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

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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

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                               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.

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         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

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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

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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

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                                 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

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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

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                                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

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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

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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

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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

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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

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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

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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

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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

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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

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      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

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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.

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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

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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

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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

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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

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      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

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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

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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

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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

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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

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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

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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

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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

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       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

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 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

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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

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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

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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

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                            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

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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

-------
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