ANIMAL INDICATORS OF AIR POLLUTION:
A REVIEW AND RECOMMENDATIONS
by
James R. Newman
Huxley College
Bellingham, Washington 98225
CERL-006
Huxley College of Environmental Studies
Western Washington State College
Bellingham, Washington 98225
Contract No. G4-729
Corvallis Environmental Research Laboratory
Corvallis, Oregon 97330
May, 1975
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DISCLAIMER
This report has been reviewed by the Corvallis Environmental Research
Laboratory, U.S. Environmental Protection Agency, and approved for publication.
Mention of trade names or commercial products does not constitute endorsement
or recommendation for use.
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ABSTRACT
The use of animals as biological monitors of air pollution is essen-
tially non-existent. Besides being used as general measures of environ-
mental quality, animals give more precise information on the quality of
the environment as it relates to human and other animal systems. This
study reviews the existing information on the effects of industrial
air pollutants on animals for the purpose of suggesting animal indi-
cators of air pollutants and various monitoring approaches based on
their responses of animals to air pollutants.
The amount of information varies on the effects of specific air pollu-
tants on animals. In general, laboratory investigations have been
conducted at conditions not found in the environment. A significant
number of episodes involving the effects of air pollutants on free-
living animals have been reported. They indicate the widespread effect
of air pollutants on animals. Numerous animal indicator systems and
approaches to development of the animal indicator systems are dis-
cussed .
This report was submitted in fulfillment of (Project //04J1P01486 and
Contract/Grant Number G4-729 (NERL/LEFOHN)) by James R. Newman,
Huxley College of Environmental Studies, Western Washington State
College under the sponsorship of the Environmental Protection Agency.
Work was completed as of February, 1975.
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CONTENTS
Page
Abstract i
List of Tables iv
Acknowledgments vii
SECTIONS
1. CONCLUSIONS 1
2. RECOMMENDATIONS 4
3. INTRODUCTION 8
4. LITERATURE SEARCH AND REVIEW PROCESS 1*
5. REVIEW OF EXISTING INFORMATION ON THE EFFECTS OF AIR
POLLUTION ON ANIMALS 20
5.1 Introduction
20
5.2 Asbestos ..................... 2;L
5.3 Arsenic ...................... 24
5.4 Barium ...................... 29
5.5 Beryllium ..................... 31
5.6 Boron ....................... 35
5.7 Cadmium ...................... 37
5.8 Carbon monoxide .................. ^2
5.9 Chromium ..................... 48
5.10 Fluoride ..................... 52
5.11 Hydrocarbons ................... 60
5.12 Hydrochloric acid .................
5.13 Hydrogen sulfide ................. 70
5.14 Iron ....................... 74
5.15 Lead ....................... 75
5.16 Manganese ..................... 82
5.17 Mercury ...................... 83
5.18 Molybdenum .................... 87
5.19 Nickel ...................... 89
5.20 Nitrogen dioxide ................. 91
5.21 Particulates ................... 101
5.22 Phosphorus .................... 108
5.23 Photochemical oxidants .............. 109
5.24 Selenium ..................... 12°
5.25 Sulfur dioxide ..................
ii
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CONTENTS (Continued)
Page
5.26 Vanadium 135
5.27 Zinc 138
6. ZOO SURVEY: RESULTS 141
7. DISCUSSION OF GENERAL SUITABILITY OF ANIMALS 150
7.1 Trends Indicated by Episodes 150
7.2 Summary of General Effects of Air Pollutants on
Animals 166
7.3 Summary of General Responses of Animals to Air
Pollution 178
iii
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List of Tables
Page
3-1 LISTS EXAMPLES OF THREE TYPES OF BIOLOGICAL INDICATORS 9
3-2 KINDS OF RESPONSES OF BIOLOGICAL INDICATORS TO POLLUTANTS 11
4-1 DESCRIPTION OF COMPUTERIZED DATA BASES 15
4-2 SELECTED AIR POLLUTION TECHNICAL PUBLICATIONS OF THE
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY 16
5.2-1 ASBESTOS: REPORTED EFFECTS ON FREE-LIVING ANIMALS 21
5.2-2 REPRESENTATIVE STUDIES OF THE EFFECTS OF ASBESTOS ON
EXPERIMENTAL ANIMALS 22
5.3-1 ARSENIC: EPISODES INVOLVING FREE-LIVING ANIMALS 25
5. 3-2 SUMMARY OF LETHAL ORAL DOSAGES OF ARSENIC TRIOXIDE IN
ANIMALS 26
5.4-1 REPRESENTATIVE LABORATORY STUDIES ON THE TOXICITY OF
BARIUM COMPOUNDS 30
5.5-1 PHYSIOLOGICAL CHANGES AND MORTALITY RESULTING FROM
INHALATION OF BERYLLIUM FLUORIDE, BERYLLIUM OXIDE, AND
BERYLLIUM SULFATE 32
5.6-1 REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF
BORON ON ANIMALS 36
5.7-1 EFFECTS OF CADMIUM AND CADMIUM COMPOUNDS ON ANIMALS 38
5.8-1 REPRESENTATIVE STUDIES ON THE EFFECTS OF CARBON MONOXIDE
ON LABORATORY ANIMALS 43
5.9-1 REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF
CHROMIUM ON ANIMALS 49
5.10-1 FLUORIDE: EPISODES INVOLVING FREE LIVING ANIMALS 53
5.10-2 REPRESENTATIVE STUDIES ON THE EFFECTS OF FLUORIDE ON
EXPERIMENTAL AND LABORATORY ANIMALS 55
5.11-1 COMPARATIVE EFFECTS OF ACUTE AND CHRONIC EXPOSURE TO
AROMATIC HYDROCARBON VAPORS IN AIR 61
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List of Tables Continued)
5.11-2 REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF
ALDEHYDES ON ANIMALS 63
5.12-1 SUMMARY OF REPORTED EFFECTS OF INHALATION OF HYDROGEN
CHLORIDE ON ANIMALS 68
5.13-1 HYDROGEN SULFIDE: EPISODES INVOLVING FREE-LIVING ANIMALS 71
5.13-2 STUDIES ON THE EFFECTS OF HYDROGEN SULFIDE ON ANIMALS 73
5.15-1 LEAD: EPISODES INVOLVING FREE-LIVING ANIMALS 76
5.15-2 REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF
INGESTED LEAD ON ANIMALS 77
5.17-1 MERCURY: EPISODES INVOLVING FREE-LIVING ANIMALS 84
5.17-2 REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF
MERCURY COMPOUNDS ON ANIMALS 85
5.18-1 MOLYBDENUM: EPISODES INVOLVING FREE-LIVING ANIMALS 88
5.19-1 REPRESENTATIVE LABORATORY STUDIES ON EFFECTS OF NICKEL
CARBANYL ON ANIMALS 90
5.20-1 NO : EPISODES INVOLVING FREE-LIVING ANIMALS 92
x
5.20-2 REPRESENTATIVE STUDIES OF TOXICOLOGICAL EFFECTS OF NITRIC
OXIDE ON LABORATORY ANIMALS AND BACTERIA 93
5.20-3 REPRESENTATIVE STUDIES OF TOXICOLOGICAL EFFECTS OF SHORT-
TERM N02 EXPOSURE ON LABORATORY ANIMALS 94
5.20-4 REPRESENTATIVE STUDIES ON TOXICOLOGICAL EFFECTS OF LONG-
TERM N0? EXPOSURE ON LABORATORY ANIMALS 97
5.21-1 PARTICULATES: EPISODES INVOLVING FREE-LIVING ANIMALS 102
5.21-2 REPRESENTATIVE STUDIES ON THE EFFECTS OF PARTICULATES ON
LABORATORY ANIMALS 105
5.23-1 PHOTOCHEMICAL OXIDANTS AND OZONE: EPISODES INVOLVING
FREE-LIVING ANIMALS 11:L
5.23-2 REPRESENTATIVE STUDIES ON THE EFFECTS OF OZONE ON
LABORATORY ANIMALS 112
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5.23-3 REPRESENTATIVE STUDIES ON THE EFFECTS OF PHOTOCHEMICAL
OXIDANTS ON LABORATORY ANIMALS 116
5.24-1 SYMPTOMS AND GROSS PATHOLOGY OF CHRONIC SELENIUM
POISONING IN LIVESTOCK I22
5.25-1 S02: EPISODES INVOLVING FREE-LIVING ANIMALS 126
5.25-2 MAXIMUM CONCENTRATIONS OF S02 DURING SPECIFIC AIR POLLU-
TION EPISODES I28
5.25-3 REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF S02
ON ANIMALS i29
5.25-4 REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF H^O^
MIST ON ANIMALS 131
5.26-1 VANADIUM: EPISODES INVOLVING FREE-LIVING ANIMALS 137
5.26-2 REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF
VANADIUM ON ANIMALS 138
5.27-1 REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF
ZINC COMPOUNDS ON ANIMALS
6.1 RESULTS OF SURVEY OF WORLD ZOOS ON THE EFFECTS OF AIR
POLLUTION ON ANIMALS 145
7.1-1 EPISODES INVOLVING AIR POLLUTANTS AND ANIMALS 152
7.2-1 TOXTCITIES OF AIR POLLUTANTS BASED ON OBSERVED AMBIENT
CONCENTRATIONS 168
7.2-2 CLASSIFICATION OF AIR POLLUTANTS BASED ON THEIR CAPACITY
TO ACCUMULATE IN BODY TISSUE
7.2-3 MAJOR SITES OF ACCUMULATIONS OF AIR POLLUTANTS 171
7.2-4 ASSOCIATION OF AIR POLLUTANTS AND GENERAL BIOLOGICAL
INDICATOR RESPONSE I72
7.2-5 THE MAJOR BIOLOGICAL TARGET AREAS OF AIR POLLUTANTS 173
7.2-6 ABNORMAL BEHAVIORS OF ANIMALS ASSOCIATED WITH AIR POLLUTANTS 174
7.2-7 CHANGES IN EXTERNAL MORPHOLOGY OR APPEARANCE DUE TO AIR
POLLUTION INTOXICATION
vi
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List of Tables (Continued)
7.2-8 EFFECTS OF A[R POLLUTANTS ON BLOOD CHEMISTRY AND
PHYSIOLOGY 176
7.2-9 ENZYMES AFFECTED BY AIR POLLUTANTS 177
7.3-1 POSSIBLE BIOLOGICAL INDICATORS OF AIR POLLUTANTS 180
vii
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ACKNOWLEDGMENTS
The support of numerous research and zoo directors who provided me
with information on their investigations on the effects of air pollu-
tants is acknowledged; in particular F. W. Adams, 0. J. Balchum,
R. E. Borchard, W. B. Buck, J. Davis, T. Eisner, J. T. Gatzy, W. E.
Giddins, Jr., C. G. Loosli, A. J. Loustalot, D. O'Meara, D. M. Morris,
M. Pollard, J. S. Reif, V. L. Sanger, I. J. Selikoff, J. L. Shupe,
R. L. Snyder. G. R. Spencer, H. E. Stokinger, W. A. Thomas, R. L.
Wood and A. Zarkower.
The efforts of Arvilla Weir and Diane Groh, Librarians, EPA Region X
and Ruth Seidman, Librarian EPA Region 1 in searching for additional
information and use of the APTIC system is much appreciated.
The literature searching of Don Disraeli and Ming-Ho Yu's review of
the manuscript is acknowledged.
1 would like to thank Jane Clark and Ann Drake of the Bureau of Faculty
Research, Western Washington State College for their great effort in
preparation of the manuscript.
A final acknowledgment is given to my family for their understanding
and patience during the project.
viii
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SECTION 1
CONCLUSIONS
Animals, both vertebrates and invertebrates, would make suitable bio-
JogLcal indicators of air pollution. They exhibit varying degrees of
sensitivity and show a wide range of diagnostic responses. However,
little research has been conducted to develop animal indicators for air
pollutants.
Several pollutants including arsenic, fluoride, lead, photochemical
oxidants, nitrogen dioxide, and sulfur dioxide, are well enough under-
stood and widespread in their effects (affecting vertebrates and inver-
tebrates) that research into developing biological indicator systems
for these particular pollutants would be fruitful. Other pollutants,
especially chromium, phosphorus, and vanadian,toxic and/or affecting
animals, need more basic information before monitoring systems can be
set up.
Development of monitoring programs requires selection of appropriate
monitoring procedures and monitoring systems. Selection of appropriate
monitoring procedures depends on the known effects or elicited re-
sponses of animals to various pollutants, and whether information is
required on specific air pollutants or general air pollution conditions.
Priorities can be established on monitoring procedures depending upon
the specificity of response, commonness of response among air pollu-
tants, ease in measuring the response, and the costs involved in
measurement.
Of the possible responses of biological indicators, four responses give
specific information on specific pollutants. These responses are:
physiological changes observed in autopsy or histology; residue accumu-
lation; changes in blood chemistry; and changes in morphology and ap-
pearance. Consideration of biological monitoring programs should con-
sider at least three responses. In addition, several responses give
more general information and are supportive of the first four. These
more generalized responses are: cellular enzyme changes, abnormal
behavior, and changes in abundance or distribution of animals. The
last two responses, although general, could serve as initial signs of
possible environmental change. They are also useful in requiring only
field observations. Depending upon the organism, i.e., birds, only
visual observations might be required.
Die-offs of animals because of air pollution have not often been re-
ported compared to reports of sickened and weakened animals. However,
die-offs do occur; for example, Prince Rupert bird die-offs. When
die-offs do occur they indicate severe conditions to which immediate
attention should be given. Reporting of die-offs is most important
and increased surveillance is needed.
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Some pollutants cause specific effects. Monitoring programs focusing
on the presence or effects of specific pollutants might use special
monitoring procedures along with more general monitoring approaches.
For example, a program interested in the effects of selenium should
employ embryonic and fetal examination of the animals, since selenium
is teratogenic. Embryonic and fetal examination would not be appro-
priate as a routine monitoring test for general pollution monitoring.
The specific response approach would also apply for those pollutants
known to be carcinogenic such as asbestos, cadmium, nickel, photo-
chemical oxidant, and vanadium. General and specific monitoring
procedures should be identified for air pollutants.
Section III discusses the general theory of biological indicators and
lists some twelve traits which biological indicators should have. The
development of monitoring programs should include consideration of
these traits in selecting indicator species.
Air pollution is a by-product of man's activities and all animal popu-
lations affected by air pollution are non-target species. Several
kinds of animal populations can serve as biological indicators: domes-
tic animals including livestock, zoo animals, and wildlife including
vertebrates and invertebrates. One of the common trends noted in
deteriorating ecosystems is impairment to predators. This apparent
sensitivity is due to the concentrating effect of pollutants in the top
of the food chain. Some of the early warning signals for pesticide
hazards were given by predators such as the Peregrine Falcon and the
Brown Pelican. Biological magnification of many air pollutants should
occur. However, only a few studies have measured levels or effects of
air pollutants on predators or top carnivores. The sensitivity of top
carnivores to other environmental hazards suggest their role as bio-
logical monitoring species.
The animals discussed in this report are fairly common in the environ-
ment and are easily sampled. Some groups, like domestic animals and
zoo animals, by the nature of their activities are the most easy to
work with. Game animals, which represent more natural conditions, are
also fairly easy to observe or collect.
The collection and examination of biological indicators should include
more than a few individuals. This is important for confirming results
and establishing the extent of the problem. Recent examination of the
distribution of pollutants in the environment, such as mercury have
often used very small sample sizes. This is due to lack of resources
and to the time involved in measurement or analysis of the pollutants
or their effects. Biological indicators, and the responses measured,
should be considered for their ease and simplicity in measurement.
Sampling of populations, including their numbers and distribution,
may be less time and resource consuming than the analyses of tissue
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samples from a few individual animals. Monitoring programs should
identify key populations whose responses would be easy to measure and
be indicative of a specific pollutant.
In urban environments observations in zoos are limited to single or a
few individuals. However, the lack of large sample sizes is compen-
sated for by the extensive life history information available for
these species. Studies of mortality and morbidity of key zoo animals
would provide excellent information on trends of urban environmental
quality. There are a large number of wildlife in urban areas. There
are numerous species of birds and insects which might make suitable
biological indicators. Pigeons, sparrows and rats have been considered
as urban biological monitors. However, their usefulness as biological
indicators has not been established. Investigation using other
species is needed.
In non-urban environment the distribution of widespread sensitive
species and especially easily observable species such as birds, would
provide a good indicator of environmental quality across geographical
areas. The observed decline in Peregrine Falcons alerted scientists to
the widespread danger of certain pesticides. Measurements of densities
of biological indicators would be time consuming but would provide
more precise information on the status of the indicator.
Diversity measures are indicative of trends of environmental quality
at the community level. However, biotic indexes similar to those de-
veloped for water quality need to be developed, since some pollutants
have shown to be associated with increase in kinds and density of or-
ganisms. In addition, this sensitivity of diversity indices to environ-
mental change needs to be studied. In general, diversity indexes would
be most suitable for vertebrates since air pollutants are toxic to
them. Bird diversity indexes would be the best because of the larger
number of avian species compared to mammals, their diurnal habits,
ease of observation and suspected sensitivity. However, it has been
pointed out repeatedly that there is a general lack of information
concerning the effects of air pollutants on birds.
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SECTION 2
RECOMMENDATIONS FOR FUTURE RESEARCH
2.1.0 Studies to develop biological monitoring systems for arsenic,
fluoride, lead, photochemical oxidants, and sulfur dioxide.
Reason: Sufficient information is available on the fate and
effects of these pollutants on the environment. The effects
are understood and so widespread that testing of biological
indicator systems would be possible.
2.2.0 Experimental studies on the effects of air pollutants at low and
chronic exposures.
Reason: Most experiments to date have been carried at con-
centrations rarely approached in nature.
2.2.1 Studies on the distribution of air pollutants in the
body.
Reason: Studies are needed on numerous pollutants to
find out their distribution and fate in animals, such
as chromium and nickel.
2.2.2 Studies on the effects of air pollutants on animals
with highly developed olfactory and visual systems
especially in birds.
Reason: Several pollutants including photochemical
oxidants and hydrocarbons are known to interfere with
these systems and animals utilizing these systems might
show high sensitivities.
2.2.3 General studies on species sensitive to air pollutants.
Reason: Little information is known on animal sensitivi-
ties to pollutants.
2.2.4 Studies to develop standard methods of diagnosis for air
pollutants.
Reason: Many pollutants appear to have well defined re-
sponses such as changes in blood chemistry or physiology.
Simple, quick and accurate methods of analysis need to
be established.
2.2.5 Studies on the combined effects of air pollutants.
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Reason: Research emphasis has been on simple effects of
air pollutants while in nature air pollution generally
involves the presence of two or more pollutants.
2.2.6 Studies on the secondary effects of air pollutants.
Reason: Available information indicates most all of the
air pollutants affect animals both physiologically and/or
behaviorally. Studies are needed to determine the resis-
tance of such animals to normal environmental stress and
the importance of such effects on the general health of
the animals.
2.3.0 Studies on the effects of air pollutants on ecological systems
particularly involving animal populations.
Reason: The effects of air pollutants have been found to be
widespread including both plants and animals, and to be both
direct and indirect so as to cause general disintegrating
effects to ecological systems; however, few comprehensive in-
vestigations have been conducted.
2.3.1 Studies on the effects of air pollution on the population
ecology of essentially sedentary populations.
Reason: No extensive investigations have been made, yet
scattered reports indicate small mammals, soil organisms
and insects do respond to air pollution.
2.3.2 Further studies on the dynamics of industrial melanism
in particular to look at shifts in melanic forms com-
pared to change in environmental quality.
Reason: Studies on industrial melanism indicate a pos-
sible rapid shift in melanic forms due to changing air
quality. More information is needed on the response
time of these shifts, relationship of specific pollu-
tants, and specific melanic forms, and the distribution
and occurrence of industrial melanism in the United
States.
2.3.3 Studies on the relationship of insect attractants and
repellants to air pollution.
Reason: Field observations indicate possible insect
pest infestations associated with air pollution. The
chemical nature of some of these plant and animal
pheromones are not too dissimilar from certain air
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pollutants such as photochemical oxidants and hydro-
carbons.
2.3.4 Studies on the concentration and effect of air pollutants
upon natural trophic level systems in particular upon top
carnivores.
Reason: Little or no information is known on the effects
of air pollutants on top carnivores. Top carnivores have
been shown to be extremely sensitive to other kinds of
pollution. They may be valuable as sentinel or detector
species.
2.3.5 Studies on the effects of certain air pollutants such as
asbestos, As, Ba, Be, Cd, Cr, Hg, Mn, Ni, and Zn on
vegetation.
Reason: Little or no information is known on the effects
or concentration of these pollutants in vegetation.
Understanding of effects of these pollutants on animals
is hindered because of the lack of this information.
2.4.0 Studies to develop biological indicator programs for urban areas.
Reason: There is a need to determine the environmental quality
of human environments and to determine the effectiveness of
the control measures implemented. Non-human biological monitors
or indicators are needed, since it is preferable to use animals
as indicators than to allow conditions to develop where humans
show adverse effects because of air pollution.
2.4.1 Development of biological monitoring programs using zoos
and other native animal populations of urban areas.
Reason: Animals dwelling in urban areas are affected by
air pollution and cases are reported where animals were
first affected. However, no systematic investigation
has been conducted to setting up such a program.
2.5.0 Studies on the concentration of certain air pollutants such as
Ba, Bo, Cr, HC1, Hg, Mn, Ni, P, and V in the environment.
Reason: Little or no information is available on the occur-
rence and distribution of these pollutants and their assessment
of the effects are hindered.
2.5.1 Studies on the concentrations of air pollutants on
vegetation.
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Reason: Only a few studies have been found which con-
sider concentrations of pollutanLs on vegetation and
other materials which free-living animals may come
into contact with. It is difficult to relate ambient
air concentrations of pollutants to hazardous condi-
tions for pollutants which can accumulate on surfaces.
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SECTION 3
INTRODUCTION
Biological indicators are organisms whose presence or absence or other
characteristic response indicate certain environmental conditions.
The concept of biological indicators is not new. Many early ecological
studies investigated various organisms as indices of succession as in-
dicators of the physical environment. ' Biological indicators have
also been used as measures of water pollution. Kolkwitz and Marsson in
1908-1909 classified plants and animals according to the extent of
water pollution.-' The present interest in environmental indices has
both governmental sanction in Public Law 91-190 Sections 102(2) Bond
209, and governmental interest.
The use of biological indicators as measures of environmental pollution
is extremely valuable for several reasons: 1) they integrate all en-
vironmental effects and reflect the total environment; 2) they correlate
physical and chemical measurements with biological effect; 3) they
reveal trends or changes in the environment; 4) they show pathways and
points of accumulation of pollutants in ecological systems^; and 5)
they allow for more realistic assessment of air quality standards.
The greatest advancement in the development and use of biological indi-
cators are in water pollution studies.^*' They are the most successful
indices of natural and cultural eutrophication and other types of
water pollution. Hundreds of species representing both plants and ani-
mals have been characterized according to their responses to certain
water quality conditions."
Biological indicators of air pollution exist. Many species of plants
are good indicators of air pollution. However most botanical indica-
tors are oramental or cultivated species." In contrast water pollution
indicators are mainly naturally occurring species. The use of animals
as biological indicators of air pollution is almost non-existent .-"-0
There are two fundamental questions which have yet to be fully an-
swered in regards to animal indicators of air pollution: (1) are
animals suitable indicators of air pollution, (2) what parameters
are good measures of an animal's response to air pollution. Animals
are sensitive to air pollution and therefore they should make suitable
indicators. For example, bees are extremely sensitive to fluoride. -1-
Novakova12 has shown that there is a shift in insect diversity and
trophic structure in areas of high SO™ and HF. Rabbits exposed to
low levels of waterborne fluoride exhibit anemia and impairment of
blood sugar regulation.^ N02 causes elevated lactic dehydrogenase
and aldolase in guinea pigs.14
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Five types of biological indicators are proposed by Jenkins based on
their response to pollution:
Sentinels: highly sensitive organisms found in the environment
and act as early warning devices to certain adverse environmental con-
ditions.
Bioassay monitors; selected organisms used as bioreagents to
detect or monitor the presence and/or concentration of a particular
pollutant.
Detectors: individual species occurring in the environment who
show a reasonably characteristic response to pollutants or some environ-
mental changes.
Thrivers: those whose presence indicates the occurrence of a
particular pollutant or existence of an environmental condition associ-
ated with that pollutant.
Accumulators: those organisms that collect and accumulate a
pollutant in reasonable and usually large quantities.
Table 3-1 lists examples of these types of biological indicators.
Table 3-1
Type of indicator
T
Organism
Sentinels
Bioassay Monitors
Detectors
Thrivers
Accumulator
Miner's Canary
Rats
Gladioli
Tub if ic id worms
Western Grebes
CO
CO
F
Heavy aquatic organic
pollution
DDT
Pollutant
Based on the knowledge of existing indicators, some generalizations
can be made concerning their desired characteristics, and strategies
for use. Useful biological indicators have some combination of the
following traits:
1) non-target species (reflect undesired changes in environ-
ment)
common or abundant in polluted situations (ease in sampling)
2)
3)
suitable for long-range surveillance and universal use
(reflect trends)
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4) indicative of ecological response to pollutants (a measure
of sum of environmental variables plus pollutant)
5) stenotolerant rather than eurytolerant (eurytolerant less
diagnostic)
6) observable or measurable (suitable for remote sensing)
7) allows for precision and accuracy (reproducible and consis-
tent results)
8) sensitive to pollution with well-defined and uniform re-
sponse (prevent non-specific or confusing results)
9) sensitive to various levels of pollution (better diagnostic)
10) discriminates between natural and induced environmental
changes (prevent non-specific or confusing results)
11) large size versus small size (slower turnover rates in
larger organisms avoid confusion with natural population
changes)
12) possible economic or ecological importance, or related to
certain important economic or ecological relationships (in-
dicates potential or real problem).
Based on studies of ecological and water pollution indicators a number
of kinds of general responses of animals to pollution are possible
(Table 3-2). These responses associated with existing biological in-
dicators represent the full expression of an organism's response to
the environment and the environmental stimulus.
The strategy for use of biological indicators, especially in water
pollution problems, employs multispecies indicators to insure a better
integration and detection of the environmental changes caused by pollu-
tion. Several types of indicators used concurrently (e.g., sentinel
and thrivers) allow for more accurate identification of the pollutant.
Diversity indices assure detection of subtle changes in abundance
which might not be observed using a single organism. These general
strategies allow for detecting changes in the populations, species
and communities.
The purpose of this report is to determine whether animals would make
suitable biological indicators of air pollution. This report attempts
to point out possible biological indicators of air pollution and to
make recommendations for further research into the problem. My ap-
proach is to review existing information on the effects of industrial
air pollutants on animals within the framework of the biological in-
dicator concept. The known responses of experimental animals to
various air pollutants are compared with typical ambient concentra-
tions of air pollutants and reported effects of air pollutants on
free-living animals. Characteristic and diagnostic responses of
animals and sensitive and responsive animal groups to various air pol-
lutants are considered.
10
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Table 3-2. KINDS OF RESPONSES OF BIOLOGICAL INDICATORS TO POLLUTANTS
Observations of abnormal behavior
Death
Avoidance of pollutant
Physiological changes observed in autopsy and histological
analysis
General growth retardation
Differential effects of life stages
Residue accumulation
Changes in energy requirements for normal activities
Genetic resistances
Changes in blood chemistry
Reduced tolerance to normal environmental stimuli or stress
Changes in morphology or appearance
Changes in taste
Changes in abundance
11
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REFERENCES
1. Clements, F. F. Plant Indicators: the Relation of Plant Communi-
ties to Process and Practice. Publications of the Carnegie Insti-
tute of Washington. 290(i-xvi):1-388, 1920.
2. Alice, W. C., 0. Park, A. E. Emerson, T. Park and K. P. Schmidt.
Principles of Animal Ecology. Philadelphia, W. B. Saunders Co.,
1949.
3. Warren, C. E. Biology and Water Pollution Control. Philadelphia,
W. B. Saunders Co., 1971. Ch. 20.
4. Curlin, J. W. National Environmental Policy Act of 1969, Environ-
mental Indices - Status of Development Pursuant to Sections 102
(2)(B) and 204 of the Act. Library of Congress. Washington Commit-
tee on Insular Affairs, U.S. Senate. December 1973. 46 p.
5. Jenkins, D. W. Global Biological Monitoring. In: Man's Effects
on Terrestrial and Oceanic Ecosystems, Mathews, W. D., F. E. Smith,
and E. D. Goldberg (eds .). Cambridge, M.I.T. Press, 1971. p. 351-
370.
6. Thomas, W. A. (ed.). Indicators of Environmental Quality. New
York, Plenum Press, 1972. 275 p.
7. Cain, J. , K. L. Dickson and G. Lanza. Rapid Biological Monitoring
Systems for Determining Aquatic Community Structure in Receiving
System. Biological Methods for the Assessment of Water Quality,
ASTM STP 528, American Society for Testing and Materials, 1973. p.
148-163.
8. Weber, C. Biological Monitoring of the Aquatic Environment by
the Environmental Protection Agency. In: Biological Methods for
the Assessment of Water Quality. ASTM STP 528, American Society
for Testing and Materials, 1973. p. 46-60.
9. Jacobson, J.S. and A. C. Hill. Recognition of Air Pollution In-
jury to Vegetation: A Pictorial Atlas. Pittsburg, Air Pollution
Control Association, 1970. 70 p.
10. Thomas, W. A., G. Goldstein and W. H. Wilcox. Biological Indica-
tors of Environmental Quality, a Bibliography of Abstracts. Ann
Arbor, Ann Arbor Publishers Inc., 1973.
11. Caparrini, W. Fluorine Poisoning in Domestic Animals (Cattle) and
Bees. Zooprofilassi 12:249-250, 1957.
12
-------
12. Novakova, E. Influence des Pollutions Tndustrielles sur les
Communautes Animals et 1'Utilisation des Animaux Comme Bioindi-
cateurs. In: Air Pollution, Proceedings of the First European
Congress on the Influence of Air Pollution on Plants and Animals.
Wageningen, Center Agricultural Publishing and Documentation,
1969. p. 41-50.
13. Maier, J. R. and D. Rose. Environmental Fluoride. National
Research Council of Canada, Ottawa. National Research Council
Publication Number 12,226. 1971. 32 p.
14. Buckley, R. D., and 0. J. Balchum. Acute and Chronic Exposures to
Nitrogen Dioxide Effects on Oxygen Consumption and Enzyme Activity
on Guinea Pig Tissues. Arch. Environ. Health. Air Quality, 1971.
10:220-223, 1965.
13
-------
SECTION 4
LITERATURE SEARCH AND REVIEW PROCESS
I have reviewed available information on the effects of air pollutants
on animals. The scope of the review includes all air pollutants of
primarily industrial origin (see Table of Contents). Radiation, pesti-
cides, and biological aerosols are not included. Pollutants arising
from primarily non-industrial sources, such as ammonia, are also not
included. All animal groups, vertebrates and invertebrates, and
domestic, laboratory and wild animals are considered.
Four approaches were taken to obtain information on the effects of air
pollution: computerized bibliographic searches, published bibliogra-
phies, review articles on air pollutants and medical and insecticide
toxicology and, finally, a survey of experts currently working on the
health aspects of air pollutants.
Five major computerized bibliographic searches were utilized: APTIC,
CAIN, MEDLINE, NTIS, and TOXLINE (Table 4-1). These searches pro-
duced some 2000 titles and abstracts. Although there was some overlap,
each of the searches did produce unique references.
Although some early references are included in the computerized data
bases, these data bases are more complete from 1970 on. There are a
number of published bibliographies which partially cover the early
literature.I"11 Additional information was obtained from general re-
view articles on specific pollutants, in particular the series of pub-
lications published by the Department of Health, Education and Welfare
and the Environmental Protection Agency (Table 4-2). Since a number
of the pollutants have been used or considered as insecticides, such
as fluorides, sulfur dioxide, ozone, and arsenic compounds12»13»1^
and since others, such as lead and other heavy metals, have long his-
tories of toxicity, veterinary and insecticide toxicological litera-
ture was reviewed.
To determine possible unpublished information, investigators currently
doing research on the effects of air pollution on animals were also
contacted. Since several studies1^' indicated possible effects of
air pollutants on zoo animals, a survey was made of all the major zoos
of the world requesting information on any observed incidents of zoo
animals being effected by air pollution (Section 6). In many cases
the responses to the survey and other inquiries included suggestions
of other individuals or institutions to be contacted.
-------
Table 4-1. DESCRIPTION OF COMPUTERIZED DATA BASES
Data Base
Description
Period
APTIC
CAIN
MEDLINE
NTIS
TOXLINE
Air Pollution Technical Information Center,
7000 periodicals, government reprints, patents,
technical papers, preprints, translation articles
from books and proceedings.
Cataloging and indexing data base of the National
Agricultural Library; journals and monographs in
agriculture and related fields as forestry,
veterinary, medicine, chemistry, consumer pro-
I tection, entomology, and others.
Medical Literature Analysis and Retrieval
System on Line: 2800 journals and includes
Index Medicus, International Nursing Index,
and Index to Dental Literature.
National Technical Information Service of the
! U.S. Dept. of Commerce: citations and abstracts
! of government-sponsored research and development
! reports plus some translations on foreign
language reports.
Toxicology Information Conversational On-Line
Network, includes Toxicity Bibliography,
Health Aspects of Pesticides Abstract Bulletin,
Chemical-Biological Abstracts, Abstracts on the
Health Effects of Environmental Pollutants,
International Pharmaceutical Abstracts, and
Hayes1 File.
1966 to
date
Jan. 1970
to
present
Jan. 1972
to
present
Jan. 1970
to
present
Jan. 1969
to
date
15
-------
Table 4-2. SELECTED AIR POLLUTION TECHNICAL PUBLICATIONS OF
THE UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
Series
Number
AP-062
AP-064
AP-084
AP-049
AP-063
AP-050
APTD-69-24
APTD-69-26
APTD-69-27
APTD-69-28
APTD-69-29
APTD-69-31
APTD-69-32
APTD-69-33
APTD-69-34
APTD-69-35
APTD-69-36
APTD-69-37
Title
Air Quality
Air Quality
Air Quality
Air Quality
Air Quality
Air Quality
Preliminary
Criteria for Carbon Monoxide. 3/70.
Criteria for Hydrocarbons. 3/70.
Criteria for Nitrogen Oxides. 1/71.
Criteria for Particulate Matter. 1/69.
Criteria for Photochemical Oxidants. 3/70.
Criteria for Sulfur Oxides. 4/70.
Air
Preliminary Air
pounds. 10/69.
Preliminary
Air
Preliminary Air
pounds. 10/69.
Preliminary
Compounds.
Pollution
Pollution
Pollution
Pollution
Air Pollution
10/69.
Preliminary Air
pounds. 10/69.
Preliminary
Compounds.
Preliminary
Preliminary
Compounds.
Preliminary
Preliminary
10/69.
Preliminary
10/69.
Pollution
Air Pollution
10/69.
Air
Pollution
Air Pollution
10/69.
Air
Air
Air
APTD-69-38 Preliminary Air
pounds. 10/69.
APTD-69-39 Preliminary
Compounds.
APTD-69-40 ; Preliminary
Pollution
Pollution
Pollution
Pollution
Air Pollution
10/69.
Air
Pollution
Survey
Survey
Survey
Survey
Survey
Survey
Survey
Survey
Survey
Survey
Survey
Survey
Survey
Survey
Survey
of
of
of
of
of
of
of
of
of
of
of
of
of
of
of
Aldehydes. 10/69.
Arsenic and Its Corn-
Asbestos. 10/69.
Barium and Its Corn-
Beryllium and Its
Boron and Its Corn-
Cadmium and Its
Chlorine Gas. 10/69.
Chromium and Its
Ethylene. 10/69.
Hydrochloric Acid.
Hydrogen Sulfide.
Iron and Its Corn-
Manganese and Its
Mercury and Its
Compounds. 10/69.
16
-------
Table 4-2 (continued) SELECTED AIR POLLUTION TECHNICAL PUBLICATIONS
OF THE UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
Series
Number
Title
APTD-69-41
APTD-69-45
APTD-69-47
APTD-69-48
APTD-69-49
Preliminary Air Pollution Survey of Nickel and Its
Compounds. 10/69.
Preliminary Air Pollution Survey of Phosphorous and Its
Compounds. 10/69.
Preliminary Air Pollution Survey of Selenium and Its
Compounds. 10/69.
Preliminary Air Pollution Survey of Vanadium and Its
Compounds. 10/69.
Preliminary Air Pollution Survey of Zinc and Its Compounds.
10/69.
17
-------
REFERENCES
1. Campbell, E. E.and H. M. Miller, 1961, 1964. Chemical Detectors:
A Bibliography for Industrial Hygienist W. Abstracts and Annota-
tions. Vol. 1 (1961); Vol. 2 (1964).
2. Cooper, A. G. Air Pollution Publications, A Selected Bibliography,
1963-66. United States Public Health Service. Washington, D.C.:
Publication Number 979. 1966.
3. Cooper, A. G. Air Pollution Publications, A Selected Bibliography,
1955-63. United States Public Health Service. Washington, D.C.:
Publication Number 979. 1964.
4. Davenport, S. J. and G. G. Morgis. Air Pollution, A Bibliography.
United States Bureau of Mines. Bulletin Number 537. 1954. p. 1-
448.
5. Gibson, J.R., W. E. Culver, and M. E. Kurz. The Air Pollution
Bibliography, Volume I. Library of Congress. Washington, D.C.
1957.
6. Jacobius, A. J., J. R. Gibson, V. S. Wright, W. E. Culver and
L. Kassianoff. The Air Pollution Bibliography, Volume II.
Library of Congress. Washington, D.C. 1959.
7. Kettering Laboratory. Effects of Atmospheric Pollution on the
Health of Man. Cincinnati. Kettering Lab. of Appl. Physiology.
Univ. of Cincinnati. 1957.
8. Effects of Atmospheric Pollution on the Health of Man. Dept. of
Preventive Medicine and Industrial Health. Univ. of Cincinnati.
Cincinnati, Ohio. 1957. p. 311-378.
9. Stokinger, H. E. Ozone Toxicity: A Review of the Literature
Through 1953. Arch. Indus. Hyg. Occup. Med. 9:366-383, 1954.
10. Murk, J. B. Ind. Eng. Chem. 47:976, 1955.
11. Biological Aspects of Air Pollution: An Annotated Bibliography.
United States Public Health Service, Division of Industrial
Hygiene Division, with United States Steel Workers of America.
12. Cory, E. N. and H. B. McDonnell. Preliminary Tests of Ozone as an
Insecticide. J. Econ. Ent. 21(3):510, 1928.
13. Marcovitch, S. and W. W. Stanley. Cryolite and Berium Fluosili-
cate: Their Use as Insecticides. Tennessee Agricultural Experi-
ment Bulletin. 140:1-19, 1929.
18
-------
14. Negherbon, W. 0. Handbook of Toxicology, Volume FT1: Insecti-
cides. Philadelphia, W. B. Saunders Co., 1959. 829 p.
15. Snyder, R. L. and H. L. Ratsliffe. Primary Lung Cancer in Birds
and Mammals of the Philadelphia Zoo. Cancer Res, 26:514-518,
March 1969.
16. Bazell, R. J. Lead Poisoning: Zoo Animals May be Just Victims.
Science 1973(3992):130-131, 1971.
19
-------
SECTION 5
REVIEW OF EXISTING INFORMATION ON THE EFFECTS OF AIR POLLUTION
ON ANIMALS
5.1 Introduction
Extensive reviews on the effects of various air pollutants have been
published under the titles of Air Quality Criteria . . . and Preliminary
Air Pollution Surveys. . . (Table 4-2). These studies document the
physical, social, and health aspects of the major air pollutants. For
the most part, these in-depth reviews provide information on the re-
sponse of laboratory and experimental animals to air pollutants.
Lillie reviewed the effects of air pollutants on domestic animals.
In some instances effects upon wildlife are reported.
The purpose of this section of the report is to review the existing
information on the effects of air pollution on animals. Utilizing this
information I have attempted to determine characteristic effects and
the feasibility of using animals as biological indicators of air pollu-
tion. In addition the known responses of animals to various pollutants
are summarized. Reported air pollution episodes involving animals are
analyzed to determine sensitive species, patterns of response of free-
living species, and any other diagnostic or characteristic measures.
Reported episodes are classed as episodes attributable to a known pol-
lutant or those episodes possibly attributable to known pollutants or
a mixture of pollutants including the specific pollutant. Laboratory
and experimental studies are evaluated according to the observed re-
sponses of laboratory animals to known concentrations of a pollutant.
Comparison of the experimental concentrations are made to determine
the likelihood of observing responses in nature. Where possible labor-
atory studies are related to reported episodes. The review of each
pollutant is divided into the six topics: sources and environmental
concentration, summary of symptoms of acute and chronic poisoning,
laboratory studies, suggested biological indicators, and areas of
needed research.
REFERENCE
1. Lillie, R. J. Air Pollutants Affecting the Performance of
Domestic Animals: A Literature Review, United States Department
of Agriculture, Washington, D.C. Agriculture Handbook Number
380. August 1970, 109 p.
20
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5.2 Air Polluta_nt_;__ Asbestos
The primary sources of asbestos emissions are through the use of
asbestos products in the construction industry and asbestos mines and
factories. No urban concentrations of asbestos could be found. Ambient
levels near industrial sources have been recorded. Asbestos dust was
found up to 50 km from an asbestos mine in Finland. The rate of fall-
out was determined to be 1.5 x 10^ ug/100ra3/month at 4 km and 36.6 x
106 yg/lOOm-Vmonth at 0.3 km. In Russia ambient levels near an asbes-
tos plant were found to be up 6,000 ug/m3 at 3 km, 3,000 to 33,000
at 1.5 km, and 6,000 to 34,000 ug/m3 at 0.5 km.1
Summary of Symptoms of Acute and Chronic Poisoning by Asbestos. The
major mode of intoxication is by inhalation. Ingestion of asbestos
dust-laden vegetation may also occur although documentation is lacking.
The primary biological target area is the pulmonary system. Acute
asbestos poisoning is characterized by fibrotic lesions of the lung.
Besides these lesions chronic poisoning results in bronchiolitis and
tumors of the lung. The lungs appear as areas of accumulation with
the presence of "asbestos bodies" being a diagnostic characteristic
of exposure.
Episodes Involving the Effects of Asbestos on Free-Living Animals. Two
incidents are reported of free-living animals being affected by asbes-
tos. These include the finding of asbestos bodies in the lungs of
cattle near an asbestos mine and in free-living monkeys and rats near
a South African mine. The population density of rats was lower than
expected.
Table 5.2-1. ASBESTOS: REPORTED EFFECTS ON FREE-LIVING ANIMALS
A. Known effects:
1) Webster, 1963. Found asbestos bodies in free ranging Rhesus
monkeys and rats near asbestos mine in South Africa. Rats
showed lower population.3
2) Kiviluoto, 1965. Asbestos bodies found in cows near asbestos
mine.
Summary of Studies on the Effects of Asbestos on Experimental Animals.
Comprehensive experimental animal studies on the effects of aspestos
have not been conducted. Asbestotic pulmonary fibrosis has been pro-
duced experimentally in rats, guinea pigs, hampsters, rabbits, mon-
keys and chickens.1' 2 Lung cancers from chrysotile dust have been
produced experimentally in rats, mice and guinea pigs. 2 However,
most experimental studies have been conducted at extremely high levels
21
-------
(Table 2.2) compared to ambient levels. In many cases asbestosis has
been induced by injection or transplantation of asbestos material into
lungs. Hampsters may be more sensitive to asbestos fibers than rats
and guinea pigs.
Table 5.2-2. REPRESENTATIVE STUDIES OF THE EFFECTS OF ASBESTOS
ON EXPERIMENTAL ANIMALS
Species
Rats
Guinea
Pigs
Hampsters
Guinea
Pigs
Rats
Substance
Chrysotile
Chrysotile
Chrysotile
Asbestos
dust
Chrysotile
Concentration
ug/m^
86,000
86,000
86,000
86,000
Length of
Exposure
60-120 hrs.
60-120 hrs.
less than
60 hrs.
14 days
few months
Effects
Asbestosis
Asbestosis
with As-
bestos
bodies
Asbestosis
Bronchioli-
tis
Minimal
References
Gross and
Detreville^
1967
6
Holt et al
Gross and
Detreville5
Suggested Biological Indicators of Asbestos. The lung appears as a
good biological monitoring system, with the presence or absence of
asbestos bodies being a diagnostic criteria for asbestos exposure.
Population changes might be correlated with asbestos contamination.
Areas of Needed Research. (1) Effects of asbestos on insects, birds
and other animals with high respiratory rates; (2) studies on urban
concentration of asbestos along with measurements of deposits on vege-
tation and its fate; (3) ecological studies on effects of asbestos on
relatively sedentary populations.
REFERENCES
1. Sullivan, R. J. and Y. C. Athanassiadis. Preliminary Air Pollu-
tion Survey of Asbestos, a Literature Review. National Air Pollu-
tion Control Administration. Publication number APTD 69-28.
October 1969. 93 p.
2. Biological Effects of Atmospheric Pollutants Asbestos. Washing-
ton, D.C. National Academy of Science-National Research Council.
1971. 40 p.
22
-------
3. Webster. I. Asbestosis in Non-experimental Animals in South
Africa. Nature 197:506, 1963.
4. Kiviluoto, R. Pleural Plaquescend Asbestos: Further Observa-
tions on Endemic and Other Non-Occupational Asbestos. Ann. N. Y.
Acad. Sci. 132:235, 1965.
5. Gross, P. and R. T. P. de Treville. Experimental Asbestosis
Studies on the Progressiveness of the Pulmonary Fibrosis Caused
by Crysotile Dust. Arch. Environ. Health 15 (5):638, 1967.
6. Holt, P. F., J. Mills and D. K. Young. Experimental Asbestos in
the Guinea Pig. J. Pathological Bacteriology 92(1):185(1966).
23
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5.3 Air Pollutant: Arsenic
Arsenic as an air pollutant is commonly found in the form of arsenic
trioxide. The primary technological sources are gold and copper smelt-
ing and agricultural activities involving the use of arsenical insec-
ticides. Non-urban concentrations of arsenic range from 0.00 to 0.01
ug/m-*. The maximum urban concentration in 1953 was 1.41 ug/ro . Higher
levels have been reported around industrial operations ranging from 60
to 13,000 ug/m^ in badly polluted areas. Arsenic is also found in
the soils and vegetation. In Montana concentrations in soils have
been found as high as 150 ppm. Pasture grasses have contained arsenic
levels up to 120 ppm wet weight.2
Summary of Symptoms of Acute and Chronic Arsenic Poisoning. In gen-
eral, the major modes of arsenic intoxication are by ingestion and
inhalation. The primary target system for arsenic is the gastro-
intestinal system and upper respiratory tract. Acute
arsenic poisoning causes inflammation of the gastrointestinal tract,
liver damage, nausea and diarrhea. Chronic symptoms include weakness,
occasional vomiting, diarrhea, inflammation of mucous membranes of
the nose and gums, skin ulcers and reduced reproduction.3 Insects
show digestive system changes and changes in blood physiology. Arsenic
is accumulated in the kidney and liver. Long-term exposures result in
arsenic being stored in the bones, skin and keratinized tissues.
Episodes Involving Arsenic Poisoning of Free-Living Animals. Numerous
episodes are reported involving arsenic poisoning in free-living ani-
mals (Table 5.3-1). These have included domestic animals and wildlife.
It would appear that large herbivores are adversely affected by indus-
trial emissions of arsenic. Bees are also affected by arsenic. In
most cases, the symptoms of the poisoning were not included. For
those episodes reporting symptoms, they were typical of arsenic poison-
ing. Several studies involving possible arsenic poisoning are re-
ported. Again herbivores (domestic) were affected, and the symptoms
were similar to those of arsenic intoxication. In two cases, respira-
tory and parasitic infections were observed.
Summary of Studies on Effects of Arsenic on Experimental Animals.
^Studies of lethal oral dosages of As-03 (Table 5.3-2) on vertebrate
and invertebrate animals indicate the ambient concentrations in pol-
luted situations are high enough to be harmful to both groups of
animals. Due to the broad toxicity of arsenic to animals, harmful
effects should occur in a considerable number of wildlife species
living under polluted conditions. Sensitivities vary within verte-
brates and invertebrates. In vertebrates sensitivity decreases
respectively in dogs, pigs, sheep, horses, cattle, and poultry.
24
-------
Table 5.3-1 ARSENIC: EPISODES INVOLVING FREE-LIVING ANIMALS
A. Known
1. Harkins & Swain, 1908. Reports arsenic poisoning in cattle and
horses near smelter in Montana. Symptoms include red line at base of
teeth (horses), garlic odor of breath, weakness, loss of hair, ulcers
of nose.^
2. Formad, 1908. (39933). Reports loss of 2000 horses in Montana
over 4 years, losses in cattle great; effects include decreases in fer-
tility and abortions, along with effects in respiratory and digestive
organs."
3. Prell, 1937. Reports 60-70% of game animals in Tharandt Forest
killed, including deer and rabbits, due to arsenic, in Germany.7
4. Tendron, 1964. Reports killing of fallow dear near silver
foundry in Germany in 1887.°
5. Rodriguez, 1965. Reports horses and asses sickened by As
fumes near industrial source in Spain.
6. Heis & Masek, 1969. (08260). Observed arsenic poisoning in
stags and roe bucks and bees; bees died up to 52 km from industry in
Czechoslovakia. °
7. Lillie, 1970. Reports several studies involving destruction
of bees and bee colonies resulting from arsenic emissions. They ap-
pear to show high sensitivity.11
B. Probable or Combined Pollutants
1. Bischoff, 1939. (12530). Reports sick cattle, sheep, horses
and poultry near copper smelter in Germany. High levels of copper and
AS203, miscarriages, sterility, loss of weight, parasitic infestations
of lungs and stomach.
2. Wiemann, 1939. (12546). Reports sick cattle (diarrhea,
abortion, loss of weight and appetite) and loss of hair in cattle due
to copper and arsenic from copper smelter in Germany.1-*
3. Masek & Hais, 1963. (12537). Report sick cattle (diarrhea and
pneumonconiosis simplex)and abortions in Czechoslovakia due to 202
and arsenic.1^
4. Lewis, 1972. (41893). Reports sick horses from Montana
near smelter, air contained arsenic, cadmium, and lead. 1-5
( ) = APTIC No.
25
-------
T;ible 5.3-2
SUMMARY OF LETHAL ORAL
IN ANfMALS
DOSAGES OF ARSENIC TRTOXIDF,
Bombyx raor L
Rabbit
Melanoplus
bivattatus
Dog
MeL.moplus
d if f erentia lis
Rat
Musca domes tica
Melanoplus femur
Apis mellifera
Dog
Fowl
Pit-
Sheep
Horse
Cow
Bass
Trout
Mussels
Plcinarians
Aquatic insects
Concentration,
mg/kg body wt.
A. Acute Exposures
15-20
20
26
85
90
138
180
137-360
0.2-0.5ug/bee
100-150 mg/animal
50-300 mg/animaJ
500 mg/ animal
850 mg/animal
2000 mg/animal
200 mg/animal
10 ppm
10 ppm
16 ppm
40 ppm
2-4 ppm
Length of
Exposure
Acute
Acute
Acute
Acute
Acute
Acute
Acute
Acute
Acute
Acute
Acute
Acute
Acute
Acute
10 days
1 month
3-16 days
?
7
Observed '
Effect(s) Reference(s)
LD50
LD50
LD50
LD50
LD50
LD50
^50
L°50
J\J
MI.D
Average
lethal
dose
Average
lethal
dose
MLD
MLD
MLD
Toxic
Harmless
Toxic
Toxic
Toxic
4
Negherborn
3
Garner
4
Negherborn
NOTE: As 03 is soluble in dilute acids, alkalis, and carbonate
solutions.
26
-------
SuRgesled Biological Indicators of Arsenic. In terms of mammalian
systems, the respiratory tract and gastrointestinal system would be
suitable monitors for arsenic intoxication. Tn particular, the kidney
and liver, along with skin, bones and keratinized tissues should be
observed. Both mammals (herbivores) and insects appear as sensitive
species . In particular, bees exhibit a high sensitivity to arsenic.
Areas of Needed Research. 1) Effect on animals with high respiratory
rates, including birds; 2) effect of arsenic on soil organisms and
wild bee populations; 3) studies on sensitivities of wildlife to
As203.
REFERENCES
1. Sullivan, R. .1. Preliminary Survey of Arsenic and Its Compounds,
a Literature Review. National Air Pollution Control Administration.
Publication Number 69-26. October 1969. 59 p.
2. Helena Valley, Montana, Area Environmental Pollution Study. En-
vironmental Protection Agency. Research Triangle Park, North
Carolina. AP-91. Office of Air Programs. January 1972. 179 p.
3. Garner, R. J. Veterinary Toxicology. London, Balliere, Tindall
and Cox. 1957. p 42-255.
4. Negherbon, W. 0. Insecticides; a Compendium. In: Handbook of
Toxicology, Vol. Ill, 1959. National Academy of Sciences, Natural
Resource Council. Philadelphia. N. B. Saunders.
5. Harkins, W. D., and Swain, R. E. The Chronic Arsenical Poisoning
of Herbivorous Animals. Amer Chem Soc Jour. 30: 928-946, 1908.
6. Formad, R. J. The Effect of Smelter Fumes upon the Livestock
Industry in the Northwest. United States Department of Agricul-
ture. Washington D. C.: Pathological Division, Report number
25. Bureau of Animal Industry. 1908. p. 237-268.
7. Prell, H. Injury to the Animal World Through the Distant Effects
of Industrial Waste Gases. Arch. Gewerbepath Gewerbehyg. 7:656,
1937.
8. Tendron. Effect of Pollution on Animals and Plants. European
Conference on Air Pollution, Council of Europe. Strasbourg.
24 June to 1 July 1964. 25-70.
9. Rodriguez, G. M. Arsenic Poisoning from Industrial Fumes and
Gases. Notic. Neoson. 127:89-92, 95, 1965.
27
-------
If) Heis, K. and J. Masek. Effects of Some Exhalations on Agricul-
tural Animals. Ochr Ovzdusl: 1969: 122-125, Aug. 1969.
11. Li Hie. R. Air Pollutants Affecting the Performance of Domestic
Animals. United States Department of Agriculture. Washington,
D.C. Handbook Number 380. 1970. p 20-23.
J2. Bischoff, 0. Poisoning of Domestic Animals Through Copper and
Arsenic Containing Fly Dust. Deut. Tierzerztl Wochschr., 47:
442-447, 1939.
13. WLemann. Copper Poisoning Due to Flue Cases. Deut. Tierzerztl
Wochschr.. 47:279-281, 1939.
14. Masek, J. and K. Hais. Negative Effects of Industrial Exhala-
tions on Cattle. Vet. Med. (Czech) 8(5):341-346, 1963.
15. Lewis, T. R. Effect of Air Pollution on Livestock and Animal
Products. Ln: Helena Valley, Montana. Area Environmental
Pollution Study. Environmental Protection Agency, Research
Triangle Park, N.C. Number AP-91. January 1972. p. 113-124.
28
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5. 4 Air Pollutajit^._ Barium
Barium emissions in the form of various salts result from mining and
some petrochemical industries. No ambient levels have been reported.1
Summary of t\\v_Symptoms of Acute and Chronic Barium Poisoning. The
primary route of experimental poisoning has been by ingestion. Poison-
ing by inhalation is possible. The primary target systems for barium
are the central nervous system and pulmonary system. y»cute barium
poisoning results in incoordination and paralysis of skeletal muscle
and heart irregularities. Chronic poisoning causes respiratory
changes and bronchiogenic carcinoma. Barium does not appear to be
readily accumulated by the body of mammals. '
Episodes Involving Barium Poisoning of Free-Living Animals. No inci-
dents have been reported.
Summary of Studies on the Effect of Barium on Experimental Animals.
Laboratory studies indicate toxicities vary with species and type of
barium compound (Table 5.4-1). Because of the lack of information on
ambient concentrations of barium, no conclusions can be reached as
to the importance of barium as an environmental hazard.
Suggested Biological Indicators for Barium. The lack of information
allows no suggestions of potential biological indicators.
Areas of Needed Research. 1) Studies on the concentration and distri-
butTon of barium in the environment; and 2) studies on the effects of
barium on animals and plants.
REFERENCES
]. Minor, S. Preliminary Air Pollution Survey of Barium and Its
Compounds, a Literature Review. National Air Pollution Control
Administration. Publication Number APTD 69-28. October 1969.
57 p.
2. Garner, R. J. Veterinary Toxicology. London, Balliere, Tindall
and Cox. 1957. p 42-255.
29
-------
Table 5.4-1 REPRESENTATIVE LABORATORY STUDIES ON TIIF. TOX1CITY OF
BARIUM COMPOUNDS ADAPTED FROM MINER.1
Species
Rnbbits
Rabbits
Mice
Rats
Rats
Rabbi ts
Pigs
Mice
Rats
Dogs
Pigeon
Horse
Hedgehog
Guinea pig
Rats
Rabbits
Substance
Ba acetate
Ba carbonate
Ba chloride
Ba fluoride
Ba silico-
f luoride
Concentration,
rag/kg body wt.
236
815
200
1480 + 340
50 - 200
170 - 300
1000
7 - 14
355 - 533
90
500
800 - 1200
4800 - 9600
350
175
175
Time oT
death
24 hrs
1.5 hrs
1-8 days
Observed
ef fect(s)
LD
LD
LD
^50
LD
LD
LD
LD
LD
LD
LD
LD
LD
LD
LD50
MLD
30
-------
5•5 Air Pollutant: Beryllium
Environmental contamination by beryllium occurs as a result of extract-
Ing, refining and machining of beryllium-containing materials. As a
pollutant, it is found in the form of oxides and halides. Maximum ur-
ban concentrations have been reported as high as 0.0003 ug/m . Atmo-
spheric concentrations near industrial sources have been higher. In
Pennsylvania and Ohio near beryllium plants, ranges of atmospheric
beryllium have been reported to range from 0.028 to 0.082 gg/m^ and
20 to 2,100 ug/ro3.1
Summary of Symptoms of Acute and Chronic Beryllium Poisoning. The ma-
jor modes of intoxication of beryllium are by inhalation and possible
ingestion of beryllium dust on vegetation. The primary biological tar-
get system of beryllium is the respiratory system. Acute poisoning re-
sults in bronchiolitis, pneumonitis, irritation to eyes and nasal pas-
sages. Chronic poisoning causes rickets, arteriosclerosis, primary
broncho-pulmonary cancer, bronchitis, anemia, and emphysema.It »J
Episodes involving Beryllium Poisoning of Free-Living Animals. No
such incidents have been reported.
Summary of Studies on the Effects of Beryllium on Experimental Animals.
Laboratory studies have been conducted at extremely hij.h concentra-
tions (Table 5.5-1). In general, reports of ambient concentrations are
much below those laboratory studies. The conditions at the Ohio beryl-
lium plant were high enough to fall within the lower range of experi-
mental studies; although the duration of the high ambient concentration
was not given, it appears that possible harmful effects could have oc-
curred to animals living within the area. Humans were adversely effected.
Suggested Biological Indicators for Beryllium. The respiratory system
appears as a possible biological system to monitor beryllium. This
system, along with monitoring of the areas of biological accumulation,
might provide a suitable monitoring system.
Areas of Needed Research. 1) Studies on the effects and sensitivities
of animals, including birds and insects, to beryllium; and 2) further
studies on the concentration and distribution of beryllium in the en-
vironment, including occurrence in or on plants.
REFERENCES
1. Durocher, N. L. Preliminary Air Pollution Survey of Beryllium and
Its Compounds, a Literature Review. National Air Pollution Con-
trol Administration. Publication Number APTD 69-29. October 1969.
79 p.
31
-------
2. Vorwald, A. J., A. L. Reeves, and E. C. J. Urbon. Experimental
Beryllium Toxicology. In: Beryllium, Its Industrial Hygiene
Aspects. H. E. Stohenger (ed.). New York, Academic Press,
1966. p 200-234.
3. Lillie, R. Air Pollutants Affecting the Performance of Domestic
Animals. United States Department of Agriculture. Washington,
D. C. Handbook Number 380. 1970. 109 p.
Table 5.5-1 PHYSIOLOGICAL CHANGES AND MORTALITY RESULTING FROM IN-
HALATION OF BERYLLIUM FLUORIDE, BERYLLIUM OXIDE, AND
BERYLLIUM SULFATE
Species
Cats
Rabbits
Rats
Dogs
Dogs
Substance
Be fluoride
Conc3
Pg/m
970
970
970
970
2000-
2400
Length of
exposure
6 hrs/day
207 days
6 hrs/day
207 days
6 hrs/day
5 days/wk
207 days
6 hrs/day
207 days
6 hrs/day
Observed effect(s)
No deaths; lung
damage
No deaths; sus-
pected macro-
cytic anemia;
lung damage
73 deaths; minimal
lung lesions
3 deaths; suspected
macrocytic anemia;
consolidation, em-
physema and slight
edema in lungs; Be
tended to accumu-
late in lungs, pul-
monary lymph nodes,
liver, skeleton,
and bone marrow
Decrease in RBC
count and Hb
levels; increase in
mean corpuscular
volume consistent
with macrocytic '
anemia
Ref erence(s)
Durocher
•
32
-------
Table 5.5-1 (Continued) PHYSIOLOGICAL CHANGES AND MORTALITY RESULTING
FROM INHALATION OF BERYLLIUM FLUORIDE, BERYLLIUM OXIDE,
AND BERYLLIUM SULFATE
Species
Rats
Rats
Rats
Rats
Rats
Rats
Rats
Cats
Substance
Be
sulfate
Cone.
UR/m3
2.8
21.0
35.0
42.0
42.0
194
424
950
Length of
Exposure
7 hrs/day
1-100 days
7 hrs/day
1-100 days
6 months
9 hrs/day
3 months
3 months
Acute
8 hrs/day
5.5 dys/wk
6 months
6 hrs/day
100 days
Observed effect(s)
No effect
Inflammatory changes.
in long-surviving
rats
Granulamatosis and
neoplasia
Produced chronic
pneumonitis
Pulmonary change —
subpleura and paren-
chyma 1 foci
Lethal
46 deaths; apparent
effect on lung tis-
sue; stimulation of
epithelial cell pro-
liferation without
provoking a connec-
tive tissue reac-
tion; foam-cell
clustering; focal
mural infiltration;
lobular septal cell
proliferation; peri-
bronchial alveolar
wall epithelization;
granulomatosis and
neoplasia
No deaths; 10% body
weight loss; yg Be/g
fresh tissue from 5
sacrificed animals;
lung, 0.6; pulmonary
lymph nodes, 0.7;
liver, 0.01; kidney,
0.003; spleen, 0.01.
Reversible macrocy-
tic anemia after 3-8
weeks; significant
changes in phosph-
lipid and free chol-
esterol of whole RBC
Reference (s)
Vorwald , et
al.,2
1
Durocher
33
-------
Table 5.5-1 (Continued) PHYSIOLOGICAL CHANGES AND MORTALITY RESULTING
FROM INHALATION OF BERYLLIUM FLUORIDE, BERYLLIUM OXIDE,
AND BERYLLIUM SULFATE
Species
Guinea
pigs
Hamsters
Monkeys
Rabbits
Rats
Rats
Rats
Rats
Substance
Be
sulfate
Cone.
u / •»
UE/m
950
950
950
950
950
4000
47.000
100,000
Length of
Exposure
6 hrs/day
100 days
6 hrs/day
100 days
6 hrs/day
100 days
6 hrs/day
100 days
6 hrs/day
5 days/wk
100 days
6 hrs/day
23 weeks
6 hrs/day
5 days/wk
5 hrs/day
5 days/wk
14 days
Observed effect(s)
tendency to hypoal-
buminemia and hyper-
globulinemia; acute
inflammatory response
in lung, with erosion
and proliferation of
bronchial epithelium.
No deaths; 18% body
weight gain
No deaths; no change
in body wt.
No deaths; 10% body
wt. gain, ug Be/g
fresh tissue from 2
sacrificed animals;
lung, 1.2; pulmonary
lymph nodes, 1.3;
liver, 0.5; kidney,
0.01; spleen, 0.1
No deaths; 15% body
weight gain, ug Be/
g fresh tissue from
5 sacrificed animals;
lung, 1.6; pulmonary
lymph nodes, 0; liver
0.004; kidney, 0.003;
spleen, 0.01
No deaths; 20% body
weight gain
Decrease in RBC count
increase in mean cor-
puscular volume con-
sistent with macro-
cytic anemia
13 deaths; no change
in body weight; leu-
kocytosis
10 deaths; 2% body
weight loss; leukocy-
tosis
Reference (s)
Durocher
34
-------
5.6 Air Pp_Llutan_t_:_ JJorpn
Boron, in the form of oxides and halides, is emitted from the indus-
trial activities involving iron, fuel, and other chemical industries.
No levels of boron in the atmosphere have been published.
Summary of the Symptoms of Acute and Chronic Poisoning by Boron. Littie
information is available on the health effects of boron. One of the
modes of intoxication is through inhalation. The primary target systems
for boron appear to be the central nervous system, res[.iratory tract,
and liver. Acute poisoning results in diarrhea, vomiting, circulatory
collapse, liver and kidney damage, and cerebral edema. Boron concen-
trates in the brain, liver, and body fat. »^
Episodes Involving Boron Poisoning of Free-Living Animals. No inci-
dents have been reported.
Summary of Studies j)n the Effect of Boron on Experimental Animals.
Most studies have been at high concentrations and acute exposures
(Table 5.6-1). These studies indicate that relatively high concentra-
tions are lethal to rodents. With the lack of field dsta on ambient
concentrations and effects on free-living animals, no conclusions can
be drawn as to its environmental importance.
Suggested Biological Indicators for Boron. The brain, liver, and body
fat appear to be accumulating sites for boron and its derivatives.
Areas of Needed Research. 1) Studies on the distribution and concen-
tration of boron in the technological environment; 2) studies of the
effects of low concentrations and chronic exposures to boron on ani-
mals, including birds and insects, and vegetation.
REFERENCES
1. Durocher, N. L. Preliminary Air Pollution Survey of Boron and Its
Compounds, a Literature Review. National Air Pollution Control
Administration. Publication Number APTD 69-31. October 1969.
45 p.
2. Garner, R. J. Veterinary Toxicology. London, Balliere, Tindall
and Cox. 1957. p. 42-255.
35
-------
5.6-1 REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF
BORON ON ANIMALS, ADAPTED FROM DUROCHER.1
Species
Mice
Rats
Rats
Rats
Rats
Mice
Dogs
Rats
Mice
Guinea pig
Mice
Rats
Mice
Rats
Mice
Rats
Guinea pig
Substance
A. Oral Dosages
Decaborane
Boron
Boranes
Boric Acid*
Borates
B. Inhaled Dosag
Borones
Decaborones
Boron halides
"one . ,
ppm
es
29
40-80
25.7
46
20-750
20-750
50-750
Con. ,
R/g
40,900
64,300
240,000
59,000-
238,000
5,140
* 4,100
> 1,000
650
2,000^
3,000
5,300
33,000
45,000-
91,000
122,000
230,000
Length of
exposure
Acute
Acute
Acute
Acute
Acute
Acute
Acute
Acute
Acute
Acute
14 days
14 days
4 hrs/day/
2 days
4 hrs/day/
2 days
5-14 hrs
5-14 hrs
5-14 hrs
Observed
effect(s)
LD50
LD50
"•so
LD50
"'so
LD50
LD50
^50
LD50
^O
LC50
"=50
LC50
LC50
Toxic; varying
mortalities
Toxic; varying
mortalities
Toxic; varying
mortalities
*Has a cumulative effect.
36
-------
5.7 Air Pollutant: _ Cadmium
As an air pollutant, cadmium is found in several forms, including a
niotal dust, an oxide, sulfate, and sulfide. Technological cadmium
emissions come from the refining of metals such as Zn, Cu, Pb, electro-
plating processes, and cadmium manufacturing products. Normal levels
of cadmium in the soil are estimated to be 0.55 to 2.45 ppra (ug/m ).
Urban levels from 1954 to 1964 have averaged 0.002 pg/m3 with a maxi-
mum reported of 0.420 ug/m3 for St. Louis. Soil near industrial
sources can have high concentrations. Soils near a battery smelter in
British Columbia had levels as high as 95 ppm.2 Levels as high as 160
ppm have been reported in the Helena Valley of Montana. Concentra-
tions of cadmium in and on vegetation can also reach high levels. 1.2
ppm to 9.8 ppm (wet weight) have been observed in pasture grasses in
Montana.3 Oat roots grown in contaminated soils had up to 205.1 ppm
cadmium. Levels as high as 30 to 55 ppm have been found on tree
leaves in the same area.^
Summary^ of Symptoms of Acute and Chronic Cadmium Poisoning. The main
modes of intoxication by cadmium are through ingestion and inhalation.
The primary target systems are the pulmonary, circulator and renal
systems (Table 5.7-1). Acute poisoning with cadmium salts causes
violent gastritis with vomiting and diarrhea. Chronic poisonings re-
sult in pulmonary inflammation and emphysema, reduction in hemoglobin
and red blood cells, arteriosclerosis, kidney and splenic disfunction.
Cadmium has been found to be teratogenic and carcinogenic. Kidney
damage is considered to be a classical syndrome of chronic cadmium
poisoning. Cadmium is concentrated in a number of tissues in the
body, including the blood and bones.^»^»5
Episodes Involving Cadmium Poisoning of Free-Living Animals. No con-
firmed reports were found on contamination of animals attributable
solely to cadmium. Horses have been reported sickened in an area in
Montana where high levels of cadmium were found along with arsenic
ami lead (Table 5.7-2).
Summary of Studies on the Effects of Cadmium on Experimental Animals.
Experimental studies indicate that possible concentrations of cadmium
in vegetation can be toxic to mammals (Table 5.7-1). No studies were
found involving birds and insects. Experimental levels of inhalation
are far above known ambient levels, and no conclusions can be reached
on effects of cadmium from inhalation. The paucity of experimental
studies on laboratory and domestic animals do not allov> for conclu-
sions to be drawn as to general effects on animals.'
Suggested Biological Indicators. The pulmonary and circulatory sys-
tems, along with the kidneys, appear as biological monitoring systems
37
-------
Table 5.7-1 EFFECTS OF CADMIUM AND CADMIUM COMPOUNDS ONANIilALS (Adapted from Athanassiades1).
Species
Rats
Rats
Cats
Rats
Rabbits
Mice
Material
Ingested Dosages
Cadmium metal
Cadmium chloride
Rabbits
Monkeys
Dogs
Mice
Guinea pigs
Dogs
Cows
Rats
B. Inhaled Dosages
Cadmium oxide
Average
Does
Length of
Exposure
Observed Effect(s)
0.1-10 ppm 1 year Cadmium content of liver and kidney
increased in proportion to quantity
of cadmium intake.
5-75 ppm Single Dose Lethal
20 ppm Single Dose Produced vomiting
135 ppm Single Dose Lethal
" 2 50y g/kg 12~2 9" wks
body wt.
4480 pg/kg 1-7 days
body wt.
630-3690
gg/m3 13-30 min.
4500-28,200
Ug/m3 _ 10-30 min.
7000pg/m 1102 hrs
660,000- 15 min.
13-30 min.
Mg/min/m
640,000-
6,450,0003
Ug/min/m
3,100,000- 10-20 min.
10,000,000
yg/min/m
3 gms/day 2 weeks
500,000 Ug/
min/m3 1 minute
Pulmonary edema
Lethal
Lethal
Retention of cadmium dust in tissues
Lethal
Decreased body and milk production;
return to normal after
Acute pulmonary edema within 24 hrs
pneumonitis in 3-10 days; permanent
lung damage and fibrosis
-------
Table 5.7-1 (Continued)
EFFECTS OF CADMIUM AND CADMIUM COMPOUNDS ON ANIMALS (Adapted from
Athanassiades 1).
W
Species Material
Rats
Rats
Mice Cadmium chloride
Dogs
Rats
Dogs
Dogs Cadmium stearate
Mice
Average
Dose
150,000-
1,300.000 vg/
min/m3
800,000-
1,000.000 pg/
min/m
85,000-170,000
ug/m3 _
320,000 ug/mJ
250,000 ug/
min/m3
9,600,000ug/
min/m3
9,310-18,570
ug/m3 day
6,000-7,570
ug/m3/dat
Length of
Exposure
10-15 minutes
1 minute
30 minutes
15 minutes
1 minute
1-7 days
1-7 days
Observed Effect(s)
Acute pulmonary edema within 24
hours; pneumonitis in 3-10 days;
permanent lung damage and fibrosis
Lethal; acute pulmonary edema
within 24 hours; pneumonitis in
3-10 days; permanent lung damage
and fibrosis _
Overall retention
Lethal
Lethal; pulmonary edema within 24
hours; pneumonitis in 3-10 days;
permanent lung damage and fibrosis
Lethal
Lethal; LD 9310 ug
Growth suppression, histological
changes in stomach, intestine,
Cadmium chloride
78,000-164.000
Ug/min/m-'
6 months
testicles, other organs
Tolerated
-------
Table 5.7-2 CADMIUM: EPISODES INVOLVING FREE-LIVING ANIMALS
A. Known
1. Nishino, 1973 (55770) high levels of Cd found in sparrows
from Areas with Cd pollution.
B. Possible or Mixed Pollutants
1. Lewis, 1972 (41893). Sick horse with high As, Cd, and Pb
levels in the hair of the horse near a smelter in Montana.
( ) = APTIC No.
in mammals.. Bleaching of rat incisors is noted at concentrations of
5 ppm CdCl. Due to the lack of studies, no conclusions can be
reached as to particular species which might be suitable biological
indicators. Sparrows, however, do accumulate cadmium.
Areas of Needed Research. 1) Studies of low and chronic exposures to
cadmium, including birds, mammals, and insects.
REFERENCES
1. Athanassiadis, Y. C. Preliminary Survey of Cadmium and Its Com-
pounds, a Literature Review. National Air Pollution Control Admin-
istration. Publication Number APTD 69-32. October 1969. 81 p.
2. Lillie, P. A Study of Heavy Metal Contamination oi Leaf Surfaces.
Environ. Pollut. 5:159-172, 1973.
3. Hondawi, I. J. and G. E. Neely. Soil and Vegetation Study. In
Helena Valley, Montana, Area Environmental Pollution Study. En-
vironmental Protection Agency, Research Triangle Park, N.C.
Number AP-91. January 1972. p. 81-94.
4. Garner, R. J. Veterinary Toxicology. London. Balliere, Tindall
and Cox. 1957. p 42-255.
5. Lillie, R. Air Pollutants Affecting the Performance of Domestic
Animals. United States Department of Agriculture. Washington,
D.C. Handbook Number 380. 1970. p 26-28.
6. Nishino, 0., M. Arari, I. Senda, and K. Kubota. Influence of
Environmental Pollution on the Sparrow. (Kankyo Osen No Suzume Ni
Oyobosu Eikyo). Nippon Koshu Eisei Zasshi (Japan J. Public Health),
20 (10), 1 p. , Oct. 1973.
40
-------
7. Lewis, T. R. Effects of Air Pollution on Livestock and Animal
Products. Tn Helena Valley, Montana, Area Environnental Pollution
Study. Environmental Protection Agency, Research Triangle Park,
N.C. Number AP-91. January 1972. p 113-124.
-------
5.8 Air Pollution: Carbon Monoxide
Carbon monixide is a product of combustion, the major sources being
transportation, fuel combustion from stationary sources, industrial
processes, solid waste, and forest fires. Urban levels average from
10 to 40 ppm (12 to 46 ug/m3). A high of 360 ppm (394 ug/m ) was
recorded at a traffic island in London.
Summary of Symptoms of Acute and Chronic Carbon Monoxide Poisoning.
The mode of intoxication is inhalation, with the central nervous
system being the primary target system. Acute exposures to carbon
monoxide result in muscular weakness, rapid respiration, possible
asphyxiation, and cherry red color in all tissues. Symptoms have been
observed at low chronic concentrations. The circulatory system is the
major area of accumulation, where carbon monoxide (CO) combines with
hemoglobin to form carboxyhemoglobin (CO-Hb)A»2
Episodes Involving Carbon Monoxide Poisoning of Free-Living Animals.
No episodes have been reported on free-living animals.
Summary of Studies on the Effects of Carbon Monoxide on Experimental
Animals. In general, laboratory and experimental studies indicate that
at concentrations of less than 50 ppm there are little or no effects
observed in mammals and chickens (Table 5.8-1). Acute exposures
of 100 ppm will change behavior and hemoglobin levels. Chronic ex-
posures of 100 ppm similarly effect hemoglobin levels, behavior and
result in changes in heart structure. The toxic level of carbon
monoxide for mammals and chickens is generally above levels found in
polluted situations, although conditions may exist where levels be-
come toxic. Susceptibility to carbon monoxide poisoning varies be-
tween toxonomic group. Sensitivities have been observed in the follow-
ing species in decreasing order of sensitivities: canary, mouse, ,
chicken, small dog, pigeon, English sparrow, guinea pig, and rabbit.
Suggested Biological Indicators for Carbon Monoxide. The circulatory
system, in particular, through changes in blood chemistry, appears to
be a very good indicator to exposure to carbon monoxide. Methods for
the measurement of carboxyhemoglobin have been>developed.
Species susceptible varies between animal groups, with some birds
more susceptible than some mammals, and vice versa.
Areas of Needed Research. 1) Studies on the effect of carbon monox-
ide on insects and animals with high respiratory rates; 2) studies
on the combined effects of carbon monoxide and other pollutants.
42
-------
Table 5.8-1 REPRESENTATIVE STUDIES ON THE EFFECTS OF CARBON MONOXIDE ON LABORATORY ANIMALS
Species
Monkeys
Dogs
Mice
Dogs
Rats
Rabbits
Dogs
Rats
CO level
55 ug/m3
(48 ppm)
58 "g/m3
(50 ppm)
58 ug/or*
(50 ppm)
58 yg/m
58 ug/m3
(50 ppra)
58 ug/m
(50 ppm)
Length of exposure
n.a.
6 wks, continuous
and intermittent
3 mo to 2 yr
6 hrs/day, 5 days/wk
for 6 wks.
24 hr/day, 7days/wk,
for 6 weeks
24 hr/day, 7 days/wk
for 3 mo.
24 hr/day, 7 Jays/wk
for 3 mo.
COHb,%
3.7 to 4.7
2.6 to 5.5
n.a.
2.6 to 5.5
Rats 1.8
Rabbits 3.2
Dogs 7.3
Effect Reference
No decrement in performance, even
at simulated altitude of 27,000 ft.
Same changes as noted with exposure
to 115 ug/m3, except EKG were not as
prominent .
No changes noted in fertility,
fetal survival, body growth, food
intake, weight and water content
of various organs, EKG, or blood
chemistries.
Brain: Mobilization of glia and
dilatation of lateral ventricles.
Necrosis and dilineation absent.
Heart: 10/15 developed EKG
changes in third week
Dogs: No changes in EKG's and
pulse rates. No histologic dif-
ference between exposed and con-
trol animals. Significant in-
creases in hemoglobin levels,
hematocrits, and RBC counts.
EKG changes in the first. 2 weeks
returning to normal in third
week. Slight increase in hemo-
globin levels, hematocrits, and
RBC counts.
HEW1
u>
-------
Table 5.8-1 (Continued)
REPRESENTATIVE STUDIES ON THE EFFECTS OF CARBON MONOXIDE ON LABORATORY
ANIMALS
Species
CO level
Length of exposure
COHb,%
Effect
Reference
JHEW]
Rats
58
(50 ppm)
1 hr
1 to 5 hr/day for
5 days
Change in EEC increasing in
severity with length of ex-
posure.
Progressive deterioration in
EEC returning to normal 48
hrs after end of exposure.
Dogs
115 pg/m
(100 ppm)
6 hr/day, 5 days/wk,
24 hr/day, 7 days/wk,
for 6 wk.
7 to 12
Brain: Mobilization of glia and
dilatation of lateral ventricles).
Necrosis and demyelination ab-
sent.
Heart: 8/8 developed abnormal
EKG's after about 2 weeks.
Autopsy: dilatation of right
heart and occasionally of left
heart; some degeneration of
heart muscle.
Dogs
115 ug/m
(100 ppm)
5-3/4 hr/day, 6 day/
wk for 11 wk.
up to 21
Brain: No changes in EEC or in
peripheral nerves. Consistent
disturbance of postural reflexes
and gait. Autopsy: 6/6 showed
some indication of cortical
damage.
Heart: 1/4 had inverted T-wave
after second week. 2/4 had in-
verted T-wave by tenth week.
Autopsy: 4/4 showed degenera-
tive changes in muscle fibers.
-------
Table 5.8-1 (Continued)
REPRESENTATIVE STUDIES ON THE EFFECTS OF CARBON MONOXIDE ON LABORATORY
ANIMALS
Species
Rats
Dogs
CO level Length of exposure
115 to Jup to 48 min.
11,500 ug/m3!
(100 to
100,000 ppm
115 ug/m
(110 ppm)
Chick-
ens
Rabbits
183 yg/m3
(115 ppra)
(2,000 ppm)
(3,600 ppm)
(600 ppm)
195 Lg/m3
(170 ppm)
i
,
i
6 wks, continuous and
intermittent
7 days
2 hrs
30 min.
?
8 weeks
COHb,%
n.a.
7 to 12
63-75
63-75
25-50
19.7 at end
of first
week
i
•
i
Effect
Impairment in time discrimin
ation.
-
EKG changes, more marked with
continuous than intermittent
exposure. Dilatation of right
cardiac chamber. Dilatation
of lateral ventricles of the
brain.
No effects chicks 1 to 42 days
old.
Death.
Death.
Distress but rapid recovery in
normal environment.
Decrease in % COHb from 19.7 to
15.1. Increase in hemoglobin
Reference
HEW1
Carson & .
Clandinin
level in first five weeks fol- :
lowed by stabilization. Ex-
posure to 400 ug/m^ (350 ppm)
caused further increase in Hb.
Rats were cholesterol fed. In-
creased total cholesterol in
aortic tissue in rabbits ex- ;
_AAA.J *• A f*r\ '
-------
Table 5.8-1 (Continued) REPRESENTATIVE STUDIES ON THE EFFECTS OF CARBON MONOXIDE ON LABORATORY
ANIMALS
Species
Dogs
Dogs
CO level
920 to
1150 g/m3
(800 to
1000 ppm)
11,452
g/m3
Length of exposure
6 to 8 hr/day, 7 days
for 36 wks
4 hrs/day for
40 days
COHb,%
Effect
Increased RBC counts, hemo-
globin, and blood volume.
Challenge with 575 g/m3
(500 ppm) in these dogs
produced the same % COHb
as in non-acclimatized
controls.
Lower resistance to strep
infection.
Reference
HEW1
Ambrosio
and Mazza
-------
REFERENCES
L. Air Quality Criteria for Carbon Monoxide. U. S. Dppt. of
Health,Education and Welfare. Washington. Publ. Number AP-62.
National Air Pollution Control Administration. Maich 1970. 138 p.
2. Garner, R. J. Veterinary Toxicology. London, Balliere, Tindall
and Cox. 1957. p 42-255.
3. Lillie, R. Air Pollutants Affecting the Performance of Domestic
Animals. United States Department of Agriculture. Washington,
D. C. Handbook Number 380. 1970. p 29-33.
4. Carson, H. C. and D. R. Clandinin. Carbon Monoxide Poisoning in
Chicks. Poultry Sci. 42:206-214. 1963.
5. Ambrosio, L. and V. Mazza. Immunological Potency in Carbon
Monoxide Intoxication. III. Behavior of the Antistreplolysentiter.
Riv. 1st. Sieroterap. Ital. 34:399-406. 1959.
47
-------
5.9 Air Pollutant: Chromium
Chromium emissions come primarily from industrial use of chromium in
mrt.-illurgical industries, in refractory materials and product use,
such as chrome plating, and tanning. Chromium as a pollutant occurs
as a number of hexavalent and trivalent compounds.*
3
Non-urban concentrations are found to average 0.002 ug/m with maxi-
mum of 0.056 pg/m reported. National urban maximum concentrations
have been found as high as 0.56 ug/m^.2 Emissions from a coal
plnnt have been found to range from 220 to 1,900 pg/m3. Air from
exhaust systems of chromium-producing plant were measured at 148,000
^.l No ambient industrial data were found.
Summary of Symptoms of Acute and Chronic Chromium Poisoning. The major
mode of chromium intoxication is through inhalation. Although informa-
tion is lacking on chromium content in plants (Sullivan op. cit.) inges-
tion of chromium dust on vegetation is possible.
The respiratory and digestive systems are the primary target areas
for chromium. Acute chromium poisoning causes congestion and inflam-
mation of lun-gs, and decreased respiratory rate. Chronic poisoning
causes bronchitis, pneumonia, congestion, inflammation and ulceration
of the stomach, and carcinogenic activity.^»^
Episodes Involving Chromium Poisoning of Free-Living Animals. No inci-
dents have been reported.
Summary of Studies on Effects of Chromium on Experimental Animals.
Rodents, cats, dogs, and monkeys have been studied (Table 5.9-1).
From these experimental studies, it appears that relatively high
levels of inhaled chromium can be tolerated. Similar results are ob-
served from exposure by ingestion. Field studies need to be under-
taken to determine if ambient concentrations occur near experimentally
determined toxic levels.
Suggested Biological Indicators of Chromium. More information is
needed concerning health effects. Probably the gastrointestinal
system would serve as a biological monitoring system.
Arc-as of Needed Research. 1) Levels and distribution of chromium
in the environment around emission sources; 2) effects of chromium
on animals, in particular birds and insects; 3) distribution of
chromium in the body.
48
-------
Table 5.9-1 REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF CHROMIUM ON ANIMALS
(ADAPTED FROM SULLIVAN1)
Species
Mice
Rabbits
Guinea
pigs
Mice
Rats
Rabbits
Cats
Material
A. Inhaled Dosages
Mixed dust containing
chromates
Mixed dust containing
chromates
Mixed dust containing
chromates
Mixed dust containing
chromates
Dichromates
Dichromate
Average
Dose
1500 ug/m3
as CrO_
3
5000 ug/m
as CrO_
3
7000 ug/m
as CrO
7000 ug/m
as CrO-
11,000-23,000
yg/ra^ as bi-"
Length of
Exposure
4 hrs/day/5
days/wk/1 yr
4 hrs/day/5
days/wk/1 yr
37 hrs over
10 days
37 hrs over
10 days
2-3 hrs for
5 days
chr ornate J
11,000-23,000 |2-3 hrs for
ug/m^ as bi-
5 days
chromate
Observed
Effect(s)
No harmful effects
No marked effects
Fatal
Barely tolerated
No effect
Bronchitis, pneumonia
Mice
Rats
Mixed dust containing
chromates
16,000-27,000
^ as CrO,
B. Ingested Dosages j
Potassium chromate
added to drinking
water
500 ppm
0.5 hr/day |
intermittently'
:Daily
Fatal to some strains
Maximum nontoxic level
-------
Table 5.9-1 (Continued) REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF CHROMIUM ON
ANIMALS (ADAPTED FROM SULLIVAN l )
Species
Rats, Mice
Young rats
Young rats
Dogs, Cats
Rabbits
Materials
Zinc chroraate in feed
Zinc chroma te in feed
Potassium chromate in
feed
, Mono- or dichro-
mates
i
j
Dogs
Dogs
Potassium dichromate
Potassium dichromate
Average
Dose
1%
0.12%
0.12%
1900-5500 ug
chromium/kg
body wt/day
(1000 ug
chromium
equivalent to
283(£ ug
1,000,000 to
2,000,000 ug
as Cr
1,000,000 to
10,000,000 ug
as Cr
Length of
Exposure
Daily
Daily
Daily
29-685 days
Daily
Daily
Observed
Effect(s)
Maximum non toxic
Maximum non toxic
Maximum nontoxic
level
level
level
No harmful effects
Fatal in 3 months
Rapidly fatal
Ln
o
-------
REFERENCES
1. Sullivan, R. J. Preliminary Air Pollution Survey of Chromium
and Its Compounds, a Literature Review. National Air Pollution
Control Administration. Publication Number APTD 69-34. October
1969. 75 p.
2. Air Quality Data for Metals, 1968 and 1969 from the National Air
Surveillance Networks and Contributing State and Local Networks.
Research Triangle Park, N.C. APTD-1467. Office of Air Quality
Planning and Standards. June 1973. var. pg.
3. Garner, R. J. Veterinary Toxicology. London, Balliere, Tindall
and Cox. 1957. p 42-255.
51
-------
5.]0 ALr Pollutant: Fluoride
Fluoride as an air pollutant occurs in numerous forms including
cryolyte, fluoroapatite, fluorosilicate, hydrogen fluoride and
aluminum fluoride. The major sources of fluoride emissions are smelt-
ing, glass making, fertilizer production, aluminum refining, and coal
combustion. Non-urban maximum concentrations are reported to be 0.16
ug/rn-^, while maximum urban concentrations have been reported as high as
1.89 ug/m^. Levels near industrial sources are much higher. In Florida
near a phosphate mining industry levels occurred as high as 200 gg/m^.
Fluoride is also concentrated in vegetation with levels as high as 500
ppra found in some areas.1
Summary of Symptoms of Acute and Chronic Fluoride Poisoning. The
primary mode of fluoride intoxication is by ingestion. The major bio-
logical target systems are the skeletal and dental systems. Acute
fluoride poisoning causes gastroenteritis, clonic convulsions, and
pulmonary congestion. Chronic exposure to fluoride leads to dental
lesions, periosteal hyperostosis, mineralization of tendons, and anemia.
The major area of accumulation for fluoride is the skeletal system.
After recent exposures high levels of fluoride can be found in the kid-
neys.1'2'3
Episodes Involving Fluoride Poisoning and Contaminations of Free-
Living Animals. Of all the air pollutants fluoride has the most re-
ported incidents of industrial contamination and the most widespread of
effects in terms of animals effected (Table 5.10-1). The bulk of the
incidents involved cattle and other domestic animals developing the
symptoms of fluoride poisoning or fluorsis. The next group of ani-
mals showing adverse effects are insects, especially silkworms and
bees. Insect pest outbreaks are associated with fluoride contamin-
ation. Elevated levels of fluoride have been found in numerous wild-
life species. In deer the symptoms of fluoride poisoning are similar
to those found in domestic animals.
Summary of Studies on the Effect of Fluoride on Experimental Animals.
Laboratory studies indicate that animals would be effected at ob-
served industrial concentrations. This is the only pollutant where
low and chronic exposure to a pollutant has been well documented and
the experimental concentration are comparable to observed
ambient concentrations. The effects observed in the field in terms
of damage to mammals are supported by laboratory observations (Table
5.10-2).
Suggested Biological Indicators. The changes in the skeletal system
including dental disfigurement are diagnostic indicators of chronic
exposure to fluoride. In particular, positive diagnosis of fluoro-
sis in cattle and other mammals can be made by tail vertebrae biopsy,
52
-------
Table 5.10-1 FLUORIDE: EPISODES INVOLVING FREE-LIVING ANIMALS
1. Known
a) Hupka and Luz, 1929 (12533) report lameness, swelling of joint,
and decreased milk production in cattle near fluoride gas
chemical plant.
b) Bardelli, 1935 (12529) reports death to silkworms then cows
near aluminum refinery in Italy, later on goats affected.5
c) Radeloff, 1939 (24024) reports death of bee population near
fluorine plant in Germany—shifting wind.6
d) Agate et al., 1949, report fluorosis in cattle and sheep near
aluminum plant in Scotland.'
e) Miller, 1952, reports infestation of Black Pine leaf scale near
manganese and aluminum refinery in Washington. Similar inci-
dences in California and Idaho.
f) Ehrlich, 1954 (12554) reports loss of weight, dental and skele-
tel abnormalities and labored breathing in cattle near aluminum
factory in Germany.9
g) Mazel, 1958 reports a decrease in insect and bird populations
in France due to fluoride.10
h) Spencer et al., 1959 (20015) report lameness in cattle in
Dallesport, Oregon, near aluminum plant.H
i) Pfeffer, 1962-63 (41482) reports infestation of fir bark lice,
wood wasp and bark beetles near aluminum plant in Czechoslo-
i fr
vakia. if-
j) Narozeny, 1963 (12538) reports cattle developed dental abnorm-
alities and shortened lifespan near Czechoslovakian aluminum
plant.13
k) Wentzel, 1965 (46733) found infestation of spruce gall lice
and bark beetles with fluoride-damaged trees near brick kiln
factory in Germany.1^1
1) Hasegawa and Yoshikawa, 1969 (20707) report death of 70 oxen
near chemical fertilizer plant in Osaka, Japan.15
m) Hasumi, 1969 (48377) reports damage to silkworms of farmer in
Japan near glass fiber manufacturing plant.16
n) Lezovir, 1969 (13203) reports fluorosis in goats and cattle
near aluminum factory in France.17
o) Bourbon et al., 1971 (29991) report fluorosis in cattle near
phosphoric acid plant in France.18
p) Karstad, 1970, reports fluorosis in White-tailed dear near
aluminum plant in Ontario, Canada.19
q) Daessler, 1971 (41439) reports dental fluorosis and decreased
milk production in cattle and reduction of bee population
living near HF plant.20
r) Dewey, 1973 (53025) reports high levels of fluoride in all
insect trophic levels near aluminum reduction plant in
Montana.21
53
-------
Table 5.10-1 (Continued) FLUORIDE: EPISODES INVOLVING FREE-LIVING
ANIMALS
s) Yamazoe, 1973 (48639) reports ill silkworm and cattle fluorosis
in Japan.22
t) Newman and Yu, 1974, report fluorosis in Black-tailed deer
living near aluminum plant in Washington.
u) Babazova and Hbachen, 1968 (25665) report high concentration
of fluoride in house sparrows with cattle showing fluorosis near
aluminum plant in Czechoslovakia.2^
2. Possible or Mixed Effects
a) Berge, 1973, reports heavy infestation of lice, mealy bugs on
F- and S0~-damaged trees, also on trees in area with high con-
centration but no damage.25
) = APTIC No.
-------
Table 5.10-2
REPRESENTATIVE STUDIES ON THE EFFECTS OF FLUORIDE ON EXPERIMENTAL AND LABORATORY
ANIMALS
Species
Sheep
Horse
Cattle
Horse
Dog
Goat
Mouse
Swine
Rabbi tt
Rat
Guinea pig
Apis mellifero
Melanophus bi-
vattus
Bombyx mori,
4th in-star
Cattle
Cattle
Horse
Cattle
Cattle
Swine
Compound
NaF
p
ppm
7 to 9.5
1
mg/K
1.8 to 2.35
13.8 to 41.4
37.5
46 to 55
50 to 100
73.7
80
153
200 to 500
200
250
6.0 ug/bee
40 yg/g
110 to 150 ug/8
4.12
5.27
7.29-10.3
12.3
23.6
;
1
Exposure
Acute
Acute
Acute
Acute
Acute
Acute
Acute
Acute
Acute
Acute
Acute
3 days
3 days
3 days
Diet several
months
In H20, 28
days
In feed, 12
days
In feed, 15
days
In feed, 27
days
In feed. 75
days
Effect
No effect
No effect
No effect
Acute fluorosis
MLD
Acute fluorosis
LD
Acute fluorosis
MLD
LD 50
MLD
LD 50
LD 50
LD 50
Marginally
acute signs
Marinally
acute signs
Marginally
acute signs
Acute fluorosis
No effect
Reference
Cass26
27
Negherbon
26
Cass
26
Cass
!
en
-------
Table 5.10-2 (Continued) REPRESENTATIVE STUDIES ON THE EFFECTS OF FLUORIDE ON EXPERIMENTAL AND
LABORATORY ANIMALS
01
; i
Species • Compound ppra mg/K •_
Swine : NaF (cont)
Japanese Quail !
•
Exposure • Effect Reference
7 to 9.5 'In feed 75 days
300
t NaSiF
Cattle
!
Cattle
Goat
Swine
Cattle
Cattle
Cattle
Cattle
Bombyx mori
Melanoplus femur-
rubrum
3Na.F-AlF,
2 3
;
I
I
1,200 to '
1,800
1,820 to
3,640
69
120 to 668
25.3
52.2
46.4
94.4
In drinking
water
Acute signs
28
High mortality iVohva
1 loss of body
! weight
7ft
Acute
Acute
Slight effects Cass
Acute fluorosisi
i
Acute . Acute fluorosis:
Acute Acute fluorosid
I
26
28 days j No effect Cass
Daily in H.O,
No effects
15 days
Daily in HO,
16 days
Daily in H20,
Acute effects ,
i
Acute signs i
27 days i 77
.05 to .07, 3 days i LD 50 Negherbon"'
i ' -12
i
|3 days ' LD 50 I
! i
-------
urinnlvsLs, radiology, alkaline phosphatase levels, accumulation or
presence of fluoride in Che bone, urine, and feed. Sensitivity to
fluoride intoxication varies. In general, sensitivities decrease
from bees to cattle, sheep, horses, swine, rabbits, and poultry.
Since fluoride was once considered as an insecticide the sensitivity
of other insects needs to be investigated. Trophic transmission of
fluoride is known but general ecosystem effects are not known.
Areas of Needed Research. 1) Effects of fluoride on birds and other
wildlife; 2) effects of fluoride on insects and pest insect behavior;
3) studies on the effects of fluoride on the ecosystem.
REFERENCES
1. Biological Effects of Atmospheric Pollutants. Fluoride. Washing-
ton, D.C. National Academy of Science. National Research Council.
1971. 306 p.
2. Garner, R. J. Veterinary Toxicology. London, Ballier, Tindall
and Cox. 1957. P 42-255.
3. Lillie, R. Air Pollutants Affecting the Performance of Domestic
Animals. United States Department of Agriculture. Washington, D.C.
Handbook Number 580. 1970. p 41-61.
4. Hupka, E. and P. Lug. Frequent Occurrence of Osteomalacia Among
Grazing Cattle Caused by Hydrofluoric Acid Contained in the Flue
Gas Discharged by a Chemical Plant. Arc Wissenschaft-Liche
Praktisch Tierheilkunde (Berlin). 60:21-39, 1929.
5. Bardelli, P. and C. Menzani. Studies of Spontaneous Fluorosis in
Ruminants: A Note on Prophylaxis. Annali D'Igiene, 45(6):399-
404, 1935.
6. Radeloff, H. Investigation and Appraisal of Flue-Gas Damage
[In German]. Hamburg Staatsinst. Angew. Botanik Jahresber.,
6:126-127, 1939.
7. Agate, J. N. et al. Industrial Fluorosis, A Study of the Hazard
to Man and Animals Near Fort William, Scotland; a Report to the
Fluorosis Committee. Medical Research Council. London. Memor-
andum Number 22. Her Majesties Stationary Office. 1949. 131 p.
8. Miller, V. L. The Effect of Atmospheric Fluoride on Washington
Agriculture. In: Air Pollution: Proceedings of the U. S.
Technical Conference on Air Pollution. New York. McGraw-Hill
Book Company, Inc., 1952. p. 116-122.
57
-------
9. KhrlLch, C. Observations and Investigation of Chronic Fluoride
Poisoning in Cattle. Deut Tier aerz H. (Wochschr). 61:225-228,
June 1954.
10. Mazel, A. Fluoraroses Industrielles Imprimerie Ouvriere.
(Toulouse) 1958, p. 141, 1958.
11. Spencer, G. R., E. C. Stone and D. F. Adams. Florides in Animals
in the Dallesport Area. Washington State University Agricultural
Experiment Station. Pullman, Washington. State circular number
353. 1959. 8 p.
12. Pfeffer, A. Insect pests on Firs in Air Pollution Areas. Z. Angew
Entomol. 51:203-207. 1962/1963.
13. Narozny, J. 1965. Dental Fluorosis of Cattle. Veterinarni
Medicina. (Prague) 7:421-424.
14. Wentzel, Karl F. Insects as Emission-Related Pests. Naturwissen-
schaffen (Berlin). 52(5):113, 1965.
15. Hasegawa, T., and H. Yoshikawa. On the Atmospheric Fluoride
Pollution. Part 1. J Japan Soc Air Pollution 4(1):147. 1969.
16. Hasurai, K. Modernization of Hygenic Laboratory. Z. Hydrogen
Fluoride Pollution. Fukushima-ken Eiser ken kyusho kenkyu Hokoku
17(3):27-30. 1969.
17. Lezovic, J. The Influence of Fluorine Compounds on the Biological
Life Near an Aluminum Factory. Fluoride Quarterly, J Intern Soc
Fluoride Res. 2(1):25-27. January 1969.
18. Bourbon, P., J. Tournut, J. Alary, J. F. Rouzaad, and F. Alengrin.
Consequences of Small Fluoride Pollution in a Mountain Valley.
Tribune Lebedeau (Cent Belg Etud Doc Eaux Air) 24(327):62-66,
Feb. 1971.
19. Karstad, L. H. A. Wildlife in Changing Environments. In:
Environmental Change, Focus on Ontario. Elrich, D. E. (ed.).
New York. Simon and Schuster, Inc., 1970.
20. Daessler. H. G. The Effect of Hydrogen Fluoride and Cryolite
Dust upon Plants and Animals Near a Hydrogen Fluoride Factory.
Fluoride. 4(l):21-24, January 1971.
21. Dewey, J. E. Accumulation of Fluorides by Insects Near an Emis-
sion Source in Western Montana. Environ. Entomol. 2(2):179-182,
April 1973.
58
-------
22. Yamazoc, F. The Effect of Air Pollution on Agriculture and
Forestry. Nogyo Oyobi Engei. 48(1):133-138, 1973.
23. Newman, J. R. and M. Yu. Fluorosis in Black-tailed Deer
(Odocoileus hemionus). Submitted to J. Wild.Dis., Feb, 1974.
24. Balazova, G. and E. Hluchan. The Effect of Floridine Exhalation
on Animals in the Surroundings of an Aluminum Plant. In: Air
Pollution Proceedings, First European Congress (on the) Influence
of Air Pollution on Plants and Animals, Wageningen. 1968.
p. 275-279.
25. Berge, H. Relationship between Tree Pests and Iranissions.
Anz Schaedlingskunde 46:155-156, 1973.
26. Cass, J. S. Fluorides, A Critical Review. W. Response of
Livestock and Poultry to Absorption of Inorganic Fluorides.
J Occup Med 3:471-477, 1961.
27. Negherbon, W. 0. Handbook of Toxicology, Volume III: Insecticides.
Philadelphia, W. B. Saunders Co. 1959. 829 p.
28. Vohra, P. Fluoride Tolerance of Japanese Quail. Poul Sci. 52:
391-3, January 1973.
59
-------
5.11 Air_ Pollutant: Hydrocarbons
Hydrocnrbons nro compounds consisting of atoms of hydrogen and carbon
only. Hydrocarbons as pollutants result from the inefficient combus-
tion of fuels such as volatile fuels (e.g., gasoline) and from the use
of process raw materials like solvents. There are three major classes
of hydrocarbons: aliphatic, alicyclic, and aromatic hydrocarbons.
Photochemical reactions can occur with these hydrocarbons, resulting in
the production of hydrocarbon derivatives known as aldehydes.
Most hydrocarbon emissions come from transportation and industrial
processes. Non-urban values range from 1.0 to 1.5 ppm (0.7 to 1.0
Ug/m-*) . Yearly averages of monthly maximum total hydrocarbon concen-
trations have ranged from 8 to 17 ppm from 1962 to 1967.*
Summary of Symptoms of Acute and Chronic Hydrocarbon Poisoning. The
mode of intoxication of hydrocarbons is through inhalation, with the
primary target systems being the mucous membranes of the eyes, upper
respiratory tract, and skin. Aliphatic and alicyclic hydrocarbons pro-
duce no effects below 500 ppra.l Acute exposure to aromatic hydro-
carbons can cause anemia and leukopenia besides irritation of mucous
membranes. Symptoms of acute aldehyde poisoning include eye irritation,
dermatitis, irritation of the respiratory tract, edematous and
hemoragic lung. No site of accumulation is known.!*2
Episodes Involving Hydrocarbon Poisoning of Free-Living Animals. None
have been reported.
Summary of Studies on the Effect of Hydrocarbon on Experimental
Animals. Few experimental studies have been conducted at low and
chronic concentrations of hydrocarbons (Tables 5.11-1,2). Based upon
ambient concentrations, the most pronounced effect is from aldehydes.
At concentrations below 20 ppm changes in cellular enzymes and
respiratory and eye irritation occur. Acrolein at low concentrations
(less than 1 ppm) appears to be extremely toxic for rats.
Suggested Biological Indicators for Hydrocarbons. Further studies
need to be made on the effects of hydrocarbons, especially for pro-
longed exposure. The skin and eyes of sensitive species may be
suitable biological monitoring systems.
Areas of Needed Research. 1) Effect of low and chronic exposures
of aromatic hydrocarbons and aldehydes on animals, especially those
with high respiratory rates and highly developed visual and olfactory
systems; 2) monitoring free-living animals for symptoms of exposure
to hydrocarbons.
60
-------
Table 5.11-1
COMPARATIVE EFFECTS OF ACUTE AND CHRONIC
VAPORS IN AIR (\DAPTED FROM HEW 1) .
EXPOSURE TO AROMATIC HYDROCARBON
Species
Mice
Mice
Mice
Mice
Rats
Mice
Mice
Mice
Rats
Guinea pig
Rats
Rabbit
Guinea pig
Guinea pig
Compound
Benzene
Toluene
Styrene
and Rat ,
Guinea pig
and Rat
Guinea pig
and Rat
Cone.
ppm
370
4700
7400
14,100
17,800
2700
6700
9500
13,500
650
1300
1300
1300
2500
5000
Cone.
Ug/m3
1180
47,993
23,696
44,979
56,782
10,166
25,226
35,768
50,828
2714
5428
5428
Length of
Exposure
Acute
Acute
Acute
Acute
Acute
Acute
Acute
Acute
Acute
8 hr/day
180 days
8 hr/day
180 days
8 hr/day
I 180 days
5428 ! 8 hr/day
180 days
10,438 ; 8 hr/day
. 1 day
,•
i
20,875 | 1 hour
1
10,000 41,750 ! 0.5-1 hour
'
! i
Observed Effect(s)
Threshold for affecting the central
nervous system.
Prostration
LC50
LC100
LC100
Prostration
LC50
LC100
T r
L 100
No effect
Eye and nasal irritation only
Eye and nasal irritation only
10% deaths
Some fatalities; varying degree of
weakness, stupor, incoordination,
tremor, unconsciousness (in 10 hrs) .
Unconsciouness in one hour.
Unconsciousness in 10 minutes; death
in 30-60 minutes
ey>
-------
Table 5.11-1 (Continued) COMPARATIVE EFFECTS OF ACUTE AND CHRONIC EXPOSURE TO AROMATIC
HYDROCARBON VAPORS IN AIR (ADAPTED FROM HEW1)
Species
Mice
Rat and
Rabbit
Rabbit
Mice
Mice
Mice
Rats
Compound
Xylene
Cone.
ppm
174
690
1150
4699
9200
12,650
17,250
Cone.
ug/rn3
755
2955
4991
20,394
39,928
54,901
74,865
Length of
Exposure
Acute
8 hr/day
130 days
8 hr/day
55 days
Acute
Acute
Acute
Acute
Observed Effect(s)
Threshold for affecting central
nervous system.
No hematological effects
Decreased leukocytes and red blood
blood cells; increased platelets
Prostration
LC50
LC100
LC100
IS)
-------
Table 5.11-2 REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF ALDEHYDES ON ANIMALS
Species
Guinea
pigs
Rats
Rats
Rats
Rats
Rats
Rabbits,
Mice,
Guinea
pigs
Rats
Rats
Rats
Rabbits
„ , 'Cone.
Compound i
r i pom
i
Formaldehyde" 0.3-
J50.0
3
0.5
0.1-
0.83
0.67
3.5
il9.0
l
\
80.0
1
i
I
Acrolein 0.5
i 0.57
i
i i
i '
0.57
i
i '
Conc3
ug/m
0.37-
61.0
3690
615
1125-
1020
815
4300
23,400
98,400
i
i
130
1520
1520
Length of
Exposure
1 hour
50 sec.
150 sec.
Continuous
0.5 hour
18 hours
10 hours
31 rain.
0.5 hour
24 days
L
t
24 days
Observed Effect(s)
Increase in resistance and de-
crease in compliance in lungs
Causes cessation of ciliary beat
in respiratory tract
Same as above
In pregnant rat, prolonged preg-
nancy 14-15% and reduced number
of fetuses; increase in organ
weights
LC
Decreased liver alkaline phos-
phates
Hemorrhages and edema in lungs;
hyperemia and pervascular edema
Death of some. Edematous and
hemorrhagic lungs, fluid in
pleural and peritoneal cavities,
pneumonic consolidation, dis-
tended alveoli and ruptured alve-
olar septa
LCcn
Til
Loss of weight, change in condi-
tioned reflex activity, decrease
in cholinesterase
No effect
i
Reference(s)
Amdur
4
Dalhamn
4
Dalhamn s
Gofmekler
6
Fasset
Murphy, 7
et.al^. ,
Salem ~&.Cal-
. • • O
lumbine
Skog
;
Fasset
Guse^, et.
al.
Gusev, et.
al.10—
OJ
-------
Table 5.11-2 (Continued) REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF ALDEHYDES
ON ANIMALS
Species
Rabbits
Mice and
Guinea
pigs
Compound
Acrolein
(Cont.)
Cone.
ppra
1.9-
2.6
10.5
ConCx
Ug/m
5110-
6995
28,245
Length of
Exposure
4 hours
6 hours
Observed Effect(s)
Enzyme alteration of eye
tissue
LC50
Reference(s)
Mettier, et.
al . 11 ~~
Pattle. et.
al." ~
-------
REFERENCES
1. Air Quality Criteria for Hydrocarbons. National Air Pollutions
Control Administration. Publication Number AP-64. March 1970.
p.
2. Lillie, R. J. Air Pollutants Affecting the Performance of
Domestic Animals: A Literature Review. United States Department
of Agriculture. Washington, D.C. Agriculture Handbook Number
380. 1970. p 62-65.
3. Amdur, M. 0. The Response of Guinea Pigs to Inhalation of Formal-
dehyde and Formic Acid Alone and with a Sodium Chloride Aerosol.
Internatl. J Air Pollut. 3(4) :201-220. 1960.
4. Dalhamn, T. Mucous Flow and Ciliary Activity in Trachea of
Healthy Rats and Rats Exposed to Respiratory Irritant Gases
(SO , H N, HCHO). Acta Physiol Scand (Stockholm). Suppl. 123.
36:1-161. 1956.
5. Gofmekler, V. A. Effect of Embryonic Development of Benzene and
Formaldehyde in Inhalation Experiments [Embriotropnoe deistvie
benzola i f ormaldegiela pri ingalyalsionnom puti vozdeistviya v
eksperimente] . Hyg. Sanit. 33:327-332, January-March 1968.
6. Fasset, D. W. Aldehydes and Acetals. In: Industrial Hygiene
and Toxicology, Patty, F. A. (ed.), Vol. II. New York,
Interscience Publishers, Inc. 1963.
7. Murphy, S. D.t et^ aj^ Altered Function in Animals Inhaling Low
Concentrations of Ozone and Nitrogen Dioxide. Amcr Ind Hyg Ass J
25:46-253, 1964.
8. Salem, H. and H. Cullumbine. Kerosene Smoke and Atmospheric
Pollutants. Arch Envir Health 2:641-647, 1961.
9. Skog, E. A. Toxicology Investigation of Lower Alephatic Alde-
hydes. I. Toxicity of Formaldehyde Acetaldehyde, Propionalde-
hyde, and Butyraldehyde; as well as of Acrolein and Crontonalde-
hyde. Acta Pharmacol. Toxicol. (Copenhagen) 6(4) :299-318, 1970.
10. Gusev, M. I. et_ al. Determination of the Daily Average Maximum
Permissible Concentration of Acrolein in the Atmosphere. Hyg.
Sanit. 31:8-13, January-March 1966.
11. Mettier, S. R. , e£ al. A Study of the Effects of Air Pollutants
on the Eye. Arch. Ind. Health. 21:1-6, January 3960.
65
-------
12. Pattle, R. E. and H. Cullumbine. Toxicity of Some Atmospheric
Pollutants. Brit. Med. J. 2(4998):913-916, October 20, 1956.
66
-------
5-12 Air Pjailut.nnj^:_ Hydrochloric Acid
Hydrochloric acid can be emitted from numerous industrial activities
such as the burning of coal, chlorinated plastics, paper, and hydro-
chloric manufacturing. No information is available on urban concen-
trations. Emissions recorded near a glass manufacturing factory after
plant death wasnnoticed ranged from 119 to 273 ppm HC1 (178,500 to
709,500
Summary of the Symptoms of Acute and Chronic Poisoning by Hydrogen
Chloride. The primary mode of intoxication is by inhalation. The
major biological target area for hydrochloric acid is the respiratory
system. Acute poisoning causes pulmonary and nasal damage, including
pulmonary edema, emphysema, necrosis of tracheal and bronchial epithe-
lium. Chronic exposures cause weight loss and irritation of eyes and
nose.1
Episodes Involving Hydrochloric Acid Poisoning of Free-Living Animals.
None reported.
Summary of Studies on the Effects of Hydrochloric Acid on ExperimentaJ_
Animals. Representative laboratory studies indicate relatively high
concentrations are harmful to mammals. Chronic exposures of less than
100 ppm cause eye and nose irritation. No studies were
found on the effects of HC1 on birds (Table 5.12-1).
Suggested Biological Indicator of Hydrochloric Acid. Not enough
field and laboratory studies are available to suggest biological indi-
cators. The irritant effect of HC1 on the eyes of mammals suggest
that birds with highly developed visual systems should be studied for
sensitivity.
Areas of Needed Research. 1) Effect of HC1 on animals with high
respiratory rates and sensitive visual systems, i.e., birds; 2)
studies on the effect of HC1 on insects; 3) studies of industrial
concentration of HC1.
REFERENCES
1. Stahl, Q. R. Preliminary Survey of Hydrochloric Acid, a Litera-
ture Review. National Air Pollution Control Administration.
Publication Number APTD 69-36. October 1969. 69 p.
67
-------
Table 5.12-1 SUMMARY OF REPORTED EFFECTS OF INHALATION OF HYDROGEN
CHLORIDE ON ANIMALS (ADAPTED FROM STAHL1)
Species
Rabbles
Rabbits
Guinea pig
Rabbit
Monkey
Pigeons
Guinea pigs
Rabbits
Guinea pigs
Rabbits
Guinea pigs
Rabbits
Guinea pigs
Rabbits
Guinea pigs
Rabbits
Cats
Guinea pigs
Rabbits
Concentra-
tion (ppm)*
30
60
33
33
33
100
100
100
100-140
100-140
300
300
670
670
1,350
1,350
1,350
3,400
3,400
Exposure
time
10 min
5 min
6 hr/day
5 days/week
for 4 weeks
6 hr/day
5 days /week
for 4 weeks
6 hr/day
5 days/week
for 4 weeks
6 hr/day
for 50 days
6 hr/day
for 50 days
6 hr/day
for 50 days
6 hr
6 hr
6 hr
6 hr
2 hr
2 hr
90 min
90 min
90 min
90 min
90 min
Effects or Comments
Cessation of ciliary activity
without recovery
Cessation of ciliary activity
without recovery
No immediate toxic effects and
no pathological changes
No immediate toxic effects and
no pathological changes
No immediate toxic effects and
no pathological changes
Slight unrest and irritation of
the eyes and nose
Slight unrest and irritation of
the eyes and nose
Slight unrest ard irritation of
the jyes and nose
Only slight corrosion of the
cornea and upper respiratory
irritation
Only slight corrosion of the
cornea and upper respiratory
irritation
Corrosion of the cornea and up-
per respiratory irritation
Corrosion of the cornea and up-
per respiratory irritation
Fatal in some cases
Fatal in some cases
Severe irritation, dyspnea,
and clouding of the cornea
Severe irritation, dyspnea
and clouding of the cornea
Severe irritation, dyspnea,
and clouding of the cornea
Death after 2 to 6 days
Death after 2 to 6 days
*1 ppm = 1,470 ug/m at 25° C.
68
-------
Table 5.12-1 (Continued) SUMMARY OF REPORTED EFFECTS OF INHALATION
OF HYDROGEN CHLORIDE ON ANIMALS (ADAPTED FROM STAHL*)
Species
Cats
Guinea pigs
Rabbits
Concentra-
tion (ppm)*
3,400
4,300
4,300
Exposure
time
90 min
30 tnin
30 min
Effects or Comments
Death after 2 to 6 days
Fatal in some cases, due to
laryngeal spasm, laryngeal
edema, or rapidly developing
jpulmonary edema
Fatal in some cases, due to
laryngeal spasm, laryngeal
edema, or rapidly developing
pulmonary edema
69
-------
5-13 Ajjr J^pH».ta.n tj Hydrogen SuJ fide
llydrn};on su 11" ide ;is a tochnologic.il pollutant can he- omitted from
krnft paper mills, industrial waste disposal ponds, sewage plants,
refineries, and coke oven plants. Natural levels are reported to
range from 0.15 to 0.46 ug/m . Average urban concentrations have
ranged from 1 to 3 ug/m3 with a maximum of 1400 vig/m3 reported. Indus-
trial sources show a wide spectrum of levels: Russian petrochemical
plant ranged from 8 to 70 ug/mj 2.5 km away to 1 to 50 ug/m3 20 km
away; Idaho kraft mill reported a two hour maximum concentration of
77 ug/m3; hourly averages ranged from 140 to 600 ug/m3 found near
burning coal piles; Indian industrial lagoon had over 460 ug/m3;
and 600 to 1600 ug/m3 near a Russian electrical power and chemical
complex.
Summary of Symptoms of Acute and Chronic Poisoning by Hydrogen
Sulfide. The primary mode of intoxication is through inhalation. The
major biological target areas are the central nervous system, respira-
tory tract and gastrointestinal system. The characteristic response
of acute poisoning is loss of muscular coordination, distended abdo-
mens, congested liver, and lung hemorrhages. Chronic symptoms include
morphological changes in brain cortex, irritation of intestinal ,
mucosa. The presence of suIfhemoglobin is a diagnostic indicator. '
Episodes Involving Hydrogen Sulfide Poisoning of Free-Living Animals.
Two episodes are ported of hydrogen sulfide effects. The first report
involved the death of all canaries and 50 percent of other plants in Posa,
Mexico from the emissions of a sulfur recovery pi ant.The second inci-
dent is less specific but involved birds and other animals which were
found dead in the vicinity of an oil field with extremely high levels
of hydrogen sulfide. A possible incident of hydrogen sulfide poison-
ing involves the death of up to 500 passerine birds in the vicinity of
a Canadian pulp mill which emitted high levels of sulfurous compounds.
1'rom these incidents it appears that birds are sensitive to hydrogen
sulfide.
Summary of Studies on the Effects of Hydrogen Sulfide on Experimental
Animals. Studies involving acute exposures on mammals reveal extreme-
ly high levels of hydrogen sulfide are needed before harmful effects
are detected in mammals (Table 5.13-2). Chronic studios are not as
extensive but tolerance for hydrogen sulfide in rodents appears high.
No studies regarding the experimentally-induced effects of hydrogen
sulfide on birds were found although field data suggest avian sensi-
tivity.
Suggested Biological Indicators of Hydrogen Sulfide. The blood, in
particular the presence of sulfhemoglobin, may be an indicative
response of hydrogen sulfide exposure. Small birds also appear to
be potential sensitive biological indicators. Confirming studies
need to be conducted.
70
-------
Table 5.13-1 HYDROGEN SULFIDE: EPISODES INVOLVING FREE-LIVING
ANIMALS
1. Known
a. Yant and Sayers, 1927. Reported death of unspecified birds
and animals near oil tank and.wells in Texas. Levels be-
tween 111,247 to 139,059 ug/in .4
b. McCabe and Clay, 1952. Reported death of all canaries and 50%
of all other animals in Poza Rico, Mexico in 1950. Source
sulfur recovery plant. Other animals affected—chickens,
cattle, pigs, geese, dogs and cats.^
2. Possible of Mixed Effects
a. Harris, personal communication. Reported death of between
200 to 500 passerine birds near pulp mill in Canada. Birds
showed inflammation of intestinal tract and hemorrhages in
the brain and trachea. High levels of sulfur compounds (HjS)
along with a fog occurred at the same time.
Areas of Needed Research. 1) Effect of low and chronic exposures of
hydrogen sulfide on birds and other animals; 2) development of diag-
nostic measures for hydrogen sulfide.
REFERENCES
1. Miner, S. Preliminary Air Pollution Survey of Hydrogen Sulfide,
a Literature Review. National Air Pollution Control Administra-
tion. Publication Number APTD 69-37. October 1969. 91 p.
2. Garner, R. J. Veterinary Toxicology. London, Balliere, Tindall
and Cox. 1957, p. 42-255.
3. Li Hie, R. J. Air Pollutants Affecting the Performance of Domes-
tic Animals: a Literature Review. United States Department of
Agriculture. Washington, D. C. Agriculture Handbook Number 380.
1970. p 66-68.
4. Yant, W. P. and R. R. Sayers. Hydrogen Sulfide as a Laboratory
and Industrial Poison. J Chem. Ed. 4:613-619, 1927.
5. McCabe, L. C. and G. D. Clayton. Air Pollution by Hydrogen
Sulfide in Poza Rica, Mexico. Arch. Indus. Hyg. Occup. Med. 6:
199-213, 1952.
71
-------
d. Harris, R. I). Ri rds Cnllocti>il (Hit— Off) at Prinro Rupert,
B.C., Sc'-ptumber L971. Cnnadian Wildlife ServLc-c. unpublished
report. 1 October 1971. 6 p.
72
-------
Table 5.13-2 STUDIES ON THE EFFECT OF HYDROGEN SULFIDE ON ANIMALS.
Species
Mice
Rabbit
Flies
Rats
Mice
Mice
Rats
Flies
Flies
Rats
Mice
Rats
Rats
Rats
Concei
ppm
ACUTE
CHRONI
itration
yg/m
.024xl06
.07xl06
.096x10
.096x106
.096xl06
.38xl06
. 38xl06
. 38xl06
1.5xl06
1.5x10
l.SxlO6
C
;8
20
1000
Exposure
16 hrs
16 hrs
03
16 hrs
23 hrs
6.8 hrs
16 hrs
716 hrs
7 min
14 min
18 min
24 hrs/day/70 days
12 hrs/day/3 mos
12 hrs/day/3 mos
•
Effects
No effect
No effect
No effect
Toxic
LC50
LD50
LD50
LD50
LD50
LD50
LD50
No effect
Slight changes in CNS
Changes in CNS, irritated
tracheal mucosa
Reference
Miner _
Lillie
^
Miner1
3
Lillie, 1970
-------
5.14 Air Pollutant: Iron
Iron as an air pollutant is emitted in many forms, especially as oxides.
The major techno Logical source of i ron is the iron and steel production
and secondarily from fossil fuel combustion. Non-urban concentrations
in 1968 ranged from 0.0 to 3.7 pg/m3.1 National urban concentrations
averaged 1.58 pg/m3 with a maximum of 22.0 pg/m3 reported. Particulate
concentrations in the vicinity of such industrial operations can become
quite high with values of 477,000 pg/m3 reported. The iron content of
particulates was not given. Tn other studies ambient concentrations of
iron near industries are reported up to 30.8 pg/m3.2
Summary of Sumptoms of Acute and Chronic Iron Poisoning. Little in-
formation is available on the toxicity of iron. The major routes of
intoxication is by inhalation or ingestion of vegetation with iron
particulate deposits. The primary target system is the respiratory
system. Intoxication results in a form of mild pneumonia, siderosis.
There is some evidence to indicate iron oxide might be carcinogenic.
Iron compounds might act synergistically with certain gases or aid in
their toxic action.^
Episodes Involving Iron Poisoning of Free-Living Animals. None re-
ported.
Summary of Studies on the Effects of Iron on Experimental Animals.
Experimental studies indicate iron oxide is not toxic at ambient
concentrations. It may be carcinogenic at high dosages especially
acting synergistically with other compounds like benzo(a)pyrene. It
does act as an inert particulate in its ability to absorb toxic
compounds like sulfur dioxide. Iron is an essential nutrient im-
portant in blood physiology and metabolism. Excess iron is stored
in the kidney and spleen.
Suggested Biological Indicators of Iron. Not enough information
available for conclusions.
Areas of Needed Research. 1) Studies on the effects of iron on
animals with high respiratory rates; 2) studies on ambient concentra-
t ions.
REFERENCES
1. Air Quality Data for Metals, 1968 and 1969 from the National Air
Surveillance Networks and Contributing State and Social Networks.
Research Triangle Park, N.C. APTD-1467. Office of Air Quality
Planning and Standards. June 1973. var. pg.
2. Sullivan, R. J. Preliminary Air Pollution Survey of Iron and
Its Compounds. Environmental Protection Agency, Raleigh, N.C.
Publication Number APTD 69-48. October 1969. 94 p.
74
-------
5.15 Air Pollutant: Lead
Lead as a pollutant occurs in many forms including halides, sulfides
and oxides. The major sources of lead emissions are from transporta-
tion, smelting and refining of heavy metals and fossil fuel combustion.
Average background levels of lead have been reported as high as 0.0005
ug/m^ in air and 10 to 15 ppm in airborne dust. Elevated levels of
lead are found in cities. Cities near heavily travelled freeways have
had concentrations that ranged from 1 to 3 pg/m3 with a maximum reported
as high as 54.3 ug/m3.1 Levels of lead in soils in cities have been
measured up to 3,357 gg/m3.1- In soils near smelters, concentrations as
high as 6800 ppm have been measured. Concentrations of lead fend other
pollutants) involving vegetation can be considered in two ways: the
amount in a plant tissue, and the amount on the surface of plants. Con-
centrations of lead in grass along freeways measured up to 225 pg/kg
dry weight, in pasture grass near smelter operations from 1.4 to 100
ppm wet weight. The concentrations of lead (and other particulates)
on the surface of plants ranged from 200 to 3500 ppm on leaves near
smelters in England.
Summary of Symptoms of Acute and Chronic Lead Poisoning. The primary
mode of lead intoxication is through ingestion of contaminated food,
either plant or animal. Inhalation is a secondary source of intoxica-
tion. The main biological target systems of poisoning are the gastro-
intestinal system and central nervous system. The most indicative
responses of acute lead poisoning in domestic animals are locomotor
impairment, convulsions, blindness, listlessness, constipation and
diarrhea of a distinctive color. Chronic poisonings result in weight
loss, partial paralysis, and anemia. »* Lead found in high levels in
blood, liver and kidneys is indicative of lead poisoning (Table 5.15-
2). The presence of basophilic stippling of red blood cells and
acid fast inclusion bodies in the kidneys are other diagnostic
characteristics.
Episodes Involving Lead Poisoning of Free-Living Animals. Numerous
episodes (Table 5.15-1) are reported on the effects of lead on free-
living animals. Most of these have been concerned with cattle near
smelters exhibiting typical symptoms of lead poisoning. A couple of
incidents have reported effects on sheep, horses, and bees. Two
incidents were reported involving zoo animals. At the Staten Island
Zoo, lead poisoning was more common in animals living out of doors.
Pinnipeds kept in an aquarium at the Detroit Zoo near a freeway
showed a higher incidence of lead poisoning than similar animals
kept at other locations.
Summary of Studies on the Effects of Ingested Lead on Experimental
Animals. Numerous lead compounds have been used in laboratory experi-
ments (Table 5.15-2). For short exposures,high dosages are required
75
-------
Table 5.15-1 LEAD: EPTSODES INVOLVING FREE-LIVING ANIMALS
1. Known
a. Having & Meyer, 1915 (40591). Roaring and paralysis of larynx,
aspiration, pneumonia in horses, from Benecia, Calif, smelter. 3
b. Pavlicevic, 1962 (57066). Young sheep developed paralysis of
extremities, craw, tongue, larynx, and neck; anemia, changes
in digestive organs, in Czechoslovakia. ^
c. Hammond & Aronson, 1964 (27118). Horses were more affected
than cattle by lead from Minnesota smelter. 10
d. losif, 1966 (10318). Cachexia, decreased milk production,
enteritis with constipation, diarrhea, colic and muscular
twitches in cattle from Rumania. H
e. Egan & O'Cuill, 1969 (2738). Death of cattle and sheep, includ-
ing newborn, in Ireland near lead mine. 12
f. Bazell, 1971 (30931). Lead poisoning in animals kept out of
doors compared to inside species in S tat en Island Zoo. 13
g. Kerin & Kerin, 1971 (31185). Lead found in miLk; also a de-
creased honey production near smelter. 1^
h. Ottoboni and Kahn, 1970 (18520). Twelve out of 30 horses died
in pasture near refinery; high level of lead found. 15
i. Schmitt, e_t al. , 1971 (32736). Six horses chronically ill.
Lead along with other metals found in forage. 1°
2. Possible or Mixed Pollutants
a. Shrenk, et al. , 1949. Sick and dying dogs and cats along
with poultry and rabbits in Donora, Penn. High levels of
SO , NO , and lead in smog.l7
( ) = APTIC No.
to be harmful. If the reported ranges of lead deposits on plants and
accumulation of lead in plants are representative, these levels
would be toxic to the rodents, rabbits and cattle only through con-
tinuous exposure. Relative sensitivities of species to lead are hard
to determine from experimental data. 5 Field studies suggest that
horses are more sensitive than cattle, and cattle more sensitive than
sheep. Swine and goats are relatively resistant.
Biological Indicators of Lead. High levels of lead in the
blood, kidneys and liver indicate lead contamination. ^16 in calves
sublethal dosages of lead causes blood levels to be two to twenty
times higher than normal. Concentrations of 25 ppm in renal cortex
and 10 ppm in liver are considered indications of lead poisoning.
Normal levels of lead in the blood of goats, sheep, horses, cows
and young calves range from 0.05 to 0.25 ppm.
76
-------
Table 5.15-2
REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF INGESTED LEAD ON ANIMALS,
SELECTED FROM NAS1
T.ead
Compound
Pb arsenate
Pb acetate,
Pb arsenate
Pb acetate
Species
Chickens
Rats
Rabbits
Rats
Mice
Sheep
Calves
Rabbits
Rats
Rats
Calves
Rats
Cone.
US/kg
450
825
125
4
0.32-
2.56
1
6
30
64
213
200-
Length of
Exposure
Acute
Acute
Acute
Acute
15-356 days
Daily
Daily
5X in 16
days
1 year
6-7 wks
Observed Effect(s) Reference (s)
LD50
LD50
LD50
Lead in blood immediately
No difference in toxicity of PbAc
or PbAr. High retention in bone,
kidney, liver, and newborn; 15 diec
of severe lead poisoning in 15-229
days, all had behavioral and CNS
changes.
Toxic, induced abortions
No effect
Killed 40-90 days later. Baso-
philic cells rose sharply — typical
lead poisoning
No change in fertility or fecund-
ity. Maternal transfer of lead.
Decreased growth rate, kidney and
spleen hypertrophy
Daily Lethal
400 :
512 • Daily . No effect
18
Voight, £t. al.
19
Calvery, et .al.
20
Blaxter
Blaxter
Bradley & Fred-
nT\
rick22
23
Morris , et al.
24
Barltrap
24
Blaxter
23
Morris, et al.
PbNO,
PbNO,
Rats
I Ducks
i Ducks
512 , 70-80 days
6 137 days
8-12 25-28 days Lethal
Lower rate of protein catabolism
in liver
No effect
Lightbody
Calvery25
Coburn, et alt
26
-------
Table 5.15-2 (Continued)
REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF INGESTED LEAD
ON ANIMALS, SELECTED FROM NAS1
Lead
Compound
Pb acetate
Pb arsenate
-t
Species
i Rats
1
. Sheep
!
Cone.
me/kg
1% of
diet
2 gm/
day
Length of
Exposure
24 wks
Observed Effect(s)
Inclusion bodies found in kidneys
.after 2 months
3.5-7.0 days
' Rats 0.25-1 3.5-35 days
gm/day!
2 died after 3.5 days, 1 after 7
days; hemorrhagic erosion of lumen
Reference (s)
Angevine, et
al 27
— ' 28
McCulloch
wall; severe enteritis, pneumonia i
5 died within 35 days; black bone
marrow; temporary polycthemia
oo
-------
Areas of Needed Research. 1) Studies on relative sensitivities of
different animals to lead; 2) studies on the effect of lead on in-
sects and wildlife; 3) studies on effects of lead on ecosystems, in
particular soil ecosystems; 4) studies on the routes of intoxication.
REFERENCES
1. Biological Effects of Atmospheric Pollutants: Lead. Washington,
D.C. National Academy of Sciences, National Research Council.
1972. 330 p.
2. Hindawi, I. J. and G. E. Neely. Soil and Vegetation Study. In:
Helena Valley, Montana, Area Environmental Pollution Study.
Research Triangle Park, N.C., Environmental Protection Agency.
January 1972. p 81-94.
3. Lillie, P. A Study of Heavy Metal Contamination of Leaf Surfaces.
Environ. Pollut. 5:159-172, 1973.
4. Garner, R. J. Veterinary Toxicology. London, Balliere, Tindall
and Cox. 1957. p 42-255.
5. Heath, R. G., J. W. Spann, E. F. Hill and J. F. Kreitzer. Com-
parative Dietary Toxicities of Pesticides to Birds. Bureau of
Sports Fisheries and Wildlife, Washington D.C. Special Scientific
Report - Wildlife. Report number 152. 1972. 57 p.
6. Lillie, R. Air Pollutants Affecting the Performance of Domestic
Animals. United States Department of Agriculture. Washington,
D.C. Handbook Number 380. 1970. p 72-80.
7. Siegmund, 0. H. (ed.). The Merck Veterinary Manual. Rahway,
N.J., Merck and Co., Inc., 1973. p 935-936.
8. Baring, C. M. and K. F. Meyer. Investigation of Live-stock
Conditions and Losses in the Sebley Smoke Zone. Bull. Bureau
Mines, no. 98:474-520, 1915.
9. Parliceric, M. The Occurrence of Lethal Paralysis in Young
Sheep as a Result of Poisoning from Factory Smoke. Vet. Glas.
11:1085-1088, 1962.
10. Hammond, P. B. and A. L. Aronson. Lead Poisoning in Cattle and
Horses in the Vicinity of a Smelter. Ann. N. Y. Acad. Sci.,
111:595-611, 1964.
11. losif, C. Acute and Chronic Lead Poisoning in Cattle. Rec Med
Ecole Alfort 142(2):95-106, Feb. 1966.
79
-------
12. Egan, D. A. and T. O'Cuill. Open East Lead Mining Areas. A
Toxic Hazard to Grazing Stock. Vet Rec 84(9):230, March 1969.
J3. Bazell, R. J. Lead Poisoning: Zoo Animals may be First Victims.
Science 173 (3992):130-131, 1971.
14. Kerin, D. and Z. Kerin. Lead Contamination of Milk and Honey
Through Lead Aerosols by the Industry. Pro Vitae, 16(2): 61-62,
Arpil 1971.
15. Ottoboni, F. and E. Kohn. Study of Benica Area Horse's Deaths,
Interim Report. California State Department of Public Health.
Berkeley. Bureau of Occupational Health and Environmental
Epidemiology. May 1, 1970. 12 p.
16. Sr.hmitt, N. , G. Brown, E. I. Devlin, A. A. Larsen, J. M. Saville,
and E. D. McCausland. Lead Poisoning in Horses. An Environmental
Health Hazard. Arch Environ Health. 23:185-95, September 1971.
17. Shrenk, H. H. , H. Heiman, G. D. Clayton, W. M. Gafafer, and H.
Wexler. Air Pollution in Donora, Pa. Federal Security Agency,
Public Health Service, Division of Industrial Hygiene. Public
Health Bull. No. 306. 1949. 173 p.
18. Voight, J. L., L. D. Edwards and C. H. Johnson. Acute Toxicity
of Arsenate of Lead in Animals. J. Amer Pharm. Assoc. Sci Ed.
37:122-123, 1948.
19. Calvery, H. 0., E. P. Long, and H. J. Morris. The Chronic Effects
on Dogs of Feeding Diets Containing Lead Acetate, Lead Arsenate,
and Arsenic Trioxide in Vary Concentration. J. Pharm. Exp.
Ther. 64:364-387, 1938.
20. Blaxter, K. L. Lead as a Nutritional Hazard to Farm Livestock.
II. The Absorption and Excretion of Lead by Sheep and Rabbits.
J. Corapar. Path, and Ther. 60:140-159, 1950.
21. Blaxter, K. L. Lead as a Nutritional Hazard to Farm Animals.
III. Factors Influencing the Distribution of Lead in the
Tissues. Jour. Compar. Path, and Ther. 60:177-189. 1950.
22. Bradley, W. R. and W. G. Fredrich. The Toxicity of Antimony:
Animal Studies. Ind Med Ind Hyg. 2(2):15-22, 1941.
23. Morris, H. P., E. P. Laug, H. J. Morris, P. L. Grant. The
Growth and Reproduction of Rals-Fed Diets Containing Lead
Autob and Arsenictrioxide and the Lead and Arsenic Contents of
Newborn and Suckling Rats. J. Pharm 64:420-445, 1938.
80
-------
24. Baltrap, D. Transfer of Lead to Human Foetus. In: Mineral
Metabolism in Paediatrus. Baltrap, D. and W. L. Barland
(eds.). Philadelphia, F. T. Davis Company. 1969. p 135-151.
25. Lightbody, H. D. and H. 0. Calvery. Variations in the Orginast
Concentrations in Livers of White Rats Caused by Administration of
Arsenic and Lead. J Pharm. 64:458-464, 1968.
26. Coburn, D. R., D. W. Metzler and R. Treichler. A Study of Absorp-
tion and Retention of Lead in Wild Waterfowl in Relation to Clini-
cal Evidence of Lead Poisoning. J Wild. Manag. 15:183-192, 1951.
27. Angevine, J. M., A. Kappas, R. L. DeGowen and B. H. Spargo.
Renal Tubular Miclear Inclusions of Lead Poisoning; A Clinical
and Experimental Study. Arch Path 73:486-492, 1962.
28. McCulloch, E. C. and J. L. St. John. Lead-Arsenate Poisoning of
Sheep and Cattle. J Am Vet Med Assoc., 96:321-326. 1940.
81
-------
5.16 Air Pollutant: Manganese
Manganese in the form of oxide and ferro-manganese dust is emitted
during smelting and refining of ore; ferro-manganese blast furnace
operations, and burning of fossil fuels high in manganese content.
Non-urban concentrations in 1968 ranged from 0.0 to 0.14 pg/mS.1 Urban
concentrations are reported to average 0.10 ug/m with a maximum of 10
ug/m3 found in 1964. No ambient concentrations could be found for in-
dustrial operations.
Symptoms of Acute and Chronic Manganese Poisoning. The major modes of
intoxication are through the inhalation, ingestion, and through the
skin. The primary biological targets are the central nervous and pul-
monary system. Poisoning by manganese is identified by chronic symp-
toms of manganese pneumonia, changes in liver, and lesions in cerebrum.
Manganese is accumulated in the liver, brain, bones, and muscles. »J
Episodes Involving Manganese Poisoning of Free-Living Animals. No con-
firmed reports of manganese affecting free-living animals were found.
An incident involving high ambient levels of manganese, along with cop-
per and lead was associated with the death of sheep and cattle near a
coke oven industry. The effects here were probably due to lead and cop-
per.
Summary of Studies of the Effect of Manganese on Experimental Animals.
Manganese is used as a mineral supplement to poultry. Information on
the adverse effects of manganese is lacking.
Suggested Biological Indicator of Manganese. Information is lacking
to suggest potential indicators. The liver, brain, bones and muscles,
however, may serve as accumulating organs in mammals.
Area of Needed Research. 1) Ambient concentration and distribution of
manganese near industrial operations; 2) manganese by animals, especial-
ly birds, insects and animals with high respiratory rates.
REFERENCES
1. Air Quality Data for Metals, 1968 and 1969 from National Air Sur-
veillance Networks and Contributing State and Local Networks.
Research Triangle Park, N.C. APTD-1467. Office of Air Quality
Planning and Standards. June 1973. var. pg.
2. Sullivan, R. J. Preliminary Air Pollution Survey of Manganese and
Its Compounds, a Literature Review. National Air Pollution Control
Administration. Publication Number APTD 69-39. October 1969. 53 p.
3. Lillie, R. Air Pollutants Affecting the Performance of Domestic
Animals. In: Agriculture Handbook Number 380. Washington. D.C.
United States Department of Agriculture, 1970. p 81.
82
-------
5.37 Air Pollutant; Mercury
Mercury as a pollutant is best known as a water pollutant and a pollu-
tant arising from the use of mercurial pesticides. This discussion,
however, will be confined to mercury derived from industrial sources.
The primary forms of mercury as an air pollutant are elemental mercury
and mercuric sulfide. The industrial sources of mercury emissions are
mercury mining and refining of the ore. The use of mercury compounds
as pesticides also contribute to ambient air concentrations. Urban
concentrations are not completely monitored. Several cities, including
Cincinnati and Charleston, have reported average concentrations of 0.10
pg/m3 and 0.17 yg/m3 respectively, and a maximum of 0.21 ug/nr* reported
for Cincinnati. In Japan, which uses organic mercury as a pesticide,
air concentrations have been reported as high as 10,000 pg/m .
Summary of Symptoms of Acute and Chronic Mercury Poisoning. The major
modes of intoxication of mercury are by inhalation and ingestion of
contaminated food. The primary biological target areas for mercury
are respiratory, renal, hepatic and gastrointestinal systems. The
characteristic symptoms of acute mercury poisoning are dyspnea, nasal
discharge, violent gastroenteritis, diarrhea, and pulmonary edema.
Chronic poisoning in addition to dyspnea and gastroenteritis results in
anorexia, lethargy, blindness, degeneration of liver, kidney and 2^
myocardium. Mercury accumulates in the liver, kidney, and stomach.
Episodes Involving Mercury Poisoning (as an air pollutant) of Free- ^
Living Animals. Mercury contamination of the environment is widespread.
However, only one reported incident involving industrial mercury poison-
ing was found. This incident involved cows and other domestic animals
which became sick near a fire in a mercury mine (Table 5.17-1).
Summary of Studies on the Effects of Mercury on Experimental Animals.
Laboratory studies on the effects of mercury vapor are varied. Exposures
of 100 ug/m3 for 83 weeks has no effects on dogs, while exposures to
rats as low as 2 ug/m3 for approximately 40 weeks causes changes in the
central nervous system. Pigeons are not affected by exposure to 80
pg/m3 for 20 weeks. Studies indicate that for cumulative poisons such
as mercury, single exposures are poor indications of relative hazards.
Although high concentrations of mercury fungicides are required to kill
animals, low concentrations over long periods of time are also lethal.5
Suggested Biological Indicators of Mercury. More study is needed to de-
termine biological monitoring systems for mercury. The stomach, kidney
and liver appear as accumulating organs, however.
Areas of Needed Research. 1) Studies of industrial emissions—concen-
tration and distribution of mercury; 2) studies on the effects of low
83
-------
Table 5.17-1 MERCURY: EPISODES INVOLVING FREE-LIVING ANIMALS
Known
1. Henderson and Haggard, 1943, reports mercury mine fire in
Yugoslavia sickened cows and other domestic animals."
and chronic exposure of mercury on animals, including insects, birds,
and other animals with high respiratory rates.
REFERENCES
1. Stahl, Q. R. Preliminary Air Pollution Survey of Mercury and Its
Compounds, a Literature Review. National Air Pollution Control
Administration. Publication Number APTD 69-40. October 1969.
95 p.
2. Garner, R. J. Veterinary Toxicology. London, Balliere, Tindall
and Cox. 1957. p 42-255.
3. Lillie, R. J. Air Pollutants Affecting the Performance of Domestic
Animals: a Literature REview, USDA Agr Handb. 380, Aug, 1970.
4. Buhler, D. R. (ed.) Mercury in the Western Environment. Corvallis,
Ore. Continuing Education Publications. 1973. 359 p.
5. McEwen, L. C. , R. K. Tucker, J. 0. Ells and M. A. Haegele. Mercury-
Wildlife Studies by the Denver Wildlife Research Center. In:
Mercury in the Environment. Buhler, D. R. (ed.). Corvallis, Ore.
Continuing Education Publications. 1973. p. 146-156.
6. Henderson, Y. and H. W. Haggard. Noxious Gases. New York,
Reinhold. 1943.
84
-------
Table 5.17-2 REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF
MERCURY COMPOUNDS ON ANIMALS
Species
Rats
Pigeons
Dogs
Dogs
Dogs
Dogs
— 'O —
Rabbits
Dogs
Pigeons
Dogs
Pheasant
Greater
Prairie
Chicken
Grey
Partridge
Coturnix
Quail
Domestic
Pigeon
Chukar
Partridge
Mallard
Mallard
Bob-White
Quail
Pheasant
Coturnix
Quail
Substance
mercuric
vapor
i
ceres an-Ma
ceresan-L*5
Concentration
2-30 u/m3
80 ug/m
100 ug/m
860 yg/m
T
3000 ug/m
3000 to 6000
Ug/m3 .
6000 yg/m
6000 to 20,000
yg/m3 _
17,000 ug/m
20,000 yg/m3
11.5 mg/Kg
(Mercury
equivalent)
11.5
17.6
21. A
24.2
26.9
30.0
^72
23.9
26.8
33.1
Exposure
9.5 mos
6 hrs/
20 weeks
83 weeks
6 weeks
40 days
40 days
6 weeks
8 days
14 weeks
few hrs
acute
acute
acute
acute
i
acute
acute
daily
acute
acute
acute
acute
Effects
high levels in
kidney & liver
affected CNS
no effects
no effects
affected brain
& kidney, but
recovered
no effect
affected CNS
digestive tract
severe damage to
kidney, heart,
lungs, brain
death
changes in
behavior
death
LD50
LD50
LD50
LD50
^50
LD50
lethal
^50
^50
LD50
LD50
leference
5hahl2
McEwan , et
1 T
alj
!
i
;
a
(
1
1
1
85
-------
Table 5.17-2 (Continued) REPRESENTATIVE LABORATORY STUDIES ON THE
EFFECTS OF MERCURY COMPOUNDS ON ANIMALS
Species
Fulvous
Free Duck
House
Sparrow
Pheasant
Mallard
Mallard
Mallard
Substance
Panogenc
Agroxd
Mema RMe
Concentration
mercury equi-
valent) mg/kg
37.8
12.7-38.1
23.9
25.2
.80
75.7
Exposure
acute
acute
acute
acute
acute
- — i
acute
Effects
LD50
LD50
LD50
W50
LD50
LD50
Reference
McEwen, et
al5 "
3N-(elhylmercuric)-p-toluene sulfonanilide
bme thy lmercuric-2,3-dehydroxy-propy liner captide and melhylmercurie acetate
Cmethylmercuric dicyandiamide
phanylmercuric urea
emelhoxyelhylmercuric acetate
86
-------
5.18 Air Pollutant: Molybdenum
Molybdenum is emitted from numerous industrial sources, in particular
steel and other metal-producing industries. Maximum urban concentra-
tions have been reported as high as 0.78 pg/m3. Levels of molybdenum
in pastures near molybdenum factories are reported to be over 200 times
normal concentrations.1 High levels of molybdenum occur naturally in
certain soils with consequent high levels in vegetation.
Symptoms of Acute and Chronic Molybdenum Poisoning. The major mode of
molybdenum intoxication is by ingestion of contaminated food. The
primary target area for molybdenum is the gastrointestinal system.
Chronic poisoning has been described as causing diarrhea, enteritis,
hyperemia of intestine, change in skin color and shift in copper balance
in body for mammals. The presence of molybdenum is a good indicator
of exposure. Storage is greatest in bones and kidney.2
Episodes Involving Molybdenum Poisoning of Free-Living Animals. All
reported incidences involving molybdenum poisoning have involved cattle
grazing near industrial sources (Table 5.18-1). They exhibit the
typical clinical symptoms of molybdenum poisoning.
Summary of Studies on the Effects of Molybdenum on Experimental Animals.
Non-ruminants are more resistant to molybdenum toxicity.z
Suggested Biological Indicators of Molybdenum. Two monitoring systems
might be established: observation of the concentrations of molybdenum
in the bone, kidney and urine, comparison of copper phosphorus balance
in animals. In cattle and sheep copper storage in the liver is reduced
by molybdenum. In pigs copper storage is increased by high molybdenum
diets. Phosphorus absorption is decreased and excretion increased in
cattle and rabbits exposed to high levels of molybdenum. This imbal-
ance leads to clinical rickets in cattle.2 Not enough information is
available to make a definitive statement on sensitivity except that
cattle appear more sensitive than horses.
Areas of Needed Research. 1) Studies on urban concentrations of
molybdenum; 2) studies on the effects of low and chronic exposure to
birds, insects and animals with high metabolic rates.
87
-------
Table 5.IH-l MOLYBDENUM: F.P1SODKS FNVOLVJNC FREE-LIVING ANIMALS
1. Known
a. Ogura, 1965 (12539) reported fifty-two cattle developed diarrhea,
malnutrition, decreased milk production and fertility near
molybdenum smelter plant in Japan, up to 484 ppm in fodder.
b. Verweij, 1971 (47792) reported cattle showed copper deficiency,
severe diarrhea, dull coat, and lameness near molybdenum plant
in Holland.5
c. Gardner and Hall-Patch, 1968 (49710) reported over a dozen
cattle sick near an oil refinery in England. Cattle suffered
from acute diarrhea and locomotor damage.6
2. Possible or Mixed Effect
None.
) = APTIC No.
REFERENCES
1. Lillie, R. Air Pollutants Affecting the Performance of Domestic
Animals. United States Department of Agriculture. Washington,
D.C. Agriculture Handbook Number 380. 1970. p 84-86.
2. Garner, R. J- Veterinary Toxicology. London, Balliere, Tindall
and Xoc. 1957. p 42-255.
3. Siegmund, 0. H. (ed,). The Merck Veterinary Manual. Rahway, N.J.
Merck Co., Inc. 1973. p 943-945.
4. Ogura, Y. Molybdenum Poisoning in Cattle Due to Air and Soil
Contamination as an Industrial Hazard. Japanese Tokyo Nat Instit
Animal Health Bull 50:24-29, 1965.
5. Verweij, J. H. P. Molybdenosis in Cattle by Air Pollution.
Tijdschr Diergenesk. 96(22):1508-151, 1971.
6 Gardner, A. W. and P. K. Hall-patch. Molybdenosis in Cattle Grazing
Downwind from an Oil Refinery Unit. Vet Rec. 82(3), January 1968.
88
-------
5.19 Air Pollutant: Nickel
The technological emission sources of nickel are metallurgical plants
using nickel, and engines burning coal and oil. As a pollutant nickel
occurs in several forms, including nickel oxide, nickel sulfate and
sulfide. Non-urban concentrations in 1968 ranged from 0.0 to 0.055
Ug/m -1 The national urban concentration is reported to average 0.032
Vjg/ro3. A maximum urban concentration of 0.690 ug/m3 was recorded in
East Chicago, Indiana, in 1964. An industrial concentration of 1.2
Ug/m3 was reported to have been found near a nickel plant in West
Virginia.2
Summary of Symptoms of Acute and Chronic Nickel Poisoning. The major
modes of nickel intoxication are by inhalation and external airborne
exposure. The primary target system is the pulmonary system. Acute
poisoning is characterized by extensive pneumonitis, pulmonary edema,
sclerosis, anaplastic carcinoma, adenocarcinoma, and kidney damage.
Chronic exposures result in kidney degeneration, adenocarcinoma,
squamous cell carcinoma and pulmonary edema. No patterns of accumula-
tion are found. The mode of excretion depends upon the mode of adminis-
tration. Ingested nickel is primarily excreted in the feces while in-
haled nickel is excreted in the urine.2
Episodes involving Nickel Poisoning of Free-Living Animals. None re-
ported.
Summary of Studies on the Effects of Nickel on Experimental Animals.
Most studies have been at concentrations far above reported ambient
levels (Table 5.19-1). These tend to indicate the toxic concentrations
of nickel metal and nickel carboxyl are very high for laboratory
animals.
Suggested Biological Indicators of Nickel. Not enough information is
available to draw conclusions.
Areas of Needed Research. 1) Effects of low and chronic concentra-
tion of nickel on animals, especially those with high respiration
rates, i.e., birds: 2) effects of low and chronic concentrations of
nickel on insects.
REFERENCES
1. Air Quality Data for Metals, 1968 and 1969 from the National Air
Surveillance Networks and Contributing State and Local Networks.
Research Triangle Park, N.C. APTD-U67. Office of Air Quality
Planning and Standards. June 1973. var. pg.
2. Sullivan, R. J. Preliminary Air Pollution Survey of Nickel and Its
Compounds, a Literature Review. National Air Pollution Control
Administration. Publication Number APTD 69-41. October 1969. 69 p.
89
-------
Table 5.19-1 REPRESENTATIVE LABORATORY STUDIES ON EFFECTS OF NICKEL
CARBONYL ON ANIMALS (ADAPTED FROM SULLIVAN2)
Animal
Rats
Mice
Rats
Cats
Dogs
Dogs or
Cats
Dose
30-60ug/liter
in 50% C H OH
&
-------
5.20 Air Pollutant:
The two primary nitrogen oxides considered as air pollutants are nitro-
gen dioxide and nitrogen oxide. Most of the nitrogen oxides are in the
form of nitrogen dioxide. The major sources of nitrogen oxides are from
transportation sources, such as motor vehicles and fuel combustion in
stationary sources, such as coal and natural gas. Levels of nitrogen
oxides are low in nature, with non-urban averages reported as 2 pg/m3
(2 ppb) for nitrogen oxide and 8 ug/m3 (4 ppb) for nitrogen dioxide.
Urban peak levels for nitrogen dioxide have been reported to be as
high as 940 yg/m3 (0.5 ppm).1
Summary of Symptoms of Acute and Chronic Nitrogen Oxides Poisoning.
The mode of intoxication by nitrogen oxides is through inhalation.
The primary target systems for birds and mammals are the respiratory
and circulatory systems. Except at extremely high levels (3,075 rag/m^
or 2500 ppm), nitrogen oxide is non- toxic. The most characteristic
responses to nitrogen dioxide are pulmonary edema and inflammation,
leucocytosis, polycythemia, increased production of methemoglobin,
and lowered resistance to respiratory diseases. Nitrogen oxides are
accumulated in the blood as completed hemoglobin (NO-hemoglobin) and
methemoglobin (NO-methemoglobin) . These complexes have a very short
half-life(2 days). The production of methemoglobin may possibly be
used as a nitrogen dioxide indicator. Studies need to be carried
out to determine its presence at chronic exposures.
Episodes Involving Nitrogen Dioxide Poisoning and Contamination of
Free-Living Animals. Nitrogen dioxide poisoning is frequently encoun-
tered in agricultural situations and is sometimes called "silo fillers"
diseases. Concentration of nitrogen dioxide during these episodes are
quite high with hazardous conditions considered to occur at 15 ppm
(28,200 yg/rn3). Levels have reached as high as 151 ppm (284,000 ug/m3),
Only one industrial episode involving only nitrogen dioxide is re-
ported. This was a pest infestation in a N02 contaminated pine forest.
No pattern of effects is apparent, except possible sensitivities of
insect pests to levels of pollutant. Episodes of possible effects of
nitrogen oxides associated with other pollutants involved inverte-
brates, two infestations of conifer trees by insects, and vertebrates,
domestic animals which became sick during the fog in Donora, Pennsyl-
vania (Table 5.20-1).
Summary of Studies on the Effects of Nitrogen oxides on Experimental
Animals. Most studies on the effects of nitrogen oxide (Tables 5.20-2,
3, 4) have been at concentrations far exceeding the highest levels re-
ported in polluted situations. These studies used laboratory rodents
rabbits, monkeys, and dogs. Concentrations of nitrogen dioxide of
91
-------
less than 1 ppra (1900 pg/m3), or twice the reported urban maximum, are
not harmful to mammals. No studies could be found on other animals.
Based upon these laboratory studies, the reported effects upon mammals
in industrial episodes are not attributable to nitrogen dioxide alone,
but are either due to other pollutants or synergistic effects of nitro-
gen dioxide with other pollutants.
Suggested Biological Indicators of Nitrogen dioxide. Based on the
available information, insects respond to ambient N02 levels and may
possibly be used as indicators; however, studies need to be conducted
to determine the mode of action. The presence of ntethemoglobin in
mammals indicates short term exposure.
Areas of Needed Research. 1) Effects of chronic exposure to low
levels of nitrogen oxide on animals with high respiratory rates, es-
pecially birds; 2) studies on feasibility of using methemoglobin as
indicator of exposure; 3) studies on the effect or relationship of
insect pests and nitrogen dioxide to determine sensitivities and re-
lationships to plant damage.
Table 5.20-1 NO : EPISODES INVOLVING FREE-LIVING ANIMALS
x
1. Known
a. Lillie, 1970. "Silo fillers" disease noticed in cattle, poul-
try, pigs, and flies; hazardous concentration of N02 as low as
15 ppm (26,200 pg/m3), levels of 151 ppm (284,000 pg/m3)
reached.'
b. Sierpinski, 1971 (51095). NOX damaged pine forest, highest
concentration of pests in lowest N02 levels in Poland.3
2. Probable or Mixed Pollutants
a. Shrenk, et al., 1949. 38/245 dogs sick, 11/38 died of respira-
tory failure; highest percent young and old, behavior changes
noted. Cats less affected than dogs; 40% mortality in poultry
flocks; 1/7 of household rabbits sick; 3/13 farms with sick
cattle in Donora, Penn. Atmospheric concentration of NOx, S02,
and Pb high.4
b. Wentzel and Ohnesorge, 1961. Report insect infestation of
spruce trees correlating with S02 and nitrogen complexes.^
c. Sierpinski, 1967 (45988). Large pine sawfly larvae increased
in moderate NOX and SOX concentrations, tut decreased in high
concentratios in Austria.**
) = APTIC No.
92
-------
Table 5.20-2 REPRESENTATIVE STUDIES OF TOXICOLOGICAL EFFECTS OF NITRIC OXIDE ON LABORATORY
ANIHALS AND BACTERIA ADAPTED FROM EPAl (Table 9-8) and ADDITIONAL SOURCES
Species
Proteus vulgaris
Rats
Proteus vulgaris
Mice
Cone.
ppm
20
10
16-40
10,000
2,500
Cone.
mg/rn^
24.6
12.3
19.7
12,300
3,075
Length of
Exposure
10 min.
1 and 9
days
4 hours
10 min.
6-7 min.
Observed Effect(s)
Reversible inhibition of
hydrogenase activity.
NO-hemoglobin and NO-methe-
raoglobin not found in blood.
Methemoglobin not examined.
No effect on respiratory
rates and tidal volumes
Irreversible inhibition of
hydrogenase activity
Death within 12 min. Re-
covered if returned to clean
air after 4- to 6- min.
exposure.
References
EPAl
-------
Table 5.20-3
REPRESENTATIVE STUDIES OF TOXICOLOGICAL EFFECTS OF SHORT-TERM NO. EXPOSURE ON
LABORATORY ANIMALS ADAPTED FROM EPA1(TABLE 9-9)AND ADDITIONAL SOURCES
Species
Rats
Rats
Rats
Rabbits
Mice
Mice
Guinea
Pigs
Mice
Monkeys
Cone.
pptn
0.5
1.0
1.0
1.0
3.5
5.0
Cone.
mg/ra^
0.9
1.9
1.9
1.9
6.6
9.4
i
5.2-, 9.8-
13.0 24.4
7.7 14.5
10 ' 18.8
Length of
Exposure
4 hours
1 hour
4 hours
1 hour
2 hours
2 hours
Observed Effect(s)
Lung shows degranulation in mast cell morph-
ology. (Possibly precedes onset of acute
inflammatory reaction.)
Lung shows degranulation in mast cell morph-
ology. (Mostly reversible 24 hrs. after
exposure. )
Lungs show lipid peroxidation. (Delayed ef-
fect. Maximum response 24 hrs after exposure.)
Lung: structural changes in collagen (by
spectroscopy) of animals sacrificed immediately
after exposure; reduced in animals sacrificed
24 hrs after exposure. (Changes suggest de-
naturation of structural protein, only par-
tially reversed.)
Enhanced susceptibility to respiratory infec-
tion demonstrated by increased mortality after
challenge with K. pneumoniae. (Threshold for
significant effect 6.6 mg/mj (3.5 ppm) for 2
hrs when challenged 1 hr after exposure. )
Increased mortality when infected with 1C.
pneumoniae either before or after N02 ex-
posure; reduced bacterial clearance from
1 lungs .
2-4 hours j Lung showed increased respiratory rates and
6 hours
decreased tidal volumes.
20% decrease in voluntary running activity.
2 hours i Lung: respiratory rate unchanged; tidal vol-
ume decreased; septal breaks, alveolar ex-
! ' pansion, and some large air vesicles with
, ' thin septal walls observed. (Tidal volume
. ; returned to pre-exposure levels within 48
Reference
EPA1
: hrs.)
VO
-------
Table 5.20-3 (Continued) REPRESENTATIVE STUDIES OF TOXICOLOGICAL EFFECTS OF SHORT-TERM
N02 EXPOSURE ON LABORATORY ANIMALS ADAPTED FROM EPA1(TABLE 9-9) AND ADDITIONAL
SOURCES
Species
Dogs
Dogs
Monkeys
Rabbits
Monkeys
Cone.
ppm
13-
190
2_
190
15
25
35-50
i
J
Cone.
mg/m3
25-
358
28.2
47.0
65.8-
94.0
Length of
Exposure
25-40 min.
25-40 min.
2 hours
3 hours
2 hours
Observed Effect(s)
} respiration
^.respiration
Lung: respiratory rate unchanged; tidal
volume decreased; moderate in albeoli
expansion, minimal septal wall thinning,
patchy lumphocytic interstitial infiltra-
tion. (Tidal volume returned to pre-
exposure levels within 48 hrs.)
Kidney: some tubular erosion.
Liver: Cell ballooning with clear cyto-
plasm and nuclear displacement; inter-
stitial congestion
Decreased inter feron production and de-
creased resistance to viral infection.
Lung: marked increase in respiratory
rate with marked decrease in tidal
volume; large areas of total alveolar
collapse, edema, and lymphocytic infil-
tration with other areas of alveolar
expansion and septal wall thinning;
bronchi inflamed, epithelial surface
erosion, and loss of cilia. (Change in
pulmonary function persisted up to 72
; i hrs.)
i Heart: interstitial fibrosis and edema.
1 ' Kidney: Glomerular-tuf t swelling and
• intercellular lymphocytic infiltration.
• Liver: Lymphocytic infiltration, conges-
tion, and centrolobular necrosis.
Reference (s)
Yokoyama, 1964 7
1
EPA
-------
Table 5.20-3 (Continued) REPRESENTATIVE STUDIES OF TOXICOLOGICAL EFFECTS OF SHORT-TERM
EXPOSURE ON LABORATORY ANIMALS ADAPTED FROM EPA1 (TABLE 9-9) AND ADDITIONAL
SOURCES
Species
Guinea
pigs
Rats,
Guinea
pigs and
Rabbits
Hamsters
Rats
Chickens ,
Pigs,
Calves ,
Flies
Rabbits,
Guinea
pigs
Cone.
ppm
40.0
75-
100
100
115-
151
Cone.
ing/m^
75.2
141.0-
150.4
188.0
188.0
216-
284
i
150 ; 282.0
,
Length of
Exposure
0.5 hr at
2-hr inter-
vals, total-
ing 4.5 hrs,
2 hours
6 hours
1 hour
very short
1 hour
Observed Effect(s)
Enzyme systems: increased 0_ consumption —
liver, spleen, kidney; increased lactic
dehydrogenase — liver, kidney, serum; in-
creased aldolase — liver, spleen, kidney,
serum.
Lung: inflammation of bronchiolar
epithelium. (Apparent recovery 2 wks
after exposure. )
Lung: epithelial proliferation in major
bronchi and more distal respiratory tract;
electron microscope evidence of depressed
mucopolysaccharide production, increased
phospholipid production, and increased
lysozymal enzyme content.
Blood: Methemoglobin present. (Disap-
peared 1 to 2 hrs after return to clean
air.)
Instantaneous death — silo door (resulted
from
Blood: methemoglobin present
Reference (s)
EPA1
8 9
Anon . '
VO
-------
Table 5.20-4
REPRESENTATIVE STUDIES ON TOXICOLOGICAL EFFECTS OF LONG-TERM NO EXPOSURE ON
LABORATORY ANIMALS ADAPTED FROM EPA1(TABLE 9-10)AND ADDITIONAL SOURCES
Species
Rabbits
Mice
Mice
Rats
Rats
Rats
Rabbits
Rats,
Monkeys
Rabbits
Cone.
ppm
0.25
0.5
0.5
•rife
^^
0.5
0.8
1.3
2.0
2.0
Rats i 2-0
Cone.
mg/m^
0.5
0.9
0.9
0.9
1.5
0.84-
5.7
2.5
3.8
3.8
3.8
Length of
Exposure
4 hrs/day/
6 days
6-24 hrs/
day/3-12
months
6-24 hrs/
day, 7 days/
week, to 12
months
2-6 weeks
Continuous ,
lifetime
6 months
Continuous
17 weeks
Continuous
3 weeks
4 days
Continuous
lifetime
1
t
'
Observed Effect(s)
Lung: structural changes in collagen (elec-
tron microscopy) . (Still apparent 7 days
after exposure.)
Lung: pneumonitis; alveolar distention.
(Possibly emphysematous condition.)
Enhanced susceptibility to respiratory
infection as demonstrated by increased
mortality after challenge with K. pneumonae.
(Significant increase after 3 mos exposure
24 hr/day and 6 mos at 6 and 18 hrs/day.
After 12 mos, increase significant at 24
hrs/day only.)
,> blood catalase — 5th week, then lower
6th and slight >in aspartic acid excretion.
Tachypnea and some terminal bronchiolar
hypertrophy.
& conditioned reflex activity, lost fur
at 5 months in spinal area.
Reduction in rate of weight gain; 2%
increase in exposed versus 8% in controls.
Blood: polycythemia. (Approximate doub-
ling of red cell number with lesser in-
creases in hematocrit and hemoglobin.)
Morphological changes in terminal bronchi-
olar epithelium.
Lung: bronchiolar epithelial changes —
loss of cilia and reduced cytoplasmic
bleeding, crystalloid inclusion bodies.
(Possibly pre-emphysematous lesion. Effect
occasionally seen at 1.5 mg/m3 (0.8 ppm).)
Reference(s)
EPA1
Ripperton &
Johnston1^
1 1
Yakimchuk11
EPA1
VO
-------
Table 5.20-4 (Continued) REPRESENTATIVE STUDIES ON TOXICOLOGICAL EFFECTS OF LONG-TERM
EXPOSURE ON LABORATORY ANIMALS ADAPTED FROM EPA1 (TABLE 9-10) AND ADDITIONAL
SOURCES
Sj>ecies
Rabbits
Guinea
pigs
Monkeys
Cone.
ppm
3.0
5.0
5.0
1
Rabbits
Monkeys
Rats
Rats
Guinea
pigs
Guinea
pigs
8-12
10.00
10-25
Cone.
mg/m-*
5.6
9.4
9.4
15-23
18.8
18.8-
47.0
12.0 ; 22.6
15.0
28.2
i
15-0 ! 28.2
i
Length of
Exposure
Continuous
15 weeks
4 or 7.5
hrs/day, 5
dys /wk , 5.5
months
Continuous
2 months
3 months
Continuous
1 month
Continuous
4-12 mons.
Continuous ,
9 months
Continuous
1 year
10 weeks
Observed Effect(s)
Loss in weight; exposed group showed 10%
decrease, 11% increase in control group.
Lung: formation of circulating substance —
possibly lung antibody; no change in expi-
ratory flow resistance. (Amounts increased
with length of exposure. )
Lung: increased respiratory rate and de-
creased tidal volume. (Minute volume un-
changed. One of three monkeys exposed to
influenza virus 24 hrs before NO. died af-
ter 5 days. )
50-60% died within 12 weeks; pulmonary con-
gestion, edema, alveolar walls, non-elas-
tic resistance of lungs (Non-elasticity).
Lung: both respiratory rate and tidal
volume increased. (Three monkeys exposed
to influenza virus 24 hrs before N0« died
with 3 days.)
Lung: voluminous emphysema- like lungs;
distended and disrupted alveoli. (Associ-
ated thoracic kyphosis and rib flaring.)
Blood: Polycythemia
Weight: decrease in rate of gain; exposed
20% below controls.
Lung: formation of circulating substance —
perhaps lung antibody.
Enzyme systems: increased 0_ consumption--
spleen, kidney; increased lactic dehydro-
Reference (s)
EPA1
12
Davidson
1
EPA
genase — lung, liver, kidney; increased \
' aldolase — liver, spleen, kidney, serum. ,
00
-------
Table 5.20-4 (Continued) REPRESENTATIVE STUDIES ON TOXICOLOGICAL EFFECTS OF LONG-TERM I
EXPOSURE ON LABORATORY ANIMALS ADAPTED FROM EPA1(TABLE 9-10)AND ADDITIONAL
SOURCES
Species
Guinea
pigs
Rats,
Rabbits
Dogs
Hamsters
Cone.
ppm
15-20
24.0
25-26
50
Cone.
rag/ra^
28.2-
37.6
45.1
47.0-
48.9
94.0
Length of
Exposure
2 hrs/day,
5 dys/wk,
for 21 mos
6 hrs/day,
5 dys/wk,
for 43 dys
(rats) or
45 dys
(rabbits)
6 months
10 weeks
i
Observed Effect(s) Reference (s)
Lung: formation of circulating sub- EPA
stance — perhaps lung antibody.
Blood: methemoglobin formation; mean:
rabbits, 2.8%; rats, 13.6%. (Animals
exposed to welding fumes, which con-
tained 3.075 to 6,150 g/nt3 (2.5-5.0
ppm) NO as well as other contaminants:
methemoglobin disappeared during post-
exposure period.)
Lung: bullous emphysema or scattered
small bullae; diffuse increase in colla-
gen. (Early lesions of pulmonary emphy-
sema produced; inclusion of ferric oxide
with the NO appeared to exert a pro-
tective effect.)
Lung: increase in volume, with a return
to normal 2 weeks after cessation of the
exposure; transitory epithelial prolifer-
ation in respiratory bronchioles. (No
! histological evidence of emphysema.)
VO
-------
REFERENCES
1. Air Quality Criteria for Nitrogen Oxides. Environmental Protec-
tion Agency. Air Pollution Control Office Publication Number
AP-84. January 1971. 170 p.
2. Lillie, R. Air Pollutants Affecting the Performance of Domestic
Animals. United States Department of Agriculture. Washington,
D.C. Handbook Number 380. 1970. p. 87-91.
3. Sierpinski, Z. Secondary Noxious Insects of Pine in Stands Grow-
ing in Areas with Industrial Air Pollution Containing Nitrogen
Compounds. Sylvan. 115(10):11-18, October 1971.
4. Schrenk, H. H., H. Heimann, G. D. Clayton, W. M. Gafafey, and H.
Wexler. Air Pollution in Donora, Pa. Washington, D.C. Federal
Security Agency, Public Health Service, Division of Industrial
Hygiene. 1949. 173 p.
5. Wentzell, K. F. and B, Ohnesorge. Occurrence of Insect Pests
with Air Pollution. Forstarchiv. 32:177-186, 1961.
6. Sierpinski, Z. Influence of Industrial Air Pollutants on the
Population Dynamics of Some Primary Pine Pests. International
Union of Forest Research Organization. Vienna (Austria), Proc.
Congr. Intern. Union Forest Research Organization, Munich, W.
Germany 5(24):518-531, 1967.
7. Yokoyama, E. Effects of Exposure to Nitrogen Dioxide on the
Mechanical Properties of the Lung in Anesthetized Dogs. Tokyo
Inst Pub Health Bui. 12:14-21, 1964.
8. Anonymous. "Silo-Fillers" Disease in Animals. Amer. Vet. Med.
Assoc. J. 128:602, 1956.
9. Anonymous. Silo-Fillers Disease. Hoard's Dairyman 101:1983,
1956.
10. Ripperton, L.A. and D. R. Johnston. Effect of Growing Animals
on a Continuous Exposure to Experienced Concentrations of
Nitrogen Dioxide. Amer. Indus. Hyg. Assoc. J. 20:324-326, 1959.
11. Yakirachuk, P. P. Experimental Basis for the Limit of Allowable
Nitrogen Dioxide Concentration in Atmospheric Air. USSR
Lit. Air. Pollut. and Relat. Occup. Dis. 9:177-184, 1963.
12. Davidson, J. T. , G. A. Lillington, G. B. Haydon and K. Wasserman.
Physiologic Changes in the Lungs of Rabbits Continuously Exposed
to Nitrogen Dioxide. Amer. Rev. Resp. Dis. 95(5):790-796, 1967.
100
-------
5.21 Air Pollutant; Particulates
Particulates are aggregates of many molecules suspended in air. These
aggregate molecules may be chemically similar or dissimilar, and range
in size from 10 urn to 0.1 urn. The effects of particulates can be con-
sidered in three ways: intrinsic toxicity of particles, particulates
activity as carriers of toxic material, and as inert particles which
interfere with the clearance of other airborne toxic material. Parti-
cles with intrinsic toxicity include S03> Pb, Be, As, and Mo.1 Discus-
sion of these and other similarly intrinsically toxic particles is
found in other sections of this report. Particulate carriers such as
soot carbon can absorb photochemical oxidants, hydrocarbons, SO and
NO -1 Their effects are also considered in other sections of the re-
port. This section considers only the effects of inert particles on
animal systems. *•
The sources of inert particulates are many and result from incineration,
open-hearth furnaces, chemical manufacturing, motor vehicles, fuel oil
combustion, cement plants, and mining activities. Non-urban averages
for particulates are reported to range from 10 ug/mJ to 60 ug/mj. Urban
values are high, ranging from 60 vg/m3 to 200 ug/m-» with a maximum of
1254 ug/ra3 recorded. A level of 470,000 ug/m for particulates of un-
known nature is reported for iron and steel production (see Section
5.14) but no other representative data was found.
Summary of Symptoms of Acute and Chronic Particulate Poisoning. The
effects of inert particulates are primarily on the respiratory system.
In cases of acute exposure blocked air passages and hemorrhagic le-
sions appear. Chronic exposure leads to pulmonary lesions typical of
non-occupational anthracosis, pneumonitis, and pulmonary fibrosis and
phagocytosis, and changes in chemistry of the lung lining (Table 3.21-
1).
Episodes Involving Particulate Poisoning of Free-Living Animals.
Episodes solely attributable to inert particulates were not found. In
one case Particulate caused soiling of white-colored zoo animals,
especially those with oily plumage in the Ruhr region of Germany. Two
reports of carbon deposits in lungs of animals living in the London
Zoo, Antwerp Zoo, and cattle from the Ruhr region were found (Table
5.21-1).
Many episodes involving possible or combined effects of Particulates
and other pollutants are known from before the turn of the century.
The Royal Commission Report of 1878, for example, states smoke from
copper works blinded 20 cattle and sheep along with other incidents.
Recent incidents have involved vertebrates, including domestic animals
(cattle and sheep) and some wildlife (rabbits and deer); and inverte-
brates, including pest infestations, in Japan and Poland in trees and
on crop alfalfa (see Table 5.21-1).
101
-------
c
Table 5.21-1 PARTICULATES: EPISODES INVOLVING FREE-LIVING ANIMALS
1. Known
a. Lillie, 1970. Reports animals, including birds, living in Lon-
don Zoo, developed carbon deposits in lungs that led to death.'
b. Vandenberg, 1974 (pers. coram.) Reports lung anthracosis regu-
larly observed in Antwerp Zoo; intensity related to time of
captivity. **
c. Gewalt, 1974 (pers. comm.). Reports quick soiling of white
animals such as white llamas and white storks from Duisburg in
the Ruhr region in Germany. Cattle in slaughterhouses fre-
quently had black lungs.^
2. Possible or combined effects.
a. Royal Commission Report, 1878. Reports smoke from copper
works blinded 120 cattle; sheep and pigs not affected.10
b. Oliver, 1912. Reports roadside dust kills trout and insects,
the latter reducing bird population.H
Scientific American, 1914. Reports cattle lungs affected and
reduced quality and quantity of wool in sheep due to smoke in
England.12
d. Doane, 1915 (40589) insect infestations in orchard within
smoke zone of Smelter.13
e. Henneman, 1931 (12558). Reports sick cattle near Mg factory
in AustriaJ-4
f. Brown, et al., 1935. Reports Kansas duststorm killed jack-
rabbits and birds. 1-5
g. Chemical Age. 1936. Reports cattle feeding reduced from 2
cows/acre to 1 cow/3 acres due to smoke from industrial
town.1**
h. Gregg, 1955. Reports Colorado dust storm killed hundreds of
geese and ducks, and also dead deer and antelope were found,
nostrils and windpipes clogged.^
i. Masek and Hais, 1963 (12537). Sick cattle in Czechoslovakia
due to ash and S02«1^ (See S02 for symptoms. Section 5.25)
j. Pfeffer, 1965 (11989). Reports change in rabbit blood
physiology and enzymes near power station in Czechoslovakia
with high levels of dust and SOX.19
k. Tendron, 1964. Reports deer adversely affected by cement
dust in Germany.2^
1. Darley, 1966. Reports infestation of alfalfa field by
aphids contaminated with cement dust near factory.21
Lillie, 1970. Reports drastic decrease in egg production
and death of laying hens housed near asphalt factory in
Japan. Soot was found to be toxic, poisonous constituent
unidentified.
102
m
-------
n,
Table 5.21-1 (Continued) PARTICULATES: EPISODES INVOLVING FREE-
LIVING ANIMALS
Gilbert, 1971. Smoke and S02 reduced lichens on trees, and
caused reduction of herbivores in England.22
Sierpinski, 1971 (51095). Reports pest infestation of trees23
in Poland near industry; high levels of dust, SOX, NOX, NH^.
Askew, et al., 1971. Reports industrial melanism in England
near industrialized areas with high concentrations of soot."
Lees, et al., 1973. Reports statistical correlation of
melanic moths with smoke in England.2^
Kawai, 1973 (52777). Reports correlation of oust and prolifer-
ation of Concha Vermin in urban areas of Japan. 2->
) = APTIC No.
103
-------
Particulates from industrial smoke and soot caused the reduction of
tree herbivores and the elimination of lichens in England. A shift
in melanic morphs of numerous species of insects due to changes in
selection forces has been attributed to particulate pollution (Indus-
trial Melanism).
Two incidents of natural episodes involving particulates were the
killing of large numbers of ducks, geese, jackrabbits, and even deer
and antelope by dust storms in Kansas and Colorado.
Summary of Studies on the Effect of Particulates on Experimental
Animals. Representative laboratory studies have been conducted at
levels far in excess of urban concentrations (Table 5.1!l-2). These
studies indicate slight to no effects on mammals at levels less than
2000 ug/m . Particulates do accumulate in the lungs.
Most laboratory studies conducted at levels below the urban maximum
(1254 pg/m^) on rats and mice have caused a reduction in ability to
produce antibodies and change in the area and chemistry of lung sur-
faces.2'3
Newton reports experimental exposure of bees to smoke causes be-
havioral changes in bees including increased engorging and aggression
and decrease in guarding behavior. No experimental studies were found
on the direct effects of inert particulates on birds and invertebrates,
although several episodes involved these organisms.
Suggested Biological Indicators of Particulates. The most suitable
animal biological system to monitor particulates is the pulmonary sys-
tem. Two of the diagnostic responses are pulmonary fibrosis and
phagocytosis. The primary collection site for particulates is the
respiratory passages and lungs. Along with the supporting laboratory
studies, the few reported incidents of particulate contamination have
involved contamination of the lungs.
Soiling of white or light colored animals could serve not only as a
biological indicator, but also as an aesthetic indicator. Rates and
degree of soiling might be correlated with concentrations of particu-
lates. Terrestrial animals with light colored and/or oily surfaces
could also serve as external collectors or accumulators. These indi-
cators could be site-specific indicators at zoos. Animals with highly
developed grooming, preening and other cleaning behaviors, would
accumulate particulates in the body.
104
-------
Table 5.21-2 REPRESENTATIVE STUDIES ON THE EFFECTS OF PARTICULATES ON LABORATORY ANIMALS
Suecies
A
Mice
Mice
Mice-Guinea
Pigs
B
Particulates
ua/m3
Acute Exposure
782-1554
50,000
664,000
. Chronic Exposures
Length of
Exposure
3 days
36-66 hours
6 hours
i
Observed Effect
Reduced ability to produce
Soot particles spread over
(s)
antibodies
lining of
bronchioles and alveoli, only slight
capillary congestion
No effect
Reference(s)
Zarkower &
» 26
Morges^"
Pattle S.
Burgess27
Salem & Cul-
lumbine28
DV*s*/4Ao £.
Rats
M Mice, Ham-
<-n sters, Rab-
bits, Guinea
Pigs, Mon- '
keys
Rats
Rats
Rats,
Rabbits
545
1600-2400
4000
570,000
4410 part. /cm
i 9 months
!
; Prolonged
i
i
•
! 16 days
5-165 days
80 days
Reduced lung surface area
No effect but accumulation
in phospholipids and lecithin
Did not increase susceptibility to
pneumococci infection
Lesions of non-occupational anthra-
cosis, non-reversible fibrous reac-
tion.
Knoaes a
Frazer^
NAPCA1
Rhodes
NAPCA1
Schnurer
Hay thorn
&
29
-------
Shifts in frequency of melanomorphs of insects exhibiting industrial
melanism could serve as measures of disintegrating or improving environ-
mental quality over larger geographical areas. Clark and Sheppard5
found shifts in morphs to coincide with attempts at pollution control
in England. The response time in melanic shifts may be rather quick.^
Areas of Needed Research. 1) Study effects of low l=vel particulates
on animals with high respiratory rates, especially birds, to determine
toxicities; 2) study direct effects of particulates on insects; 3) de-
termination of rates of soiling of light colored animals with concen-
tration levels and of methods of collecting of particulates from the
hair or feathers of animals; 4) determination of response times of
shifts of industrial melanomorphs with changing ambient concentrations
of particulates.
REFERENCES
1. Air Quality Criteria for Particulate Matter. National Air Pollu-
tion Control Administration Publication Number AP-049. January
1969. 180 p.
2. Rhodes, R. A. Effect of Inhaled Carbon on Surface Properties of
Rat Lung. Life Science 11:33-42, 1972.
3. Rhodes, R. A. and D. G. Frazer. Influence of Inhaled Carbon
Particulates on Pulmonary Surface Area. Proc. Soc. Exp. Biol Med.
140:1045-1048, 1972.
4. Newton, D. C. Behavioral Response of Honey Bees (Apis Mellifera
L.) To Colony Disturbance by Smoke, Acetic Acid, 1sopentyl Ace-
tate, Light, Temperature and Vibration. Illinois Univ., Urbana,
Dept of Entomology, Thesis (Ph.D.) Ann Arbor, Mich., Univ.
Microfilms, Inc., 1967, 68 p.
5. Clark, C. A. and P. M. Sheppard. A Local Survey of the Distri-
bution of Industrial Melanic Forms in the Moth Biston betularia
and Estimates of the Selective Values of these in an Industrial
Environment. Proc. R. Soc. B, 165: 424-39, 1966.
6. Askew, R. R. , L. M. Cook, and J. A. Bishop. Atmospheric Pollu-
tion and Melanic Moths in Manchester and Its Environs. J. Appl.
Ecol. 8:247-256, April 1971.
7. Lillie, R. Air Pollutants Affecting the Performance of Domestic
Animals: A Literature Review. United States Department of
Agriculture. Washington, D.C. Agriculture Handbook Number 380.
1970. p.8-10.
106
-------
8. Van den berg, W. Director, Societe de Zoologie, Antwerp,
Belgium. Letter dated 6 August 1974.
9. Gewalt. Director, Zoo Duisburg, Duisberg, Germany. Letter
dated 4 September 1974.
10. Noxious Vapors. Her Majesty's Stationery Office. London. Royal
Commission Report 614:72. 1878.
11. Oliver, T. Dust and Fume, Foes of Industrial Life. Lancet 183:
365. 1912.
12. Scientific American. Smoky Air and Animals. Vol. Ill p. 299,
1914.
13. Doane, R. W. Insect Pests in the Selby Smoke Zone. United
States Bureau of Mines. Washington, D.C. Bulletin Number 98.
1915. p. 428-450 and p. 503-520.
14. Henneman, J. Frequent Occurence of Stomach and Intestinal
Diseases in Cattle Caused by Iron Containing Flue Gases. Wien.
Tieraerztl. Monatsschr., 18(8):225-231, 1931.
15. Brown, E. G.. S. Gottlieb, and R. L. Laybam. Dust Storms and
Their Possible Effect on Health, With Special Reference to the
Dust Storms in Kansas in 1935. Pub. Health Rpts. (U.S.) 50:
1369-83, 1935.
16. Chemical Age. Smoke Abatement from the Point of View of Public
Health. 33 p. 333, 1935.
17. Gregg, R. F. Effects of Dust Storms on Wildlife, Soil Conser-
vation 20:22-23, 1954.
18. Masek, J. and K. Heis. Negative Effects of Industrial Exhala-
tions on Cattle. Vet. Med. (Prague) 8(5):341-346, 1963.
19. Pfeffer, S. The Effect of Air Polluted with SO on the Coun-
tryside. In: Preprints of Czechoslovak Reports. Internation-
al Symposium on the Control and Utilization of SO and fly-ash
from flue gases large thermal power plants. Libiice House of
Scientific Worker, 1965. p. 171-183.
20. Tendron. Effect of Pollution on Animals and Plants. European
Conference on Air Pollution. Council of Europe (Strasburg)
24 June - 1 July, 1964. p. 25-70.
21. Darley, E. F. Studies on the Effects of Cement kiln dust on
Vegetation. Jour. Air Pollut. Control Assoc. 16:145-51, 1966.
107
-------
22. Gilbert, 0. L. Some Indirect Effects oC Air Pollution on Bark-
Living Invertebrates. J Appl Ecol. 8(l):77-84, April 1971.
23. Sierpinski, Z. Secondary Noxious Insects of Pine in Stands
Growing in Areas with Industrial Air Pollution Containing Nitrogen
Compounds. Sylwan 115(10):11-18, October 1971.
Ik. Lees, R. R. , E. R. Creed, and J. G. Duckett. Atmospheric Pollu-
tion and Industrial Melanism. Hereditz (London) 30:227-32,
April 1973.
25. Kawai, S. A Study on Urban Environment and the Growth of Concha
Vermin Parasites. In: Study on Animals and Plants as Human
Environmental Indices under Urban Environments. Japan Environ-
mental Agency. March 1973. p. 18-57.
26. Zarkower, A. and W. Merges. Alteration in Antibody Response
Induced by Carbon Inhalation: A Model System. Infect. Immun.
5(6):915-920, 1972.
27. Pattle, R. F. and F. Burgess. Toxic Effect of Mixtures of Sulfur
Dioxide and Smoke with Air. J. Pathiol Bacteriol. 73:411-419,
1957.
28. Salem, H. and H. Cullumbine. Kerosene Smoke and Atmospheric
Pollutants. Arch. Envir. Health. 2:641-647, 1961.
29. Schnurer, L. and S. R. Hawthorn. The Effects of Coal Smoke of
Known Conposition on Lungs of Animals. Amer. J. Path. 13:799,
1937.
108
-------
5 - 22 Ai_^_P(^llu^tnnC: Phosphorus
Phosphorus is emitted as a result of mining activities and fertilizer
plant operation. The major types of phosphorus emissions are phosphorus
vapor, super-phosphate and other phosphorus oxides. Urban concentrations
of phosphorus as a vapor have been reported as high as 9.23 pg/m in Los
Angeles in 1959. No concentrations of phosphorus were reported in the
vicinity of industrial operations.
Summary of Symptoms of Acute and Chronic Phosphorus Poisoning. The
primary mode of intoxication is through inhalation and possibly by in-
gestion of phosphorus particulates on vegetation. The major biological
target areas for phosphorus are the respiratory and renal systems.
Acute poisoning is characterized by pulmonary edema, convulsions,
nephrosis of the kidney. Chronic poisoning results in ulceration of the
stomach, hemorrhaging of the pancreas, thymus and tubular nephrosis.
Phosphorus dust is accumulated in the lungs.•"•
Episodes Involving Phosphorus Poisoning of Free-Living Animals. None
reported.
Summary of Studies on the Effects of Phosphorus on Experimental Animals.
Detailed laboratory studies of low and chronic exposure to inorganic
phosphorus were not found.
Suggested Biological Indicators of Phosphorus. Not enough information
is available to draw conclusions as to sensitivity of species. The
lungs may be an accumulating site.
Areas of Needed Research. 1) Concentration and distribution of phos-
phorus near industrial operations; 2) studies on the effects of phos-
phorus on insects and animals with high respiratory rates, especially
birds.
REFERENCES
1. Athanassiadis, Y. C. Preliminary Air Pollution Survey of Phos-
phorus and Its Compounds, a Literature Review. National Air
Pollution Control Administration. Publication Number APTD 69-45.
October 1969. 73 p.
109
-------
5.23 Air Pollutant: Photochemical Oxidants
The main types of photochemical oxidants are ozone and peroxyacetyl
nitrate. These are produced by the action of solar energy on atmo-
spheric oxygen, NO and hydrocarbons from transportation and stationary
fuel combustion sources. Maximum natural background levels of ozone
range from 0.01 ppm to 0.05 ppm (20 to 100 ug/m ). Urban maximum
concentrations, as one-hour averages, are as high as 0.13 to 0.58 ppm
(250 to 1,140 ug/m^) with one short-term peak as high as 0.67 ppm
(1,310 pg/m ) reported.1
Summary of Symptoms of Acute and Chronic Photochemical Oxidant Poison-
ing. The mode of intoxication of animals by photochemical oxidants
is through inhalation. The primary target systems in mammals are the
pulmonary systems and eyes. Intoxication by photochemical oxidants
results in pulmonary damage such as bronchiolitis, bronchitis, emphy-
sematous and fibrotic changes in lung tissue, and eye irritation with
changes in the cornea. Photochemical oxidants are carcinogenic,
causing lung adenoma in lung-tumor-susceptible mice. Tn rabbits,
chronic exposure induces premature aging in the form of calcification
of cartilage. Another indicative response of ozone is to act as a
bacteriocide on E. coli. Photochemical oxidants also increases the
susceptibility of mammals to respiratory disease. »2'-*
Episodes Involving Photochemical Oxidants Poisoning and Contamination
of Free-Living Animals. Investigators report bark beetle infestations
in conifers, and lung edema and high incidence of lung cancer in cat-
tle, due to photochemical oxidants. A correlation has been found
between heavy oxidant pollution and blindness in bighorn sheep in
California. Incidents involving the effects of mixed pollutants in-
cluding oxidants include infestations of pest insects, reduced dragon-
fly and butterfly population, and change in liver cells of house
sparrows. An extensive study at the Philadelphia Zoo showed a high
incidence of lung cancer among wild ducks and geese kept out of
doors (Table 5.23-1).
No pattern of sensitivities can be established from these incidents
other than that both vertebrates and invertebrates respond to oxi-
dants. Invertebrates showed both positive and negative population
responses to oxidants.
Summary of Studies on the Effects of Photochemical Oxidants on
Experimental Animals. Most laboratory studies have beon conducted
at levels far exceeding the reported ambient levels (Tables 5.23-2-
3). However, studies at low and chronic levels show that photo- _
chemical oxidants as concentrations of less than 1 ppm (1960 jjg/m )
are toxic to animals. Acute exposure ( <1 ppm for A hours) results
in changes in respiratory rate and increased susceptibility to
110
-------
Table 5.23-1 PHOTOCHEMICAL OX1DANTS AND OZONE; EPISODES INVOLVING
FREE-LIVING ANIMALS
1. Known
a. Cobb, et al.. 1968 (20911). Increased infestaiion of bark
beetles in Ponderosa pine damaged trees in California.
b. Liebenow, 1971. In Germany, report lung edema and high
incidence of lung and skin cancer in cattle from areas with
high ozone levels.°
c. Light, et al., 1971. Correlation found between heavy oxidant
air pollution and totally or partially blind bighorn sheep
(Ovis canadensis nelsoni) cataracts in San Bernadino Mountains.
2. Probable or Mixed Pollutants
a. Snyder and Ralstiffe, 1966. High incidence of lung cancer in
birds and mammals, Philadelphia Zoo. High incidents in ducks and
geese exposed the longest. "
b. Wellings, 1970 (25577). Changes in liver cells of house spar-
rows in urban areas of California vs. non-urban areas.
c. Aichi Prefecte Gov., 1972 (56986). Reports reduced dragonfly
and butterfly populations in Nagoya, Japan.
d. Kawai, 1973 (52777). Increased numbers of concha vermin in
urban Japan; decrease in their natural enemies.1J
) = APTIC No.
Ill
-------
Table 5.23-2 REPRESENTATIVE STUDIES ON THE EFFECTS OF OZONE OK LABORATORY ANIMALS.
INJ
Animal
A.
Mice
Guinea Pigs
0
Guinea Pigs
Dogs, Cats
Rabbits
Rabbits
Mice
Guinea Pigs
Mice-
Hamsters
Rats
Rats
Rats
Rats
Cats
Rabbits
Guinea Pigs
Ozone,
ug/m^
Acute EXF
160
670
1330
1960
1960
1960
1960
2120
2550
3900
4880
5860
41,000
67,980
Ozone
ppm
tosures
0.08
0.34
0.68
1.00
1.00
Length of
Exposure
3 hours
2 hours
2 hours
2 hours
1 hour
j
1.00
1.00
1.08
1.30
2.00
6 hours
4 hours
Observed Effect(s)
Increased susceptibility to strep-
tococcus (Group C)
30% increase in frequency of
breathing; 20% decrease in tidal
volume
No significant increase in flow
resistance
Irritation to respiratory tract
Chemical changes in ground sub-
stance and lung protein
Fatal
Engorged blood vessels and excess
| leucocytes in lung capillaries
2 hours Increased flow resistance
3 hours i Increased susceptibility to
Klebsiella pneumoniae
3 hours Increased lung weight, decreased
tidal volume, decreased minute
. ventilation.
2.5 ' 4 hours ' No effect
3.00
21.80
Reference(s)
Athanassia-
T
dis1
1
•Hill &Flechx
Athanassia-
1 /
dis14
Dizzle &
Gage15
4 hours High Cu and Zn content and glulath- Dixon, i£
lone in lungs
3 hours
50% Mortality
34.50 ! 3 hours ; 50% Mortality
71,000 36.00 3 hours 50% Mortality
.101,370 51.70 , 3 hours 50% Mortality
. et al..-*-"
• Mittler,
et al.,17
-------
Table 5.23-2 (Continued) REPRESENTATIVE STUDIES ON THE EFFECTS OF OZONE ON LABORATORY
ANIMALS.
u>
Animal
B.
Guinea Pigs
Rabbits
Mice,
Hamsters
Mice
Mice, Rats,
Hamsters,
Pigs, Dogs
Chickens
Rats
Rats
Mice
Rats
Guinea Pigs
Mice,
Rabbits
Ozone,
Ozone
ppm
Chronic Exposures
400
800
1680
1960
1000-
4580
2000-
7900
12,000
<6000
6290
8780
9800
9800
0.2
0.4
0.84
i i.oo
t
i
1
;0.5-2.34
i
!
1-4
i
; 6.00
•
<3.00
3.20
4.5
5.00
, 5.00
•
Length of
Exposure
9 mo. contin.
6 hrs/day/5
days/week 10
months
4 hrs/5 days/
2 weeks
continuous
6 hrs/day/5
days/433 days
5 days contin
18 hours
24 hours
4 hours
4 hours
2 hours
3 hours
i
Observed Effect(s)
Death
> Serum protein esterase, emphy-
sematous and vascular lesions
present, >thickening of pulmon-
ary arteries
Reference (s)
Shrenk18
Jejier1^
Increased susceptibility to Kleb-jAthanassia-
giella pneumoniae
Bronchitis, bronchiolitis, em-
physematous and fibrotic
changes; acceleration of lung
tumor development
Bronchitis, bronchiolities; in
all species but dog mild
irritability
.50-99% mortality. LD5Q = 53.5
ppm hours
Edema
No effect
Gross pulmonary edema
Respiratory distress
Increased lung compliance,
increased susceptibility to
histamine
Decreased activity of bacterio-
cidal lysozyme.
disA
Stokinger,
et al.20
Quilligan,
- 91
et al.21
Hill &
T /.
Fleck14
Athanassia-
^
dis1
Dizzle &
1 C
Oage15
Athanassia-
1
dis1
i
-------
Table 5.23-2
(Continued) REPRESENTATIVE STUDIES ON THE EFFECTS OF OZONE ON LABORATORY
ANIMALS.
Animal
Rats
Rats
Rats
Ozone,
yig/m
13,700
19,650-
23,550
11,800
Ozone
ppm
6.00
10-12
6.00
Length of
Exposure
18 hours
Observed Effect(s)
Edema
4 hours ! LD
'
4 hours Gross pulmonary edema, increased lung
Reference(s)
Athanassia-
dis1
Dizzle &
Gage15
Athanassia-
dis1
Goats
Goats
Rabbits
Goats
Mice
Dogs, Cats
Rabbits
Rabbits,
Rats, Mice
Mice
Rats
Rats
Mice
Rats
13,760 7.00
17,660 9.25
29,400 15.00
29,400- 15-20
39,300
41,000 21.00 i
i
i
29,400- 15-20
39,300
15,700- 8-45
88 ,.000
:Stokinger22
3.5 hours . Dyspnia
3-3.5 hours Dyspnia
0.5 hours Decreased tidal volume, decreased 0^ ;Athanassia-
A A_B m •«**« #• •! *^*« Q 1_S
consumption
2 hours Death, pre-coughing, edema
3 hours 50% mortality
2 hours Death
1 hr/wk to Damage to epithelium of the lower
49 weeks ( trachea and bronchioles; fibrosis
disj
Hill &
Fleck14
Athanassia-
dis1
C. Systemic Effects. Short-term Exposures
390 i 0.20
390
1960
0.20
1.00
6100 • 3.10
7800 4.00
11,800 6.00
0.5 hour , Increased sphering of red blood cells Athanassia-
' when irradiated dis1
6 hours ' Decreased voluntary running activity ,
6 hours ' 60% increase in mortality as a result
• of exercise for 15 min/hour
20 hours > Increased liver weight; increased liver
alkaline phosphatase
4 hours Decreased mortality with age: young 50%
mortality, old 10% mortality
4 hours i Decreased brain serotinin
-------
Table 5.23-2 (Continued) REPRESENTATIVE STUDIES ON THE EFFECTS OF OZONE ON LABORATORY
ANIMALS.
Animal
Ozone I Ozone
yg/m ! ppm
Length of
Exposure
Observed Effect(s)
'Reference(s)
Mice
D. Systemic Effects. Long-term Exposures
390
0.20
5 hr/day/3 'Structural changes in heart rayocardial Ath^nassi-
weeks .fibers dis
wn
-------
Table 5.23-3
REPRESENTATIVE STUDIES ON THE EFFECTS OF PHOTOCHEMICAL OXIDANTS ON LABORATORY
ANIMALS.
Animals
Oxidant
ug/m3
Oxidant
ppm
A. Acute Exposures
Mice
Guinea pigs
Mice
> 240
650-
1610
> 780
>0.12
0.33-
0.82
>0.4
B. Chronic Exposures
Guinea pigs
Mice
Mice
> 980
1960-
7470
5488-
16,856
>0.5
1.0-3.8
Source
Irr.auto
exhaust
Irr. auto
exhaust
Smog
Smog
Ozonized
gasoline
2.8-8.6
i
PAN
Length of
Exposure
4 hours
4 hours
2-3 hours
Continu-
ous
Continu-
ous
6 hrs/day
5 days
Observed Effect(s)
Increased mortality from strep-
tococal pneumonia
Increased expiratory flow re-
sistance 20-120%; increased in-
spiratory flow resistance 40%;
decreased respiratory frequency
15-35%.
Alveolar tissue changes in ani-
mals aged 9 mos or over. In-
creased severity with age.
Damage at 9 mo. reversible, at
21 irreversible. Disruption
of epithelial walls; cytoplas-
mic fragments and proteinaceous
material in alveoli.
Increase in flow resistance (in-
crease also occurred at lower
oxidant levels)
Increased frequency of lung
tumors seen after 24 weeks.
All concentrations depressed,
voluntary running activity.
i
Reference (s)
Coffin &
1 O
Blommer^
Athanassia-
dis1
Campbell,
et al.23
-------
Table 5.23-3 (Continued) REPRESENTATIVE STUDIES ON THE EFFECTS OF PHOTOCHEMICAL OXIDANTS ON
LABORATORY ANIMALS.
Animals
Mice
Mice
Oxidant
Ug/m^
Oxidant
pom
C. Systemic Effects,
650-
1610
0.33-0.82
D. Systemic Effects,
200-
980
Mice
390-
1960
i
Mice • 590-
1960
0.1-0.5
0.2-1.0
(inlet)
0.3-1.0
Source
Short-term
Irr. auto
exhaust
Length of
Exposure
Exposures
6 hours
Long-term Exposures
Irr. auto
exhaust
Auto ex-
haust
Irr. auto
exhaust
16 hrs/
day/46
days
Continu-
ous
Observed Effect(s)
8-80% decrease in spontaneous
running activity
Decrease in fertility.
Doubling of non-pregnancy
average
Stress adaptation response,
i.e., reduction in spontaneous
running activity returning to
pre-exposure levels
16 hrs/ 1 Increased neonatal mortality
day/46 !due to preconditioning of
days
1
males
Reference(s)
Athanassia-
dis1
Athanassia-
i
dis1
i
-------
respiratory infection. Chronic exposures of less than 1 ppm, in addi-
tion to causing the acute symptoms, cause bronchitis, emphysema, lung
tumors, and depressed running activities (Table 3.23-3). Dogs are
more resistant to low chronic exposures than small rodents. At one
time ozone was used as an insecticide. It is lethal at 4 mg/1 at ex-
posures ranging from 25 seconds to 5 minutes for houseflies, honeybees,
beetles, aphids, and meal worms.^ The general class of oxidants and
hydrocarbons are important to insects. Certain types of oxidants and
hydrocarbons are known to act as attractants and repellants for insects
and other animals.5 Studies on the relationship of industrial photo-
chemical oxidants and hydrocarbons to insects do not exist. In general,
photochemical oxidants affect both vertebrates and invertebrates. The
symptoms of effect on free-living animals are similar to those found in
the laboratory due to toxic photochemical oxidant exposure.
Suggested Biological Indicators for Photochemical Oxidants. Changes in
the pulmonary system and increased frequency of respiratory infections
and cancers appear as a general class of indicator. Blindness and
other eye damage in animals might also serve as an indicator system.
Because of the relatively sensitive nature of the respiratory system,
birds and other animals may prove to be suitable biological indicators
of oxidants. Birds of prey, because of their highly developed eyes,
might prove useful indicators. The established importance of chemical
oxidants as attractants and repellants^
infestation of plants by insects in polluted situations, suggest insect
sensitivity as possible indicator systems.
Areas of Needed Research. 1) Effects of chronic levels of photo-
chemical oxidants on birds and insects with development of indicator
criteria; 2) effect of low chronic levels of oxidants on animals with
high respiratory rates; 3) relationship of photochemical oxidants and
insect attractant and repellant mechanism; 4) continued monitoring of
zoo populations as fixed indicators with studies relating concentra-
tions to disease patterns of effect; 5) effects of photochemical
oxidants and infestation of plants by insects, looking for sensitivi-
ties and synergistic effects of vegetation damage, insect damage,
oxidant levels.
REFERENCES
1. Air Quality Criteria for Photochemical Oxidants. National Air
Pollution Control Administration. Publication Number AP-63.
March 1970. 180 p.
2. Stokenger, H. E., and D. L. Coffin. Biological Effect of Air
Pollutants. In: Air Pollution. Stern, A. C. (ed.). New York.
Academic Press. 1968. Vol. 1:446-467.
118
-------
3. Coffin, D. L. and D. E. Gardner. Interaction of Biological
Agents and Chemical Air Pollutants. Ann Occup Hyg. 15:219-
235, November 1972.
4. Cory, E. N. and H. B. McDonnell. Preliminary Tests of Ozone as an
Insecticide. J. Econ. Ent. 21(3):510, 1928.
5. Eisner, T. Chemical Defense Against Predation in Anthropods.
In: Chemical Ecology, Sondheimer, E. and J. B. Simeone (eds.).
New York, Academic Press, 1970. p. 157-217.
6. Norris, D., J. E. Baker, T. K. Borg, S. M. Ferhovich, and J. M.
Rozental. An Energy-Transduction Mechanism in Chemoreception by
the Bark Beetle, Scolytus Multistriatus. Contrib. Boyce Thompson
Inst. 24(13)263-274, 1970.
7. Cobb, F. W., Jr., D. L. Wood, R. W. Stark, and J. R. Parameter, Jr.
Photochemical Oxident Injury and Bark Beetle (Coleoptera: Scoly-
tidae) Infestation of Ponderosa Pine. In: Theory on the Relation-
ships between Oxident Injury and Bark Beetle Infestation.
Hilgardic. 39(6):141-152. May 1968.
8. Lieberow, H. Bearings of Emissions on Plants and Livestock.
Moratsh. Veterinaermed, 26(3):106-111, February 1, 1971.
9. Light, J. T. Effects of Oxidant Air Pollution on the Forest
Ecosystem of the San Bernadino Mountains. In: Oxidant Air Pollu-
tion Effect on a Western Coniferous Forest Ecosystem, Task B
Report: Historical Background and Proposed Systems Study of the
San Bernadino Mountains Area. Taylor, 0. C. (ed.)- Air Pollu-
tion Research Center, University of California, Riverside. Jan.
1973. p. Bl-12.
10. Snyder, R. L. and H. L. Ratsliffe. Primary Lung Cancers in
Birds and Mammals of the Philadelphia Zoo. Zoo Cancer Res. 26:
514-518. 1966.
11. Wellings, S. R. Respiratory Damage Due to Atmospheric Pollutants
in the English Sparrow, Passerdomesticus. In: Project Clean
Air. California University, Davis., Dept. of Pathology.
Calif. Univ. Res. Proj. S-21. September 1, 1970.
12. Annual Report on the State of Environmental Pollution. Aichi
Prefectural Government. Environmental White Paper. 1972.
355 p.
13. Kawai, Shozo. A Tudy on Urban Environment and the Growth of
Concha vermin Parasites. In: Study on Animals and Plants as
Human Environmental Indices under Urban Environment. Japan
Environ. Agency, p. 18-57, March 1973.
119
-------
14. Hill, L. and M. Flack. The Physiological Influence of Ozone.
Roy. Soc. London, Proc., Ser. B., 84:404-415, 1912.
15. Diggle, W. M. and J. C. Gage. The Toxicity of Ozone in the
Presence of Oxides of Nitrogen. Brit J Ind Med. 12:60-4, 1955.
16. Dixon, J.R., W. D. Wagner and T. D. Martin. Metal Shifts as
Early Indicators of Response from Low-Grade Pulmonary Irritation.
Toxicol and Appl Pharmacol. v. 225-223. 1966.
17. Mittler, S. et al. Toxicity of Ozone. I. Acute Toxicity.
Indus Med Surg. 25:301-306, 1956.
18. Shrink, H. H. Industrial Hygiene: Toxicity of Ozone and Oxides
of Nitrogen. Ind Eng Chem. 46:111A-114A, 1954.
19. Jegier, Z. Ozone as an Atmospheric Pollutant. Can J Public
Health. 64: 161-6, March 1973.
20. Stokinger, H.E., W. D. Wagner, and 0. J. Dobrogorski. Ozone
Toxicity Studies. III. Chronic Injury to Lungs of Animals Follow-
ing Exposure at a Low Level. Arch Ind Health. 16(6):514-522,
December 1957.
21. Quilligan, J. J., Jr., R. D. Boche, H. L. Falk, and P. Koten.
The Toxicity of Ozone for Young Chicks. Arch. Indus. Health.
18:16-22, 1958.
22. Stokinger, H. E. Ozone Toxicity; a Review of the Literature
Through 1953. Arch. Indus. Hyg. Occup. Med. 9:366-383, 1954.
23. Coffin, D. L. and E. J. Blommer. Acute Toxicity of Irradiated
Auto Exhaust. Arch Environ Health. 15:36-38, 1967.
120
-------
5.24 Air Pollutant; Selenium
The primary technological sources of selenium emissions are from refin-
ing of such metals as copper, gold, nickel and silver, cumbustion of
industrial and residential fuels, and the incineration of waste products
containing selenium. Selenium occurs naturally and is accumulated by
certain plants. Detailed information on ambient concentrations of
selenium is lacking. Urban concentrations have been measured as high
as 0.06 ug/m • Certain plants grown on seleniferous soils can accumu-
late up to 10,000 ppm of selenium.1
Summary of Symptoms of Acute and Chronic Selenium Poisoning. The major
modes of intoxication are through ingestion and inhalation. The pri-
mary target areas are the central nervous system and gastrointestinal
system. Acute selenium poisoning results in abnormal movements,
diarrhea, mucous discharge, emesis, paresis and respiratory failure.
There are two degrees of chronic poisoning: subacute and chronic
poisoning (Table 5.24-1). In addition to the symptoms seen in acute
exposure, necrosis, atrophy, cirrhosis of the liver and loss of hair
occur. Selenium causes cancer of the liver and is possibly terato-
genic. The greatest accumulation of selenium is in the liver, next the
spleen, and kidneys. Prolonged exposures result in high concentrations
in keratinized tissue, such as hair and hooves.1»2»3
Episodes Involving^ Selenium Poisoning of Free-Living Animals. Although
selenium poisoning occurs from natural sources, no reported incidents
of industrial poisoning have been reported.
Summary of Studies on the Effects of Selenium on Experimental Animals.
Because of the lack of information on environmental concentrations of
selenium and reported industrial episodes, it is difficult to draw
conclusions as to the importance of laboratory responses of animals
to selenium. Concentrations greater than 5 ppm of selenium are con-
sidered harmful to livestock. Chronic seleniosis is produced experi-
mentally in animals if drinking water contains between 7 and 16 ppm
selenium. Subacute seleniosis results from drinking water between 20
and 30 ppm.
Feeds containing more than 5 ppm selenium are teratogenic to poultry.
This results in a decrease in hatchability of eggs because of
deformities of the embryos. At concentrations of 10 ppm hatchability
is zero.
Selenium has insecticidal properties, and certain species of insects
have shown sensitivities to selenium compounds, including aphids,
leaf nematodes, and certain mites. In areas with natuially high
levels of selenium, insect resistance to selenium has been found in
certain beetles and wasplike insects.3
121
-------
Table 5.24-1
SYMPTOMS AND GROSS PATHOLOGY OF CHRONIC SELENIUM POISONING IN LIVESTOCK, FROM
STAHL1
Blind Staggers
Alkali Disease
'Experimental Selenoisis
Selenium source
Symptoms
ro
K9
Gross pathology
Certain selenium "indicator"
plants
1st stage: increased desire
to eat, animal staggers; 2nd
stage: increased loss of muscu-
lar control, front legs become
very weak, does not eat or
drink; 3rd stage: paralysis,
nearly blind, abdominal pain,
body temperature drops, emancia-
tion, eyes swollen and inflamed,
cornea cloudy, death usually oc-
curs in 3rd stage.
Necrosis (with cirrhosis of
liver, nephritis (sub-acute and
chronic), enlarged gall bladder,
soft and flabby heart, impacted
intestinal tract with irrita-
tion.
Seleniferous grains
and grasses
Lameness, loss of
vitality, elongated
and hardened hoofs,
loss of hair from
mane and tail, anemia
stiffness of joints,
roughened coat.
Selenite and selenate
inorganic salts
Emanciation, some loss of
muscle control, trembling
of skeletal muscles,
anorexia.
Atrophy and cirrhosis
of liver; chronic
nephritis; soft,
flabby, and atrophied
heart; edema of
lungs.
Necrosis with occasional
cirrhosis of liver, acute
nephritis, ulceration and
gangrene of intestinal
tract.
-------
Table 5.24-2 REPRESENTATIVE LABORATORY STUDIES ON THE EFFECT OF SELENIUM ON ANIMALS
Species
~
A.
Sheep
Calf
Cattle
Horses &
Mules
Pigs
B.
Rats
Rats
Rats
Cattle
Guinea pigs
Concentration
ppm tug/kg
Acute Exposures
400-
800
600
3
3.3
1.2-2.0
Chronic Exposures
5
9
10
10-20
192
Length of
Exposure
Acute
Acute
Acute
Acute
Acute
10-30 days
10-30 days
10-30 days
7-8 wks
4-21 days
Observed Effect (s)
Acute poisoning
Lethal
Minimum lethal dose
Minimal lethal dose
Minimum lethal dose
Prevented normal growth
i
Death in young animals
Reduced food intake
Subacute poisoning: "blind staggers'
Loss of weight, anorexia, death
Reference (s)
Rosenfeld &
Beath.3
Garner
Rosenfeld &
Beath3
10
-------
Suggested Biological Indicators of Selenium. The affi-nity of the
selenium for the hepatic system and keratinized tissues, might be used
as biological monitoring system. Not enough information is available
to precisely determine the sensitivity of various vertebrates. It
would be expected, however, that wild herbivores such as deer would be
affected similarly as sensitive domestic herbivores. The teratogenic
effect of selenium poultry raises questions as to the effects on free-
living seed-eating birds.
The insecticidal properties of selenium suggest that mites, aphids,
and leaf nematodes might be used as sentinels. Beetles (bruchids) and
seed chalcids might be considered as species which might thrive under
conditions of selenium pollution. Because of the varied responses of
insects to selenium, various ecological measures, such as species rich-
ness and diversity, might also prove useful indicators.
Areas of Needed Research. 1) Studies on the concentration and distri-
bution of selenium from technological sources; 2) studies on the effects
of low and chronic exposures to selenium on insects, birds, and other
animals to determine sensitlvites and responses; 3) field studies on
responses of wildlife to selenium emissions, including studies on in-
sect population ecology and determination of diagnostic procedures for
mammals.
REFERENCES
1. Stahl, Q. R. Preliminary Air Pollution Survey of Selenium and Its
Compounds, A Literature Review. National Air Pollution Control
Administration. Publication Number 69-47. October 1969. 75 p.
2. Garner, R. J. Veterinary Toxicology. London Valliere, Tindall
and Cox. 1957. p. 42-255.
3. Rosenfeld, I. and 0. A. Beath. Selenium. New York: Academic
Press. 1964. 411 p.
4. Siegmund, 0. H. (ed.) The Merck Veterinary Manual. Rahway, N.J.,
Merch and Co., Inc. 1973. p.947-949.
124
-------
5.25 Air Pollutant: Sulfur Oxides
Sulfur oxides are common atmospheric pollutants arising mainly from com-
bustion processes. Sources of sulfur oxide include such activities as
combustion of fossil fuels, refining of petroleum, smeltering of ores
containing sulfur, manufacture of sulfuric acid, burning of refuse, and
paper-making. Mean annual urban averages have ranged from 0.01 ppm
(29 yg/m3) to 0.18 (514 yg/ra3). Higher concentrations have been re-
ported in various episodes (Table 5.25-2) although most levels are
generally below 10 ppm.l
Symptoms of Acute and Chronic Sulfur Oxide Poisoning. The mode of
intoxication by sulfur oxides is by inhalation. Theprimary target sys-
tem for SO in mammals and birds is the respiratory sys-tem and secondary
effects inXthe eyes. The symptoms of acute sulfur dioxide intoxication
include bronchial constriction, salivation, pulmonary edema, emphysema,
and hemorrhages along with change in size of gall bladder and heart.
No diagnostic symptoms have been established for chronic exposures at
low levels. SO is widely distributed throughout the body, and no
specific accumulation sites are known.
Episodes Involving Sulfur Oxide Poisoning and Contamination of Free-
Living Animals. Numerous episodes are reported involving intoxication
and other effects on animals. These reports include cattle showing
signs of emphysema, pneumonia, and reduced productivit>. Sulfur diox-
ide has caused changes in blood physiology of wild rablits. Insects
show evidence of sensitivity to SO by having reduced populations and
also of exhibiting population explosions (Table 5.25-1). The melanic
morph of Biston betularia in Manchester, England, makes up 90 percent
of the population when SO is greater than 100 ug/m (letter dated 19
July, 1974 from L. M. CooR, Dept. of Zoology, Univ. of Manchester,
Manchester, England).
The probable or mixed efforts of SO and other pollutants follows the
same pattern: sickened domestic animals and both reduction and in-
festations of various insect pests.
Summary of Studies on the Effects of Sulfur Oxides on Experimental
Animals. Acute laboratory and experimental studies (Tables 5-25^3-4)
conducted at concentrations of SO of less than 40 ppm (120 vg/m )
show animals to have some eye irritation and emphysema. Toxicities
of S00 in some insect species occur at very high concentrations.
Chronic exposure to concentrations of less than 40 ppm generally re-
sults in no effect. Only slight changes in the epithelial lining
of lungs are observed. Studies involving a combination of SO™ and
particulates generally give the same results. The results or labor-
atory studies and reported episodes do not support one another.
125
-------
Table 5.25-1 SO : EPISODES INVOLVING FREE-LIVING ANIMALS
x
1. Reported
a. Rubay, 1932 (12544). Observed subcutaneous emphysema, dyspnea, _
cyanosis, asphyxia, and increased CO. and decreased 0 in blood.
b. Masek & Hais, 1963 (12537). Observed frequent diarrhea, ^
pneumoconiosis, simplex and abortion in cattle in Czechostrava.
c. Pfeffer, 1965 (11989). Reports infestations of insects on fir
and spruce trees in air-damaged areas.-*
d. Pfeffer, 1965 (11989). Reports changes in blood composition and
chemistry of rabbits in SO area.5
e. Sierpinski, 1967 (45988). Reports 2° insect, the night moth.
exhibiting epidemic behavior in S0_-damaged trees."
f. Bassus, 1968 (24063). S0? emissions change ph of soil and
change the composition of nematode populations.
g. Przybylski, 1968 (36218). Reports reduction in bee population
around sulfur producing plant in Poland, with resulting reduc-
tion in fruit yield.8 .
h. Liebenow, 1971 (35877). Levels of S02 (0.15 mg/m ) in air re-
duced milk production 9% and fat content of milk 8% in cattle
in Germany."
i. Hilliman, 1972. Reports increase in aphids in alfalfa field ._
with high S0_ and decrease in Apidae and parasitic Hymenoptera.
j. Freitag, et al., 1973 and Freitag and Hastings, 1973. Reports
five-fold reduction in ground beetle (Carabidae) population
with increase in S0_ concentration near Kraft Mill.
k. Cook, pers. comm, 1974. Melanic form of the Peppered Moth
(Biston betularia) makes up 90% of the population of Peppered
moths when S02 concentrations are greater than 100 ug/m^.
2. Probable or Mixed Pollutants
a. Schrenk, et al., 1949 (63-Cinn). Sick and dead dogs, cats,
rabbits, poultry, and cattle from Donora, Penn., with high
levels of SO anil other pollutants (NO, Pb).12
b. Wentzel & Ohnesorge, 1961 (48393). Report heavy infestation
of spruce trees by sawfly in areas with S0? and smoke at
levels below vegetation damage. •*
"c. Parliceric, 1962. Reports catarrhal bronchitis in sheep in
areas with high SO and Pb.1*
d. Sierpinski, 1967 (55988). Reduction of large pine sawfly
larvae infestation in areas of highest S02 levels.^
e. Gilbert, 1971. With reduction of lichens by smoke and S02>
reduced bark lice populations.1
126
-------
Table 5.25-1 (ConLinued) SO : EPISODES INVOLVING FREE-LIVING
X ANIMALS
2. Probable or Mixed Pollutants (Continued)
f. Pfeffer, 1971 (57486). SO and F found to cause increase in
several groups of forest pest insects, including Homoptera,
Heteroptera, Coleoptera, Lepidoptera, Hymenoptera, and
Orthoptera.17
g. Sierpinsky, 1971 (51095). Infestation of air pollution-
damaged trees in Poland (see NO
Berge, 1973. Heavy infestation of tree lice ai:d mealy bugs in
areas contaminated by SO- and HF but without observable tree
damage. Some species appear sensitive (spider mite). 19
Lees, Creed, and Duchett, 1973. Industrial melanism in several
moth species; Bis ton correlated with S0_.20
) = APTIC No.
127
-------
Table 5.25-2 MAXIMUM CONCENTRATIONS OF SO DURING SPECIFIC AIR
POLLUTION EPISODES 2
Location
New York, Thanksgiving, 1966
London. 1952
Australian Copper Smelter
Norwegian Pulp Mill
Iranian Oil Refinery
Concentration
ppra
1.02
13.5
2-37
up to
100
. 3
mg/m
2.9
4.0
38.6
5.7-102.9
286
128
-------
Table 5.25-3 REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF S0x ON ANIMALS.
NJ
VO
Species
Cone. ';
Dom !
Cone,.
me/m
A. Acute Exposures
Swine
Guinea pigs ;
Mice
Mice
Guinea pigs
Sitophilus
granorius
5-40 '
130
150
1000
1000
1995
Cimex lee- j 2065
tularis
Tribalium : 2100
confusum
Syrian | 3250
hamster
Sitophilus 5600
oryzea
13-114
f\
370 mg/m
430
1 2800
2800
i 5700
t
'' 5900
6000
i
| 9300
1
! 17,000
Length of
exposure
8 hours
154 hours
|
847 hours
i
i
4 hours
20 hours
5 hours
i
5 hours
Observed Effect(s) Reference (s)
Slight eye irritation and salivation
at 5 ppm >at > levels; hemmorhage and
emphysema within 24 hours at 40 ppm.
LD . Symptoms at high concentra-
tions: coughing, moderate dyspnea,
thinitis, lachrynation, conjuncti-
vitis, abdominal distention,
lethargy, weakness, paralysis of
hind quarters, visceral congestion,
pulmonary edema, distention of gall
bladder and stomach, hemmorhage of
O'Donoghue &
tn
Graesser'1"
Setter^.
Strom
lung and stomach.
LD _. Same symptoms as above
LD _. Same symptoms as above.
LD ?. Same symptoms as above.
LC^° at 25° C.
jU
LC at 25° C.
Weed on, ^o
et al.
23
Negherborn
[
5 hours ' LC5Q at 20° C.
•1.5 hours ' LD_0 within 24 hours
5 hours , LC5Q at 25° C.
Goldrine. et
et al.24
23
Negherborn
'
-------
Table 5.25-3 (Continued) REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF S0x ON ANIMALS
OJ
o
Cone.
Species ppm
Cone. Length of
ma/m3 F.vnosure '. Observed Effect(s) Reference (s)
B. Chronic Exposures
,
White rats j .3 to 70
i
i
Dogs ! 4.5
Rats
Rats
Rabbits
Rats
Hampster
10
40
140
300-
400
650
0.1-20 i 4 hrs/day for
13.4
30
1, 114, 144,
& 165 days
21 hrs/day/
620 days
6 hrs/5 days
+ 3 hrs Satur/
18-67 days
i
114 5 hrs/5 days
400
900-
1100
1850
for 3 months
6 hrs/4 days
same as above
75 days
1 25
blood
ascorbic acid.
> number of mucus-secreting cells;
< ciliary activity
no significant histophathological
changes in lung.
* 29
An
28
Reid
Goldring,
et al.24
-------
Table 5.25-4
REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF H0SO, MIST ON ANIMALS
2 4
Species
Guinea pigs
1-2 months
Guinea pigs
18 months
Guinea pigs
200-250 gm
Guinea pigs,
200-250 gm
Guinea pigs ,
200-250 gra
Cone.
ppm
Cone.
mg/m
18
50
27
! 60
i
i
Length of
Exposure
8 hours
8 hours
8 hours
8 hours
Observed Effect(s)
LC,.g. H.SO. promotes laryngeal and
bronchial and parenchymal lung damage.
LC50
LC... Large particles
Ref erence(s)
. . ,30
Amdur , et al.
Pattle, et al.
LC _. Small particles !
47 •' 8 hours LC,.-. Small particles at 0° C.
i '
Guinea pigs
Mice
Rats
Rabbits
22.1 89
140 561
178 714
296 1186
2.75 hours Killed. Degenerated epithelium of j Treon, et al.
respiratory tract, pulmonary hyper- {
mimo, edema, emphysema, alelectosis,
and sometimes local pulmonary hemmor-
' hages.
3.5 hours Same as above
7 hours Same as above
103 hours Same as above
32
-------
Suggested Biological Indicators of Sulfur Oxides. The respiratory sys-
tem is the key system to monitor, although the responses are non-
specific. S0_ is present in respiratory tissue for a short time after
exposure. This fact, coupled with physiological response, might be
used to develop diagnostic criteria.
No particular species can be suggested as a good indicator because of
the lack of studies. Some mammals are more sensitive than others but
the number of species studied is small. Industrial melanism in Biston
betularia is correlated with SO levels. Shifts in frequency of
melanic forms might be a measure of environmental quality over geo-
graphical areas for some species like the Peppered Moth (Biston
betularia). For other melanics the selective agents are not suffi-
ciently understood (Cook, pers. comm.).
Areas of Needed Research. 1) Studies on the effects of chronic expo-
sure to low concentrations of SO on animals with high respiratory
rates, especially birds; 2) studies to determine sensitivities of
animals to SO ; 3) studies on the effects of SO on insect populations,
considering pest and nonpest types; 4) further studies on industrial
melanism in Biston betularia and S0_ concentration.
REFERENCES
1. Air Quality Criteria for Sulphur Oxides. National Air Pollution
Control Administration. Publication Number AP-50. April 1970.
178 p.
2. Lees, D. R., E. R. Creed, and J. G. Duckett. Atmospheric Pollu-
tion and Industrial Melanism. Hereditz (London) 30227-32,
April 1973.
3. Rubay, M. About the Fog Observed in the Mense Valley in December
1930 and Its Noxious Effects on Animals. Ann. Med. Vet. 77:
145-158. April 1932.
4. Masek, J. and K. Hais. Negative Effects of Industrial Exhalations
on Cattle. Vet Med. 8(5):341-346, 1963.
5. Pfeffer, A. The Effect of Air Polluted with SO on the Country-
side. In: Preprints of the Czechoslovak Reports. International
Symposium on the Control and Utilization of SO. and Fly-Ash from
the Flue Gases of Large Thermal Power Plants. Liblace House of
Scientific Workers, p. 171-183. 1965.
132
-------
6. Sierpinski, Z. Influence of Industrial Air Pollutants on the
Population Dynamics of Some Primary Pine Pests. International
Union of Forest Research Organization, Vienna (Austria),
Proc. Congr. Intern. Union Forest Research Organization, 14th
Munich, West Germany 5(24):518-531, 1967.
7. Bassus, W. On the Effects of Industrial Emissions on the Popula-
tion of Nematodes in the Soil of Pine Forests. Redbiol.
(Germany) 8:289-295, 1968.
8. Przybylski, Z. Result of Consecutive Observation:? of Effects of
SO , SO , and H SO Gases and Vapors on Trees, Shrubs, and Entomo-
fauna of Orchards in the Vicinity of Sulfur Mines and Sulfur
Processing Plants in Machow. [In Polish]. Postepy Nauk Roln.
(Warsaw), 15(6):131-138, 1968.
9. Liebenow, H. Bearings of Emissions on Plants and Livestock.
Monatsh. Veterinaermed., 26(3):106-111, Feb. 1, 1971.
10. Hilliman, R. C. Biological Effects of Air Pollution on Insects,
Emphasizing the Reactions of the Honey Bee. (Apis Mellifera L.)
to SO . Penn State Univ., Univ. Park,Dept. of Entomology thesis,
(Ph.D.), Ann Arbor, Mich. Univ. Microfilms, Inc. p. 5-44,
March 1972.
11. Freitag, R. L., L. Hastings, W. R. Mercer, and A. Smith.
Ground Beetle Populations Near a Kraft Mill. Can. Ent. 105:
299-310, 1973.
12. Schrenk, H. H., H. Heiman, G. D. Clayton, W. M. Gafafer, and H.
Wexler. Air Pollution in Donora, Pa. Federal Security Agency,
Public Health Service, Division of Industrial Hygiene, Washington
D.C., Public Health Bull. No. 3066,1949. 173 p.
13. Wentzel, K. F. and B. 0. Ohnesorge. Occurance of Insect Pests
with Air Pollution. Forstarchiv 32:177-186, 1961.
14. Porliceric, M. The Occurance of Lethal Paralysis in Young
Sheep as a Result of Poisoning from Factory Smoke. Vet. Glas.
2:1085-1088, 1962.
15. Sierpinski, Z. Influence of Industrial Air Pollution on Popula-
tion Dynamics of Some Primary Scotch Pine Pests. Inter. Union
Forest Res. Org. (IUFRD Congress) Proc. 14 (vol. 3 sect. 24):
518:531, 1967.
16. Gilbert, 0. L. Some Indirect Effects of Air Pollution on Bark
Living Invertebrates. J. Appl. Ecol. 8(1)77-84, 1971.
133
-------
17. Pfeffer, A. Insects as Bioindicators. Ustav Krajinne Ekologie
Czav, Bioendikatory Deteriorizace Krajiny, Sbornek Z. Mezin-
arodne Konference, Prague, Czechoslovakia, 1971. p. 83-85.
18. Sierpinski, Z. Secondary Noxious Insects of Pine in Stands
Growing in Areas with Industrial Air Pollution Containing Nitrogen
Compounds. Sylwan 115(10):11-18, Oct. 1971.
19. Berge, H. Relationship between Tree Pests and Inunission. Amz.
Schaedlingskunde. 46:155-156, 1973.
20. O'Donoghue, J. G., and Graesser, F. E. Effects oJf Sulphur
Dioxide on Guinea Pigs and Swine. Canad Jour Compar Med and
Vet. 26:255-263, 1962.
21. Setterstrom, C. Effects of Sulphur Dioxide on Plants and
Animals. Ind Eng Chem 32:478-479, 1940.
22. Weedon, F. R. , Hartzell, A., and Setterstrom, C. Toxicity of
Ammonia, Chlorine, Hydrogen Cyanide, Hydrogen Sulphide, and
Sulphur Dioxide Gases. V. Animals. Contrib Boyce Thompson
Institute. 11:365-385, October-December 1940.
23. Negherborn, W. 0. Insecticides; a Compendium. In: Handbook of
Toxicology, Volume 3: National Academy of Sciences. Philadelphia.
W. B. Saunders. 1959.
24. Goldring, I. P., Cooper, P., Ratner, I.M., and Greenburgh, L.
Pulmonary Effects of Sulfur Dioxide Exposure in the Syrian
Hamster. Arch Environ Health. 15:167-176, 1967.
25. Lobova, E. K. Effect of Low So Concentrations on the Organism
of Animals. In: VOPr. Gigieny Atmosf. Vozdukha. L. 14-24.
1959; and Effect of Low Sulfur Dioxide Concentration on the
Animal Organism. U.S.S.R. Lit. Ait Pollut. and Rolat. Occup
Dis. 8:79-89, 1963.
26. Lewis, T. R., W. J. Morrman, W. F. Ludmann, and K. I. Campbell.
Toxicity of Long Term Exposure to Oxides of Sulfur. Arch
Environ Health. 26:16-21, January 1973.
27. Dalhamn, T. and J. Rhodin. Mucous Flow and Ciliary Activity in
the Trachea of Rats Exposed to Pulmonary Irritants. Brit J
Ind Med. 13:110-3, 1956.
28. Reid, L. An Experimental Study of Hypersecretion of Mucus in
the Bronchial Tree. Brit. J. Exp. Pathol. 44:437-445, Aug. 1963.
134
-------
29. An, A. S. Effect of Sulfur Dioxide on Vitamin C Balance in the
Animal Organism. Gigiena i Sanitariya 25(3):34-40, 1960.
30. Amdur, M. 0., Schulz, R. Z., and Drinker, P. Toxicity of Sulfuric
Acid Mist to Guinea Pigs. A.M.A. Arch Ind Hyg Occup Med. 5:
318-329, April 1952.
31. Pattle, R. E., F. Burgess, and H. Cullurabine. The Effects of
Cold Environment and of Ammonia on the Toxicity of Sulphuric Acid
Mist to Guinea Pigs. J Pathol Bacteriol. 72:219-232, July 1956.
32. Treon, J. F., F. R. Dutra, J. S. Cappel, J. Sigmon, W. Younker.
Toxicity of Sulfuric Acid Mist. Arch Ind. Hyg. Occup Med. 2:
716-734, 1950.
•135
-------
5.26 Air Pollutant; Vanadium
Vanadium as an air pollutant is found as V 0 and V 0-. The technologi-
cal sources of vanadium result from uranium ore mining and its use as
an oil catalyst. Concentrations of vanadium from industrial sources
are not reported* Non-urban concentrations of vanadium has ranged from
0.0 to 0.18 ug/m .! Maximum urban concentrations in New York City have
been as high as 9.98 ug/m3.
Summary of Symptoms of Acute and Chronic Vanadium Poisoning. The
primary mode of vanadium intoxication is through inhalation. The major
biological target systems are the circulatory and pulmonary systems.
Symptoms of acute exposure to vanadium include hypochronic anemia and
decreased leucocytes, congestion of liver and lungs, and degeneration
of the kidneys. Chronic symptoms include, along with acute symptoms,
suppurative bronchitis, bronchitis, pulmonary emphysema, pulmonary
cellular dust and changes in the kidney. Greatest accumulations of
vanadium are in the kidney, followed by the liver and spleen.-*
Episodes Involving Vanadium Poisoning of Free-Living Animals. Only
one study has been reported involving vanadium toxicity on free-
living animals. This occurred among cattle grazing in areas exposed to
fuel oil soot high in vanadiam (Table 5.26-1).
Summary of Studies on the Effects of Vanadium on Experimental Animals.
Few studies have been made, and these have been conducted at high con-
centrations (Table 5.26-2).
REFERENCES
1. EPA 1973.
2. Athanassiadis, Y. C. Preliminary Air Pollution Survey of Vanad-
ium and Its Compounds, a Literature Review. National Air Pollu-
tion Control Administration. Publication Number APTD 69-48.
October 1969. 91 p.
3. Lillie, R. J. Air Pollutants Affecting the Performance of
Domestic Animals, a Literature Review. United States Department
of Agriculture, Agriculture Research Service. Agriculture
Handbook Number 380. August 1970. p. 98-99.
4. Stokinger, H. E. Vanadium. In Industrial Hygiene and Toxicology,
F. A. Patty (ed.). New York: Interscience Publishers.
136
-------
Table 5.26-1 VANADIUM: EPISODES INVOLVING FREE-LIVING ANIMALS
1. Known
a. Lillie, 1970. Reports weakness and ataxia in cattle grazing
in area exposed to fuel oil soot. Hematological findings
revealed vanadium toxicity, high levels in the liver (1.5-24
ppm) and kidneys (3-4.7 pptn).^
2. Possible or Mixed Pollutants
a. None reported.
137
-------
Table 5.26-2 REPRESENTATIVE LABORATORY STUDIES ON THE EFFECTS OF VANADIUM ON ANIMALS.
U)
00
Species
Rabbits,
Rats
Cone.
ppra
Rats 100
Rats
Cone.
other
40,00^-70,000
Ug/m
23,000 ug/kg
body weight
56,000 ug/kg
body weight
1000 ;
• i
Length of
Exposure
9-12 months
t
|
1
Observed Effect(s)
Hypochronic anemia, change in ;
body chemistry and respiratory
malfunction, V 0 3 to 5 times
as toxic.
MLD of V205
MLD of V203
V 0 toxic in suboptimum diet
V 0 toxic in optimal diet
Reference (s)
2
Athanassiadis
4
Stokinger
-------
5.27 Air Pollutant: Zinc
The primary form of zinc emission is zinc oxide resulting from smelting
operations, especially copper and brass production. Average urban
concentrations are reported as 0.67 yg/m . Maximum urban concentra-
tions are reported as high as 58 Mg/m . 1 Industrial concentrations
are much higher. Concentrations of 9000 ppm dry weight were found on
tree leaves in England.2 Zinc concentrations in Montana soils near
smelting operations ranged up to 5200 ppm dry weight. Pasture grasses
had up to 232 ppm wet weight.-*
Summary of Symptoms of Acute and Chronic Zinc Poisoning. The major
mode of zinc intoxication is by ingestion. The primary target system
is the gastrointestinal system. Acute poisoning results in violent
vomiting, abdominal pain, dypspnea, anorexia, subcutaneous emphysema
of neck and chest. Chronic poisoning causes a variety of symptoms, -
including constipation, and arthritis. Zinc is stored in the liver.
Episodes Involving Zinc Poisoning of Free-Living Animals. No defini-
tive reports wete found. One episode involving zinc, lead, and
sulfuric acid caused spotted teeth and decreased milk production in
cattle. (See Leibetseder in Section 5.15 on Lead.)
Summary of Studies on the Effects of Zinc on Experimental Animals.
Laboratory studies have been conducted at very high and acute concen-
trations (Table 5.27-1). These studies indicate very high concentra-
tions are required for intoxication of rodents and rabbits. Generally
zinc is found in combination with other metals, like lead. Based on
laboratory studies the adverse effects observed in these situations
are due to pollutants other than zinc.
Suggested Biological Indicators of Zinc. The liver is a possible
accumulating site for monitoring zinc ingestion. Exposure by inhala-
tion can be monitored by concentrations in the lung. Due to the lack
of low and chronic studies on animals further suggestions on monitor-
ing systems are impossible.
Areas of Needed Research. Studies on the effects of low and chronic
exposure of zinc on animals including birds, insects and other
animals with high respiration rates.
139
-------
Table 5.27-1
REPRESENTATIVE LABORATORY STUDIES ON THE
ANIMALS FROM ATHANASSIADIS1
EFFECTS OF ZINC COMPOUNDS ON
Species
Rats
Guinea Pigs
Dogs, Cats
Rats
Rats
Rats
Rabbit
Rabbit
Compound
ZnO
ZnNH.SO.
4 4
ZnO
zinc acetate
zinc phos-
phide
zinc carbon-
ate
zinc diathvl-
dithiocar - i
Concentration
ug/rn3
400 to 600
1000
175,000 to
1,000,000
yg/kg
10,000 to
15,000
46,700
500,000 to
500,000
600,000
bamate
zinc acetate 976,000 to
I 1,966,000
Exposure
Inhalation
10-120 min.
60
3 to 53 wks
Ingestion
4 months
acute
daily (?)
acute
Effects
Death to some rats; fall in
body temperature; high
levels in lung
Increased pulmonary resis-
tance
Tolerated but produced
glycosuria in dogs; and
pancreatic degeneration
in some cats
No intoxication
LD50
Change in liver enzymes
"so
1
acute • LD_n
Rabbit
Rat
zinc sulfate
zinc sulfate
lapprox.
I 2,100,000
'. 2,200,000
acute
acute
LD
LD
-------
REFERENCES
1. Athanassiades, Y. C. Preliminary Air Pollution Survey of Zinc and
its Compounds, A Literature Review. National Air Pollution Control
Administration Number APTD 69-49. October 1969. 49 p.
2. Lillie, P. A Study of Heavy Metal Contamination of Leaf Surfaces.
Environ. Pollut. 5:159-172, 1973.
3. Miesch, A. T. and C. Huffman, Jr. Abundance and Distribution of
Lead, Zinc, Cadmium, and Arsenic in Soils. In Helena Valley,
Montana, Area Environmental Pollution Study. Research Triangle
Park, N.C. Environmental Protection Agency. 1972. p. 65-81.
141
-------
6. ZOO SURVEY
A survey of the major world zoos was made to determine if these facili-
ties had observed any incidents of animals being affected by air pollu-
tion (Table 6.1). This survey was undertaken after Bazell^ and Snyder
and Ratsliffe2 reported zoo animals dying of lead poisoning and lung
cancer resulting from air pollution. Zoos would appear as potential
biological monitoring sites because they are often located in the urban
areas. They contain a wide variety of species which are cared for
and whose health is monitored.
Inquiries were sent to 340 world zoos registered in the International
Zoo Yearbook. Eighty-four were in the United States and the rest were
from other parts of the world, including Africa, Republic of China,
and Russia. Information was requested on any known incidents of ani-
mals being affected by air pollution including possible secondary ef-
fects, such as high incidents of respiratory disease.
The returns on the inquiries were low, with only 66 zoos reporting.
Of the reporting zoos 25 were in the U.S. Only eight zoos (3 U.S.,
4 European and 1 Australian) reported definite incidents attributable
to air pollution. Lead poisoning was observed to occur in a high in-
cidence of animals kept out-of-doors in the Staten Island Zoo. The
principal animals affected were leopards, cats, and primates.1 Snyder
and Ratsliffe^ reported higher incidents of lung cancer in birds and
mammals kept out-of-doors than other animals. Snyder (pers. comm.)
indicates lung cancer was associated with animal species with be-
haviors which would bring them into greater contact with pollution
than other animals. In particular, racoon-like animals or those with
noses close to the ground, developed malignant tissue tumors in the
nose (neuralepitheloma). Ducks like Redheads and Shovelers, which
feed on the bottom and the surface of ponds developed cancer, while
other species did not. Snyder reports that since 1966 they have no
incidents of cancer in ducks and, coincidentally, they have no Red-
heads or Shovelers in captivity since then.
Pinnepeds, in particular seals and sea lions from the Detroit Zoo
which were kept in a pool adjacent to a highway (300 feet away) died
of lead poisoning. Sea lions kept in the other pools further away
from the traffic had no accumulations (letter dated 21 August,
1974 from K. K. Kreog, Zoological General Curator, Detroit Zoological
Park, Detroit, Michigan).
A fourth incident was reported from Jungle Larry's Safari in Cedar
Point, Ohio (letter dated 4 August, 1974 from L. E. Tetzloff, Jungle
Larry's Safari, Cedar Point, Ohio). He reported that his monkeys,
birds and chimps start coughing when he takes them to a TV studio
near Cleveland, Ohio.
142
-------
The Soctete Royal de Zoologie, Antwerp, Belgium, reports lunganthracio-
sis in unspecified animals. The intensity of the disease is dependent
upon the length of captivity (letter dated 6 August, 1974, W. Vanden-
bergh, Director, Societe Royale de Zoologie, Antwerp, Helgium). Some
lunganthracicosis was found in primates kept in Melbourne zoo (letter
dated 9 August, 1974, J. H. Sullivan, Director, Melbourne Zoological
Gardens, Victoria, Australia). Soiling of white colored animals,
especially white llamas and storks, is common in the Ruhr-Valley zoo
at Dusburg, Germany (letter dated 4 September, 1974, Dr. Gewalt,
Zoo Duisburg, Germany). Dr. Gewalt reports frequent occurrence of
lunganthraciosis found in cattle from the same region. Anthracosis was
found to occur in animals from the Prague and Barcellona zoos.
The low number of responses may be due partly to incorrect or incom-
plete addresses. A number of letters were returned for these reasons.
The low number of reported incidents is not a true indication of the
sensitivities of zoo populations. No attempt was made to select zoos
in cities with heavy air pollution. A number of respondents (19/60)
said their zoos did not occur in polluted environments. A nearly
equal number of respondents (13/60) indicated they did not carry out
studies which would detect effects of air pollutants. Seven zoos
indicated they did some studies. In the United States only three
zoos do extensive autopsies and examination of all their animals.
They are the Philadelphia Zoo, National Zoo in Washington, D.C., and
the San Diego Zoo.
Conclusions and Recommendations
The few positive responses indicate zoo animals are affected by air
pollution and can act as biological monitors. Besides acting as
sentinals or early warning devices they can be used as a measure of
environmental quality and a measure of effectiveness of environmental
control attempts for urban areas. In particular, they could be indi-
cators of trends of environmental quality, especially for hitman
health. However, a monitoring system should be established to stand-
ardize the collecting of monitoring data. Certain biological monitor-
ing zoos should be designated. Choice would depend upon geographical
location and demographical criteria and existing environmental quality.
Standard diagnostic methods should be established for particular
pollutants. Similar or nearly similar species should be designated
as bioassay monitors. Besides monitoring health or condition of
particular species, records ought to be kept on mortality and mor-
bidity rates of zoo animals. These would be useful in determining
trends and additional species which might serve as monitors. This
information might lead to monitoring of free-living counterparts.
A system of environmental monitoring zoos should be established in
143
-------
the U.S. With existing zoological societies an international monitoring
system could be developed. In addition, many zoos are found within
botanical gardens and parks. Besides potential plant indicators plant-
insect-pollution relationships could be monitored.
REFERENCES
1. Bazell, R. J. Lead Poisoning: Zoo Animals may be First Victims.
Science 173(3992):130-131, 1971.
2. Snyder, R.L. and H. L. Ratsliffe. Primary Lung Careers in Birds
and Mammals of the Philadelphia Zoo. Zoo. Cancer Res. 26:514-518,
1966.
3. International Zoo Yearbook 1973. Duplay, H.N. (ed.) London.
Zoological Society of London. 1973.
-------
Table 6.1 RESULTS OF SURVEY OF WORLD ZOOS ON THE EFFECTS OF AIR
POLLUTION ON AMIMALS
Zoo and
Location
Zoological Gardens
Pert, Australia
Zoological Board
of Victoria, Vic-
toria, Australia
Royal Zoological
Soc. of So. Aus-
tralia, Adelaide,
Australia
Salzburger Tier-
garten Hellbrunn
Salzburg, Austria
Socle te Royal De
Zoologie, Antwerp,
Belgium
Jarden Zoolo-
gique, Orsain-
ville, Ontario,
Canada
Jarden Zoologies
Viejo, Chile
Parque Zoologico
Santa Fe Sociedad
De Mejoras Publi-
cas, Medellin,
Columbia
Severoceska Zool-
oglcka Zehrada,
Liberec,
Czechoslovakia
Zoologicka Zah-
rada, Praha,
Pollution
Effects
Yes
?
X
No
X
X
X
X
X
X
X
,
X
i
Czechoslovakia
'
Effects
some anthracosis
noted in primates
decrease in Swallows
due to poisoning of
insects
lunganthracosis in an-
imals, intensity re-
lated to captivity
not in pollution zone
Moni
Yes
X
tor
No
?
?
?
?
7
?
{
some anthracosis in
old aninals. Giraffe
and Wildhorse.2 Para-
keets killed 6 hours
1
X
1
1
j
i
•
Other
Comment
little pollu-
tion in city
little pollu-
tion near zoo
industrial
city
clean envi-
ronment
industrial
area
little pol-
lution
145
-------
Table 6.1 (Continued) RESULTS OF SURVEY OF WORLD ZOOS ON THE EFFECTS
OF AIR POLLUTION ON ANIMALS
Zoo and
Location
Zoologlcka Zah-
rada, Praha,
Czechoslovakia
(continued)
Zoological Society
Briston, England
Zoological Soc. of
London, London,
England
Pare Zoologique,
Paris France
Tierpark Hella
Brunn, Munich,
Germany
Zoologicher Garten,
Frankfurst, Germ-
any
Zoo Duisburg,
Duisburg, Germany
Krefelder Zoo
Krefeld, Germany
Zoologischer Gar-
ten, Wuppertal,
Germany
Pollut
Effec
Yes
?
X
7
Burgers Zoo, •
Arnheim, Holland
i
Royal Rotterdam
Zoological & Bo-
tanical Garden,
:ion
:ts
No
X
X
X
X
X
Effects
after 30 min. expo-
sure to asphalt smoke
from source 200
meters.
none observed during
"London Fog"
white animals soiled
(llamas, storks)
incident of unfertil-
ized eggs of fish
eating birds
.
Moni
Yes
tor
No
Other
Comment
i
No informa-
tion
x observed recent
• bats in cen-
, ter of Lon-
X
x
don
not in city
located in
city
1
x polluted re-
gion; cattle
; from area
have black
. lungs
i
:
x not in pollution zone
source of
problem un-
known
! ' !
X
1
X
1 !
Rotterdam, Hoi.
146
-------
Table 6.1 (Continued) RESULTS OF SURVEY OF WORLD ZOOS ON THE
EFFECTS OF AIR POLLUTION ON ANIMALS
Zoo and
Location
Natura Artis Magis-
tra, Koopermans-
bank, Holland
Dierenpark Wassen-
aar Zoo, Wassenar,
Holland
Peshav Park Zoo,
Poona, India
Belfast Zoological
Gardens, Belfast,
No. Ireland
Biblical Zoo, Jer-
usalem, Israel
Zoological Garden
Soc., Tel-Aviv,
Israel
Giardino Zoologi-
ca, Rome, Italy
Aberdeen Zoo, Ab-
erdeen, Scotland
Scottish National
Zoological Park,
Royal Zoological
Soc. of Scotland,
Edinburg, Scot-
land.
Calderpark Zoo
Glasgow, Scotland
National Zoologi-
ollution
Effects
es No
cal Gardens,
Pretoria, South
Africa
X
X
X
X
X
X
X
X
X
X
1 ;
Effects
not in pollution zone
not in pollution zone
no pollution in area
Moni
Yes
?
tor
No
X
?
?
i
i
?
Other
Comment
do post-
mortems
little air
pollution
'
1
l
147
-------
Table 6.1 (Continued) RESULTS OF SURVEY OF WORLD ZOOS ON THE
EFFECTS OF AIR POLLUTION ON ANIMALS
Zoo and
Location
Parque Zoologico
Barcelona, Spain
National Zoologi-
cal Gardens of
Sri Lanka, Deli-
wala, Sri Lanka
Kolmardens Djur-
park, Kolmorden,
Sweden
Zoo ZUrich, Zlir-
ich, Switzerland
SjBfartsmuseet
Akvarium, GBte-
borg, Sweden
Aksel Aland,
Izmir, Turkey
Zoological Parks
Caracas, Vene-
zuela
Institut des Jar-
dins, Zooloique
et Botanique,
Kinshasa, Zaire
United States
Birmingham Zoo
Birmingham, Ala.
Arizona-Sonora
Desert, Tucson,
Pollu
Effe
Yes
X
i
tion
cts
No
X
X
X
X
X
X
X
:
Effects
anthracosis in some
animals
slight elevation in
Pb levels in Blue-
berry wires in a
Safaripark compared
to deep forested
region
fish are dying
dogs killed near
bullet producing
factory
x not in pollution zone
X
!
Monitor
Yes No
,
9
X
X
9
some
Arizona '
9
,
Other
Comment
forested
area
148
-------
Table 6.1 (Continued) RESULTS OF SURVEY OF WORLD ZOOS ON THE
EFFECTS OF AIR POLLUTION ON ANIMALS
Zoo and
Location
San Diego Zoologi-
cal Garden, San
Diego, Ca.
San Francisco Zo-
ological Gardens,
San Francisco, Ca.
Denver Zoological
Foundation, Denver,
Colorado
Cheyenne Mountain
Zoological Park;
Colorado Springs,
Co.
Pollution
Effects
fes No
Jacksonville Zo- !
ological Soc. and !
Park, Jacksonville,
Fl.
Busch Gardens,
Tampa, Fl.
National Zoologi-
cal Park, Wash-
ington, D.C.
Atlanta Zoologi-
cal Park, Atlanta,
Ga.
Indianapolis Zo-
ological Soc. ,
Indianapolis, In.
Zoological Park
Commission, De-
troit, Mi.
St. Paul's Corao
X
X
X
X
X
X
X
; | X
! 1 X
Effects
some long pigmentation
not in pollution zone
not in polluted area
snakes killed by gas
fumes
not in polluted area
i !
X
1
1
1
pinnepeds in pool
near highway died
of Pb poison
x
Zoo, St. Paul, :
Mn. i . |
Kamper Park, x
Hattiesburg, ' ;
Monit
Yes |
x
some
?
some
:or
No
7
?
7
7
?
x
•
f
Other
Comment
Mass.
149
-------
Table 6.1 (Continued) RESULTS OF SURVEY OF WORLD ZOOS ON THE
EFFECTS OF AIR POLLUTION ON ANIMALS
Zoo and
Location
Kansas City Zoo,
Kansas City, Mo.
Buffalo Zoologi-
cal Gardesn,
Buffalo, N.Y.
Staten Island
Zoo, New York,
N.Y.
Cleveland Zoologi-
cal Soc. , Cleve-
land, Ohio.
Jungle Larry's Af-
frican Safari,
Sandusky, Ohio
Philadelphia Zoo,
Philadelphia, PA
Fort Worth Zo-
ological Park,
Fort Worth, Texas
San Antonio Zo-
ological Gardens
and Aquarium,
San Antonio Texas
Lafayette Park v
Zoo, Norfolk, VA.
Pollu
Effe
Yes
?
x
tion
cts
No
x
X
X
X
X
X
X
Effects
not in polluted area
lead poisoning in leo-
pards, high levels in
other cats and pri-
mates
animals including mon-
keys cough on way to
Cleveland
high incidence of can-
cer in ducks and ra-
Moni
Yes
7
?
x
coon-like animals
jungle snakes sensi- '
tive to dust '
i
tor
No
x
X
Woodland Park and x ! x
Zoological Gar-
dens, Seattle, WA | ,
Milwaukee County ' j x , x
Zoologicak Park, i
Milwaukee, WI. , ! •
fc !
Other
Connnen t
soil at zoo
contained
3900 ug/mg
clean air
150
-------
7. DISCUSSION OF GENERAL SUITABILITY OF
ANIMAL INDICATORS OF AIR POLLUTION
7.1 Trends indicated by episodes
Nearly one hundred episodes have been reported since the end of the 19th
century of animals being adversely affected by industrial air pollution
(Table 7.1-1). Seventy-five percent occurred in the last 25 years. The
preponderance of recent episodes do not reflect the status of the en-
vironment, but modern technology, communications, and greater interest
in reporting such incidents. Early reported episodes, such as Royal
Commission Report7^ indicate damage to animals was not uncommon. Law
suits and other types of litigation occurred because of industrial air
pollution. The most documented or reported incidents involve intoxica-
tions by arsenic, fluoride, lead particulates, and sulphur dioxide. The
most commonly affected animals are domestic animals, in particular cat-
tle, followed by insects such as bees and silkworms ranked third in re-
ported episodes. Besides being adversely affected by air pollutants
there are a large number of episodes involving insect pest infestations
associated with air pollution. The majority of work involving plant
insect-pest-air pollution relationship are from European investigators.
If a causal relationship exists, and there is evidence to indicate it
does, then our understanding of pest infestations bears some reexamin-
ation. Finally, general wildlife, including deer and small birds are
reported affected by air pollution. Caution has to be taken on drawing
conclusions as to the sensitivities based on these episodes. Many of
the published reports do not involve extensive monitoring of ambient
air for concentrations of pollutants. Secondly, there is an economic
bias to notice and study effects on domestic animals. Of all the
animal groups affected, domestic animals and beneficial insects are
the most often reported. If insect pests of plants are included in
this group nearly 85 percent of the reported animal groups are repre-
sented.
After reading accounts of these episodes involving dome-stic animals
and beneficial insects, an equal or greater number of wildlife must
have also been affected although not reported. Wildlife generally do
not live in optimum conditions as do domesticated species. They should
show a lower resistance to environmental stresses. Arsenic and lead
most often affected vertebrate animals. Particulates and sulfur diox-
ide affected vertebrates and invertebrates nearly equally.
Finally, in many cases two or more toxic elements were found occur-
ring at the same time, such as S02 and fluoride, S02 and particulates,
arsenic and SO-, and lead, zinc, arsenic, and cadmium. Investigatins.
both experimental and field, should consider not only the individual
effects of air pollutants but the combined effects of air pollutants.
151
-------
Table 7.1-1 EPISODES INVOLVING AIR POLLUTANTS AND ANIMALS
Ln
Species
Cow
Monkey and
Rat
Bees
Po
Type
Asbes-
tos
Asbes-
tos
As
i
Fallow deer
As
Stags, Roe- As 0
llutant
Concentration
.0001 to
.0017% as in
pollen
bucks, Bees
.
!
Deer, Wild
Rabbits,
Fishes,
j
As
Cattle, ' !
Location
and Date
South
Africa
Europe
Germany
Czecho-
slovakia
Saxony ,
Germany
Source
Asbestos
Mine
Asbestos
Mine
Electri-
city pro-
ducing
plant
Silver
foundry
C Indus-
try
Effects |Reference
1 i
Asbestos bodies found in cow
Monkeys and rodents in the area
Kiviluto
2
Webster
had asbestos bodies, rodent
pop. less than expected ; ,
452 bee colonies destroyed and jLillie
171 weakened because of arsen- J
ic surrounding power plant j
Killed fallow deer in 1887
Observed cachexy, loss of hair.
baldness, resulting in in-
! creased loss of fluids(?),
Indus-
trial
'
Silkworms • ',
i
i
Horses
As ?
Deer . Cu smel-
\
ter
leading to freezing to death
in winter. Roe-bucks less re-
sistent. Bees died up to 52
km from sources.
Frequently killed 60-70% game
in Tharandt Forest; defective
hair growth, cirrhosis of
liver & spleen, eraanciation;
effects on nucosa, connective
tissue and antlers.
Reduction of herd by 2024
horses (2447 in 1902 to 423 in
1906) in four years, cattle
losses greater; effects in-
: eluded sterility and abortions
30-60%; death from chronic
: ' 'p , catarrhal inflammation of sto-
4
Tend r on
Ha is and
Masek
6
Prell0
mach, intestine, lungs, kidneys;
-------
Table 7.1-1 (Continued) EPISODES INVOLVING AIR POLLUTANTS AND ANIMALS
Ln
Species
Po
Type
Horses (Continued)
Horses &
Asses
As
Cattle 1 As,
Cu
llutant
Concentration
Location
and Date
Polode
j Lena,
?
Spain
Germany ,
1938
Source
Industry
Cu smel-
ter
Effects
inflammation of mucous mem-
branes of some
16 horses and asses sick and
died of As fumes. Symptoms
included intense pain with
head banging, diarrhea, hard
skin, colic, weakness, para-
plegia, and cacheria
Diarrhea, < appetite, <; weight,
no milk, running eyes initial-
ly, hair loss, miscarriage
Reference
8
Rodriguez
9
Wiemann
in
Cattle, As, j ? ; Germany Cu smelt- Miscarriage, sterility < milk, I Bischoff ~~
sheep, i Cu
; ing plant
horses, ' |
running eyes, < weight, ;
/• liver, > number of worms
poultry i 1
, i
Sparrow ! Cd ! j Japan Refinery
Mice,
Rats,
Cats
Dog ticks
Birds
i
i
;
in lungs & stomach with > Cu i
content ;
Level of contamination in j Nishino et
area X = 2.2 ppm vs. control
x=0.47, caused mortality —
al.LJ-
good indicator because of J
| i sensitivity ^
Car- i Germany Produce | Animals died in stable 50 • Herman
bonic plant ; yards from produce plant '•
Oxide ''
CO
£.
U.S. Automo-
Tick numbers > next to road
' bile i corrollated with CO-
4 J
traffic
concentration
1 . '
F
Czecho- Al f ac- Nesting bird sp v. with r> F
Slovakia tory levels. Transient birds >
McEnroe
Feriancova-
Masarova &.. ,
Kalivodova
with > F. Reflects compe-
tition.
-------
Table 7.1-1 (Continued) EPISODES INVOLVING AIR POLLUTANTS AND ANIMALS
Species
Cattle
Cattle
Cattle
(Oxen)
Cattle
Cattle
Cattle (12)
Cattle
Goats,
Cattle
P
Type
F
F
F
F
F
F
F
F
ollutant
Concentration
0 to lOmb/m
31 to 56 times
more than
control
Up to 20 ppm
in grass
Up to 43/mg%
in vegetation
Location
and Date
France
Germany
Osaka ,
Japan
1928
Czecho-
slovakia
Germany
1
!
0-8. 3ppm in
hay
15-234.8 mg/
ra^ in snow
Dalles-
port,
Ore.
mountain
valley
m
Source
Phosphoric
acid plant
Aluminum
factory
Chemical
fertilizer
ceramics,
and other
industries
Flue gas
chemical
plant
Aluminum
products
factory
Hydroflu-
oric acid
plant
Aluminum
reduction
plant
Aluminum
factory
Effects
Typical fluorosis for animals
living three years in area
<" weight, retardation of
young cattle; lusterless
skin; lameness; dental de-
formity; irregular breath-
ing; abnormal bone growth
Death of 70 oxen, 1953-
1964; expert analysis could
not find cause; F> amounts
in bone
Lameness, swelling joints;
< milk product; effect
< winter w/change in forage
Dental abnormalities; < life
span
Dental disfigurement,
locomotion, no fertility or
milk products; exp of keep-
ing 12 cows near plant 3.5
Reference
Bourbon,
et al."
Ehrlich16
Hasegawa &
Yoshikawa17
1 O
Hupka & Luy
19
Narozeny
Rosenberger
& Gruender^O
years 1
Only one cow wiLli lameness
95% goats, cattle affected
by fluorosis; 2 years after
plant installed, cattle
Spencer, et
al.21
22
Lezovir
weight decreased to cachexia ;
(malnutrition). Swine,
horses, poultry < sensitive.
-------
Table 7.1-1 (Continued) EPISODES INVOLVING AIR POLLUTANTS AND ANIMALS
Species '
Sheep, Cat-
tle
Sparrows,
Cattle
Deer
Deer, Red Fox
Cottontail
Rabbit ,
Muskrat,
Ground Hog,
House Spar-
row
Cows, bees
Silkworms,
cows, goats
Silkworms,
cattle
Bees
Silkworms
Pollutant
rype Concentration
-J-K.
F
I
F '0.02-O.U
mg/m3
F 3900 ppm in
raetatarsals
F
:
,
iF j 20 mg in
', leaves
F
F
F : ?
j
F 19.1 to 23.3
ppm in air;
39 to 40 ppm
in mulberry
Location
and Date
Scotland
Europe-
Poland
or Czech-
oslovakia
Washing-
ton
Ontario
?
Italy
Japan
Central
, Germany
Japan
Source
Aluminum
plant
Aluminum
plant
Aluminum
•plant
Aluminum
•plant
JHF plant
sAl refin-
jery
'Fluorine
plant
\
!Glass fi-
:ber manu-
facturing
iplant
Effects
Dull coats, dental disfigure-
ment, stiffness, lameness
H. sparrows had 7 to 12 times
F than controls; pigeons not
affected; cattle - fluorsis.
excessive damage to teeth,
high cone, in bones
Fluorosis in deer and high
concentrations in other
animals
£ milk, dental fluorosis:
< bee population.
Death first to worms, then
cows; cathexia, < milk, lame-
ness; later goats
Silkworms ill with plant > 30
ppm: cattle, fluorosis
Bees of migrating stand died
same day with wind ^ in their
direction
damage to silk worms on farm
Reference
Agate, et
al.23
Balazova and
Hlachan24
Newman and
•ic
Vii^-5
26
Karstad
27
Daessler
Bardelli
and 2g
Menzani2g
Yamazoe
30
Radeloff
31
Hasumi
1/1
-------
Table 7.1-1 (Continued) EPISODES INVOLVING AIR POLLUTANTS AND ANIMALS
Species
Pollutant
type Concentration
ocation
and Date
Source
Effects
Reference
Bees,
Silkworms
Insects (pol- F
linators, j
predators, !
foliage feed-j
ers)
Insects
(Lepidoptera,
Coleoptera)
Insects:
Fir Bark '
M Lice (Drey- ;
J£ fusia picea,
JO. musslini);,
Woodwasp ,
(Paururus !
juveniles
Insect | F
(spruce gall j
lice) j
Cattle j Fe
|(du£t
Sparrows,
Warblers,
Thrushes
France
Aluminum
plant
Montana !A1 reduc-
'tion plant
France
Czecho- Industry:
Slovakia Aluminum
PlantC?)
Germany Ifirick kiln
Austria
Prince
Rupert
B.C.
Mg factory
Pulp mill
forms of animal fluorosis
per-acute, bees; sub-acute,
silkworms; chronic ruminants
>levels in all trophic
levels: pollinators, 58 to
585 ppm; predators, 6.1 to
170 ppm; foliage feeders,
8.5 to 52.5 ppm
Number of insects, -*
number of bird species
Infestation of fir bark lice
and wood wasps in trees,
decrease in bark beetles
genus Pityokteines.
Tendron**
Dewey
33
Mazel
Pfeffer'
> pollution \ tree damage
>spruce gall lice infesta-
tion.
Stomach and intestinal
problems; ; milk; severe
case -> liver, no effect on
respiratory organs
200-500 songbirds died near
pulp mill during fog and
high cone, of H S, birds had
internal hemorrhaging in
lungs and liver.
Uentzel
35
Henneman
36
Harris
37
-------
Table 7.1-1 (Continued) EPISODES INVOLVING AIR POLLUTANTS AND ANIMALS
Species
Canaries
Birds and
Animals
Cattle
Cattle
Cattle
Bighorn
Sheep
Bark beet-
les (Cole-
optera,
Scolytidae)
Cattle
Pollutant Location
Type .Concentration and Date
H0S
2
H_S
2
Mb
Poza,
Mexico
111,247 to - Texas
139,059 mg/in
U.S.
Source
S recover-
ing plant
Oil field
Oil refin-
ery
r !
Mb up 484 ppm in Japan
•
Mb
Oxi-
dant
air
fodder
Mb smelt-
ing fac-
— _ -i
Effects
All canaries dead in area;
50% of all other animals
Killed large number of birds
and animals (unspecified)
near oil field.
Molybdinous wattle
acute diarrhea, locomotor
damage
52 cattle developed Diarrhea,
malnutrition, v milk product;
tory <. fertility
Holland JMo-Ox pro- {Cattle showed Cu deficiency;
t
,'
i
heavy !San Gab-
Srlel Mts.
Calif.
pollu-|
tion
Ozone
.
? Calif.
I
ducts "severe diarrhea; dull coat;
plant
Urbaniza-
< growth; discoloration of
hair; lameness
blind or totally blind sheep
tion of Losfound only in mountain
Angeles
areas of heavy oxidant pollu-
tion
I
i ^ number in damaged Ponderosa
pine trees
i
i
j
i 1
Pd iaverage 26 rag/ Romania
'lOOgm; vegeta-
tion near plant
up to .16% by
weight; 1.2x
106 part/m2 -
grd lead 2x10
part/m^at 40m.
Lead
refinery
Cachexis; < milk product
pale mucosa, enteritis with
Reference
McCabe &g
Clayton
Yont and
Sayers
Gardner &
Hall-40
Patch™
Ogura
42
Verweij
43
Light"
Cobb. et
al.
45
losif
constipation and diarrhea; i
:most severe -12 animal colic;
muscular twitches
i
i
1
in
-------
Table 7.1-1 (Continued) EPISODES INVOLVING AIR POLLUTANTS AND ANIMALS
Species
Cattle,
Horses
Cattle,
Sheep
Horses
Horses
Horses
Pollutant
Type .Concentration
Pb
Pb
Pb
Pb
Pb
t
Sheep
Zoo ani-
mals:
Leopards
and other
cats and
primates
Cows, bees
Pb
Pb
Pb,
PbO
Location !
and Date !
Source
Minneso- .Smelter
ta '
Effects
Horses show less adverse
than cattle
i i
Reference
Hammond &
Aronson
Dublin, 'Opencast Death and death of newborn Egan & A7
?
Soil up to
4200 ppm; for-
age up to 2800
ppm
7
Ireland
lead jvia utero and milk transfer ;0'Cuill
, mining
Benicia '
& Valle- •
jo, Cal.
Selby Lead
Smelter
i
Causes roaring and paralysis
of larynx, aspiration, pneu-
monia
Benecia, iQil refin- 12 out of 30 horses died in
Calif.
i
Trail, !
B.C. :
Serbo- \
Croatia
3900 yg/mg in Staten
soils Island,
New
York
ery
smelter?
Smelter
Haring_&
Meyer
Ottobone &
1 Q
Kaha*9
Six foals became sick; loss iSchmitt,
;of weight, weakness, pro- et al.JW
!gressively arched backs,
cachectic effected young
• animals
Industry Young sheep — paralysis of
extremities, craw, tongue,
' larynx; rigidly held neck,
anemic mucous membrane, cone .
> digestive and respiratory
1 organs .
Air — urban | Lead poisoning, animals out-
doors > levels
Roasting
station,
sulfide
[lead ore
1
> levels in milk, honey
51
Pavlicevic
52
Bazell
Kerin &
Kerin"
00
-------
Table 7.1-1 (Continued) EPISODES INVOLVING AIR POLLUTANTS AND ANIMALS
Species
Aphid s,
mites, leaf-
hoppers.
Pollutant
Type Concentration
Smoke
& Pb
Location | |
and Date 'Source Effects
iSelby lead
jsmelter
Poor orchards attributed to
insects, not smoke (later
work shows damage > insects)
i
•Reference
iDoane
VO
thrips,
beetles
Cattle
Cattle,
Horses
Cattle,
Horses
Rabbit
Insects
Insects
SO +
Asfi
"Fog"
prob.
S09
"F5g"
Czecho-
slovakia
(Ostrava).
Meuse 'Factories
Meuse, Factories
1929,
1930
Czecho- [Power sta-
slovakia Itions
dust
Smoke,up to 224 yg/m
SO SO and 391 \g/
m3 smoke, Rural < 20
for both.
so,, :
Frequent diarrhea and pneu- ,Masek &
moconiosis simplex, frequent JHais
jabortion 55
I Subcutaneous emphysema, >CO 'Rubay
!and <0 in blood, dyspnea,
cyanosis, asphyxia . 57
Subcutaneous emphysema, fever iRubay
irregular breating, cows more '
sensitive than horses
England
Pennsyl-
vania
i
Jrbaniza-
jtion and
•industry
Coal fire
power
plant
Changes in eosinophils, tend- |Pfeffer
;ency to polyglobulitis, j
imarked disorders of eukolid- j
lites among protein fraction |
!of blood serum, higher trans-j
laminases and cholinesterase '
[Reduction in lichens on trees Gilbert
[cause reduction in herbivores
i (barklice—Psocids)
58
Increased number of aphids in
high pollutants, decrease in
parasitic hymenoptera, de-
crease in Apidae, no change
in Diptera or Cicadellidea
Hilliman
60
-------
Table 7.1-1 (Continued) EPISODES INVOLVING AIR POLLUTANTS AND ANIMALS
Species
Insects
Po
Type
30.
2
Insects: SO.
Gd. Beetle . l
Carabidae
Insects
Insects
1° parasites:
pine trunk
beetle, blue
spruce wood
wasp.
2° parasites:
large forest
gardner, roon
longicorn
beetle, com-
mon timber
50
X
Llutant
Concentration
up to 35+ mg/
m-* during day
Location
and Date
Czecho-
Source
Effects
Thermal !SOn reduced number and kind
slovakia : power of bare-bodied insects and
Canada
Poland
Poland
plant insects on surface of trees;
large number of insects liv-
ing in galls or buds, e.g.,
Reference
PfefferO-L
jSaccliphanlos abictis, S.
iviridis, Evetria buoliana,
E. turionana, Eratolea, ded-
ocella; also larger number
of bark borers in subcortical
areas than bark; multiplica-
ition if in cocoons and pro-
tected by waxy secretions
Kraft mill [Reduced ground beetle popula-
'tion 1.5 miles around stack,
jno effect on body size
1
Sulfur pro-lReduction in bees — and <
cessing
plant
fruit yield.
Parasites infest crowns of
thinnest trees — weakening &
jthinning more ^penetration
jof pollutants.
2° parasites: timber bark
[beetles settle in dense
stands not exposed to indus-
trial emissions
Freitag, et.
al.b2
Przybylski63
64
Sierpinski
bark beetle
-------
Table 7.1-1 (Continued) EPISODES INVOLVING AIR POLLUTANTS AND ANIMALS
Species
Nematoda
Pollutant
Type "Concentration
Location
and Date
S00 + ' i Germany
dust ;
i
Insects:
Phigalia
pedaria,
Adalia bi-
punctata.
Biston
betularia
Cattle
Insects
Insects
( Aphid s)
Fallow
Deer
(lime)1
Smoke
and
so.
2
'•
l
England
V il ppm in soot [Germany?
Road-
side
dust
Dust-
Cement
Kiln
Cement
Cust
England
1
Hanover ,
Germany
1
Source
Industrial
Air
Industry
Effects
A pH of humus from 3.7 to
7 resulted in % semisapro-
phage and saprophage and
predatory nematodes
>, unaffected area semi-
parasitic nematodes >
Local smoke correlated
with melanic forms of
Phigalia and Adalia; SO,,
correlated with Biston
statistical tests
From fuel j several cows grazing in area
oil soot
Traffic
Cement
factory
Cement
plant
exposed to fuel oil soot ex-
hibited weakness and Ataxia.
Hematological studies reveal
V. toxicity. Levels in kid-
ney 3 to 4.7 ppm, Liver 1.5
to 2.4 ppm.
Dust from roads kills trout
and insects and .'. reduces
number of birds, especially
Reference
Bassusaj
Lees, Creed,,
and Ducket t
t\
Lillie^
67
Oliver
goldfinch. fiR
Investation of alfalfa field
subjected to dust; other
areas free of dust and
aphids; theorize decrease in
predators.
Darley
L
Deer adversely affected 'Tendron'
i
-------
Table 7.1-1 (Continued) EPISODES INVOLVING AIR POLLUTANTS AND ANIMALS
Species
Insects: 4
species of
moth
Hens
Pollutant
Type (Concentration
Soot [83-535 yg/mj
Location
and Date
Manches-
i i tgr>
soot
as-
phalt
i
'
:
Cattle
Cattle
Fog,
smog
Smoke;
Air
England
i
Pol.
Cattle
Smoke
| i
Cattle
Smog
Japan
Meuse
Valley,
Belgium
Europe (?)
England
London
Source Effects
Reference
Industrial-Jlndustrial melanism seen in JAskew, et.
Lzation [all species, in area where jal.69
'control implemented, lighter
iforms increasing in frequen-
icy. i 3
Asphalt 50% drop in egg production [Li Hie
factory land 59% death and decrease (pg-8)
!in several thousand Leghorn
jHens near asphalt factory in
Japan. Soot determined to
[be toxic-poisonous constitu-
;ent not identified. Patholog-
ical findings: congestion,
Industry
hemorrhage or catarrh of
lungs, gullet ovaries, intes-
tine, trachea, kidneys 1/2-
2-1/2 normal size.
Large number of cows died.
jAutopsy on 12 showed pulmon-
Industrial
towns
Copper
works
Urbaniza-
tion and
industry
ary edema.
Reduced feeding, 2 cows /acre
to 1 cow/3 acres; cows defi-
cient in calcium
70
Alexander
Chemical
Age7!
Blinded up to 120 cattle; iRoyal Corn-
caused bone damage in cattle miss ion _
sheep, not pigs.
1952 killer fog; first indi-
cations of problem seen in
respiratory stress of cattle
at Smithfield Stock Show; 5
Report'''
Schwabe7^
cattle died, 51 sick, 11 j
needed to be slaughtered; 1873
same phenomena at cattle show
(preceding killer smog.
l
NJ
-------
Table 7.1-1 (Continued) EPISODES INVOLVING AIR POLLUTANTS AND ANIMALS
Pollutant
Species Type [Concentration
Location
and Date
Source
'Effects
Reference
Cattle,
Sheep
Dogs
Dogs
Mammals
and birds
(Ducks and
geese)
E.Sparrow
Smoke
Air i
Pollu.!
Air
Pollu.j
Urban !air pollution
Insects
(dragon-
flies, but-
terflies,
fireflies)
Insects
(Concha
vermin-
parasites)
Air
Pollu.
Air
Pollu
Leeds, , Industry?
England '
Phila- I Urbaniza-
delphia tion
London j Urbaniza-
1 tion
Phila- ; Urbaniza-
delphia j tion,
Davis/ !Urbaniza-
Sacremen*-tion
to, Cal.
area vs.
Bodege
Nagoya, jIndustry
Japan
Urban JAir pollution
and |
dust I
|Affected lungs of cattle and
ireduced wool production and
;quality of wool in sheep
Japan
Urban
areas
Scientific
American^
igland and
U\J.Ci. dill
(Cohen76
jSnyder & 7?
JRatsliffe"
[Higher incidence of tonsilar (_._.„_
•cancer in urban (Philadelphia)jGorham75
|dogs than rural (Wash. St.) |
Higher incidence of tonsilar iRief and
cancer in urban dogs, al-
though low absolute number
300/1900 species had lung
jcancer; in bird species,
!ducks and geese, .> number—
jmight be due to > exposure
iyear round
Pulmonary anthracosis and
cytoplasmic fat vaculation
in some hepatic parenchymal
cells in urban birds
mento vs. coast birds
Dragonflies and butterflies
drastically reduced in num-
bers, general decrease in
wildlife.
Wellings
78
Aichi Pre-
fectural
Gov.79
Air pollution and deteriora-
tion of soil hatching of
parasite concha vermin, also
in their natural enemies;
close correlation between
dust and proliferation.
Kawai
80
-------
Table 7.1-1 (Continued) EPISODES INVOLVING AIR POLLUTANTS AND ANIMALS
Po
Species ; Type
Cattle SO_,F
Ozone
Dogs, Cats,
Smog-
Poultry, SO ,
Rabbits, NO,Pb
Cattle
Insects:
Small
Spruce
Sawfly
Pristiphora
abientina
Insects:
Plant lice
Mealy Bugs
S°2
and
smoke ;
tar
and
organi
acids
so
i
HF
llution Location
Concentration and Date
! Germany
i
i
i
Donora,
i PA
!
0.19-0.38 mg/
m3 S0_
i
c
•J
6-8 mg/m F;
1.5-2.0 mg/m
S00
2
-
i
Source Effects _
.15 mg/m SO in air > milk
product; fluorosis in cattle,
ozone-lung edema plus inci-
dents in lung and skin cancer
Industrial jDogs: 38/245 were sick, 11/38
Reference
Liebenow8!
Schrenk.
plant: Zn died; respiratory and be- let al.°^
and Steel havior changes % young and
old. Cats less affected j
than dogs. 40% mortality in
poultry flocks of 4 farmers.
'1 of 7 households w. rabbits
were sick. 3 of 13 farms had
t |
isick cattle. j
Feldberg, (charcoal ;Heavy infestation of spruce (Wentzel and
Boden- [plant sawfly in area of smoke and |0hnesorge83
felde,
|S00 contamination; levels of
Germany i pollutant below damage
levels to trees.
i Heavy infestation of air dam-
aged trees — Abies concolor
and Abies neitchi — trees with
pesticide, no air damage.
Ilex aquafolium showed F and
S09, often attacked by the
fly Phytomyza ilices, some
1 spider mites on Picea omorchi;
lot her pest Blaslethia turion-
fella found in air pollution
Iprotected part of tree.
84
Berge
1
-------
Table 7.1-1 (Continued) EPISODES INVOLVING AIR POLLUTANTS AND ANIMALS
Species
Insect
(large pine
sawf ly)
I
Type
NO ,
sox
x
'ollutant
Concentration
7
| Location
:and Date
; Austria
I
i
Source
Industry
i
Effects
Pine sawfly
moderate NO
< with > SO"
larvae >
and SO ,
V
in
but
!
Reference
Sierpinski03
i
en
Insects: ] S09,
Night Moth
(Lymantria
monacha)
Insects
(Xylopha-
gous)
Insects
(Pests)
Insects:
Hemoptera
Heteroptera
Coleoptera
Lepidoptera
Hymenoptera
Orthoptera
Cattle
Cattle and
Sheep
*•
some
N+C1
Indust
NHV
NO4!
S°x
dust
SO ,F
Zn
Pb
S0_
2
Mn,
Pb
Cu
jSilesia, Industrial [Night moth exhibits epidemic
I Poland plant [behavior in heavy pine dam-
i iaged zones
Sierpinski
85
Poland Industry?
(Silesia)'
(Invasion of insect in
damaged trees, but insect
!in levels of pollution
!Poland
I
Czecho-
slovakia
ilndustry Damage to trees with NO Sierpinski
; [invade by insect—35% of
j |130 ha. stand, cone, of
insects in zone of lowest
exposure, least in highest. „,
86
SO and F associated number Pfeffer
Phaenop cyanea F, Exotelea
dodecella L., Paururus noc-
Austria
jZn, Pb,
Isulfuric
tilis, Dreyfusia picea Ratzb.
lylurgops palliatus gyll.,
)ryocoetes autographus ratzb.
jTrypodendron lineatum ol. ,
Pissodes harcyniai, FIssodes
jscabricollis mill.
bpots on teeth, milk pro-
Iduct. No other effects
88
lacid plantsj
i i
ICoke-oven Death of sheep and cattle
[industry ^near industry with high con-
\ jpentration of Mn, Cu, and Pb,
Leibetseder
•Dunn and Blo-
kam89
I
-------
Table 7.1-1 (Continued) EPISODES INVOLVING AIR POLLUTANTS AND ANIMALS
Species
Sheep
Horses
Horses
Fallow
Deer,
Cattle
Annelids
(Earth-
worm)
PoJ
Type (
Pb.SO
L
As,Cd,
Pb
Lead
Zn,F
As.Cd
As, SO.
2
9
Auto
Exhaus
Zn.Pb
Llutant
Concentration
?
t
Location
and Date Source
Zvechan Pb Smelter
Helena Smelting,
Valley, refining
Montana
Trail, Smelter
B.C.
Germany Arsenious
(Frei- acid and
burg, silver
Saxony)? foundry
? Automobile
traffic
1
Effects (Reference
During lambing season Pb |Parlicericyu
caused paralysis of extremi-
ties, craw, tongue, change in
mucous membrane of digestive
tract, inflammation of lung; '
also catarrhal bronchitis due!
to SO., dead sheep. Shepherd
took nerd out of area. > g-|
> levels in mane, older ani-
mals > chronically impaired
Chronic debilitating disroder
in 6 horses. Found horse
greater sensitivity than old-
er horses and cattle. Symp-
toms include lameness, re-
duced adipose tissues, edema-
tous synovial membranes,
necrosis of nerve cells,
hepatic cell degeneration and
nephrosis
1880 's deer and cattle re-
ported adversely affected in
Saxony
High levels of Zn and Pb
found in earthworms within
160 feet of roadway; 330+
ppm Pb, 670 ppm Zn
Lewis
Schmitt et
no
al.92
4
Tendron
Gish and
Christen-
Q 1
sen^J
ON
-------
7.2 General effects of air pollution on animals
Tn this section of the Report I will attempt to summarize the general
effects of air pollutants based upon the responses of animals to these
air pollutants. I will describe responses of animal indicators which
are most appropriate for the recognition of air pollutants. The pur-
pose of this discussion is to point out which pollutants are most likely
to have suitable animal indicator systems and which animal systems are
most suitable for monitoring their presence.
Air pollutants can be classified according to their degree of toxicity,
accumulating capacity, biological target systems and other special
characteristics.
Three degrees of toxicities are recognized: toxic to free-living
animals; non-toxic but effect free-living animals; and no affect on
free-living animals (Table 7.2-1). For some pollutants such as cadmium,
hydrochloric acid, mercury, nickel, selenium, chromium, phosphorus, and
vanadium, information on their effects or environmental concentrations
is lacking to draw any conclusions as to their toxicity (see Section
5). Information is needed on industrial sources, ambient concentra-
tions, and observed effects in the field for these pollutants. The
majority of air pollutants reviewed are toxic to free-living animals.
In addition they may influence the abundance and distribution of ani-
mal populations. For example, photochemical oxidants are toxic to
mammals at observed ambient concentrations. They are also associated
with insect pest infestation and may directly induce such outbreaks.
(See Section 7.3on insect-air pollution relationships.) Six of the
air pollutants are nontoxic at expected ambient concentrations and,
unless concentrated in other organisms, would have no effect on free-
living populations. One of the major failings of most laboratory
studies is that they have been carried out at exceedingly high concen-
trations. Proper understanding of the action of most of these pollu-
tants needs to be demonstrated by low and chronic exposures to a
variety of animals. Such studies might change the classification of
some of the nontoxic pollutants.
Air pollutants can also be classed in terms of their accumulating
capacity. Understanding of these characteristics will allow for more
effective monitoring. Most of the pollutants studied are accumulated
by certain parts of the mammalian system. Three classes of pollutants
can be considered based on their capacities for accumulation in
animals: permanent, temporary, and nonaccumulators (Table 7.2-2).
Permanent accumulators are pollutants which are held in the body for
long periods of time, even for the life of the animal, such as fluor-
ide in bones. Three pollutants, are temporary accumulators:
CO, H S, and NO . These pollutants are accumulated for only
short periods or time in the blood. Presence of these pollutants
would indicate recent exposure. A number of the permanent
167
-------
Table 7.2-1 TOXICITIES OF AIR POLLUTANTS BASED ON OBSERVED AMBIENT
CONCENTRATIONS
Toxic to free-
living animals
Nontoxic but affect
free-living animals
Nontoxic
asbestos
arsenic
beryllium
cadmium
carbon monoxide
fluoride1
hydrocrabons
f
hydrochloric acid1*
hydrogen sulfide
lead
2
mercury
molybdenum
nickel2
photochemical
oxidants^
selenium
nitrogen dioxide
particulates (inert)
barium
boron
chromium
iron
manganese
zinc
also affect populations in nontoxic manner
potentially toxic but corroborating information lacking
laboratory studies suggest nontoxic classification; however, field
studies suggest otherwise.
168
-------
Table 7.2-2 CLASSIFICATION OF ATR POLLUTANTS BASED ON THEIR CAPACITY
TO ACCUMULATE IN BODY TISSUE
Accumulators
Permanent
asbestos
arsenic
beryllium
boron
cadmium*
fluoride*
iron
lead
manganese
molybdenum
particulates
selenium
vanadium
Temporary
carbon monoxide
hydrogen sulfide
nitrogen dioxide
Non-accumulators
barium
chromium
hydrocarbons
hydrochloric acid
iron (ingested)
nickel (ingested)
photochemical oxid&nts
*also temporary accumulators
169
-------
accumulators have temporary accumulating sites, i.e., the kidney for
fluoride. The five most common accumulating sites for air pollutants
are blood, skeletal tissue, lungs, hair and the kertonized tissue,
kidney and the liver. Table 7.2-3 indicates associations of each
pollutant with these various sites.
Table 7.2-4 shows the general kind of biological indicator response
described in Section 3 possible for each of the pollutants. The table
is not complete and represents a generalized picture. Further research
is needed to provide information on pollutants where information is
scarce. As would be expected, the induced response of air pollutants
are varied. Some patterns are apparent. The majority of the pollu-
tants affect the respiratory and the pulmonary systems. The next most
common systems affected are the central nervous system and gastro-
intestinal system. A number of pollutants, in particular asbestos. F,
As, CO, hydrocarbons, Fe, Mo, Ni, Zn, and particulates, have single
target areas (Table 7.2-5).
Nearly all pollutants cause changes in behavior of exposed animals.
These abnormal behaviors range from listlessness and lethargy to vio-
lent movements such as jerking, and running into objects (Table .2-6).
Certain abnormal behaviors of domestic animals are symptomatic of
specified chemical poisonings,94 but for the most part many of the
abnormal behavioral responses are non-specific. External changes in
morphology and appearance are good diagnostic indicators of exposure.
This is particularly true for certain pollutants (Table 7.2-7).
However, more research is needed to test the universality of some of
these changes.
Besides specific areas of accumulation there are several other in-
ternal indicator responses. Two of these, cellular enzyme changes,
and changes in blood chemistry and physiology, may be used as diag-
nostic tests. Novakova and Roubal95 report a correlation in the
phosporus and calcium rates in the blood of rabbits with various
concentrations of SO-. The calcium ratio decreases in rabbits from
areas of high S02- The phosphorus ratio was higher from these
areas. It appears that changes in blood chemistry and physiology
are more diagnostic of specific pollutants than cellular enzyme
changes (Tables 7.2-8 and 7.2-9). Standard sampling techniques
should be developed.
Only four of the pollutants reviewed are carcinogenic: asbestos,
nickel, photochemical oxidants, and vanadium. At least one pollutant,
selenium, is tetragenic in birds. Observations of egss of free-living
seed-eating birds might prove a good sampling procedure for determin-
ing selenium exposure.
170
-------
Table 7.2-3 MAJOR SITES OF ACCUMULATION OF AIR POLLUTANTS
Asbestos
Arsenic
Barium
Beryllium
Boron
Cadmium
Carbon Monoxide
Chromium
Fluoride
Hydrocarbon
Hydrochloric Acid
Hydrogen Sulfide
Iron
Lead
Manganese
Mercury
Molybdenum
Nickel
Nitrogen Dioxide
Particulates
Phosphorus
Photochem. Oxide
Selenium
Sulfur Dioxide
Vanadium
Zinc
Adipose
tissu.
X
•o
o
3
fa
X
X
X
X
X
CO
.
0)
c
•o
•H
X
X
X
X
X
X
Liver
X
X
X
X
X
X
X
X
00
c
hJ
X
X
X
X
Muscle
X
e
•H
.*
C/}
X
c
0)
0)
iH
0.
C/3
X
X
171
-------
Table 9.2-4 ASSOCIATION OF AIR POLLUTANTS AND GENERAL BIOLOGICAL INDICATOR RESPONSE
General Responses
Avoidance of pollutant
Changes in abundance
Changes in blood chemistry
and physiology
Changes in cellular enzymes
Changes in energy requirements
for normal activities
Changes in morphology or appearance
Changes in taste
Death
Differential effects on life stages
Effect on reproduction
General growth retardation
Genetic resistance
Observations of abnormal behavior
Physiological changes observed in
autopsy & histological analysis
Reduced tolerance to normal en-
vironmental stimuli or stress
Residue accumulation
Tetragenic and/or carienogenic
\sbestos |
X
X
X
X
Arsenic |
X
X
X
X
X
X
Barium |
X
X
Beryllium ]
X
X
X
Boron |
X
X
Cadmium |
X
X
X
Darbon I
Monoxide {
X
X
X
Chromium |
X
Fluoride |
x
X
X
X
X
X
X
Hydrocarbon |
X
Hydrochloric
A.
X
X
Hydrogen
Sulfate
X
X
X
X
c
o
M
X
X
X
•o
CO
0)
X
X
X
X
Manganese |
X
X
Mercury |
X
X
Molybdenum |
X
X
X
X
X
Nickel I
X
Nitrogen I
Dioxide f
X
X
X
X
X
X
Particulate^
y
X
X
Phosphorus |
X
X
X
X
o
6
0)
4=
(J
O
4J
0
x
X
X
X
X
X
Selenium |
X
X
X
X
Sulfur Dioxj
X
X
Vanadium (
X
X
v
u
c
•rl
Nl
X
X
K5
-------
Table7.2-5 THE MAJOR BIOLOGICAL TARGET AREAS OF AIR POLLUTANTS
Asbestos
Arsenic
Barium
Beryllium
Boron
Cadmium
J2g.rh°ri tyn"ox.
Chromium
Fluoride
Hydrocarbon
Hydrochloric A.
Hydrogen Sul.
Iron
Lead
Manganese
Mercury
Molybdenum
Nickel
Nitrogen Diox.
Particulates
Phosphorus
Photochera.Ox.
Selenium
Sulfur Dioxide
Vanadium
Zinc
Eyes
X
X
X
Central
nervous
system
X
X
X
X
X
X
X
Circula-
tory
system
X
X
Diges-
tive
system
X
i
•
Gastro-
intestinal
system
X
X
X
X
X
',
' X
I
I
1 X
Hepatic
system
X
X
i
!
Pulmon-
ary
system
X
X
X
X
X
X
1
X
i
X
Respir-
atory
system
X
X
X
X
X
X
X
X
X
X
! X
[
X
X
Renal
system
X
X
i x
,
Skeletel
& dental
system
X
i
-------
Table 7.2-6
ABNORMAL BEHAVIORS OF ANIMALS ASSOCIATED WITH AIR
POLLUTANTS
Pollutant
Observed abnormal behavior
Arsenic
Carbon monoxide
Chromium
Barium
Beryllium
Boron
Fluoride
Hydrocarbons
Hydrogensulfide
Lead
Manganese
Mercury
Molybdenum
Phosphorus
Selenium
incoordination of gait, muscular paralysis
breath of garlic odor
incoordination of gait and movements, re-
duced appetite in chickens, impairment
of learned activities in rats
stiffness, loss of appetite
incoordination of movements, twitching,
tremors, muscular paralysis
temporary lethargy in dogs
incoordination, tremors, listlessness,
coma
lameness, stiffness, weakness
dizziness, fatigue, loss of appetite
lethargy, gasping
bellowing, roaring, staggering about
with rolling eyes, frothing of mouth,
grinding of teeth, ataxia, maniacal ex-
citement, lethargy, loss of appetite,
delirium
lethargy, tremors
incoordination of movements, paralysis
anorexia, lethargy, blindness
stiffness in legs and back
restlessness, nervousness
abnormal movement and posture, fear,
nervousness, opisthotonos
Sources:
al.,
Buck et,al
Sullivan,111'112
Garner, Lillie, Miner, Sigmund et
174
-------
Table 7.2-7 CHANCES IN EXTERNAL MORPHOLOGY OR APPEARANCE DUE TO
AIR POLLUTION INTOXICATION
Air pollutant
Change
Arsenic
Barium
Fluoride
Lead
Molybdenum
Particulates
Photochemical oxidants
Selenium
- rough haircoat, brick red coloration of
visible mucous membranes, sometimes skin
necrosis
- darkening of comb in poultry
- dental disfigurement
- blue-black discoloration of gums found
in horses, carnivores and sheep on occa-
sion
- fading of haircoat
- soiling of haircoat and feathers
- dull cornea, sagging conjunctivae
- loss of hair from mane and tail in horses
along with cracking of hoof at coronary
band, deformed hooves in cattle and swine
Sources: Buck et al.,108 Garner,109; Sigmund et al..
175
-------
Table 7.2-8 EFFECTS OF AIR POLLUTANTS ON BLOOD CHEMISTRY AND
PHYSIOLOGY
Air pollutant
Changes in blood chemistry and physiology
Arsenic
Cadmium
Carbon monoxide
Hydrogen sulfide
Lead
Molybdenum
Nitrogen dioxide
Photochemical oxidant
Sulfur dioxide
Vanadium
- reduces haemocyte count in Blatta and
Locusta
- reduces hemoglobin and RBC
- formation of carboxy hemoglobin
- reduces sulphaemoglobin
- causes basophilic stippling of RBC
- changes copper balance in blood
- formation of methemoglobin
- change in number of rat neutrophils and
lymphocytes
- changes in blood vitamin C
- reduces hemoglobin and leucocyte
176
-------
Table 7.2-9 ENZYMES AFFECTED BY AIR POLLUTANTS
Air pollutant
Cellular enzymes affected
Arsenic
Beryllium
Fluoride
Hydrocarbon
Hydrogen sulfide
Iron
Photochemical oxidants
- sulfhydryl enzymes
- alkaline phosphatase, ATPase and others
- chloinesterase, bone-alkaline
phosphatase
- rat liver alkaline phosphatase
- alkaline phosphatase, acid phosphatase,
and others
- metabolic oxidative enzymes
- 5-nucleotidase, alkaline phosphatase of
lungs, RBC acetylcholenesterase
177
-------
The most common effect of air pollution is sickened or weakened ani-
mals. For animals in particular wildlife the toxic effect of a pollu-
tant may not be the proximate cause of death but the ultimate cause by
weakening the resistance of the animal to other environmental stres-
ses. This is one parameter which should be studied. Nitrogen dioxide
and photochemical oxidants have been shown to weaken the resistance
of laboratory animals to respiratory infections. This lowered resis-
tance probably occurs in the field and probably extends to other envir-
onmental stresses besides respiratory infections. For example,
fluoride intoxication results in a lower nutritional state for cattle.
Deer effected by fluoride may die because of fluoride induced malnu-
trition.
Only four of the pollutants As, F, H_S, and Pb have been associated
with animal die-offs (Table 7.2-4). Tlost of these involve domestic
animals. To date the Center for Short-lived Phenomena of Smithsonian
Institution has recorded no such events. From the review of air pollu-
tion episodes death of wildlife attributable to air pollution are prob-
ably a more common occurrance than reflected in the reported dieoffs.
In most cases few attempts were made to examine wildlife species.
178
-------
7.3 Summary of General Response of Animals to Air Pollutants
Several animal species have been suggested as biological indicators of
air pollution. Pigeons96 and city rats97 have been proposed as moni-
tors of lead and asbestos, however, confirming studies have not been
conducted. Sparrows9** and wild hares9^ as monitors of atmospheric
pollutants have only been recently studied. The preliminary investi-
gations, however, show strong correlation between atmospheric pollu-
tion and physiological changes in these species.
Further studies need to be undertaken to determine specific biological
indicator organisms. The available information suggests some bio-
logical indicators species and general groups of indicators (Table
7.3-1). Specific accumulator sites have been discussed in previous
sections. These sites apply to mammals and birds. A few studies99'100
using mammals as accumulators have been conducted. Insects are known
to accumulate fluorideJOl These studies show the accumulating capacity
is as much a function of the ecology of the animals as it is a function
of their physiology. The characteristic behaviors of animals are a
clue to indicator species. The incidence of cancers in ducks in zoos
is correlated with feeding behaviors. Studies on dogs and cats102
have correlated the type of cancers (oropharyngeal) with panting and
licking of fur. Although of very low incidence, the cancers in dogs
are found at a significantly higher frequency in urban canine popula-
tions than in rural canine populations. The concentration of roadside
lead in three species of rodents varied according to their food and
behavior.
Because of the many studies on the effects of pollutants on domestic
animals1 and associated episodes involving livestock (Table 7.1-1),
domestic animals would make suitable bioassay monitors. Extensive
information on their physiology and anatomy is known so that compara-
tive diagnosis or analyses can be done. Sufficient information on
game animals such as pheasants, deer, rabbits, etc., also exists to
allow them to be used as monitors. However, not all pollutants have
been characterized as to their effect on this latter group.
Detectors are different from bioassay monitors in that they show a
reasonably characteristic response to a pollutant but do not neces-
sarily require extensive understanding of the physiology and health
of the animal. Based on the limited number of anima] studies,
birds and mammals are likely to be found as reliable detectors
(Table 7.3-1).
The final category of biological indicators are those species who
thrive or survive under polluted conditions. Here much work needs
to be done and the list developed is not based on experimental data
but on field observations. The mechanisms of responses are not
179
-------
Table 7.3-1 POSSIBLE BIOLOGICAL INDICATORS OF AIR POLLUTANTS
Indicator type
Air pollutant
Organisms
Sentinel carbon monoxide
fluoride
hydrogen sulfide
nitrogen dioxide
sulfur dioxide
Bioassay monitors arsenic
fluoride
lead
molybdenum
particulates
photochemical
oxidants (acrolein)
selenium
sulfur dioxide
Detectors arsenic
carbon monoxide
fluoride
nitrogen dioxide
particulates
photochemical
oxidants
selenium
sulfur dioxide
vanadium
Thrivers fluoride
nitrogen dioxide
photochemical
oxidants
canary, other birds (?)
bees, silkworms
small birds
tree insects (?)
bees
horses and domestic rumin-
ants, poultry, dogs
cattle, other domestic
herbivores
horses and domestic livestock
domestic ruminants
animals with behaviors that
would tend to accumulate
particulates in body by
sniffers and groomers
rats
domestic livestock & poultry
rabbits and domestic animals
mammalian herbivores—
domestic and wild
birds and mammals
mammalian herbivores,
domestic and wild
birds and mammals
white or light colored birds
and mammals
birds and mammals
ruminants and gallinacious
birds
birds and mammals
ruminants
coniferous tree insects such
as fir bark lice, wood
wasps, bark beetles, spruce
gall lice, mealy bugs
coniferous tree insects such
as large pine sawfly larva
coniferous tree insects such
as bark beetle
180
-------
Table 7.3-1 (Continued) POSSIBLE BIOLOGICAL INDICATORS OF AIR
POLLUTANTS
Indicator type Air pollutant Organisms
Thrivers (continued)
selenium genetic resistant insects
such as beetles and seed
chalcids
sulfur dioxide coniferous tree insects such
as night moths and aphids
Accumulators see Table 7.2-3 for generally birds and mammals;
specific pollutants high levels of fluoride have
been found in insects.
181
-------
known, but the numerous reports suggest certain animal groups may
serve in the role of indicator species. Insects are not only adverse-
ly affected by air pollution but may work together with air pollution
in damaging plants, or may actually be attracted to plants by pollu-
tants .themselves. Pfeffer58 and Sierpinski64 report invasion or
proliferation of insect pests in forests contaminated by air pollution.
Wentzel and Ohnesorge8^ have found invasion of spruce sawfly (Priste-
phora abientina) occurs prior to any detectable damage to spruce trees
by hydrogen fluoride.
Figure 7.3-1 diagrams several possible mechanisms for responses of
insects associated with polluted conditions. First air pollution may
eliminate natural controls. Secondly, it reduces resistance of plants
to insects through direct damage to plants. Thirdly, plant herbivores
may be reduced by air pollution.58 A fourth possible mechanism in-
volves the attraction and stimulation of insects to feed on plants by
air pollutants themselves. This mechanism is suggested by the fact
that chemicals such as hydrocarbons and oxidants have been found to
act as attractants and repellants for insects.1*^, 105,106 It is
possible that the industrial hydrocarbon, photochemical oxidants, and
other pollutants might illicit similar responses. Wentzel and
Ohnesorge's study may be supportiving field evidence for this
mechanism. In all cases the air pollutants had an adverse effect on
plants. This insect-air pollution association would contribute to this
plant damage.
182
-------
1.
AIR
POLLUTION
2.
AIR
POLLUTION
\
\
PLANT INSECT
PREDATORS
REDUCE
PREDATION
PLANT INSECT
HERBIVORES
I
INCREASE
CONSUMPTION
PLANTS
PLANT INSECT
PREDATORS
PLANT INSECT
HERBIVORES
I
INCREASE
CONSUMPTION
PLANTS
3.
AIR
POLLUTION
KNOWN EFFECT
POSSIBLE EFFECT
PLANT INSECT
PREDATORS
REDUCE
rPREDATION
PLANT INSECT
HERBIVORES
REDUCE
,CONSUMPTIOIS
PLANTS
4.
PLANT INSECT
PREDATORS
AIR
POLLUTION
REDUCE
RESISTENCE
OR ATTRACT TO
DAMAGED PARTS
ATTRACT
I
PLANT INSECT
HERBIVORES
I
INCREASE
CONSUMPTIOI
PLANTS
7.1-1
FOUR POSSIBLE MECHANISMS OF AIR POLLUTION- INSECTS. AND PLANT RELATIONSHIP
-------
REFERENCES
1. Kiviluto, R. Pleural Plagues and Asbestos. Further Observations
on Endemic and Other Non-Occupational Asbestosis. Ann. N.Y.
Acad. Sci. 132:235, 1965.
2. Webster, I. Asbestosis in Non-Experimental Animals in South
Africa. Nature 197:506, 1963.
3. Lillie, R. J. Air Pollutants Affecting the Performance of Domes-
tic Animals. A Literature Review, USDA Agr. Handb. 380, Aug.
1970.
4. Tendron. Effect of Pollution on Animals and Plants. European
Conference on Air Pollution. Council of Europe (Strasburg).
24 June-lst July, 1964. p. 25-70.
5. Hais, K. and J. Masek. -Effects of Some Exhalations on Agricultur-
al Animals. Och Ouzdusi. 1969:122-125, August 1969.
6. Prell, H. Injury to the Animal World Through the Distant Effects
of Industrial Waste Gases. Arch. Gewerbepath. Gewerbehyg.
7:656. 1937.
7. Fornad, R. J. The Effect of Smelter Fumes upon the Livestock
Industry in the Northwest. United States Department of Agricul-
ture. Washington, D.C. Report Number 25. Pathological Division,
Bureau of Animal Industry 1908. p. 237-268.
8. Rodriquez, G. M. Arsenic Poisoning from Industrial Fumes and
Gases, Notic. Neoson. 127:89-92, 95, 1965.
9. Wieman. Copper Poisoning Due to Flue Gases. Dent Tieraerzh
Wochschr. 47:279-281, 1939.
10. Bischoff, 0. and F. R. Hana. Poisoning of Domestic Animals
Through Copper and Arsenic Containing Fly Dust. Deut.Tieraerztl
Wochenscher. 17(28):442-447, July 15, 1939.
11. Nishino, 0., M. Arari, I. Senda, and K. Kuboto. Influence of
Environmental Pollution on the Sparrow (Kankyo Osen No Suzume Ni
Oyobosu Eikyo). Nippon Koshei Eisei Zasshi (Japan J. Public
Health), 20(10), 1 p., Oct. 1973.
12. Herman, Douglas. Notes on Poisoning by Carbonic Oxide. Journ
Soc Chem Ind. 15:854, 1884. abs. Persifor Frazer, Trans
Am Inst Min Eng. 38:537, 1907.
184
-------
13. McEnroe, W. D. The Effect of Automobile Traffic on American Dog
Tick Distribution (Permacenter Variabilis: Acarina, Ixodidae.
Environ Pollut., 2(2):135-143, October 1971.
14. Feriancova-Maserova, Zora and Eva Kalivodova. The Effect of
Exhalations from the Aluminum Plant in Ziar N/Hronora on the
Spectrum of Bird Species in the Vicinity of the Plant. Biologic
(Bratislava), 20(2):109-121, 1965.
15. Bourbon, P., J. Tournot, J. Alary, J. F. Rouzard, and F. Alengrin.
The Effects of Low Level Fluorine Pollution in a Mountain Valley.
Tribune Cebedean (Cent Belg Etud Doc Eviron Air). 24(327):62-66,
February 1971.
16. Ehrlich, C. Observations and Investigations of Chronic Fluorine
Poisoning in Cattle. Deut Tieraerztl. (Wochschr). 61:225-228,
June 1954.
17. Hasegawa, T. and H. Yoshikawa. On the Atmospheric Fluoride
Pollution, Part 1, J. Japan Soc Air Pollution. 4(1):147, 1969.
18. Hupka, E. and P. Luy. Frequent Occurrence of Osteomalacia Among
Grazing Cattle Caused by Hydrofluoric Acid contained in the Flue
Gas Discharged by a Chemical Plant. Arch. Wissenschaff-Liche
Praktisch Tierheilkunde (Berlin). 60:21-39, 1929.
19. Narozeny, J. Dental Fluorsis of Cattle. Vet Med. 7:421-424,
1965.
20. Rosenberger, G., and H. D. Gruender. Investigations into the
Effects of Fluorine Itranissions on Cattle in the Neighborhood
of a Hydrofluoric Acid Plant. Franklin Inst. Research Labs.
Philadelphia, Science Info. Services, Contract No. CPA 22-69-30,
Project No. C2939. 1968.
21. Spencer, G. R., E. C. Stone, and D. F. Adams. Fluorides in
Animals in the Dallesport Area. Washington State University
Agricultural Experiment Station. Pullman. State Circular
Number 353. 1959.
22. Lezovir, J. The Influence of Fluorine Compounds on the
Biological Life Near an Aluminum Factory. Fluoride Quarterly,
J. Intern Soc. Fluoride Res. 2(1):25-27, Jan. 1969.
23. Agate, J. N., et al. Industrial Fluorosis, A Study of the
Hazard to Man and Animals Near Fort William, Scotland. A Report
to the Fluorosis Committee. Medical Research Council Memorandum
No. 22, p. 131. London. H. M. Stationary Office. 1949.
185
-------
24. Balazova, G., and F. Hlachan. The Effects of Fluorine Inhalation
on Animals in the Surrounding of Aluminum Plant. Air Pollution
Proc. 1st European Congress. Influence Air Pollution: Plant,
Animals, Wageningen. 1968.p. 275-279.
25. Newman, J. R. and M. Yu. Fluorosis in Black-tailed Deer (Odo-
colleus hemionus). Submitted to J. Wild. Dis., Feb. 1974.
26. Karstad, L. H. A. Wildlife in Changing Environments, in:
Elrich, D. F. (ed). Environmental Change, Locus on Ontario,
N.Y. New York: Simon and Schuster, Inc. 1970.
27. Daessler, H. C. The Effect of Hydrogen Fluoride and Cryolite
Dust upon Plants and Animals Near a Hydrogen Fluoride Factory.
Fluoride 4(l):21-22, January 1971.
28. Bardelli, P. and C. Menzani. Studies of Spontaneous Fluorosis
in Ruminants: A note on Prophylaxis. Annali D'Igiene.
45(6):399-404, 1935.
29. Yamazoe, F. The Effect of Air Pollution on Agriculture and
Forestry. Nogyo Oyobi Engei 48(1):133-138, 1973.
30. Radeloff, H. Investigation and Appraisal of Flue-Gas Damage.
[In German] Hamburg Staatsinst. Angew. Botanik Jahresber., 6:
126-127, 1939.
31. Hasumi, K. Modernization of Hygenic Laboratory. 2: Hydrogen
Fluoride Pollution. Fukushima-ken Eisen Ken Kyusho Kenkyu
Hokoku 17(3):27-30, 1969.
32. Dewey, J. E. Accumulation of Fluoride by Insects Near an Emis-
sion Source in Western Montana. Environ. Entomol. 2(2):179-
182, April 1973.
33. Mazel, A. Fluoruroses Industrelles Imprimeril Ouvriere.
(Toulouse). 2nd ed., p. 141, 1958.
34. Pfeffer, A. Insect Pests on Firs in Air Pollution Areas.
Z Angew Entemol. 51:203-207, 1962/1963.
35. Wentzel, K. F. Insects as Emission-Related Pests. Naturwis-
senchaffen (Berlin) 52(5):113, 1965.
36. Henneman, J. Frequent Occurrence of Stomach and Intestine
Diseases in Cattle Caused by Iron Containing Flue Gases. Wien.
Tierderztl. Monatsschr., 18(8):225-231, 1931.
186
-------
37. Harris, R. D. Birds Collected (Die Off) at Prince Rupert, B.C.,
September 1971. Canadian Wildlife Service, unpublished report.
1 October 1971. 1971. 6 p.
38. McCabe, L. C. and G. D. Clayton. Air Pollution by Hydrogen Sul-
fide in Poza Rica, Mexico. Arch. Indus. Hyg. Occup. Med. 6:199-
213, 1952.
39. Yont, W. P. and R. R. Sayers. Hydrogen Sulfide as a Laboratory
and Industrial Poison. Jour. Chem. Ed. 4:613-619, 1927.
40. Gardner, A. W. and P. K. Hallpatch. Molybdenosis in Cattle Grazing
Downwind from an Oil Refinery Unit. Vet. Rec., 82: January, 1968.
41. Ogura, Y. Molybdenum Poisoning in Cattle Due to Air and Soil
Contamination as an Industrial Hazard. Japanese Tokyo National
Institute of Animal Health Bulletin. 50:24-29, 1965.
42. Verwiej, J. H. P. Molybdenosis in Cattle by Air Pollution.
Tojaschr Diergeneesk., 96(22):1508-1515, 1971.
43. Light, J. T. Effects of Oxidant Air Pollution on Forest Ecosys-
tem of the San Bernadino Mountains. In: Oxidant Air Pollution
Effect on a Western Coniferous Forest Ecosystem, Task B Report:
Historical Background and Proposed Systems Study of the San
Bernadino Mountains Area. Taylor, 0. C. (ed.). Air Pollution
Research Center, University of California, Riverside. Jan. 1973,
p. Bl-12.
44. Cobb, F. W. Jr., D. L. Wood, R. W. Stark, and J. R. Parameter, Jr.
Photochemical Oxident Injury and Bark Beetle (Coleoptera: Scoly-
tidae) Infestation of Ponderosa Pine IV. Theory on the Relation-
ships Between Oxident Injury and Bark Beetle Infestation.
Hilgardia 39(6):145-152. May 1968.
45. losif, C. Acute and Chronic Lead Poisoning in Cattle. Rec. Med.
Vet. Ecol. (Alfort) 142(2):95-106, February 1966.
46. Hammond, P. B. and A. L. Aronson. Lead Poisoning in Cattle and
Horses in the Vicinity of a Smelter. Ann. N. Y. Acad. Sci. Ill:
595-611, 1964.
47. Egan, D. A. and T. O'Cuill. Open East Lead Mining Areas—A
Toxic Hazard to Grazing Stock. Vet Rec. 84(9):230. March 1969.
48. Haring, C. M. and K. F. Meyer. Investigation of Live Stock
Conditions and Losses in the Selby Smoke Zone. Bull. Bureau
Mines, No. 98. 1915. 474-520.
187
-------
49. Ottobone, F., and E. Kohn. Study of Benica Area Horses' Death,
Interim Report. California State Department of Public Health.
Berkeley. Bureau of Occupational Health and Environmental
Epidemiology. May 1, 1970. 12 p.
50. Schmitt, N., G. Brown, E. L. Devlin, A. A. Larsen, J. M. Saville
and E. D. McCausland. Lead Poisoning in Horses. An Environ-
mental Health Hazard. Arch. Environ. Health 23:185-95, Sept.
1971.
51. Parliceric, M. The Occurrence of Lethal Paralysis in Young Sheep
as a Result of Poisoning From Factory Smoke. Vet Glas. 11:1085-
1088, 1962.
52. Bazell, R. J. Lead Poisoning: Zoo Animals May be First Victims.
Science 173(3992):130-131, 1971.
53. Kerin, D., and Z. Kerrin. Lead Contamination of Milk and Honey
Through Lead Aerosols by the Industry. Prot. Vitae. 16(2):61-62,
April 1971.
54. Doane, R. W. Insect Pests in the Selby Smoke Zone. Bull.
Bureau Mines, No. 98:428-450 and 503-520, 1915.
55. Masek, J. and K. Hais. Negative Effects of Industrial Exhalations
on Cattle. Vet. Med. (Czech) 8(5):341-346, 1963.
56. Rubay, M. About the Accidents Caused by Fog in the Meuse area.
Ann Med Veterinaire. 77:390-391, 1932.
57. Rubay, M. About the Fog Observed in the Meuse Valley in December
1930 and Its Noxious Effects on Animals. Ann Med Veterinaire.
77:145-158, April 1932.
58. Pfeffer, A. The Effect of Air Pollution with S02 on the Country-
side. In Preprints of the Czechoslovak Reports. International
Symposium on the Control and Utilization of S0_ and Fly-Ash from
Flue Gases of Large Thermal Power Plants. Liblace House of
Scientific Workers p. 171-183, 1965.
59. Gilbert, 0. L. Some Indirect Effects of Air Pollution on Bark-
Living Invertebrates. J. Appl Ecol. 8(1):77-84, 1971.
60. Hilliman, R. C. Biological Effects of Air Pollution on Insects,
Emphasizing the Reactions of the Honey Bee. (Apis Mellifera L.)
to S0_. Penn State Univ., Univ. Park, Dept. of Entomology,
Thesis, (Ph.D.), Ann Arbor, Mich., Univ. Microfilms,Inc. March,
1972.
188
-------
61. Pfeffer, A. The Effects of Air Polluted with SO on the Coun-
tryside. In: Preprints of the Czechoslovak Reports. Interna-
tional Symposium on the Control and Utilization of SO and Fly-
Ash from the Flue Gases of Large Thermal Power Plants. Liblace
House of Scientific Workers, p. 171-183, 1965.
62. Freitag et al. Ground Beetle Populations Near a Kraft Mill.
The Canadian Entomol. 105:299-310, 1973.
63. Przylbylski, Z. Result of Consecutive Observations of Effects of
SO , SO and H SO Gases and Vapors on Trees, Shrubs, Entomo-
fauna of Orchards in the Vicinity of Sulfur Mines and Sulfur
Processing Plants in Mochow [In Polish] Poslepy Nauk Robn.
(Warsaw) 15(6):131-138, 1968.
64. Sierpinski, Z. The Significance of Secondary Pine Parasites in
Areas of Chronic Exposure to Industrial Pollution. M. H. Forst.
Bundesuers. 97:609-615. 1972.
65. Bassus, W. On the Effects of Industrial Emissions on the Popula-
tion of Nematoda in the Soil of Pine Forests. Pedo Biol. 8:289-
295, 1968.
66. Lees, D. R., E. R. Creed and J. G. Duckett. Atmospheric Pollu-
tion and Industrial Melanism. Heredity (landon) 30:227-32.
April 1973.
67. Oliver, T. Dust and Fumes, Foes of Industrial Life. Lancet
183:365, 1912.
68. Darley, E. F. Studies on the Effects of Cement-kiln Dust on
Vegetation. Jour. Air Pollut. Contr. Assoc. 16:145-51, 1966.
69. Ashew, R. R., L. M. Cook, and J. A. Bishop. Atmospheric Pollution
and Melanic Moths in Manchester and Its Environs. Jour. Appl.
Ecol. 8:247-256, April, 1971.
70. Alexander, J. Fatal Belgian Fog. Science 73:96, 1931.
71. Chemical Age. Smoke Abatement from the Point of View of Public
Health, 33 p.333, 1935.
72. Noxious Vapors. Her Majesty's Stationery Office. London. Royal
Commission Report 614:72, 1878.
73. Schwabe, C. W. Veterinary Medicine and Human Health. Baltimore,
Williams and Wilkins Co. 1969.
189
-------
74. Scientific American. Smoky Air and Animals. Vol. Ill, p. 299,
1914.
75. Ragland, W. L. and J. R. Gorham. Tonsillar Carcinoma in Rural
Dogs. Nature 214:925-926, 1967.
76. Reef, J. S. and D. Cohen. The Environmental Distribution of
Canine Respiratory Tract Neoplasms. Arch. Environ. Health 22.
136-140, 1971.
77. Snyder, R. L. and H. L. Ratsliffe. Primary Lung Cancers in Birds
and Mammals of the Philadelphia Zoo. Cancer Res. 26:514-518, 1966.
78. Wellings, S. R. Respiratory Damage Due to Atmospheric Pollutants
in the English Sparrow, passerdomesticus. In: Project Clean
Air. California University of Davis, Department of Pathology,
California University Research Project S-25, Sept. 1, 1970.
79. Annual Report on the State of Environmental Pollution. Aichi
Prefectural Government. Environmental White Paper 1972. 355 p.
80. Kawai, Shozo. A Study on Urban Environment and the Growth of
Concha Vermin Parasites. In: Study on Animals and Plants as
Human Environmental Indices under Urban Environment. Japan
Environmental Agency. March, 1973. p. 18-57.
81. Liebenow, H. Bearings of Emissions on Plants and Livestock.
Monatsh. Veterinaermed. 26(3):106-111, Feb. 1, 1971.
82. Schrenk, H. H. , H. Heimann, G. D. Clayton, W. M. Gafefer, and H.
Wexler. Air Pollution in Donora, Pa. Washington, D. C. Federal
Security Agency, Public Health Service, Division of Industrial
Hygiene. Public Health Bull. No. 306, 1949. 173 p.
83. Wentzel, K. F. and B. Ohnesorge. Occurance of Insect Pests with
Air Pollution. Forslavchiv. 32:177-186, 1961.
84. Berge, H. Relationship Between Tree Pests and Emissions.
Anz. Schaedlingskunde 46:155-156, 1973.
85. Sierpinski, Z. Influence of Industrial Air Pollutants on the
Population Dynamics of Some Primary Pine Pests. International
Union of Forest Research Organizations, Vienna (Austria), Proc.
Congr. Intern. Union Forest Research Organization, Munich,W.
Germany 5(24):510-531, 1967.
86. Sierpinski, Z. Secondary Noxious Insects of Pine Stands Growing
in Areas with Industrial Pollution Containing Nitrogen Com-
pounds. Sylwan 115(10):11-18, October 1971.
190
-------
87. Pfeffer, A. Insects as Bioindicators. (Insekten als Bioindika-
toren). Terplan-Statni Ustav Pro Uzemni Planovani, Ustav
Krajinne Ekologie Czav, Bioindikatory Deteriorizace Krajiny,
Sbornik Z Mezinarodni (Conference, Prague, Czechoslovakia, 1971.
p. 83-85.
88. Leibetseder, J. , M. Skalicky, A. H. Said, A. Kraent, E. Glawi-
schnig, and G. Schlerka. Studies of the Toxic Effect of Hay on
Cattle in Smoke-Injured Areas. Z. Erzbergbau Metallhue Henwessen,
25(10): 498-505, 1972.
89. Dunn, J. T. and H. C. L. Blokam. The Occurrence of Lead, Copper,
Zinc, and Arsenic Compounds in Atmospheric Dusts, and the Sources
of these Impurities. J Soc Chem Ind. 52:189T-92T, 1933.
90. Parliceric, M. The Occurrence of Lethal Paralysis in Young
Sheep as a result of Poisoning from Factory Smoke. Vet. Glas.,
11:1085-1088, 1962.
91. Lewis, T. R. Effects of Air Pollution on Livestock and Animal
Products. In: Helena Valley, Montana, Area Environmental Pollu-
tion Study, Environmental Protection Agency Research. Triangle
Park, N.C. Publication Number AP-91, 1972. Office of Air Pro-
grams, p. 113-124.
92. Schmitt, N., G. Brown, E. L. Devlin, A. A. Larson, E. D. McCaus-
land, and J. M. Saville. Lead Poisoning in Horses. Arch.
Environ Health 23:185-197, 1971.
93. Gish, C. D. and R. E. Christen. Cadmium, Nickel, Lead, Zinc in
Earthworms in Roadside Soil. Env. Sci. Tech. 7:1060, 1973.
94. Sigmund, 0. H. The Merck Veterinary Manual. Rahway, N.J.
1973. 1600 p.
95. Novakova, E. and Z. Roubal. Calcium and Phosphorus Ratios in
the Blood Serum of Hares Subject to Air Pollution. Union In-
ternat. des Biologistes du Gibier, Acles du X Congres, Paris
3-7 Mai. p. 530-536.
96. Tansey, M. F. and R. P. Roth. Pigeons. A New Role in Air
Pollution. J. Air Poll. Constr. Ass. 20:307-6. 1970.
97. Selikoff, I. J. and E. C. Hammond. 1968. Community Effects of
Non-occupational Environmental Asbestos Exposure. Am. J. Public
Health 58(9):1658.
191
-------
98. McArn, G. E., M. L. Boardman, R. Munn and S. R. Wellings. Rela-
tionship of Pulmonary Particulates in English Sparrows to Gross
Air Pollution. J. Wild. Dis. 10:335-340, Oct. 1974.
99. Huckabee, J. W., F. 0. Car tan, and G. S. Kenning ton. Environ-
mental Influence on Trace Elements in Hair of 15 Species of
Mammals. Oak Ridge, Tenn. ORNL-TM-37 47, Oak Ridge National
Laboratory. June, 1972. 38 p.
100. Jefferies, D. J. and M. C. French. Lead Concentration in Small
Mammals Trapped on Roadside Verges and Field Sites, Environ.
Pollut. 3:147-156, 1972.
101. Carlson, L. E. and J. E. Dewey. Environmental Contamination by
Airborne Fluorides in Montana. Phytopathology 61(8):887, 1971.
102. Nielson, S. W. Environmental Pollutants Pathogenic to Animals.
J Am Vet Med Assoc. 159:1103-7, November 1971.
103. Jefferies, D. J. and M. C. French. Lead Concentrations in Small
Mammals Trapped on Roadside Verges and Field Sites. Environ.
Pollut. 3:147-156. 1972.
104. Lillie, R. Air Pollutants Affecting the Performance of Domestic
Animals. United States Department of Agriculture. Washington.
D.C. Handbook Number 380. 1970. 109 p.
105. Dethier, V. G. Chemical Interactions Between Plants and Insects.
In: Chemical Ecology. Sondheimer, E. and J. B. Simeone (eds.).
New York, Academic Press, 1970. p. 83-102.
106. Gilbert, B. L. and D. M. Norris. A Chemical Basis for Bark
Beetle (Scolytus) Distinction Between Host and Non-Host Trees.
J. Insect Physiol. 14:1063-1068, 1968.
107. Eisner, T. Chemical Defense Against Predation in Arthropods.
In: Chemical Ecology. Sondeheimer, E. and J. B. Simeone (eds.)
New York. Academic Press. 1970. p. 157-217.
108. Buck, W. B., G. D. Osweiler, and G. A. Van Gelder. Clinical and
Diagnostic Veterinary Toxicology. Dubuque, Iowa. Kendall/Hunt
Publ. Co. 1973. 233 p.
109. Garner, R. J. Veterinary Toxicology. London, Balliere, Tindall
and Cox. 1957. p. 42-255.
110. Miner, S. Preliminary Air Pollution Survey of Barium and Its
Compounds, a Literature Review. National Air Pollution Control
Administration Publication Number APTD 69-28. October 1969.
57 p.
192
-------
111. Sullivan R. J. Air Pollution Aspects of Manganese and Its
Compounds. Litton Systems, Inc., Bethesda, Md, Environmental
Systems Div., Sept. 1969.
112. Sullivan, R. J. Preliminary Air Pollution Survey of Chromium
and its Compound. A Literature Review. National Air Pollution
Control Administration Publication Number APTD 69-34. October
1969. 75.
193
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