg/
24 h
19.95
2.85
1.08
-
6.83
4.83
0.38
0.85
9.73
0.92
0.28
11.86
2.72
1.13
—
14.04
3.66
0.32
yg/
100 ml
40.5
4.5
21.5
—
49.0
13.5
5.0
6.5
38.0
10.0
6.0
78.0
12.5
13.5
—
34.5
13.5
7.0
yg/
24 h
425
34
22
-
125
95
5
8
266
15
3
718
100
34
—
449
105
6
(continued)
-------
TABLE A-l. (continued)
Subject
and
Family re-
community lationship Age
H.A.
H.M.
H.A.
H.S.
K.A.
K.M.
K.D.
S.J.
S.A.
S.A.
S.J.
G.F.
G.M.
G.R.
G.J.
K.S.
K.A.
K.B.
K.S.
C3
C3
C3
C3
A
Bi
A
D
D
D
D
C2
C2
C2
C2
Bi
Bi
Bi
Bi
f.
m.
d.
s.
f.
m.
s.
f.
m.
d.
d.
f.
m.
s.
d.
f.
m.
s.
d.
35 yr
28 yr
7 yr
3 mo
29 yr
22 yr
9 yr
36 yr
30 yr
7 yr
2 yr
32 yr
31 yr
7 yr
4 yr
38 yr
34 yr
11 yr
3 yr
Hb
g/
100 ml
15.6
15.6
13.0
11.8
16.6
15.6
14.6
17.9
16.2
15.6
15.2
14.9
14.0
13.0
13.4
12.2
13.8
-
13.9
Hct
%
42.5
43.0
39.0
36.0
44.0
42.0
40.0
45.5
40.5
42.0
40.0
40.5
41.0
38.7
39.0
39.0
40.0
-
40.0
B
BPE/
10 6E
2400
0
700
1200
800
0
0
1500
0
0
0
0
0
0
0
500
1500
0
1700
L 0 0 D
Ret
%o
14
24
13
15
16
16
8
17
30
13
7
7
11
7
10
13
16
15
16
EP
yg/ioo
ml E
851.2
46.2
65.9
60.1
436.2
203.6
389.2
309.7
45.0
127.2
86.7
106.6
23.6
87.1
107.1
807.8
297.6
-
99.0
ALAD
units/
ml E
8.8
68.8
54.4
64.2
7.3
43.1
16.2
16.4
52.7
37.7
47.8
45.6
115.2
47.8
33.3
5.1
23.4
-
68.9
Pb
yg/
100 ml
122.7
49.8
48.3
22.9
124.8
70.0
127.3
86.8
44.3
64.8
54.3
31.8
29.3
25.7
29.3
84.4
60.1
-
52.9
U R I N
E
ALA Coproporphyrin
mg/
100 ml
2.93
0.79
0.78
—
1.21
-
0.41
0.64
0.37
0.47
0.44
0.61
0.16
0.48
0.19
2.29
0.83
0.23
0.18
mg/
24 h
16.11
4.74
1.95
—
8.47
-
4.10
6.08
2.59
2.35
1.10
6.10
1.56
1.92
1.33
6.87
9.13
1.15
0.36
yg/
100 ml
113.0
7.5
3.5
—
40.5
-
10.5
10.5
7.5
6.5
9.0
18.5
8.0
8.5
6.5
56.5
9.0
15.5
12.5
yg/
24 h
622
45
9
-
284
-
105
100
53
33
23
185
78
34
46
170
99
78
25
(continued)
-------
TABLE A-l. (continued)
00
BLOOD
Subject
and Family re-
community lationship Age
S.L.
S.M.
V
S.D.
V
S.T.
G.R.
G.A.
G.R.
£ • "~
m. -
s. -
d. -
D f.
D m.
D s.
D s.
D f .
D m.
D s.
father
mother
son
daughter
32 yr
30 yr
8 yr
2 yr
24 yr
22 yr
2 yr
Hb
g/
100 ml
13.4
14.5
15.0
13.3
17.1
14.4
13.3
Hct
%
39.0
42.0
42.5
38.0
43.5
38.5
38.0
BpE/
106E
0
0
0
200
0
900
1400
Ret
%o
31
9
6
11
15
10
17
EP
yg/ioo
ml E
517.1
9.3
59.1
160.6
272.6
8.7
179.4
ALAD
units
ml E
4.8
62.5
54.7
29.6
21.6
95.8
71.1
Pb
yg/
100
51.
25.
40.
50.
116.
38.
47.
ALA
mg/
ml 100 ml
5 2.50
7 0.55
3 0.24
7
2 0.79
2 1.37
6 0.65
URINE
Coproporphyrin
mg/ yg/ yg/
24 h 100 ml 24 h
22.50 45.0 405
5.06 9.0 83
1.20 7.0 35
6.32 5.0 40
5.48 3.5 14
0.82
-------
TABLE A-2. LEAD-EXPOSED GROUP 2
ȣ>
Subject
and
Family re-
community lationship Age
T.M.
T.S.
T.B.
T.Z.
D.M.
D.J.
D.M.
D.S.
C.F.
V
C.M.
V
c.s.
V
C.S.
S.G.
S.M.
S.D.
B.D.
B.H.
B.K.
B.H.
A
A
A
A
D
D
D
D
D
D
D
D
D
D
D
D
D
D
D
f.
m.
s.
s.
f.
m.
d.
d.
f .
m.
s.
d.
f .
m.
d.
f.
m.
s .
d.
38 yr
25 yr
6 yr
1 yr
36 yr
35 yr
12 yr
2 yr
29 yr
27 yr
7 yr
2 yr
30 yr
29 yr
9 yr
33 yr
29 yr
7 yr
1 yr
Hb
g/
100 ml
16.6
14.5
14.4
13.2
17.9
12.6
16.2
14.2
16.6
15.3
16.3
14.5
15.7
14.8
13.8
16.0
15.7
15.5
14.7
Hct
%
45.0
40.0
38.5
38.0
43.5
37.5
37.0
38.5
44.5
40.0
42.0
40.0
41.0
40.0
38.0
43.0
39.5
41.5
39.0
B
BpE/
10 6E
200
0
0
800
2400
0
1000
0
0
0
0
0
700
200
0
500
1300
0
3600
L 0 0 D
Ret
%o
10
31
15
14
20
12
15
24
9
14
8
14
11
10
10
14
23
10
20
EP
ug/ioo
ml E
115.1
205.1
442.0
90.3
69.7
113.8
29.6
74.1
80.6
25.5
76.0
86.2
43.8
30.7
112.2
17.7
31.3
66.6
58.9
ALAD
units
ml E
31.1
19.4
22.7
65.8
102.0
98.3
123.6
47.1
19.6
83.4
52.1
53.1
57.9
103.1
55.6
82.8
129.7
71.9
86.5
Pb
yg/
100 ml
87.9
27.8
73.0
53.6
54.0
18.6
22.0
28.4
69.2
21.5
59.7
47.7
45.8
26.5
32.8
59.7
25.8
50.0
39.8
URINE
ALA Cqproporphyrin
mg/
100 ml
0.66
0.38
1.29
0.35
0.22
0.37
0.35
0.52
0.34
0.33
0.38
0.17
0.41
0.29
0.54
0.29
0.52
0.51
0.24
mg/
24 h
6.27
3.04
1.94
-
1.54
1.66
0.70
-
1.87
0.66
0.95
0.17
4.10
2.90
2.70
2.90
4.16
2.55
-
Ug/
100 ml
12.5
8.5
22.5
-
8.5
6.5
3.5
-
12.5
10.0
3.0
6.5
10.5
5.5
11.0
4.5
8.5
7.0
-
MS/
24 h
119
68
34
-
60
29
7
-
69
20
8
7
105
55
55
45
68
35
-
(continued)
-------
TABLE A-2. (continued)
CO
O
Subject
and
Family re-
community
D.J.
D.M.
D.F.
D.H.
M.J.
M.J.
M.D.
M.N.
P.T.
P.LJ.
P.S.
P.J.
P. IS.
P. A.
P.M.
J.J.
J.M.
J.M.
J.N.
D
D
D
D
C3
C3
C3
C3
D
D
D
C3
C3
C3
C3
Bi
Bi
Bi
BI
lationship Age
f.
m.
s.
d.
f.
m.
d.
d.
m.
d.
s.
f .
m.
d.
d.
f.
m.
s.
d.
38 yr
33 yr
7 yr
1 yr
32 yr
27 yr
6 yr
8 mo
31 yr
11 yr
1 yr
30 yr
28 yr
6 yr
3 yr
33 yr
32 yr
7 yr
2 yr
Hb
g/
100 ml
18.5
14.9
14.1
11.8
17.5
15.2
15.3
13.4
14.0
15.9
14.8
17.8
15.8
14.4
14.9
16.5
15.5
14.7
10.4
Hct
%
43.0
40.0
38.5
37.0
44.0
41.0
39.5
39.5
39.5
42.0
42.5
45.5
43.0
40.5
40.0
44.5
42.5
40.0
36.5
B
BpE/
10 6E
0
0
0
0
0
0
0
700
0
0
5100
0
0
0
0
0
0
•o
0
L 0 0 D
Ret
%o
12
5
7
16
5
25
13
5
13
7
24
12
20
24
13
6
9
8
13
EP
ug/ioo
ml E
130.0
58.4
101.4
112.5
69.2
71.8
320.3
83.4
95.5
37.3
83.7
91.8
75.7
166.0
69.3
36.2
36.9
153.4
532.0
ALAD
units
ml E
31.9
165.0
56.4
136.8
59.6
78.6
27.2
109.1
118.0
123.5
60.5
68.1
120.6
100.3
107.8
36.7
73.8
25.9
34.2
Pb
yg/
100 ml
90.5
47.2
44.0
47.9
69.8
50.2
78.8
54.3
41.1
51.5
63.8
101.6
44.3
59.4
67.2
42.9
32.9
47.2
39.7
ALA
mg/
100 ml
0.57
0.38
0.93
0.49
0.32
0.24
0.41
-
0.29
0.40
-
0.15
0.20
0.17
0.43
0.38
0.33
0.45
0.03
URINE
Coproporphyrin
mg/
24 h
5.70
4.18
0.93
-
4.48
2.40
2.05
-
2.75
2.00
-
1.05
2.00
0.93
1.72
1.90
2.31
2.25
-
]yg/
100 ml
7.5
5.5
9.5
13.5
10.5
6.0
4.5
-
9.0
5.5
-
6.5
8.0
6.0
6.0
5.0
2.0
7.0
-
yg/
24 h
75
61
10
-
147
60
23
-
86
28
-
46
80
33
24
25
14
35
-
(continued)
-------
TABLE A-2 (continued)
u>
Subject
and
community
V.A.
V.A.
V.P.
V.A.
V.F.
V.M.
V.E.
V.L.
P.H.
P.M.
P.T.
P.M.
T.J.
T.A.
T.M.
T.J.
K.J.
K.E.
K.M.
K.M.
Bi
Bi
BI
Bi
A
A
A
A
B2
B2
B2
B2
D
D
D
D
D
D
D
D
Family re-
lationship Age
f.
m.
s.
s.
f.
m.
s .
s.
f.
m.
s .
d.
f .
m.
d.
d.
f.
m.
s.
s.
29 yr
31 yr
7 yr
2 yr
35 yr
24 yr
5 yr
2 yr
32 yr
32 yr
8 yr
2 yr
40 yr
38 yr
15 yr
2 yr
34 yr
33 yr
10 yr
2 yr
Hb
g/
100 ml
17.0
14.1
14.1
13.8
16.6
13.8
13.6
14.8
15.7
14.4
15.3
14.9
18.2
13.8
15.1
11.8
17.3
11.0
14.2
13.6
Hct
%
44.0
39.5
40.0
40.0
44.0
41.0
40.0
41.0
43.0
40.5
42.0
41.0
46.0
42.0
42.0
37.8
45.0
35.5
39.5
38.0
B
BpE/
106E
1000
2100
5300
0
0
0
0
0
500
400
0
0
0
0
0
0
300
0
0
1400
L 0 0 D
Ret
%o
22
15
12
13
9
8
6
7
11
12
13
7
10
11
9
10
12
8
7
15
EP
yg/ioo
ml E
84.1
31.9
61.3
-
282.0
117.3
179.3
185.9
153.2
120.7
305.0
231.1
85.0
69.3
72.9
88.0
116.1
80.3
90.9
43.3
ALAD
units
ml E
52.5
31.6
44.3
24.6
7.1
52.1
29.3
43.9
29.3
91.0
21.7
30.4
38.5
73.8
81.8
114.6
93.6
221.8
71.8
83.2
Pb
yg/
100 ml
35.0
21.4
37.2
32.3
123.7
31.6
39.0
38.6
79.4
41.5
65.3
68.5
95.8
44.3
81.0
55.7
57.2
32.7
48.3
45.8
URINE
ALA Coproporphyrin
mg/ mg/
100 ml 24 h
0.43
0.25
0.54
-
0.62
0.22
0.36
0.15
0.25
0.20
0.16
0.08
0.43
0.38
0.31
0.20
0.51
0.29
0.38
0.32
3.01
3.00
2.63
-
4.96
2.20
1.80
-
3.12
2.50
2.40
-
6.02
2.68
2.17
0.20
4.08
1.59
1.90
—
yg/
100 ml
9.5
9.5
10.0
-
10.5
7.0
16.0
-
12.0
12.0
6.5
-
15.5
7.0
10.5
11.5
12.5
10.0
10.5
—
yg/
24 h
66
114
45
-
84
70
80
-
150
150
98
-
217
49
74
12
100
55
53
-
(continued)
-------
TABLE A-2. (continued)
Subject
and
Family re-
community
M.F.
M.M.
M.D.
M.R.
P.J.
P.M.
P.M.
P.T.
P.O.
P. A.
P.M.
P.N.
L.S.
L.R.
L.M.
L.A.
D.D.
D.A.
D.B.
D.J.
C3
C3
C3
C3
B2
B2
B2
B2
D
D
D
D
D
D
D
D
D
D
D
D
lationship Age
f.
m.
d.
s .
f.
m.
s.
s.
f .
m.
d.
d.
f .
m.
s .
d.
f .
m.
s.
s.
41 yr
36 yr
10 yr
2 yr
35 yr
27 yr
8 yr
1 yr
35 yr
39 yr
11 yr
2 yr
35 yr
35 yr
10 yr
2 yr
38 yr
30 yr
8 yr
2 yr
Hb
g/
100 ml
16.7
16.3
15.1
12.8
15.0
14.4
14.4
13.5
17.5
12.6
14.2
13.4
16.1
14.1
13.0
12.3
17.7
15.3
15.1
12.3
Hct
%
45.7
42.5
42.5
39.0
42.0
40.0
40.5
39.0
44.0
39.0
38.0
38.0
43.7
41.0
39.0
37.7
45.0
44.5
43.2
37.2
B
BpE/
106E
1600
0
0
0
3200
0
0
0
300
0
0
0
1400
200
0
0
0
0
0
0
L 0 0 D
Rtc
%o
17
17
12
9
19
14
7
7
12
10
10
8
18
14
9
11
10
9
8
11
EP
yg/100
ml E
410.9
25.0
87.0
217.6
371.7
48.1
87.8
125.9
45.4
75.6
87.9
188.5
69.7
67.8
144.7
150.1
21.8
12.8
64.6
81.0
ALAD
units/
ml E
13.1
131.4
68.8
66.3
5.9
67.1
48,7
73.7
61.9
100.9
101.3
64.8
55.7
55.1
66.9
94.1
145.5
86.2
90.8
64.5
Pb
yg/
100 ml
110.1
43.3
55.1
35.5
62.1
21.5
38.4
36.5
52.3
32.4
27.7
40.5
66.7
21.5
43.6
29.3
35.0
33.8
42.2
33.6
ALA
mg/
100 ml
0.72
0.38
0.15
-
1.00
0.51
0.45
0.40
0.28
-
0.35
0.13
0.47
0.29
0.68
0.49
0.67
0.38
0.46
-
URINE
Coproporphyrin
mg/
24 h
3.60
2.66
0.98
-
7.00
4.08
2.25
-
1.40
-
1.75
0.26
0.94
2.03
4.62
-
6.16
3.80
2.99
-
yg/
yg/
100 ml 24 h
_
6.0
3.5
-
210.0
15.0
12.5
-
10.0
-
3.0
11.0
10.0
8.0
9.5
-
9.0
9.5
10.0
-
__
42
23
-
1470
120
63
-
50
—
15
22
20
56
65
-
83
95
65
-
(continued)
-------
TABLE A-2. (continued)
Subject
and Family re-
community lationship
K.V. D
K.S. D
K.D. D
f. - father
m. - mother
s. - son
d. - daughter
f.
m.
d.
Hb
g/
Age 100 ml
42 yr 15.6
41 yr 14.5
11 yr 14.7
B
Hct BpE/
% 106E
44.0 0
41.0 0
41.7 0
LOO
Rtc
%o
8
8
10
D
EP
yg/ioo
ml E
294.2
71.4
246.5
U R I N
ALAD
units/
ml E
16.6
102.1
62.9
Pb
yg/
100 ml
65.1
31.6
61.9
ALA
mg/
100 ml
0.79
0.64
0.49
E
Coproporphyrin
mg/
24 h
7.11
3.20
3.43
yg/
100 ml
6.5
21.6
6.0
yg/
24 h
59
108
42
-------
TABLE A-3. CONTROL GROUP
OJ
Subject
and
Family re-
community
O.D.
O.A.
O.M.
H.A.
H.M.
H.A.
H.R.
V.F.
V.C.
V.A.
V.M.
P.F.
P.M.
P.J.
P.M.
P.I.
P.S.
P.G.
P.B.
E
E
E
F
F
•F
F
F
F
F
F
E
E
E
E
E
E
E
E
lationship Age
f .
m.
d.
f .
m.
d.
s.
f.
m.
d.
d.
f.
m.
d.
d.
f.
m.
d.
d.
44 yr
44 yr
2 yr
36 yr
35 yr
9 yr
3 yr
35 yr
35 yr
7 yr
3 yr
38 yr
36 yr
10 yr
2 yr
46 yr
40 yr
14 yr
2 yr
Hb
g/
100 ml
18.1
15.2
14.1
16.7
15.9
14.1
12.3
16.6
13.5
13.4
13.2
16.7
13.7
13.9
13.8
16.6
16.1
16.1
13.2
Hct
%
46.0
42.0
45.0
45.0
42.0
40.5
38.0
44.5
38.5
38.5
36.0
45.0
40.0
37.5
38.0
38.0
44.0
40.0
39.5
B L
BpE/
106E
0
0
0
0
0
0
400
0
0
0
0
0
0
0
0
0
0
600
200
0 0
Rtc
%o
7
13
10
12
10
9
12
7
11
7
8
13
10
10
16
11
10
14
10
D
EP
yg/ioo
ml E
11.6
9.9
9.4
20.9
22.3
7.2
24.6
17.8
11.6
17.9
12.6
10.4
9.2
10.8
15.1
11.6
10.3
11.2
9.3
U R I N
ALAD
units
ml E
160.1
177.1
170.6
147.2
173.2
173.1
161.8
91.0
212.7
170.5
205.6
129.2
178.4
195.0
172.0
185.9
156.5
190.0
199.1
Pb
yg/
100 ml
50.6
44.4
29.3
49.1
39.7
35.4
29.1
30.0
31.9
24.4
28.8
47.2
33.0
35.4
26.4
42.2
24.6
29.9
22.8
ALA
mg/
100 ml
0.50
0.49
0.42
0.67
0.28
0.45
0.31
0.19
0.54
0.23
0.39
0.38
0.29
0.41
0.35
0.19
0.29
0.28
0.23
E
Copjroporphyrin
mg/
24 h
3.00
2.70
0.84
3.35
3.36
1.40
1.09
3.04
6.75
0.92
1.56
0.68
1.31
4.72
0.28
3.42
4.06
0.48
0.55
yg/
yg/
100 ml 24 h
21
9
11
21
13
17
15
9
8
9
6
12.
6
8
20
4
9
20
12
126
50
22
105
156
53
53
144
100
36
24
23
27
92
16
72
126
34
29
(continued)
-------
TABLE A-3. (continued)
OJ
Oi
Subject
and
Family re-
community lationship Age
V.I.
V.A.
V.J.
V.E.
N.I.
N.H.
N.M.
N.A.
V.S.
V.A.
V.H.
V.S.
K.F.
K.M.
K M.
K.F.
J.F.
J.M.
J.L.
* _
F
F
F
F
G
G
G
G
F
F
* F
* F
F
F
F
F
G
G
G
twins
f .
m.
d.
d.
f.
m.
s.
s.
f .
m.
d.
d.
f.
m.
s.
s.
f.
m.
d.
43 yr
41 yr
6 yr
3 yr
39 yr
37 yr
9 yr
1 yr
35 yr
25 yr
2 yr
2 yr
38 yr
32 yr
10 yr
3 yr
46 yr
43 yr
1 yr
Hb
g/
100 ml
19.0
14.8
12.7
13.4
18.3
14.1
13.4
12.7
18.1
14.6
15.0
14.5
17.0
15.7
14.3
13.5
18.1
15.2
12.7
Hct
%
40.0
42.0
40.0
36.0
40.0
41.0
40.5
37.0
46.0
40.0
40.0
40.0
45.0
42.0
39.0
37.0
46.0
43.5
36.0
B L
BpE/
106E
800
0
0
0
0
0
0
0
0
800
4600
600
0
0
0
400
0
0
0
0 0
Rtc
%o
22
34
25
9
8
8
8
8
9
24
10
12
10
8
7
12
7
10
7
D
EP
yg/ioo
ml E
18.2
9.0
11.6
10.9
12.9
11.5
10.4
10.6
12.6
15.4
11.4
12.0
10.6
5.6
5.9
8.9
11.9
16.9
17.0
ALAD
units
ml E
195.6
179.8
176.5
217.0
202.9
213.4
170.4
152.0
174.7
153.1
217.5
206.9
162.2
129.8
158.7
185.1
145.7
162.9
204.9
Pb
yg/
100 ml
49.3
37.3
31.0
32.4
50.8
29.6
26.0
28.2
22.4
18.8
13.2
29.4
28.2
24.8
23.5
32.6
31.5
19.1
29.5
U
ALA
mg/
100 ml
0.73
0.31
0.19
0.38
0.27
0.28
0.14
—
0.25
0.28
0.38
0.47
0.29
0.39
0.28
0.32
0.45
0.30
0.25
R I N
E
Coproporphyrin
mg/
24 h
5.11
1.86
0.67
0.57
2.43
2.80
0.42
-
2.65
3.64
0.76
0.71
2.12
1.95
1.26
0.64
4.05
1.38
0.25
yg/ yg/
100 ml 24 h
12
13
8
10
13
21
10
—
15
12
12
8
12
15
8
8
7
10
8
(continued)
84
78
28
15
117
210
30
-
158
156
24
12
88
80
36
16
63
46
8
-------
TABLE A-3. (continued)
Subject
and
community
P.J.
P.V.
P.M.
D.F.
D.E.
D.E.
A.G.
A.J.
A.T.
J.F.
J.A.
J.T.
K.F.
K.E.
K.A.
H
H
H
H
H
H
H
H
H
H
H
H
E
E
E
Family re-
lationship Age
f .
m.
s .
f.
m.
d.
f .
m.
s.
f.
m.
d.
f.
m.
s.
29 yr
27 yr
2 yr
39 yr
38 yr
1 yr
25 yr
21 yr
2 yr
29 yr
31 yr
2 yr
25 yr
22 yr
11 mo
Hb
g/
100 ml
17.3
14.6
13.3
17.3
14.8
12.7
14.3
15.9
12.7
17.3
15.5
13.7
16.4
11.9
12.8
Hct
45.0
41.0
39.0
44.5
42.0
36.5
49.0
44.0
38.0
44.5
43.0
39.5
44.0
38.5
38.0
B L
BpE/
106E
0
0
0
0
0
0
0
0
0
0
0
600
0
0
0
0 0
Rtc
%o
10
9
18
12
11
7
9
10
9
12
8
12
7
9
8
D
EP
yg/ioo
ml E
14.1
29.5
16.9
9.5
8.6
18.6
9.0
13.8
9.3
12.6
10.6
13.1
10.5
76.0
13.5
ALAD
units
ml E
144.2
178.4
200.6
143.3
162.8
206.8
157.1
184.4
180.9
121.6
178.8
190.1
142.3
198.1
165.5
Pb
yg/
100 ml
32.5
27.3
31.8
38.4
20.2
33.6
31.5
22.4
35.0
36.6
29.3
35.9
31.5
19.4
30.8
U
R I N E
ALA Coproporphyrin
mg/
100 ml
0.28
0.30
0.35
0.57
0.14
0.53
0.25
0.18
0.30
0.41
0.39
0.29
0.27
0.47
mg/
24 h
2.24
1.20
3.15
3.42
0.04
4.24
1.25
0.54
2.70
4.92
0.19
1.31
1.62
0.28
yg/ yg/
100 ml 24 h
7
10
9
22
-
4
17
11
4
13
-
20
12
-
56
40
81
132
-
32
85
33
36
156
-
90
72
-
(continued)
-------
TABLE A-3. (continued)
P.J.
BLOOD
URINE
Subject
and
community
P.J. I
P.P. I
Family re-
lationship Age
f. 31 yr
m. 29 yr
Hb
g/
100 ml
15.7
14.4
Hct
%
44.0
40.0
BpE/
106E
0
0
Rtc
%o
11
6
EP
yg/100
ml E
13.8
17.5
ALAD
units
ml E
116.5
204.4
Pb
yg/
100 ml
30.6
19.9
ALA
mg/
100 ml
0.32
0.38
Coproporphyrin
mg/
24 h
2.56
2.81
yg/
100 ml
10
8
yg/
24 h
80
59
8.
3 yr 13.6
39.0
0 11 21.2
170.2 42.0
0.37
0.52
10
f.
m.
s.
d.
- father
- mother
- son
- daughter
-------
TECHNICAL REPORT DATA
(Please read Instructions on the reverse before completing)
1. REPORT NO.
EPA-600/1-78-067
2.
3. RECIPIENT'S ACCESSION NO.
4. TITLE AND SUBTITLE
STUDY OF CHILDREN'S BLOOD-LEAD LEVELS WITHIN FAMILIES
5. REPORT DATE
November 1978
6. PERFORMING ORGANIZATION CODE
7. AUTHOR(S)
Danica Prpic-Majjic
8. PERFORMING ORGANIZATION REPORT NO.
9. PERFORMING ORGANIZATION NAME AND ADDRESS
Institute for Medical Research and Occupational
Health
Zagreb, Yugoslavia
10. PROGRAM ELEMENT NO.
1AA601
11 CONTRACT/GRANT NO.
SFCP-JF-3-570-3
12. SPONSORING AGENCY NAME AND ADDRESS
Health Effects Research Laboratory
Office of Research and Development
U.S. Environmental Protection Agency
Research Triangle Park, N.C. 27711
13. TYPE OF REPORT AND PERIOD COVERED
14. SPONSORING AGENCY CODE
EPA 600/11
15. SUPPLEMENTARY NOTES
16. ABSTRACT .
Comparative studies of the biological indices of elevated exposure to lead in
children and adults were conducted with the intention of reaching a better under-
standing of lead absorption in children. Three family groups were examined. Group 1
consisted of families who lived in the vicinity of a lead smelter and whose fathers
were occupationally highly exposed to lead. Group 2 consisted of families settled
in the same area, but whose fathers had no supplemental occupational exposure to lead.
The third was the control group consisting of families who lived in an area with very
low exposure and whose fathers were not occupationally exposed to lead. Families
were selected with one child under 4 years and, If possible, another child of school
age. In the environmental survey lead in air, dustfall, household-dust, and
drinking-water were analyzed. Three biological parameters, erythrocyte school-age children - children up to 4 years > mothers. Children with
fathers occupationally exposed to lead had a slight additional lead exposure in
comparison with children whose fathers had no supplemental occupational exposure to
lead. It was found that the population living near a lea,d smelter, except for the
fathers occupationally exposed to lead, had biological findings at the level of a
while the
tionally exposed
GKCGS01VG
17.
exposure.
KEY WORDS AND DOCUMENT ANALYSIS
DESCRIPTORS
b.IDENTIFIERS/OPEN ENDED TERMS
c. COSATI Held/Group
lead (metal)
children
blood analysis
occupational diseases
environmental surveys
06 F, T
DISTRIBUTION STATEMENT
RELEASE TO PUBLIC
19. SECURITY CLASS (ThisReport)
UNCLASSIFIED
20- s,^y!".T^.CLASSttTM, page)
21. NO. OF PAGES
153
3. SECURITY CLASS ('
UNCLASSIFIED
22. PRICE
EPA Form 2220-1 (Rev. 4-77) PREVIOUS EDITION is OBSOLETE
138
------- |