ENVIRONMENTAL ASSESSMENT OF THE
DOMESTIC PRIMARY COPPER, LEAD
AND ZINC INDUSTRIES
VOLUME II - APPENDICES
PEDCo ENVIRONMENTAL
-------
PEDCo- ENVIRONMENTAL
SUITE 13 • ATKINSON SQUARE
CINCINNATI. OHIO 45246
513/77 1-433O
ENVIRONMENTAL ASSESSMENT OF THE
DOMESTIC PRIMARY COPPER, LEAD
AND ZINC INDUSTRIES
VOLUME II - APPENDICES
Prepared by
PEDCo-Environmental Specialists, Inc.
Suite 13, Atkinson Square
Cincinnati, Ohio 45246
Contract No. 68-02-1321
Task No. 38
EPA Project Officer
Margaret J. Stasikowski
Prepared for
U.S. ENVIRONMENTAL PROTECTION AGENCY
Industrial Environmental Research Laboratory
5555 Ridge Avenue
Cincinnati, Ohio 45268
November, 1976
BRANCH OFFICES
Suite 110, Crown Center Suite 107-B Professional Village
Kansas City, Mo. 64108 Chapel Hill. N.C. 27514
-------
DISCLAIMER
This report has been reviewed by the Industrial Environmental 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 con-
stitute endorsement or recommendation for use.
-------
ABSTRACT
This report presents the results of a multi-media (air, water, and
solid waste) study of the environmental impacts from the U.S. primary
copper, lead and zinc industries. The open literature was surveyed to
identify and describe all processes employed by these industries and to
characterize pollutant effluents and environmental effects from those
processes. Various pollution control systems are described and eval-
uated for domestic application, and alternate production processes are
reviewed.
Principal environmental impacts from the copper industry are air
emissions of S02 and trace metals from smelting operations. Insuffi-
cient markets for by-product sulfur compounds are a disincentive for SO?
control. Water pollution problems include acid drainage and trace metal
contamination of wastewaters from ore beneficiation processes. The fact
that many mines and smelters are located in remote arid regions tends to
mitigate the severity of these pollution problems. Newer hydrometallur-
gical processes may produce leach residues that will require further
efforts to control.
Lead is produced by six pyrometallurgical smelters in this country.
There are large lead deposits in the State of Missouri so that a large
percentage of future lead supplies are expected to originate in that
state. Mining and concentrating operations produce metal-laden waste-
waters that are effectively controlled in the Missouri area by biotic
degradation and natural precipitation at high pH. Principal smelter
emissions include S02 and particulates from sintering and blast furnace
operations. Electrostatic precipitators, baghouses, and sulfuric acid
plants are used for pollution control.
Zinc smelters are mainly located in populated areas and have large-
ly been forced to clean up their emissions in recent years. Economic
prospects have forced several smelters to close in recent years. SC>2 is
controlled at all smelters by means of acid plants. Particulates are
controlled by electrostatic precipitators and baghouses. There is some
concern that volatile metals may pass through these control devices in
the vapor phase.
Several programs for further research and development are indi-
cated.
-------
IV
-------
CONTENTS
Pacje.
ABSTRACT
FIGURES
TABLES
ACKNOWLEDGMENT
1.0 INTRODUCTION
2.0 COPPER INDUSTRY
Industry Description
Industry Analysis, Copper
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
Process
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
No.
1,
2,
3,
4,
5,
6,
7,
8,
9,
10,
11,
12,
13,
14,
15,
16,
17,
18,
19,
20,
21,
22,
23,
24,
25,
26,
27,
28,
29,
30,
31,
32,
33,
34,
35,
36,
37,
38,
39,
Mining
Concentrating
Multiple-Hearth Roasting
Fluidization Roasting
Drying
Reverberatory Smelting
Electric Smelting
Flash Smelting
Peirce-Smith Converting
Hoboken Converting
Noranda
Slag Treatment
Contact Sulfuric Acid Plant
DMA S02 Absorption
Elemental Sulfur Production
Arsenic Recovery
Fire Refining and Anode Casting
Electrolytic Refining
Electrolyte Purification
Melting and Casting Cathode Copper
Slime Acid Leach
CuSO, Precipitation
Slimes Roasting
Slime Water Leach
Dore Furnace
Scrubber
Soda Slag Leach
Selenium and Tellurium Recovery
Dore Metal Separation
Heap and Vat Leaching
Cementation
Solvent Extraction
Electrowinning
Sulfation Roasting
Sponge Iron Plant
CLEAR Reduction
CLEAR Regeneration - Purge
CLEAR Oxidation
39, Cymet Leaching
1
12
12
27
30
35
42
50
53
55
64
67
70
77
79
81
83
90
93
95
98
106
110
114
117
119
121
123
125
127
129
131
133
135
138
140
142
144
146
148
150
152
154
-------
CONTENTS (Continued)
Process No.
No.
3.0
Process
Process No.
Process No.
Process No.
Process No.
LEAD INDUSTRY
Industry Description
Industry Analysis
40,
41,
42,
43,
44,
45,
Cymet Crystallization
Cymet Reduction
Cymet Solvent Regeneration
Arbiter Leaching
Arbiter Precipitation
Arbiter Decomposition
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
4.0
Process No
ZINC INDUSTRY
Industry Description
Industry Segment Analysis
1, Mining
2, Concentrating
3, Sintering
4, Acid Plant
5, Blast Furnace
6, Slag Fuming Furnace
7, Dressing
8, Dross Reverberatory Furnace
9, Cadmium Recovery
10, Reverberatory Softening
11, Kettle Softening
12, Harris Softening
13, Antimony Recovery
14, Parkes Desilverizing
15, Retorting
16, Cupelling
17, Vacuum Dezincing
18, Chlorine Dezincing
19, Harris Dezincing
20, Debismuthizing
21, Bismuth Refining
22, Final Refining and Casting
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
Process No
1, Mining
2, Concentrating
3, Multiple-Hearth Roasting
4, Suspension Roasting
5, Fluidized-Bed Roasting
6, Sintering
7, Horizontal Retorting
8, Vertical Retorting
9, Electric Retorting
10, Oxidizing Furnace
11, Leaching
12, Purifying
13, Electrolysis
Process No. 14, Melting and Casting
Page
156
157
158
159
161
163
165
165
169
172
176
184
193
195
203
208
212
214
215
218
220
222
224
226
228
230
232
233
235
237
239
241
241
253
256
259
268
272
275
279
285
293
299
303
307
311
313
318
VI
-------
CONTENTS (Continued)
Process No. 15, Cadmium Leaching 320
Process No. 16, Cadmium Precipitation 323
Process No. 17, Cadmium Purification and Casting 325
5.0 AIR MANAGEMENT 328
Emission Characteristics 328
Emission Control Systems 330
Fugitive Emissions 333
6.0 WATER MANAGEMENT 335
Sources of Secondary Water Pollution 335
Concentrator Effluent 337
Sulfide Weathering 338
Waste Characteristics 340
Waste Handling and Treatment 341
Advanced Treatment 352
7.0 EMERGING TECHNOLOGY 359
8.0 RECOMMENDED RESEARCH AND DEVELOPMENT PROGRAMS 382
APPENDICES
A. HEALTH EFFECTS OF PRIMARY COPPER, LEAD AND ZINC SMELTING 398
1. SELECT REVIEW OF PUBLISHED TOXICOLOGY AND EPIDEMIOLOGY 399
2. AN EPIDEMIOLOGICAL ANALYSIS OF DISEASE SPECIFIC MORTALITY 447
ASSOCIATED WITH PRIMARY Cu, Pb and Zn SMELTING
3. CONCLUSIONS AND AN ASSESSMENT OF THE PUBLIC HEALTH 480
HAZARD OF PRIMARY Cu, Pb and Zn SMELTING
B. ECOLOGICAL EFFECTS 482
-------
LIST OF FIGURES
No. Page
1-1 Yearly Copper, Lead, and Zinc Commodity Prices, 1962-1976 5
1-2 Primary U.S. Nonferrous Smelting and Refining Locations 9
2-1 Copper Industry Flow Sheet 28
3-1 Lead Industry Flow Sheet 170
4-1 Zinc Industry Flow Sheet 254
vm
-------
LIST OF TABLES
No. Page
1 Copper Industry Summary of Process Waste Streams 4
2 Lead Industry Summary of Process Waste Streams 11
3 Zinc Industry Summary of Process Waste Streams 16
1-1 By-Product Elements of The Industries - 1975 3
1-2 By-Products - Primary Non-Ferrous Smelter and 6
Refineries
1-3 Mine Production of Copper, Lead, and Zinc by States 10
(1975)
2-1 Copper Minerals Important in U.S. Production 13
2-2 Typical Analysis of Copper Ore Used at White Pine 15
Copper Company, Michigan
2-3 Consumption of Refined Copper in 1975 16
2-4 Salient Statistics of the Primary Copper Industry in 18
the United States in 1974
2-5 Largest By-Product Sulfuric Acid Producers - 1974 19
2-6 U.S. Primary Copper Producers (Conventional Smelting/ 20
Refining Operations)
2-7 Twenty-Five Leading Copper Mines in the United States 21
in 1974
2-8 1976 Survey of Mine and Plant Expansions in the 23
United States
2-9 Annual Generation of Hazardous Pollutants from Primary 24
Copper Industry - 1968 (metric tons)
IX
-------
LIST OF TABLES (continued)
No. Page
2-10 Raw Waste Load in Water Pumped from Selected Copper 31
Mines
2-11 Analysis of Copper Concentrate 37
2-12 Typical Flotation Collectors 38
2-13 Typical Size Profile of Multiple-Hearth Copper Roaster 44
Effluents
2-14 Concentration and Weight Analysis of Particulate 45
Effluents from a Multiple-Hearth Copper Roaster
2-15 Typical Levels of Volatile Metals in Domestic Copper 46
Ore Concentrations
2-16 Composition of Reverberatory Furnace Exhaust Gases 58
2-17 Effluents from Slag Granulation (mg/1) 59
2-18 General Range of Reverberatory Furnace Slag Com- 60
position
2-19 Material Balance on Converters - Smelters in Arizona 71
(percent)
2-20 Composition of Converter Dust 72
2-21 Particle Size Distribution in Converter Dust 73
2-22 Particulate Emissions Analysis at Stack Outlet for 73
Reverberatory Furnace and Converter
2-23 Converter Off-Gas Composition 74
2-24 Estimated Maximum Impurity Limits for Metallurgical 85
Off-Gases Used to Manufacture Sulfur Acid (Approxi-
mate limit, (mg/Nm3)
2-25 Raw Waste Characterization: Acid Plant Slowdown 86
2-26 Acid Plant Slowdown Control and Treatment Practices 88
2-27 Analysis of Arsenic Plant Washdown Water 97
-------
LIST OF TABLES (continued)
No. Page
2-28 General Range Analysis of Anode Copper 99
2-29 Water Requirements for Copper Refineries 101
2-30 Waste Effluents from Anode Cooling Water 102
2-31 Contact Cooling Water Control and Treatment Practices 103
2-32 General Range Analysis of Electrolyte, Refined Copper 108
and Anode Slime
2-33 Waste Effluents from NiSO, Barometric Condenser 112
2-34 Analysis of Water Used to Cool Refinery Shapes 116
(Concentrations in mg/1)
2-35 Dore Metal Analysis 125
3-1 Lead Minerals, By Name, and Composition 166
3-2 Domestic Primary Lead Producers 168
3-3 Analysis of a Missouri Mine Water 174
3-4 Typical Southeastern Missouri Lead Concentrate 178
Analyses (Percent by weight)
3-5 Western Lead Concentrate Analyses 179
3-6 Flotation Chemicals 180
3-7 Lead Mill Wastewater Analysis 181
3-8 Sinter Analysis 185
3-9 Sinter Machine Feed 185
3-10 Grain Loading and Weight Analysis of Input Feed and 188
Effluents-Updraft Lead Sintering Machine
3-11 Typical Size Profile of Effluents, Updraft Lead 188
Sintering Machine
-------
LIST OF TABLES (continued)
No. Page
3-12 Analysis of Sinter Machine Exhaust Gases (Missouri 189
Lead Operating Company)
3-13 Atmospheric Control Systems on Primary Lead Sintering 190
Machines
3-14 Wastewater Treatment at Primary Lead Acid Plants 194
3-15 Scrubber Wastewater Treatment at Primary Lead Plants 194
3-16 Lead Bullion Composition 196
3-17 Typical Blast Furnace Slag Analysis 197
3-18 Typical Blast Furnace Charge 198
3-19 Atmospheric Control Systems on Primary Local Blast 200
Furnaces
3-20 Waste Effluents from Slag Granulation 204
3-21 Primary Lead Slag Granulation Wastewater Treatment 206
3-22 Lead Bullion Analysis Basic: As drossed 209
3-23 Typical Compositions of Softened Lead Bullion and 216
Slag (Amounts in weight percent)
3-24 Typical Retort Analysis 226
4-1 Mining, Production, and Consumption of Zinc and 242
Cadmium (metric tons)
4-2 Twenty-Five Leading Zinc Mines in the United States 243
4-3 Common Ores Mines for Their Zinc Content 246
4-4 U.S. Slab Zinc Consumption - (1975) 248
4-5 Grades of Commercial Zinc 248
4-6 Primary Zinc Processing Plants in the United States 250
4-7 Range of Compositions of Zinc Concentrates 261
XII
-------
LIST OF TABLES (continued)
No. Page
4-8 Typica.1 Flotation Reagents Used for Zinc Concentra- 262
tions
4-9 Ranges of Constituents of Wastewaters and Raw Waste 264
Loads for Five Selected Mills
4-10 Product Sinter Composition (percent) 280
5-1 Elemental Analysis of Particulate Size Fractions 329
1-1 A Classification of the Effects of Metals 400
1-2 Target Organs of Metals 402
•3
1-3 Acceptable Average Concentrations (v>g/m ) of 403
Occumpational Expsoure Based on 8-Hours Exposures
1-4 Tolerance Levels for Metals in Drinking Water and 404
Results of Sampling of Community Water Supplies
(969) in 1969
1-5 Metal Carcinogenesis in Experimental Animals 405
1-6 Effects of Metals on Reproduction 406
1-7 Body Burden and Human Daily Intake and Content in 407
the Earth's Crust of Selected Elements
1-8 Some Toxic Levels of Cadmium Exposure 411
1-9 Effects of Inorganic Lead Salts in Relation to 414
Absorption
1-10 Distribution of Sequelae Following Various Modes of 416
Onset in 425 Patients with Plumbism
2-1 Causes of Death used to Generate Mortality Profiles 449
for Counties Containing Cu, Pb, or Zn Smelters
2-2 Cancer Mortality Rates from 1950-1969 for Counties 450
in the ARea of the Bunker Hill Lead Smelter
2-3A Liver and Biliary Passages Cancer Mortality Rankings 452
for Counties in the Area of the Bunker Hill Lead
Smelter
xm
-------
LIST OF TABLES (continued)
No. Page
2-3B Trachea, Lund and Bronchus Cancer Mortality Rankings 453
for Counties in the Area of the Bunker Hill Lead
Smelter
2-3C Kidney Cancer Mortaility Rankings for Counties in the 454
Area of the Bunker Hill Lead Smelter
2-3D Bladder Cancer Mortality Rankings for Counties in the 455
Area of the Bunker Hill Lead Smelter
2-3E Thyroid Cancer Mortaility Rankings for Counties in the 456
Area of the Bunker Hill Lead Smelter
2-3F Mortaility Rankings for all Cancers Combined for 457
Counties in the Area of the Bunker Hill Lead Smelter
2-4 Lead Smelter Cancer Mortality Data Summary 458
2-5 Zinc Smelter Cancer Mortality Data Summary 459
2-6 Copper Smelter Cancer Mortality Data Summary 460
2-7 Lead Smelter Non-Cancer Mortality Data Summary 461
2-8 Zinc Smelter Non-Cancer Mortality Data Summary 462
2-9 Copper Smelter Non-Cancer Mortality Data Summary 463
2-10 Observed Mortality Associations for Counties 466
Containing Primary Lead Smelters
2-11 Observed Mortality Association for Counties 467
Containing Primary Zinc Smelters
2-12 Observed Mortality Associations for Counties 468
Containing Primary Copper Smelters
2-13 Copper, Lead or Zinc Smelter-Containing Counties with 472
Significantly Elevated Cancer Mortality Rates
2-14 Definition of Ranges of Element Concentrations in Cu 474
and Zn Smelter Ore Concentrates
2-15 Quantities of Nine Elements in Zn Smelters Ore 475
Concentrates
2-16 Quantities of Nine Elements in Cu Smelter Ore 476
Concentrates
xiv
-------
ACKNOWLEDGMENT
This report was prepared by PEDCo-Environmental Specialists, Inc.,
under the direction of Mr. Timothy W. Devitt. Principal authors were
Dr. Gerald A. Isaacs, Mr. Thomas K. Corwin, Mr. Hal M. Drake, Mr.
Douglas J. Morell, and Mr. Jeffrey A. Smith.
Project officer for the U.S. Environmental Protection Agency was
Ms. Margaret J. Stasikowski.
The authors appreciate the efforts and cooperation of everyone who
participated in the preparation of this report.
xv
-------
XVI
-------
APPENDIX A
HEALTH EFFECTS OF PRIMARY COPPER,
LEAD AND ZINC SMELTING
-------
1.0 SELECT REVIEW OF PUBLISHED TOXICOLOGY AND EPIDEMIOLOGY
TOXICOLOGY OF METALS
In order to realistically assess the toxic potential of residual
metals emitted from smelters or other sources, several general concepts
must be appreciated. Smelter residual metal emissions differ widely in
both composition and quantities of individual metals. Although the
toxic properties of each individual metal within an emission stream may
be known, the combined toxic effect of the stream is not necessarily the
simple sum of the effects of the components. Some elements such as Ca
and Zn seem to mitigate the toxic effects of other metals such as Cd and
Pb, while other combinations of metals probably produce greater than
additive adverse effects. Another dilemma is encountered when consid-
ering carcinogenic or teratogenic effects of metals. Although occupa-
tional exposure limits for carcinogens such as As, Ni and Cr and tera-
togens such as Cd and Se have been established, no one really knows what
concentration of a given carcinogen or teratogen is safe. With these
considerations in mind, the toxic potentials of individual metals are
discussed, and supposed safe levels of exposure to carcinogens are
presented.
Summary of the Toxicity of Metals
Table 1-1 lists of types of effects various metals would be ex-
pected to produce. Metals indicated as possible "Factors in Environ-
mental Nonoccupational Disease" are generally those which tend to accu-
mulate in animal tissue. As shown in Table 1-1, most metals which are
probable factors in environmental disease are also moderate to severe
industrial hazards. Another significant point illustrated by the table
is that some of the metals which play a role in environmental disease
are also essential elements for mammals. As is generally true for most
substances, metal toxicity is dependent upon concentration and length of
exposure. Thus, Table 1-1 reflects current knowledge concerning the
quantities and concentrations of metals usually encountered.
As discussed in the introduction to this section, typical sources
of metal emissions do not emit only one element, and the effects of a
combination of metals in an emissions stream can only very rarely be
predicted. For this reason, one of the most important aspects of en-
vironmental toxicology is to indicate what types of disease may be
caused by complex combinations of metals so that epidemic!ogical inves-
399
-------
Table 1-1. A CLASSIFICATION OF THE EFFECTS OF METALS'
Matal
Aluminum
Antimony
Arsenic
Barium
Beryllium
Bismuth
Boranes
Cadmium
Cesium
Chromium (III)
Chromium (VI)
Cobalt
Copper
Gallium
Germanium
Gold
Hafnium
Indium
Iridium
Iron
Lanthanons
Lead
Magnesium
Manganese
Mercury
Metal hydrides
and Carbonyla
Molybdenum
Nickel
' Niobium
!
Palladium
Platinum
Rhenium
Rubidium
Selenium
Silver
Strontium
Tantalum
Tellurium
Thallium
Tin (organic)
Titanium
Tungsten
Uranium
Vanadium
Zinc
Zirconium
Essential
For Mammals
+
+•
+•
+•
+
+
_)_
+
+
+
+•
Moderate to
Severe
Industrial
Hazard
+
t
+
+
+•
+
+
+
+
*
+
*
+
+
*
*
*
+
. Factors in
Environmental
Nonoccupational
Disease
+
+
+
+
+
+
+
+
+
7
Accidental
Poisoning
+ •
4-
>
x_-
+
4-
+
+ .
+
*
7
Limited
Industrial
Hazard
+
+
+
+
+
+
+
+
+
+
+
+
+
+
•f
I
4-
+
+
+
+
+
7
+
400
-------
tigations will have a starting point. Table 1-2 lists the target organs
of individual metals. Knowledge of which organs are affected by which
metals is essential for the success of any epidemiological analyses of
sources emitting residual metals.
Maximum allowable concentrations for metals in both workroom air
and drinking water have been established and are listed in Tables 1-3
and 1-4. It must be emphasized that these values represent probable
safe values only in the absence of all other toxic substances. For
example, a worker exposed to 500 yg As/m3, 200 yg/m3 Cd dust, 1000 yg
Ni/nr, 500 yg Sb/m3 and 500 yg/m3 V205 dust simultaneously would prob-
ably develop respiratory disease if exposure continued long enough.
Each one of those respiratory disease producing metals at its maximum
allowable concentration (Table 1-3) would probably be safe (disregarding
carcinogenic potentials), but all five present together at their maximum
allowable concentrations probably would not. Values listed in Table 1-3
do not apply to 24 hour/day - 7 day/week exposures, and even values
lowered proportionately to the increased exposure time may not be suf-
ficient to protect the public health. Although the exposure limits
summarized in Tables 1-3 and 1-4 have severe limitations when consid-
ering the environmental toxicology of metals, an idea of relative toxic-
ity may be safely extracted. For example, from Table 1-3, it is clear
that molybdenum is less toxic than mercury.
In Section 2.0, the associations between Cu, Pb and Zn smelters and
increases in mortality from cancers is presented. It is now apparent
that As, Ni and Cr cause respiratory cancers in man, but at this point,
human cancer of the liver, kidney, bladder and thyroid have not been
linked to metals. However, animal studies have linked many other malig-
nant neoplasms besides respiratory cancers to metal exposure, and the
associations presented in Section 2.0 link Cu, Pb and Zn smelting to
many cancers as well as respiratory ones. For these reasons, the car-
cinogenic potential of metals upon experimental animals is detailed in
Table 1-5. Similarly, the teratogenic potential of metals upon animals
is presented in Table 1-6. Even though sufficient statistical data to
adequately evaluate the teratogenic associations of smelters is lacking,
the large number of associations between cancers and smelters would
indicate that metals emitted from Cu, Pb and Zn smelters may be linked
with human teratogenesis.
As a final note, it should be kept in mind that environmental
exposure to metals from smelters of some other facility is not the sole
source of metal intake. Metals are contained in food, water and are
normal components of the earth's crust. Table 1-7 lists typical human
intake and body burden of metals as well as natural abundance of the
various metals.
401
-------
Table 1-2. TARGET ORGANS OF METALS'
Gastro-
intestinal
Metals Tract
Aluminum
Antimony +
Arsenic +
Barium +
Beryllium
Bismuth
Boranes
Boron -f
Cadmium . +
Chromium
Cobalt +
Copper
Gallium
Germanium +
Gold
Hafnium
Indium
Iron +
Lanthanons
Lead +
Lithium +
Magnesium
Manganese
Mercury
M«tal hydride*
' Molybdenum
Nickel
Niobium
Osmium
Palladium
Platinum
Rhodium
Rubidium
Ruthenium
Selenium +
Silver
Strontium
Tantalum
Tellurium
Thallium +
Tin (organic) +
Titanium
Tungsten
Uranium
Vanadium
Cine +
Zirconium
Respira-
tory
Tract
+
+
+
•f
•«•
+
+
+
+
•¥
+
+
+
+
+
+
•f
+
+
+
+
•f
+
CNS
+
+
+
+
+ •
.+
+
+
+
+
+
+
.'+
+
+
*
+
+
+
+
+
*
*
Cardio-
vascular
System
+
+
+
+
+
+
+
+
*
Liver
+
+
•f
+
+
'
+
. +
+
+
+
*
*
*
+
-------
Table 1-3. ACCEPTABLE AVERAGE CONCENTRATIONS (yg/M ) OF
OCCUPATIONAL EXPOSURE BASED ON 8-HOUR EXPOSURES*1
Antimony and compounds (as Sb) 500
Stibine (SbH3) 500 (0.1 ppm)
Arsenic and compounds (as As) 500
Arsine (AsHa) 200 (0.05 ppm)
Arsenate, calcium 1,000
Arsenate, lead 150
Barium (soluble compounds) 500
Beryllium and compounds 2 (5t)
Boron oxide 15,000
Boron trifluoride 3,000t
Diborane 100
Pentaborane (0.005 ppm)
Decaborane (skin) 300
Cadmium fume 100 (3000t)
Cadmium dust 200 (600t)
Chromic acid and chromates lOOt
Chromium, soluble salts 500
Chromium, metal and insoluble salts 1,000
Cobalt, metal fume and dust 100
' Copper fume 100
Copper, dusts and mists 1,000
Hafnium 500
Iron oxide fume 10,000
. Ferban (ferric dimethyldithiocarbamate) 15,000
Perrovanadium dust (FeV) 1,000
Lead and its inorganic compounds 200
Lead arsenate 150
Lead, tetraethyl (as Pb-skin) 75
Lead, tetramethyl (as Pb-skin) 75
Lithium hydride 25
Magnesium oxide fume 15,000
Manganese 5,000t
Mercury lOOt
Mercury (organo alkyl) 10 (40t)
Molybdenum (soluble compounds) 5",000
Molybdenum (insoluble compounds) 15,000
Nickel, metal and soluble compounds as Ni 1,000
Nickel carbonyl 7
Osmium tetroxide . 2
Silver, metals and soluble compounds 10
Tantalum . 5,000
Tellurium 100
Tellurium hexafluoride 200 (0.02 ppm)
Thallium (soluble compound:-skin as Tl) 100
Tin (inorganic compounds except oxides) 2,000
Tin (organic compounds) 100
Platinum (soluble salts as Pt) 2
Rhodium, metal fume and dust as Rh 100
Rhodium (soluble salts) 1
Selenium compounds as Se 20
Selenium, hexafluoride 400 (0.05 ppm)
Titanium dioxide 15,000
Uranium (soluble compounds) 50
Uranium (insoluble compounds) 250
Vanadium (V20S dust) 500t
.Vanadium (V205 fume) lOOt
Yttrium 1,000
Zinc chloride fume 1,000
Zinc oxide fume 5,000
Zirconium compounds as Zr 5,000
From Federal Register, Vol. 36, No. 157;
tCeilings.
Friday, Aug. 13, 1971.
403
-------
Table 1-4. TOLERANCE LEVELS FOR METALS IN DRINKING WATER AND RESULTS OF
SAMPLING OF COMMUNITY WATER SUPPLIES (969) IN 1969*
Element
Arsenic
Barium
Boron
Cadmium
Chromium (Cr6*)
Copper
Iron
Lead
Manganese
Selenium
Silver
Uranium (Uranyl) t
Zinc
LIMITS IN rag/liter
Mandatory
Upper
0.05
1.0
5.0
0.01
0.05
0.05
0.01
0.05
Desirable
Upper
0.01
1.0
1.0
0.3
0.05
5.0
5.0
Maximum
Concentrations
Found
0.10
1.55
3.28
3.94
0.79§
8.35
26.0
0.64
1.32
0.07
0.03
Not included
13.0
NUMBER OF SAMPLES
OF A TOTAL OF 2595
EXCEEDING
Mandatory
5
2tt
0
4
5
37
10
0
Desirable
10
20
42
223
211
8
*From U.S. Public Health Service:
Community Water Supply Study;
U.S. Department of Health, Education, and Welfare, Washington7 D.C.,
tProposed.
ttNot measured in all samples.
ITotal Chromium measured.
Analysis of Nation Survey Findings.
1970.
-------
Table 1-5. METAL CARCINOGENESIS IN EXPERIMENTAL ANIMALS*
Metal
Compound
Species
Rabbits, mice, rats
Monkeys, rats
Rats, mice
Chicken
Rabbits
Rats, mice
Rats
Rats, .rabbits
Chickens
Rats, mice, rabbits
Rats ,
Mice
Rats, mice
Guinea pigs, rats
Rats
Cats
Rats
Rats
Chickens
Rats, mice
Rats
Rats
Rats
Rats
Route
Type of Tumor
Beryllium
Cadmium
Chromium
Cobalt
Copper
Iron
Lead
Nickel
Selenium
Zinc
Titanium
Aluminum
Silver
Mercury
AnBeSiOj, BeO
BeO, BeS04, BeHPOi,
CdS, CdO, CdCl2, CdSO,,
Cd powder
CdCl2
Metallic Cr
Roasted chroraite ore
CaCrOi., Cr03/ Na2Cr207
Cr203
CaCrO,,
Metallic Co, Co powder
CoO, CpS
CuSO,,
Iron-carbohydrate
complexes
Pbj(PO,.)2, Pb(C2H302)2
Tetraethyl lead
Pb(C2H302)2, 2Pb(OH)2
Ki dust, Ni(CO)
Nickelocene, Ni dust
Ni3S2 dust, NiO dust
Ni pellets
Ni3S2 discs
NH,,KSe, grain with Se,
Na2, SeOi,, bis-4-acet-
aminophenyl Sehydroxide
ZnCl2
ZnSOi, ZnClj
Titanocene
Al foil
Ag foil
Ag colloid
Liquid mercury
IV
Inhalation
SC, IM
Intratesticular
Intraosseous
IM, IP, SC
Intrapleural
Intrabronchial
SC, Im
Intraosseous
Intratesticular
IM, SC
SC
SC
Dietary
Inhalation
IM, SC
Implantation in
nasal sinuses
Dietary
Intratesticular
Intratesticular
IM
Implantation
Implantation
IV
IP
Osteosarcomas
Pulmonary carcinomas
Sarcomas
Leydigiomas
Teratoma
Sarcomas
Sarcomas
Squamous
Cell carcinomas
Squaraous cell and adeno-
carcinomas
Sarcomas
Teratoma
Sarcomas
Renal adenomas and carcin-
omas
Lymphomas
Renal adenomas
Renal and testicular
carcinomas
Anaplastic and adeno-
carcinomas
Squamous cell, anaplastic
and adenocarcinomas
Sarcomas
Squamous cell and adeno-
carcinomas
Hepatomas
Sarcomas
Thyroid adenomas
Leydigiomas, serminoma
Chorionepithelioma
Teratomas
Fibrosarcomas, hepatomas
Lymphomas
Sarcomas
Fibrosarcomas
Tumors (?)
Spindle cell sarcomas
*Data from Furst and Haro, 1969; Sunderman, 1971.
-------
Table 1-6. EFFECTS OF METALS ON REPRODUCTION*'
Metal
Species
Test
Results
O
OY
Arsenic
Cadmium
Cobalt
Copper
Indium
Lead
Lithium
Manganese
Mercury
Molybdenum
Nickel
Selenium'
Tellurium
Titanium
Zinc
Mouse
Hamster, rat
Mouse
Hamster
Hamster
Hamster
Hamster
Mouse
Rat
Hamster
Mouse
Hamster
Human
Mouse( rat
Hamster
Mouse
Hamster
Rat
Hamster
Livestock
Hamster
Mouse
Rat
Rat
Hamster
Rat
5 ppm arsenite in drinking water, 3
generations
Teratogenic parenteral
10 ppm in drinking water, 3
generations
Teratogenic parenteral
Teratogenic
Teratogenic
Teratogenic parenteral
25 ppm in drinking water, 3 -
generations
25 ppm in drinking water, 3
generations
Teratogenic parenteral
Teratogenic
Teratogenic
Epidemiologic •
Teratogenic (methyl mercury)
Teratogenic (mercuric acetate and
phenylmercuric acetate)
10 ppm (molybdate) in drinking
water, 3 generations
Teratogenic
5 ppm in drinking water, 3
generations
Teratogenic parenteral
in drinking water,
Epidemiologic
Teratogenic
3 ppm (selenate)
3 generations
Teratogenic (dietary 500 to 3500 ppm)
5 ppn (titanate) in drinking water,
3 generations
Terntogenic parenteral
Dietary administration dam
Increased male to female ratio, reduced
litter size
Head changes, exencephaly, urogenital
abnormalities
Failure to reproduce 3 generations,
congenital abnormality of the tail,
runting, death before weaning
Abnormalities face and palate
Not teratogenic
Not teratogenic
Abnormalities of limb buds
Failure to reproduce 3 generations,
runting, death before weaning
Death before weaning, runting
Malformation tail bud
Resorption, cleft palate
Not teratogenic, embryocidal
Mental retardaion, neuromuscular
effects
Behavior effects, CNS changes
No clear-cut effects
Deaths before weaning, runting
Not teratogenic, embryocidal
Death before weaning, runting, reduced
litter size, reduced number of males
in third generation
Embryotoxic, few general malforma-
tions
Teratogenic
Not teratogenic
Increased male to female ratios, death
before weaning, runting
Hydrocephalus
Runting, death before weaning, male to
female ratio reduced
Mild teratogenic effect
Increased hydrocephalus
•Data largely from Schroeder and Mitchner, 1971b; Perm, 1972
-------
Table 1-7. BODY BURDEN AND HUMAN DAILY INTAKE AND
CONTENT IN THE EARTH'S CRUST OF SELECTED ELEMENTS*"1
Element
Aluminum
Antimony
Arsenic
Barium
Boron
Cadmium
Calcium
Cesium
Chromium
Cobalt
Copper
Germanium
Gold
Iron
Lead
Lithium
Magnesium
Manganese
Mercury
Molybdenum
Nickel
Niobium
Potassium
Rubidium
Selenium
Silver .
Sodium
Strontium
Tellurium •
Tin
Titanium
Uranium
Vanadium
Zinc
Zirconium
Human
Body
Burden
(mg/70 kg)
100
<90
<100
16
<10
30
1,050,000
<0.01
<6
1
100
trace
<1
4,100
120
trace
20,000
20
trace
9
<10
100
140,000
1,200
15
<1
105,000
140
600
30
<15
0.02
30
2,300
250
Daily
Intake
(mg)
36.4
0.7
16
0.01-0.02 •
0.018-0.20
0.06
0.3
3.2
1.5
15
0.3
2
500
5
0.02
0.35
0.45
0.60
10
0.06-0.15
2
0.6
17
0.3
2.5
12
3.5
Earth's
Crust
(ppm)
81,000
0.2
2
400
16
0.2
36,000
1
200
23
45
1
0.005
50,000
15
30
20,900
1,000
0.5
1
80
24
25,900
120
0.09
0.1
28,300
450
0.002
3
4,400
2
110
65
70
*Data largely from Schroeder, 1965a.
407
-------
Toxicology of the Major Residual Metals Emitted from Primary Cu, Pb
and Zn Smelters1»z»3»4
Antimony - Antimony compounds are absorbed slowly from the gastro-
intestinal tract and tend to produce vomiting. Trivalent forms accumu-
late in the liver and are mainly excreted in the feces, while pentava-
lent forms tend to concentrate in the liver and spleen and are excreted
in the urine. Acute human poisoning produces symptoms similar to those
of arsenic poisoning, namely vomiting, watery diarrhea, collapse, irreg-
ular respiration and hypothermia. Chronic administration of potassium
antimony tartrate (5 ppm) in drinking water to rats increased the mor-
tality rates and decreased serum glucose levels. Toxicity data derived
in connection with the therapeutic use of antimonials include cardiac
effects, in a few cases atrial fibrillation due to a direct effect on
the heart and death, liver toxicity, characterized by jaundice and fatty
degeneration, pulmonary congestion and edema, and papular skin erup-
tions. Indications of industrial antimony poisoning include upper
respiratory tract irritation, pneumonitis, dizziness, diarrhea, vomit-
ing, and dermatitis. Antimony may generate stibine (antimony hydride)
under reducing conditions. The lethal concentration of stibine in air
for mice is about 100 ppm for 1.6 hours, and stibine may be expected
like arsine to cause rapid hemolysis, hemoglobinuria, and anuria.
Dernehl and his colleagues (1945) quote Feil who, in 1939, found
among workers in antimony smelters the following symptons: conjunctivi-
tis, tracheitis, pharyngitis, anemia, headache, anorexia, and vomiting.
Feil ru.led out arsenic as the cause since the ore contained less than 10
mg per kilogram. Taylor (1966) described acute antimony trichloride
intoxication causing gastrointestinal symptoms with persistent nausea
and respiratory tract irritation. In 1953 Renes reported 69 cases of
illness among workers in an antimony smelter where they were exposed to
dust and fume at high levels (5 to 12 mg/m3); particle size was less
than one micron allowing rapid absorption. Since the arsenic concentra-
tions in this exposure were low, the toxic effect was attributed to
antimony. Inflammation of the skin and upper respiratory tract occurred
most frequently, and in six cases an acute pneumonitis was demonstrated
by chest x-ray and was completely reversed by penicillin and freedom
from exposure.z
A serious toxic effect of exposure to antimony as the compound
Sb2S3 was reported by Brieger et al. in 1954. He studied 125 workers
who had been employed in the abrasive industry for less than two years.
Of these, 6 died suddenly of heart failure, and 37 of 75 examined showed
abnormal electrocardiograms (EKG's). The chief abnormality was found in
T wave changes. The use of antimony had to be stopped as values of 3 to
5.5 mg/m3 of antimony were found in the air and up to 9.6 mg/L in urine,
in spite of engineering control.2
408
-------
Arsenic - Arsenic compounds may be absorbed by an oral or inhala-
tion route with trivalent compounds usually more toxic than pentavelant
ones. Arsenate is the valence form most prevalent in nature and in this
form tends to be rapidly excreted by the kidneys, thus, probably not
accumulating. Arsenites bind to proteins and are concentrated in leuko-
cytes. In the body, they accumulate primarily in the liver, muscles,
hair, nails and skin. Arsenic is both teratogenic and embryotoxic for
mice; a level of 10 mg/Kg sodium arsenite was sufficient to produce
these effects, while 25 mg/Kg sodium arsenate was without effectJ
Similarly, no dogs fed arsenic (125 ppm) as arsenite survived a two year
study, but only one dog died when fed the same level of arsenic as
arsenate.
Symptoms of acute inorganic arsenic poisoning include burning and
dryness of the oral and nasal cavities, gastrointestinal disturbance,
and muscle spasms; vertigo, delirium and coma may also occur. Chronic
arsenic intoxication initially produces malaise and fatigue and may
ultimately cause gastrointestinal disturbances, hyperpigmentation,
peripheral neuropathy, anemia and leukopenia. Industrial poisoning
generally follows the same pattern, although skin changes such as nasal
septum ulceration may occur more frequently than the hematologic
changes. Epidemiological studies link arsenic by industrial exposures
to skin and lung cancer and by oral intake with goitrogenesis and black-
foot disease, a severe form of peripheral arteriosclerosis in Taiwan.
Arsine, one of the most toxic arsenic compounds, is the principal source
of industrial arsenic poisoning today and has been reported in connec-
tion with the refining or processing of tin, lead and zinc. Arsine, a
gas with a slight garliclike odor detected only above safe levels,
produces massive hemolysis and renal failure; exposures of as low as 10
ppm have been lethal in humans.
Bismuth - Most bismuth compounds commonly encountered are insoluble
and poorly absorbed. There have been no reports of industrial poisoning
from bismuth, and the bismuth compounds do not present a hazard by
dermal application, inhalation or ingestion. Bismuth administered
therapeutically is concentrated priamrily in the kidney and to a lesser
extent in the liver. Urine is the major route of excretion. Symptoms
of chronic bismuth toxicity in man include anorexia, weakness, rheumatic
pain, diarrhea, metal line on the gums, foul breath, gingivitis and
dermatitis. Although rare, nephritis signaled by albuminuria, jaundice
and conjunctival hemorrhage have been reported.
Cadmium - In biologic systems, the metabolism of zinc and cadmium
are closely related, so much so that cadmium can be considered an anti-
metabolite of zinc. About 6 to 10 percent of ingested cadmium is ab-
sorbed, and most accumulation occurs in the kidney except in cases of
409
-------
large exposures where the liver may contain more. Inhaled cadmium dusts
and fumes have retention rates from 5 to 50 percent and have a half-life
in the lungs of about 5 days. Inhaled cadmium is distributed to other
parts of the body probably through the action of the carrier protein
metallothionen. Normal cadmium blood levels are below 1 -pg/lOO ml and
normal urinary cadmium values range from 0.5 to 11 vg/1. The urine is
the primary route for cadmium excretion, but hair loss and fecal excre-
tion also contribute.
The toxic effects of cadmium are fairly well documented, and some
toxic levels of exposure are listed in Table 1-8. Large oral doses of
cadmium produce vomiting, while acute inhalation exposures may result in
pulmonary edema and death by anoxia within 3 days. The second stage of
acute intoxication consists of cellular proliferation in the alveoli as
well as hyperplasia of the lining cells sometimes accompanied by intra-
alveolar hemorrhage. Delayed lung effects which may occur are peri-
vascular and peribronchial fibrosis along with emphysema. Lethal levels
of cadmium exposure are estimated to be 50 mg Cd/rn^ for one hour for
cadmium oxide dust and about one-half that for the fume. Cadmium is
also teratogenic for hamsters if administered during the proper gesta-
tional period, and simultaneous administration of zinc can greatly
mitigate these teratogenic effects.5
Chronic cadmium inhalation exposure may result in proteinuria and
emphysema, differing from chronic bronchial emphysema in that it is not
preceded by a history of bronchitis and coughing. Chronic oral cadmium
poisoning can also drastically alter human calcium and zinc metabolism
as exemplified by the outbreak of Itai-itai (ouch-ouch) disease in the
Toyama Bay area of Japan. The disease occurred most frequently in
postmenopausal women who has histories of several pregnancies. Lumbar
and leg pain were characteristic. Skeletal deformities with markedly
decreased body height, susceptibility to multiple fractures after slight
physical stress such as coughing, and waddling gait caused by bone
deformities may precede complete inability to walk. The abnormal clini-
cal pathologic parameters produced in this disease are proteinuria,
glucosuria, reduced urinary phosphate, low serum inorganic phosphorus
and calcium, increased serum alkaline phosphatase, urinary amino acids,
and decreased urinary and blood zinc levels. Additional symptoms and
signs of chronic cadmium poisoning attributed to industrial exposures
are anosmia, watery nasal discharges, loss of weight, low hemoglobin
values, bone fractures and rickets.
Cadmium (5 ppm) added to the drinking water of rats or mice re-
sulted in a high tumor incidence, shortened life-span, hepatic cirrhosis
with fatty degeneration, arteriosclerosis of the kidney and heart,
proteinuria, neurologic disorders, severe vestibular disturbances,
410
-------
Table 1-8. SOME TOXIC LEVELS OF CADMIUM EXPOSURE'
Species
Man
Man
Man
Rats
Rats
Dogs
Route
Oral
(insoluble salts)
Inhalation
(CdO fume)
Inhalation
(occupational
exposure)
(CdO fume and dust)
Oral
(drinking water)
Oral
(diet)
Oral
(drinking water)
Concentration
> 15 mg
0.5-2.5 mg/ra
Unknown ,
but > 0.2 mg/m
10-50 ppm
135 ppm
5-10 ppm
Time
Single dose
Intermittent
2-3 days
Chronic
(many years)
1 year
6 months
4 years
Effects
Vomiting
Pneumonitis
Emphysema
Mild anemia
Proteinuria
Anemia and reduced
growth rate
Anemia and poor
' growth
No significant
toxic effects
-------
hypertension and left ventricular hypertrophy. It is interesting to
note that hypertension induced in female rats by cadmium exposure can,
as can many other effects, be reversed by the administration of zinc.
Although the kidney is frequently the target organ in occupational
diseases related to cadmium exposure, there is some eivdence that acute
industrial exposure can cause myocardial infarction and cor pulmonale
without necessarily influencing the kidney.
Cobalt - Cobalt salts are generally well absorbed orally, but large
doses usually do not significantly accumulate. Of the ingested cobalt,
about 80 percent is excreted in the urine and another 15 percent is
eliminated in the feces. Cobalt which does accumulate does so in the
liver, heart and hair. The normal levels in human urine and blood are
about 98 and 0.18 yg/1, respectively. Ingestion of large amounts of
cobalt can produce polycythemia, and goiter when taken chronically.
Adverse reported effects from cobalt taken therapeutically include
vomiting, diarrhea, and a sensation of warmth, flushing of the face,
hypertension, slowed respiration, giddiness, tinnitus and deafness.
Cardiomyopathy has been caused by ingestion of beer containing 1 ppm
cobalt; why such a small amount of cobalt could produce such effects in
the course of only one month is not known. Industrial exposure to
cobalt salts leads to respiratory effects, although there is some ques-
tion as to whether cobalt is the sole agent responsible for these ef-
fects. Skin and eye lesions similar to allergic dermatitis have also
been reported following industrial exposures.
Copper - Absorption of copper is regulated by the intestinal muco-
sa; absorbed copper is initially bound to albumin and finally to cerulo-
plasmin. Excretion of excess copper by the bile usually maintains serum
copper at between 120 to 145 yg/1. Excess copper is normally deposited
in the liver and in bone. Man is not very sensitive to copper, conse-
quently, it is felt that excessive copper exposure in normal persons
does not result in any chronic disease. Industrial exposure to copper
appears to only be responsible for metal fume fever. Acute poisoning
resulting from ingestion of large amounts of copper salts produce vomit-
ing, hematemesis, hypotension, melena, jaundice, coma and sometimes
death. Hemolytic anemias have also been induced by using topical cop-
per - containing compounds for burns and copper - containing dialysis
equipment.
Germanium - Sodium germanite is rapidly absorbed from the gastro-
intestinal tract; and germanium levels of 0.65 and 0.29 -pg/ml have been
reported as normal values for erythrocytes and serum, respectively. The
urine is the major route of germanium excretion (normal range of urinary
germanium may be 0.40 to 2.16 yg/ml), but milk and feces are secondary
routes. Germanium and its compounds have a low toxicity, and exposure
412
-------
to germanium is not considered an industrial hazard or a cause of chron-
ic disease in man. The acute effects of high doses of germanium admin-
istered to animals are hypothermia, listlessness, diarrhea, respiratory
and cardiac depression, edema, and hemorrhage in the lungs and gastro-
intestinal tract.
Indium - Indium is poorly absorbed from the gastrointestinal tract
and is excreted in the urine and feces. No industrial injury has been
reported from the use of indium, and human absorption from the use of
indium plated silver in utensils is without known toxic effect. Subcuta-
neous and intravenous injection of indium is followed by hindleg paraly-
sis, convulsions and death. Autopsies of such animals revealed necrotic
and hemorrhagic livers and kidneys and muscle degeneration.
Lead - The average daily intake of lead depends upon the source of
food, but a good estimate is about 300 iig/day. Children, however, may
have a greater relative lead intake due to higher metabolic needs per
kilogram of body weight. Absorption of lead from the gastrointestinal
tract appears to be regulated to some extent by the mechanism control-
ling calcium and phosphorous absorption, and under normal conditions, 5
to 10 percent of ingested lead is absorbed. Although calcium antago-
nizes lead absorption, at levels of ingested lead above 20 mg, signifi-
cant quantities are not eliminated. Inhalation absorption of lead from
the atmosphere is dependent upon normal physiologic parameters, but as
an average about 37 percent of inhaled lead is retained within the
lungs. From long-term studies, it appears that fecal and urinary excre-
tion play equally important roles in eliminating the body lead burden.
Over 90 percent of the lead body burden is stored in bone, but the
aorta, liver, kidney, pancreas and lungs have higher lead concentrations
than bone. Urinary lead levels of 150 yg/100 ml and blood levels of 80
yg/100 ml are indicative of hazardous exposure.
A great deal is known about the toxic effects of lead on humans,
and the amount of lead which needs to be absorbed before such effects
occur. The various effects and sequelae of lead intoxication are sum-
marized in Tables 1-9 and 1-10. Symptoms of acute lead poisoning are
thirst, a metallic taste, nausea, vomiting, black stools and circulatory
collapse. Several days following acute lead poisoning muscular weak-
ness, acute hemolytic crisis and kidney damage may occur preceding
death. Colic, one of the most common symptoms, constipation, and weak-
ness in the upper limb, wrists and fingers are the earliest symptoms of
chronic lead poisoning. Lead has a devastating effect upon red blood
cells. Impairment of the enzymes delta aminolevulinic acid synthetase
and dehydrase, coproporphyrinogen oxidase, and heme synthetase along
with lead's direct hemolytic action are responsible for the anemia of
plumbism. Severe and permanent kidney, central nervous system and
413
-------
Table 1-9. EFFECTS OF INORGANIC LEAD SALTS IN RELATION TO ABSORPTION"
A. Metabolic:
(accumulation
and excretion
of heme
precursors)
(a) Classification of Levels and Types of Effects
1 2 3 4
Types of Effects:
No demon-
strable
in vivo
effect
Minimal
Subclinical
metabolic
effect
Compensatory
biologic
mechanisms
invoked
Mild ,
Late effects of
Acute chronic or recurrent
lead acute lead
poisoning poisoning
Severe
normal
slight in-
crease in
urinary
ALA may be
present
progressive
increase in
ALA, UCP,
FEP
increased increased if excessive
5 to 100 . exposure recent, but
fold may not be increased
if excessive exposure
remote
B. Functional
Injury:
1. Hematopoiesis none none
2. Kidney (renal none none
tubular
function)
3. Central none • none
nervous
system
4. Peripheral none none
nerves
shorterited
RBC life
span, reti-
culocytosis
(+).(rever-
sible)
shortened RBC
life span and
.reticulocytosis
with or without
anemia (rever-
sible)
Anemia (+)
(reversible)
? aminoaciduria,. Fanconi chronic nephropathy
glycosuria(;O syndrome (permanent)
(reversible) (reversible)
mild injury
(??? reversi-
ble)
rare
severe
injury
(perma-
nent)
rare
severe injury
(permanent)
Impaired conduction
(wrist, foot drop
usually improve
slowly, but may be
permanent)
-------
Table 1-9 (continued). EFFECTS OF INORGANIC LEAD SALTS IN RELATION TO ABSORPTION'
Ul
(a) Classification of Levels and Types of Effects
123 4
No demon- Minimal Compensatory
strable Subclinical biologic
in vivo metabolic mechanisms
effect effect . invoked
Acute
lead
poisoning
Late effects of
chronic or recurrent
acute lead
poisoning
Types of Effects:
C. Clinical
Effects:
Mild Severe
Blood Level
(yg Pb/100 gm
whole blood)
Urine Lead
(adults only)
(pg Pb/L)
none
none
Non- colic, irri- ataxia,
specific tability, stupor,
mild symp-vomiting coma,
toras (may convul-
be due in sions
part to co-
existing
diseases)
mental deficiency
(may be profound)
seizure disorder
renal insufficiency
(gout) (permanent)
(b) Index of Recent or Current Absorption by Level of Effect
< 40 ug Pb 40-60 yg Pb Level III. 60 100 + ug Pb
Level IV with anemia, intercur-
rent disease. 60 100 + ug Pb
Level IV. > 80 ug Pb
< 80 ug Pb/L < 130 ug Pb/L
may be normal
> 130 ug Pb/L endogenous excretion
(may be less may be normal
in /severe
illness)
CaEDTA mobilization
test: chronic nephro-
pathy-positive per-
manent CNS injury +_
(see text)
Pb=lead; ALAD-a-
coproporphyrin;
•aminolevulinic acid dehydratase; ALA«o-aminolevulinlc acid; UCP»urinary
FEP»free erythrocyte protoporphyrin; RBC-red blood cell.
-------
Table 1-10. DISTRIBUTION OF SEQUELAE FOLLOWING VARIOUS MODES
OF ONSET IN 425 PATIENTS WITH PLUMBISM3
CTi
Sequelae
None
Mental
retardation
Seizures
Cerebral palsy
Optic atrophy
All cases
Moae of onset
Enceph.
11(18)
23(38)
32(54)
8(13)
4( 6)
59
Seizures
14(33)
14(33)
17(39)
0
0
43
Ataxia
7(41)
5(29)
6(35)
K 6)
1 ( =6)
17
G.I.
159(69)
43(19)
30(13)
0
0
232
Febrile
13(81)
3(19)
0
0
0
16
Asympto-
matic
53(91)
5( 9)
0
0
0
58
Total
257(61)
93(22)
85(20)
9( 2)
5( 1)
425
Data in parentheses are percentages of cases with that mode of onset developing
the sequelae. The percentages in any column may total more than 100 because
the one patient may develop more than one sequela.
-------
peripheral nerve damage are well documented in chronic lead poisoning.
Other reported effects of chronic lead poisoning are a reduction in
iodine uptake by the thyroid, a decrease in pulmonary resistance to
infectious disease when inhaled, and the induction of renal cancer in
rats. Lead has also been associated with sterility, abortion, still
births, and neonatal deaths in man. Although the toxicity of organic
lead is interesting, it is not relevant to lead emitted from copper,
lead and zinc smelters; a good summary discussion of the toxicology of
organic lead can be found in Reference 1.
Perhaps the most disturbing aspect of chronic lead poisoning is the
frequency with which disabling diseases occur in spite of normal urinary
and blood lead levels. Permanent gout, renal insufficiency, mental
deficiency and seizure disorders can all occur with normal urinary and
blood lead levels. Although Ca EDTA mobilization tests can confirm the
etiology of these diseases, normal screening procedures for lead intoxi-
cation would not. Thus the above mentioned effects as well as less
specific effects of chronic lead poisoning may occur and go unrecognized
to a frightening extent.
Magnesium - Calcium and magnesium are competitive with respect to
their absorptive sites, and excess calcium may limit the already poor
absorption levels of magnesium salts. Serum levels of magnesium are
remarkably constant, however, there is an apparent obligatory urinary
loss (the primary route of excretion) of about 12 mg/day. Endocrine
activities influence magnesium levels, and there is an inverse relation-
ship between the concentration of calcium and magnesium in bone. If
exposure is sufficient, magnesium oxide fume can cause metal fume fever.
Conjunctivitis, nasal catarrh, and coughs productive of discolored
sputum have also resulted from industrial inhalation exposures. Subcu-
taneous injection of magnesium into animals produces gas gangrene, while
oral poisoning of animals results in hypotension, renal impairment and
respiratory parlysis.
Manganese - Although the body burden of manganese has been esti-
mated at 20 mg with the liver, kidney, intestine and pancreas having the
highest concentrations, no significant changes in tissue concentration
occur with age. Manganese has a rapid turnover in the body, and the
lungs do not accumulate manganese with age despite significant concen-
trations in urban air. Manganese is excreted mainly through the gastro-
intestinal tract via the bile. Orally or dermally administrated manga-
nese is of low systemic toxicity, but industrial toxicity from inhala-
tion exposures may be severe. Acute exposure to manganese dioxide
causes pneumonitis, and men working in plants with high concentrations
of manganese dust show an incidence of respiratory disease 30 times
greater than normal. Chronic inhalation exposure to manganese dioxide,
417
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generally over a period of more than two years, involves the central
nervous system. Symptoms of chronic manganese poisoning (manganism)
include a masklike face, retropulsion or propulsion and a Parkinson-like
syndrome. The pathophysiology of manganism is also remarkable similar
to that of Parkinson's disease. Degenerative lesions of the basal
ganglia and markedly decreased levels of dopamime and serotonin in the
caudate nucleus occur in both disease states. As a final note, L-Dopa,
a drug pharmacologically designed to treat Parkinson's disease, has been
effective in the treatment of manganism
Mercury - Mercury is a somewhat unique environmental toxicant for
two reasons, volatility and biotransformation. In areas containing soil
with high mercury levels (10 ppm), atmospheric concentrations of 20 to
200 yg Hg/nr result. These levels are sufficient to produce central
nervous system effects under conditions of chronic exposure. Biotrans-
formation of mercury into shortchain alkyl mercury compounds by bacteria
contributes to the environmental hazard posed by mercury. The high
concentration of methyl mercury in fish, the food source containing the
most mercury, is probably attributable to this phenomenon.
Absorption of elemental mercury after ingestion is minimal, but
elemental mercury undergoes almost complete absorption from inhaled air.
Mercury absorbed in pulmonary tissue may be oxidized in situ to inor-
ganic mercury, arid in rats, mercury has a half-life in the lungs of
about five hours. Elemental mercury may dissolve in blood, and in this
form, it may be transported acorss the blood-brain barrier to be oxi-
dized in brain tissue. Brain levels of mercury are higher after ex-
posure to mercury vapor than after ingestion of a similar dose of mercu-
ric salts. Mercury tends to accumulate in the central nervous system
and in the kidneys. Elimination of mercury from the dentate nucleus of
the cerebellum is particularly slow. In rats, excretion of mercury
after acute exposure is characterized by a rapid phase mediated by fecal
excretion, and a slow phase where urinary and fecal excretion play equal
roles. In the central nervous system, mercury is eliminated nvre rapid-
ly from the cortex than from the medulla.
Alkyl mercury compounds differ drastically from the other organic
mercurials, and methyl mercury which can be environmentally transformed
from other forms of mercury is the most serious hazard in this group.
Like elemental mercury vapor, methyl mercury is well absorbed through
the lungs and skin, but in diametric opposition to elemental mercury,
methyl mercury is nearly completely absorbed from the gastrointestinal
tract after ingestion. Alkyl mercurials are preferentially accumulated
in erythrocytes, and the change to inorganic mercury characteristic of
the other organic mercurials is slowest after doses of methyl mercury.
In rats, excretion of methyl mercury primarily occurs through the feces
418
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via the bile, and due to rapid reabsorption, enterohepatic recirculation
-maintains a large pool of methyl mercury within the bile. Perhaps the
most insidious aspect of alky 1 mercurials is their ability to cross the
placenta! barrier. Levels of methyl mercury can be 20 percent higher in
fetal blood than in maternal blood, and much higher levels are found in
fetal as compared to maternal brain tissue.
Symptoms of prenatal mercury toxicity due to maternal ingestion of
mercury-containing fish as in Minamata include mental disturbance,
ataxia, impairment of gait, speech and mastication. Postmorten examina-
tion of these cases revealed hypoplasia and atrophy of the brain tissue.
Symptoms of postnatal intoxication from short-chain alKyl mercurials
usually have a latent period of weeks to months and include gustatory
disturbances, sensory deficits of the lip and extremities, ataxia,
constriction of the visual field, impairment of hearing, extrapyramidal
disturbances, and mental impairment. These types of cases have been
reported as a result of excessive intake from fish (Minamata), occupa-
tional exposure, and ingestion of seeds treated with organic mercury
compounds. The metabolic interrelationship of metals is again illus-
trated by experimental work which indicates selenium can decrease the
toxicity of methyl mercury in birds and rats.
Ingestion of mercuric chloride leads to an ashen-gray appearance of
the mouth, vomiting, a metallic taste in the saliva, excessive saliva-
tion, gingivitis, and possibly death as a result of damage to the renal
tubule epithelium. Acrodynia (pink disease) has occurred in children
exposed to inorganic mercury salts and is believed to be a hypersensi-
tivity reaction. Following a latent period of one to two weeks, cardio-
vascular manifestations, pink color of the extremities, edema, blister-
ing and desquamation of cells, photophobia, apathy, and hypotonia re-
sult. Organic or inorganic mercucy produces similar renal toxicity, and
in experimental situations, point mutations. Although no good criterion
for judging the extent of mercury exposure exists, the lowest whole-
blood concentration for toxicity related to methyl mercury intake is 0.2
yg/g» and urinary and blood levels above 0.3 mg/1 and 5 yg/100 ml,
respectively probably indicate excessive exposure to elemental mercury.
Molybdenum - Soluble hexavalent forms of molybdenum are well ab-
sorbed from the gastrointestinal tract. Excretion of molybdenum is
rapid, and over half of that excreted is found in the urine. Of the
approximately 9 mg molybdenum body burden, most is concentrated in the
liver, kidney, adrenal and omentum. Although there are no recorded
cases of molybdenum toxicity in man due to industrial exposure, there
are some interesting diseases and metabolic interrelationships of molyb-
denum with other metals, found in animals. Cattle and sheep grazing in
pastures containing 20 to 100 ppm molybdenum may develop a disease
419
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called "teart" which may be prevented by copper or sulfate fortified
diets. Teart is characterized by anemia, poor growth rate and diarrhea;
prolonged exposure has also led to deformities of the joints. Experi-
mental studies have shown molybdenum trioxide to be more toxic than the
sulfide. Molybdenum trioxide has induced fatty degeneration of the
liver and kidney if given in sufficient quantity to animals.
Nickel - Absorption of nickel salts from the gastrointestinal tract
is limited by their astringent and irritant properties. Although die-
tary nickel is excreted largely in the feces, inhalation of nickel
carbonyl results in the appearance of significant increases in urinary
nickel. Normal urine values of 2.3 iig Ni/100 ml have been reported, and
urinary nickel values of 0.5 mg/1 are considered serious. Dermatitis
(nickel itch) is the most frequent effect of exposure to nickel. The
dermatitis is a hypersensitivity reaction, and in some cases, nickel may
produce paroxysmal asthmatic attacks and pulmonary eosinophilia. Nickel
carbonyl is the most toxic of nickel compounds, and 30 ppm for 30 min-
utes is lethal for man. Nickel carbonyl intoxication causes headache
and vomiting initially, and after 12 to 36 hours, dyspnea, cyanosis,
leukocytosis, fever and chemical pneumonitis. If death is to occur, 4
to 11 days following exposure is the most likely time. Chronic exposure
to nickel carbonyl has been implicated epidemiologically in human cancer
of the nasal passages and lungs; experimental work with inhalation
exposures to animals have confirmed these findings. In addition, in-
halation exposure to nickel and nickel oxide have produced malignant
pulmonary neoplasms in guinea pigs and rats.
Selenium - Elemental selenium is probably not absorbed from the
gastrointestinal tract. Of the 15 mg average body burden of selenium,
the greatest concentrations are found in the kidney, liver and hair.
Selenium is excreted in the urine, which normally contains about twice
as much as the feces. Normal urinary selenium values are 0 to 15 yg/100
ml. Industrial exposure to hydrogen selenide produces garlic breath,
nausea, dizziness, lassitude, and eye and nasal irritation. Aujte
selenium poisoning causes central nervous system effects such as drowsi-
ness, nervousness and sometimes convulsions. Pallor, coated tongue,
gastrointestinal disorders, nervousness, garlic breath, liver and spleen
damage, anemia, mucosal irritation and lumbar pain are all symptoms of
chronic inhalation exposure to selenium. Selenium is considered embryo
toxic and teratogenic in animals, and some reports claim these effects
have also been observed in humans. Selenite is more toxic than selenate
in animals and has been shown to increase the number of aortic plaques
in rats. Many of the symptoms of selenium toxicity can be prevented by
arsenic, by high-protein diets, and by methionine in the presence of
Vitamin E.
420
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The complexity of the interrelationships of the metals has been
further illustrated in an experimental investigation of selenium metabo-
lism in rats. In this study arsenic, mercury, and thallium Inhibited
the pulmonary excretion of volatile selenium compounds. Mercury in-
creased the blood, kidney and spleen concentrations. Thallium increased
renal and hepatic retention. Arsenic increased biliary excretion,
lowered selenium tissue levels, and prevented selenium induced liver
damage. Lead was without apparent effect.'
Tellurium - Tellurium is stored in greatest quantity in bone, while
the kidney has the largest soft tissue concentration. Soluble tetrava-
lent tellurites absorbed into the body after oral administration are
reduced to tellurides, partly methylated, and then exhaled as dimethyl
telluride (responsible for the garlic odor in persons exposed to tellu-
rium). The urine is the principal route of excretion, while sweat and
milk are secondary routes. Tellurates and tellurium are of low toxic-
ity, but tellurites are usually more toxic. Acute inhalation exposure
can cause sleeplessness, anorexia, nausea, a metallic taste, and a
garlic odor of the breath and perspiration. In rats, chronic exposure
to tellurium dioxide has produced decreased growth and necrosis of the
liver and kidney. One of the more toxic tellurium compounds, tellurium
hexafluoride, in concentrations of 5 ppm is lethal to rats exposed for
four hours. Five hundred ppm tellurite diets fed to pregnant rats have
also produced hydrocephalus in the offspring.
Thallium - Thallium is not normally present in animal tissues, but
it can be easily absorbed through the skin and gastrointestinal tract.
After poisoning, the highest concentrations of thallium are found in the
kidneys and urine, while the intestines, thyroid, testes, pancreas,
skin, bone and spleen have lesser amounts. Acute exposure induces large
amounts of thallium to be excreted in the urine during the first 24
hours. Following the initial period after exposure, fecal excretion may
play the greatest role in elimination of thallium from the body. Acute
thallium poisoning is characterized by gastrointestinal irritation,
acute ascending paralysis and pyschic disturbances. The estimated
lethal dose of thallium for humans is 8 to 12 mg/kg body weight. In
man, fatty infiltration and necrosis of the liver, nephritis, gastro-
enteritis, pulmonary edema, degeneration of adrenals, peripheral and
central nervous systems, alopecia, and in some cases death have occurred
from chronic systemic thallium intake.
Tin - At most, only 10 percent of ingested soluble tin salts are
absorbed through the gastrointestinal tract, but the majority of inhaled
tin or its salts remains in the lungs, most extracellularly. Of the
average U.S. daily intake of 17 mg tin, most is excreted by the kidneys,
and the normal urinary tin level 1s about 14 yg/100 ml. Tin which does
421
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accumulate after ingestion is found in the liver and kidneys. Chronic
inhalation of tin dusts or fumes usually only cause a benign pneumo-
coniosis, but tin hydride is more toxic than arsine and produces central
nervous system effects. Orally, inorganic tin or its compounds require
massive doses to be toxic. On the other hand, organic tin compounds are
considerably more toxic. Excessive industrial exposure to triethyltin
has caused headaches, visual defects, and EEG changes which were only
very slowly reversed. Acute burns or sub-acute dermal irritation can
result from tributyltin exposure, and triphenyl tin has been shown to be
a portent immunosuppressant.
Vanadium - The average body burden of vanadium is about 30 mg with
most being stored in adipose tissue. In most forms, vanadium is moder-
ately absorbed from the gastrointestinal tract, and urine is the prin-
cipal means of vanadium excretion. Normal serum levels of vanadium are
considered to be 35 to 48 -pg/100 ml. The toxic action of vanadium is
largely directed toward the respiratory system as attested to by the
unusually high incidence of bronchitis and bronchopneumonia in workers
exposed to vanadium compounds. Symptoms also linked with industrial
vanadium exposure include eye and skin irritation, gastrointestinal
distress, nausea, vomiting, abdominal pain, cardiac palpitation, tremor,
nervous depression and kidney damage. Acute vanadium poisoning also
causes hemorrhage, paralysis, convulsions and respiratory depression in
animals. Epidemiological analyses suggest that heart disease is related
to vanadium air pollution and vanadium may act with cadmium to produce
these effects.
Zinc - Large concentrations of zinc are found in muscle, liver,
kidney, pancreas, epididymis, prostate, testes and eyes. Excretion of
zinc is through the gastrointestinal tract; pancreatic fluid contains
significant amounts, while the bile contains somewhat less. The urine
contains only 20 percent as much zinc as is found in the feces. Acci-
dental oral poisoning with large doses of zinc has produced fever,
vomiting, stomach cramps and diarrhea. The main consequence of indus-
trial exposure to zinc compounds is the metal fume .fever produced by
inhaling freshly formed fumes of zinc oxide. ZnCl2 fumes may produce
cyanosis, dermatitis and ulceration of the nasal passages. As zinc is
an essential element, there is a homeostatic mechanism for regulating
body zinc levels. Thus, orally administered zinc is not toxic to rats
unless more than 0.25 percent of their diet is composed of zinc.
SELECT REVIEW OF PERTINENT PUBLISHED EPIDEMIOLOGICAL STUDIES
Many good epidemiological studies dealing with the health effects
of metals emitted from Cu, Pb and Zn smelters have been published. In
fact, so many have been published that a detailed synopsis of each would
422
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be both redundant and nearly impossible to read. For this reason, only
about a dozen of the most relevant and applicable studies are summarized
in this section. It is realized that some important work has been
omitted, but the included works cover most of the well documented health
effects of metals epidemiologically associated with Cu, Pb and Zn smelt-
ing. Many other good epidemiological studies with some relevance to the
question at hand are included in the list of general references at the
end of this section.
Arsenic
Human Arsenic Exposure in Relation to a Copper Smelter - Children
living near a copper smelter in Tacoma, Washington, were shown to have
increased levels of arsenic in hair and.urine. The urinary arsenic
level decreased with distance of residence from the smelter stack.
House vacuum-cleaner dust showed a similar distance relationship. Urine
arsenic levels in children varied synchronously over a 5-week period,
indicating that inhalation was the most likely exposure route. In
children urinary arsenic level showed an inverse relationship to age
with younger children showing consistently higher urine arsenic levels.
A death-record analysis indicated an increased respiratory cancer
incidence in men working at this smelter. Since published urinary
arsenic levels for men working at this smelter were similar to those
seen in people residing near the smelter, it was felt that the community
surrounding the smelter might be exposed to an increased respiratory
cancer risk. Accordingly, action was taken to reduce arsenic emissions
from the smelter.
Respiratory Cancer and Occupational Exposure to Arsenicals - The
proportionate mortality experience of 173 decedents exposed primarily to
lead arsenate and calcium arsenate was compared with that of 1809 dece-
dents not exposed to those compounds. A significant increase in respi-
ratory cancer was found among the exposed employees. The relationship
between cumulative arsenic exposure and the ratio of observed to ex-
pected respiratory malignancy deaths was estimated using a least squares
approach. The predicted/expected ratio exceeded six-to-one for indivi-
duals exposed to compounds containing an equivalent level of 1 mg/m^
arsenic for a period of more than eight years. For the more heavily
exposed individuals, an excess of respiratory cancer was observed 35+
years after the initial exposure. Observations based on the propor-
tionate study were supported by an analysis of the same target popula-
tion, employing the prospective study in a retrospect approach.
Prevalence of Skin Cancer in an Endemic Area of Chronic Arsem'cism
in Taiwan** - In a limited area on the southwest coast of Taiwan where
artesian well water with a high concentration of arsenic has been used
423
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for more than 45 years, a high prevalence of chronic poisoning has been
observed in recent years. The total population of this endemic area,
which is defined by the presence of both patients and contaminated
wells, is approximately 100,000. A general survey of 40,421 inhabitants
(19,269 males and 21,152 females) of the area was made. The overall
prevalence rates for skin cancer, hyperpigmentation, and keratosis were
10.6, 183.5, and 71.0/1000, respectively. The male-to-female ratio was
2.9:1 for skin cancer and 1.1:1 for hyperpigmentation and keratosis,
respectively. Generally speaking, the prevalence increased steadily
with age in all three conditions, though there was a decline in age
groups above 69 in females with cancer or hyperpigmentation. The preva-
lence rate for skin cancer showed an ascending gradient according to the
arsenic content of the well water, i.e., the higher the arsenic content,
the more patients with skin cancer. The results were the same for
hyperpigmentation and keratosis. Blackfoot disease, so-termed locally,
a peripheral vascular disorder resulting in gangrene of the extremities,
especially of the feet, had an overall prevalence rate of 8.9/1000. A
dose-response relationship between this disease and the amount of ar-
senic in the well water was similar to that observed for skin cancer.
The association of Blackfoot disease with hyperpigmentation, keratosis,
and skin cancer was significantly higher than expected. The causal
relationship between Blackfoot disease and chronic arsenicism is dis-
cussed.
Cadmium
Some Facts and Documents Relating to the Health Aspects of
Cadmium Pollution in Japan^ - An investigation near mines and smelters
in several prefectures in Japan prompted by discovery of cadmium induced
Itai-itai (ouch-ouch) disease in the Jinzu River Valley, and the result-
ant promulgation of regulations is presented. Investigations showed
that ingestion of rice and water, polluted by cadmium through mine
drainage and/or smelter participate fallout, was the main source of
intake. Rice tended to concentrate the cadmium which had buiK up in
the soil. Cadmium toxicity was greatest in women who had given birth to
several children and been a resident longer than 30 years.
Seven separate areas, under the influence of three (3) mines and
four (4) smelters were observed. Conclusions indicated that: (1) farm-
ers in the areas should not eat rice containing 1.0 ppm Cd (wet weight);
(2) no case of Itai-itai disease or cadmium poisoning were found other
than that mentioned in the Jinzu River Valley; and (3) local pollution
of ambient air by cadmium and lead was found at Annaka (smelting plant).
Due to the results obtained in these areas, and the publicity that
was generated, regulations were promulgated giving acceptable standards
and the grounds for these standards. The standards are: (1) 0.01 ppm
424
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cadmium for water; (2) 0.1 ppra Cd in liquid effluent (assuming dilution
factor of 10); (3) 1.0 ppra Cd in unpolished rice; 0.9 ppro Cd in polished
rice; (4) l.Omg/nm-* Cd atmospheric emission standard; and (5) soil
pollution control for agricultural land on which the rice contains
levels of cadmium greater than 1.0 ppro. In addition, where the above
designated levels are exceeded, the cadmium concentration in urine of
not less than 30 adult persons in the area should be examined; urinal-
ysis diagnosis is to include protein, and cadmium tests, if possible.
Measurement of blood pressure was also advocated. Guidelines for "areas
requiring observation" produced standards of 9 -pg/1 Cd 1n the urine as a
primary screening test and 30 iig/1 Cd, based on the average concentra-
tion in food of 0.99 ppm as a secondary screening level. Total diseased
patients from 1967-1972 totaled 123, including 40 dead. Control of
damage, both physical and agricultural is discussed.
Lead
The Consequences of Chronic Lead Poisoning - Workers in various
professions exposed to lead vapors or dust in concentrations exceeding
0.01 mg/cubic meter were examined and working capability was evaluated
on the basis of clinical symptoms and general condition. In the earlier
stages of poisoning, temporary transfer to working places without ex-
posure to lead is recommended. Where the symptoms do not disappear,
then permanent retirement must be recommended. The average exposure
time before retirement due to chronic poisoning was 11.6 years for men
and 12 years for women. Retirement of women was less frequent than for
men, which is attributed to the less hazardous conditions for women.
EPA's Position on the Health Effects of Airborne Lead11 - Clinical
manifestations of mild lead intoxication (loss of appetite, irritabil-
ity, drowsiness, apathy and abdominal pain) are mentioned, citing spe-
cific cases, especially with regard to children. Levels of lead concen-
tration below that considered toxic may contribute to minimal brain
damage. The metabolic effects of low levels of lead (below 40 yg/100 g
blood) which include enzyme inhibitation may impact the central nervous
system or cause genetic damage. Chromosomal abnormalities were found in
13 of 15 randomly selected individuals located near a lead smelter.
Lead blood levels of 40 vg/100 g blood for adults are acceptable evi-
dence that excessive exposure to lead has occurred, and the possibility
that lower levels in children may cause significant damage is discussed.
Sources of lead exposure among the general population include
paint, dirt, and dust. Ninety percent of airborne lead emissions comes
from leaded gasoline which in turn contributes to lead levels in dust
and dirt. Airborne lead exposures were more relevant in adults than
small children, whose primary exposure comes from ingestion of house
dirt and dust as well as leaded paint.
425
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The report indicates that: (1) levels of 30^g/100 g blood are
considered excessive for pregnant women; (2) a safe blood level for
children should not be above 40-yg/lOO g; (3) blood levels of 30/yg/100
g obtained from umbilical cord blood is excessive; (4) airborne lead
levels of 2 yg/m have been demonstrated to contribute to high blood lead
levels; (5) individuals within groups may be excessively exposed to lead
even though the average exposure is well within normal limits; and (6)
every effort should be made to reduce all preventable lead exposure.
Occupational and Environmental Lead Poisoning in Association with
a Secondary Lead Smelter'^ - Employees at a secondary lead smelter,
household occupants of neighboring residences, cows, horses, dogs and
cats quartered nearby, and plants, soil and water from the adjacent area
were surveyed to determine the public health significance of lead pollu-
tion originating from this factory. Eighty-six percent of company
laborers were found to have blood lead levels at or greater than 80
yg/100 ml, and in two years since the installation of a blast furnace by
the company, .at least nine employees had been hospitalized for treatment
of lead poisoning, primarily but not exclusively lead colic. Illnesses
and deaths from lead poisoning have been demonstrated in cows, horses,
dogs and cats quartered in the vicinity of the smelter. A case of
chronic plumbism in a survivor of bovine lead poisoning has been de-
scribed. Cows foraging on land within 400 yards downwind of the smelter
furnace have been determined to be in danger of dying from lead poison-
ing. Lead poisoning has also been found to present a significant threat
to the health of children residing within 100 yards downwind. Apparent
deviations from good practice are a major obstacle to controlling lead
pollution by the company and in instituting proper medical supervision
of its workers. Blood protoporphyrin has been suggested as a better
measure of cumulative lead-induced physiologic damage than blood lead.
Normal blood protoporphyrin values for cattle and a correlation between
elevated blood lead and elevated blood protoporphrin in these animals
have been established for the first time. Normal values for hair lead
of cattle, horses and dogs have also been determined.
Neuropsychologic Dysfunction in Children with Chronic Low-Level
Lead flbsorptipnla ^ The relationship between low-level lead absorption
and neuropsychologic function is not clearly defined. To investigate it
further, neurologic and psychologic evaluations were undertaken of 50
asymptomatic children, ages 3 to 15 years, with blood lead concentra-
tions of 40 to 60 vg/100 ml (mean, 49 yg/100 ml) and of 81 controls with
levels less than 40 yg/100 ml (mean, 27 yg/100 ml). Groups were matched
by age, sex, ethnic background, and socioeconomic status. All children
lived within 4 miles of a large smelter, and smelter emissions were a
major source of absorbed lead. Lead exposure was chronic (mean, 6.6
years) and, in many instances, lifelong.
426
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Performance I.Q. was found to be significantly lower in the chil-
dren with lead levels greater than or equal to 40 -pg/TOO ml (mean scores
94 versus 102, p <0.01j. Children 1n this group also showed subclinical
weakness of wrist muscles as compared to controls. Verbal I.Q., activ-
ity and behavior ratings, and other neurologic functions did not differ
significantly. . These findings suggest that Tow-level lead absorption,
at least when it is of sufficiently early onset and long duration, may
produce definite neuropsychologic impairment. Whether the impairment
noted in this study will be reversible remains to be determined.
Non-Professional Saturnism: A Pollution Epidemic from Industrial
Emission^ - An epidemic of lead poisoning occurred among residents of a
small Italian community, Stanghella, in the proximity of a plant for the
fusion of lead from used automobile batteries. Of the 179 persons
examined, 30.7 percent had urinary lead levels between 30 to 60 micro-
grams/I and 37.2 percent had significantly high levels. Such levels are
not generally encountered in individuals without occupational exposure
to lead. High levels of erythrocytic protoporphyrins proved the exis-
tence of very high lead concentrations in the tissues of about two-
thirds of the population. Only one-third of the cases showed a definite
increase in urinary coproporphyrins; however, the majority of the sub-
jects were examined 3 months after the plant was closed and urinary
coproporphyrins are known to decrease rapidly following cessation of
lead exposure. Pronounced iron anemia was registered in 12 cases. Most
subjects lived 300 to 700 feet downwind from the plant, suggesting that
the lead poisoning was brought about by direct contamination of their
houses and front yard vegetable gardens.
Chromosome Aberrations Observed in Male Workers Occupational1y
Exposed to Lead!5 - Chromosome observations were performed on periphera1
blood lymphocytes of 14 workers from a zinc industry who have presented
signs of lead poisoning of different degrees. According to type and
duration of exposure, workers examined were divided into three groups:
those exposed to a high level of zinc and low levels of lead and cad-
mium; those exposed to high levels of the three minerals; and those
exposed to high levels of lead and cadmium in the absence of zinc. The
aberrations were dicentrics, rings, chromatid exchanges, as well as gaps
and fragments. Exposure to zinc and cadmium does not seem to increase
the number of cells with severe chromosome anomalies, and lead intoxica-
tion can be considered to be responsible for the chromosome aberrations.
Manganese
Industrial Hygenic Studies on Manganese - Forty-one workers in
the manganese railing manufacturing process were examined to see the
effects of traceable manganese dusts on their health. Their medical
427
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histories, conscious symptoms, chest x-rays, manganese excretion in
urine, and other nervous and physiological symptoms were examined. Air
samplings were taken by a hi-volume sampler, particle size was measured
by the Andersen air sampler, and the Mn content in dusts and urine was
measured by atomic absorption spectrophotometry. The total amount of
dusts in three areas were 9550, 4058, and 2834 mg/cu m and the dust
particle sizes were generally large (only 13.3% were less than 2 mi-
cron). The Mn content in dust was 0.963 percent: by individual sam-
plers, Mn in dust was 1.467 mg/cu m. It was far below the maximum
allowable concentration in the working environment which is 5 mg/cu m.
The workers average age was 43.2 years, the average duration of work in
the same environment was 15.6 years, 65.9 percent were older than 40
years, and 75.6 percent had worked more than 10 years. The chest x-ray
revealed 12 workers (29.3%) with pneumoconiosis. They were all older
than 40 years old and had worked more than 15 years in the same environ-
ment. Significant differences from the control group were noted in the
complaints of hip pains (39.0%) and the average on the total number of
complaints (12.6%). Other symptoms with high rates of complaints were
increased sputum (41.5%), wheezing (7.3%), chest pain (9.8%), fatigue
(29.3%), and pain in the joints (34.2%).
Nickel
Some Statistical Materials on Carcinogenic Hazards in the Produc-
tion of Nickel17 - The increased mortality rates due to carcinoma and
sarcoma among workers of a nickel combine were statistically investi-
gated and compared with similar rates for the city population and en-
virons. Lung cancer accounted for the highest mortality rate at a
factor of 2.8 greater than that expected among males 40 years old and
older working at the roasting-reduction and cobalt shops and exposed to
dusts containing nickel sulfides, nickel oxides, cobalt and arsenic
compounds. The average service period for workers employed in nickel
shops who died of pulmonary carcinoma was 13 years. Femoral end pulmo-
nary sarcomas were most often encountered among the men at the combine.
Copper, Lead, or Zinc Smelters
18
Occupational Lung Cancer Among Copper Smelters ° - Because a high
lung cancer mortality rate was noted among males in a town, a case
control study was carried out on the basis of mortality cards. The case
group consisted of 19 males who died from lung cancer and a control
group of 19 males who died of other causes. The only significant dif-
ference found is that 11 of the 19 subjects with lung cancer had been
employed as smelters in a local copper refinery, and exposed to arsenic
and other compounds. In all 11 cases, the disease became manifest after
the men had stopped working in the refinery.
428
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1 9
An Environmental Impact Study of a Zinc Smelter - It is the
conclusion of this report that the Asarco zinc smelter 1n Araarillo,
Texas 1s emitting participate and heavy metal contaminants to the atmo-
sphere. This report finds that:
a. Zinc, cadmium, lead and mercury are being emitted by the
plant.
b. There is sufficient information to suggest a direct connection
between the plant emissions and blood cadmium levels in chil-
dren of the area.
c. Concentrations of zinc, lead and cadmium are building up in
the soils adjacent to the plant.
d. Zinc emissions from the plant contribute about 20 percent of
the atmospheric lead burden in the area.
e. Lead emissions from the plant contribute about 20 percent of
the atmospheric lead burden in the area.
f. Stack emissions appear to be in compliance with Air Control
Board regulations.
g. It is undisputed by the staff and Asarco that fugitive emis-
sions are in violation of present Air Control Board regula-
tions and will also be in violation of new regulations to be
enforced after December 31, 1973.
The following conclusions are drawn by this report:
a. No significant toxic effects should result from zinc oxide
emissions by the plant.
b. Lead levels in the Amarillo area are not above normal urban
levels.
c. If retort emissions contain 50 percent by weight zinc, it is
technologically and economically feasible for the plant to
install abatement equipment.
429
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430
-------
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431
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432
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433
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436
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Cadmium and Lead. Reprinted from Trace Substances in
Environmental Health - VL 1973. A symposium, D. D.
Hemphill, Ed., University of Missouri, Columbia.
100. Poetzl, K. and R. Reiter. Study of Retention of
Chemical Components of Industrial Aerosols. (Zur
Retinierbarkeit der chemischen Komponenten von Indus-
trieaerosolen.) Text in German. Zentr. Arbeitsmed.
Arbeitsschutz. 19 (9):1-8, 1969.
101. Posner, E. Diagnosis and Management of Industrial
Chest Disease (Respiratory Tract Disease). British
Med. J. 1(5486):525-529, February 26, 1966.
102. Puget Sound Air Pollution Control Agency. The Concen-
tration of Lead, Arsenic, Mercury, Cadmium, S02 and
Suspended Sulfates Downwind from the Tacoma Smelter,
the Impact and Control Status, and Benefits from
Reduction. (Presented to the ASARCO Impact Task
Force. January 1, 1975.)
0103. Rajner, V. Effect of Vanadium on the Respiratory Tract.
(Vliv Vanadu na Dychaci Cesty.) Translated from Czech.
(Presented at the National ORL (Otolaryngolocical)
Conference. Karlovy Vary, Czechoslovakia. October 8,
1959.) Cesk. Otolaryngol. 9:202-204, August 1960.
104. Reiter, R., K. Poetzl, and W. Carnuth. An Automatic
Retention Simulator. (Bin automatischer Retentions-
simulator.) Text in German. Staub, Reinhaltung
Luft. 32(10):392-399, October 1972.
105. Roschin, A. V. Industrial Aerosols of Rare Metals and
Their Hygienic Significance. British Occupational
Hygiene Society. (London) 2:811-817, 1971.
442
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106. Roschiiri/. I. V. Hygienic Aspects of Industrial Vanadium
Aerosol. Translated from Russian. Literature on Air
Pollution and Related Occupational Disease. 4:109-
114, August 1960.
107. Rossano, A. T. and H. McClannan. Concentrations of
Arsenic and Lead in Airborne Particulates and House-
hold Dust in The Vicinity of a Copper Smelter - A
Preliminary Report. PNWIS-APCA Paper 74-AP-31. Boise,
Idaho. November 18, 1974.
108. Sahagian, B. M., et al. Transmural Movements of Zinc,
Managanese, Cadmium and Mercury by Rat Small Intestine.
Dept. of Internal Medicine, Washington Univ. School
of Medicine and Cochran Veterans Admin. Hospital,
St. Louis, Missouri. May 1967.
109. Saito, K., T. Sato, Y. Sato, and K. Niizuma. Effect
of Low Lead Concentration on Human Body. Ind. Health
(Japan). ll(3):85-93, Sept. 1973. (Presented at
the 31st Japanese Society of Public Health. Sapporo,
Japan. October 25027, 1972.)
110. Sawinsky A., J. Durszt, and G. Pasztor. Leukocyte
Damage Through Exposure to Lead. (Leukozytenschaed-
igung bei Bleiexposition.) Text in German. Z. Ges.
Hyg. Grenzg. (Berlin) 17(4):239-240, 1971.
111. Sayre, J. W., M.D., et al. House and Hand Dust as a
Potential Source of Childhood Lead Exposure. Am J.
Dis Child. Vol 127, February 1974.
112. Schegel, H., G. Kufner, and H. Leinberger. The Practice
of Lead-Damage Prevention in the Metal-Working Indus-
try. Translated from German. Lead and Environment
1972. West German Federal Ministry of Health, Commis-
sion for Environmental Dangers Lead Working Group.
p. 111-130, 1972.
113. Schroeder, H. A. and D. K. Darrow. Relation of Trace
Metals to Human Health. Environmental Affairs.
11(1):222-236.
114. Schuetzle, D. Arsenic in the Air in Puget Sound Area.
Air Resources Division, University of Washington,
Seattle. 1971.
115. Schulz, E. J. Arsenic as a Cause of Skin Cancer, with
Notes on Its Occurrence in Pretoria. S.A. Medical
Journal. (Presented at the Conference on Chemical
Carcenogenesis. Johannesburg. July 1966.) p. 819-822,
443
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116. Secchi, G. C., L. Alessio, and G. Cambiaghi. Studies
on Ala-Dehydratase Activity of Erythrocytes in Subjects
Not Occupationally Exposed to Lead, Living in Urban
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sica eritrocitaria di soggetti non exposti a contatto
professionale con piombo ed abitanti in zone rurali
ed urbane.) Text in Italian. Med. Lavoro. (Milan)
62:435-450, October 1971.
117. Selikoff, I. J., Ed. Hazards of Mercury. Academic
Press. 4(1), March 1971.
118. Selyankina, K. P. and L. N. Alekseeva. Selenium and
Tellurium in the Atmosphere Around Electrolyte Copper
Plants. Hygiene and Sanitation. EPA and National
Science Foundation. Washington, D.C. 35(3):431-432.
119. Statnick, R. M. Measurement of Sulfur Dioxide, Parti-
culate, and Trace Elements in a Copper Smelter (Tacoma)
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Research Triangle Park, N.C. July 1974.
120. Sullivan, R. J. Preliminary Air Pollution Survey of
Arsenic and Its Compounds. HEW. Raleigh, N.C.
October 1969.
121. Sullivan, R. J. Preliminary Air Pollution Survey of
Nickel and Its Compounds. HEW. Raleigh, N.C. October
1969.
122. Symon, K. and V. Bencko. Health Aspects of Air Pol-
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Air Congress. Duesseldorf, West Germany. 1973.)
p. A53-A55.
123. Tammes, P. M. and M. M. DeLint. Leaching of Arsenic
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Persons Working in the Nickel Industry. (Rak dykha-
telynyky putei u rabot ayushchikh s nikelom.) Text
in Russian. Vopr. Onkol. 13(6):58-60, 1967.
125. The Spector of Cancer. Environmental Science and Tech-
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444
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Rtuti, K Volrosu o Sovmestnom Deistvii Taksicheskogo
I Temperaturiogo Fakorov.) Text in Russian. Gigiena
Truda I Prof. Zabolevaniya. 9:7-12, December 1965.
129. Tsuchiya, K. Results of a Long-Term Observation of
Cadmium Workers. Japan Public Health Assoc. (Pre-
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Translated from Japanese. Redwood City, Calif.
p. 170-185, April 1973.
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Montana, Area Environmental Pollution Study. June 1971,
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the Forested Ozarks of Missouri. Environmental Science
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445
-------
138. Yukio, S., N. Keitaro, M. Yutaka, 0. Masahiro, K.
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446
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2.0 AN EPIDEMIOLOGICAL ANALYSIS OF DISEASE SPECIFIC MORTALITY
ASSOCIATED WITH PRIMARY Cu, Pb AND Zn SMELTING
As illustrated in Section 1.0, the health effects which could be
produced as a result of copper, lead and zinc smelting are both varied
and numerous. A rough estimate of the composition and quantities of
residual metal emissions from existing smelters is available but it is
only extensive enough to provide a general idea of what types of disease
may be produced. In order to obtain a realistic idea of what diseases
are occurring as a result of smelting, mortality data for 16 diseases
has been examined for all counties containing and those surrounding
primary Cu, Pb or Zn smelters which have been operational for at least
35 years. This approach was taken so that mortality profiles for coun-
ties containing smelters could be constructed. By generating a mortal-
ity profile, an overview of the mortality characteristics and potential
health problems of the exposed population can be obtained.
Several cautionary notes must be made in relation to the analysis
which follows. As in all statistical studies with wide scopes, many
variables which could influence the associations discovered could not be
investigated due to a lack of both available data and knowledge concern-
ing all the pertinent variables. Precise quantification has not been
attempted in this study because of the wide scope and limited accuracy
of data concerning smelter characteristics employed. For example, the
data utilized for smelter ore concentrate compositions is only consid-
ered to be of order of magnitude accuracy and is used accordingly.
Also, it was not possible to adjust county mortality rates for such
factors as population, population density, income, and other factors
known to influence disease rates. Thus, the nature of this study does
not lend itself to the computation of confidence intervals or other
classical statistical methods for determining significance. This anal-
ysis was designed to determine what disease specific mortality is linked
with primary Cu, Pb, and Zn smelting. In depth epidemiological analyses
involving clinical evaluations of the affected members of the exposed
populations will be required to substantiate the validity of the asso-
ciations presented.
DATA AND METHODS
The basic strategy of this analysis was to generate mortality
profiles for counties containing smelters as compared to all surrounding
counties. A justification for this type of approach rests with the fact
447
-------
that a smelter can be considered a point emissions source within a given
county. Thus, if smelter emissions were producing adverse health ef-
fects, the county containing the smelter would be expected to bear the
largest adverse effect as compared to all surrounding counties. All
primary Cu, Pb or Zn smelters which have been operational for at least
35 years have been examined by comparing smelter-county mortality data
for sixteen diseases. The sixteen diseases used to construct smelter-
county mortality profiles are listed in Table 2-1 along with their ICD
(International Classification of Diseases) Code. These diseases were
chosen upon the basis of availability of data and known target organs of
metal toxicity (Table 1-2). A 35 year period of continuous smelter
operation was included as a necessary condition to allow sufficient time
for the scope of the mortality data, and the latency periods for chronic
diseases and cancer.
Mortality data for this analysis were taken from two sources which
employed two different revisions of the ICD Code, but the procedures
used for data reduction were completely analogous for both data sets.
The most specific county mortality data were taken from the HEW publica-
tion, U.S. Cancer Mortality By County: 1950-1969.1 This data source
contained average annual age-adjusted cancer mortality rates and yielded
information about the magnitude of death rates. The other source of
data employed, Vital Statistics of the U.S. 1971 Volume II - Mor-
tality, Part B,2 had the advantage of not being limited to only cancer
mortality. However, only the actual number of deaths which occurred in
the counties were reported. Consequently, average annual age-adjusted
mortality rates were not available, and no accurate estimate of the
absolute magnitude of mortality rates could be made. As an alternative,
percentages of total deaths in a county which were caused by specific
diseases were calculated and substituted for absolute mortality rates
for non-cancer causes of death. Although the latter mortality parameter
is not as desirable or sensitive as mortality rates, it can still indi-
cate excess disease specific mortality within a given county. For
convenience, the summarized mortality data are presented in two parts
with each part corresponding to the sources from which the data were
taken. Preceding the summarized cancer mortality data, a detailed
example of the data reduction procedure is given. No example of the
reduction procedures used in data taken from the second source is pre-
sented because the two procedures were totally analogous except for a
substitution of percentages of total deaths for mortality rates.
The following series of tables will demonstrate the procedure used
in working up published mortality data. Table 2-2 was prepared by first
listing the county containing the Bunker Hill lead smelter and then all
counties contiguous to that county. All cancer mortality rates in
Table 2-2 were taken from the reference footnoted in the table. Tables
448
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Table 2-1. CAUSES OF DEATH USED TO GENERATE MORTALITY
PROFILES FOR COUNTIES CONTAINING Cu, Pb OR Zn SMELTERS
International
Classification
of Disease
(ICD) Code
8th Revision
Causes of Noncancer Deaths
Major cardiovascular disease
Hypertensive heart disease
Ischemic heart disease
Other forms of heart disease
Hypertens ion
Cerebrovascular disease
Arteriosclerosis
Other small vessel disease
Influenza and pneumonia
Bronchitis, emphysema and asthma
Causes of Cancer Deaths
All cancers combined
Cancer of the liver and biliary
passages
Cancer of the trachea, lung and
bronchus
Cancer of the kidney
Cancer of the bladder
Cancer of the thyroid
390 - 448
402 & 404
410 - 413
420 - 429
400, 401, 403
430 - 438
440
441 - 448
470 - 474, 480 - 486
490 - 493
ICD Code
6th revision
140 - 205
155
162, 163
180
181
144
449
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Table 2-2. CANCER MORTALITY RATES FROM 1950-1969 FOR COUNTIES
IN THE AREA OF THE BUNKER HILL LEAD SMELTER**
County, State
*
Shoshone , Idaho
Latah, Idaho
Kootenai , Idaho
Benewah, Idaho
Clearwater, Idaho
Bonner, Idaho
Mineral , Montana
Sanders, Montana
Average Annual Age-Adjusted Cancer Mortality
Rates Per 100,000 Population (Male/Female)
Liver and
Biliary
Passages
(ICD-
155)
5.7/6.8
3.9/4.1
4.0/5.0
4.6/5.2
5.0/3.4
1.6/6.2
3.5/0
2.7/7.0
Trachea,
Lung and
Bronchus
(ICD-
162,163)
37.6/8.2
16.5/2.1
26.4/4.9
27.6/5.5
21.6/0
24.5/4.5
33.4/9.7
21.5/4.0
Kidney
(ICD-
180)
7.6/1.8
3.2/3.1
.9/.7
3.9/3.5
2.9/1.2
6.6/1.2
0/0
3.9/1.4
Bladder
(ICD-
181)
6.0/1.8
7.7/2.1
4.5/1.8
1.2/0
3.0/0
S.4/.6
9.7/1.9
2.2/1.0
Thyroid
(ICD-
144)
1.5/1.8
.5/1.5
1.3/2.1
0/1.8
1.0/0
.5/.6
0/0
0/0
All
Combined
191.5/121.2
145.3/107.5
139.0/120.0
143.9/134.5
124.4/94.1
134.1/115.6
163.4/78.3
127.8/100.3
*>.
Ul
o
County contains Bunker Hill Pb smelter.
All cancer rates were taken from the HEW publication: U.S. Cancer Mortality
by County; 1950-1969. This source used the 6th revision of the ICD Code.
-------
2-3A through 2-3F are simply a ranking of the average male and female
cancer mortality rates for individual cancers and are based upon Table
2-2; "1" indicates the county with the lowest observed rate while "8"
implies the highest cancer rate. For ease in comparison of the cancer
mortality rankings of Shoshone County with that of other smelter con-
taining counties, the numerical rankings in Table 2-3A through 2-3F can
be converted to normalized percentfle rankings. Thus Shoshone County
was ranked sixth in bladder cancer out of 8 counties in the area (Table
2-3D) so its percentile ranking is 6/8 • 100 -0.5 (1/8) or 69. Simi-
larly, Shoshone County ranked eighth out of 8 counties in liver, lung,
kidney and all cancers so its percentile ranking for these categories is
8/8 • 100 - 0.5 (1/8) or 94. The percentile cancer mortality rankings
for Shoshone County have been summarized in the first entry of Table 2.4
denoted simply "Bunker Hill-Kellog, Idaho." Tables 2-4, 2-5 and 2-6
list only the percentile cancer mortality rankings for all Pb, Zn and Cu
smelters examined, however, analogous procedures were used to obtain
each table entry. Similarly, Tables 2-7, 2-8 and 2-9 list only the
percentile non-cancer mortality rankings for all Pb, Zn and Cu smelters
examined. For some diseases, there were an insufficient number of
deaths in a particular cluster of counties to compute meaningful per-
centile mortality rankings; these cases are denoted with a dash (-) in
Tables 2-4 through 2-9.
451
-------
to
Table 2-3A. LIVER AND BILIARY PASSAGES CANCER MORTALITY RANKINGS FOR COUNTIES
IN THE AREA OF THE BUNKER HILL LEAD SMELTER**
County, State
*
Shoshone, Idaho
Latah, Idaho
Kootenai, Idaho
Benewah, Idaho
Clearwater, Idaho
Bonner, Idaho
Mineral, Montana
Sanders, Montana
Average Annual Age-Adjusted Cancer
Mortality Rates Per 100,000 Population
(Male Rate + Female Rate)/2
6.25
4.0
4.5
4.9
4.2
3.9
1.75
4.85
Ranking
8
3
5
7
4
2
1
6
County contains Bunker Hill Pb smelter.
**
All cancer rates were taken from the HEW publication:
U.S. Cancer Mortality by County; 1950-1969. This source
used the 6th revision of the ICD Code.
-------
ui
co
Table 2-3B. TRACHEA, LUNG AND BRONCHUS CANCER MORTALITY RANKINGS FOR COUNTIES
IN THE AREA OF THE BUNKER HILL LEAD SMELTER**
County, State
*
Shoshone , Idaho
Latah, Idaho
Kootenai , Idaho
Benewah, Idaho
Clear-water, Idaho
Bonne r , I daho
Mineral , Montana
Sanders, Montana
Average Annual Age-Adjusted Cancer
Mortality Rates Per 100,000 Population
(Male Rate + Female Rate)/2
22.9
9.3
15.65
16.55
10.80
14.5
21.55
12.75
Ranking
8
1
5
6
2
4
7
3
County contains Bunker Hill Pb smelter
**A11 cancer rates were taken from the HEW. publication:
U.S. Cancer Mortality by County; 1950-1969. This source
used the 6th revision of the ICD Code.
-------
Table 2-3C. KIDNEY CANCER MORTALITY RANKINGS FOR COUNTIES
IN THE AREA OF THE BUNKER HILL LEAD SMELTER**
County, State
*
Shoshone, Idaho
Latah, Idaho
Kootenai , Idaho
Benewah, Idaho
Clearwater, Idaho
Bonner, Idaho
Mineral, Montana
Sanders, Montana
Average Annual Age-Adjusted Cancer
Mortality Rates Per 100,000 Population
(Male Rate + Female Rate)/2
4.7
3.15
0.8
3.7
2.05
3.9
0.0
2.6
Ranking
8
5
2
6
3
7
I
4
County contains Bunker Hill Pb smelter.
**A11 cancer rates were taken from the HEW publication:
U.S. Cancer Mortality by County: 1950-1»69. This source
used the 6th revision of the ICD Code.
-------
Table 2-3D. BLADDER CANCER MORTALITY RANKINGS FOR COUNTIES
IN THE AREA OF THE BUNKER HILL LEAD SMELTER**
Ol
Ul
County, State
*
Shoshone, Idaho
Latah, Idaho
Kootenai , Idaho
Benewah, Idaho
Clearwater, Idaho
Bonner, Idaho
Mineral , Montana
Sanders, Montana
Average Annual Age-Adjusted Cancer
Mortality Rates Per 100,000 Population
(Male Rate + Female Rate)/2
3.9
4.9
3.15
0.6
1.5
2.0
5.8
1.6
Ranking
6
7
5
1
2
4
8
3
County contains Bunker Hill Pb smelter.
**A11 cancer rates were taken from the HEW publication:
U.S. Cancer Mortality by County; 1950-1969. This source
used the 6th revision of the ICD Code.
-------
Table 2-3E. THYROID CANCER MORTALITY RANKINGS FOR COUNTIES
IN THE AREA OF THE BUNKER HILL LEAD SMELTER**
County, State
*
Shoshone, Idaho
Latah, Idaho
Kootenai, Idaho
Benewah, Idaho
Clearwater, Idaho
Bonner , Idaho
Mineral, Montana
Sanders , Montana
Average Annual Age-Adjusted Cancer
Mortality Rates Per 100,000 Population
(Male Rate + Female Rate)/2
1.65
1.0
1.70
0.9
0.5
0.55
0.0
0.0
Ranking
7
6
8
5
3
4
1.5
1.5
County contains Bunker Hill Pb smelter.
**A11 cancer rates were taken from the HEW publication:
U.S. Cancer Mortality by County; 1950-1969. This source
used the 6th revision of the ICD Code.
-------
Table 2-3F. MORTALITY RANKINGS FOR ALL CANCERS COMBINED FOR COUNTIES
IN THE AREA OF THE BUNKER HILL LEAD SMELTER**
County, State
*
Shoshone, Idaho
La tab, Idaho
Kootenai , Idaho
Benewah, Idaho
Clearwater, Idaho
Bonner, Idaho
Mineral, Montana
Sanders, Montana
Average Annual Age-Adjusted Cancer
Mortality Rates Per 100,000 Population
(Male Rate + Female Rate)/2
156.4
126.4
129.5
139.2
104.3
124.9
120.9
114.1
Ranking
8
5
6
7
1
4
3
2
County contains Bunker Hill Pb smelter.
**A11 cancer rates were taken from the HEW publication:
U.S. Cancer Mortality by County; 1950-1969. This source
used the 6th revision of the ICD Code.
-------
Table 2-4. LEAD SMELTER CANCER MORTALITY DATA SUMMARY
Facility
Bunker Hill-
Kellog, Idaho
Asarco-E. Helena,
Montana
Asarco-El Paso,
Texas
St. Joe-Herculaneum,
Missouri
Percentile Cancer Mortality Rankings
Liver and
Biliary
Passages
(ICD-
155)
94
79
88
42
Trachea ,
Lung and
Bronchus
(ICD-
162,163)
94
50
88
75
Kidney
(ICD-
180)
94
79
88
42
Bladder
(ICD-
181)
69
93
63
75
Thyroid
(ICD-
144)
82
-
88
25
All
Combined
94
93
88
59
en
oo
All cancer rates were taken from the HEW publication: U.S. Cancer Mortality
by County; 1950-1969. This source used the 6th revision of the ICD Code.
All entries in the above table are percentile cancer mortality rankings of counties
containing smelters as compared to all contiguous counties. The ranking was accomplished
using average annual age-adjusted mortality rates per. 100,00.0 population fo.r.Jthe years
1950 through 1969. A representative county cancer rate was obtained by averaging white
male and female rates.
-------
Table 2-5. ZINC SMELTER CANCER MORTALITY DATA SUMMARY
Facility
Bunker
Hill-
Kellog,
Idaho *
Asarco-
Amaril-
Jo, Texas
Asarco-
Corpus
Christi,
Texas
Araax-
Blackwell,
Dkla.
National
Zinc-
Bartles-
ville,
Okla.
N. J.Zinc-
Palmerton ,
Pa.
St . Joe-
Monoca,
Pa.
Percentile Cancer Mortality Rankings
Liver and
Biliary Passages
(ICD-155)
94
45
32
57
22
88
32.
Trachea
Lurig and
Bronchus
(ICD-
162-163)
94
95
94
82
79
13
69
Kidney
(ICD-180)
94
95
19
69
79
92
82
Bladder
(ICD-181)
69
40
82
69
64
21
94
All
Combined
94
95
94
94
79
38
57 •'
*This facility is also a Pb smelter.
All cancer rates were taken from the HEW publication; U.S. Cancer
Mortality by County: 1950-196'9. This source used the 6th revision
of the 1CD Code.
All entries in the above table are percentile cancer mortality
rankings of counties containing smelters as compared to all con-
tiguous counties. The ranking was accomplished using average annual
age-adjusted mortality rates per 100,000 population for the years
1950 through 1969. A representative county cancer rate was obtained
by averaging white male and female rates.
459
-------
Table 2-6. COPPER SMELTER CANCER MORTALITY DATA SUMMARY
Facility
*Asarco-Tacoma ,
Washington
Anaconda-
Anaconda , Mon .
Kennecott-
McGill, Nevada
Kennecott-
Garfield, Utah
Cities Service-
Copperhill,
Tennessee
Asarco-El Paso,
Texas***
Kennecott-
Hurley, New
Mexico
Inspiration-
Miami, Ariz.
Asarco-
Hayden, Ariz.
**
Phelps Dodge -
Morenci, Ariz.
Phelps Dodge-
Douglas, Ariz.
Percentile Cancer Mortality Rankings2
Liver and
Biliary Passages
(ICD-155)
63
64
69
64
96
. 88
70
79
75
36
93
Trachea, Lung
and Bronchus
(ICD-162,163)
79
93
32
50
79
88
90
93
95
50
79
Kidney
(ICD-180)
46
36
82
93
63
88
90
93
95
50
22
Bladder
(ICD-181)
59
50
82
57
79
63
30
93
80
64
93
All Combined
88
50
69
79
96
88
90
93
'95
22
79
Average ranking of Pierce and King Counties. Two of six contiguous counties also contain
Cu smelters. ***This facility is also a Pb smelter.
IAH cancer rates were taken from the HEW publication: U.S. Cancer Mortality by County^ 1950-1969.
This source used the 6th revision of the ICD Code.
2A11 entries in the above table are percentile cancer mortality rankings of counties containing
smelters as compared to all contiguous counties. The ranking was accomplished using average annual
age-adjusted mortality rates per 100,000 population for the years 1950-1969. A representative
county cancer rate was obtained by averaging white male and female rates.
-------
Table 2-7. LEAD SMELTER NON-CANCER MORTALITY DATA SUMMARY'
Facility
Bunker Hill -
Kellog, Idaho
Asarco -
E. . Helena,
Montana
Asarco -
El Paso,
Texas
St. Joe -
Herculaneum,
Missouri
Percentile Mortality Rankings for Percentages
of Total Deaths Due to the Indicated Disease2
ICD Code3
390-
448
19
22
38
25
402 &
404
44
36
88
50
410-
413
57
64
13
43
420-
429
7
36
63
25
400, 401,
403
-
64
63
25
430-
438
19
64
63
59
440
94
7
63
25
441-
448
480-486
19
79
63
75
470-
474
7
36
63
75
490-
493
32
79
63
42
1. All mortality data was taken from: Vital Statistics of the U.S. 1971. Volume II-
Mortality, Part B. This source used the 6th revision of the ICD Code.
2. All entries in the above table are percentile non-cancer mortality rankings of
counties containing smelters as compared to all contiguous counties. The ranking
was accomplished by using the percentages of total deaths due to the above
indicated diseases for each of the counties examined.
3. See Table 2.1 for the ICD Code key.
-------
Table 2-8. ZINC SMELTER NON-CANCER MORTALITY DATA SUMMARY"
CPi
Facility
Bunker Hill -
Kellog, Idaho*
Asarco -
Amarillo,
Texas
Asarco -
Corpus Christi,
Texas
Amax -
Blackwell,
Oklahoma
National Zinc -
Bartlesville,
Oklahoma
N.J. Zinc -
Palmerton ,
Pennsylvania
St. Joe -
Monaca,
Pennsylvania
Percentile Mortality Rankings for Percentages
of Total Deaths Due to the Indicated Disease2
ICD Code 3
390-
448
19
77
44"
82
64
38-
19
402 &
404
44
68
63
7
93
71
82
410-
413
57
95
69
82
64
13
19
420-
429
7
50
19
32
7
46
94
400, 401,
403
.-
77
82
82
79
34
32
430-
438
19
59
19
57
50
96
94
440
94
40
57
44
64
46
44
441-
448
19
59
32
69
7
63
44
ffl-
480-486
7
68
32
32
36
96
94
490-
493
32
31
44
57
50
4
57
* This facility is also a Pb smelter.
1. All mortality data was taken from:
Vital Statistics of the U.S. 1971. Volume II-
Mortality, Part B. This source used the 6th revision of the ICD Code.
2. All entries in the above table are percentile non-cancer mortality rankings of
counties containing smelters as compared to all contiguous counties. The ranking
was accomplished Ly using the percentages of total deaths due to the above indicated
diseases for each of the counties examined.
3. See Table 2.1 for the ICD Code key.
-------
Table 2-9. COPPER SMELTER NON-CANCER MORTALITY DATA SUMMARY
u>
Percentile Mortality Rankings for Percentages
of Total Deaths Due to the Indicated Disease2
Facility
Asarco -
Tacoma ,
Washington
Anaconda -
Anaconda,
Montana
Kennecott -
McGill,
Nevada
Kennecott -
Garfield,
Utah
Cities Service -
Copperhill,
Tennessee
Asarco -
El Paso*, Texas
TCD Code3
i :
390-
448
63
93
19
36'
54
38
402 &
404
29
79
_.
79
54
88
410-
413
71
93
94
22
63
13
420-
429
38
79
13
50
63
63
400, 401,
403
29
_
—
79
21
63
430-
438
79
50
44
50
38
63
440
21
36
57
64
79
63
441-
448
13
22
82
50
54
63
470-
474
480-486
29
7
82
50
54
63
490-
493
79
'93
13
36
29
63
* This facility is also a Pb smelter.
1. All mortality data was taken from: Vital Statistics of the U.S. 1971. Volume II -
Mortality, Part B. This source used the 6th revision of the ICD Code.
2. All entries in the above are percentile non-cancer mortality rankings of counties con-
taining smelters as compared to all contiguous counties. The rankings was accomplished
by using the percentages of total deaths due to the above indicated diseases for each
of the counties examined.
3. See Table 2.1 for the ICD Code key.
-------
Table 2-9 (continued). COPPER SMELTER NON-CANCER MORTALITY DATA SUMMARY
it*
Percentile Mortality Rankings for Percentages
of Total Deaths Due to the Indicated Disease2
Facility
Kennecott -
Hurley,
New Mexico
Inspiration -
Miami, Arizona
Asarco -
Hayderi ,
Arizona
Phelps Dodge -
Morenci ,
Arizona?1*
Phelps Dodge -
Douglas,
Arizona
ICD Code3
':>
390-
448
50
50
55
22
50
402 &
404
90
64
75
-
29
•'
410-
413
70
50
55
36
22
420-
429
10
22
25
79
36
400, 401,
403
30
93
95
_
79
430-
438
50
7
15
36
64
440
70
7
5
64
50
441-
448
20
50
65
64
79
470-
474
480-486
50
64
75
7
36
490-
493
70
36
35
22
64
1971. Volume II -
3.
Two of six contiguous counties also contain Cu smelters.
All mortality data was taken from: Vital Statistics of the U.S.
Mortality, Part B. This source used the 6th revision of the ICD Code.
All entries in the above are percentile non-cancer mortality rankings of counties con-
taining smelters as compared to all contiguous counties. The rankings was accomplished
by using the percentages of total deaths due to the above indicated diseases for each
of the counties examined.
See Table 2.1 for the ICD Code key.
-------
OBSERVED MORTALITY ASSOCIATIONS FOR COUNTIES CONTAINING Cu, Pb, OR Zn
SMELTERS
Tables 2-4 through 2-9 presented mortality profiles for each county
which contained a Cu, Pb or Zn smelter chosen for this analysis. Cer-
tain disease specific mortality associations appeared when the summary
data in these tables was inspected closely; these mortality associations
are listed in Tables 2-10 through 2-12. It should be emphasized again
that the basis for determining excess mortality was a comparison between
mortality parameters in smelter-containing versus all contiguous coun-
ties. It is interesting to note that only two excess mortality associa-
tions, cancer of the trachea, lung and bronchus and all cancers com-
bined, were observed for the majority of Cu, Pb and Zn smelters exam-
ined. Another particularly striking industry specific association was
the association of excess mortality due to hypertension and hypertensive
heart disease with only the majority of zinc smelters.
The five diseases for which excess mortality was associated with
the majority of lead smelters were (Table 2-10):
1. All cancers combined.
2. Cancer of the liver and biliary passages.
3. Cancer of the trachea, lung and bronchus.
4. Cancer of the kidney.
5. Cancer of the bladder.
If mortality from these diseases was not associated with counties
containing primary lead smelters, then the average disease specific
percentile mortality ranking of all these counties would be expected to
be 50 for each of the five diseases. From Tables 2-4 and 2-7, the
average percentile mortality ranking of all the counties containing lead
smelters examined, for each of the five diseases can be calculated to
be:
1. 76 = (94 + 79 + 88 + 42)/4 for cancer of the liver and biliary
passages,
2. 77 for cancer of the trachea, lung and bronchus,
3. 76 for cancer of the kidney.,
4. 75 for cancer of the bladder,
465
-------
Table 2-10. OBSERVED MORTALITY ASSOCIATIONS FOR
COUNTIES CONTAINING PRIMARY LEAD SMELTERS
1. An increase in the percentage of total deaths or high
absolute mortality rates for the following causes of
death are associated with the majority of Pb smelters
examined (_> 75%) :
a. All cancers combined.
b. Cancer of the liver and biliary passages.
c. Cancer of the trachea, lung and bronchus.
d. Cancer of the kidney.
e. Cancer of the bladder.
2. Both the Asarco-El Paso/ Texas and the Asarso-East
Helena, Montana Pb smelters have associated, elevated
percentages of total deaths due to bronchitis, emphysema
and asthma.
3. The St. Joe-Herculaneum, Missouri and the Asarco-El Paso
Pb smelters have associated, elevated percentages of total
deaths due to influenza and pneumonia.
4. The Bunker Hill-Kellog, Idaho and the Asarco-El Paso,
Texas Pb smelters have associated, elevated percentages
of total deaths due to arteriosclerosis.
5. The Asarco-E. Helena, Montana and the St. Joe-Herculaneum,
Missouri Pb smelters have associated, elevated peicentages
of total deaths due to small vessel disease other than
arteriosclesosis.
6. St. Joe-Herculaneum, Missouri is the only Pb smelter
which does not have associated high mortality rates for
cancer of the kidney, thyroid and liver and biliary
passages.
466
-------
Table 2-11. OBSERVED MORTALITY ASSOCIATIONS FOR
COUNTIES CONTAINING PRIMARY ZINC SMELTERS
1. An increase in the percentage of total deaths or high
absolute mortality rates for the following causes of
death are associated with the majority of Zn smelters
examined (>_ 67%) :
a. Hypertension.
b. Hypertensive heart disease.
c. All cancers combined.
d. Cancer of the trachea, lung and bronchus.
e. Cancer of the kidney.
f. Cancer of the bladder.
2. Both the Asarco-Amarillo, Texas and the Amax-Blackwell,
Oklahoma Zn smelters have associated, elevated percent-
ages of total deaths due to major cardiovascular disease
and ischemic heart disease.
3. Both the New Jersey Zinc-Palmerton, Pennsylvania and the
St. Joe-Monaca, Pennsylvania Zn smelters have associated,
elevated percentages of total deaths due to cerebrovas-
cular disease and influenza and pneumonia.
4. New Jersey Zinc-Palmerton, Pennsylvania and St. Joe-
Monaca, Pennsylvania are the only Zn smelters examined
which do not have associated, elevated percentages of
total deaths due to hypertension.
5. Both the Asarco-Amarillo, Texas and the Asarco-Corpus Christi,
Texas Zn smelters have associated, extremely high mortality
rates for cancer of the trachea, lung and bronchus.
NOTE: The Bunker Hill-Kellog, Idaho facility is both a
zinc and lead smelter. For this reason, the
Bunker Hill facility was not used in constructing
zinc smelter mortality associations.
467
-------
Table 2-12. OBSERVED MORTALITY ASSOCIATIONS FOR
COUNTIES CONTAINING PRIMARY COPPER SMELTERS
1. High, absolute mortality rates for the following causes of
death are associated with the majority of Cu smelters
examined (>_ 70%) :
a. All cancers combined.
b. Cancer of the liver and biliary passages.
c. Cancer of the trachea, lung and bronchus.
2. Increased percentages of the total deaths due to hypertensive
heart disease are associated with the following Cu smelters
(40% of those examined):
a. Anaconda - Anaconda, Montana.
b. Kennecott - Garfield, Utah.
c. Kennecott - Hurley, New Mexico.
d. Asarco - Hayden, Arizona.
3. Increased percentages of the total deaths due to hypertension
are associated with the following Cu smelters (40% of those
examined):
a. Kennecott - Garfield, Utah.
b. Inspiration - Miami, Arizona.
c. Asarco - Hayden, Arizona.
d. Phelps Dodge - Douglas, Arizona.
4. Increased percentages of the total deaths due to ischemic
heart disease are associated with the following Cu smelters
(30% of those examined):
a. Anaconda - Anaconda, Montana.
b. Kennecott - McGill, Nevada.
c. Kennecott - Hurley, New Mexico.
468
-------
Table 2-12.(continued) OBSERVED MORTALITY ASSOCIATIONS FOR
COUNTIES CONTAINING PRIMARY COPPER SMELTERS
5. Increased percentages of the total deaths due to bronchitis,
emphysema and asthma are associated with the following Cu
smelters (30% of those examined):
a. Asarco - Tacoma, Washington.
b. Anaconda - Anaconda, Montana.
c. Kennecott - Hurley, New Mexico.
6. Both the Anaconda - Anaconda, Montana and the Kennecott -
Hurley, New Mexico Cu smelters have associated, elevated
percentages of total deaths due to hypertensive heart disease,
ischemic heart disease, and bronchitis, emphysema and asthma.
7. The Kennecott - Garfield, Utah and the Asarco - Hayden,
Arizona Cu smelters have associated, elevated percentages of
total deaths due to hypertension and hypertensive heart
disease.
8. High, absolute mortality rates for cancer of the kidney are
associated with the followimg Cu smelters (50% of those
examined):
a. Kennecott - McGill, Nevada.
b. Kennecott - Garfield, Utah.
c. Kennecott - Hurley, New Mexico.
d. Inspiration - Miami, Arizona.
e. Asarco - Hayden, Arizona.
9. High, absolute mortality rates for cancer of the bladder are
associated with the following Cu smelters (50% of those
examined):
a. Kennecott - McGill, Nevada.
b. Cities Service - Copperhill, Tennessee.
c. Inspiration - Miami, Arizona.
469
-------
Table 2-12. (continued) OBSERVED MORTALITY ASSOCIATIONS FOR
COUNTIES CONTAINING PRIMARY COPPER SMELTERS
d. Asarco - Hayden, Arizona.
e. Phelps Dodge - Douglas, Arizona.
NOTE: The Asarco - El Paso, Texas facility is both a
copper and lead smelter. For this reason, the
Asarco facility was not used in constructing
copper smelter mortality associations.
470
-------
5. 84 for all cancers combined.
It is clear that the average percentile mortality ranking for each
of these five diseases is above 50. Similar calculations for the excess
disease-specific mortality associated with the majority of either Cu or
Zn smelters lead to an identical conclusion.
The only comparison which can be made between mortality rates in
smelter-containing counties and national mortality rates is for cancer
mortality data. For this purpose, a companion document to the one used
for generating cancer mortality profiles for smelter-containing coun-
ties, Atlas of Cancer Mortality for U.S. Counties: 1950-T969.4 can be
emp1oyecTThis atlas has tabulated the counties which have si gn i fi-
cantly elevated cancer mortality rates as compared to national rates. A
county with a significantly elevated cancer rate was considered to be
one whose 95 percent confidence interval for a specific cancer mortality
rate did not overlap with the 95 percent confidence interval for the
national mortality rate for that same cancer. For three of the five
cancers which were examined for all Cu, Pb and Zn smelters, large per-
centages of smelter-containing counties with significantly high mortal-
ity rates as compared to the percentages of counties in the continental
U.S. with significantly high mortality rates were found. For cancer of
the liver and biliary passages, 3 percent of all continental U.S. coun-
ties had significantly elevated male rates and 7 percent had signifi-
cantly elevated female rates. Of the twenty Cu, Pb or Zn smelter-
containing counties examined in this study, 10 percent had significantly
elevated male mortality rates for cancer of the liver and biliary pas-
sages and 20 percent had significantly elevated female rates. Simi-
larly, the percentage of continental U.S. counties which had signifi-
cantly elevated male/female rates versus the percentage of smelter-
containing counties with significantly elevated male/female rates was 7
percent/5 percent versus 20 percent/20 percent for cancer of the tra-
chea, lung and bronchus and 5 percent/5 percent versus 10 percent/10
percent for all cancers combined.
Table 2-13 lists the smelters and smelter-containing counties which
had significantly elevated cancer mortality rates as compared to na-
tional mortality rates. Only the three cancers mentioned previously are
included in the table because kidney and bladder cancer mortality rates
in smelter-containing counties were not significantly elevated when
compared to national rates. The copper smelter located in Tacoma,
Washington is situated on the border of two counties. For this reason,
both of the counties which the smelter borders were considered as smelt-
er-containing counties.
471
-------
Table 2-13. COPPER, LEAD OR ZINC SMELTER-CONTAINING COUNTIES WITH
SIGNIFICANTLY ELEVATED CANCER MORTALITY RATES
Facility
Asarco-El Paso,
Texas
St. Joe-
Herculaneuin,
Missouri
Asarco -
Amarillo,
Texas
Asarco-Corpus
Christi, Texas
N.J. Zinc-
Palmerton,
Pennsylvania
St. Joe-
Monaca,
Pennsylvania
Asarco-Tacoma ,
Washington
Anaconda-
Anaconda,
Montana
Phelps Dodge-
Douglas ,
Arizona
County of
Location
El Paso
Jefferson
Potter
Nueces
Carbon
Beaver
King**
Deerlodge
Cochise
Type of
Smelter
Lead/
copper
Lead
Zinc
Zinc
Zinc
Zinc
Copper
Copper
Copper
Significantly Elevated Mortality Rates
As Compared to National Mortality Rates*
Cancer of the Liver
& Biliary Passages
Male
t
N
t
Female
t
t
t
t
Cancer of the Trachea
Lung and Bronchus
Male
t
t
t
t
Female
t
t
t
t
All Cancers Combined
Male
t
t
Female
t
t
to
All data for this table was taken from Reference 4. Significance is defined to be the non-
overlap of 95% confidence intervals for county and national mortality rates.
King County is one of the two counties on which this smelter borders.
-------
EXPLANATIONS FOR THE OBSERVED MORTALITY ASSOCIATIONS OF COUNTIES
CONTAINING Cu, Pb OR Zn SMELTERS
Although knowledge of which diseases are claiming the lives of
inhabitants of smelter-containing counties is important, knowledge of
why certain disease specific excess mortality is associated with primary
Cu, Pb and Zn smelting is of far greater importance. In an attempt to
explain the mortality associations presented in the previous section,
two sets of fundamental smelting characteristics were examined. First,
the unit processes employed in smelting which are detailed in the main
body of this report were listed for each facility investigated, and
observed smelter mortality associations were compared with this list to
see if unit processes influenced disease specific mortality. To avoid
redundancy, no descriptions of the unit processes associated with excess
mortality will be presented in this section; readers are therefore urged
to refer to the appropriate sections of the main body of this report for
unit process descriptions. The second set of smelter characteristics
examined were the compositions of the ore concentrates smelted. Un-
fortunately, lead smelter ore concentrate compositions were not avail-
able and were necessarily omitted. All ore concentrate composition data
were taken from unpublished EPA sources and are only considered to be of
order of magnitude accuracy. Consequently, Tables 2-15 and 2-16 only
list ranges of element concentrations in zinc and copper ore concen-
trates for the nine elements examined. Table 2-14 gives the definitions
of levels of element concentrations in ore concentrates used for this
analysis.
No associations between disease specific excess mortality which was
observed for the majority of either Cu, Pb or Zn smelters and unit
processes could be determined from this analysis. In other words, the
disease specific excess mortality linked with the majority of either
primary lead, copper or zinc smelters is probably not a result of the
unit processes employed. The most probable explanation for these indus-
try specific mortality associations (see Tables 2-10, entry [1]; 2-11,
entry [1]; and 2-12, entry £1]) is the common chararacteristics of a
lead, copper or zinc ore concentrate. For example only zinc ore concen-
trates characteristically contain high concentrations of both zinc and
cadmium (Table 2-15).
Due to a lack of ore concentrate composition data for lead smelt-
ers, the ability to explain the observed mortality associations of these
facilities was severely limited. However, the absence of one lead
smelting unit process was found to be associated with the absence of
excess mortality from three diseases. The St. Joe smelter located in
Herculaneum, Missouri was the only lead smelter examined in this study
which did not use slag fuming furnaces, a significant emissions source
473
-------
Table 2-14. DEFINITION OF RANGES OF ELEMENT CONCENTRATIONS
IN Cu AND Zn SMELTER ORE CONCENTRATES
Element
Range of Element Concentration
in Ore Concentrates
(All entries are in ppm
unless otherwise noted)
Low (L) Medium (M) High
(H)
As
Hg
Cd
Pb
Ni
Mn
Zn
Sb
Se
< 200
< 1
< 100
< 1000
< 20
< 100
< 1%
< 100
< 5
200 - 999
1 - 9.9
100 - 999
1000 - 9,999
20 - 99
100 - 999
1% - 29.9%
100 - 999
5-99
>_ 1000
> 10
1000
1%
100
1000
30%
>_ 1000
> 100
474
-------
Table 2-15. QUANTITIES OF NINE ELEMENTS IN
Zn SMELTERS ORE CONCENTRATES
Facility
Quantities of Elements in
Ore Concentrates
(see Table .2.14)
As Hg Cd Pb Ni Mn Zn Sb
Se
Bunker Hill -
Kellog, Idaho
Asarco -
Amarillo, Texas
Asarco -
Corpus Christi,
Texas
Amax -
Blackwell,
Oklahoma
National Zinc -
Bartlesville,
Oklahoma
N. J. Zinc -
Palmerton, Pa
St. Joe -
Monaca, Pa
HHHMLMHL
HMHMLHHM
LMHMMMHLL
MLHMLMHLL
LLHLLMHL
LHHLLMHLM
NOTE: L = Low, M = Medium, H = High
475
-------
Table 2-16. QUANTITIES OF NINE ELEMENTS IN
Cu SMELTER ORE CONCENTRATES
Facility
Asarco -
Tacoma,
Washington
Anaconda -
Anaconda ,
Montana
Kennecott -
McGill,
Nevada
Quantities of Elements in
Ore Concentrates
(See Table 2.13)
As Hg
H H
H L
L M
Cd Pb Ni
M M H
M M M
L L H
Mn Zn Sb
H M H
M M M
M L M
Se
"
M
M
Kennecott,
Garfield,
Utah
Cities
Service -
Copperhill,
Tennessee
*Asarco -
El Paso,
Texas
Kennecott,
Hurley,
New Mexico
Inspiration -
Miami,
Arizona
Asarco -
Hayden,
Arizona
Phelps Dodge
Morenci,
Arizonz
Phelps Dodge
Douglas,
Arizona
MLLMHMLMH
LLLHHMLL
LLLLHMLMM
LMMMHMML
LMLLMMLLM
LMMMMMMMM
NOTE: L = Low, M = Medium, H = High
*Also a Pb smelter
476
-------
for As, Pb, Zn and Cd. This same smelter was also the only lead smelter
examined which did not have associated elevated mortality rates for
cancer of the kidney, thyroid, and liver and biliary passages.
Upon comparison of zinc ore concentrate compositions and zinc
smelter mortality associations, several significant facts appeared.
Excess mortality from hypertension and hypertensive heart disease was
noted for 4 out of the 6 primary zinc smelters investigated (Table 2-
11). The only two zinc smelters examined which did not have associated
excess hypertension mortality, New Jersey Zinc - Palmerton, Pennsylvania
and St. Joe - Monaca, Pennsylvania, were also the only two that smelted
ore concentrates with low levels of lead. These same two primary zinc
smelters were the only two examined which had associated excess mortal-
ity from cerebrovascular disease, and influenza and pneumonia. It
appears that low levels of lead in zinc ore concentrates drastically
alters the mortality profiles for counties containing these facilities.
Only 2 of the 6 smelters examined which only smelt zinc ores, Asarco -
Corpus Christi, Texas and Asarco - Amarillo, Texas, had percentile
cancer of the trachea, lung and bronchus mortality rankings greater than
90 (Table 2-5). In fact, the Asarco - Corpus Christi facility had
significantly elevated rates for both male and female cancer of the
trachea, lung and bronchus, while the Asarco - Amarillo smelter had
significantly elevated male cancer mortality rates for the same disease
(Table 2-13). These same two zinc smelters are also the only two which
process zinc ore concentrates with high levels of arsenic, an element
previously linked epidemic!ogically with human lung cancer (see Section
1.0). The counties containing smelters which process zinc ore concen-
trates with high levels of arsenic thus seem to be at great risk of
having significantly high mortality rates for cancer of the trachea,
lung and bronchus.
Explanations for the mortaility associations of copper smelters
based upon unit processes and ore concentrate compositions are not
nearly as strong as those presented for lead and zinc smelters. No
associations between unit processes and copper smelter associated mor-
tality could be determined from this analysis. Although copper ore
concentrate composition data yielded some clustering of ore concentrate
characteristics and disease specific excess mortailty, no clear cut
associations such as those found for zinc smelters could be determined.
The reader is thus cautioned against overinterpretation of the ore
concentrate composition versus excess mortality associations presented
for copper smelters.
Most of the copper smelters which had associated excess mortality
from hypertension or hypertensive heart disease smelted ore concentrates
with medium levels of lead and high levels of nickel. Both of the
477
-------
copper smelters which had associated excess mortality from hypertension
and hypertensive heart disease, Kennecott - Garfield, Utah and Asarco -
Hayden, Arizona, also had medium levels of lead and high levels of
nickel in their ore concentrates. All copper smelters with associated
excess mortality from ischemic heart disease had medium levels of both
antimony and selenium in the ore concentrates which they smelted.
Excess mortality from cancer of the kidney around copper smelters was
always accompanied by ore concentrates high in nickel. Once again, the
reader is cautioned against overinterpretation of these copper smelter
mortality versus ore concentrate composition associations.
478
-------
Specific References for Section 2.0
1. Mason, T.J., et al. U.S. Cancer Mortality by
County: 1050-1969. DHEW Publication # (NIH)
74-615.
2. Vital Statistics of the U.S. 1971. Volume II -
Mortality, Part B. Table 7-9. P.H.S. HEW (HRA)
75-1102. Rockvilie, Maryland. 1974.
3. Daniel, W.W. Biostatistics: A Foundation for
Analysis in the Health Sciences. John Wiley and
Sons, Inc., New York, 1974.
4. Mason, T.J., et al. Atlas of Cancer Mortality
for U.S. Counties: 1950-1969. DHEW Publication
# (NIH) 75-780.
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3.0 CONCLUSIONS AND AN ASSESSMENT OF THE PUBLIC HEALTH HAZARD
OF PRIMARY Cu, Pb AND Zn SMELTING
It is clear from the epidemiologlcal analysis presented in the
previous section that excess mortality is associated with counties
containing primary Cu, Pb and Zn smelters. Elevated rates of cancer of
the trachea, lung and bronchus and all cancers combined have been found
in association with the majority of Cu, Pb and Zn smelters. Excess
mortality from cancer of the kidney and bladder was linked with the
majority of Pb and Zn smelters, while elevated rates of cancer of the
liver and biliary passages was associated with the majority of the Pb
and Cu smelters. Only the majority of Zn smelters had associated excess
mortality from hypertension and hypertensive heart disease. Perhaps one
or two of these associations could be attributed to some strange quirk
of probability, but the implication of all these mortality associations
combined is undeniable. Counties containing primary Cu, Pb or Zn smelt-
ers are exposed to a significant public health hazard.
The two elements contained in smelter ore concentrates which were
most strongly linked with excess mortality by the analysis presented in
Section 2.0 are arsenic and lead. Smelting zinc ore concentrates with
high levels of arsenic was clearly associated with significantly ele-
vated rates of cancer of the trachea, lung and bronchus. Numerous
previously published epidemic!ogical studies have suggested the rela-
tionship between excessive cadmium exposure and hypertension. The
results of this study strongly show that a relatively narrow range of
lead exposure must also be present before excess hypertension mortality
is observed. Excess hypertension mortality was only noted in associa-
tion with facilities which processed ore concentrates with medium levels
of lead. The smelting of ore concentrates with either low or high
levels of lead was not associated with excess hypertension mortality
regardless of the levels of cadmium present.
The solution for arsenic induced lung cancer around facilities
which smelt high arsenic zinc ore concentrates is fairly straight
forward. Sufficient reduction of the levels of arsenic emitted by these
facilities should solve the problem. Excess mortality from hypertension
as a result of a synergistic relationship between cadmium and lead poses
a somewhat more complex regulation problem. Zinc and copper smelters
which have intermediate concentrations of lead in their ore concentrates
will probably need to reduce lead emissions to prevent excess hyperten-
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sion and hypertensive heart disease mortality. However, lead smelters
which have much higher lead emissions will need to achieve a far greater
relative emissions reduction to bring lead emissions to a safe absolute
level. If lead smelters were only required to achieve a percent lead
emissions reduction equivalent to that required to eliminate Pb asso-
ciated excess mortality around Cu or Zn smelters, excess mortality from
hypertension or hypertensive heart disease which was not found to be
associated with lead smelters might result.
Three other elements present in copper ore concentrates were more
weakly linked with disease specific excess mortality by this study. The
possible synergistic action of antimony and selenium in relation to
excess mortality from ischemic heart disease should be investigated, and
appropriate emissions standards set as necessary. Along the same lines,
the association of high nickel levels in copper ore concentrates and
elevated levels of cancer of the kidney should be examined further.
Nickel has previously been linked epidemiologically with occupational
induced cancers (see Section 1.0). Thus, its possible role in induction
of kidney cancer, and the possible need for regulation of nickel emis-
sions is not a great surprise.
One specific smelting unit process was linked with excess mortality
by this study. The use of slag fuming furnaces by lead smelters was
strongly associated with elevated rates of cancer of the kidney, thy-
roid, and liver and biliary passages. It is probable that strict emis-
sions control of slag fuming furnaces or unit process modifications will
be required to eliminate this public health risk.
In conclusion, it must be stated that the associations made con-
cerning smelter induced excess mortality and its most probable causes
reflect the current state of knowledge as embodied in the literature and
as established by the epidemiological analysis undertaken by this study.
Further investigations involving clinical evaluations of the exposed
populations should validate and expand many of the associations just
presented.
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APPENDIX B
ECOLOGICAL EFFECTS
In the past several years efforts have been made to determine the
ecological impacts resulting from mining, milling, transport, and smelt-
ing of nonferrous metals. There are five major sources of pollutants
from the copper, zinc, and lead industries; (1) mine water, (2) mill
waters, (3) solid wastes from both mining and milling (tailings and
spoil), (4) concentrates resulting from the milling process, and (5)
smelter emissions.
Water from mining and milling operations often receives treatment
in at least a single tailing pond before release to receiving streams;
the discharge does, however, cause some changes in receiving streams.
Turbidity and suspended solids are usually increased greatly. Heavy
metals are often associated with these suspended solids. Chemicals
related to flotation processes often cause excessive productivity such
as algae blooms or excessive growth in aquatic vegetation which can
cause blocking of photosynthetic energy input and thus eliminate normal
stream populations. The effects or toxicity of heavy metals on algae,
benthic organisms, and various fish species have been studied for many
years. Most studies have been in the form of bioassays. Though they
often yield varying results, the bioassays have shown that heavy metals
such as copper, lead, and zinc may be toxic to aquatic life in the
concentrations reached in receiving streams. Bioassays, however, are
only indicators of what may actually take place, and to date very
little on-site work has been done. Until this is accomplished, the
effects of mining and milling on aquatic life will not be known con-
clusively.
For the past 60 years the Sudbury, Ontario, area has been an impor-
tant center for mining and smelting of metals, including copper, nickel,
and cobalt. This is one of few areas where field studies of the ter-
restrial and aquatic impacts of smelters have been undertaken. The area
has been heavily contaminated by a number of heavy metals, notably
nickel, copper, and iron.
Contamination of water bodies has occurred in four principal ways:
1. Aerial contamination occuring directly with dust fallout into
water bodies. Metal-containing dust is blown off the land.
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2. As a result of the loss of terrestrial vegetation cover, the
soil is subject to extreme leaching and erosion. This, to-
gether with the increased acidity of the soil, which increases
the solubility of heavy metals in the soil, causes runoff into
the water bodies. This runoff water carries large quantities
of heavy metals.
3. Water percolates through slag heaps and mine tailings dumped
from the mining operation and thus transfers heavy metals to
water bodies.
4. Acidic mine streams enter water bodies or are pumped to the
surface adding a further source of metals.
The flora and fauna of several lakes in the mining and smelter area
have been severely depleted.! Since copper, and particularly copper
sulfate, is the most commonly used algicide in reservoirs and water
supplies, this depletion of algal flora is hardly surprising.
A study of copper pollution in the Churnet and Dove Rivers in the
United Kingdom showed that discharge from copper works severely reduced
algal numbers. Effects on species numbers and composition could be
detected for a distance of 30 miles downstream, at which point levels of
0.1 ppm Cu were recorded.2 Animal numbers were similarly affected, and
animal life was eliminated for a distance of 10 miles.
The Sudbury studies also indicate that a combination of high
concentrations of copper and nickel is likely to be especially harmful
to living organisms, since it has been shown that copper and nickel act
synergistically in their toxicity to algae and that this synergism is
increased at low pH levels. Nickel by itself, at a concentration of 0.5
ppm, has killed laboratory strains of algae.
Little information is available on the effects of lead smelters on
local ecology. To date the only field study has been in the area of the
New Lead Belt in Missouri. Temporary excessive algae and aquatic
vegetational growth has been observed in receiving streams. Diversity
in species has been reduced in some receiving streams. Though this does
not necessarily mean that the quality of the stream has been degraded,
it does mean that species used in the index have changed.
Other studies have shown that in soft water lead may be very toxic
to fish at a concentration of 0.1 milligram per liter. In hard water
this concentration is not toxic.3
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Zinc exhibits its greatest toxicity toward fish and aquatic organ-
isms. In soft water, concentrations of zinc ranging from 0.1 to 1.0
milligram per liter have been reported to be lethal, but calcium is
antagonistic toward such toxicity. Sensitivity to zinc varies with
species, age, and condition of the fish, as well as the physical and
chemical characteristics of the water.4
Though arsenic is generated in most smelter operations and its
effects on humans are well known, little field data are available as to
its effects on aquatic organisms. A study pertaining to sewage treat-
ment processes showed that arsenic concentrations of 3 to 20 milligrams
per liter have not harmed aquatic insects such as immature dragonflies,
damsel flies, and mayflies.5
The terrestrial environment, like the aquatic environment, is
affected by smelter operation. A study near a copper smelter in Wollon-
gong, New South Wales, Australia, showed statistically significant
relationships between distance from the smelter and concentrations of
heavy metals in the vegetation. Significant relationships were found
between distance from the smelter (for a radius of 3 kilometers and
beyond) and the levels of easily extractable copper and zinc in the
soil, and also between distance from the smelter and the content of
copper and zinc in herbage.6»7 over a 0.5 kilometer distance, signifi-
cant correlations were found for copper and nickel. Highly significant
correlations were found between distance from the chimney and the levels
of easily extractable copper, zinc, lead, and cadmium in the soil.
Some bioassays have shown that selected plants absorb these metals
into their various structures; toxic effects have been shown. However,
few field-documented cases of excessive damage due to heavy metals have
been reported. Several cases have been reported in which terrestrial
plants have developed metal tolerances and have adapted to high metal
concentrations. The evolution of metal resistant species or ecotypes
has also been demonstrated in relation to man's industrial activities.8
Much work remains to be done, however, on the effects of relat'vely
high, frequent intakes of particular heavy metals, and also on the
aggregate and interaction effects of two or more heavy metals when
individually they are at sublethal levels.
Research indicates that sulfur dioxide fumigation resulting from
smelter operations will inflict serious damage on local vegetation.
Usually the fumigation must reach the interior of the leaf to inflict
injury. The sulfur dioxide is partially converted to sulfurous and
sulfuric acids. As a result of these chemicals, the cells lose their
capacity to hold and translocate water; thus they dry out and die.
Critically impaired water conduction is particularly evident in broad-
leaf plants; tissues between the veins are generally the first to
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shrink and die. In addition, the chlorophyll of leaf cells is destroyed,
possibly by the strong reducing properties of sulfur dioxide and sul-
furous acid. Evidence of damage is early loss of green color in the
affected areas, even while the leaves are still turgid. Defoliation
occurs last.
The severity of injuries to plants exposed to a given dosage of
sulfur dioxide varies with different species. Plants are most likely to
be injured by sulfur dioxide when there is a favorable growing tem-
perature, high relative humidity, bright weather, and protracted wind
from the direction of the sulfur dioxide source. Although these factors
in combination may have a slight to moderately additive effect, their
primary influence is more analogous to links in a chain; a critical de-
ficiency in any one of them may preclude injury despite the adequacy of
the other factors for it. Apparently it is the rate, not the amount, of
sulfur entry into the leaf that determines whether injury occurs.
In a study of smelter injury to forest trees in Washington and
Montana, reproduction was scarce. This appeared to be a result of
reduced cone crops and of the susceptibility and increased mortality of
seedlings.9
Eighteen years after the initiation of sulfur dioxide abatement
measures in the Columbia Rfver Valley area, there was no evidence of
current injury to timber or plants. Moreover, the appearance of in-
dividual trees did not suggest residual effects of earlier damage.
Timber stands in zones of greatest damage were still thinner than else-
where but there was no denuded area so large as to preclude fairly
prompt restocking.
Conclusions and Recommendations
Some adverse environmental impacts may result from the mining,
milling, and smelting of primary metals. Most evidence thus far is in
the form of bioassays, with very little field documentation of finds.
It is therefore obvious that full scale long range field documentation
studies are required. These studies must look not only at the short-
term ecological effects, but more importantly at the long-term effects.
The following are basic questions to be studied: (1) Can biotic life in
receiving streams and terrestrial habitats adapt to slightly higher
concentrations of heavy metals? (2) How are the quality and quantity of
biotic life altered as a result of mining, milling, and smelting opera-
tions? and (3) Can aquatic and terrestrial life recover their original
stable states after mining operations cease?
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REFERENCES
1. Stokes, P.M., T.C. Hutchinson, and K. Krauter. Heavy-metal Tol-
erance in Algae Isolated from Contaminated Lakes Near Sudbury,
Ontario. Canadian Journal of Botany. Volume 51:2155-2168. 1973.
2. Butcher, R.W. Studies on the Ecology of Rivers. VI. The Aglol
Growth of Highly Calcareous Streams. Journal of Ecology 33:268-283.
1946.
3. Dourdoroff, P. and M. Katz. Critical Review of Literature on the
Toxicity of Industrial Wastes and Their Components to Fish. II.
The Metals, as Salts. Sewage and Industrial Wastes. 25. 1953.
4. Schneider, Robert F. The Impact of Various Heavy Metals on the
Aquatic Environment. U.S. Environmental Protection Water Quality
Office. NTIS, Springfield Virginia.
5. Rudolfs, W., G.E. Barnes, G.P. Edwards, H. Heukelekian, E. Hurwitz,
C.E. Renn, S. Steinberg, and W.F. Vaughan. Review of Literature on
Toxic Materials Affecting Sewage Treatment Processes, Streams and
BOD Determinations. Sewage and Industrial Wastes. 22. 1950.
6. Beavington, F. Contamination of Soil with Zinc, Copper, Lead, and
Cadmium in the Wollongong City Area. Australian Journal of Soil
Resources 11:27-31. 1973.
7. Beavington, F. Some Aspects of Contamination of Herbage with
Copper, Zinc, and Iron. Environmental Pollution. 8:65-'/l. 1975.
8. Antonovics, J., A.D. Bradshaw, and R.G. Tuner. Heavy Metal Toler-
ance in Plants. Advanced Ecological Research 7:1-85. 1971.
9. Scheffer T.C., and G.G. Hedgecock. Injury to Northwestern Forest
Trees by Sulfur Dioxide from Smelters. U.S. Department of Agri-
culture, Forest Service. Technical Bulletin No. 1117. June 1955.
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