AIR  QUALITY CRITERIA
FOR

SULFUR OXIDES
   U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFA1
                  Public Health Service
         Consumer Protection and Environmental Health Service

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                                      AP50
          AIR QUALITY CRITERIA
                       FOR
               SULFUR  OXIDES
U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE
                 Public Health Service
    Consumer Protection and Environmental Health Service
            National Air Pollution Control Administration
                    Washington, D. C.
                      January 1969

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National Air Pollution Control Administration Publication No. AP-50

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                                      Preface
  Air quality criteria tell us what science has
thus far been  able to meaure of the obvious
as well as the insidious effects of air pollution
on man and his environment. Such criteria
provide  the  most  realistic basis that  we
presently have for determining to what point
the levels of pollution must be reduced if we
are to protect the public health and welfare.
  The  criteria  that we  can  issue  at  the
present time do not tell us all that we would
like to know. If all of man's previous experi-
ence in  evaluating  environmental  hazards
provides us with a guide, it is likely that im-
proved knowledge will show that there are
identifiable health and welfare hazards  as-
sociated  with  air pollution levels that were
previously  thought to be innocuous.  As our
scientific knowledge grows,  air quality  cri-
teria will have  to  be reviewed  and, in all
probability, revised.  But the  Congress  has
made it clear  that we are  expected, without
delay, to make the most effective use of the
knowledge  we now have.
  The Air  Quality Act of 1967 requires that
the Secretary of Health, Education, and Wel-
fare ". . . from time to time, but  as soon as
practicable, develop  and issue to  the  States
such criteria of air quality as in his judgment
may be requisite for  the  protection of the
public health  and  welfare.  . . Such criteria
shall. . . reflect the latest scientific knowledge
useful in indicating the kind and extent of all
identifiable effects  on  health and  welfare
which maybe expected from the presence of
an air pollution agent. . ."
  Under the Air Quality Act, the issuance of
air  quality criteria is  a vital step in a pro-
gram designed to assist the States in taking
responsible technological, social, and political
action to protect the public from the adverse
effects of air pollution.
  Briefly, the  Act calls for the Secretary of
Health,  Education, and Welfare to define the
broad  atmospheric areas  of  the  Nation in
which climate, meteorology, and topography,
all of which  influence the  capacity of air to
dilute and disperse pollution,  are generally
homogeneous.
  Further, the Act requires the Secretary to
define those geographical regions in the coun-
try where air pollution is a problem—wheth-
er interstate or  intrastate. These  air quality
control  regions  will be designated  on the
basis of meteorological, social, and political
factors  which suggest that a  group of com-
munities should  be treated as a unit for set-
ting limitations  on concentrations of atmos-
pheric pollutants.  Concurrently,  the  Secre-
tary is  required to issue air quality criteria
for those pollutants he believes may be harm-
ful to health or welfare, and to publish re-
lated information  on the  techniques  which
can  be  employed  to  'control the  sources of
those pollutants.
  Once these steps have been taken for any
region, and for any pollutant or combination
of pollutants, then the State or States respon-
sible for the  designated region are on notice
to develop  ambient air quality standards ap-
plicable to the region for  the  pollutants in-
volved,  and to develop plans  for  action for
meeting the standards.
  The Department of Health, Education, and
Welfare will review, evaluate, and approve
these standards  and plans,  and once they are
approved, the States will be expected to  take
action to control pollution sources in the man-
ner outlined in their plans.
  At the direction of the Secretary, the Na-
tional Air  Pollution Control Administration
has  established  appropriate  programs to
carry out the several Federal responsibilities
specified in the legislation.
  The Air Quality Act of 1967 requires  that
". . . criteria issued prior to enactment of this
section  November 21,  1967  shall  be re-
                                                                               in

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evaluated in accordance with the consultation
procedure . . . and, if necessary, modified and
reissued." Air  Quality Criteria for  Sulfur
Oxides was first published in  March 1967.
This edition reflects the reevaluation, and re-
sulting modification called for by the Act.
  In accordance with the Act, a National Air
Quality Criteria Advisory  Committee was
established,  having  a  membership broadly
representative of industry, universities, con-
servation interests, and all levels of govern-
ment. The committee, whose members  are
listed  following this  discussion,  provided
invaluable advice on policies and procedures
under which to issue criteria, and provided
major assistance in reevaluating the original
document.
  With the help of a Subcommittee on Sulfur
Oxides, expert  consultants were retained to
rewrite and edit portions  of the document,
with other segments being revised by staff
members of the National Air Pollution Con-
trol  Administration. After the initial revi-
sions, there followed a  sequence of review by
the subcommittee, and  by the full committee,
as well as by individual reviewers especially
selected for their competence and  expertise
in the  many fields of science and technology
related to the problems of atmospheric pollu-
tion by sulfur oxides. These efforts, without
which  this  document  could  not have been
completed  successfully,  are  acknowledged
individually on the following pages.
  As also required by the Air Quality Act of
1967,  appropriate Federal  departments and
agencies, also listed on the following pages,
were consulted prior to issuing this criteria
document. A Federal consultation committee,
comprising members designated by the heads
of seventeen departments and agencies, re-
viewed the document, and met with staff per-
sonnel of the National Air Pollution Control
Administration to discuss their comments.
  This Administration is pleased to acknowl-
edge the efforts of each of the persons speci-
fically  named, as well as the many not named
who contributed  to the publication of this
volume.  In  the  last analysis,  however,  the
National Air  Pollution Control Administra-
tion is responsible for its content.
            JOHN T. MIDDLBTON,
 Commissioner, National Air Pollution
                  Control Administration
       IV

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         NATIONAL  AIR QUALITY CRITERIA ADVISORY COMMITTEE

                                     Chairman
                        DR. JOHN T. MIDDLETON, Commissioner
                     National Air Pollution Control Administration
Dr. Herman R. Amberg
Manager, Manufacturing Services Dept.
Central Research Division
Crown Zellerbach Corp.
Camas, Wash.

Dr. Nyle C. Brady
Director, Agricultural Experiment
  Station
Cornell University
Ithaca, N.Y.

Dr. Seymour Calvert
Director, Statewide Air Pollution
  Research Center
University of California, Riverside
Riverside, Calif.

Dr. Adrian Ramond Chamberlain
Vice President
Colorado State University
Fort Collins, Colo.

*Dr. Raymond F. Dasmann
Senior Ecologist
Conservation Foundation
Washington, D.C.

Mr. James R. Garvey
President and Director
Bituminous Coal Research, Inc.
Monroeville, Pa.

Dr. David M. Gates
Director
Missouri Botanical Gardens
St. Louis, Mo.
  * Resigned, October 14, 1968
Dr. Neil V. Hakala
President
Esso Research & Engineering Co.
Linden, N.J.

Dr. Ian T. Higgins
Professor, School of Public Health
The University of Michigan
Ann Arbor, Mich.

Mr. Donald A. Jensen
Executive Engineer
Ford Motor Co.
Dearborn, Mich.

Dr. Herbert E.  Klarman
Professor of Public Health Administration
  and Political Economy
School of Hygiene and Public Health
Johns Hopkins University
Baltimore, Md.

Dr. Leonard T. Kurland
Professor of Epidemiology
Mayo Graduate School of Medicine
Head, Medical Statistics
Epidemiology and Population Genetics
Section, Mayo Clinic
Rochester, Minn.

Dr. Frederick Sargent II
Dean, College of Environmental
  Sciences
University of Wisconsin
Green Bay, Wis.

Mr. William J. Stanley
Director, Chicago Department of
  Air Pollution Control
Chicago, 111.

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                       CONTRIBUTORS  AND  REVIEWERS
Dr. Mary 0. Amdur
Associate Professor of Toxicology
Department of Physiology
School of Public Health
Harvard University
Boston,  Mass.

Dr. Rodney R. Beard
Executive Head, Department
  of Preventive Medicine
Stanford University Medical School
Palo Alto, Calif.

Dr. Francis E. Blacet
Emeritus Professor of Chemistry
University of California, Los Angeles
Los Angeles, Calif.

Dr. L. J. Brasser
Head, Atmospheric Pollution Division
Research Institute for
  Public Health Engineering
Delft, The Netherlands

Dr. Robert Carrol
Professor of Epidemiology
Albany Medical College
Albany, N.Y.

Dr. Eric J. Cassell
Associate Professor of Community Medicine
The Mount Sinai Hospital
Mt. Sinai School of Medicine
New York, N.Y.

Dr. R. E. Eckardt
Director
Medical Research Division
Esso Research and  Engineering  Co.
Linden, N.J.

Dr. James G. Edinger
Professor of Meteorology
University of California
Los Angeles, Calif.

Dr. David W. Fassett
Director, Laboratory of Industrial Medicine
Eastman Kodak Co.
Rochester, N.Y.

Dr. Lars Friberg
Chief, Department of Hygiene
Karolinska Institute of Hygiene
Stockholm, Sweden
Dr. John R. Goldsmith
Chief, Environmental Hazards
  Evaluation Unit
Department of Public Health
State of California
Berkeley, Calif.

Dr. Leonard Greenburg
Professor of Preventive and
  Environmental Medicine
Albert Einstein College of Medicine
New York, N.Y.

Mr. John H. Jacobs
Principal Research Physicist
Bell & Howell Research Center
(Chicago, 111.)
Pasadena, Calif.

Dr. P. E. Joosting
Medical Service
Research Institute for
  Public Health Engineering
Delft,  The Netherlands

Dr. Herbert Landesman
Consulting Chemist
Pasadena, Calif.

Mr. Benjanmin Linsky
Professor, Department of Civil Engineering
West Virginia University
Morgantown, W. Va.
Dr. Harold MacFarland
Professor, York University Faculty of
  Arts and Sciences
Toronto, Ontario

Dr. Robert Mason
Graduate Department of
  Community Planning
University of Cincinnati
Cincinnati, Ohio

Dr. James R. McCarroll
Professor of Preventive Medicine
School of Medicine
University of Washington
Seattle, Wash.

Dr. James N. Pitts, Jr.
Professor of Chemistry
University of California, Riverside
Riverside, Calif.

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Mr. Alexander Rihm, Jr., P.E.
Assistant Commissioner
Division of Air Resources
New York State Department of Health
Albany, N.Y.
Dr. Bernard Saltzman
Kettering Laboratory
University of Cincinnati
Cincinnati, Ohio

Mr. Jean J. Schueneman
Chief, Division of Air Quality Control
Maryland State Department of Health
Baltimore, Md.

Dr. William S.  Spicer
Director, Division of Respiratory Diseases
University of Maryland School of Medicine
Baltimore, Md.
Dr. Wayne T. Sproull
Consultant in Physics
Pasadena, Calif.

Dr. E. Stephens
Research Chemist
Air Pollution Research Center
University of California,  Riverside
Riverside, Calif.
Dr. 0. Clifton Taylor
Associate Director
Statewide Air Pollution Research Center
University of California, Riverside
Riverside, Calif.

Dr. Moyer D. Thomas
Editor, Inter-Society Committee Manual of
  Methods for Ambient Air Sampling and
  Analysis
Riverside, Calif.

Dr. Paul Urone
Professor
Department of Chemistry
University of Colorado
Boulder,  Colo.

Mr. Hans K. Ury
Special  Consultant
Environmental Hazards Evaluation Unit
California State Department of Public Health
Berkeley, Calif.

Mr. Ralph C. Wands
Director, Advisory Center on Toxicology
National Research Council
Washington, D.C.

Dr. Richard P. Wayne
Oxford  University
London, England
Visiting Professor in Photochemistry
University of California, Riverside
Riverside, Calif.
                                                                              VII

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               FEDERAL AGENCY LIAISON REPRESENTATIVES
Department of Agriculture
Kenneth E. Grant
Associate Administrator
Soil Conservation Service

Department of Commerce
Paul T. O'Day
Staff Assistant to the Secretary

Department of Defense
Colonel Alvin F. Meyer, Jr.
Chairman
Environmental Pollution Control Committee

Department of Housing and Urban
  Development
Charles M. Haar
Assistant Secretary for Metropolitan
  Development

Department of the Interior
Harry Perry
Mineral Resources Research Advisor

Department of Justice
Walter Kiechel, Jr.
Assistant Chief
General Litigation  Section
Land and Natural Resources Division

Department of Labor
Dr. Leonard R. Linsenmayer
Deputy Director
Bureau of Labor Standards

Department of Transportation
William H. Close
Assistant Director for Environmental
  Research
Office of Noise Abatement
Department of the Treasury
Gerard M. Brannon
Director
Office of Tax Analysis
Federal Power Commission
F. Stewart Brown
Chief
Bureau of Power
General Services Administration
Thomas E. Crocker
Director
Repair and Improvement Division
Public Buildings Service
National Aeronautics and Space
  Administration
Major General R. H. Curtin, USAF (Ret.)
Director of Facilities
National Science Foundation
Dr. Eugene W. Bierly
Program Director for Meteorology
Division of Environmental Sciences
Post Office Department
Louis B. Feldman
Chief
Transportation Equipment Branch
Bureau of Research and Engineering
Tennessee Valley Authority
Dr. F.  E.  Gartrell
Assistant Director of Health

Atomic  Energy Commission
Dr. Martin B. Biles
Director
Division of Operational Safety

Veterans Administration
Gerald M. Hollander
Director of Architecture and Engineering
Office of Construction
       vm

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AIR  QUALITY  CRITERIA FOR  SULFUR  OXIDES
                    TABLE OF  CONTENTS
 Chapter
       Preface                                                    iii
       Introduction                                                  x
    1  Physical and Chemical Properties and the Atmospheric Reactions
       of the Oxides of Sulfur                                         1
    2  Sources and  Methods  of Measurements of  Sulfur Oxides in the
       Atmosphere                                                 17
    3  Atmospheric Concentrations of Sulfur Oxides                      31
    4  Effects of Sulfur Oxides in the Atmosphere on Materials             49
    5  Effects of Sulfur Oxides in the Atmosphere on Vegetation             59
    6  Toxicological Effects of Sulfur Oxides on Animals                  71
    7  Toxicological Effects of Sulfur Oxides on Man                     89
    8  Combined Effects of Experimental Exposures to Sulfur Oxides and
       Particulate Matter on Man and Animals                         103
    9  Epidemiological Appraisal of Sulfur Oxides      .........         113
   10  Summary and Conclusions                       .             151
 Appendices
   A  Symbols                                           .        164
   B  Abbreviations                                               165
   C  Conversion Factors              .                             166
   D  Glossary                                              .167
      Author Index                                               172
      Subject Index [[[    175

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                                 INTRODUCTION
  Pursuant to  authority  delegated to  the
Commissioner of the National Air Pollution
Control Administration, Air Quality Criteria
for Sulfur  Oxides is issued in accordance
with Section 107bl of the Clean Air Act  (42
U.S.C. 1857c-2bl).
  Air  quality criteria are an expression of
the scientific knowledge of the relationship
between various concentrations of pollutants
in the air and their  adverse  effects on man
and his environment. They are issued to as-
sist the States in developing air quality stand-
ards. Air quality criteria are descriptive; that
is, they describe the effect that have been ob-
served to occur when the ambient air level of
a pollutant has reached or exceeded a specific
figure  for a specific time period. In develop-
ing criteria, many factors have to be con-
sidered. The chemical  and physical  charac-
teristics of the pollutants and the techniques
available for measuring these characteristics
must   be  considered,  along  with  exposure
time, relative humidity, and other conditions
of the  environment.  The criteria must con-
sider the contribution of all such variables to
the effects of air pollution on human health,
agriculture, materials, visibility, and climate.
Further, the individual characteristics of the
receptor must be taken into account. Table A
is a listing of the major factors that need to
be considered in developing criteria.1
  Air   quality standards  are  prescriptive.
They  prescribe pollutant exposures which a
political jurisdiction determines should  not
be exceeded in a specified  geographic area,
and are used as one of several factors in de-
  1 Calvert S. Statement for air  quality  criteria
hearings held by the Subcommittee on Air and Water
Pollution  of the  U.S. Senate Committee on Public
Works, July 30, 1968, published in "Hearings Before
the Subcommittee on Air and Water Pollution of the
Committee on Public Works, United  States Senate
(Air Pollution-1968, Part 2)."
signing legally  enforceable  pollutant  emis-
sion standards.
  This document focuses on the sulfur oxides
commonly found in the atmosphere—sulfur
dioxide, sulfur trioxide, their acids, and the
salts of their acids.  Other oxides of sulfur
are well known in the laboratory, but their
presence in  the atmosphere has not been
demonstrated. Futher, this document consid-
ers the effects of the sulfur oxides in conjunc-
tion with other pollutant classes, especially
particulate matter,  where important syner-
gistic  effects are  observed.  (Atmospheric
particulate matter is treated in  detail in  a
companion document:  Air Quality Criteria
for Particuldte  Matter.)
  This publication reviews the chemical  and
physical characteristics of the sulfur oxides,
and considers the various analytical methods
for measuring them in the atmosphere. Also
discussed are the effects of the sulfur oxides
on  visibility, vegetation,  and materials.  The
toxicological effects of sulfur oxides on  ani-
mals and on man are considered  in separate
chapters.  Finally,  there  is  a discussion of
epidemiological studies that assesses the dose-
population  response  and the  response of
population  subgroups  (i.e.,  children,  the
elderly, respiratory cripples, etc.)  to sulfur
oxides and to sulfur dioxide in the presence
of particulate matter.
  In general, the terminology employed  fol-
lows usage recommended in  the publications
style guide of the American Chemical Society.
A glossary of terms, list of  symbols and ab-
breviations,  list of  conversion  factors  for
various units of measurement, author index,
and subject index are provided.
  The literature has been generally reviewed
through June 1968. The results and conclu-
sions of foreign investigations are evaluated
for their possible application to the air pollu-
tion problem in the United States. This docu-

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ment is not intended as  a complete, detailed
literature review, and  it does not cite every
published article relating to sulfur oxides in
the ambient atmosphere.  However, the litera-
ture has been reviewed thoroughly for infor-
mation related to the development of criteria,
and the document not only summarizes  the
current scientific knowledge of sulfur oxides
air pollution, but also points up the major
deficiencies in that knowledge and the needs
for further research.
   The technological and  economic aspects of
air pollution control are  considered  in com-
panion volumes  to  criteria  documents.  The
best methods and techniques for controlling
the sources of sulfur oxides emissions, as well
as the costs of applying these techniques, are
described in: Control  Techniques for Sulfur
Oxide Air Pollutants.

  Table A.—FACTORS  TO BE CONSIDERED  IN
     DEVELOPING AIR QUALITY CRITERIA

Properties  of Pollution:
    Concentration
    Chemical composition
    Mineralogical structure
    Adsorbed  gases
    Coexisting pollutants
    Physical state of pollutant
        Solid
        Liquid
        Gaseous
    Rate of transfer to receptor domain
Measurement Methods:
    Hi-Vol sampler
    Spot tape sampler
    Dust fall bucket (rate of deposition)
    Condensation nuclei counter
    Impinger (liquid filled)
    Cascade impactor
    Electrostatic precipitator
    Light scattering meter
    Chemical analysis
    Gas analysis (non-adsorbing)
    Adsorbed gas analysis
    Light scattering or attenuation
        (Ringelmann or visibility observation)
    Colored suspension
    Nucleation of precipitation
    Stabilization of fog
    Odor
    Taste
Exposure Parameters:
    Duration
    Concomitant conditions,  such as
        Temperature
        Pressure
        Humidity
Characteristics of Receptor:
    Physical characteristics
    Individual  susceptibility
    State of health
    Rate and site of transfer to receptor
Responses:
    Effects on  health  (diagnosable  effects,  latent
      effects, and effects predisposing the organism
      to disease)
        Human health
        Animal health
        Plant health
    Effects on  human comfort
    Soiling
    Other objectionable surface deposition
    Corrosion of materials
    Deterioration of materials
    Effects on  atmospheric properties
    Effects on radiation and  temperature
                                                                                       XI

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                   Chapter 1
  PHYSICAL AND CHEMICAL PROPERTIES AND THE
ATMOSPHERIC REACTIONS OF THE OXIDES OF SULFUR

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Table

     Acid Solutions in Equilibrium with Water Vapor at Different Rela-
     tive Humidities                                                       10
1-3  Scattering Ratios for Various Size Droplets of Sulfuric Acid Mist in
     Equilibrium with Water Vapor at Various Relative Humidities           11

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                                      Chapter 1

     PHYSICAL AND CHEMICAL  PROPERTIES  AND  THE ATMOSPHERIC
                   REACTIONS OF  THE  OXIDES  OF SULFUR
           A. INTRODUCTION
  Sulfur dioxide,  sulfur  trioxide,  and the
corresponding acids  and salts  (sulfites and
sulfates) are common atmospheric pollutants
which  arise mainly  from combustion  proc-
esses. In this chapter, the chemical and phys-
ical properties of  these substances are dis-
cussed in relation to  their  chemical reactions
in the atmosphere and their effect in reducing
visibility through the atmosphere, and with
respect to the methods employed for their es-
timation.  Analytical methods are described
more  fully  in Chapter 2.  More  extensive
treatments of  the chemistry of sulfur oxides
are to  be found in most works on inorganic
chemistry (e.g., references 1 and 2).

            B. OCCURRENCE
  The  oxides  S02  (sulfur dioxide)  and S03
(sulfur trioxide), with  the  corresponding
acids  H2S03  (sulfurous  acid) and  H2S04
(sulfuric acid) and  the salts of these acids,
are well known in atmospheric studies. Other
sulfur  oxides—SO, S203, S207, and S04—are
known in laboratory studies, but their  ex-
istence in the atmosphere has not been  de-
monstrated. It has been suggested, however,
that S207 may exist  in some atmospheres as
a result of  the reaction between sulfur di-
oxide and ozone.3
  Solid and liquid fossil fuels generally con-
tain appreciable quantities of sulfur, usually
in the form of inorganic sulfides and/or sul-
fur-containing organic compounds. Combus-
tion of the fuel in power plants forms sulfur
oxides in the ratio of 40 to 80 parts of sulfur
dioxide to  1 part of sulfur trioxide. Aside
from  naturally occurring oxides of sulfur,
the burning of fossil fuels such as coal and
petroleum in  the  United  States  constitutes
the major source of sulfur oxides in the
atmosphere.

     C. PHYSICAL PROPERTIES OF
           SULFUR DIOXIDES
  Sulfur  dioxide is a  nonflammable, non-
explosive, colorless gas.  In  concentrations
above 0.3 ppm to 1 ppm in air, most people
can  detect  it by taste;  in  concentrations
greater than  3  ppm  it has  a  pungent, ir-
ritating  odor  to most  people.4"7 The gas is
highly soluble in water:  11.3 g/100 ml  at
20°C, as compared to 0.004, 0.006, 0.003, and
0.169 g/100 ml for  oxygen, nitric oxide,
carbon  monoxide, and  carbon dioxide,  re-
spectively. The physical properties of sulfur
dioxide are listed in Table 1-1.

Table 1-1.—PHYSICAL PROPERTIES OF  SULFUR
                 DIOXIDE
Molecular weight 	   64.06
Density (gas), g/liter .       2.927 at 0°C; 1 atm
Specific (liquid)  gravity   .   1.434 at —10° C
Molecular volume (liquid),
  ml        .         .44
Melting point, °C .       —75.46
Boiling point, °C   ...    —10.02
Critical temperature, °C     157.2
Critcal pressure, atm ..  .    77.7
Heat of fusion, Kcal/mole    1.769
Heat of vaporization,
  Kcal/mole    	    5.96
Dielectric constant (prac-
  tical  units) ...      ..    13.8 at 14.5 °C
Viscosity, dyne sec/cm2       0.0039 at 0°C
Molecular boiling point
  constant, °C/1000g    .    1.45
Dipole moment,  Debye
  units     .      	    1.61

D.  CHEMICAL PROPERTIES OF SULFUR
    DIOXIDES AND  SULFUROUS ACID
  Sulfur  dioxide  is a gas  under ambient
atmospheric conditions and can  act as a re-

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ducing agent or as  an oxidizing agent. Of
considerable importance to the problem of
air pollution is the ability of the gas to react
either photochemically or catalytically with
materials  in the atmosphere to  form sulfur
trioxide, sulfuric acid, and salts of sulfuric
acid. These atmospheric reactions  are dis-
cussed separately in  Section G.
  Laboratory experiments  demonstrate that
sulfur dioxide may act as an oxidizing or as
a reducing agent at room temperature. In the
gaseous state, sulfur dioxide oxidizes hyrogen
sulfide to  form elemental sulfur and water.
A catalyst is generally used for this process,
which is known as the Glaus reaction.
     2H2S + S02	>3S + 2H20.     (1-1)
As a reducing agent,  the gas reacts very slow-
ly with  oxygen at 400 °C to yield sulfur tri-
oxide, but catalytic  oxidation to sulfur tri-
oxide occurs at temperatures as low as room
temperature.
                                                                    PbS04.
                                                          (1-5)
       so,-
           catalyst
S03.
                                    (1-2)
Catalysts  effective in this oxidation include
finely divided  platinum,  charcoal, vanadic
oxide (V205), graphite, chromic oxide, ferric
oxide, and the nitrogen oxides. The nitrogen
oxides are used as the catalyst in the chamber
process of manufacturing sulfuric acid from
sulfur dioxide.
  Ferrous sulfate   (FeSO4)  catalyzes  the
direct oxidation of sulfur dioxides to sulfuric
acid in the presence of oxygen and water.
     H2O + S02
    H2S04.     (1-3)
                FeS04
  Some metal oxides oxidize sulfur dioxide
directly to sulfate. Magnesium oxide (MgO),
ferric oxide (Fe203), zinc oxide (ZnO), man-
ganic oxide (Mn203), cerous oxide (Ce203),
and cupric oxide (CuO) are examples. A sul-
fide is also formed as a product if the metal
ion is not reduced to a lower valence state.
 4MgO  +  4S02	>3MgS04  + MgS
                                    (1-4)
Magnesium Sulfur  Magnesium Magnesium
  oxide     dioxide     sulfate     sulfide
  Lead  peroxide (Pb02) is an active oxidiz-
ing agent and is used to obtain an estimate of
the amount of oxidizable sulfur compounds
in air, e.g.,
  Hydrogen peroxide (H202) is used exten-
sively as an oxidizing agent in the analysis
of air  samples for sulfur  dioxide: sulfuric
acid is formed,  and is  estimated conducto-
metrically or by titration.
  Sulfur dioxide reacts  with  the halogens.
With chlorine, the product is thionyl chloride
(SOC12). On  the  other  hand,  the reaction
with iodine in aqueous  solution yields sul-
furic acid and hydrogen iodide, and the de-
colorization of a starch-iodine mixture is used
in one of the methods for the  determination
of atmospheric S02.
  Sulfur dioxide reacts with water to form
sulfurous acid (H2S03)

       S02 + H20  •   ..  H2S03.     (1-6)
The pure acid is unstable and exists only in
aqueous solution.  Sulfurous acid can react
directly with many organic dyes. The West-
Gaeke  method for the determination  of at-
mospheric  sulfur dioxide  takes advantage
of this property; pararosaniline is used as the
organic dye.

   E. PHYSICAL AND CHEMICAL PROP-
     ERTIES  OF  SULFUR TRIOXIDE
   Sulfur trioxide in ambient  air is  either
derived from  combustion sources directly or
from the oxidation of atmospheric sulfur di-
oxide.  Sulfur  trioxide may exist in the air
as a vapor if  the water vapor concentration
in the air is low enough; but if sufficient wa-
ter vapor is present  (as there probably al-
ways is in ambient air), the sulfur  trioxide
combines  immediately with water to  yield
sulfuric acid in the form of droplets.
       S03 + H20	> H2S04.        (1-7)
Sulfuric acid,  rather than  sulfur trioxide, is
thus the compound normally found in the at-
mosphere. Because of the difficulty of measur-
ing  free sulfur  trioxide in the air,  little is
known about how much may be present under
various  circumstances;  presumably,  it  is
present in the unhydrated form only in trace
amounts.
   Sulfur trioxide is a strong acid and readi-
ly converts basic oxides to  sulfates. It is also
a dehydrating agent. When phosphates, car-
bonates, perchlorates, and salts of other oxy-

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acids react with sulfur trioxide, the  cor-
responding  anhydride  of  the  oxy-acid is
formed  by  extraction  of the  elements of
water. Sulfur trioxide  may also  act  as an
oxidizing  agent,  giving free halogens  (ex-
cept fluorine)  with many  metal and non-
metal halides.  Sulfur trioxide  reacts as a
Lewis acid  with  a variety  of nitrogen-con-
taining organic ring systems to form addition
complexes.  Gilbert8 recently reviewed the
numerous and diverse reactions of sulfur tri-
oxide with organic compounds.

    F. ATMOSPHERIC  REACTIONS  OF
            SULFUR OXIDES

       1. Laboratory Investigations
  Sulfur dioxide is oxidized in  the  atmos-
phere by two main processes: photochemical
and catalytic. Gerhard and Johnstone 9 deter-
mined that the oxidation of sulfur dioxide in
30 percent sulfuric acid droplets of 0.3-/i dia-
meter in the absence of catalysts proceeds
at a rate negligible compared to the rate of
photochemical oxidation.  They pointed  out,
however, that even in  the  absence of  cat-
alysts the rate of liquid-phase oxidation in a
water fog might  be faster than in a photo-
chemical smog if the rate depends upon the
total amount of  dissolved sulfur  dioxide.
  Junge and Ryan10 studied the  oxidation of
sulfur dioxide in  solution and found that es-
sentially no  reaction occurred in the absence
of a catalyst. When ferric chloride was used
as a catalyst, oxidation did  take place.  The
final amount  of  sulfate formed  was only
slightly  dependent  on the concentration of
catalyst but was  a linear function of  sulfur
dioxide concentration. Johnstone and Cough-
anowr " estimated  from their study  of sul-
fur dioxide  oxidation in small droplets that,
if manganese sulfate was present as 1-p crys-
tals, the oxidation rate in fog droplets at 1
ppm S02 would be about 1 percent per min-
ute. Both investigators found that manga-
nese salts were more effective catalysts than
iron salts.   Bracewell and Gall12  also mea-
sured rates  of  catalytic oxidation of  sulfur
dioxide in droplets and estimated that, in the
presence of  ferric or manganous ions, rates
of oxidation could be sufficient to account for
the sulfuric acid  content of urban fogs  (as-
suming  sulfur  dioxide  concentrations  of
1750 jug/m3 or about 0.6 ppm; see appendix
for conversion factors).
  The oxidation of sulfur dioxide  essentially
stopped when the pH of the water droplets
approached 2 in Junge and Ryan's experi-
ments,10  and they suggested that the effect
is due, at least in part, to the low solubility
of sulfur dioxide in strongly acidic solutions.
If ammonia was present  in the air to neu-
tralize the acid as it was formed, oxidation
of sulfur dioxide continued. Van den Heuvel
and  Mason 13  found that  for given concen-
trations  of ammonia and  sulfur dioxide the
mass of  sulfate formed was proportional to
the product of the surface area of the drops
and the time of exposure.
  The catalytic oxidation  of sulfur dioxide
may also proceed after adsorption of the gas
on the surfaces of suspended solid particles.
Smith et  al.u demonstrated  preferential
chemisorption of  sulfur dioxide at ambient
concentrations on iron oxide and  aluminum
oxide aerosols followed by multilayered phys-
ical adsorption at  higher concentrations. Li-
berti and associates " were unable to desorb
sulfur dioxide from atmospheric  dust  sam-
ples  and  concluded  from  analyses  of these
samples that adsorbed sulfur dioxide is either
oxidized to sulfate or reacts to form a variety
of organic compounds. The interaction of
sulfur dioxide with atmospheric aerosols is
important also from the point of view of the
toxicological effects of such pollutant combi-
nations (see Chapter 8).
  Gerhard and Johnstone 9 found  the photo-
oxidation rate of  sulfur dioxide  in air and
sunlight  to be 0.1  percent to 0.2 percent per
hour; the rate did not depend upon the  pres-
ence of sodium chloride nuclei  or nitrogen
dioxide, or on changes of  relative humidity
between  30 percent to 90 percent.  Renzetti
and Doyle 16 found appreciable formation of
H2S04 aerosol by  irradiation, at 3130 A, of
sulfur dioxide at concentrations below 1 ppm
and  at relative humidity  below 50 percent.
More recently Urone et al." investigated re-
actions of sulfur dioxide in air in the  pres-
ence of water vapor with irradiation at 3100
A-4200 A;  their  results  indicate a faster
photooxidation rate when  hydrocarbon and
nitrogen dioxide are present.

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  Of primary interest in the photochemical
oxidation of sulfur dioxide is the formation
of participate matter in hydrocarbon-nitro-
gen oxides systems.  In the absence of sulfur
dioxide, little  or no  aerosol is formed when
mixtures of nitrogen oxides and most hydro-
carbons  (all at atmospheric  concentrations)
are irradiated.  (Varying amounts of par-
ticulate matter are, however, formed when
nitrogen oxides are irradiated with any of
several particular hydrocarbons  such as cy-
clic olefins.) 18-20  In the absence of nitrogen
oxides, Johnstone and  Dev  Jain 21 obtained
particulate matter when they irradiated sul-
fur oxide with %-butane both at 20 mm Hg
partial pressure;  but Kopczynski and Alt-
shuller 22  were unable to detect  any forma-
tion of particular matter when sulfur  diox-
ide at atmospheric concentration  together
with  atmospheric  concentrations of either
olefins or paraffins were irradiated. In fact,
Renzetti and Doyle1S and Dainton and Ivin 23
demonstrated that olefins can suppress the
production of particulate matter during ir-
radiation of sulfur dioxide in the absence of
nitrogen oxides.
   On  the other  hand,  mixtures of olefins,
nitrogen dioxide, and sulfur dioxide definitely
form an aerosol in the presence of sunlight.
Thus a major product of the complex photo-
chemical reaction is sulf uric acid,16 24~26 which
is a hygroscopic material that adsorbs water
to form light-scattering droplets of sulfuric
acid mist. The density of such a haze obvious-
ly will depend on the prevailing relative hu-
midity. Sulfuric acid is sufficiently nonvolatile
to self-nucleate even at realistic  atmospheric
concentrations but  this may not be neces-
sary in view  of the large numbers of nuclei
present even  in "clean" air.  The exact mech-
anism by which sulfur dioxide is converted to
sulfuric  acid  mist remains unclear.  Even
more uncertain is the chemical nature of the
aerosol  reportedly formed  in hydrocarbon-
nitrogen  oxide systems without sulfur di-
oxide.
   For detailed reviews  of photochemical air
pollution, the work of Leighton,27 Altshuller
and Buffalini,28 and Stern 29 should be con-
sulted. The basic spectroscopy  and photo-
chemistry of  sulfur dioxide  are  discussed by
Calvert and Pitts.30
          2.  Field Investigations

  Gartrell et al.31 studied the oxidation of sul-
fur  dioxide in  coal-burning  power plant
plumes. Soluble  sulfates were  collected on
membrane  filters,  and  sulfur  dioxide  was
collected in hydrogen peroxide. The sulfur
trioxide concentration in the stack gas  was
15 ppm to  40 ppm and the sulfur dioxide
concentration was about 2200 ppm. Thus, on
a weight  basis, the ratio of sulfuric acid to
sulfur dioxide  as  initially about  0.03. In
successive samples  collected from the plume,
the investigators found oxidation rates rang-
ing from  zero to 2 percent per minute. In-
creasing  rates  of  oxidation  were  observed
with increasing relative humidity, and the in-
vestigators  concluded that moisture within
the plume  of the  ambient strata was the
most important  factor affecting the rate of
oxidation.
  Katz32  made  simultaneous  collections of
two air samples in  the Sudbury, Ontario,
nickel-smelting area to determine sulfur di-
oxide and "total sulfur contaminants," which
he  interpreted as sulfur dioxide, sulfur tri-
oxide, and  sulfuric  acid.  The sample for
"total sulfur  contaminants" was collected in
a dilute solution of sulfuric acid  and hydro-
gen peroxide,  and  the sulfur dioxide equiv-
alent was determined from electroconductivi-
ty  measurements.  The second sample  was
collected  in a starch-iodine solution so  that
sulfur dioxide could be determined idometri-
cally. Katz  found that (1)  the average ratio
of sulfur  dioxide to total sulfur contaminants
or to net  gaseous acid was highest when the
concentration  of gases was highest and (2)
the ratio  decreased from about  95 percent in
1 hour to 65 percent in 12 hours residence
time of the pollutant.32 33  Although reserva-
tions exist  about the quantitative nature of
these ratios because of a number of apparent-
ly uncontrolled or uncontrollable  parameters
in  the experiments,  they  nevertheless in-
dicate  qualitatively  that sulfur dioxide  is
oxidized  in the atmosphere. In the experi-
ments, interferences  may  arise  from  the
possible presence of the acidic  gas, nitrogen
dioxide, the possible selective removal of ba-
sic substances in the air with time, the vari-
able  effectiveness  of  the  filter in removing
       8

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particulate matter and sulfuric acid from the
air, etc.  Analysis  of  the  data presented  by
Katz shows that over the relatively narrow
range of conditions studied the rate of de-
crease in the ratio of sulfur dioxide to total
sulfur contaminants appears to be independ-
ent of concentration of contaminants, of the
time of day at which the measurements were
made, and  of ambient temperature. The rate
was  about  0.035 percent  per  minute.  From
this  oxidation  rate it  follows that, if the
initial concentration of sulfur  dioxide were 1
ppm (2860 /xg/m3 at 0°C), the concentration,
assuming no dilution, would be approximate-
ly 2850 yug/m3 after 10 minutes, 2800 ^g/m3
after 1 hour, and 2300 /tg/m3 after 10 hours.
The  cjrresponding sulfur trioxide  (as sul-
furic acid) concentrations would be approxi-
mately 15 /xg/m3, 90 ^g/m3, and 830 jug/m3,
and the weight ratios of sulfuric acid to sul-
fur dioxide at the  respective times would be
approximately  0.005, 0.032, and  0.358.
   This rate, obtained  from the work of Katz,
is much   smaller   than  that reported  by
Gartrell and associates,31 perhaps in part be-
cause Gartrell  had more efficient sulfuric
acid  collection  and perhaps in part because
atmospheric conditions were not the same. As
noted previously, Gartrell and his associates
concluded  that  moisture  within  the plume
of the ambient air  strata is the primary rate-
determining factor in the oxidation.
   The effect of concentration on reaction rate
also must be considered. Whereas Katz' data
indicated that the  rate of loss of sulfur di-
oxide was  independent of concentration, the
sulfur dioxide concentrations of the samples
(taken in the open air) generally  were less
than 2 ppm. Although Gartrell et al. did not
indicate concentrations of the contaminants
in their  plume samples,  concentrations  in
such a plume would be much  higher than 1
ppm to 2 ppm; at  the higher  concentrations
the reaction rate may be  faster  and concen-
tration  dependent.

   3.  Particulate Sulfate in Polluted Air

   The oxidation of atmospheric  sulfur di-
oxide results  in the  formation of sulfuric
acid  and  other sulfates that typically account
for about 5 percent to 20 percent of the total
suspended  particulate matter in urban air.
In general, as expected, there  is a relation-
ship (Commins;34 see also Chapter 3, Section
C)  between  the  concentrations  of  sulfuric
acid or sulfate and sulfur dioxide.
  In  recent  years, some studies have been
made of the particle size distribution of sus-
pended  atmospheric sulfate. This  property
determines visibility reduction 3r> and is  an
important factor in physiological responses
because of its relation to the degree of pene-
tration and  retention  of particles in  lungs.
Roesler et al.3K reported sulfate size distribu-
tions in  downtown  Chicago and Cincinnati
based  on 24-hour  samples collected  with
cascade impactors.  They found  values for
mass median  diameter  (MMD),  i.e., for
equivalent spheres of unit density, that aver-
age 0.3,u to 0.4/x in the two cities.  These were
within the range of average MMD value for
total sulfur  (0.2it to 0.9/u.) found by Ludwig
and  Robinson 3T in the Los Angeles and San
Francisco Bay areas.  From 8-hour  samples
collected continuously  for a week in each of
four cities, Wagman et al.3S found values for
average sulfate MMD  (i.e., 0.42/x  in Chicago,
Cincinnati, and Fairfax, and 0.60/x in  Phila-
delphia)  that were in good agreement with
these measurements. They  also  found that
sulfate particle sizes generally increased with
increasing relative humidity, whereas sulfate
concentration was more closely correlated
with absolute humidity. Of particular signifi-
cance is the fact that  all of these investiga-
tions showed that a major fraction (generally
80 percent or more)  of urban atmospheric
sulfate is associated with particles below 2^
in diameter.  Suspended sulfate is therefore
largely in the respirable fraction of  particu-
late  matter  and  is  associated mainly with
particles that cause the most pronounced re-
duction in visibility.

 G.   EFFECTS  OF SULFUR OXIDES ON
LIGHT  TRANSMISSION IN ATMOSPHERE
  One of the most noticeable physical effects
of air pollution is the reduced visibility in
polluted atmospheres.  Comprehensive treat-
ments of the subject include those  of Stef-
fens,39 Middleton,35 and Robinson.40 A com-
panion document, Air  Quality Criteria for
Particulate Matter,  also discusses the sub-
ject  in Chapter 3, "Effects of Atmospheric

-------
Particulate Matter on Visibility." Since the
meteorological effects, as well as reduction of
visibility, are considered in detail in the above
document, only  the salient features of this
problem are summarized here.

 1.   Reduction of Visibility by Air Pollutants

  Visibility in the  atmosphere is reduced by
the scatter and  absorption of visibile radia-
tion by air molecules and aerosol  particles.
Attenuation by scatter and absorption of the
light passing from objects  to  observer re-
duces the brightness and contrast  between
objects  with the result that the eye's ability
to distinguish objects from their background
is reduced.
   In addition to reducing visibility by at-
tenuation, aerosols that scatter light efficient-
ly are effective  in reducing object contrast
and visibility because they also scatter light
from the sky and  sun  into the line  of sight
of an observer.  It is a common observation
that  dark  objects,  for  example  mountain
ridges, become progressively lighter in  shade
as they  become more distant.  The most dis-
tant mountain  that one can  distinguish is
typically almost as light or bright as its sky
background. Since particulate sulfur oxides
are  most effective in scattering light,27 they
represent air pollutants that play an impor-
tant role in reducing visibility in the atmos-
 phere.

 2.  Scattering of Light by Sulfuric Acid and
              Sulfate Particles
   The quantitative contribution made by the
 oxides  of  sulfur to the total  scattering of
 light in various atmospheres has  not been
 resolved, but sulfuric acid mist and other sul-
 fate particulate matter are  recognized  as
 important sources of scattering. The  latter
 arise, as noted  earlier, from complex  oxida-
 tion processes,  some  of  which are photo-
 chemical in nature.
   Regardless of the mechanism by which the
 particulate matter is formed, one can, never-
 theless,  formulate an expression for the dis-
 tance we can see through the atmosphere. The
 visual range, Lv, along a given path  is de-
 fined 41 as the greatest distance a  black ob-
 ject may be  seen when viewed against the
sky  at  the horizon,  and  for  monodisperse
particles  and  monochromatic light  at  a
threshold contrast of 2 percent, is given by
the relation
          Lv=-
                3.92
 3.92
NAE
(1-8)
where a is the scattering coefficient (per unit
     path length),
  N is the number of particles per unit vol-
     ume of atmosphere,
  A is the cross-sectional area of the parti-
     cles, and
  E is the particles scattering ratio.40
  The particles  scattering ratio, E, is the
ratio of  the area of the wave front acted on
by  the particles to the geometric  area of the
particle. This ratio depends on the particle's
refractive index, its shape, and its size  rela-
tive to the wave-length of the light. Refrac-
tive indices  of  sulfuric acid in equilibrium
with water vapor at various relative humidi-
ties are  given in Table 1-2 and in Table 1-3,
values for E when A = 0.54/x  are given for
 Table 1-2.—DENSITY, PERCENT SULFURIC ACID,
  AND REFRACTIVE INDEX OF SULFURIC ACID
  SOLUTIONS  IN EQUILIBRIUM WITH WATER
  VAPOR  AT DIFFERENT RELATIVE HUMIDI-
  TIES42"
Relative
humidity,
percent
0
2
5
10
20
30
40
50
55
60
65
70
75
80
85
90
95
97.5
98
H2SO<,
percent
100.00
84.41
69.44
64.45
57.76
52.45
47.71
43.10
40.75
38.35
35.80
33.09
30.14
26.79
22.88
17.91
11.08
7.42
4.99
Density
1.8305
1.7615
1.6015
1.5485
1.4775
1.4205
1.3705
1.3305
1.3105
1.2885
1.2665
1.2435
1.2205
1.2025
1.1645
1.1265
1.0745
1.0385
1.0315
Refractive
index
1.440
1.434
1.421
1.414
1.407
1.399
1.393
1.387
1.384
1.381
1.378
1.374
1.370
1.366
1.362
1.356
1.347
1.343
1.340
       10

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Table  1-3.—SCATTERING RATIOS FOR VARIOUS SIZE DROPLETS OF SULFURIC ACID MIST IN EQUI-
   LIBRIUM WITH WATER VAPOR AT VARIOUS RELATIVE HUMIDITIES (INTERPOLATED FROM
   REFERENCE NO. 44)
Percent relative humidity
d"
0.1
0.2
0.3
0.4
0.5
0.6
0.7
0.8
0.9
1.0
1.1
1.2
1.3
1.4
1.5
1.6
1.7
1.8
1.9
2.0
50
0.02
0.24
0.88
1.63
2.50
3.18
3.63
3.94
4.00
3.84
3.30
2.84
2.33
2.20
1.78
1.66
1.92
2.11
2.47
2.43
55
0.02
0.24
0.87
1.60
2.42
3.13
3.58
3.92
4.00
3.85
3.33
2.93
2.50
2.23
1.85
1.61
1.91
2.12
2.42
2.40
60
0.02
0.23
0.85
1.58
2.43
3.11
3.52
3.91
3.99
3.85
3.31
2.98
2.54
2.22
1.81
1.62
1.91
2.10
2.39
2.43
65
0.02
0.23
0.84
1.56
2.41
3.06
3.53
3.89
3.98
3.85
3.38
3.02
2.58
2.29
1.88
1.68
1.91
2.08
2.35
2.40
70
0.02
0.22
0.81
1.53
2.36
3.02
3.50
3.87
3.97
3.86
3.42
3.53
2.65
2.33
1.90
1.71
1.90
2.04
2.30
2.32
75
0.02
0.22
0.80
1.50
2.32
2.93
3.46
3.81
3.98
3.87
3.45
3.14
2.71
2.38
1.92
1.72
1.90
2.01
2.25
2.33
80
0.02
0.21
0.78
1.47
2.27
2.92
3.42
3.84
3.97
3.87
3.48
3.21
2.78
2.37
1.95
1.76
1.90
1.98
2.21
2.29
85
0.02
0.21
0.76
1.44
2.23
2.88
3.39
3.82
3.97
3.87
3.52
3.27
2.84
2.46
1.99
1.79
1.90
1.94
2.16
2.26
90
0.02
0.20
0.73
1.40
2.17
2.81
3.34
3.78
3.95
3.88
3.58
3.35
2.93
2.52
2.05
1.86
1.90
1.89
2.08
2.20
95
0.02
0.19
0.69
1.33
2.07
2.69
3.23
3.72
3.94
3.89
3.67
3.49
3.07
2.63
2.16
1.90
1.90
1.82
1.91
2.10
98
0.01
0.18
0.66
1.28
1.99
2.60
3.16
3.67
3.92
3.89
3.73
3.59
3.16
2.70
2.27
2.08
1.90
1.75
1.88
2.03
    a Diameter in microns.
various concentrations of sulfuric acid mist
of various particle sizes.
a. Droplet Size
  When  particles of different sizes and dif-
ferent refractive indices are involved, the
equation Lv = 3.9/NAE  for visual  range,
must be modified as follows:
                  3.9p
                                     d-9)
where Lv   is the visual range  in  standard
           units  with  a   contrast   limit
           (threshold)  of 0.02,
      i&j  identify  a class of particles of a
           given diameter (d)  and a given
           refractive index (n),  respectively,
      NU   represents the number of ij par-
           ticles per unit volume,
      AJJ   represents   the   cross-sectional
           area of an ij particle,
      E;j   is the  scattering ratio  of  the  ij
           particle,
      p    is unity if Lv is in the same units
           as N and A,  e.g., LY is in meters
           if N,J is number of particles per
           cubic meter and A^ is cross-sec-
           tional area in square meters, but
           p is 62.14xlO"5 if Lv is in'miles,
           Nij is in number of particles per
           cubic meter,  and AU is in square
           meters.
  Waller  and  co-workers43 4G  studied acid
droplets  in urban air and  presented data
pertaining to a 39 /^g/m3 sample of sulfuric
acid mist with a  mass median diameter of
0.5/u and a geometric  standard deviation of
8.  The  relative humidity at  the  time the
sample  was  collected  was  85  percent. The
number of particles of various  sizes was cal-
culated from the density of sulfuric acid in
equilibrium with water vapor at 85 percent
relative humidity,  and the mass distribution
of the sample.
                                                                               11

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  Given the diameter  dDT1 of particles at a
                        i\.n.
specific relative humidity RH, the diameter
d'    of particles at relative humidity RH'
can be determined from the relationship
                                     (1-10)
where C and C' are weight percent of H2S04
in droplets at  relative humidities  RH and
RH',  respectively, P and  P' are densities  of
droplets at relative humidities RH and RH',
respectively.
  Equation  (1-10)  shows  that there  is  a
shift  of the particle size distribution toward
larger sizes with  increasing relative humidi-
ty. Data from Waller's sample were used to
calculate mass median diameters for various
relative humidities  (Figure  1-1).
6. Number of Droplets Per  Cubic Meter
  In  general,  the increase  in mass median
diameter  with increase in relative humidity
      0  10  20  30  40  50  60  70  80  90 100
                RELATIVE HUMIDITY, %

  Figure 1-1. Calculated Mass Median Diameter of Sus-
           pended Sulfuric Acid Mist Droplets as a
           Function of Relative Humidity.
results in greater numbers of particles (Fig-
ure 1-2)  in the size range  of O.l/t to 2.0/u,
the sizes  that  cause significant reduction in
visual range. The consequences are shown in
Figure  1-3 where, for  example, it can  be
seen that at 30 /xg/m3 of sulfuric acid mist
the visual range is calculated to be 31 miles
at 50 percent relative humidity but only 3.1
miles at 98 percent relative humidity. This
result is  not  inconsistent with the data of
Robinson.40
c. Use of Sulfur Dioxide/Sulfuric Acid Ratio
   to  Calculate Visual Range Reduction
   Since several investigators have reported
increasing ratios of sulfuric  acid mist to sul-
fur dioxide with increasing relative humidity,
and since correlations between sulfur dioxide
and suspended particulate matter also have
been shown, it is possible, given the sulfur di-
oxide concentration and the  relative humidi-
ty, to calculate visual range by using the fol-
lowing:
                                                 1 x 1011
                                                   X10°
                                                          0.2  0.4 0.6 0.8  1.0 1.2  1.4 1.6 1.8  2.0
                                                                  PARTICLE SIZE, JU
 Figure 1-2. Calculated Number of Droplets per m3 in
          Various Size Intervals at Different Relative
          Humidities in a Sulfuric Acid Mist Sample
          Having a Concentration of 39 jig/m3.
        12

-------
  1. Figure 1-4 shows the average concen-
trations of sulfuric acid mist  (measured as
HjS04)  associated  with various  concentra-
tions of sulfur  dioxide  at various  relative
humidities  as  calculated  from  the ratios
reported by Bushtueva.47 4S Ratios similar to
those reported by Bushtueva have also  been
reported  by  Coste  and  Courtier,49 30  Com-
mins,"'1 and Thomas.:>-
  2. The average  contribution  of  sulfuric
acid mist to the denominator  of the visual
range equation
                 2.4 xlQ-3
                                     (1-11)
varies with  relative humidities  as follows:
at 50 percent relative  humidity, 0.26x10-'
per jug/nr1; at 90 percent relative humidity,
0.69x 10-' per /*g/m3; and at 98 percent rela-
tive humidity, 2.55 X 10-' per /*g/m3.
  3.  From  National Air Surveillance Net-
work data for New  York City (1964-1965)
a typical ratio of suspended particulate mat-
  10'
 a
 D i
  10-'
                       RELATIVE HUMIDITY, %
     10U
                 10n
                             102
      SULFURIC ACID MIST CONCENTRATION, p_g / m3
 Figure 1-3. Calculated Visibility (Visual Range) in Miles
          at Various Sulfuric Acid Mist Concentrations
          and Different Relative Humidities.
 This graph shows that visibility decreases with increas-
 ing acid mist concentration, and with increasing relative
 humidity.
ter to sulfur dioxide concentration  is  1200
i«.g/ni3 to 1 ppm. If the components of the
suspended particulate matter other than sul-
furic acid are assumed nonhygroscopic, their
contribution to the denominator of the visibil-
ity equation, determined from  the investiga-
tions  of   Charlson,"'5   may  range  from
0.16x10  ' to 0.66x10 ' per /xg/m3 with a
mean value of 0.33 x 10-' per ^g/m3.
   For example,  in New York City, at  0.3 ppm
sulfur dioxide concentration, the suspended
particulate matter  other than sulfuric acid
is 0.3 X 1200 or 360/xg/m!. At 90 percent rela-
tive humidity the sulfuric  acid mist  content
is 78Aig/m3.
   Then,
L/y— -
                     2.4x10-'
     (360) (0.33x10--

    2.4x10
                          (78)  (0.69xlO->)

   =	= 1.4 miles            (1-12)
    173 X 10--'
   The results of a series of such calculations
applicable to New York City (1964-1965) are
shown  in  Figure  1-5. Estimates  of visual
                                                   300
                                                            0.2      0.4     0.6     0.!
                                                                SULFUR DIOXIDE, ppm
 Figure 1-4. Ratios of Sulfuric Acid to Sulfur Dioxide
          Concentrations at Different Relative
          Humidities.
                                                                                          1.0
                                                                                  13

-------
   10'
w
z
cc
w  10°
   10"
     10
      ,-3
                 TO''
                              10-
                                           10°
                SULFUR DIOXIDE, ppm
      Figure 1-5. Calculated Visibility (Visual Range) in Miles
               at Various Sulfur Dioxide Concentrations
               and at Different Relative Humidities in
               New York City.


      This graph shows that visibility decreases with increasing
      sulfur dioxide concentration, and with increasing relative
      humidity.  It is based on a calculation combining the re-
      lationships shown in Figure 1-3 with those shown in
      Figure 1-4.
    range can be obtained for various concentra-
    tions of sulfur dioxide. The data become par-
    ticularly significant in relation to aircraft op-
    erations. At  a  visual range  of  less than  5
    miles, operations are slowed  at airports be-
    cause of the need to maintain larger distances
    between aircraft; Federal Aviation Adminis-
    tration restrictions on aircraft operations be-
    come increasingly severe as the visual range
    decreases below 5 miles.

                 H.  SUMMARY

      The burning  of coal and fuel oil, which
    contain inorganic sulfides and sulfur-contain-
    ing  organic compounds, results in the  emis-
    sion  of appreciable  quantities of sulfur di-
    oxide into  the  atmosphere. Other oxides of
    sulfur are also emitted, but in quantities that
    are small by comparison; for  example, about
40 to 80 parts of sulfur dioxide to one part of
sulfur trioxide are emitted from fossil-fueled
power plants.  Sulfur dioxide is a nonflam-
mable, nonexplosive, colorless gas that most
people can taste at concentrations from 0.3
ppm to 1 ppm in air. At concentrations above
3 ppm the gas has a pungent, irritating odor.
In the atmosphere, sulfur dioxide, an acid an-
hydride, is partly converted to sulfur trioxide
or to  sulfuric acid and  its salts by photo-
chemical  or  catalytic processes. Sulfur tri-
oxide  is immediately converted to sulfuric
acid in the presence of moisture. Laboratory
and field investigations have shown that the
oxidation of sulfur dioxide  may proceed by
several types of mechanism including (1) ho-
mogeneous gas phase reactions,  (2) homoge-
neous catalysis in liquids, (3) heterogeneous
gas-solid interactions, and (4) heterogeneous
gas-liquid  interactions.   The   predominant
mechanism and the degree  of oxidation are
determined by a number of factors, including
the concentration,  the residence time in the
atmosphere,  the temperature, the humidity,
the intensity and spectral distribution of in-
cident radiation, and the presence of  other
pollutants  such as  metal   oxides,  hydro-
carbons, and oxides of nitrogen.
  Visibility in the  atmosphere is reduced by
the scatter and absorption of visible radiation
by small  particles  in the size  range  from
O.lj« to l,u in  radius. This phenomenon is also
described in  Chapter 3 of a companion  docu-
ment,  Air Quality  Criteria for Particulate
Matter. The  attenuation of light from an ob-
ject and the  illumination of the air between
the object and the observer reduce the con-
trast  of object  and hence  reduce its visi-
bility.  Of the  total  suspended particulate
matter in urban air,  about  5 percent  to 20
percent consists of sulfuric  acid  and  other
sulfates, and generally 80 percent or more of
these particles by weight  are smaller than 1
n radius.  Suspended sulfates in  the air con-
sequently  are very effective in reducing vis-
ibility.
  The contribution of sulfuric acid mist and
other suspended sulfates to the total scatter-
ing of light and therefore to reduced visibility
can be estimated from data on the concentra-
tion and particle size distribution.  Generally,
a good correlation  exists between the con-
          14

-------
centrations of sulfuric acid or sulfate and the
concentrations  of sulfur  dioxide.  Increases
in the humidity  result in  increases  in the
ratio of  sulfuric  acid to sulfur dioxide, ac-
companied by a shift of the mass median di-
ameter  of  sulfuric  acid   droplets  toward
larger sizes and an increase of sulfuric acid
concentration in the size range characteristic
of acid fogs.  Since correlations between sul-
fur  dioxide levels and  suspended  particu-
late matter can be found, it is possible for a
given  relative humidity to estimate the vis-
ibility from the sulfur dioxide concentration.
The relationship  between  the visual  range,
which is the greatest distance a black object
may be  seen when viewed against the sky at
the horizon, and the sulfur dioxide concentra-
tion is shown in  Figure 1-5 for  a ratio of
concentrations of sulfur dioxide and particu-
late matter typical of New York City (1964-
1965).

              I.   REFERENCES

 1. Brasted,  R.  C.  "Comprehensive   Inorganic
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    U.S.  Bureau  of Mines, Information  Circular
   7836, 1958, 22 pp.
 8. Gilbert,  E.  E. "The  Reactions  of  Sulfur Tri-
   oxide  and of  its Adducts,  with Organic  Com-
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   Ind. Eng. Chem.,  Vol. 47, pp. 972-976, May 1955.
10. Junge, C. E. and Ryan, T.  "Study  of the SO.
   Oxidation in  Solution  and its Role in Atmos-
   pheric Chemistry."  Quart. J. Roy.  Meteorol.
    Soc., Vol. 84, pp. 46-55, Jan. 1958.
11.  Johnstone, H. F. and Coughanowr, D. R. "Ab-
    sorption of Sulfur Dioxide from Air.  Oxidation
    in Drops Containing Dissolved Catalysts."  Ind.
    Eng. Chem., Vol. 50, pp. 1169-1172, 1958.
12.  Bracewell, J.  M. and  Gall, D.  "The  Catalytic
    Oxidation of Sulfur Dioxide in Solution at Con-
    centrations Occurring  in Fog Droplets." Pro-
    ceedings  Symposium  on the  Physico-chemical
    Transformation of Sulfur  Compounds  in  the
   Atmosphere and the  Formation of Acid  Smogs.
    Organization for Economic Cooperation and  De-
    velopment, Mainz, Germany,  June 1967.
13.  Van Den Heuvel, A. P. and Mason, B. J. "The
    Formation of Ammonium Sulfate in Water Drop-
    lets Exposed  to Gaseous  Sulfur Dioxide  and
    Ammonia." Quart.  J. Roy. Meteorol.  Soc., Vol.
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14.  Smith, B. M.,  Wagman, J., and Fish, B. R.  "In-
    teraction of  Airborne  Particles  with Gases."
    Presented  at Symposium on Colloid and Surface
   Chemistry  in  Air and  Water Pollution, 156th
    National Meeting of American Chemical Society,
    Atlantic City, New Jersey, September 11, 1968.
    Submitted for publication in Environmental Sci-
    ence and Technology, 1968.
15.  Liberti, A. and Devitofrancesco, G. "Evaluation
    of  Sulfur Compounds  in  Atmospheric  Dust."
    Proceedings of the  Symposium on the Physico-
    chemical Transformation of  Sulfur Compounds
    in the Atmosphere  and the Formation of Acid
    Smogs. Organization for Economic Cooperation
    and Development, Mainz, Germany,  June 1967.
16.  Renzetti, N. A. and Doyle, G. J. "Photochemical
    Aerosol Formation in Sulfur  Dioxide-Hydrocar-
    bon Systems." Intern. J. Air Pollution,  Vol. 2,
    pp. 327-345, June 1960.
17.  Urone, P., Lutsep, H., Noyes, C. M., and Parcher,
    J. F.  "Static  Studies  of Sulfur  Dioxide Reac-
    tions in Air."  Environ.  Sci. Technol., Vol. 2,  pp.
    611-618, 1968.
18.  Shuck, E.  A.  and Doyle, G. J. "Photooxidation
    of Hydrocarbons in Mixtures Containing Oxides
    of Nitrogen and Sulfur Dioxide."  Air Pollution
    Foundation, San Marino, California, Report 29.
19.  Doyle, G. J., Endow, N., and Jones, J. L. "Sulfur
    Dioxide Role in Eye  Irritation." Arch. Environ.
    Health, Vol. 3, pp. 657-667, Dec. 1961.
20.  Prager, M. J., Stevens,  E. R., and Scott, W. E.
    "Aerosol  Formation from Gaseous  Air Pollu-
    tants." Ind. Eng. Chem., Vol. 52, pp. 521-524,
    June 1960.
21.  Johnston, H. S. and Dev Jain, K.  "Sulfur  Di-
    oxide  Sensitized Photochemical  Oxidation  of
    Hydrocarbons."  Science, Vol.  131, pp. 1523-1524,
    May 20, 1960.
22.  Kopczynski, S. L. and Altshuller,  A. P. "Photo-
    chemical Reactions of Hydrocarbons with Sulfur
    Dioxide."  Intern. J. Air Water Pollution, Vol.
    6, pp.  133-135, March-April 1962.
23.  Dainton, F. S. and Ivin, K.  J. "Photochemical
    Formation of  Sulfinic Acids from Sulfur Diox-
    ide and  Hydrocarbons."  Trans. Faraday Soc.,
    Vol. 46, pp. 374-381, 1950.
                                                                                         15

-------
24.  Shuck,  E. A. Doyle, G. J.,  and Endow, N. "A
    Progress  Report on the Photochemistry of Pol-
    luted Atmospheres."  Air Pollution Foundation,
    San Marino, California, Dec. 1960.
25.  Endow, N., Doyle, G. J., and Jones, J. L. "The
    Nature of Some Model  Photochemical  Aerosols."
    J. Air Pollution Control Assoc., Vol. 13, pp. 141-
    147, April 1963.
26.  Goetz, A. and Pueschel, R.  F. "Basic Mecha-
    nisms of Photochemical  Aerosol  Formation."
    Atmos. Environ., Vol. 1, pp. 287-306, 1967.
27.  Leighton, P.  A.  "Photochemistry  of Air Pol-
    lution."   Academic Press,   New  York,  1961,
    300 pp.
28.  Altshuller,  A. P. and  Buffalini,  J. J.  "Photo-
    chemical  Aspects  of Air Pollution: A Review."
    Photochem. Photobiol.,  Vol.  4, pp.  97-146, 1965.
29.  Stern, A. C. (ed.)  "Air Pollution." 2nd edition,
    Vols. I and II, Academic Press, New York, 1968.
30.  Calvert, J.  G. and Pitts, J.  N., Jr. "Photochem-
    istry."  John  Wiley and Sons,  Inc., New York,
    1966, pp. 209-211.
31.  Gartrell,  F. E., Thomas, F. W., and  Carpenter,
    S.  B. "Atmospheric Oxidation of S02  in Coal-
    Burning  Power Plant  Plumes." Am.  Ind. Hyg.
    Assoc. J.,Vol. 24, pp. 113-120, March-April 1963.
32.  Katz, M. "Photoelectric Determination  of At-
    mospheric  Sulfur Dioxide,  Employing  Dilute
    Starch-Iodine Solutions."  Anal. Chem., Vol.  22,
    pp. 1040-1047, 1950.
33.  Katz, M.  "Sulfur Dioxide in the Atmosphere and
    its  Relation  to Plant  Life."  Ind.  Eng. Chem.,
    Vol.  41,  pp.  2450-2465, Nov. 1949.
34.  Commins, B.  T. "Some Studies on the Synthesis
    of  Particulate Acid Sulfate from the Products
    of  Combustion of Fuels and Measurement of the
    Acid in Polluted  Atmospheres." Proceedings of
    the Symposium on the Physico-chemical Trans-
    formation of Sulfur Compounds in the Atmos-
    phere and  the  Formation  of Acid Smogs, Or-
    ganization  for  Economic  Cooperation and De-
    velopment,  Mainz, Germany, June  1967.
35.  Middleton,  W.  E.  K.  "Vision  through  the
    Atmosphere."  Univ.  of Toronto Press,  Toronto,
    1952, 250 pp.
36.  Roesler,  J. F.,  Stevenson, H. J. R., and Nader,
    J.  S.  "Size Distribution of Sulfate Aerosols in
    the Ambient  Air."  J.  Air  Pollution Control
    Assoc., Vol. 15, pp. 576-579, 1965.
37.  Ludwig,  F. L. and Robinson, E. "Size Distribu-
    tion of Sulfur-Containing Compounds in  Urban
    Aerosols."  J. Colloid  Sci.,  Vol. 20, pp.  571-584,
    1965.
38. Wagman, J., Lee, R. E., Jr., and Axt, C. J. "In-
    fluence of  Some  Atmospheric  Variables on the
    Concentration and Particle  Size Distribution of
    Sulfate in  Urban Air." Atmospheric Environ-
    ment, Vol.  1, pp. 479-498,  1967.
39. Steffens,  C. "Visibility and Air Pollution." In:
    Air  Pollution  Handbook, P. L. Magill,  F. R.
    Holden, and C. Ackley (eds.), McGraw-Hill, New
    York, 1956, pp. 6-1 to 6-43.
40.  Robinson, E.  "Effects of Air Pollution on Visi-
    bility."  In: Air Pollution, 2nd edition, Vol.  I,
    A. C. Stern (ed.), Academic Press, New York,
    1968, pp. 349-400.
41.  Huschke,  R.  E.   (ed.)   "Glossary  of Meteor-
    ology." American Meteorological Society, Boston,
    Massachusetts, 1959.
42.  Lange, N. A. and Forker, G. M.  (eds.) "Hand-
    book of Chemistry," 10th edition, McGraw-Hill,
    New York, 1961, 1969 pp.
43.  Weast, R.  C., Selby,  S. M., and Hodgman, C. D.
    (eds.)  "Handbook of Chemistry and  Physics,"
    45th edition,  The  Chemical Rubber Co.,  Cleve-
    land, 1964,  1495 pp.
44.  Tendorf, R. B.  "New Table of Mie Scattering
    Functions.  Part  6."  Geophys.  Res. Paper  45,
    Air Tone Cambridge Research  Laboratory, Bed-
    ford, Massachusetts, AFCRC-TR-56-20416,1956.
45.  Waller, R. E. "Acid Droplets in Town Air." Int.
    J. Air Water Pollution,  Vol. 7,  pp. 773-778, Oct.
    1963.
46.  Waller,  R.  E., Brooks, A. G. F., and Cartwright,
    J. "An Electron  Microscope Study  of Particles
    in Town Air."  Int. J. Air Water Pollution, Vol.
    7, pp. 779-786, Oct. 1963.
47.  Bushtueva, K. A.  "Ratio of Sulfur  Dioxide and
    Sulfuric  Acid Aerosol  in  Atmospheric Air,  in
    Relation to Meteorological  Conditions."  Gig.  i
    Sanit., Vol. 11, pp. 11-13, 1954.  In:  U.S.S.R.
    Literature  on Air Pollution and Related Occu-
    pational  Diseases.  A  Survey.  Vol. 4.  Trans-
    lated by B. S. Levine, U.S. Dept. of Commerce,
    Office of Technical Services, Washington, D.C.,
    Aug. 1960, pp.  193-196.
48.  Bushtueva, K.  A.  "The  Determination of  the
    Limit of  Allowable Concentration  of Sulfuric
    Acid in Atmospheric Air." In: Limits of Allow-
    able Concentrations  of  Atmospheric Pollutants.
    Book 3, 1957. Translated by B. S. Levine, U.S.
    Dept. of Commerce, Office of Technical Services,
    Washington,  D.C., pp. 20-36.
49.  Coste, J. H.  "Investigation of  Atmospheric Pol-
    lution." Cong.  Int. Quim.  Pura  Aplicada (Ma-
    drid), Vol. 6, pp. 274-287, 1934.
50. Coste, J. H. and  Courtier, G. B. "Sulfuric Acid
    as a Disperse Phase in Town Air." Trans. Fara-
    day Soc.,  Vol.  32,  pp.  1198-1202,  1936.
51.  Commins, B. T.  "Determination of Particulate
    Acid in Town  Air." Analyst, Vol. 88, pp. 364-
    367, May 1963.
52. Thomas, M. D.  "Sulfur Dioxide, Sulfuric Acid
    Aerosol and  Visibility in Los Angeles."  Int. J.
    Air Water Pollution, Vol.  6, pp. 443-454, Nov-
    Dec. 1962.
53. Charlson, R. J., Ahlquist, N. C., and Horvath, H.
    "On the Generality of Correlation of Atmospheric
    Aerosol Mass Concentration and  Light Scatter."
    Atmospheric  Environment,  Vol. 2, pp. 455-464,
    1968.
        16

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                Chapter 2
SOURCES AND METHODS OF MEASUREMENT OF
    SULFUR OXIDES IN THE ATMOSPHERE

-------
                          Table of Contents
                                                                   Page
 A. INTRODUCTION                                                 19
 B. SOURCES OF ATMOSPHERIC  SULFUR OXIDES                   19
 C. MEASUREMENT OF GASEOUS SULFUR DIOXIDE
      CONCENTRATIONS                                           20
   1. Sampling Techniques                                            20
   2. Colorimetric Method: Pararosaniline                              21
   3. Conductometric Methods                                         21
   4. Acid Titration Method: Hydrogen Peroxide                         22
   5. Spectroscopic Methods                                           22
   6. Other Methods            	                              23
   7. Use and Comparison of Methods                                  23
 D. MEASUREMENT OF SULFURIC ACID AND SULFATES            24
 E. OTHER  METHODS  OF MEASURING  POLLUTION BY SULFUR
      OXIDES                                                      24
   1. Sulfation Rates of Lead Peroxide Candles                  .         24
   2. Suspended Sulfate                               .                25
   3. Sulfate in Dustfall                                              25
   4. Sulfuric Acid Mist                                              25
 F. SUMMARY                                                      25
 G. REFERENCES                                                   27
                             List of Tables
 Table
 2-1   Atmospheric Sulfur Dioxide Emissions in 1963 and 1966 by Source       20
18

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                                      Chapter  2

          SOURCES AND METHODS OF  MEASUREMENT OF  SULFUR
                         OXIDES IN THE  ATMOSPHERE
          A.   INTRODUCTION

  Oxidized sulfur in the atmosphere exists in
several different chemical and physical forms.
Under normal  conditions, the  predominant
state is gaseous sulfur dioxide, together with
smaller amounts of non-volatile sulfuric acid
mist or sulfate salts.
    Since the proper and efficient establish-
ment of criteria and standards ultimately  de-
pends upon reliable analytical data, it is par-
ticularly important that proper attention be
given to (1) the  sampling  techniques, and
(2)  the  analytical procedures   employed.
These have been reviewed recently by Hend-
rickson 1 and Katz.2
  If gaseous sulfur dioxide were the sole pol-
lutant in the atmosphere,  its quantitative
determination,  even in the  fractional ppm
range, would not  be  unduly difficult. The
presence of both sulfuric  acid mist and sul-
fate salts adds complications to the analytical
procedures. These are further complicated by
real or potential interferences from a variety
of additional air pollutants often found in
conjunction with sulfur dioxide.
  Some of the methods used for determining
S02 are specific, while others are general and
depend on a general property such as acidity
or conductivity and are subject to errors  be-
cause of interferences. This has led  to some
problems in  the interpretation  of analyses
from  different  laboratories using  different
techniques.
  In the following discussion, the man-made
sources  of atmospheric oxides of sulfur will
be outlined, and the more important methods
of their determination, including recent tech-
niques involving remote sensing of S02, will
be discussed.
  Agreement between the various  methods
of measurement is not always good, because
each method is subject to interference from
differing causes which  may lead to  either
high or low results.
  Sulfuric  acid mist is  determined by the
separation  of  the  mist  from sulfur dioxide
and the subsequent measurement of the acid
or of the sulfate content. Measurements  of
suspended particulate sulfate and sulfate  in
dustfall are obtained by means  of conven-
tional sulfate determinations.

    B.  SOURCES OF  ATMOSPHERIC
            SULFUR OXIDES

  Sulfur dioxide pollution results primarily
from the combustion of  fossil fuels, the re-
fining of petroleum, the smelting of  ores con-
taining sulfur, the manufacture  of sulfuric
acid, the burning  of refuse, paper making,
and the burning or smoldering of coal refuse
banks. In  all  of  these  processes,  a  small
amount of sulfur  trioxide  or sulfuric acid
also  is emitted. Sulfur  trioxide  is  normally
present in the  atmosphere in extremely small
concentrations  because  it  is converted  to
sulfuric acid soon  after its entry into the at-
mosphere.
  Specific reviews  covering the coal  industry,
petroleum  refineries, fuel  oil  combustion,
burning coal mine  refuse banks, sulfuric acid
manufacture, the iron and steel industry, and
sulfite  pulping have   been  published.3-12
Sources of sulfur  oxides in the atmosphere
also  have been reviewed by Rohrman and
Ludwig.13
  Of considerable  importance to the meteor-
ological  and  chemical  behavior of  sulfur
oxides in the atmosphere, as well as to their
                                                                             19

-------
measurement,  are the  kinds  of  emitters,
whether large or small and whether disperse
or point sources. The trend of operations has
been away from sulfur dioxide pollution by
low-level disperse sources and toward large
point sources, except for space heating and
diesel trucks using fuels of high sulfur con-
tent.  The  large  source  emissions  contain
lower concentrations of polynuclear  hydro-
carbons and  higher concentrations of nitro-
gen oxides and sulf uric acid. Particulate mat-
ter which interacts with the oxides of sulfur
can be  controlled to a  greater extent when
emitted from the  larger  sources.  Further,
emissions from  large  sources usually are
emitted from higher stacks and although this
practice appears to reduce average ground
level concentrations and the frequency of air
pollution episodes, 910  14~17 it may result  in
early morning fumigations.
  Sources of atmospheric sulfur oxides can
be considered  from the  viewpoint of their
annual production. Obviously, sulfur-contain-
ing coal and fuel oil utilized for heating dur-
ing the winter will produce a seasonal  in-
crease in atmospheric S02. This is in contrast
with industrial sources, such  as power sta-
tions and factories, whose effluents are more
or less constant throughout the year.
  Major sources of sulfur dioxide released to
the atmosphere in  1963 13 and in  1966 18 are
presented in Table 2-1.

    C.   MEASUREMENT OF GASEOUS
            SULFUR  DIOXIDE
            CONCENTRATIONS

         1.  Sampling Techniques
  Before discussing specific analytical meth-
ods, it is important to recognize that regard-
less of how accurate the technique may be,
the validity of the  final results is dependent
upon  the sampling technique employed for
the determination.  For example, considera-
tion must be given to factors such as adsorp-
tion on, and desorption from, inlet tubes uti-
lized in  the sampling  apparatus.19 Teflon *,
Tygon *, glass, stainless steel and aluminum
have been tested for various lengths and flow
rates; in general, a conditioning period is re-
* Mention of commercial products does not constitute
  endorsement by the National Air Pollution Control
  Administration.
     Table 2-1.—ATMOSPHERIC SULFUR DIOXIDE EMISSIONS IN 1963 AND 1966 BY SOURCE

                                                              Sulfur dioxide a
                                                         1963              1966
Process
Burning of coal:
Power generation (211,189,000 tons, 1963 data)
Other combustion (112,630,000 tons, 1963 data)
Subtotal
Combustion of petroleum products:
Residual oil
Other products .. ..
Subtotal 	
Refinery operations
Smelting of ores
Coke processing 	 	
Sulfuric acid manufacture
Coal refuse banks ....
Refuse incineration .
Total Emissions
Tons

9,580,000
4,449,000
14,029,000

3,703,000
.. 1,114,000
4,817,000
1,583,000
1,735,000
462,000
451,000
183,000
100,000
. 23,360,000
Percent of
total
emissions

41.0
19.0
60.0

15.9
4.8
20.7
6.8
7.4
2.0
1.9
0.8
0.4
100.0
Percent of
Tons total
emissions

11,925,000
4,700,000
16,625,000

4,386,000
1,218,000
5,604,000
1,583,000
3,500,000
500,000
550,000
100,000
100,000
28,562,000

41.6
16.6
58.2

15.3
4.3
19.6
5.5
12.2
1.8
1.9
0.4
0.4
100.0
    a A small amount of this tonnage is converted to sulfuric acid mist before discharge to the atmosphere.
 The rest is eventually oxidized and/or washed out. Only under unusual meteorologic conditions (Chapter 3)
 does accumulation occur. The increasing output of sulfur oxides due to increasing power demand is evident.
       20

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quired by Tygon and aluminum tubing. For
relatively high flow rates (28.3 1/min), alu-
minu required a conditioning period of about
5 hours  at 0.2 ppm and Tygon  required a
much longer  period  and should be avoided.
Neither adsorption nor desorption was sig-
nificant in glass or stainless steel tubing at
various flow rates for tubing lengths as great
as 30.5 meters. Teflon tubing  falls into this
same class. Any of these three materials can
be used for sampling sulfur dioxide at suffi-
ciently high flow velocities (greater than 3.7
m/sec) without prior conditioning and with-
out effect by temperature or humidity.
  Both continuous and intermittent sampling
are commonly used for sulfur  dioxide.  To a
large extent the type of  instrument selected
is dependent upon the measurement principle
desired. The  West-Gaeke and  the Conducto-
metric methods are most commonly employed
in the United States. Many agencies  in  the
country use intermittent or manual sampling
where the collected sample is returned to the
laboratory for analysis.  Intermittent samp-
ling can be used to provide integrated samples
of from 1 hour to 24 hours and is less expen-
sive than continuous monitoring. Continuous
monitoring is necessary where it is important
to show  diurnal changes or the influence of
local sources  and meteorology.

  2.  Colorimetric Method: Pararosaniline
  In the West-Gaeke method,  sulfur dioxide
is absorbed in dilute aqueous  sodium tetra-
chloromercurate  to  form  the  nonvolatile
dichlorosulfitomercurate   ion,   which  then
reacts with formaldehyde and bleached para-
rosaniline to  form red-purple pararosaniline
methylsulfonic acid.  This reaction is specific
for sulfur dioxide and sulfite salts. The color
intensity of the dye, which is proportional to
the concentration of sulfur dioxide, is meas-
ured at a wavelength of 560 m/x. The method
can be used to determine concentrations in
the air from 0.002 ppm to 5 ppm. Ozone and
nitrogen  dioxide reduce the apparent concen-
tration  by  destroying   some   of the  dye,
although interference by nitrogen dioxide can
be eliminated by adding sulfamic acid after
sample collection or just prior to analysis.
Heavy metal  salts,  especially  iron  salts,
oxidize dichlorosulfitomercurate,  which also
results in a lowering of the apparent sulfur
dioxide  concentration.  This  effect can be
eliminated by a membrane prefilter or by
including the disodium  ethylenediaminete-
traacetic  acid in the absorbing  reagent to
sequester metallic ions.   Hydrogen  sulfide
precipitates mercuric sulfide from the collect-
ing reagent, and such a precipitate must be
removed by centrifugation from  the sample
before proceeding with color development.
  Recently two improved West-Gaeke (para-
rosaniline) methods  were developed for the
determination of sulfur dioxide  in ambient
air.20  These  give  greater  sensitivity and
reproducibility, as well as adherence to Beer's
Law throughout a  greater  working  range,
than does the original West-Gaeke method.
The improvements  resulted from optimiza-
tion of several important parameters.  Speci-
fically the pararosaniline dye  was purified
and standardized   to  reduce   variability.
Phosphoric acid  was used in the final color
development to control pH.  The pararosani-
line methylsulfonic acid produced  in the reac-
tion exhibits a hypsochromic spectral shift
with increasing pH.  Hence the reaction pro-
duct behaves as a two-color pH indicator, and
regardless of the pH condition under which
the reaction is carried out, the spectra can be
interchanged by addition of acid or base. The
sharp peak with an absorbance maximum at
A = 548 niju (rose-red) at the higher pH value
(1.68)  shifts to  A = 575 m/t  (magenta)  at a
lower pH value  (1.02). Interferences from
nitrogen oxides, ozone, and heavy metals are
minimal,  and  laboratory results  are  repro-
ducible to within 4.9 percent (at 95 percent
confidence level)  if recommended precautions
are taken. It is noted that these modifications,
although  specifically developed  for  sulfur
dioxide in the atmosphere, can be applied to
determination of sulfite in  other materials.
This method has been adopted as the standard
or reference method by the NAPCA.

       3.   Conductometric  Methods

  The basis of these  methods is the oxidation
of sulfur dioxide to sulfuric acid  by aqueous
hydrogen  peroxide,  and   the  subsequent
measurement of the  increased electrical con-
ductivity  of the solution.  This is a  general
technique and one must take special precau-
                                                                              21

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tions  to eliminate other  pollutants which
could  affect the  conductivity of the solution.
For example, acidic gases such as the hydro-
gen halides will increase the conductivity of
the solution so that, in the presence of such
gases,  incorrectly high  S02 values will be
indicated. Weakly acidic gases such as hydro-
gen sulfide cause practically no intereference
because of  their slight solubility and  poor
conductivity, and nitrogen dioxide  produces
minimum interference  because  it is poorly
absorbed. Sulfuric acid mist is not efficiently
collected in the  usual  gas "scrubber"  and
therefore is not  measured. Salt spray from
ice and snow control may give high readings.
Ammonia interferes with electroconductivity
measurements by neutralizing the  acid  and
forming the ammonium ion which has a high
transport number of the opposite charge.
2NH3   +
Ammonia
H,S04
Sulfuric
 Acid
              (2-1)
Ammonium
   Sulfate
Conductivities  that are  too  low  are  then
recorded, since the transport number of all
other cations is several times less than that of
the hydrogen ion.
  Conductometric methods can be automated
readily so that one can obtain instantaneous
readings. Air is drawn through either acidic
hydrogen peroxide solution or through deion-
ized water, and the sulfur dioxide concentra-
tion is estimated from the conductivity of the
final  solution.  The interference  effects of
various gases on the conductivity have been
described. 21 -'-

    4.  Acid Titration Method: Hydrogen
                 Peroxide

  In this method, the air sample is bubbled
through  O.OSN hydrogen peroxide solution
adjusted to pH 5. Any sulfur dioxide present
forms  sulfuric acid,  which is  then titrated
with standard alkali.  The presence of other
acidic  gases in the sample will lead to  erron-
eously high  results, and alkaline gases or re-
active  basic solids give erroneously low re-
sults.  Generally, a filter is placed in front of
the  sampling bottle  so that no particulate
matter or other aerosols are absorbed in the
hydrogen peroxide solution.  It is important
that this be an efficient filter.
  This technique is straightforward and the
apparatus is inexpensive. It may be auto-
mated, if desired. Often, it is used to obtain
24-hour  averages,  particularly  in  Europe,
where it is widely employed  as the standard
apparatus and procedure.


         5.   Spectroscopic Methods

  In addition to  techniques for making "on-
the-spot" analyses for  atmospheric sulfur
dioxide, it would be a great advantage to have
additional  methods by  which  atmospheric
concentrations   of SO., could be determined
by means of an instrument remote from the
emission source or from the actual air mass
being investigated. Recently, there have been
developed several  spectroscopic  techniques
which provide such remote sensing capability.
Two of the  most important are the multiple
scan infrared interference spectrometer and
the correlation spectrometer. Such instru-
mentation, though expensive, yields data  in
a uniquely useful form for a variety of appli-
cations.
  A commercial model of a multiple-scan in-
frared  interference spectrometer  has  been
developed by  Block  Engineering Corpora-
tion*  and its utilization  in the field has been
discussed by Low.-1  With  this  instrument,
remote  detection of SO^ and COo  in the stack
effluent of a power plant has been reported by
Low and Clancy.24
  A correlation spectrometer mounted in an
airplane recently has been used by Barringer
and associates to estimate atmospheric sulfur
dioxide "contours" for several U.S. cities.25"27
The instrumental technique  utilizes sunlight
reflected from the earth's surface as a "light
source" and, in a sophisticated fashion, meas-
ures the absorption of this reflected solar ra-
diation  by the  sulfur dioxide in the air. The
method depends on the fact that  sulfur diox-
ide has a clearly structured absorption spec-
trum  in the region near 3100A and it  gives
                                   1 Mention of commercial products does not constitute
                                   endorsement by the National Air Pollution Control
                                   Administration.
       22

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the total sulfur dioxide concentration in the
"line  of  sight" of  the spectrometer. While
work  to date has been carried out primarily
from  aircraft, correlation spectrometry need
not be limited to airborne applications.

            6.   Other Methods

  The earliest methods for determining  sul-
fur dioxide were based on its ability to reduce
a  starch-iodine  solution. This method  was
considered to be  reasonably accurate in the
range 0.8 ppm to  3  ppm and it later was
modified to cover the range 0.1  ppm to 60
ppm.  This method has now been automated.28
These and other methods are discussed by
Katz.29 He also reported a method of measur-
ing the titratable acidity of the air by absorb-
ing acid components  in  a water  solution of
hyperol, a compound formed by reacting hyd-
rogen peroxide with urea. The oxidizable acid
components react with the peroxide.
   Sulfur dioxide can be determined by a fuch-
sin-formaldehyde method reviewed by Hoch-
heiser 3tl and reported by Alekseeva and Sam-
orodiva.31  The sample is collected in  0.1N
sodium  hydroxide in glycerol-water solution.
Another procedure, reported by Bushtueva,32
made use of collection in a potassium chlorate
solution. The method of analysis was not stat-
ed, but  it probably  was by nephelometric
analysis of barium sulfate  or turbidimetric
analysis of lead sulfate. Lyubimov 33 describ-
ed a  monitoring instrument in which sulfur
dioxide is absorbed in a solution of  barium
chloride, and light  transmission through the
turbid solution, inversely related to the sulfur
dioxide concentration, is recorded.
   A  further method  for determining ozone
and sulfur dioxide has been reported  recent-
ly.34 The measurement principle involves lib-
eration of iodine by  ozone from an iodide
solution in  one channel  of the analyzer and
the consumption of iodine by sulfur  dioxide
in a second analyzer channel.

    7.  Use and Comparison of Methods

   The hydrogen peroxide acid titration meth-
od or an automatic  conductometric  version
of the same method is used most frequently
in Europe;  in the United States, the colori-
metric pararosaniline and automated conduc-
tometric (using either acidified peroxide or
deionized water) methods are used most fre-
quently.
  The values obtained by the various methods
of measuring gaseous sulfur dioxide in ambi-
ent air  may not always correlate well with
one another, since they do not measure the
same thing and because interfering substan-
ces are present in varying amounts from time
to time  and from place to place. It is gener-
ally assumed that sulfur dioxide is the major
constituent in  air that will respond to any of
the methods discussed;  that  the assumption
may not be entirely valid is shown in some
recent studies.35-4"
  Recently the conductivity  and colorimetric
pararosaniline techniques have been evalu-
ated in  depth,41 "2  and others have reported
on comparisons between the  methods.41-45 In
one study, no consistent relationship between
the two measurements  was  found, although
the conductometric method usually gave high-
er values.44
  There is  evidence  that hydrochloric acid
may contribute significantly to the values ob-
tained by the hydrogen peroxide method in
England, but  this  may not  be  true for cer-
tain  sections of the United States because of
the negligible amounts  of chloride found in
the coal burned.43^48
  Recently  a  flame  photometric  instrument
was  reported for the detection of total sulfur
compounds  in the  atmosphere.49 The  instru-
ment is based  on the principle that when sul-
fur compounds in air are introduced into a
hydrogen-rich flame, they emit  light between
300  m/j. to  425  m/*.  A  photomultiplier tube
looks at the  light  of  wavelength 394 m/*
through a  narrow-band  optical filter. The
quantity of light is  proportional to the con-
centration  of sulfur  compounds. This instru-
ment is readily automated  for continuous
monitoring.
   Several  commercial instruments are also
available  which are based  on coulometry.
These  instruments  measure  the  reducing
properties  of  sulfur dioxide and, with the
use of a suitable scrubber, can provide rela-
tively specific and continuous measurements
of sulfur dioxide. The principle of this method
involves the titration of sulfur dioxide by
electrogenerated bromine or  iodine.
                                                                              23

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D.  MEASUREMENT OF SULFURIC ACID
             AND SULFATES

  These forms of sulfur are always found in
the particulate phase in polluted air, either as
suspended matter which can be removed by
special measurement techniques or in dust-
fall. The acidity may be measured by titra-
tion or by a related procedure; alternatively,
sulfate ion may be measured (frequently by
conversion to the  insoluble barium salt).
Since the particle size is very small, the'ini-
tial collection of the sample requires special
techniques.  Any  technique  for  separating
particulate matter from air may be used, but
filtration  and impaction usually have  been
employed.
  A system capable of filtering 50 cubic feet
to 60 cubic  feet of air in 1 hour through
Whatman No. 4  filter paper (1-inch diam-
eter)  that had previously been washed  with
distilled  water until the washing had a pH
of 7 ± 0.10, is described by Mader.50 The test
filter  holding the pollutants was  macerated
in 20 ml of distilled water, and the pH of the
resulting solution was determined. Total acid-
ity (sulfuric acid) was determined by titra-
tion of  0.002^ sodium  hydroxide to an end
point equivalent to the pH of carbon-dioxide-
free distilled water and corrected by a blank
determination.
   Commins51 has  described a  method  in
which sulfuric acid in the air was collected by
filtering air through Whatman No. 1  filter
paper. The amount  of  acid  was determined
by immersing the collected sample in a known
excess of 0.012V sodium tetraborate in deion-
ized water of pH 7 and titrating back to pH
7 with Q.01N sulfuric acid.
   Sulfuric acid aerosol  has been collected by
impaction or filtration to separate sulfuric
acid from sulfur dioxide.52 The acid is decom-
posed at  controlled  temperatures under a
nitrogen, stream, and the liberated sulfur tri-
oxide is then reduced with hot  copper to sul-
fur  dioxide.  Sulfur dioxide is determined
spectrophotometrically, coulometrically, or by
flame photometry. The method  measures sul-
furic acid in the presence of 10 to 100  times
as much sulfur  dioxide and inert sulfates.
Ammonium  sulfate, a primary lung irritant,
is also  measured as sulfuric acid; however,
this sulfate probably originates in the atmos-
phere from the reaction of sulfuric acid and
ammonia. The sensitivity is in the parts per
billion range using 1 m3 of air as a sample.
DuBois has described a method in which sul-
furic acid is collected on glass fiber filters and
titrated following thermal separation at 200°
C  in a nitrogen atmosphere.  This method
measures free sulfuric acid and does not in-
clude ammonium  sulfate  or sulfuric  acid
which reacts with particles on the filter.

 E.  OTHER METHODS  OF MEASURING
    POLLUTION BY SULFUR OXIDES

1.   Sulfation Rates of Lead Peroxide Candles

   A method for measuring sulfation involves
use  of the lead peroxide  "candle." A paste
made of lead peroxide in a gum tragacanth
solution is applied to a cotton gauze wrapped
around a glass or porcelain form; the product
is the lead peroxide candle. The  candle  is
exposed to the ambient air  in a louvered shel-
ter for an extended period of time, usually a
month, and the lead sulfate formed in the
candle is then determined. It is abvious that
the  method cannot give any information on
short-term variations in sulfur oxides pollu-
tion levels and  that it is  only an  empirical
estimate  of the average concentration. The
method measures sulfuric acid, hydrogen sul-
fide, and other  sulfur-containing compounds
which can form sulfate. In  spite of these limi-
tations,  sulfation  measurements have corre-
lated well with  data on biological effects and
the  deterioration of materials.
   A small, dish-type lead peroxide measuring
device termed a "sulfation plate," which can
be exposed  without a  protective shelter, has
been described.53 The  plates are more reac-
tive than candles, and it is proposed that ex-
posure periods  could be shortened to 1 day
with more sensitive analytical methods. Tur-
 bidimetric  determination  of  sulfate  was
found, not unexpectedly, to be less time-con-
 suming  than gravimetric analysis, though
 not  as accurate.
   The primary  application of the lead perox-
 ide  candle is for mapping  sulfur pollution in
 a given area as  related to sources and meteor-
 ology. It is convenient since a simple shelter
 requiring no electrical power is used. A major
       24

-------
problem with the lead peroxide candle is that
results are influenced by wind movement and
humidity. Another  major  drawback  to the
lead peroxide candle is that the laboratory
preparation  and analysis is quite time con-
suming. The cost of preparing and analyzing
a lead peroxide  candle is approximately the
same as  for  collecting and analyzing a 24-
hour integrated sulfur dioxide sample by the
West-Gaeke  procedure. Also, the lead perox-
ide candle provides  intelligence on the oxi-
dizable sulfur compounds in the atmosphere
which seldom can be directly related to sulfur
dioxide. It has been observed that in many
cases monthly averages of sulfur dioxide rise
and fall somewhat parallel  to monthly sulfa-
tion values.
   Sulf ation rates in United States cities have
been  observed to  range from a  few  hun-
dredths of a milligram to about 8 mg of sul-
fur trioxide per 100 cm2 of exposed lead per-
oxide candle surface per day (mg S03/100
cm2-day).35~37 35

          2.  Suspended Sulf ate
   Sulf ate (sulfuric acid and sulfate salts) in
suspended particulate matter has been exten-
sively measured for a number of years by the
National  Air  Surveillance  Networks.48 56
Sulfates  are  extracted from the  particulate
matter on the glass fiber filter by refluxing
with distilled water.  Sulfate in the extract is
determined by the methyl thymol  blue auto-
mated method  or  by  the  turbidimetric
method. The maximum 24-hour average con-
centration estimated from  2,197 samples
collected  over the  years 1957 to  1960 is  94
/tg/m3, and  the national  average for this
period is  11.8 /tg/m3. There is considerable
geographic variation. The  observed average
concentrations of  18.8  ^g/m3, 15.0  /tg/m3,
14.5 /tg/m3, and  13.3 /tg/m3 occur in the Mid-
Atlantic, Midwest, Mideast, and  New Eng-
land areas, respectively. Lower average con-
centrations  of 10.7  /tg/m3, 9.0  /tg/m3, 8.7
f*g/m3, 7.4 /tg/m3, and 5.8  /tg/m3 have  been
observed  in  the  Southeast,  Pacific  coast,
Great Plains,  Gulf south, and Rocky Moun-
tain areas, respectively. As with sulfur diox-
ide,  the  highest concentrations occur most
frequently in the fall and winter  months.
          3.  Sulfate in Dustfall
  The register of Air Pollution Analyses 5e
lists only  four organizations which  have
measured and reported sulfate in dustfall in
the United States. This measure may be ex-
pressed either as percent sulfate in total dust-
fall or as tons of sulfate per square mile per
month. In a southwestern city, where 32  col-
lecting stations were used, sulfate averaged
10.8 percent of the  total dustfall,  or  15.5
tons/mi2-month over a 3-month period. In a
northwestern city, sulfate averaged 27 per-
cent of the total dustfall, or 7.4  tons/mi2-
month, which is similar to the 32 percent of
the total  dustfall and 7.8 tons/mile2-month
observed in a New England  town.54 57~59

          4.  Sulfuric Acid Mist
  Few attempts have been made to measure
sulfuric acid mist in the United States. Con-
centrations  measured in Los  Angeles  aver-
age about 25 /xg/m3,  and a high concentra-
tion of 50 /tg/m3 has  been observed.50 60 61 In
Chicago, during the months of November and
December 1964, the average for the hours 10
a.m. to 4 p.m. was 9.2 /tg/m3.62

             F.  SUMMARY

  In 1966, an estimated 28.6 million tons of
sulfur dioxide were  emitted  to the atmos-
phere, as compared with 23.4 million tons in
1963.  The principal share, i.e., 58.2 percent,
came  from  the combustion of coal,  most of
which was used to generate electrical power.
The combustion of residual fuel oil and other
petroleum products accounted for 19.6 per-
cent of the  total, while the remainder came
from the refining of petroleum (5.5 percent),
the smelting of sulfur-containing ores  (12.2
percent), the manufacturing of sulfuric acid
(1.9 percent), the burning of refuse (0.4 per-
cent) , and the burning or smoldering of coal
refuse banks (0.4 percent).  Paper-making
and some  other industrial operations  also
contributed minor amounts to the total. In all
of these  processes, small  amounts of sulfur
trioxide or sulfuric acid are emitted also.
  In the United States,  the two most com-
mon methods of measurement are  the color-
metric West-Gaeke (pararosaniline)  and the
                                                                              25

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conductometric methods.  The  former  is a
specific method and the latter is  a general
method. The colorimetric West-Gaeke method
employs a chemical reaction in which a red-
purple dye is produced; the intensity of the
dye, which is proportional to the concentra-
tion of sulfur dioxide, is then measured. This
method is specific for sulfur dioxide and sul-
fite salts.  While nitrogen  oxides, ozone, and
heavy  metal salts in the  sample  can  affect
the measurement, there are ways to eliminate
these interferences. For intermittent as well
as continuous  sampling, the modified West-
Gaeke  (pararosaniline) procedure is the most
satisfactory, and it  is the standard method
of the National Air Pollution Control Admin-
istration.
  Conductometric methods  may  employ an
acidified peroxide solution in which the elec-
trical conductivity changes directly with the
concentration of sulfur dioxide in the absorb-
ing solution. Although conductometric meth-
ods can be readily automated to obtain read-
ings over long durations,  they are general
techniques and the user must be fully aware
that other pollutants can  affect the conduc-
tivity of the solution. Since often it is not
known what other interfering pollutants may
be  present  in  the sample,  the results are
sometimes very approximate, particularly at
high and very low sulfur  dioxide concentra-
tions.
  The  technique  most frequently used  in
Europe is the hydrogen peroxide approach,
in which  sulfur dioxide forms sulfuric acid
which  is then  titrated with standard alkali;
this approach may be considered a general
method, since the presence of other acidic or
alkaline gases  in  the sample may give er-
roneously high or low results.
  An approach that has been widely used is
the lead peroxide candle technique, which de-
termines a "sulfation rate." The method gives
integrated values for relatively long periods,
but, unlike continuous monitoring instru-
ments, provides no indication of short-term
fluctuations. While the lead candle method is
inexpensive in terms of equipment, the pre-
paration and  analysis costs are  about the
same as for collecting and analyzing 24-hour
integrated sulfur dioxide  samples by the
West-Gaeke procedure. In general, the dis-
advantages of lead candles far outweigh their
advantages. They are useful only in relatively
localized studies where the meteorology and
exposure do not vary, and then only if great
care is exercised  to keep the construction of
the candles and the chemistry of the analyses
constant. In addition, the lead candle provides
only a rough indication of sulfur dioxide con-
centrations, since it is  a general approach
that may respond to a large number  of oxi-
dizable sulfur-containing compounds found in
the atmosphere.
  Recently, two long-path spectroscopic tech-
niques have been introduced that sense sulfur
dioxide  concentrations remotely. A multiple-
scan interference spectrometer detects from
a distance  the characteristic infrared sulfur
dioxide  emissions in heated plumes; a corre-
lation spectrometer looks at the character-
istic absorption by sulfur dioxide that occurs
near 3100A. Although these instruments are
complex and expensive, they possess a poten-
tial for determining the sulfur dioxide "pollu-
tion contours" over large areas of the city, as
well as the concentrations at different eleva-
tions.
  Other techniques are  still being perfected
and may have much promise. Coulometric in-
struments involve the titration of sulfur diox-
ide by  electrogenerated  bromine  or  iodine.
With the aid of suitable scrubbers, the tech-
nique may provide a method for determining
sulfur  dioxide  that is both  continuous and
relatively specific. A  newly developed flame
photometric instrument measures total sulfur
and is therefore not specific for any one sul-
fur-containing pollutant. In  this method sul-
fur compounds undergo reduction in a hydro-
gen-rich flame; the light emitted at a charac-
teristic  wavelength  is  proportional  to  the
total atmospheric sulfur.
  Other methods are  available for analyzing
other sulfur-containing compounds. For ex-
ample, sulfuric acid aerosol in suspended par-
ticulate material  may be measured by titra-
tion or by controlled decomposition to sulfur
dioxide. This then can be measured by  a num-
ber of methods, including spectrophotometry,
coulometry, and  flame photometry. Particu-
late sulfate may be analyzed by spectrophoto-
metric or turbidimetric methods.
  Each  method is  unique in terms  of  the
      26

-------
measuring time resolution, the costs, the skill
and time  required for the analysis, and  the
kinds of pollutants which may cause inter-
ference and  thus impair the accuracy of  the
results. The  techniques selected, therefore,
are usually a compromise. Moreover, a single
program often will make use of both general
and specific methods. In selecting a technique,
it is  especially important to consider the  de-
gree  to which the resulting data can  be con-
verted for comparison with  results obtained
from  other  instruments and  at other time
periods.

              G.   REFERENCES

 1. Hendrickson, E.  R.  "Air Sampling and  Quan-
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22. Rodes, C. F.,  Elfers, L. A., Palmer, H.  F., and
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    Air Pollution Control Association, St. Paul, Min-
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23. Low,  M. J. D. "Multiple-Scan Infrared Inter-
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    p. 637, 1966.
24. Low,  M. J. D.  and Clancy,  F. K.  "Remote  Sens-
    ing and Characterization of  Stack Gases by In-
    frared Spectroscopy. An Approach  Using Mul-
    tiple-Scan Interferometry." Environ. Sci.  Tech-
    no!., Vol. 1, pp. 78-74, 1967.
25. Barringer, A. R. and Newberry, B. C. "Remote
    Sensing Correlation  Spectrometry for Pollution
    Measurements."  Ninth Conference on  Methods
    in Air Pollution and Industrial Hygiene, Pasa-
    dena, California, Feb. 7-9,  1968.
26. Barringer, A.  R. and Newberry, B.  C.  "Molec-
    ular  Correlation  Spectroscopy for Sensing Gas-
    ous Pollutants." 60th Annual Air Pollution Con-
    trol Association Meeting, Paper 67/196,  1967.
27. Barringer, A. R. and Shock,  J. P. "Progress in
    the Remote Sensing of Vapors for  Air Pollu-
                                                                                          27

-------
    tion, Geologic, and Oceanographic Applications."
    Proceedings  of  the 4th  Symposium  on Remote
    Sensing of  the  Environment,  April 1966,  pp.
    779-791.
28.  Bokhoven, C. and Niessen,  H. G. L.  "The  Con-
    tinuous  Monitoring of Traces  of  Sulfur  Diox-
    ide in Air on the  Basis of Discoloration of the
    Starch-Iodine Reagent with  Prior  Elimination
    of  Interfering Compounds."  Int. J.  Air Pollu-
    tion, Vol. 10, pp. 223-243, 1966.
29.  Katz,  M.  "Sulfur Dioxide  in  the  Atmosphere
    of  Industrial Areas." In:  Effect of Sulfur Di-
    oxide on Vegetation,  National Research Council,
    Ottawa, Canada, 1939, pp. 14-50.
30.  Hochheiser,  S.   "Methods   of  Measuring   and
    Monitoring Atmospheric Sulfur Dioxide."  U.S.
    Dept. of Health, Education, and Welfare, Public
    Health Service,  PHS-Pub-999-AP-6, Aug. 1964.
31.  Alekseeva,  M. V.  and Samorodiva,  R. Ya. S.
    "Determination  of Sulfur  Dioxide  Colorimetri-
    cally with the Aid of Fuchsin-Formaldehyde So-
    lution."  Gig. i  Sanit, Vol. 10,  p. 42, 1953.  In:
    Limits  of Allowable  Concentrations of Atmos-
    pheric  Pollutants, Book  2,  Office of Technical
    Services, Washington, D.C.,  1955, pp. 90-95.
32.  Bushtueva, K. A.  "Ratio of Sulfur Dioxide and
    Sulfuric  Acid Aerosol in  Atmospheric Air, in
    Relation  to  Meteorological  Conditions."  Gig.  i
    Sanit.,  Vol.  11,  pp.  11-13,  1954.  In: U.S.S.R.
    Literature on Air Pollution  and Related  Occu-
    pational Diseases.  A Survey. Vol. 4.  Translated
    by B.  S.  Levine, U.S. Dept. of  Commerce, Office
    of  Technical Services, Washington,  D.C.,  Aug.
    1960, pp. 193-196.
33.  Lyubimov, N. A.  "A Nephelometer with an Au-
    tomatic 24-Hour Device for Continuous Record-
    ing of  Sulfur Dioxide Concentrations in Atmos-
    pheric  Air." In:  Limits of Allowable Concen-
    trations  of Atmospheric   Pollutants.  Book 5.
    Translated by B. S.  Levine, U.S. Dept. of  Com-
    merce,  Office of Technical  Services, Washington,
    D.C., 1962, pp. 120-127.
34.  Schulze,  F.  "Versatile Combination Ozone and
    Sulfur  Dioxide  Analyzer."  Anal.  Chem.,  Vol.
    38, pp. 298-752, May 1966.
35.  McCaldin, R. 0. and  Bye, W. E. "Air Pollution
    Appraisal—Seward and New Florence, Pa." U.S.
    Public Health Service, Robert A. Taft Sanitary
    Engineering Center, 1961.
36.  Stalker, W. W., Dickerson, R.  C., and Kramer,
    G. D.  "Atmospheric Sulfur Dioxide  and  Par-
    ticulate Matter—A  Comparison  of  Methods of
    Measurements." Am. Ind.  Hyg. Assoc. J.,  Vol.
    29, pp. 68-79,  Jan.  and  Feb.  1963.
37.  Farmer, J.  R.  and Williams, J. D.  "Interstate
    Air Pollution Study, Phase II Project Report,
    Section III, Air Quality  Measurements."  Inter-
    state  Air  Pollution  Study  St. Louis-East St.
    Louis Metropolitan Areas.  U.S. Dept. of Health,
    Education, and Welfare, Public Health Service,
    Dec. 1966.
38. Hochheiser, S.,  Santner, J. T.,  and Ludman, W.
    F.  "The  Effect of  Analytical  Method on  Indi-
   cated  Atmospheric S02 Concentration."  J.  Air
   Pollution Control Assoc.,  Vol. 16, pp. 266-270,
   May  1966.  (Presented at Annual Meeting,  Air
   Pollution  Control  Association,  Toronto, June
   1965.)
39. Greenburg, L. and  Jacobs, M. B.  "Sulfur Di-
   oxide in New York City Atmosphere." Ind. Eng.
   Chem., Vol.  48,  pp. 1517-1521, Sept. 1956.
40. Tabor, E.  C. and Golden, C. C. "Results of Five
   Years' Operation of the National Gas Sampling
   Network." J. Air Pollution Control Assoc.,  Vol.
   15, pp. 7-11, Jan. 1965.
41. Terabe, M.,  Comichi,  S., Benson, F. B.,  Newill,
   V.  A.,  and Thompson, J. E.  "Relationships Be-
   tween Sulfur Dioxide  Concentration Determined
   by the West-Gaeke and Electroconductivity Meth-
   ods."  J. Air Pollution  Control Assoc.,  Vol. 17,
   pp. 673-675, Oct. 1967.
42. Shikiya, J. M. and McPhee, R. D.  "Multi-Instru-
   ment  Performance  Evaluation of Conductivity
   Type  Sulfur  Dioxide  Analyzers." Presented at
   61st Annual Meeting, Air Pollution Control As-
   sociation, St.  Paul, 1968.
43. Trieff, N.  M., Wohlers, H. C., O'Malley, J. A.,
   and Newstein, H.  "Appraisal and Modification
   of  West-Gaeke Method for Sulfur Dioxide Deter-
   mination."  J. Air  Pollution Control Assoc.,  Vol.
    18, pp. 329-331, May 1968.
44. Booras, S. G. and Zimmer, C.  E.  "A Comparison
   of  Conductivity  and  West-Gaeke Analyses for
    Sulfur Dioxide." J. Air Pollution  Control Assoc.,
    Vol. 18, pp. 612-615, Sept. 1968.
45. "Air  Quality Data (1963)  National Air Sam-
   pling  Network."  U.S. Dept.  of Health, Educa-
   tion,  and  Welfare, Public Health Service, 1965.
46. Gorham, E.  "Atmospheric Pollution  by Hydro-
   chloric  Acid."  Quart.  J. Roy.   Meteorol.  Soc.,
    Vol. 84, pp. 274-276, July 1958.
47.  Cummins,  B. T.  "Chemistry  in Town Air." Re-
    search, Vol. 15,  pp. 421-426,  Oct. 1962.
48.  "Air  Pollution   Measurements  of the National
    Air Sampling Network, Vol.  I. Analyses of  Sus-
   pended Particulates,  1953-1957."  U.S.  Dept. of
    Health, Education, and Welfare, Public Health
    Service, PHS-Pub-637, 1958.
49.  Stevens, R. K.,  O'Keeffe, A. E., and  Ortman,
    G. C.  Title not known, Environ. Sci.  Technol.
    (In press, 1968.)
50.  Mader, P. P., Hamming, W.  J.,  and Bellin, A.
    "Determination  of  Small Amounts  of  Sulfuric
    Acid in the Atmosphere." Anal.  Chem., Vol. 22,
    pp. 1181-1183, Sept.  1950.
51.  Cummins, B. T.  "Determination of Particulate
    Acid  in Town Air."  Analyst, Vol. 88,  pp.  364-
    367,  May  1963.
52. Scaringelli,  F. P.  and Rehme, K. A. "Determi-
    nations of Atmospheric Concentrations of  Sul-
    furic Acid  by   Spectrophotometry,  Coulometry,
    and  Flame  Photometry."  (To be published  in
    Anal. Chem.)
53. Huey, N.  A.  "The Lead Peroxide Estimation  of
    Sulfur Dioxide Pollution." J. Air Pollution  Con-
    trol  Assoc., Vol. 18, pp. 610-611, Sept.  1968.
        28

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64.  Kenline, P. A. "In Quest of Clean Air for Ber-
    lin, New Hampshire."  U.S. Public Health Ser-
    vice,  Robert A.  Taft Sanitary  Engineering
    Center, Tech. Kept. A62-9,  1962.
55.  "Air  Pollution  Measurements of  the  National
   Air Sampling  Network, Vol.  II.  Analyses  of
    Suspended Particulates, 1957-1961." U.S. Dept.
    of  Health,  Education, and  Welfare,  Public
    Health  Service, PHS-Pub-978, 1962.
56.  "Register of Air Pollution Analyses." U.S. Dept.
    of  Health,  Education, and  Welfare,  Public
    Health  Service, PHS-Pub-610, Vol. I,  1958 and
    Vol. II,  1961.
57.  "Air  Pollution in  the El Paso, Texas Area. Re-
    port  on a Two-Year  Study under a Community
    Air Pollution Demonstration Project Grant."  El
    Paso City-County  Health Unit, 1959.
58.  Tyler, R. G. "Report on an Air Pollution Study
    for City of  Seattle." Univ. of Washington, En-
    viron. Res. Lab., March 15, 1952.
59.  Anderson, D. M., Lieben, J., and Sussman, V. H.
    "Pure  Air  for  Pennsylvania."  Pennsylvania
    Dept. of Health and  U.S. Dept. of Health,  Edu-
    cation, and Welfare,  Public Health Service, Nov.
    1961.
60.  Chaney, A. L. "Investigations to Detect the At-
    mospheric Conversion of Sulfur Dioxide  to Sul-
    fur  Trioxide."  Am.  Petrol.  Inst, Vol. 38, pp.
    306-312, 1958.
61.  Thomas, M.  D. "Sulfur  Dioxide, Sulfuric  Acid
    Aerosol, and  Visibility in Los Angeles."  Int. J.
    Air  Pollution, Vol.  6. pp. 443-454,  Nov.-Dec.
    1962.
62.  Boone, R.E.  and Brice, R. M. "Continuous  Mea-
    surement of Acid  Aerosol in the  Atmosphere."
    APCA  Paper 65-119.   (Presented  at Annual
    Meeting Air  Pollution Control  Association, To-
    ronto, June 1965.)
                                                                                            29

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                   Chapter 3
ATMOSPHERIC CONCENTRATIONS OF SULFUR OXIDES

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                            Table of Contents                          Page
A. INTRODUCTION                                                    33
B. ATMOSPHERIC CONCENTRATIONS OF SULFUR DIOXIDE           33
   1.  Concentrations in Urban Areas                       .         .      33
   2.  Concentrations Related to Point Sources                     ...       42
      a. Copper Smelter, Australia, 1962                    .         .      42
      b. Oil Refinery, 1965           .                                    42
      c. Smelter, Canada, 1958                       .                    42
      d. Smelter, Trail, Canada, 1931 to 1937           	      42
      e. Power Plant, 1966          .                 .         ...      42
      f. Power Plant,  Pennsylvannia, 1961            .      .      ...      42
C. SULFURIC ACID AND ITS RELATION TO SULFUR DIOXIDE          42
D. ACIDITY OF RAINWATER AND PARTICULATE MATTER            45
E. SUMMARY                          .           .                    45
F. REFERENCES                                             	      47


                              List of Figures
Figure
3-1   Long-time Average  Sulfur Dioxide  Concentrations (ppm)  and As-
      sociated Maximum Average Concentrations for Various Time Periods
      for 12 Sites in 11 Cities                   .              . .           36
3-2   Frequency Distribution of  Sulfur Dioxide Levels in Selected Ameri-
      can Cities, 1962 to 1967          .                                   37
3-3   Annual  Average Sulfur Dioxide Concentrations for Eight American
      Cities                                                       ..39
3-4   Concentrations of Sulfur Dioxide  in Chicago for Various Averaging
      Times and Frequencies, from December 1,1963, to December 1, 1964      41


                              List of  Tables
 Table
3-1   CAMP Data on Sulfur Dioxide Concentrations (ppm by Volume)         34
3-2   Comparison of Calculated  and Observed Maximum Sulfur Dioxide
      Concentrations for Various Averaging Times in 1964 in Chicago  ..       41
3-3   Concentration of Sulfur  Dioxide and Sulfuric Acid Mist  Observed in
      the Air         .                   ...       	     43
3-4   Concentrations of Sulfur Dioxide and Sulfuric Acid Mist Observed
      in 1961 in Air over Los Angeles and One of its Suburbs, El Segundo....     44

       32

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                                      Chapter  3

           ATMOSPHERIC CONCENTRATIONS OF SULFUR  OXIDES
           A.   INTRODUCTION

  This chapter discusses the short and long-
term measured concentrations of sulfur ox-
ides in  urban areas and in the vicinity of
point sources such as power plants, refineries,
and smelters.  The relation of sulfur  oxides
in the atmosphere to the acidity of rainwater
and of particulate matter also is reviewed.

 B.  ATMOSPHERIC CONCENTRATIONS
          OF  SULFUR  DIOXIDE

     1.   Concentrations in Urban Areas
  Two major programs sponsored by the U.S.
Public  Health  Service have  provided the
largest body of data on atmospheric  sulfur
dioxide  concentrations  in  urban areas. The
Continuous Air Monitoring Project (CAMP)
use the electroconductirity method for S02
determination  in  six large cities;  more re-
cently, CAMP has installed and is operating
continuous,  colorimetric SO. monitoring de-
vices at all sites in addition to electroconduc-
tivity instruments. The National Air Surveil-
lance Networks (NASN) use the colorimetric
(West-Gaeke)  method  to provide 24-hour-
sample data for about 100 locations on a 26-
times-per-year basis.
  Extensive monitoring programs yield large
quantities of data which need to be reduced
to a useful form. Maximum or average  values
alone do not provide a total picture  of air
quality.  Distribution plots, showing the per-
centage of the time sulfur dioxide concentra-
tions are above certain levels,  give a more
complete insight into the distribution  of sul-
fur dioxide  concentrations  for  a given site.
  The frequency distributions obtained from
CAMP measurements (for example, see Zim-
mer and Larsen a) show that sulfur dioxide
concentrations  are not  symmetrically  dis-
tributed but follow a log-normal distribution.
This also has been established by Brasser,
Joosting, and van Zuilen.2 CAMP data are
plotted as  a frequency  ditribution for six
cities in Figure 3-2. The lower levels of sulfur
dioxide that prevail in Los Angeles and San
Francisco,  as compared  with some  Eastern
cities, are clearly evident.
  Table 3-1 gives sulfur dioxide  concentra-
tions, in  ppm (determined by the hydrogen
peroxide  method), for 1962 to 1967 at the
CAMP sites  in eight  cities for six different
averaging times:  5 minutes, 1 hour,  8 hours,
1 day, 1 month, and 1 year. For some years,
the monitoring systems were not in operation
at some  locations, and this is  indicated by
asterisks in  the columns. The  first  column
gives the calculated maximum concentration
using the  approach  of  Larsen3 described
later in the chapter. Listed in the second and
third columns are the geometric mean and the
standard geometric deviation,  similarly cal-
culated, which describe the statistical distri-
bution of the data. Columns 4 and 5 list the
range of maximum values that were recorded
during the 6-year period, while the maximum
for each year is listed in  columns  6 to 11.
  From the data shown in Table 3-1, it is ap-
parent that higher maxima are obtained as
the averaging time becomes shorter. This is
because, for shorter averaging times, the in-
stantaneous fluctuations  have much greater
influence on the resulting values.  This trend
is shown  quite clearly in Figure 3-1, in which
the maximum  average  concentrations are
plotted against the averaging time for differ-
ent cities. The standard geometric deviation
(column 3 of Table 3-1) indicates  the degree
to which  a given set of samples  deviate  from
their geometric mean, and therefore it in-
                                                                             33

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  Table 3-1.—CAMP DATA ON SULFUR DIOXIDE CONCENTRATIONS (ppm by volume)
City and
averaging
time
Chicago:
5 min
1 hr
8 hr
1 day
1 mo
1 yr
Cincinnati:
5 min
1 hr
8 hr
1 day
1 mo
1 yr 	
Denver:
5 min
1 hr
8 hr
1 day
1 mo
1 yr
Los Angeles:
5 min
1 hr
8 hr
1 day
1 mo
1 yr
Philadelphia:
5 min
Ihr 	
8 hr
1 day _ _
1 mo
1 yr
St. Louis:
5 min
1 hr
8 hr
1 day
1 mo
1 yr
San Francisco:
5 min
1 hr
8 hr
1 day
1 mo
1 yr
Washington:
5 min
1 hr
8 hr
1 day
1 mo
1 yr

1962-1967
Calc.
annl.
max.
(1)
3.33
1.60
0.87
0.64
0 24
0.14
1.85
0.70
0.31
0.21
0.06
0.03
0 36
0.18
0 10
0 07
0.03
0.02
0.47
0.22
0.12
0.09
0.03
0.02
2.60
1.16
0.60
0.42
0.15
0.08
2.40
0.96
0.45
0.30
0.09
0.05
0.56
0.22
0 10
0.07
0.02
0 01
1.19
0.58
0.32
0.23
0.09
0.05

Geo
mean
(2)
0.104
0.111
0.118
0.121
0.133
0.142
0.016
0.018
0.020
0.021
0.025
0.029
0.013
0.014
0.015
0.015
0.017
0.018
0.013
0.014
0.015
0.015
0.017
0.018
0.055
0.060
0.064
0.067
0.075
0.081
0.028
0.031
0.034
0.036
0.042
0.047
0.005
0.006
0.007
0.007
0.008
0.010
0.039
0.042
0.044
0.046
0.050
0.050
SGD
(3)
2.20
2.01
1.84
1.75
1.44
1.00
2.94
2.60
2 31
2.16
1.65
1.00
2.11
1.94
1.79
1.71
1.41
1.00
2.28
2.07
1.90
1.80
1.46
1.00
2.40
2.17
1.98
1.87
1.50
1.00
2.75
2.45
2.20
2.06
1.60
1.00
2.87
2.54
2.27
2.12
1.63
1.00
2.17
1.99
1.83
1.74
1.43
1.00
Maxima
Max.
(4)
1.94
1.69
1.02
0.79
0.35
0.18
1.15
0.57
0.38
0.18
0.06
0.04
0.96
0.36
0.14
0.06
0.03
0.02
0.68
0.29
0.13
0.10
0.03
0.02
1.25
1.03
0.71
0.46
0.15
0.10
1.42
0.96
0.36
0.26
0.08
0.06
0.33
0.26
0.10
0.08
0.03
0.02
0.87
0.62
0.35
0.25
0.11
0.05
Min.
(5)
1.11
0.86
0.45
0.36
0.13
0.09
0.65
0.41
0.14
0.10
0.04
0 02
0.33
0.17
0.05
0.02
0.01
0.01
0.24
0.13
0.08
0.06
0.02
0.02
0.79
0.66
0.43
0.35
0.12
0.06
0.85
0.55
0.24
0.18
0.05
0.03
0.16
0.11
0.06
0.05
0.01
0.01
0.42
0.35
0.22
0.15
0.07
0.04
62
(6)
1.13
0.86
0.45
0.36
0.18
0.10
0.84
0.46
0.14
0.11
0.04
0.03





0.24
0.13
0.08
0.06
0.03
0.02
1.25
1.03
0.56
0.35
0.13
0.09





0.16
0.11
0.06
0.05
0.01
0.42
0.38
0.23
0.18
0.10
0.05
63
(7)
1.94
1.69
0.87
0.71
0.33
0.14
0.99
0.48
0.23
0.11
0.06
0.03





0.51
0.19
0.09
0.07
0.03
0.02
1.05
0.85
0.58
0.46
0.12
0.06





0.33
0.26
0.07
0.05
0.02
0.01
0.56
0.48
0.35
0.25
0.11
0.05
Maximum for year
64 65 66
(8)
1.62
1.12
1.02
0.79
0.35
0.18
0.88
0.55
0.27
0.14
0.06
0.04





0.68
0.29
0.13
0.10
0.02
1.00
0.84
0.54
0.43
0.15
0.09
1.16
0.73
0.31
0.26
0.08
0.06
0.26
0.16
0.10
0.08
0.03
0.02
0.87
0.62
0.32
0.22
0.09
0.04
(9)
1.59
1.14
0.74
0.55
0.27
0.13
1.15
0.57
0.38
0.18
0.06
0.03
0.95
0.36
0.14
0.06
0.03
0.02





1.11
0.94
0.71
0.35
0.13
0.08
1.42
0.96
0.36
0.19
0.06
0.05





0.44
0.35
0.27
0.20
0.08
0.05
(10)
1.11
0.98
0.63
0.48
0.27
0.09
0.70
0.41
0.18
0.10
0.05
0.03
0.96
0.26
0.10
0.05
0.02
0.01





0.79
0.66
0.43
0.36
0.13
0.09
1.25
0.84
0.33
0.18
0.06
0.04





0.47
0.45
0.34
0.25
0.10
0.04
Perct.
data
avail.
67
(11)
1.62
1.11
0.80
0.65
0.32
0.12
0.65
0.42
0.18
0.13
0.04
0.02
0.33
0.17
0.05
0.02
0.01






1.12
0.77
0.56
0.35
0.13
0.10
0.85
0.55
0.24
0.21
0.05
0.03





0.44
0.37
0.22
0.15
0.07

82
82
84
85
93
100
82
82
83
83
86
100
84
84
85
86
92
100
59
67
71
71
64
67
75
76
77
79
86
100
81
81
82
84
88
100
64
64
65
65
75
67
69
69
70
71
75
83
34

-------
Table 3-1 (continued).—CAMP DATA ON SULFUR DIOXIDE CONCENTRATIONS (ppm by volume)
City and
time

Chicago:
o mm
1 hr 	
8 hr 	
1 day 	
1 mo
1 yr 	
Cincinnati:
5 min . _ . .
1 hr 	
8hr 	
1 day
1 mo
1 yr
Denver:
5 min . _ _
1 hr 	
8hr 	
1 day 	
1 mo _____
1 yr_ 	
Los Angeles:
5 min _ _
1 hr 	
8hr 	
1 day 	 _
1 mo 	
1 yr 	
Philadelphia:
5 min
1 hr 	
8 hr
1 day_ 	 	
1 mo 	 	
1 yr
St. Louis:
5 min 	 _
1 hr
8 hr __ ...
1 day 	 .
1 mo _ _ .
1 yr
San Francisco:
5 min
Ihr 	
8 hr _ ___
1 day 	 ___
1 mo_ 	 _ .
1 yr
Washington:
5 min_ _ 	 	
Ihr 	
8hr 	
1 day . _ 	
1 mo 	 	
lyr 	
Percent of time concentration is exceeded
.001 0.01
(12) (13)

1.75 1.34
_.- 	 1.12





0.90 0.70
... 	 0.53





0.64 0.33
_.- 	 0.26





0.56 0.38
.__ 	 0.25





1.18 0.95
0 85





1.23 0.96
-- 	 0.73





0.30 0.18
... 	 0.16





0.65 0.49
.. 	 0.46




0.1
(14)

1.03
0.96
0.76




0.42
0.35
0.22




0.18
0.11
0.08




0.15
0.13
0.10




0.72
0.66
0.49




0.58
0.50
0.29




0.13
0.11
0.09




0.36
0.35
0.26



1
(15)

0.68
0.65
0.57
0.50



0.19
0.17
0.12
0.10



0.07
0.06
0.04
0.04



0.08
0.08
0.07
0.06



0.47
0.45
0.37
0.29



0.29
0.25
0.19
0.14



0.07
0.07
0.06
0.05



0.22
0.21
0.19
0.17


10
(16)

0.33
0 33
0.32
0.31
0.27


0.07
0.07
0.06
0 06
0.05


0.03
0.03
0.03
0.03
0.02


0.04
0.04
0.04
0.04
0.02


0.21
0.21
0.19
0.18
0.12


0.11
0,11
0.09
0.09
0.06


0.03
0.03
0.03
0.03
0.02


0.11
0.10
0.10
0.10
0.09

30
(17)

0.16
0.16
0.16
0.16
0.17


0.03
0.03
0.04
0.04
0.04


0.01
0.02
0.02
0.02
0.02


0.02
0.02
0.02
0.02
0.02


0.09
0.09
0.10
0.10
0.10


0.05
0.05
0.06
0.05
0.05


0.01
0.01
0.02
0.02
0.01


0.06
0.06
0.06
0.06
0.05

50
(18)

0.08
0.08
0.09
0.09
0.09
0.12

0.02
0.02
0.02
0.03
0.03
0 03

0.01
0.01
0.01
0.01
0.01
0.01

0.01
0.01
0.02
0.02
0.02
0 02

0.05
0.05
0.06
0.07
0.08
0 09

0.02
0.03
0.04
0.04
0.04
0 04

0.01
0.01
0.01
0.01
0.01
0 01

0.03
0.03
0.04
0.04
0.04
0.04 .
70
(19)

0.03
0.03
0.04
0.05
0.06


0.01
0.01
0.02
0.02
0 02


0.00
0.00
0.00
0.00
0.01


0.01
0.01
0.01
0.01
0.01


0.03
0.03
0.04
0.04
0.07


0.01
0.01
0.02
0.02
0.03


0.00
0.00
0.00
0.00
0.01


0.02
0.02
0.02
0.02
0.03

90
(20)

0.01
0.01
0.01
0.02
0.03


0.00
0.00
0.01
0.01
0.01


0.00
0.00
0.00
0.00
0.00


0.00
0.00
0.00
0.00
0.01


0.01
0.01
0.01
0.02
0.03


0.00
0.00
0.00
0.01
0.02


0.00
0.00
O.ffl
0.00
0.00


0.01
0.01
0.01
0.01
0.02

                                                                          35

-------
    10.0
         2 -
     1.0
  a
  a
        2 -
 <
 or
    0.10
 o
 z
 o
 o
 LLI
 13
 <
 cc
 111
     0.01
    0.001
                                                "1    T
                                  N.Y.C
                          S.F.
            NEW YORK  -i
               CITY

             LONDON
       WINDSOR 2
         PHILADELPHIA  -I
     WINDSOR 1         ~
        .WASHINGTON. D.C.
         LOUIS
        CINCINNATI

       LOS ANGELES

      SAN FRANCISCO    —

   DENVER
                             I
         3 sec     30 sec     5 min      1 hr       8 hr 1 day  4 days
                                              AVERAGING TIME
                                                                   1 mo
1 yr
10 yr
     Figure 3-1. Long-time Average Sulfur Dioxide Concentrations (ppm) and Associated Maximum Average Con-
                centrations for Various Time Periods for Twelve Sites in Eleven Cities.
For each of the given lines, the last point on the right is the long-term average over the interval specified, while the
other points represent the maxima within the interval for the averaging periods shown.  If, for example, one complete
year of data were available in terms of hourly averages, there would be one maximum hourly value for that year.  If
five years of data were available, in terms of hourly averages, five maxima (one for each year) would be obtained,
and the highest of these five maxima would constitute the maximum hourly average  for the five-year period.
     36

-------
0.01
    0.01   0.05 0.1  0.2    0.5
 12       5     10       20    30    40   50
PERCENT OF TIME CONCENTRATION IS EXCEEDED
                                                                                60
                                                                                      70
                                                                                            80
          Figure 3-2.  Frequency  Distribution of Sulfur Dioxide Levels in Selected American Cities,
                      1962 to 1967 (1-Hour Averaging Time, Data From Table 3-1).
          The approximate log normality of the distribution of sulfur dioxide concentrations is shown by
          the rather straight lines of the distribution functions when these are plotted on a logarithmic
          scale (concentrations) against a normal distribution frequency.
                                                                                                37

-------
creases as the time period becomes shorter.
For 1-year averages, the geometric mean co-
incides with the arithmetic mean (standard
geometric  deviation  of   unity).   For  1-
hour-duration samples,  the  standard geo-
metric deviation varies from about 2 (1.94
in Denver) to 2.6 (in Cincinnati). When the
standard geometric deviation for 1-hour-dur-
ation samples is 2, the expected annual maxi-
mum for 1-hour-duration samples is about 10
times  the annual mean. When the standard
geometric deviation is 2.5, as it is for San
Francisco, the 1-hour maximum is about 20
times  the annual mean. Thus, for the data
shown, the highest  1-hour average concentra-
tion is expected to be from about 10 to 20
times the annual mean as the deviation varies
from 2 to 2.5. Therefore, if a 1-hour average
concentration is  not to exceed 0.3 ppm more
than once a year, the annual mean associated
with this concentration would  be between
0.015 ppm and 0.03 ppm, depending on whe-
ther the standard geometric deviation for 1-
hour averages is 2.5 or 2,  respectively. Simi-
larly,  the maximum  24-hour concentration
encountered once a year is expected to be be-
tween about 4 and 7 times the annual mean
concentration for the cities shown, and the
monthly maximum ranges from 1.5  to 2 times
the annual average. Other cities might have
deviations  lying outside  these  boundaries,
and, for such cases, the maxima for different
time periods and  the other  relevant para-
meters could be calculated.3
   Data from the NASN stations, which cover
more  cities  than  the CAMP network,  are
based on measurements over 24 hours made
on 20  to 26 selected dates throughout the
year.  The highest NASN  annual average
 (0.17 ppm)  was recorded in New York City,
which  also experienced the highest 24-hour
average  (0.38 ppm); the  lowest NASN an-
nual average  (0.002  ppm) was in  Kansas
City, Mo., while the lowest 24-hour averages
were below the minimum value detectable by
the instruments, i.e., below about 0.001 ppm.
In general,  at a typical NASN station, the
maximum 24-hour average is about 3 times as
high as the annual average, but at some sta-
tions can be as high as 6 to 8 times the annual
averages. These ranges are similar to those of
the CAMP stations in Table 3-1. Geographi-
cally, the highest values are recorded at sta-
tions in cities in the northeastern part of the
United  States,  especially those east of the
Mississippi  River  and  north of  the  Ohio
River.  In  these areas, the  major  source of
energy is fossil fuels of high  sulfur content,
such as domestically-mined coal and imported
residual oils. Maxima in the diurnal concen-
tration curve usually occur about 8 a.m.
  Figure 3-1 is a  graphical  counterpart of
Table 3-1, without the frequency distributions
but  with  four  stations added  (New  York
City, London," and two stations in Windsor,
Ontario) .6 For each of the 12 stations, maxi-
mum average concentrations are shown for
various averaging times. Since the averaging
times are  not comparable in some  cases, the
time points  for which maxima are available
have been connected in order to approximate
the relationship between the corresponding
maxima. As expected, a station with a rela-
tively high maximum concentration for one
averaging time is likely to  show, in propor-
tion, an equally high maximum concentration
for other averaging times.  A station with a
low maximum concentration for one averag-
ing time likewise shows an equally  low maxi-
mum  concentration  for   other  averaging
times.
  The  last nine columns of Table 3-1 give the
frequency distribution of concentrations for
each of these averaging times (or subsets of
these values; for example, for 1 year, with at
most six  measurements available,  only the
median, or  50-percentile   concentration,  is
given). While  the maximum of columns 6
to 11 were tabulated on a year-by-year basis,
the frequency data  shown here (columns 12
through 20) are applicable to the entire  6-
year period. The value listed in a  given col-
umn is the  concentration which is exceeded
the stated percentage of the time. For ex-
ample, the values listed in  the 0.1  percentile
columns are those concentrations which were
exceeded 0.1 percent of the time; this means
that, for 99.9 percent of the time, the con-
centrations measured were  less than or equal
to this value. In general, this value is differ-
ent  for different  averaging times. At the
lower percentiles, this value increases as the
averaging time is shortened;  in Chicago, for
example,  the   0.1   percentile concentration
      38

-------
changes from 0.76 ppm to 1.03 ppm as the av-
eraging interval is shortened from 8 hours to
5 minutes. At the higher percentiles, the op-
posite occurs: the concentration decreases as .
the averaging time is shortened.  The 30-per-
centile point (which is very close to the arith-
metic mean) apparently represents an equili-
brium  condition,  since  the  concentration
associated with this point is approximately
the same for all  averaging times. Thus, the
30-percentile  concentration,  i.e., the value
which is not exceeded for 70 percent of the
time, might be used as a simple  indicator of
the "general sulfur dioxide level" of a city,
irrespective of the  averaging  time.  For the
eight cities tabulated, using this index, Chi-
cago  clearly shows the highest level  (0.16
ppm), followed by Philadelphia,  Washing-
ton,  St. Louis, Cincinnati, Los Angeles, Den-
ver,  and San Francisco. That this is a good
index  is  borne out by Figure 3-3, which
shows the annual average sulfur dioxide con-
centrations, by  year, for these same cities.
The  ordering of the cities, from most severe
to least severe, appears to be the same, with
Chicago on the top and San Francisco on the
bottom.
   The conversion  of  the maximum concen-
tration for one averaging time to that for an-
other  may  be approached in  a number of
  I
  CO
  O
  DC

  Z
  LLJ
  CJ

  O
  O
  111
  Q
  X
  O
  DC
  D
  03
  UJ
  DC
  LLI
         1962
                        1963
                                       1964
                                                      1965
                                                                      1966
                                                                                    1967
          Figure 3-3. Trends in Sulfur Dioxide Concentration for Eight Cities.

          This figure shows that the sulfur dioxide concentrations for the years 1962-1967 were
          highest in Chicago and Philadelphia.  (Sampling periods begin on December 1 of the
          preceeding year and run until November 30 of the year shown).
                                                                                 39

-------
ways. Brasser, Joosting, and van Zuilen 2, in
a manner similar to that described above, at-
tempt to establish empirically the relationship
between  maxima  for different  averaging
times from measurements carried out over
long periods and  under  different meteoro-
logical conditions.
  Larsen 3  computes the expected maximum
concentration (C) for a given averaging time
by using the geometric mean (Mg), the stand-
ard geometric deviation (
-------
expect to be exceeded half the time at differ-
ent averaging  times. For example, for a 1-
hour  averaging  time  this concentration is
about 0.12 ppm. At several points, percentile
lines  will coincide with maximum or mini-
mum  concentration lines. For instance, when
the averaging time is 0.88 hour and the total
time period is 1 year, the 0.01 percentile will
correspond to the maximum, since there are
10,000 of these  time-units in a year; simi-
larly, the 99.99 percentile corresponds to the
minimum.
                  Table 3-2.—COMPARISON OF CALCULATED AND
                   OBSERVED MAXIMUM SULFUR DIOXIDE CON-
                   CENTRATIONS  FOR VARIOUS   AVERAGING
                   TIMES IN 1964 IN CHICAGO.

                                        Predicted    Observed
                  Averaging time          maximum,   maximum,
                                           ppm        ppm
       10
         -2
5 minutes
1 hour
8 hours
1 day
1 month
1 year
3.151
1.646
0.963
0.728
0.310
0.192
1.62
1.12
1.02
0.79
0.35
0.18
                     MINUTE
                  5  10 15  30
                  t
                 3.151
HOUR
 4   8 12
       I
                        DAY
                         4   7
                                                            14
MONTH
 236
 I  I    I
YEAR
  3
      10
1.646
                                        0.963 0.728
                                                              0.310
                                                                           0.192
              EXPECTED ANNUAL MAXIMUM CONCENTRATION IN ppm
                                                            ANNUAL MAXIMUM
                                                  -W
                                      4-  + BI-
                                                           ANNUAL MINIMUM
               GEOMETRIC MEAN FOR 1 HOUR AVERAGE IS 0.160 ppm
               STANDARD GEOMETRIC DEVIATION IS 1.84
               87 PERCENT OF HOURS HAVE DATA AVAILABLE
                                                           10'
                                                                                        101
                                                                                        10C
                                                                                        10'
                                                               Q.
                                                               a
                                                              'z
                                                              O
                                                                                        10
                                                                                          -2 :
                                                                                            UJ
                                                                                            O
                                                                                        10
                                                                                          -3
                  10-
                              10L
                                   10J
                                                                                        10
                                                                                          -4
                                     AVERAGING TIME, HOURS
Figure 3-4. Concentration of Sulfur Dioxide in Chicago for Various Averaging Times and Frequencies, from
December 1, 1963 to December 1, 1964.

For brief intervals, the concentration reached values as high as 1 ppm or 2 ppm, but for increasing
averaging times, the upper and lower limits converge to a value near 0.2 ppm.
                                                                                 41

-------
2.  Concentrations Related to Point Sources

  An  industry which  emits large quantities
of sulfur dioxide  is  described as a  point
source. The area near such sources may ex-
perience  high concentrations or immeasur-
ably small values, depending on the prevail-
ing winds, throughput differences, intermit-
tent operations, intermittent pressure releas-
es, and differences in  velocity and tempera-
ture of  emissions. Several studies of  such
situations have been reported.4 s
a. Copper Smelter, Australia, 1962
  Sullivan 9 reported that the maximum daily
average concentrations  were from 8 to  17
times the annual average concentration.  At
a station located 1.5 miles from the smelter,
the hydrogen peroxide method gave a maxi-
mum  daily average of 0.60  ppm, while the
annual average was  0.036 ppm. A Thomas
Autometer (conductometric) indicated  peak
     concentrations  from 1 ppm to 5 ppm on 30
     occasions during  a 6-month period  and a
     maximum peak of 13.5 ppm.
     6. Oil Refinery, 1965
       Concentrations  in excess of  0.5  ppm for
     10 hours during 1 month with momentary
     peaks over 2 ppm in an area near an oil re-
     finery were reported by Linzon.7
     c. Smelter,  Canada, 1958
       A station located 8  miles from a smelter
     recorded an  average concentration of  0.03
     ppm  during a  4-month study (May-August
     1958). Measureable concentrations were pre-
     sent about 20 percent of  the time,  and  con-
     centrations above 0.25 ppm occurred 4  per-
     cent of the time.10
     d. Smelter,  Trail,  Canada,  1931  to 1937
       During the 6-month growing season, a sta-
     tion 15 miles  south of the smelter recorded
     these  data:
Average SCK, ppm
Hours with S0,>0.25 ppm
1931   1932  1933   1934   1935   1936   1937
0.032  0.007  0.008  0.012  0.023  0.022   0.013
 140    8.5    18    32.5    36    47    7
  The concentrations are  6-month averages
and the hours during which more than 0.25
ppm of sulfur dioxide was measured consti-
tute from 0.2 percent to 3.5 percent of the
total  time.  Maximum  concentrations  that
lasted from 4 minutes to 54 minutes ranged
from  0.48 ppm to 1.30 ppm or from 30 times
to 160  times the respective 6-month aver-
ages.*-  The latter represents a  considerably
higher ratio  than those which can be calcu-
lated  from Table 3-1 and demonstrates the
impact  of point  sources  versus  multiple
sources.
e. Power Plant, 1966
  Sulfur  dioxide  from  a 1,000-megawatt
power station burning 430 tons of 1.5 percent
sulfur coal per hour was studied by Martin
and Barber." Sixteen sulfur dioxide record-
ers were spaced around  a ring  of radius
about 3 miles to 4 miles centered on the sta-
tion, i.e., near the zone of calculated maxi-
mum ground-level pollution. The maximum 3-
minute  concentration during the year was
about 0.62 ppm, the maximum  hourly aver-
age was about 0.47 ppm, the maximum daily
     average was 0.11 ppm, and the annual aver-
     age was about 0.027 ppm.
     /. Poiver Plant, Pennsylvania, 1961
       One  of the few  studies of  sulfur dioxide
     concentrations near a coal-fired power plant
     was made by McCaldin and Bye.13 A Thomas
     Autometer 1/2 mile from this plant indicated
     an average concentration of 0.17 ppm from
     January to April  (0.09 ppm by colormetric
     West-Gaeke)  with  a maximum hourly aver-
     age of  2.9 ppm and a momentary peak con-
     centration of 4.7 ppm.

     C.  SULFURIC ACID AND ITS RELATION
              TO SULFUR DIOXIDE
       Measurements of sulfuric acid along with
     sulfur dioxide estimations are of interest be-
     cause of the higher irritant potential of sul-
     furic acid, and because the ratio of the con-
     centrations of the two pollutants found under
     various conditions helps in our understanding
     of the  mechanism of the oxidation of sulfur
     dioxide to sulfuric acid in the atmosphere.
       Coste1314  made  simultaneous  measure-
     ments of sulfuric  acid and sulfur dioxide in
      42

-------
London, England.  Sulfur  dioxide concentra-
tions ranged from 0.13 ppm to 0.58 ppm (371
i»g/m-! to 1657 iig/m3); sulfuric acid concen-
trations ranged  from 4 /xg/m3  to  20 /xg/m3.
The weight ratio of sulfuric acid to sulfur
dioxide was 0.011 at the higher concentration
of sulfur dioxide and 0.013 at the lower con-
centration. The highest ratio of sulfuric acid
to sulfur dioxide was 0.023 on a misty day.
  A  maximum sulfur dioxide concentration
of 1.47 ppm (4200 iig/m3) in London during
the period December 2 through December 5,
1957,  was reported  by Commins.15 During
the same period the maximum concentration
of sulfuric acid was 222 /xg/m3. The ratio of
maximum sulfuric acid to maximum sulfur
dioxide  was  0.053. Commins also reported
that sulfuric acid could be as much as 10 per-
cent  of  the total sulfur,  corresponding to  a
weight ratio of sulfuric acid to sulfur dioxide
of 0.167.
  An extensive  study of the  simultaneous
presence of sulfur dioxide and  sulfuric acid
mist in  the air was made by Bushtueva.101T
Between August 1953 and January 1954, she
collected 198  paired samples for sulfur diox-
ide and sulfuric acid determination. The data
are presented in Table 3-3. The sulfuric acid
and sulfur dioxide were originally reported
in mg/m3 rather than in /xg/m3 as shown in
the table.  The concentrations of sulfur diox-
ide in ppm have been added for convenience
of comparison  with other data reported in
ppm. These data show that as the sulfur diox-
ide concentration increases so does  the  sul-
furic acid concentration, although at a slower
rate.
  Bushtueva also studied the effect  of wind
speed and relative humidity on the concentra-
tions of sulfur dioxide and sulfuric acid. Both
the sulfuric acid concentration and the ratio
of sulfuric acid to sulfur  dioxide were high-
est during periods of fog, and lowest during
periods of precipitation.  In  the  absence of
precipitation, the ratio of sulfuric acid to sul-
fur dioxide increased from  about 0.045 at
60 percent relative humidity to about 0.090
at 90  percent relative humidity, and to 0.15
at relative humidities above 91 percent. At
wind speeds below about 4.5  miles per hour,
the ratio  of  sulfuric acid to  sulfur dioxide
was 0.173, and at  wind speeds greater than
about 9 miles per hour, the ratio was only
0.068.  Thus calm  days, high  humidity, and
especially foggy weather are associated with
high concentrations  of sulfuric acid.
  Although they did not  study the  relation
of sulfuric acid to sulfur dioxide, Mader et
al.^ found that the  sulfuric  acid concentra-
tion at Los Angeles  increased as the relative
humidity  increased.
  Chaney 19 studied the relationship  between
sulfur dioxide   (West-Gaeke measurement)
and sulfuric acid  in the  Los Angeles area.
Table 3-3.—CONCENTRATION OF SULFUR DIOXIDE AND SULFURIC ACID MIST OBSERVED IN AIR M
           SO2 concentrations
                                                    Average concentration


/xg/m3
24-hour samples :
25-100
101-250
251-500
501-750
751-1000
Over 1000
Single samples :
Up to 250
251-750
Over 750 ...


ppm

0.009-0.035
0.035-0.088
0.088-0.175
0.176-0.263
0.264-0.350
over 0.35

up to 0.088
0.088-0.263
over 0.263
i\umoer
£
OI
tests


6
18
38
20
6
11

15
8
2


SO,
ppm

0.01
0.06
0.14
0.23
0.30
0.43

0.05
0.15
0.48
/xg/m"

30
176
387
663
866
1220

128
428
1380

H,SO4
/xg/m3

12.6
19.6
20.0
31.0
29.0
43.0

17.5
41.6
326.0
n?a\jt : ou2
\\Tf\t rfl*±
W eight
ratio


0.420
0.112
0.051
0.045
0.033
0.035

0.137
0.097
0.235
                                                                               43

-------
During the time of the study, sulfur dioxide
values were generally very low  and some-
times there was no measurable sulfate. The
weight ratios of sulfuric acid to sulfur diox-
ide ranged from 0.037 to 3.0 and  the sulfate
levels were relatively high compared to the
sulfur dioxide concentrations. In the data of
the National Air Surveillance Network, there
is also a large amount of sulfate per unit of
sulfur dioxide as measured by  the West-
Gaeke technique. In  the strongly oxidizing
atmosphere  of Los Angeles, sulfur dioxide
may be rather rapidly oxidized. On the other
hand,  the high  ozone and nitrogen dioxide
concentrations  in  Los Angeles may signifi-
cantly interfere with the  West-Gaeke pro-
cedure so that if the  sulfamic acid modifica-
tion is not used, values lower than actual sul-
fur dioxide concentrations  may be recorded;
consequently, oxidation of sulfur dioxide may
be more apparent than real.
   Thomas20  used an automatic  electrocon-
ductivity measuring instrument for the sim-
ultaneous measurement of sulfur dioxide and
 Table 3-4.—CONCENTRATIONS  OF SULFUR  DIOXIDE AND SULFURIC ACID  MIST OBSERVED IN
          1961 IN AIR OVER LOS ANGELES AND ONE OF ITS SUBURBS, EL SEGUNDO M
sulfuric acid mist concentrations during the
winter of 1961 in Los  Angeles.  Concentra-
tions of sulfur dioxide up to 0.21 ppm  (600
/ig/m3)  and of sulfuric  acid up to 50 /*g/m3
were observed. Thomas originally  reported
the data in ppm; but to make them compar-
able with other data in this report they  have
been converted to /ug/m3 and are presented
in Table 3-4.  The weight ratios  of sulfuric
acid to  sulfur dioxide lie between 0.032 and
0.246; these ratios  are  within the range of
values  reported by  other  investigators for
other places.
   Thomas' data indicate a nonlinear relation-
ship between sulfur dioxide and sulfuric acid
concentrations.  Sulfuric acid  increases  as
sulfur  dioxide increases up to some critical
value, depending upon  the location. Beyond
the critical value, sulfuric  acid decreases as
sulfur  dioxide increases. In El  Segundo, a
maximum  sulfuric  acid  concentration  of
about 25 /ug/m3 was observed when the sul-
fur dioxide concentration was between 0.15
ppm and 0.20 ppm (425 /*g/m3 to 570 jm
Date
El Segundo-
26 Jan
6 Feb
22 Jan
8 Feb
10 Feb
31 Jan
11 Feb
28 Jan
15 Feb
9 Feb .
30 Jan
2 Feb
Los Ang-eles:
24 Mar
21 Mar
22 Mar
10 Mar
9 Mar
13 Mar
14 Mar
22 Mar .
13 Mar
Sulfur dioxide
Ppm t

0.065
0.061
0.062
0.062
0.055
0.120
0.102
0.110
0.125
0.130
0.205
0.194

0.057
0.067
0.063
0.057
0.064
0.065
0.050
0.122
0.122



185
174
177
177
158
342
291
313
356
371
584
553

162
191
180
162
182
185
143
348
348
Sulfuric acid
ppm

0.0016
0.0031
0.0050
0.0054
0.0050
0.0046
0.0047
0.0055
0.0068
0.0075
0.0048
0.0098

0.0048
0.0070
0.0072
0.0080
0.0092
0.0099
0.0084
0.0072
0.0126

/ig/m3

6.4
12.4
20.0
21.6
20.0
18.4
18.8
22.0
27.2
30.0
19.2
39.2

19.2
28.0
28.8
32.0
36.8
39.6
35.2
28.8
50.4
H=SO4 : SO2
Weight ratio

0.035
0.071
0.112
0.112
0.127
0.054
0.064
0.070
0.076
0.081
0.032
0.071

0.118
0.146
0.160
0.200
0.201
0.214
0.246
0.082
0.145
       44

-------
whereas, in downtown Los Angeles, a maxi-
mum sulfuric acid concentration of about 30
/ig/m3 was observed when the sulfur dioxide
concentration was between 0.05 ppm and 0.10
ppm (140 jug/m3 to 280 /*g/m3).
  During the past several years the National
Air Surveillance Networks have taken simul-
taneous measurements  of  24-hour average
sulfur dioxide and suspended sulfate in vari-
ous cities.-' JJ Unpublished analyses of these
data show that correlation  coefficients be-
tween sulfur dioxide  and suspended sulfate
(sulfuric  acid and sulfate salts)  range be-
tween 0.5 and 0.9. Manganese and iron in the
suspended particulate matter, relative hum-
idity, and temperature were studied as vari-
ables that might affect this  correlation. As
relative humidity  and the concentration  of
metals increased,  so  did suspended  sulfate.
Temperature had no effect on suspended sul-
fate concentrations.
  The  data from field studies thus agree es-
sentially with data from laboratory  investi-
gations; both show that sulfur dioxide can be
oxidized  to sulfuric acid or a salt of the acid
in the atmosphere. The field studies show,
from  evidence  taken in a number  of  geo-
graphical locations, that a relationship exists
between sulfur dioxide and sulfuric acid con-
centrations in  the air. The relationship is
dependent partly upon the amount of moist-
ure in the air, partly upon the time the sulfur
contaminants have been in the  atmosphere,
the amount of  catalytic particulate  matter
present in the air, the amount (intensity and
duration) of sunlight, the amounts of hydro-
carbons  and oxides  of nitrogen, and  the
amount of directly reactive  and adsorptive
materials in the air, as  well as on the extent
of recent precipitation.

   D.  ACIDITY OF  RAINWATER AND
         PARTICULATE MATTER

  Gorham 24 studied the acidity (pH) of rain-
fall in two cities of England and found that
it was more strongly related to  the chloride
content than to the sulfate content. Such a
study apparently  has not been  made in the
United States; however, examination of some
rainfall samples collected by the National Air
Surveillance  Network  showed   pH  values
around 3. The National Air Surveillance Net-
work data indicate that the chloride content
of suspended particulate matter is generally
very  low in  atmospheres of  the United
States '-•"'  except along coastal areas.
  In another set of unpublished data collect-
ed by the National Air Pollution Control Ad-
ministration, sulfate accounted for 21 percent
of the variation in pH of solutions of the sus-
pended particulate matter, with an increase
of 12 /u,g/m3 of sulfate reducing the pH by 1
unit.  The pH values  in  both sets of data
ranged from approximately 4 to 7.5. In  the
presence of substantial amounts of ammonia,
calcium carbonate, hydroxide, or other alka-
line  material,  most of the sulfate is in salt
form. The similarity of the magnitude of at-
mospheric sulfuric acid concentrations, when
compared with the magnitude of total sulfate
concentrations, indicates that in some atmos-
pheres a large part of the total sulfate may
be sulfuric acid.19"22 -6
  Measurements of acidity of dustfall, though
seldom reported, indicate that dustfall may be
capable of providing a few pounds of hydro-
gen ions and a few hundred pounds of sulfate
ions per acre per year.-'7'29 The importance
of this to soil management is difficult to evalu-
ate because of the heterogeneity of soils, their
generally great  buffering  capacity, and  the
probable large,  though unknown, buffering
capacity of  the  dustfall itself. An order of
magnitude estimation of the effect of acidity
in dustfall  is that approximately twice as
much lime might have to be applied to the
soil  in areas near large cities, as to the  soil
of rural areas. This assumes that the near-
urban areas have average annual sulfate de-
posits of eight to twelve tons per square mile
per  month (300 to 450 pounds per acre per
year). An approximately tenfold reduction in
sulfate deposit would be required to reduce it
to about the amount  removed by plants and
leaching.30 31 Even though sulfur in some com-
pounds  is a major plant nutrient and is used
as a fertilizer element under certain condi-
tions, it would seem that uncontrolled deposi-
tion of sulfate from air pollution is undesir-
able.32
              E.  SUMMARY
   Two major programs for the surveillance
of atmospheric  sulfur dioxide on a nation-
                                                                              45

-------
wide basis are operated  by the  U.S. Public
Health Service and are (1) the National Air
Surveillance Networks  (NASN),  in which
24-hour samples  are obtained from  about
100 sites 26 times a  year, and (2) the Con-
tinuous Air Monitoring Project (CAMP), in
which  5-minute average concentrations are
recorded continuously in six large U.S. cities
—Washington,   Philadelphia,   Cincinnati,
Chicago, St. Louis, and  Denver.  The NASN
program employs  the colorimetric (i.e., West-
Gaeke) method of analysis, while the CAMP
program  uses  the electro-conductivity  tech-
nique and recently  has added  continuous,
colorimetric (West-Gaeke)  SO-,  monitoring
devices at all six locations.
  Levels  recorded in CAMP cities over the
period from 1962  to  1967 show mean annual
concentrations ranging  from  0.01 ppm, in
San Francisco, to 0.18 ppm, in Chicago, with
the averages exceeding,  for 1 percent of the
time,  a concentration range  between 0.09
ppm and  0.68 ppm for  the different cities.
The  NASN annual  average concentrations
ranged from 0.002 ppm,  in Kansas City, Mis-
souri, to  0.17  ppm, in New York  City. The
highest 24-hour average concentration was
0.38 ppm, also in New York City, while the
lowest 24-hour avearges were below the mini-
mum value detectable by the instruments—
below approximately 0.001 ppm. Geographi-
cally, the highest  values  were recorded in the
northeastern part of the United States,  es-
pecially east of  the Mississippi  River and
north of the Ohio River, where large quanti-
ties of high-sulfur fossil fuels are burned.
  Extensive monitoring programs, such as
those described above, yield large quantities
of data. Information expressed  in terms of
average or maximum values does not give as
complete a picture of air quality as does fre-
quency distribution information, which shows
the percentage of  time that concentrations ex-
ceed specified  levels. For a given averaging
time, measurements of sulfur dioxide concen-
trations follow a log-normal frequency dis-
tribution.   The two  statistical  parameters
commonly used to describe this  distribution
are the geometric mean and the standard geo-
metric deviation.  CAMP data  covering eight
cities from 1962 to  1967 show that, as aver-
aging times become  shorter, higher maxima
and lower minima are obtained. This happens
because, for shorter intervals, instantaneous
fluctuations have greater effect on the record-
ed values. The standard geometric deviation,
which  is an  index  of  the  deviation of the
samples from their geometric mean, there-
fore is greater for shorter averaging periods.
  Based on data from eight CAMP cities, the
1-hour maximum value  for the year is expect-
ed to be about 10 to 20 times the annual aver-
age,  corresponding to standard geometric
deviations of 2 and 2.5, respectively. Thus, if
the highest hourly average concentration for
the year  is 0.3 ppm, the annual mean would
be about one-twentieth  of this value, or 0.015
ppm,  for a city with a standard geometric
deviation of 2.5 and about  one-tenth of this
value, or 0.03 ppm, for a city with a standard
geometric deviation  of 2. Similarly,  the  8-
hour maximum ranges from about 6 to 10
times the annual mean;  the one-day maximum
ranges from 4 to 7 times the annual mean;
and the maximum monthly average ranges
from about 1.5 to 2 times the annual mean.
  The CAMP data appear to be fairly repre-
sentative of  large U.S. metropolitan areas,
but, for a city with  a deviation outside these
boundaries, a method exists to  calculate the
expected maximum concentrations, providing
the averaging times are 1 hour  or greater.3
It is possible also to calculate the minimum
concentration for a  given averaging time, as
well as the  concentrations at various percen-
tiles.  These  calculations make  use of the
geometric  mean and  the  standard geo-
metric  deviation of  samples  obtained   at
a particular  averaging time, and it is pos-
sible to derive the  geometric mean and the
standard geometric deviation for one aver-
aging  time from  samples obtained  at other
averaging times. The accuracy of methods for
calculating  expected  maxima,   minima,   or
other concentrations from observed data for
the same or for different averaging times de-
pends  on the number  of air samples taken
relative to  the number  of samples that could
be taken if air sampling were continuous. It
appears that a fairly good approximation  of
the frequency  distribution of hourly aver-
ages  over  a  year  may be  obtained with
samples covering 24-hour periods on 22 ran-
domly selected days.
       46

-------
  Frequency data on the percent of the time
that certain concentrations are exceeded usu-
ally necessitate the use  of a  computer but
provide  a  very detailed  description  of air
quality.  For  a  given percentile,  the concen-
trations measured over  different averaging
times  usually  vary. However, for the 30-
percentile point, i.e., the value which is not
exceeded for 70 percent of the time, the con-
centration appears to be about the same for
all  averaging times. Thus the 30-percentile
value might be used as an indicator  of the
"general sulfur dioxide level" of a city,  an
index useful for ranking one city against an-
other.
  The ratio of the maximum sulfur dioxide
concentration to  the average  value may be
greater for measurements made near a single
point source  than for a city  as a whole. For
averaging periods from 4 to  54 minutes, for
example, the maximum concentrations en-
countered near a  point source were, respec-
tively, 30 to  160 times the 6-month average
value.  These ratios are considerably  higher
than those  calculated from the data for eight
cities and  6  years shown in  Table 3-1, and
they demonstrate  the kind of impact that a
point source may have.
  Hourly average concentrations  of sulfur
dioxide as  high as 2.9  ppm have been meas-
ured T>/) mile from a coal-fired power plant.
In  general, concentrations decrease as  (1)
the distance  from sources increase, and (2)
the averaging  time is extended. When aver-
aged over many hours or days, concentrations
measured several  miles from a large source
may be  only a  few hundredths of a part per
million.  Near the  point of discharge, power
plants,  oil  refineries,  smelters, and sulfuric
acid production units may yield high ground-
level sulfur dioxide concentrations.
  Sulfur dioxide is partially oxidized to sul-
furic acid  in the  atmosphere. The  ratio be-
tween  the  two   substances  is  dependent,
among  other things, on the  oxidation  rate,
which in turn  is  dependent  on the sunlight
available and the  concentration of moisture,
catalysts, hydrocarbons, nitrogen oxides, and
the quantity of directly reactive and adsorp-
tive materials in the air. Recent precipitation
also has an effect, as does the time various
sulfur contaminants have been in the atmos-
phere.
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                                    47

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    "The Nature and  Properties of  Soils." 6th edi-
    tion, Macmillan, New York, 1960, 567 pp.
31.  Bertramson, B. R.,  Fried, M., and Tisdale, S. L.
    "Sulfur  Studies of Indiana  Soils and  Crops."
    Soil Sci., Vol. 70,  pp. 27-41, 1950.
32.  Katz, M. "Sulfur Dioxide in the Atmosphere and
    its  Relation to  Plant Life."  Ind. Eng.  Chem.,
    Vol. 41, pp. 2450-2465, Nov. 1949.
        48

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                  Chapter 4
EFFECTS OF SULFUR OXIDES IN THE ATMOSPHERE
               ON MATERIALS

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                         Table of Contents
                                                                 Page
A. INTRODUCTION              .                                  51

B. EFFECTS ON  PAINTED  SURFACES                             51
C. DAMAGE TO METALS                                          51

D. EFFECTS ON  BUILDING MATERIALS                           54

E. EFFECTS ON TEXTILE FIBERS,  DYES, AND MISCELLANEOUS
   MATERIALS                                                    54

F. SUMMARY                                                     55

G. REFERENCES                                                  56


                         List of Figures
Figure
4-1  Relationship Between Corrosion of Mild Steel  and Corresponding
     Mean  Sulfur Dioxide Concentration  for 3-, 6-, and 12-Month Ex-
     posures at Seven Chicago  Sites  (September 1963-1964)                53
 50

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                                     Chapter  4

   EFFECTS OF  SULFUR  OXIDES  IN  THE  ATMOSPHERE  ON MATERIALS
          A.   INTRODUCTION
  In reviews of the effects of air pollution on
materials, Yocom 1 and Burdick and Bark-
ley - discuss the damage to metals,  building
materials, leather, paper, and textiles by the
oxides of sulfur. Much of this damage is due
to the conversion of  sulfur oxides to highly
reactive sulfuric acid. The combined action
of sulfur oxides  and particulate matter  is
discussed in the companion report Air Qual-
ity Criteria for Particulate Matter.

 B.   EFFECTS ON  PAINTED  SURFACES
  Holbrow 3 found that the drying  times of
linseed,  tung, and bodied dehydrated castor
oil paint films  exposed to 1  to 2 ppm  SO,
were increased  by 50-100 percent. At higher
concentrations,  7 to 10 ppm, drying was de-
layed by up to two  to three days.  Time of
exposure to  SO; was not mentioned. It may
be assumed, however, that the exposure last-
ed until the paint films were  dry. Oleoresin-
ous and alkyd paints pigmented with titan-
ium dioxide had both their touch- and hard-
dry times increased substantially.
  Based  on these results Holbrow concluded
that concentrations  of  SO? encountered in
fogs or near industrial sites can increase the
drying time and  hardening time of certain
kinds of paint  systems. Some films become
softer and others more brittle than those
dried in the absence of SO,—a factor likely
to influence subsequent durability.
  Holbrow3 also found  that when several
types of paints  (simple  oil, oleoresinous or
alkyd) were allowed to dry in  clean air for
24 hours, then  exposed to moisture and ab-
normally high levels  of SO, (12,000 ppm or
more; exposure time  not specified),  followed
by  exposure to warmth  (temperature not
stated) and moisture (quantity not indicat-
ed) for one hour, a  significant reduction in
gloss  developed. Depending on the type of
paint, the reduction in gloss, expressed as a
percentage of the original value, ranged from
85 percent to  10  percent. Alone, S02  and
moisture caused no more than a small reduc-
tion in gloss; it is only after exposure to fur-
ther  moisture  and  warmth  that  a  large
change occurred. It appeared that SO, rend-
ered the films  water sensitive. Control ex-
periments  omitting- SO, showed no loss of
gloss. Sensitivity to S02 is gradually lost the
longer paint is allowed to dry prior to ex-
posure.
  The blueing  of  Brunswick green occurs
when freshly applied paint is exposed to S02
levels of 0.2 ppm (duration of exposure not
indicated)  and subsequently  exposed  to
warmth and moisture.3
  Another troublesome  paint defect is crys-
talline bloom which results when  paints are
exposed  to SO,, moisture,  and  ammonia.
Bloom is due to the formation of very small
crystals  of ammonium sulfate.  Calculated
SO... levels of 0.1 ppm (duration of exposure
not indicated)   could cause moderate bloom.

        C.   DAMAGE TO  METALS
  Under normal conditions damage to metals
by the  oxides  of sulfur increases with in-
creasing relative humidity  and temperature.
Particulate matter in the air also contributes
to the deleterious effects. Sulfur oxides gen-
erally accelerate corrosion by first being con-
verted to sulfuric acid,  either in the atmos-
phere itself or on metal surfaces. The  cor-
rosion products are  mainly sulfate salts of
the exposed metals.4"7  In  addition,  atmos-
pheric sulfuric  acid can  react with some sus-
pended  particles to form sulfate salts that
also can accelerate corrosion of many metals.
                                                                             51

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  Laboratory  studies were  conducted by
Preston and Sanyal" using bare and varnish-
ed steel test panels, which were properly pol-
ished and degreased  and  then inoculated
with  finely  divided   particles  of  various
dusts. The dusts  were powdered oxides and
chloride,  sulfate,  and chromate salts, and
boiler and flue  dusts  like  those commonly
found in the atmosphere. The metal test pan-
els were then exposed to atmospheres of pure
clean air  and  air containing S02 (very low
concentration  but not specified)  at various
humidities, and the resulting  corrosion was
measured. Filiform corrosion, characterized
by a filamental configuration, the  primary
phase in electrolytic corrosion, was noted in
all cases. Corrosion at relative humidities be-
low 70 percent is low, but it increases at high-
er humidities/' s~u In  most  of the  cases  in
this  study,s corrosion increased with humid-
ity even in clean air. The addition  of traces
of SOL,  to the test atmospheres  greatly in-
creased the rate of corrosion in all instances.8
  Atmospheres polluted  with  sulfur dioxide
have been found  to be among the most cor-
rosive of all atmospheres studied, and to  be
even more corrosive than some marine atmos-
pheres.11 '- A striking  example is the almost
fourfold reduction in  the corrosion rate  of
zinc  in  Pittsburgh associated with a three-
fold  reduction in sulfur dioxide, from annual
levels of 0.15  ppm to  0.05 ppm, and a two-
fold  reduction in dustfall in the period  1926
to I960." 13
  Schikorr 14 observed that steel panels ex-
posed in Berlin during the winter months ini-
tially corroded five times faster than similar
panels  first  exposed  during  the  summer
months.  The  particulate levels were  much
higher in winter and this resulted in the pro-
duction of a greater abundance of corrosion
nuclei. Nevertheless, Schikorr  attributed this
greater rate of corrosion primarily to the
greater concentrations of gaseous combus-
tion  products,  including sulfur oxides, in the
air and to the longer periods of specimen wet-
ting during the winter.
  Foran et al.™ and Gibbons 1617 found that,
among several metals exposed to atmospheres
ranging from  rural to heavy industrial, car-
bon  steels were  most affected, followed  in
descending order by zinc, copper, aluminum,
and stainless steel. Furthermore, they observ-
ed rather direct  relationships  between cor-
rosion and oxides of sulfur pollution  in sev-
eral  ambient atmospheres in which  2-year
average lead peroxide candle sulfation rates
ranged approximately  from essentially 0 to
12 mg S03/100 cm-'-day. The increase in cor-
rosion per  unit  increase  in sulfation was
greater at lower  sulfation rates, e.g. of the
maximum  corrosion noted  at  12 mg S03/
100 cm--day, approximately one-half had oc-
curred with steel and about one-fifth with
zinc  at 2  mg S03/100 cm2-day. In terms of
the measurements made by these investiga-
tors, a lead peroxide sulfation  rate of 2 mg
SOs/100  cm2-day is roughly equivalent to
0.08  ppm  of sulfur dioxide.
  Upham ls reported on studies in St. Louis
and  Chicago where mild low-carbon steel
panels were exposed to the atmosphere at a
number of sites. It was assumed that meteor-
ological conditions within one  metropolitan
area are sufficiently uniform that the air pol-
lution level  is the major  site variable influ-
encing observed corrosion rates, and concom-
itant measurements of the pollution levels at
each site were made. In both cities, high cor-
relations were found between corrosion rates,
as measured by weight loss, and sulfur diox-
ide concentrations measured by the West-
Gaeke method.  Sulfation  rates  in St. Louis,
measured by lead peroxide candles, also cor-
related well with weight loss due to corro-
sion. In St. Louis, except for one exceptional-
ly polluted site, corrosion losses averaged 30
percent to 80 percent more then in nonurban
locations.
  Figure  4-1 shows the weight loss in 100-
gram panels exposed  in  Chicago  at seven
sites for 3-, 6-,  and 12-month periods and the
corresponding mean concentration of sulfur
dioxide measured at each site.  Over the 12-
month exposure period, the corrosion  rate at
the most  corrosive site (mean  S02 level of
0.12  ppm) was  about 50 percent more than at
least corrosive  site (mean SO2  level of 0.03
ppm). A  regression analysis on the Chicago
data  relating  corrosion,  as  measured  by
weight loss, to  mean S02 concentrations re-
sulted in  the following regression equation:

             y = 54.1 s + 9.5
      52

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  18.0

116.0
en

UJ14.0
  12.0-
oc
U10.0-
8
K 8.0
HI
Q_
$ 6.0
  4.0
§2.0
                                  3 months
         I    I    I    I
    "0  0.02  0.04 0.06 0.08 0.10 0.12  0.14  0.16  0.18
     MEAN SULFUR DIOXIDE CONCENTRATION; ppm
Figure 4-1. Relationship between corrosion of mild
         steel and corresponding mean sulfur
         dioxide concentration for 3-, 6-, and
         12-month exposures at seven Chicago
         sites (Sept. 1963-1964).

 where
 y = corrosion weight loss  in grams per hun-
 dred  gram panel  (4" X 6" x 0.035" dimen-
 sions)  and

 s = mean S02 concentration in ppm.

   The regression coefficient was  statistically
 significant at the one-percent level. The linear
 relationship expressed by this equation would
 be valid only over the range of the observed
 data (i.e., from 0.03 to 0.12 ppm mean annual
 concentration)  and in locatons  with  topog-
 graphy and climate similar to that of  Chica-
 go.  The relationships were linear also in St.
 Louis, although the slope for the  3-month ex-
 posure period was greater than  that in Chi-
 cago,  presumably because the 3-month  ex-
 posure took place during the winter months
 in St. Louis and during the autumn in Chica-
 go.  Differences between the two  cities  in
 terms of climate and exposure site configura-
 tion also may have been influential.
   Suspended particulate levels  were meas-
 ured in Chicago at all seven sites with high-
 volume samplers, and these values correlated
 with  corrosion rates.  Since  sulfur dioxide
concentrations and particulate concentrations
themselves tend  to correlate, a  covariance
analysis  was  carried  out to determine  the
relative  influence of  these  two  pollutants.
This  adjusted analysis  indicated that  the
difference in corrosion rates at  the  various
sites resulted  primarily from  differences in
sulfur dioxide concentrations  and not from
differences in  particulate levels. Thus, sulfur
dioxide levels appeared to have the dominant
influence on corrosion  rates. Dustfall meas-
urements made in St. Louis did not show a
statistically significant correlation with cor-
rosion rates.
  The economic  significance  of  metal cor-
rosion has not been adequately investigated.
In England, it has been estimated that about
one-third of the annual replacement  cost for
steel  rails  is caused  by  air   pollution.19
Couy2°-22 investigated the effect of  atmos-
pheric corrosion on maintenance and econom-
ics of overhead line hardware  and guy wires
in Pittsburgh. The  conditions  of actual ma-
terials in use over the period roughly from
1920 to  1940  were  determined for areas of
severe and average pollution. Areas of severe
pollution included valleys traversed  by rail-
ways and areas  in  direct windline with in-
dustrial fumes. Formulae were developed to
determine the amount of inspection required,
the materials  needed,  and the  costs involved
for a particular situation. No direct cost esti-
mates were made but it appeared that the life
of the materials in the severely polluted areas
was  reduced to about  two-thirds of that of
the materials in  the areas of  average pollu-
tion. The average annual sulfur dioxide con-
centration during the period  of the study was
initially  high (0.15 ppm) but had declined
to approximately 0.05 ppm by 1940 (0.04
ppm in 1963).13
  The effects  of air pollution on  electric con-
tacts result in increased costs  because of the
losses associated with  increased resistance of
contacts  having corrosion films and  because
more costly,  less reactive,  metals  must be
used. The use of gold instead of silver for
contacts  costs about 14.8 million dollars an-
nually. If  gold could  be replaced by palla-
dium, an annual  savings of  8 million dollars
would result, but palladium tarnishes in a
sulfur dioxide atmosphere.23
                                                                                 53

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D.  EFFECTS ON BUILDING MATERIALS

  There has  been little recent investigation
of effects of ambient concentrations of sulfur
oxides on building materials. Early work2 25~27
shows that sulfur oxides may be associated
with  damage to various building materials.
Sulfur dioxide, in the presence  of moisture
is converted  to  sulfurous  or sulfuric acids
which are capable of attacking a wide variety
of building materials,  including limestone,
marble, roofing slate, and mortar. 2S~30 Any
carbonate-containing stone is  damaged by
having the carbonate converted to relatively
soluble sulfates, and then being leached away
by rainwater.21130 Other types of stone, such
as granite and certain sandstones, in which
the grains are cemented together with ma-
terials containing no carbonate, are relatively
unaffected by sulfur oxides in the  atmos-
phere.28
   Building stones erode to a greater or lesser
degree according to their chemical composi-
tion. Softer building stones, such as the lime-
stones and dolomites, are attacked more read-
ily by the acids formed by the interaction of
industrial smokes (even in small quantities)
and  moisture.31  The dolomites contain both
calcium  and magnesium  carbonates,  the
latter being  readily soluble in  an acid  en-
vironment;  the  dolomitic stones are thus
more vulnerable.26 3132  The calcium  sulfate
formed on the surface of  masonry is about
twice as bulky as the carbonate of the stone
from which it was formed, so the stone ap-
pears to grow leprous.31 Granites, gneiss, and
many sandstones, which do not  contain car-
bonates, and well-baked bricks, glazed bricks,
and  glazed tiles are attacked less readily by
the sulfurous and sulfuric acids from the at-
mosphere. Additionally, serious disintegra-
tion of stone, caused in part by the expansion
due to corrosion of iron tie rods, can occur.26
Slates containing  carbonates and the  cal-
careous sandstones often used as roofing ma-
terials are also attacked by polluted acid at-
mospheres.26  Decay  occurs  mainly  on  the
undersides,  especially  between  the laps,
where moisture is held as a thin film.
   Baines 25 reported that the expansive force,
which developed from the crystallization of
calcium and magnesium salts along the cleav-
age planes of stones in the buildings in vari-
ous English cities, slowly opened up the old
sealed vents where they could be attacked by
atmospheric acid, and even lifted fragments
of stone several tons in weight. On the Brit-
ish Houses of  Parliament, which  were ap-
proximately 90 years old  when  the  survey
was made, he found sulfate, which could only
have  been derived from the attack upon the
stone by atmospheric acid, in cracks and fis-
sures as much as 20 inches from the surface.
He observed that the increase in the volume
of crystallization of from 1 to 4.2 had thrown
off great pieces of  stone. Over  35 tons of
stone were picked off portions of the building
without using tools.
   The  deterioration  of some  of  the finest
monuments of  antiquity and  thousands of
pieces of  sculpture and carving in the open,
on public  buildings, and on  cathedrals is a
matter  of increasing  concern. The rate of
decay has accelerated  in recent years be-
cause of  the  increased pace of  Twentieth
Century industrialization  and larger emis-
sions of combustion products containing sul-
fur oxides and particulate matter. Cleopat-
ra's Needle, the large  stone obelisk  moved
from Alexandria, Egypt, to London, has suf-
fered more deterioration in the damp,  smoky
acid atmosphere of London in 70 to 80 years
than  in the earlier 3,000 or more years of its
history.

   E.   EFFECTS ON TEXTILE FIBERS,
      DYES, AND MISCELLANEOUS
                MATERIALS
   The  vulnerability of textile fabrics  and
furnishings to acid products of combustion,
which are often sorbed on the particles emit-
ted  simultaneously  by combustion sources,
depends on the chemical composition  of the
textiles.32 Cellulosic vegetable fibers, such as
cotton,  linen,  hemp, jute, rayons, and syn-
thetic nylons,  are particularly sensitive to
acid  products of combustion such as sulfur-
ous and  sulfuric acids.  After exposure to
these acids, such fibers lose tensile strength.33
..Animal fibers,  such as wool and furs, are
more resistant to acid  damage.32
   Dyed fabrics containing certain classes of
dyes  are attacked  by acid compounds often
sorbed  on atmospheric  particles;  the  dye
       54

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coloring  is reduced or sometimes destroyed
entirely.  Color changes of dyed  fabrics ex-
posed without sunlight to the atmospheres of
Los Angeles, Chicago, Phoenix, and Sarasota,
Florida, were studied  during the period Octo-
ber through  December, 1961.34 35 For some
dyes,  maximum and severe fading occurred
in Chicago, where sulfur  dioxide concentra-
tions  were highest (NASN annual  average
about 0.09 ppm).3637
  In  controlled environment studies,38 se-
lected dye-fabric combinations were exposed
to a variety of pollutants  (in the absence of
light)  in order to assess  dye  fading char-
acteristics. Auto exhaust showed no fading;
clean  air plus SOL,  (1 ppm) showed no fad-
ing; irradiated auto exhaust produced signifi-
cant fading in some dyes; and irradiated auto
exhaust plus S02 (1 ppm)  gave rise to fading
in  additional  dyes as  well as  more  pro-
nounced  fading in those dyes that faded with-
out S02.  This shows the positive  synergistic
effect of SO-, and again emphasizes  that in
many  cases  damage  is a function of pol-
lutants  working together rather  than  by
themselves.
  Leather  has  a  strong  affinity for  S02,
which causes it to lose much of its strength
and ultimately to disintegrate. The storage of
valuable leather-bound books in city libraries
can pose a serious problem. Book bindings
stored in rooms with  a free exchange of pol-
luted  air were found to  deteriorate much
more  rapidly  than those  stored  in  confined
spaces or inside of glass cases.26
  Paper also absorbs  SO- which is oxidized to
sulfuric  acid. The  sulfuric acid  causes dis-
coloration and renders the paper brittle and
fragile.26 Exposures to S02 (2-9 ppm) for 10
days  resulted  in  embrittlement  and a de-
crease in folding resistance of both book and
writing paper.2

              F. SUMMARY
  Although more  quantitative data  present-
ing dose-response relationships are needed,
sufficient evidence exists to conclude that  at-
mospheres polluted with oxides of sulfur  di-
rectly and indirectly attack and damage a
wide  range of materials and property. Much
of this damage is due  to the conversion of sul-
fur oxides to highly reactive sulfuric acid.
  In the laboratory, steel test panels dusted
with particles  commonly found  in  polluted
atmospheres  (e.g.,  powdered oxides,  boiler
and  flue  dusts, and chloride, sulfate,  and
chromate salts) corroded  at a  low rate in
clean air at relative humidities below 70
percent.  The corrosion rate increased at
humidities higher than  70  percent, and it
greatly increased when traces of sulfur diox-
ide were added to the laboratory air.
  Corrosion  rates of most  metals  and es-
pecially iron, steel, and zinc are accelerated
by sulfur dioxide-polluted environments. Par-
ticulate matter, high humidity, and tempera-
ture also play an important synergistic part
in this corrosion reaction,  Atmospheric  cor-
rosion studies show increased corrosion rates
in industrial areas where air pollution levels,
including sulfur dioxide and related pollut-
ants, are higher. Further, corrosion rates are
higher in the fall  and winter seasons when
particulate and sulfur  oxides  pollution is
more severe due to a greater consumption of
fuel for  heating. Depending on the kind of
metal exposed as well as location and dura-
tion of  exposure, corrosion rates were  1-1/2
to 5 times greater in polluted atmospheres
than in  rural environments. In  Pittsburgh,
from 1926 to 1960, when annual sulfur diox-
ide levels were reduced from 0.15 ppm to  0.05
ppm, zinc corrosion rates  exhibited a four-
fold reduction.  In Chicago  and  St.  Louis,
where steel panels were exposed at a number
of sites, high correlations were found in each
city between  corrosion  rates, as measured
by weight loss, and sulfur dioxide concentra-
tions measured by the West-Gaeke  method.
In St. Louis, except for one exceptionally pol-
luted site, corrosion losses averaged 30  per-
cent to 80 percent more than in nonurban
locations. Over a 12-month exposure period
in Chicago, the corrosion  rate  at the most
corrosive site (mean S02 level of 0.12 ppm)
was about 50 percent more than at the least
corrosive site (mean S02 level of 0.03 ppm).
These correlations were statistically signifi-
cant at the one-percent level. Sulfation rates
in St. Louis,  measured by lead peroxide  can-
dle, also  correlated well with weight loss due
to corrosion.  Although suspended particulate
levels measured in Chicago with high-volume
samplers correlated with corrosion  rates, a
                                                                               55

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covariance analysis indicated that sulfur di-
oxide concentrations were the dominant in-
fluence on corrosion. Measurements of dust-
fall in St. Louis did not correlate significantly
with corrosion rates. Based on these data, it
appears that considerable corrosion may take
place  (i.e., from  11  percent to  17 percent
weight loss in steel panels) at annual sulfur
dioxide concentrations  in the range of  0.03
ppm to 0.12 ppm, and although high particu-
late levels tend to accompany high sulfur di-
oxide levels, the sulfur  dioxide concentration
has a greater influence on the degree of cor-
rosion that takes place.
   Qualitative examples of effects  resulting
from corrosion by sulfur dioxide include:

     1.  a  one-third reduction  in  the life  of
        overhead power  line hardware  and
        guy wires;
     2.  the necessary use of more expensive,
        less corrodible metals such as gold in
        some  electrical contacts; and
     3.  one-third of the annual  damage  to
        steel rails  in England.
   Atmospheres  containing oxides  of  sulfur
also attack  and damage a  wide  variety  of
building materials—limestone, marble, roof-
ing  slate, and  mortar—as well as  statuary
and other works of art, causing discoloration
and actual  physical deterioration. Certain
textile  fibers—such  as  cotton,  rayon,  and
nylon—are also harmed by atmospheric sul-
fur oxides, and  in the presence of other pol-
lutants, fading  of dyed  fabrics  may occur.
Severe fading  was  noted for some dyes  in
fabrics exposed in  Chicago,  where annual
average sulfur dioxide levels were 0.09 ppm.
Leather exposed to sulfur dioxide may lose
much of its  strength  while paper becomes
discolored and brittle.
   Concentrations of 1 ppm S02 can increase
the drying time of some oil-based paints  by
50 percent to 100 percent. Some films become
softer and others more brittle, a factor likely
to influence subsequent durability.  Sulfur  di-
oxide also appears to render some paint films
water  sensitive, resulting  in reduced gloss.
Under certain conditions,  S02 levels of  0.1
ppm to 0.2  ppm can  cause the  blueing of
Brunswick green, and in the presence of am-
monia  produce  a troublesome defect called
crystalline bloom, due  to the formation  of
very small ammonium sulfate crystals.

             G.  REFERENCES
1.  Yocum, J. E. and McCaldin, R. O. "Effects of Air
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 2. Burdick, L. R. and Barkley, J. F. "Effect of Sul-
   fur Compounds in the Air on Various Materials."
   U.S. Bureau of Mines, Information  Circular
   7064, April 1939.
 3. Holbrow,   G.  L.  "Atmospheric Pollution:  Its
   Measurement and Some Effects on Paint." J.  Oil
   Colour Chem. Assoc., Vol. 45, pp. 701-718, Oct.
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 4. Serada,  P. J.  "Atmospheric Factors Affecting
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 5. Greenblatt, J. H. and Pearlman, K. "The Influ-
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 7. Sanyal, B. and Bhardwar, D. V. "The Corrosion
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10. Vernon, W. H. J.  "The Atmospheric Corrosion
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11. Tice,  E.  A.  "Effects of Air Pollution on  the
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13. Anderson, D. M., Lieben, J., and Sussman,  V. H.
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   1961.
14. Schikorr, G. "The Atmospheric Rusting of Iron."
   Korrosion and Metallschutz., pp. 305-313, Sept.
    17, 1941.
15. Foran, M. R., Gibbons,  E. V., and  Wellington,
   J. R.,  "The Measurement of Atmospheric Sul-
   phur  Dioxide  and Chlorides."  Chem.  Canada,
   Vol. 10, pp. 33-41, May 1958.
       56

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16. Gibbons, E. V.  "Atmospheric Corrosion Testing
   of  Metals in  Canada."  Corrosion,  Vol. 17, pp.
   318-320, 1961.
17. Gibbons, E. V.  "The Corrosion Behavior of the
   Major Architectural and  Structural  Metals in
   Canadian Atmospheres.  Summary of Two-Year
   Results."   National Research  Council,  Ottawa,
   Canada, Feb. 25, 1959.
18. Upham,  J.  B.   "Atmospheric Corrosion Studies
   in  Two Metropolitan  Areas."  J. Air Pollution
   Control Assoc.,  Vol. 17,  pp. 398-402, June 1967.
19. "Committee on Air Pollution, Beaver, H., Chair-
   man, Report."   Her Majesty's  Stationery Office,
   London, 1954.
20. Couy, C.  J. "Effect of Atmospheric Corrosion
   on Maintenance and Economics of Overhead Line
   Hardware and  Guy Strand, Part 1." Corrosion
    (Natl. Assoc. Corr. Eng.), Vol.  4,  pp. 133-140,
   April 1948.
21. Couy, C J.  "Effect of Atmospheric Corrosion on
   Maintenance and  Economics  of  Overhead  Line
   Hardware and  Guy Strand, Part 2." Corrosion
    (Natl. Assoc. Corr. Eng-.), Vol.  4,  pp. 207-218,
   May 1948.
22. Couy, C. J. "Effect of Atmospheric Corrosion on
   Maintenance and  Economics  of  Overhead  Line
   Hardware and  Guy Strand, Part 3." Corrosion
    (Natl. Assoc. Corr. Eng.), Vol.  4,  pp. 287-303,
   June 1948.
23. Gilbert, P.  T.  "The Protection of Steel Against
   Atmospheric Corrosion  by Metallic  Coatings."
   Ind.  Chem., Beige., Vol. 19, pp.  405-415, Sept.
   1963.
24. Antler, M.  and Gilbert,  J.  "Effects  of Air  Pol-
   lution on  Electric Contacts."  J. Air Pollution
   Control Assoc.,  Vol. 13,  pp. 405-415, Sept. 1963.
25. Baines, F. "Examination into Effects of Air Pol-
   lution on Building-Stones, etc." National Smoke
   Abatement  Society, Manchester, England, 1934.
26. Parker, A.  "The Destructive Effects of Air  Pol-
   lution on Materials."  In:  Proceedings, 1955 An-
   nual Conference, National Smoke Abatement So-
    ciety,  London,  1955,  pp.  3-15.   (Presented at
    Sixth  Des  Voeux  Memorial  Lecture.)
27.  McBurney,  J. W.  "Effect  of the Atmosphere on
    Masonry  and Related  Materials."  In: Sympo-
    sium on Some Approaches  to Durability in  Struc-
    tures, Boston, Massachusetts, June 23,1958, Spec.
    Tech.  Pub. 236, pp. 45-52.
28.  Yocum, J. E.  "The Deterioration of Materials in
    Polluted Atmospheres."  J. Air Pollution Control
    Assoc., 8(4) :203-208, Nov.  1958.
29.  Benner, R. C.,  IV.  "The Effect of  Smoke on
    Stone."  In: Papers on  the  Effect of Smoke on
    Building  Materials,  University of  Pittsburgh,
    Mellon Institute  of  Industrial  Research  and
    School of  Specific Industries, Bulletin 6, 1913.
30.  Turner, T.  H. "Damage to Structures by Atmos-
    pheric Pollution."  Smokeless  Air,  Vol. 23,  pp.
    22-26, Autumn 1952.
31.  Regan, C. J.  "A Chadwick Lecture on Air  Pol-
    lution." Smokeless Air,  Vol. 88, pp. 67-76, 1953.
32.  Petrie, T. C. "Smoke and  the Curtains." Smoke-
    less Air,  Vol. 18, pp.  62-64, Summer  1948.
33.  Waller, R.  E.  "Acid Droplets in Urban Air."
    Int. J. Air  Water Pollution, Vol. 7,  pp. 773-778,
    1963.
34.  Salvin, V. S.  "Effect of Air Pollutants on Dyed
    Fabrics." J. Air  Pollution Control Assoc.,  Vol.
    13, pp. 416-422, Sept. 1963.
35.  Salvin, V.  S.   "Relation  of Atmospheric Con-
    taminants  and  Ozone to Lightfastness."  Am.
    Dyestuff  Rep., Vol. 53,  pp.  33-41, Jan. 6, 1964.
36.  "Air  Quality Data (1962)  National Air Sam-
    pling  Network." U.S. Dept. of Health,  Educa-
    tion, and Welfare, Public Health Service, 1964.
37.  "Air  Quality Data (1963)  National Air Sam-
    pling  Network." U.S. Dept. of Health,  Educa-
    tion, and Welfare, Public Health Service, 1965.
38.  Ajax, R. L., Conlee,  C. J., and  Upham, J. B.
    "The  Effects of Air Pollution on the Fading of
    Dyed  Fabrics."  J.  Air Pollution Control Assoc.,
    Vol. 17, pp. 220-224, April 1967.
                                                                                            57

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                  Chapter 5
EFFECTS OF SULFUR OXIDES IN THE ATMOSPHERE
              ON VEGETATION

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                           Table of Contents
                                                                 Page
A. INTRODUCTION                                                61
B. SYMPTOMS IN VEGETATION OF EXPOSURE TO SULFUR
   DIOXIDE                                                       61
   1. Acute Injury                                     .             61
   2. Chronic Injury                                                62
   3. Physiological Effects                                           62
   4. Mechanism of Injury                                           63
C. SUSCEPTIBILITY OF VEGETATION TO SULFUR DIOXIDE         63

D. FACTORS AFFECTING PHYTOTOXICITY                         65
   1. Temperature                                                  65
   2. Relative Humidity            .                                 66
   3. Soil Moisture                                                  66
   4. Light Intensity                                                66
   5. Nutrient Supply                                               66
   6. Age of Plant Tissue                                            66
E. SYNERGISTIC EFFECTS OF SULFUR DIOXIDE AND OZONE        66

F. EFFECTS OF SULFURIC ACID MIST ON VEGETATION             66

G. SUMMARY                                                     67
H. REFERENCES                                          ...    68

                           List of Figures
Figure
5-1. Curves Showing Concentrations of Sulfur Dioxide Which Will Pro-
      duce Three Different Stages of Acute Alfalfa Leaf Damage in Differ-
      ent Time Periods under Conditions of Maximum Absorption          64
 60

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                                     Chapter  5

  EFFECTS OF  SULFUR OXIDES IN  THE ATMOSPHERE ON  VEGETATION
          A.   INTRODUCTION
  Extensive experiments  and  observations
have been made for over one hundred years
on the effects of sulfur dioxide on vegetation
by investigators in all parts of  the world.
Substantial  reviews  of  vegetation  injury
from the oxides of sulfur have been made by
Thomas,1-4 Sheffer and Hedgcock,5 Brandt
and Heck,6  and Katz  and McCallum,7  and
Daines.8  Summaries of acute  effects on a
large  number of plant species susceptible to
sulfur dioxide  injury are given  by Wood9
and in the Environmental Biology Volume of
Biological Handbooks.10 Although Thomas4
stated that the effects of  sulfur  dioxide on
plants are fairly well understood, there are
still some points of unresolved controversy
in the  literature. The response  of plants
to sulfur dioxide  presents a many faceted
problems and  involves the interactions of
plant  characteristics,  environmental condi-
tions,  and dosage of the toxicant.
  According to  Katz,11 one of  the first  de-
scriptions of sulfur dioxide injury to plants
was by Schroeder and Ruess in 1883.  De-
scriptions of injury have appeared in numer-
ous publications since that time.6-812^14 Two
general types of injury are produced by sul-
fur dioxide, acute and chronic.16~s Any over-
all effect on growth and  production is ap-
parently associated with some degree of acute
injury from sulfite or sulfurous  acid or to
chronic  injury  resulting from accumulation
of sulfates.14

  B.  SYMPTOMS IN VEGETATION OF
   EXPOSURE TO SULFUR DIOXIDE

             1.  Acute Injury

  Acute  injury results from the  rapid ab-
sorption of toxic concentrations of sulfur di-
oxide.14  Immediately after exposure, tissues
in sharply denned marginal and intercostal
area take on a dull water-soaked appearance.1'
These areas subsequently dry out and bleach
to an ivory color. On some species the lesions
finally become brown to reddish-brown.4 61516
A sharp line usually separates the  injured
lesion from surrounding, apparently healthy,
leaf tissue. Injury seldom extends across the
veins of broad-leafed plants unless the injury
is severe.2
  Acute  injury in pine usually occurs in
bands on the tips of needles with the injured
area taking on a red-brown  color.7  The  in-
jured area changes from the usual dark green
color to a lighter green, then definite areas
turn yellow-brown and finally red-brown,
giving the banded appearance. The discolora-
tion in conifers may involve the whole needle
or limited areas of any portion. Abscission
may follow  after some  interval and the  af-
fected trees  are often deficient in needles.
   The basic bleached and collapsed blotches
described  on broad-leafed plants are,  how-
ever, also typical on grass  foliage.1718 The
final bleached pattern between the  parallel
veins of grass leaves gives a streaked effect.
Often only  the  principal vein or/'midrib"
remains intact. The collapsed lesion generally
extends uniformly though the entire thick-
ness of the leaf blade.
   Holmes et al.12 found that barley, growing
in the field,  was severely injured by  fumiga-
tions with 5 ppm sulfur dioxide administered
one hour a day on six successive days. If the
same total  dosage was applied for much
shorter  intervals during the  six days,  there
was  much  less injury.  Apparently injury
could be repaired if sufficient periods free of
toxicant were provided.  It was also reported
that injury  to very young barley plants  did
not reduce final yield but that injury late in
                                                                             61

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the life of the plants caused significant reduc-
tion in yield. No yield reduction occurred un-
less visible damage symptoms were detected
on the foliage.
            2.   Chronic Injury
  Sublethal concentrations of sulfur dioxide
may require several days or weeks to cause
the development of the gradual yellowing or
chlorotic  symptom of chronic injury.2 The
slow fading of green color over a period of
several  days suggests that the  chlorophyll-
making mechanism  is being  destroyed  and
that the green pigment cannot be replenished.
If only a few cells in an area are affected, the
area may become chlorotic or brownish-red.
A large amount of sulfate is found in leaves
with  chronic  symptoms,14  whereas  leaves
which are acutely injured show  only a small
increase in  sulfate content. Large quantities
of sulfate may be accumulated in leaf tissue
without causing injury.14 2r Yet, if excessive
amounts are absorbed rapidly, acute injury
results.
   Sulfur dioxide is very soluble in water and
is absorbed by leaves. If absorbed slowly it
is oxidized or perhaps reduced to a small ex-
tent.14 The  sulfuric acid resulting from  oxi-
dation and hydrolysis in the leaf tissue  is
rapidly metabolized by organic  bases. Acids
formed in  the  leaf tissue  may reduce the
buffer capacity  without  changing pH  and
when  the  buffering capacity  is  exceeded,
chlorosis  results. A recent report19 indicates
that the reduction of sulfur dioxide in the leaf
tissue may  have more significance than pre-
viously proposed by Thomas,14 since  consid-
erable  hydrogen  sulfide  was given  off by
tomato  plants  during, and for a time after,
fumigation with sulfur dioxide.
          3.  Physiological Effects
   The "invisible injury" theory suggesting
that suppression of growth and yield may oc-
cur because of  long-term low concentration
exposure  to sulfur  dioxide,  even  if visible
symptoms of foliage injury  do  not develop,
was proposed by Stoklasa.20 According to Set-
terstrom,21 this theory was supported by sev-
eral investigators,  including Wieler,  Brede-
mann, Janson, and Bleasdale. Many investi-
gators accept the thesis that growth and yield
are not affected unless visible symptoms of
injury occur on the foliage.12 6 22~24 There is
a straight-line  relationship between yield of
alfalfa and either the total area destroyed by
acute symptoms or the area  covered by the
chlorotic symptom.25 The amount of yield
reduction produced by sulfur dioxide symp-
toms can be duplicated by clipping a compa-
rable amount  of leaf area  from healthy
plants.16 Destruction of portions of the leaf
area and accompanying defoliation not only
reduces yield  of  the current crop but may
adversely affect the next one or two clippings.
  Reduction in growth of pine trees in the
vicinity of sulfur dioxide sources has  been
reported.7 26 2r   This  growth  reduction  was
evidently due  to heavy defoliation and de-
struction of portions of needles during pro-
longed exposure  to  levels of sulfur dioxide
sufficient to kill cells and tissue or to build
sulfate  concentrations to a level which de-
stroyed chlorophyll. Needles of  many coni-
fers are normally retained for three or more
years and accumulate sulfate from continued
low concentrations of sulfur dioxide. Needle
drop is stimulated by high levels of sulfates,
and  trees  growing  near  sulfur dioxide
sources often  have very sparse foliage.27
  Defoliation  of  citrus trees exposed to sul-
fur dioxide has  been  observed  in  Japan.28
Defoliation  increased  with increasing con-
centrations, and  increased sulfur content of
foliage coincided  with the rate of defoliation.
It was concluded that leaf analyses for sulfur
content may be useful for evaluating chronic
injury,  but  such  analyses could not be used
for evaluating acute injury. A lower rate of
absorption may produce symptoms of chloro-
sis  and reduce  CO2 exchange, causing tempo-
rary disruption of photosynthesis and respi-
ration. The rate  of carbon dioxide exchange
returns to normal soon after the toxicant is
removed if visible symptoms do not develop.
At  very low concentrations, the sulfur oxides
may be utilized by plants deficient in sulfur
causing stimulation of growth  and produc-
tion.14 2124 Bleasdale,29 in  a study conducted
near Manchester, England, found that yields
of  rye  grass  grown in  unfiltered air were
significantly lower than similar plants grown
in filtered air. The S02 levels in the unfiltered
air ranged from  0.01 ppm to 0.06 ppm with
exposure periods varying  from 46 to 81 days.
       62

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No visible symptoms were  observed on the
plants exposed to S02; it is not known wheth-
er other gaseous pollutants  were present.
         4.  Mechanism of Injury
  The mechanism by  which  sulfur  dioxide
causes injury to leaf tissue is not thoroughly
understood, although a number of sugges-
tions  have been made. The  acute symptoms
are generally attributed to  excessive sulfite
or sulfurous acid in the tissue.1 " With  a
high rate of absorption, sulfite is thought to
accumulate; sulfurous acid is then  formed
and subsequently attacks the cells. Sulfur di-
oxide enters the leaf  through  the stomata
and  is  thought to  be  oxidized, perhaps by
oxygen, a by-product of photosynthesis."' Sul-
furic acid is then  formed  and reacts  with
organic bases.14  The resulting  sulfates are
apparently translocated with  the transpira-
tion stream and deposited at the tip or edges
of the leaf. Haselhoff 30 suggested that sulfur
dioxide attaches itself  to aldehydes and sug-
ars in the leaf and as these products degrade,
sulfurous or sulfuric acid is formed  and in-
jury  results. Dorries3t reasoned that  local
acidity  from the sulfur dioxide  split  magne-
sium  from the  chlorophyll  molecule  and
formed  pheophytin.  Noack 32 suggested that
iron in the chloroplasts was  inactivated by
sulfur dioxide,  causing interference with the
assimilation of organic compounds  by the
plant.
 C.   SUSCEPTIBILITY OF VEGETATION
          TO  SULFUR DIOXIDE
   Different species, different varieties within
a plant species, and even individuals within
a plant variety  vary considerably in their sus-
ceptibility to sulfur dioxide.6 K ]' Thomas -~4
tabulates many plants according to  their sen-
sitivity to sulfur dioxide.  Since alfalfa is one
of the most sensitive plants, it was used as a
reference species and all other species and
varieties were  compared  with it. The order
of sensitivity  was  calculated by Thomas 25
from unpublished data of O'Gara  on resist-
ance  factors for over 300 plants. According
to Thomas,25 O'Gara's method of determining
resistance consisted of fumigating the plants
for one hour with a measured concentration
of  sulfur  dioxide  just  sufficient  to cause
traces of injury. A  corrected threshold  con-
centration for injury was calculated for 100
percent relative  humidity. This  calculated
value was then divided by 1.25 ppm, which
was the concentration required for incipient
marking on alfalfa in the 1-hour period. The
ratings range from alfalfa,  barley, endive,
and cotton,  the most sensitive, with ratings
of 1, through celery, citrus, and cantaloupe,
with ratings of about 7, to privet leaves, the
most resistant with a rating of 15.
  O'Gara's unpublished data and his funda-
mental equation for the  "Law of gas action
on the plant cell"33 have been used extensive-
ly by  Thomas ' 3 412 23 to  calculate relative
sensitivity of various plants to sulfur dioxide
fumigation  and  to determine the  effect on
yield. O'Gara's formula was:

             t(C-C0)=K             (5-1)
where    t  is  time  (hrs)  through which
             the gas acts  to  produce a cer-
             tain effect,
          C  is the  concentration (ppm) of
             the gas,
          C0 is  the threshold concentration
              (ppm) of the gas for injury to
             the plant, and
          K  is a  constant.
  According to Thomas 25 the amount of in-
jury caused by a given quantity of sulfur di-
oxide varies with the rate of absorption; that
is, a given amount of gas, absorbed in a short
time period, will cause more leaf destruction
than if the absorption were to occur over a
longer period. General  time-concentration-
absorption equations for data obtained  from
fumigations of alfalfa are proposed. By ap-
plying these equations to data from numer-
ous fumigations, it was possible to calculate
the dosage required to produce any observed
degree of injury  under  conditions of maxi-
mum sensitivity. For example, equations rep-
resenting incipient marking, 50 percent leaf
destruction and  100 percent leaf destruction,
under conditions of  maximum sensitivity
were:
           tC = 0.94 + 0.24t  (traces of  leaf
           destruction appear),
           tC = 2.1 + 1.4t  (50 percent  leaf
           destruction occurs), and
           tC = 3.2 + 2.6t  (100 percent leaf
           destruction occurs).
                                                                               63

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   Injury thus begins after four hours of ex-
posure to 0.45 ppm, etc. Curves constructed
from these calculations are plotted in Figure
5-1. Guderian et al?- did not believe that the
O'Gara equation fitted their observations and
suggested that an exponential equation of the
form
            t=ke-a(C-r)             (5-2)
where k, a,  and r are  parameters varying
with species and degree of injury, best de-
scribed their data.
   An  apparatus was  developed by  Spier-
ings 3r' whereby  susceptibility of trees and
shrubs to air pollutants could be determined
under natural conditions without disruption
of  prevailing climates.  Fumigation  experi-
ments with sulfur dioxide showed that apple
and pear varieties were the most susceptible
                     100% LEAF DESTRUCTION
                          t (C - 2.6) = 3.2
                     50% LEAF DESTRUCTION
                         t(C- 1.4) = 2.1
                     TRACES OF LEAF
                     DESTRUCTION APPEAR
                        t (C - .24) = .94
            1         2         3
           TIME (t) OF FUMIGATION - HOURS
 Figure 5-1. Curves Showing Concentrations of Sulfur
         Dioxide Which Will Produce Three Different
         Degrees of Acute Alfalfa Leaf Damage in
         Different Time Periods Under Conditions
         of Maximum Absorption.

These curves from experimental data may be used to
estimate the extent of damage to alfalfa at any sulfur
dioxide concentration and exposure time.
of the fruit trees and that mountain-ash was
one of the most susceptible of the deciduous
forest trees. Six-hour exposures of the fruit
varieties to 0.48 ppm produced injury, where-
as injury to the mountain-ash was produced
by three-hour exposures to 0.54 ppm of sul-
fur dioxide.
  Sheffer and Hedgcock5 reported injury to
ponderosa pine, western larch, Pacific nine-
bark, and creambush  rockspirea  during an
exposure  to 0.5 ppm for 7 hours. They con-
cluded that the lowest concentration of sulfur
dioxide  that  injures  conifers  is  0.25  ppm.
Alfalfa  is generally considered to be one of
the  most  sensitive plants,  and  Thomas16
reported that photosynthesis or  respiration
by alfalfa plants  was not affected by concen-
trations up to 0.3  ppm unless the exposure
was  so long  that  sulfate injury  occurred.
Katz and  McCallum 7 reported that larch, one
of the  most  sensitive  conifers,  developed
slight symptoms from 0.3 ppm sulfur dioxide
in an 8-hour exposure. They concluded that
if concentrations higher than 0.3 ppm to 0.5
ppm do not occur and if the duration of con-
centration at the 0.3 ppm level is short in a
single gas exposure, plant damage should not
occur.
  In the  vicinity  of the  smelter at Trail,
British  Columbia, which in 1929 emitted an
average of 18,600 tons  of sulfur dioxide per
month,  plant injury was noted as far  as  52
miles south of the smelter.26 Three zones of
injury were  delineated on the basis  of the
percentage injury to ponderosa pine, Douglas
fir, and forest shrubs: in Zone 1 there was 60
percent to 100 percent injury; in Zone 2,  30
percent to 60  percent injury^ in Zone 3, 1
percent to 30 percent injury. Zone 1, in which
injury was acute,  extended about 30  miles
south of the smelter in a river valley; Zone 3,
at higher elevations, extended 52 miles south
of the smelter and  contained trees with rela-
tively slight  markings and trees  suffering
from slow but progressive deterioration. Aft-
er sulfur  dioxide  control devices were in-
stalled,  measurements in 1934 and  again in
1935 -" showed that the injury to broadleaf
trees and to  shrubs had  dropped to 20 per-
cent in the former Zone 1 and to 4 percent in
the former Zone 3. Appraisal of ponderosa
pine cone production in 1936 revealed that 81
       64

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percent of the pines in Zone 1 had no cones
and that outside the zone, 16 percent of the
pines had no cones/' Sulfur dioxide concen-
trations 15 miles south of the smelter in Zone
1 averaged about 0.03 ppm  during- the sum-
mer  with occasional peak concentrations in
excess of 0.5 ppm for a total time of 5 to 10
hours.
  Linzon "" reported marked growth suppres-
sion  and chlorotic needles on white pine at
locations 25  miles and less from the Sudbury,
Ontario, smelter where measurable sulfur di-
oxide concentrations were  present from 10
percent to 20 percent of the time. Concentra-
tions  of sulfur dioxide above 0.25 ppm were
present less than 1 percent  of the time; the
remainder of the measurable concentrations
were  less than 0.25 ppm. The annual aver-
age concentrations apparently ranged down-
ward from 0.03 ppm.
  Sullivan 'IT reported damage to 36 percent
of the home gardens in an area near a smel-
ter in Australia where  the annual average
sulfur dioxide concentration was 0.009 ppm
and the maximum daily average  0.155 ppm.
In another area more influenced by the smel-
ter, 89 percent of the gardens were damaged;
there the annual average was 0.033 ppm and
the maximum daily average 0.60 ppm. In the
latter area,  during  brief  fumigations, sulfur
dioxide concentrations ranged up to 10 ppm.
  Injury to at least 15 tree species, includ-
ing both conifers and hardwoods, in the vi-
cinity of petroleum refineries  processing
crude oil, which used 3 percent sulfur pitch
residue in   the  refinery  furnaces, was re-
ported by Linzon.Js Concentrations of  sul-
fur dioxide  measured in  the atmosphere ex-
ceeded 0.5 ppm during 10 hours in one month
in this  area with  momentary peaks over 2
ppm.  Slight to severe acute injury was re-
ported for all species within 1  to 2  miles
from  the refineries.
  Reports of deteriorated vegetation in areas
polluted by sulfur dioxide -3 3G 3S make it clear
that  injury  can occur where annual  aver-
age concentrations  are  very low when the
sources of pollution and/or  the meteorologi-
cal  conditions are  such  that  threshold for
injury  is exceeded  occasionally.  There is
some  evidence  of  growth  suppression and
particularly  chronic injury, where concen-
trations never  exceed  0.1 ppm.-9
  In Eastern Tennessee some mortality  of
white pine has occurred from a disease called
post-emergence  chronic  tipburn.  The dis-
ease has been noted only in industrial areas,
generally  within about 20  miles  of plants
with substantial stack emissions.  The af-
fected  area in  Eastern Tennessee contains
several large plants, including a large coal-
fired power plant, a major  uranium refine-
ment operation,  a  pulp mill, a ferro-alloy
reduction  plant, and an iron foundry. There
is convincing evidence that the causal agent
of the disease is atmospheric. While SOL, was
considered by some as the most likely cause
of the disease, the cause was regarded by
the investigators to be repeated  or long con-
tinued  low-level fumigations with  some un-
identified  gas or gases produced in the af-
fected area. Whatever the causal agent, some
white pine are  so sensitive  to it  that they
have developed striking foliage symptoms at
distances  many  miles  from the  pollution
source.39

        D.  FACTORS AFFECTING
            PHYTOTOXICITY
  The  response of vegetation to sulfur diox-
ide  as  an  air pollutant is influenced greatly
by temperature, relative humidity, light in-
tensity, soil moisture,  nutrient  supply, and
age of plant or tissue exposed. Each of these
factors is  discussed below.

             1.   Temperature
  A plant is much more resistant to sulfur
dioxide at temperatures below 5°  C  (40°
F)t2i =4 40  4i  Setterstrom and Zimmerman40
found  that buckwheat plants were equally
susceptible to injury at 65°  F and 105°  F.
Several investigators" 21 -" have  reported
greater resistance in winter and have related
this  to lower physiological  activity  of the
plants. Physiological activity of broad-leafed
plants  declines  sharply as the leaves become
senescent  and drop in fall and  winter, but
activity is much higher in spring  and early
summer. Sensitivity to sulfur dioxide injury
is similarly higher in spring.11 Weaver and
Morgensen 4L' found that transpiration from
conifers in winter was scarcely greater than
from  the  defoliated stems  of broad-leafed
                                                                              65

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trees.  Apparently  the  conifers are  essen-
tially dormant  in winter and gas  exchange
by the needles  is very low, thus increasing
resistance to toxicants.

          2.   Relative Humidity
  Although  reports of various investigators
do not show good agreement,  susceptibility
of plants to sulfur dioxide generally tends
to increase with increases in relative humid-
ity, providing light and soil moisture are not
limiting." -1 -*4a

             3.  Soil Moisture
  Minor variations in soil moisture  during
exposure  have  no detectable effect on  sus-
ceptibility if there is sufficient moisture for
normal plant  growth.40  When plants ap-
proach the wilting point, resistance increases
significantly. Plants  grown  with  an ample
water supply are much more susceptible than
plants grown with inadequate water.

            4.  Light Intensity
  Plants in complete darkness are highly re-
sistant to sulfur dioxide and the  resistance
decreases as the light intensity is increased
up to  3,000 candles.  Plants  grown in shade
before exposure to the toxicant  are more
susceptible   than  those  grown  in  full
sun.13 2123 40
            5.   Nutrient Supply
  Alfalfa plants grown in a deficient nutri-
ent  supply  were more susceptible to sulfur
dioxide than plants receiving adequate nu-
trients.40
          6.   Age of Plant Tissue
  Young plants and newer foliage are much
more resistant to sulfur dioxide than older
leaves. Middle-aged leaves have highest sus-
ceptibility.40

E.   SYNERGISTIC EFFECTS OF SULFUR
          DIOXIDE AND  OZONE
   Menser  and Heggestad43  demonstrated
synergistic  action  between  sulfur  dioxide
and ozone.  Combinations  of sublethal con-
centrations of sulfur dioxide (0.24 ppm) and
ozone (0.03 ppm)  in two-hour fumigations
produced injury to tobacco plants.  When the
exposure time was  doubled (4 hours), the
                                      severity of response was approximately dou-
                                      bled, but there was no response when  fumi-
                                      gation consisted of either sulfur dioxide  or
                                      ozone alone.  Heck 44 found  moderate to se-
                                      vere injury on tobacco from 4-hour expos-
                                      ures to 0.03 ppm of ozone  in combination
                                      with 0.1 ppm of sulfur dioxide. Middleton
                                      et al}~' reported that the addition  of  small
                                      amounts of sulfur dioxide to polluted atmos-
                                      pheres in the Los Angeles Basin reduced the
                                      amount of injury  produced in plants.  He
                                      also reported  that a ratio of sulfur dioxide
                                      to ozone less than 4:1 made the plants less
                                      susceptible to ozone damage; but if the ra-
                                      tio was 6:1 or higher, there was no evidence
                                      of  interference with  ozone susceptibility.
                                      Studies by Hindawi43 substantiate the syner-
                                      gistic responses reported for ozone and sul-
                                      fur dioxide.  Heck 44 reported  a synergistic
                                      reaction between nitrogen dioxide and sulfur
                                      dioxide.  A 4-hour exposure  to a mixture of
                                      0.1 ppm of nitrogen dioxide and 0.1 ppm of
                                      sulfur dioxide  produced moderate injury to
                                      a sensitive tobacco variety. If there is a
                                      synergistic response between ozone and sul-
                                      fur dioxide or other pollutants, it  offers a
                                      partial explanation for occasional inconsist-
                                      encies between findings  in  the laboratory
                                      with single agents and findings on  plant  re-
                                      sponse in  the  natural environment.

                                       F.  EFFECTS OF SULFURIC ACID  MIST
                                                  ON VEGETATION
                                         Thomas et al.2  discussed  experiments in
                                      which plants  were exposed  to sulfuric acid
                                      mists in concentrations of from 108 mg/m3
                                      to 2160 mg/m3. Sulfuric acid droplets have
                                      settled on dry leaves without causing injury,
                                      but when the leaf surface was wet  a spotted
                                      injury has developed.  Middleton et al.15 and
                                      Thomas 2 reported that this type of injury
                                      occurred in the Los Angeles area during  pe-
                                      riods of heavy air pollution  accompanied by
                                      fog when the surface of the leaf may be wet.
                                      Injury may also occur in the absence  of fog
                                      near combustion effluents containing  sulfur
                                      oxides when the gas affluent dew point per-
                                      mits acid droplet formation.
                                         The sequence of symptom development is
                                      one in  which  the exposed  surface, usually
                                      the upper surface, shows the initial necrosis.
                                      The pH  of the leaf-surface  moisture may be
66

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less than  three.  Cellular collapse in many
small  spots  develops  progressively through
the upper epidermis,  mesophyll,  and lower
epidermis of the leaf, leaving scorched areas.
No glazing  or bleaching accompanies  this
injury, and  leaf areas  covered  by exposed
leaves show no marking. In the Los Angeles
area, swiss chard and beets have shown the
most  typical  injury  (described  above) of
all plant species examined. Alfalfa has also
developed a spotted injury pattern. Spinach
is  more  uniformly wetted by fog and has
shown a more diffuse  type of injury.

              G.   SUMMARY
  Sulfur  dioxide  absorbed  by plants  may
produce  two  types of  visible  leaf injury,
acute  and chronic. Acute injury, which  is
associated  with  high  concentrations  over
relatively short intervals, usually  results in
the injured tissues drying to an ivory color,
but sometimes  they  darken to a reddish-
brown.  Brownish discoloration occurs in the
tips of pine needles, which may be followed
by abscission, while broad-leaved plants and
grasses show necrotic blotching.  Chronic in-
jury,  which  results from lower concentra-
tions over a number of  days or weeks, leads
to a  gradual yellowing  (i.e., chlorosis, in
which the chlorophyll-making mechanism is
impeded)  or  pigmentation of  leaf  tissue.
Generally, for growth and production to be
affected,  visible symptoms of injury, such as
acute lesions,  chronic chlorosis, or excessive
leaf drop, also occur.
  The mechanism by which acute  injury oc-
curs apparently involves  the plant's  ability
to transform  absorbed  sulfur  dioxide  into
sulfuric acid and then into sulfates which are
deposited at the tip  or edges of the  leaf;
with  a  high  rate of absorption, sulfite  is
thought to accumulate, and sulfurous  acid
is  then  formed which subsequently attacks
the cells.  Chronic injury,  on the other hand,
results from the gradual accumulation of ex-
cessive amounts of sulfate in the leaf tissue.
Sulfate formed in the leaf from sulfur diox-
ide absorbed  from the  atmosphere is addi-
tive to sulfate absorbed through  the roots.
Although levels of sulfate in some leaf tis-
sue five to ten times above normal have  been
noted with  no  detectable symptoms of in-
jury,  very high levels cause chronic symp-
toms and  stimulate leaf drop.
  The amount of acute injury caused by sul-
fur dioxide depends on the absorption rate
of the gas, which  is a function of the con-
centration. Thus a given amount of gas ob-
sorbed in  a short period (at a  high concen-
tration)  will  cause more leaf destruction
than if the same  amount  of gas were ab-
sorbed over a longer period (at a lower con-
centration). Mathematical expressions have
been worked out which, for some plant spe-
cies, may  be  used to relate concentration,
time of exposure, and  amount of damage.
Different  varieties of plants vary widely in
their  susceptibility to sulfur dioxide injury.
The threshold  response of alfalfa to acute
injury is  1.25 ppm over one hour, whereas
privet requires  15  times this concentration
for the same  amount of injury to develop.
Some species of trees and shrubs have shown
injury at  exposures of 0.5 ppm  for seven
hours, while injury has  been  produced in
other species at 3-hour sulfur dioxide expo-
sures of 0.54 ppm and, in  still others, at 8-
hour exposures of  0.3 ppm. From such stud-
ies, it appears  that acute symptoms will not
occur if the maximum concentration for the
year  does not exceed 0.3 ppm.   From the
data on the CAMP cities (Chapter 3), an 8-
hour  maximum concentration  of  0.3 ppm
would correspond  to a mean annual concen-
tration of between 0.03 ppm and  0.05 ppm.
  Chronic symptoms and excessive leaf drop
may be produced by long-term exposures to
lower concentrations and have been reported
in locations where the mean annual concen-
tration  is  below about 0.03 ppm.  Because
chronic injury results from the slow build-
up  of sulfate in the tissue, leaf sulfate analy-
ses may  be a useful  index for evaluating
chronic injury.
  The suppression of  growth and yield  us-
ually is  accompanied  by  visible  symptoms
of  injury. A  straight-line relationship, for
example,  has  been found between the yield
of  alfalfa and the total area  destroyed by
acute symptoms or the area covered by the
chlorotic  symptoms.  However,  it  has been
suggested that, in  some cases, sulfur dioxide
might suppress growth and yield without
causing visible injury.  One investigator re-
                                                                              67

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ported that yields of rye grass grown in un-
filtered  air  were  significantly  lower  than
similar plants grown in filtered  air, with no
visible  symptoms in the  plants.  Sulfur  di-
oxide levels in the unfiltered air ranged from
0.01 ppm to 0.06 ppm with exposure  periods
ranging from 46 to 81 days, although it is
not known whether other gaseous pollutants
were present.
  Sensitivity of plant materials is affected
significantly  by such  environmental  condi-
tions as temperature, relative humidity, soil
moisture,  light  intensity,  nutrient level, and
by  sulfate content of the soil and irrigation
water.  At locations in the vicinity of  point
sources  of sulfur dioxide, high concentra-
tions occur with greater frequency and dam-
age to plants is more likely to  occur. Plant
damage has been noted as much as 52 miles
downwind from a smelting operation which
emitted large  quantities  of  sulfur dioxide.
Slight-to-severe  injury was  reported  to  at
least 15 tree species, including  both conifers
and hardwoods, in the vicinity of petroleum
refineries  where concentrations  exceeded 0.5
ppm during 10 hours in  one  month with
momentary  peaks as high as  2 ppm.  ft,  f
  Sulfur  dioxide  concentrations  from  0.05-
to  0.25  ppm will react synergistically with
either  ozone  or  nitrogen  dioxide in  short
term exposures (e.g., 4  hours)  to produce
moderate-to-severe  injury  on certain sensi-
tive plants.
  Sulfuric acid mist, which may occur in
polluted fogs and mists, also damages leaves.
The acid  droplets cause a spotted injury to
leaves which are wet due to fog conditions.
Such injury may occur at concentrations of
0.1 mg/m3.

             H.   REFERENCES
  1.  Thomas, M. D.  "Gas Damage to Plants." Ann.
    Rev. Plant Physiol., Vol. 2, pp. 293-322, 1951.
  2.  Thomas, M. D., Hendricks, R.  H., and Hill, G. R.
    "Some  Impurities in the  Air  and Their Effects
    on  Plants."  In:  Air Pollution,  L.  C.  McCabe
    (ed.), McGraw-Hill, New York,  1952, pp. 41-47.
  3.  Thomas, M. D. and Hendricks, R. H. "Effect of
    Air Pollutants on  Plants."  In:  Air  Pollution
    Handbook, McGraw-Hill,  New York, 1956.
  4.  Thomas, M.   D.  "Effects of  Air Pollution on
    Plants." In:  Air Pollution, W. H. 0. Monograph
    Series  46, Columbia  Univ.  Press,  New York,
    1961, pp.  233-275.
 5. Sheffer,  T. C. and Hedgcock, G. G. "Injury to
   Northwestern Forest  Trees by Sulfur Dioxide
   from Smelters."  U.S.  Dept. Agri., Forest Ser-
   vice, Tech. Bull. 1117,  1955.
 6. Brandt,  C. S. and Heck, W. W. "Effects of Air
   Pollutants on Vegetation."  In:  Air  Pollution,
   2nd edition, Vol. I, A.  C. Stern (ed.),  Academic
   Press, New York-London, 1968, pp. 401-443.
 7. Katz, M. and McCallum, A. W.  "The Effect of
   Sulfur   Dioxide on  Conifers." In: Air  Pollu-
   tion, Chapt.  8, L. C.  McCabe  (ed.),  1952, pp.
   84-96.
 8. Daines,  R.  H. "Sulfur Dioxide  and  Plant Re-
   sponse."  Preprint.   (Presented  at Symposium
   on  Air  Quality  Criteria,  New  York, June 5,
   1968.)
 9. Wood, F. A.  J. Occup. Med., Vol. 10, pp. 92-102,
   1962.  (Discussion at Symposium on Air Quality
   Criteria, New York, June 4-5, 1968.)
10. Altaian, P. L. and Dittner, D.  S. (eds.)  "En-
   vironmental  Biology  (Biological  Handbooks)."
   Federation  of American  Societies for Experi-
   mental  Biology,  Bethesda, Maryland,  1966, p.
   315.
11. Katz, M. "Sulfur Dioxide in the Atmosphere and
   its  Relation  to  Plant  Life."   Ind. Eng. Chem.,
   Vol. 41,  pp. 2450-2465,  1949.
12. Holmes, J. A., Franklin,  E. C., and Gould, R. A.
   "Selby Report." U.S. Bureau of Mines, Bulletin
   98, 1915.
13. Solberg, R. A. and Adams, D. F.  "Histological
   Response of  Some Plant  Leaves  to  Hydrogen
   Fluoride and Sulfur Dioxide."  Amer. J. Bot.,
   Vol. 43, pp.  755-760,  1956.
14. Thomas, M. D., Hendricks,  R. H., and Hill, G. R.
   "Sulfur Metabolism  of Plants: Effect of Sulfur
   Dioxide  on  Vegetation."  Ind.   Eng.  Chem.,
   42(11) :2231-2235, 1950.
15. Middleton, J.  T., Darley, E. F., and Brewer, R. F.
   "Damage  to  Vegetation from  Polluted Atmos-
   pheres." J. Air Pollution Control Assoc., Vol. 8,
   pp. 9-15, 1958.
16. Thomas, M. D. and Hill, G. R. "Relation of Sul-
   fur Dioxide in the Atmosphere to Photosynthesis
   and Respiration of  Alfalfa."  Plant Physiol.,
   Vol. 12, pp.  309-383, 1937.
17. Brennan, L.  and Daines, R. H. "Investigation of
   S0< Effects on Rubber Trees as a Means of Fore-
   stalling  Injury  to  Malayan  Plantations  from
   Refinery Emissions."  J.  Air  Pollution Control
   Assoc., Vol. 14, pp. 229-233, 1964.
18. Massey,  L.  M.  "Similarities Between  Disease
   Symptoms  and  Chemically Induced  Injury to
   Plants." In:  Air Pollution, Chapt. 3, L. C. Mc-
   Cabe, (ed.),  McGraw-Hill, New  York, 1952, pp.
   48-58.
19. "Plants Absorb Sulfur Dioxide, Release Hydro-
   gen Sulfide." Sulfur Institute J., 4(2) :17, 1968.
20. Stoklasa, J.   "Die Beschadigung der Vegetation
   durch   Rauchgase   und   Fabriksexhalationen."
   Urban und Schwartzenberg, Berlin, 1923.
       68

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21.  Setterstrom, C.  "Effects of Sulfur  Dioxide  on
    Plants and  Animals." Ind.  Eng. Chem., Vol. 32,
    pp. 473-479, 1940.
22.  Swain, K. E. and Johnson, A. B. "Effect of Sul-
    fur Dioxide on Wheat Development; Action at
    Low  Concentration."  Ind.  Eng. Chem.,  28(1) :
    42-47, 1936.
23.  Wells, A. E.  "Results of Recent Investigations
    of  the  Smelter Smoke  Problem."   Ind.  Eng.
    Chem., Vol. 9, pp. 640-646, 1917.
24.  Zimmerman, P. W.  "Chemicals Involved in Air
    Pollution and  their  Effects  upon Vegetation."
    Professional Papers,  Boyce Thompson Institute,
    New  York  2(14) : 124-145,  1955.
25.  Thomas, M. D. and  Hill, G. R. "Adsorption of
    Sulfur  Dioxide by Alfalfa and its  Relation to
    Leaf Injury."  Plant Physiol., Vol. 10, pp. 291-
    307, 1935.
26.  "Effects of Sulfur  Dioxide  on Vegetation."  Na-
    tional Research Council of Canada, Ottawa, Pub.
    815, 1939, p. 447.
27.  Whitby, G. S.  "The Effects of Sulfur Dioxide on
    Vegetation." Chem. Ind., Vol. 58, p. 99, 1939.
28.  Matushima, J. and Horada, M. "Sulfur Dioxide
    Gas Injury to Fruit Trees.  V. Absorption of Sul-
    fur Dioxide by Citrus  Trees and its Relation to
    Leaf Fall and Mineral Contents  of Leaves." J.
    Soc. Hort. Sci. (Tokyo), 35(3) :241-246, 1966.
29.  Bleasdale, J. K.  A.   "Atmospheric Pollution and
    Plant Growth."  Nature, Vol. 169, p. 376, 1952.
30.  Haselhoff, E. and Lindau, G. "Die Beschadigung
    der Vegetation durch Rauch."  Verlagsbuchhand-
    lung Gebrueder Borntraeger,  Leipzig, 1903, p.
    412.
31.  Dorries, W. "Uber die Brauchbarkeit der spec-
    troscopischen  Phaophytinprobe in der  Rauch-
    schaden-Diagnostik."  Z.  Pflanzenkrankheiten u.
    Gallenkunde, Vol. 42, pp. 257-273, 1932.
32. Noack, K.  "Damage  to Vegetation from Gases in
    Smoke." Z. Angew.  Chem.,  Vol. 42, pp. 123-
    126,  1929.
33.  O'Gara, P. J.  Ind.  Eng. Chem., Vol. 14, p. 744,
    1922.
34.  Guderian, R., von Haut, H., and Stratman, H. Z.
    Pflanzenkrankh.  Pflanzenschutz,  Vol. 67, p.  257,
    1960.  (Quoted in ref. 6, p. 421.)
35.  Spierings, F. "Method for Determining the Sus-
    ceptibility of Trees to Air Pollution by Artificial
    Fumigation."  Atmos. Environ., Vol. 1,  pp. 205-
    210, 1967.
36.  Linzon, S. N.  "The Influence of Smelter Fumes
    on the Growth of White Pine in the Sudbury Re-
    gion." Ontario Dept. of Lands and Forest, On-
    tario Dept.  of Mines, Toronto, 1958, pp. 1-45.
37.  Sullivan, J.  L.  "The Nature and Extent of Pol-
    lution by Metallurgical  Industries in Port Kem-
    bla."  In: Air Pollution by Metallurgical Indus-
    tries,  Dept.  of Public Health, Div.  of Occupa-
    tional Health,  Sydney,  Australia, Vol. 1, pp.
    1-59,  1962.
38.  Linzon, S. N. "Sulfur Dioxide Injury to Trees in
    the Vicinity of Petroleum  Refineries." Forest
    Chronicle, Vol. 41, pp. 245-250, 1965.
39.  Berry, C. R. and Hepting, G. H. "Injury to East-
    ern White Pine by Unidentified Atmospheric Con-
    taminants."  Forest Sci., Vol. 10, pp. 2-13,  1964.
40.  Setterstrom, C. and Zimmerman, P. W.  "Factors
    Influencing Susceptibility of Plants to Sulfur Di-
    oxide  Injury."  Boyce Thompson Institute, New
    York, Vol. 10, pp. 155-181, 1939.
41.  Swain, R. E.  "Atmospheric Pollution  by Indus-
    trial  Wastes." Ind.  Eng. Chem.,  Vol. 15, pp.
    296-301, 1923.
42.  Weaver,  J.  E.  and  Morgenson,  A.   "Relative
    Transpiration of Coniferous  and Broad-Leafed
    Trees in Autumn and Winter."  Bot. Gaz., Vol.
    68, pp. 393-424, 1919.
43.  Menser, H.  A. and Heggestad, H. E.  "Ozone and
    Sulfur Dioxide  Synergism:  Injury to Tobacco
    Plants."  Science, Vol. 153, pp. 424-425, 1966.
44.  Heck, W.  W.  "Discussion  of  O. C.  Taylor's
    Paper:  Effects of  Oxidant Air Pollutants."  J.
    Occup. Med., Vol. 10, pp. 497-499, 1968.
45.  Hindawi, I. J. "The Effects  of  Sulfur Dioxide
    on  Vegetation  Grown in the Washington,  D.C.
    Metropolitan Area." Preprint.  (Presented at the
    Washington, D.C. Area Air Pollution Abatement
    Activity Conference, Dec. 13, 1967.)
                                                                                             69

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               Chapter 6
TOXICOLOGICAL EFFECTS OF SULFUR OXIDES
              ON ANIMALS

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                       Table of Contents
A. INTRODUCTION                                       .      73
B. EVALUATION BY MORTALITY AND PATHOLOGY         .      73
   1. Sulfur Dioxide Exposure               .  .                     73
   2. Sulfuric Acid Aerosol                              .          75
C. EVALUATION BY PULMONARY FUNCTION                     76
   1. Sulfur Dioxide Exposure                                 . .    76
   2. Mechanism of Response                              ...      79
   3. Sulfuric Acid and Particulate Sulfate Exposures       	    80
D. EFFECTS OF SULFUR DIOXIDE ON CILIARY ACTION           81
E. LIFETIME EXPOSURE OF ANIMALS TO SULFUR DIOXIDE        82
F. ABSORPTION AND DISTRIBUTION OF SULFUR DIOXIDE         82
G. MISCELLANEOUS BIOCHEMICAL EFFECTS OF SULFUR
   DIOXIDE                   .                 .     .       .    84
H. SUMMARY                               .      ....         84
 I. REFERENCES                               	    85
 72

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                                     Chapter 6

       TOXICOLOGICAL  EFFECTS  OF SULFUR OXIDES  ON  ANIMALS
          A.   INTRODUCTION
  The  toxicology of  oxides of sulfur  is re-
viewed in Chapters 6 to 8 of this document.
Unfortunately,  published data generally re-
fer to concentrations far in excess of those
likely to be  found in polluted atmospheres,
and  therefore have  little relevance to  cri-
teria for atmospheric pollutants. Even where
the animal studies are carried out at more
realistic levels,  it is  certain that the health
hazard associated  with  community air  pol-
lution can only be evaluated directly in  epi-
demiologic terms (chapter 9).  Nevertheless,
toxicological  experiments  do  indicate  the
kinds of physiological  and pathological re-
sponse of which animals and man are ca-
pable.  Studies  have  been chosen for review
in Chapters  6 to 8 on the basis of their pos-
sible relevance to air pollution problems, and
the  chapters are not comprehensive  treat-
ments of sulfur oxide toxicology.
  While unreliable conversions and extrap-
olations  are  necessary  in  assessing health
effects  on man from  toxicological experi-
ments  on  animals,  such  experiments do,
however, permit the use of higher concen-
trations, longer exposure times, larger num-
bers of subjects, surgical procedures,  post-
mortem examinations, and other liberties not
open to the experimenter with human sub-
jects.  Since  man  is an animal, the results
of  such animal experiments should  have
some relation to man, even though it is only
qualitative.   Therefore, this  chapter deals
with the toxicology  of the oxides of sulfur
in animals.
  Methods of evaluation include challenging
animals with the pollutant  or pollutant com-
binations and  examining mortality  and
changes in lung function that precede irre-
versible pathology. Absorption, distribution,
and retention of sulfur oxides have also been
examined, as have biochemical change and
ciliary response in the organism. The effects
of oxides of sulfur on animals have been re-
viewed by Setterstrom 1  and by Negherbon.2

B.   EVALUATION BY  MORTALITY AND
              PATHOLOGY
       1.  Sulfur Dioxide Exposure
  The response of various species including
guinea pigs,  mice, grasshoppers, and cock-
roaches to sulfur dioxide13 4 5 has been stud-
ied.  Concentrations  from 10  ppm to 1,000
ppm  (~30 mg/m3 to 30,000  mg/m3) were
monitored and duplicate chambers were used
for control animals.6 Exposures were con-
tinuous up to the time of death of 50 percent
of the animals or until no progressive symp-
toms appeared after  a considerable time. At
concentrations of 25 ppm (~72 mg/m3) no
mortality was produced by treatment up to
about 45  days. At concentrations of 150 ppm
(430 mg/m3) and below, mice were more re-
sistant than guinea pigs. For example, it re-
quired 847 hours to kill 50  percent of the
mice at 150 ppm, whereas 50 percent of the
guinea pigs  exposed to  130  ppm  (~370
mg/m3)  died in  154 hours.  At concentra-
tions  of  300 ppm (~860 mg/m3) to 1,000
ppm mice were less resistant than  guinea
pigs.  At levels  of around 1,000 ppm,  50 per-
cent of the mice died in about 4 hours where-
as about 20 hours were needed to kill guinea
pigs.  The susceptibility of  the  two  insect
species approximated that of the mice.  It
is thus apparent that  extrapolations from
high to lower concentrations  of such param-
eters as species sensitivity are frequently not
reliable.
  No significant  mortality or signs  of dis-
tress  were noted  among healthy animals ex-
                                                                             73

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posed  to  concentrations  of 33  ppm  (94
mg/m3)  or below.  Longer  exposure was
needed to cause mortality when the exposures
were  intermittent.  Exercise  increased sus-
ceptibility of guinea pigs exposed to 1,000
ppm but had no effect  at lower concentra-
tions.
  Symptoms produced by the higher concen-
trations included coughing,  moderate dysp-
nea,  rhinitis,  lachrymation,  conjuctivitis,
abdominal  distension,   lethargy,  weakness,
and paralysis of the hind quarters.  Patho-
logic  changes included  slight to  moderate
visceral congestion, slight to moderate pul-
monary edema,  and distension of the gall
bladder and stomach.  Higher concentrations
produced hemorrhages of lungs and stomach
and acute dilation of the right heart.
  The mean survival time of mice, guinea
pigs,  and rats was measured as  a means of
evaluating the  effect of pretreatment with
histamine,  or of adrenalectomy,  on the tox-
icity  of sulfur  dioxide.7  Concentrations in
the range of 600 ppm  to 5,000  ppm (1700
mg/mH  to  14,000 mg/ms) were  used, pre-
sumably because it was the aim to kill nor-
mal animals within a  convenient time  in-
terval.  For normal animals the susceptibil-
ity was highest in mice, intermediate  in
guinea pigs and least in  rats.  At the con-
centrations  used in these experiments the
relative  susceptibility of mice and guinea
pigs  is in  agreement with the earlier data
of Weeden  et «/." mentioned above.  Hista-
mine given by  intraperitoneal injection at
levels of  200 mg/kg of  animal  weight 10
minutes  before  exposure  significantly  de-
creased the survival time of rats  and mice.
Adrenalectomy in rats also reduced survival
time.
  The extent of changes  in  lung  pathology
and the amount of fluid in  the alveoli were
primarily dependent upon the exposure time.
In  normal  animals, pulmonary edema  and
areas of consolidation were usually observed,
while animals whose survival time had been
reduced by pretreatment, exhibited bronchial
obstruction.  Two mechanisms of death were
observed in guinea pigs.  A portion  of each
test group  succumbed  rapidly when intro-
duced into  the  sulfur  dioxide atmosphere.
Occlusion of the bronchioles and venous con-
gestion with  little or no fluid in the alveoli
were  the  pathological  changes observed in
these animals.   Those animals which sur-
vived 2 to 4 hours showed fluid in the alveoli,
distended  bronchioles and partially desqua-
mated mucosal membranes.
  Goldring et al.9  reported that 10,000 ppm
(29.000 mg/mj) produced 100 percent mor-
tality of Syrian hamsters within 8 to 10 min-
utes.  Exposures to 3,250 ppm (9,300 mg/m3)
for periods up to 1 '/•> hours produced 50 per-
cent mortality within  24 hours.  Exposures
of 650 ppm (1,850 mg/ms)  for 75  days did
not  produce  significant  histopathological
changes in the  pulmonary tree of hamsters.
Sodium chloride aerosol  was also present in
all exposures. (See Chapter 8 and Air Qual-
ity  Criteria for Particulate Matter, a com-
panion document,  for a discussion of syner-
gistic effects.)
  A limited  number of  swine was exposed
to 5,  10, 20,  and 40 ppm (about  14, 29, 57,
and 114 mg/nr') sulfur dioxide for 8 hours.10
Symptoms at 5  ppm  were limited  to slight
eye  irritation  and  excess  salivation.  At
higher concentrations  there was excess sali-
vation, excess nasal secretion and shallower,
more rapid  respiration  during the first  4
hours, after which  the symptoms abated.
Twenty-four hours after exposure the lungs
showed hemorrhage and emphysema.  The
changes were less marked in animals  killed
a week after exposure. Two animals exposed
to 40 ppm  and one  animal exposed  to 20
ppm, which  were killed 160 days after ex-
posure,  showed  some  areas of fibrosis, and
the lungs were a  darker color and  less well
inflated than in normal animals.
  Reid "  attempted to produce hypertrophy
of the goblet cells and  mucous glands of rats
which would simulate  chronic  bronchitis.
Initially,  animals were  exposed  5  hours  a
day, 5 days a week, to about 40 ppm sulfur
dioxide.  Since no great change  was found
in the lungs after 3 months, the dose was
increased to 300 ppm to  400 ppm  (about 900
mg/m3 to 1,100 mg/m3), in order to produce
the desired  changes.  There followed an in-
crease in the number of mucus-secreting cells
both in the main bronchi, where  goblet cells
are  normally frequent,  and  in the fine pe-
ripheral airways from which they are nor-
       74

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mally absent.  Excessive mucus was seen in
the bronchial lumen,  probably reflecting an
increased  number of mucus-secreting-  cells
as well as greater secretory  activity, asso-
ciated  with reduced ciliary activity leading
to retention. The changes apparently were
not mediated through  infection, as pathogens
were not more frequently found in the bron-
chi and lungs of animals exposed to the ir-
ritant than in the controls.  Although infec-
tion may act as an irritant, these experiments
indicate that it is by  no means an essential
factor  in  the development of  excessive mu-
cous cells  characteristic of  chronic bron-
chitis.
  In one experiment,  the reaction was great
in all but 2 animals, whereas  in another ex-
periment  only half the  animals  responded.
At  the  time of  the diminished  responsive-
ness, however, the supplier had made an at-
tempt  to   breed  a strain of animals  less
susceptible to bronchiectasis.  It is likely that
there is considerable  difference  in  response
between strains.
  The excess of goblet cells persisted for at
least 3  months  after exposure to  the  irri-
tant had ceased,  even in the  absence of in-
fection. Most of the goblet  cells were dis-
tended with secretion, suggesting that  they
discharged  less mucus than  during the ex-
posure.  The cessation of irritant  exposure
seemed to arrest the increase in cells.
  Dalhamn 1- studied  the morphology of tra-
cheal mucosa in rats following exposures for
periods of 18 to 67 days to about  10  ppm
(about 30 mg/m-1) sulfur dioxide.  Exposures
were 6 hours a day for  5 days a week, and
3 hours on Saturday;  there was no exposure
on Sunday.
  Severe  morphologic changes  of the epi-
thelium and lamina propria were observed.
The epithelial  surface  was  irregular  with
deep crypts, probably produced by cell pro-
liferation.  Since  the cilia lining these crypts
could not contribute to  transport of mucus,
such changes were a probable cause of ob-
served retarded  mucus  flow.  The  changes
were present at 18 days as well as at 67 days,
and they  had not regressed  4 weeks after
exposure  in six  animals examined at  that
time.  Support is  thus lent to Reid's finding "
of slow reversibility.  There  was  no alter-
ation of the  ciliary  ultrastructure although
the  surrounding  tissues  including  ciliary
cells showed severe changes. There was more
mucus in the trachea of exposed animals.  In
healthy rats  the mucus blanket was  about
5-/x thick and the secretion contained only a
few cellular  elements.  After sulfur dioxide
exposure  the mucus blanket  was  20-/x  to
25-/x thick and  the secretion  appeared more
compact and contained  numerous elements
such  as shed  cells  and  white blood cells.
Since the trachea is  the main site  of absorp-
tion of  sulfur dioxide these changes are not
surprising at 10 ppm.

         2.   Sulfurie Acid Aero*ol
  Treon ct «/." exposed rabbits, rats, mice,
and guinea  pigs  to sulfuric  acid  mist  of
which 95 percent was below 2 /*. Only a few
animals were used in the exposures, and the
concentrations  were at  levels of 87 to 1,600
mg/m'; nevertheless, a  clear-cut species dif-
ference emerged.  The  order of  increasing
sensitivity was:  rabbits, rats,  mice, and
guinea  pigs.  Mathur and Olmstread " also
found that mice were much more resistant
than guinea pigs.
  Amdur et  alS'' found  the 8-hour LCr>l,  of
sulfuric acid  (MMD I-//,) to be  18 mg/m'! for
one- to two-month-old  guinea  pigs and  50
mg/m'  for 18-month-old  animals.  Pattle et
flZ.1" determined the 8-hour LC.-)()  for  200 g
to 250 g guinea pigs exposed to sulfuric acid
of two particle  sizes, MMD 2.7-fi  and  MMD
0.8-y*. The LC,(, was 27 mg/m'1 for the large
particles and 60 nag/m"1 for the small  parti-
cles.  At 0°  C  with  0.8-/* particles the LC,-)(,
was 47 mg/m3, a value significantly different
from that at room temperature. The guinea
pig is a tropical animal  and the  difference
in effect is considered a direct action of cold
on the animals. Ammonium carbonate suffi-
cient to provide an excess of ammonia in the
chamber gave protection  from  levels of sul-
furic acid which, in the absence of ammonia,
would have caused 50 percent mortality, em-
phasizing that  the  toxicity is  related  to
acidity.
  The pathological findings were  similar in
the two investigations.  Animals dying after
short exposure (less than 2  hours)  show
grossly distended and emphysematous lungs
                                                                              75

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with no  other  serious lesions."1  The cause
of death in these animals  appeared to be
asphyxia caused by bronchoconstriction and
laryngeal spasm.  Animals dying- after longer
exposures showed gross pathological lesions
including capillary engorgement and hemor-
rhage.1' "' It is suggested that these obser-
vations were mainly sequelae of the com-
bined effects of anoxia and  increased intra-
thoracic pressure caused by bronchoconstric-
tion  and laryngeal  spasm."1  That animals
succumbing quickly show a pathology differ-
ent from those surviving longer exposures
is similar to the findings of Leong ct 
-------
The methods employed in all these studies
are documented in the original paper deal-
ing- with  sulfur  dioxide -" and  in a paper
dealing- with physiological methods of mea-
surement.^  The  method has the advantage
that the animal is unanesthetized and breath-
ing- spontaneously. The information obtained
in these experiments is,  however,  limited in
comparison  with studies of  irritant action
using anesthetized larger species. The meth-
od  is  suitable  for routine daily  use by  a
carefully  trained  technician,  and data on
numbers of animals exposed only once to  a
specific irritant can readily be obtained. This
eliminates the need for  re-exposure follow-
ing "recovery" which is necessary in com-
plicated physiological  experiments.
  Amdur and her co-workers used a stand-
ard exposure time of 1  hour;  thus the  ap-
plicability to air  pollution  criteria would be
in  connection with the possible  effects of
short-term peak  values.  Although the ani-
mals were unanesthetized during the control
and exposure periods,  an intrapleural cathe-
ter was used, and this was put  in place with
the animals  under  light  ether anesthesia.
Mead -- used another method which measured
flow resistance without the need for an intra-
pleural catheter to measure the resistance of
guinea pigs before and after intubation,  and
found that the  procedure had caused an in-
crease.  It was  not determined  whether this
increase was caused by the presence of  the
catheter or by the recent exposure to ether.
  The method yields information on pulmo-
nary flow-resistance and compliance (a mea-
sure of the elastic behavior of the lungs),-°  -3
as  well as  tidal  volume, respiratory fre-
quency, and  minute volume.  One-hour  ex-
posures produced statistically significant in-
creases in resistance ranging from about 10
percent at 0.16 ppm (460 /xg/m3)  to about
265 percent at 835 ppm  (2,390 mg/m3).24
For most normal  human subjects, an  in-
crease in  resistance of 300 percent or  less
would  have no marked physiological conse-
quences.
  After exposure was terminated,  resistance
decreased and  at  concentrations up to  100
ppm (~290 mg/m3) it  returned  to pre-ex-
posure levels in the course of an  hour.  Re-
sistance was back  to normal 2 hours after
exposure to 300 ppm (860 mg/m1).-''  A de-
crease in  respiratory  frequency  was  ob-
served, and it became statistically significant
at concentrations above 25 ppm.
  The pattern of response produced by sul-
fur dioxide is typical -'  of  the response  of
the guinea  pig  to  a group of respiratory
irritants which  includes acetic acid,  form-
aldehyde,   and  droplets  of  sulfuric  acid
smaller than 1/x. At levels  of 2 ppm (~6
mg/m1 to 14 mg/m'), the other irritants all
evoked a  greater response  than did sulfur
dioxide.  For this  group  of  irritants,  in-
creased flow  resistance is the most sensitive
indicator of response.
  Pulmonary  edema is  a  relatively minor
factor in the pathology of sulfur dioxide and
similar  irritants (although  it is important
for ozone and oxides of nitrogen) .-'•  The pat-
terns of pathological response may relate to
the ability of the irritant to penetrate  to pe-
ripheral areas of the lung. Penetration is an
important factor, but is  not the only expla-
nation, since irritant aerosols, of a size ex-
pected to penetrate readily, produced the pat-
tern  typified  by sulfur dioxide and  alde-
hydes.-7
  Amdur  and her co-workers also measured
the response of guinea pigs breathing irri-
tants through a tracheal cannula.-" -3 24 The
response to a given concentration of sulfur
dioxide was  greater  when the gas  reached
the lungs  through a tracheal cannula at con-
centrations of 2 ppm (~6 mg/m3) and above.
At  concentrations near 0.4  ppm to 0.5 ppm
(1.1 mg/m3 to 1.4 mg/mj)  the response was
not altered by  the  tracheal cannula.  This
supports the data of Strandburg -s indicating
that low concentrations of sulfur dioxide are
not efficiently removed by the upper respira-
tory tract.
  Exposures of guinea pigs breathing nor-
mally and via a tracheal cannula to sulfur
dioxide at 5 ppm  to  10  ppm  (about 14
mg/m3 to 29 mg/m3) are reported  by  Davis
et al.-s  Exposures  of normal animals pro-
duced increases  in  resistance and tidal vol-
ume and  decreases in respiratory  rate and
minute volume.  Insufficient data  are  given
to evaluate the  specific  effects of  the irri-
tant.  There were no changes in respiratory
function in animals exposed via tracheal can-
                                                                              11

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nula.  Such  animals did,  however,  respond
with a resistance  increase to inhalation of
histamine aerosol.  The authors conclude that
sulfur  dioxide is without  effect on the lung
and the entire response seen in normal ani-
mals is due to  an increase in resistance of
the upper airways.
  This  interpretation may  be questioned
since the pulmonary function tracings show
evidence of  technical  errors where flow and
volume appear completely out of phase with
the pressure tracing.  The results are not in
agreement with those of Amdur and Mead -"
and of Amdur Ji obtained on guinea pigs, nor
with the  results  discussed below for  other
species.
  Balchum  et  al."'-'"  exposed  anesthetized
dogs to sulfur  dioxide by nose and  mouth
breathing and by  means of a tracheal can-
nula.   Concentrations  ranged from  around
1 ppm to around 140  ppm (about 3 mg/m'1
to 400 mg/nr1), and  exposure periods were
20 minutes  to  40 minutes.  The dogs were
not breathing spontaneously,  but were venti-
lated at constant stroke volume following a
dose of  intravenous  nembutal sufficient to
stop spontaneous  respiration.  This  repre-
sents  an unusually deep  level of anesthesia.
A decrease  in  compliance and an  increase
in resistance was found at all concentrations
used.   These alterations were also produced
when  only  an  isolated segment of  trachea
was exposed to sulfur dioxide.5" The resist-
ance change was greatest in animals breath-
ing via a tracheal  cannula, intermediate in
those nose-breathing,  and least in those dogs
in which  only  a  tracheal segment  was ex-
posed. The  compliance changes, on the other
hand, were  of the same order of magnitude
in all  cases. The compliance changes were
possibly caused by some extraneous  influ-
ence and  not by  sulfur dioxide, since spon-
taneous compliance decreases are a common
phenomenon in dogs lying on their backs dur-
ing prolonged  physiological experiments.14
   Salem  and  Aviado '<•• ventilated  dogs by
pump  through  a  tracheal cannula  and mea-
sured  the "dynamic" pressure-volume char-
200 ppm. to 850 ppm (570 mg/m1  to 2400
mg/nr1)  sulfur dioxide for periods  of 1 to
4  minutes.  The  changes that  ensued were
acteristics of the lungs during exposures of
consistent with bronchoconstriction preceded
and  followed by  bronchodilation.   These
changes were interpreted as protective meas-
ures leading to a  reduction in the amount of
sulfur  dioxide absorbed  via the pulmonary
circulation.  They also observed pulmonary
vasoconstriction,  increase in pulmonary ar-
terial blood pressure, a depression of myo-
cardial force of contraction accompanied by
brachycardia, and systemic shock.
  Yokoyama and  Ishikawa '"'  measured the
effect of sulfur  dioxide  on  the mechanical
behavior of the lungs of dogs  exposed to 50
ppm  to  350  ppm  (140 mg/m3  to  1,000
mg/m1) via a tracheal cannula. There was
consistent increase, occasionally as much as
tenfold, in flow  resistance.  There were no
consistent changes in pulmonary compliance.
  Frank and  Speizer !7 compared  the func-
tional response of several levels of the res-
piratory system  to  inhaled sulfur dioxide.
Dogs were lightly anesthetized and exposed
by nose, by tracheal cannula, and by an iso-
lated segment of trachea.  Concentrations
ranged from 7 ppm to 230 ppm (20 mg/m3
to 660 mg/m1), and routine exposures were
for 15 minutes. Intervals of at least 20 min-
utes were allowed between exposures, and
no animal was exposed more  than 4 times.
In eight animals  exposed by nose the nasal
resistance was measured.  At levels of 7 ppm
to 61 ppm  (175 mg/m:)), the nasal resistance
increased in a manner roughly proportional
to the concentration, and at concentrations
above 25 ppm (about 70 mg/m:i)  it became
progressively greater with  duration  of  ex-
posure. One animal showed a Deduction in
nasal resistance in the first 2  exposures and
an increase in the second 2 exposures. Dur-
ing  recovery, which lasted 15 to 40 min-
utes, the  values  reverted partially or com-
pletely to control values. The authors specu-
late that  these   changes  probably  reflect
mucosal swelling, increased secretion  of mu-
cus  or  both.  The resistance  of the  larynx
appeared to rise and fall about an equal num-
ber  of times during exposure and recovery.
A significant change in one direction or the
other occurred in about 45 percent  of  the
observations.  During nose-breathing  the re-
sistance of the lungs rose and fell about an
equal number of times  and  the direction of
       78

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change  was not related to concentration of
gas nor to duration of exposure.  About one-
third of these changes were  considered sta-
tistically significant.  Significant  changes in
either direction occurred more frequently at
higher concentrations. During recovery the
lung resistance tended to increase above con-
trol  levels.  Compliance was only  slightly
lower during  exposure.  Minute  ventilation
fell owing to  slight reduction in both tidal
volume  and  respiratory frequency.
  When exposure was by tracheal cannula,
pulmonary  flow   resistance   rose   rapidly,
reaching a peak within several minutes, and
then decreased. Limiting the  exposure to the
larynx and upper trachea produced  a much
less pronounced increase in lung resistance.

        2.  Mechanism of Response
  Basic information on the mechanism of re-
sponse to  irritants is important in the com-
plex task  of assessing the irritant potential
of air pollution.   This is the realm of  the
physiologist, who  may, for example, experi-
ment with the effects of an irritant material
on nerve  fibers, or with the specific block-
ing effect of drugs.  Exposures are usually
brief, sometimes  only a  single breath, and
quite frequently   the  concentration  is  not
specified, but can be assumed to be very high.
  Widdicombe 38 studied, in cats, the cough
reflex  elicited  by  mechanical stimulation,
powdered  talc or  starch,  and sulfur  dioxide.
He  found that sulfur dioxide  elicited  the
cough reflex when given  through an endo-
bronchial  catheter so that the gas came in
contact only with the lungs and smaller bron-
chi, and not with  the trachea and extrapul-
monary bronchi.  The cough reflex produced
in this way was always stronger than when
the gas  was applied to the trachea and main
bronchi alone.  After several inhalations  of
sulfur dioxide the cats  became  completely
refractory to  the  gas but  gave  normal re-
sponses to mechanical stimulation   of  the
trachea.  This result  suggested that the re-
ceptors  sensitive to mechanical stimuli were
not being  stimulated by sulfur dioxide. Fur-
ther evidence  that the two receptors were
distinct was provided by the fact that  pro-
caine solution sprayed  into  the  trachea
blocked the mechanical cough reflex  but did
not affect the response to sulfur dioxide.
  Widdicombe 39 also made a systematic ex-
amination of different nerve endings in the
tracheobronchial  tree.  One hundred single
vagal fibers, which were excited by inflation
of the lungs, were dissected, and the response
was  studied under various conditions.  One
group of these fibers was first sensitized, then
inhibited, by sulfur dioxide. This particular
group  of fibers was distributed  throughout
the lower trachea  and main  bronchi.  The
responses of these fibers were  not inhibited
by procaine; this results parallels the obser-
vation  that the cough reflex  elicited by sul-
fur dioxide is not inhibited by procaine.24
Another group of fibers was sensitive to me-
chanical stimuli but insensitive to sulfur di-
oxide;  this sensitivity parallels the finding24
that the mechanical  cough reflex was still
present in animals  rendered  refractory  to
sulfur  dioxide. Vagal temperatures  of 7° C
to 10°  C blocked the fibers sensitive to sulfur
dioxide.  As with mechanical stimuli, sulfur
dioxide acts via the sympathetic nervous sys-
tem  as well  as  the vagus nerves, and the
group of fibers sensitive to  sulfur dioxide has
been shown to connect with the sympathetic
trunk.
  The   mechanism  of  bronchoconstriction
produced by sulfur dioxide in  cats was also
examined.40  The animals were  anesthetized,
the respiratory muscles were paralyzed with
gallamine triethiodide, and the  animals were
ventilated with a pump  via a  tracheal  can-
nula.   Sulfur  dioxide  was delivered either
to the  lungs or to the upper airways. Total
pulmonary resistance was measured.  Sulfur
dioxide delivered to the lower  airways and
lungs  during  a single inflation  cycle  pro-
duced an increase in resistance which began
during  the first breath  after exposure and
returned to control levels  within 1  minute.
Exposing only the  upper airways also  pro-
duced  a resistance increase.   During  cool-
ing of the cervical vagosympathetic nerves
the response was abolished whether the sul-
fur dioxide was delivered  to the lung or to
the upper airways. After rewarming of the
nerves, the response was re-established.  The
response was also abolished by the intra-
venous  injection of atropine.   The rapidity
of the response and its reversal  suggests that
                                                                              79

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changes in smooth muscle tone are the cause
of the bronchoconstriction.  This response de-
pends  upon  intact motor parasympathetic
pathways.  Similar results  were reported by
Widdecombe  et  al.™41 for bronchoconstric-
tion caused  by  inhalation of  fine charcoal
dust.

  3.  Sulfuric Acid and Particulate Sulfate
                Exposures
  The respiratory  response  of guinea pigs
to sulfuric acid mist was studied by Amdur.42
Concentrations ranged from 2 mg/m3 to 40
mg/m3. Three particle sizes were used, 0.8/*,
2.5/j., and  1^ MMD. The 1-p particles even
at a concentration of 30 mg/m3 caused only
a slight increase in resistance and no other
detectable alterations.  Particles  of this size
would not penetrate to any  extent beyond
the nasal  passages.  The 0.8-/i particles pro-
duced an increase in resistance (accompanied
by  a  lesser  decrease in compliance and an
increase  in  work  of breathing)  which was
statistically  significant at  the lowest con-
centration tested,  1.9 mg/m3.  The response
was prompt  in onset and resembled the pat-
tern observed in response  to sulfur dioxide.
The 2.5-/J particles produced  a  greater re-
sistance  increase at concentrations  of 40
mg/m3 than  the smaller particles.  This fits
with the finding of Pattle et al.16 that par-
ticles of 2.7/i were more lethal than those of
O.Sju, when the LC,-)0 was the criterion  of re-
sponse. On the other hand, at concentrations
about  2  mg/m3, the smaller particles pro-
duced  a  greater response. This underlines
once again the fact that data obtained using
only high concentrations can fail to predict
accurately the  response  to  low  concentra-
tions.  Response to the larger particles was
much  slower in onset  with minimal  alter-
ation during the first 15 minutes of exposure.
Response to the smaller particles in  10 to
15  minutes  had  reached  levels similar to
those  prevailing at the end of 1-hour ex-
posure to the larger particles.  The delayed
response  suggests the  possibility of  a dif-
ferent mechanism of  action,  and this pos-
sibility is borne out by both the mechanical
behavior  of  the lungs and the post-mortem
appearance of the lungs. In the animals ex-
posed  to  the 2.5-fi particles,  resistance in-
creases  were accompanied by more marked
compliance changes than  those produced by
the smaller particles or  by  sulfur  dioxide.
Such changes are consistent  with the devel-
opment of obstruction of major airways. At
post-mortem  the  animals exposed  to  high
concentrations of the large particles showed
areas of atelectasis frequently involving an
entire  lobe.  The lungs from these  animals
showed a lung weight to body weight  ratio
greater than  in control animals.  Such alter-
ations  were not produced by the exposures
to sulfur dioxide or smaller sulfuric acid
droplets.  The  large  particles  probably act
by  producing  mucosal swelling, secretion,
and  exudation of fluid which leads to ob-
struction of major  airways,  whereas the
smaller particles act via bronchoconstriction.
  The response shown by 2 mg/m3  (a  50
percent increase in  resistance for the 0.8-/x
sulfuric  acid)  is well above the sensitivity
of the method for detection of  response in
the guinea pig. Data on concentrations lower
than this are not currently available.
  The irritant potency  of  zinc  ammonium
sulfate  (which may be regarded as the proto-
typical acid sulfate) was  studied at 4 differ-
ent  particle  sizes  between  0.29^ and 1.4^
 (mean  size  by  weight) .2T  Concentrations
were from 0.25  mg/m3  to  3.6 mg/m3, and
all levels tested produced an  increase in flow
resistance  in guinea  pigs. The  irritant po-
tency increased as the particle size decreased,
a small increment in concentration  of  small
particles producing a greater increment in
response than  did the larger particles. The
importance of particle size  emphasizes the
inadequacy of using mass concentration data
alone when attempting to assess  the irritant
potency of particulate material.  Zinc sulfate
and ammonium sulfate were  also irritant but
their potency was much less  than that of the
double salt.  The authors, while  not advanc-
ing an "explanation" of the Donora disaster,
indicate that  the  zinc  ammonium sulfate,
zinc sulfate,  and ammonium  sulfate reported
by Hemeon 43 as constituents of  the Donora
fog could have been contributors to respira-
tory effects if  present as 0.3-/* to 0.5-/x par-
ticles;  if the particles were 1.4/x or larger,
the substances would have contributed little
 to the effects.
       80

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  Nadel et ol" studied the effect of aerosols
of histamine and zinc ammonium sulfate (as
an example of an irritant aerosol)  admin-
istered to anesthetized and artificially venti-
lated cats.  The aerosol particles were smaller
than lj« and the concentration for the sulfate
was  40 mg/nv!  to  50 mg/nr'.   The sulfate
aerosol  produced  a physiological response
similar to that  of  histamine  but lesser  in
degree.  The response to 3-minute inhalation
included increased pulmonary resistance, de-
creased  pulmonary  compliance, and  in-
creased end-expiratory transpulmonary pres-
sure.  Injection of atropine did  not  prevent
the changes in compliance but decreased the
changes  in  resistance.   A  bronchodilator
given intravenously  or  as an aerosol  prior
to administration of the irritant prevented
the changes, suggesting that they were due
to smooth muscle contraction.   Cardiac ar-
rest during histamine inhalation did not pre-
vent the  changes, suggesting that histamine
acts  directly on the airway smooth muscle
and is not dependent on the circulatory route.
To correlate with the physiological responses,
anatomical  studies  were  made  after  rapid
freezing  of the lungs in the open  thorax.
These showed that the principal sites of con-
striction  were the  alveolar ducts and ter-
minal  bronchioles.  Bronchioles  up  to  400/j,
were narrower than in  control animals and
showed longitudinal furrowing  of  the mu-
cosa.  Bronchi and bronchioles  larger than
400ju were  not  significanty  different  from
controls.  The authors conclude:  "It remains
to be demonstrated  that  acute  changes re-
ported  here at aerosol concentrations  of 40
mg/m3 to  50 mg/m3 are  exaggerated, but
similar in nature to those produced, if any,
at lower concentrations."
  Amdur  and Underhill4r> have recently re-
ported  that 1 mg/m3 of ferric  sulfate pro-
duced a 77 percent increase in flow resistance
in guinea  pigs, which classified it as irritant.
On  the other  hand,  neither ferrous sulfate
nor manganous sulfate at this concentration
produced  any alteration in resistance,  sug-
gesting that the irritant potency is not re-
lated to the sulfate ion as such. In experi-
ments on  guinea pigs with sulfuric acid  or
particulate  sulfate,23 -142  the  response  re-
mained above control values following expos-
ure instead of  reverting to control values
within an hour in the manner seen with ex-
posure to sulfur dioxide. This difference aris-
es since the irritant  particle is cleared less
rapidly from the lung than  the irritant gas.

D.  EFFECTS OF SULFUR DIOXIDE ON
            CILIARY ACTION
   Cralley 4" studied the effect of irritant gas-
es, among them sulfur dioxide, on the ciliary
activity of excised rabbit trachea. Tempera-
ture and humidity were  controlled  and  the
gas to be studied was passed over the tissue
at a rate comparable  to  that of breathing by
the animal. The time  needed for cessation of
ciliary activity  following irritant exposure
was related to the  concentration of  irritant
administered.  There was a rough correlation
between the concentrations of sulfur dioxide
needed to produce ciliary cessation in 10 min-
utes in the rabbit trachea  (18 ppm to 20
ppm), and the values reported for  concen-
trations causing immediate  irritation of  the
throat in human subjects (8  ppm to 12 ppm).
   The most extensive studies of the effect of
sulfur dioxide and other irritant gases on
ciliary activity of experimental  animals have
been made by Dahamn  and his co-workers,
using rats 12 '7 and rabits.47-30
   The original work with rats 12 51 developed
methods for measuring both rate of trans-
port of mucus and the  frequency of ciliary
beat in the trachea of living animals under
carefully controlled conditions of tempera-
ture and humidity. The action of sulfur diox-
ide on ciliary  activity was tested at  50 ppm,
25 ppm, and 12 ppm  (140 mg/m3, 70 mg/m3
and 35 mg/m3). The time required for cessa-
tion of ciliary beat varied with the concentra-
tion, being 50 seconds at  50 ppm, 2  minutes
at 25 ppm, and 4 to 6 minutes at 12 ppm. Rats
which  had been exposed  to 10 ppm (about
30 mg/m3) for  48  days were examined  for
acute response to 20 ppm (about 60  mg/m3)
to compare their response with that of con-
trol rats not previously  exposed. The results
indicated that the previous exposure had not
altered the reactivity of the cilia to the  20-
ppm exposure. In all these  experiments  the
cilia regained mobility a  few minutes after
exposure ceased.
   There  was  a marked  slowing  of mucus
                                                                              81

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transport and a complete cessation of flow in
some rats exposed for 18 to 67 days to about
10 ppm sulfur  dioxide. On  the other hand,
the rate of ciliary beat was slightly diminish-
ed in the shorter term exposures and unaffec-
ted in  the longer exposures. These findings
were readily accounted for  by the  morpho-
logical changes which included a  thickening
of the mucus blanket from 5^ to 25/x and evi-
dence of excess secretion.. The rate of trans-
port of mucus remained depressed in animals
examined a  month or so after the termina-
tion of exposure, in agreement with the per-
sistence  of  the  observed  morphological
changes.
   Dalhamn studied the acute effect of sulfur
dioxide on ciliary activity on  the trachea of
the rabbit in vivo and in vitro. The in vivo
studies were made with the animals breath-
ing spontaneously through the nose. Concen-
trations of the order of 300 ppm  (about 860
mg/m3)  were required  to produce cessation
of ciliary beat in the spontaneously breath-
ing rabbits. Obvious explanations for the con-
trast of this finding with the earlier findings
on rats were either that the cilia of the rabbit
trachea were relatively insensitive to sulfur
dioxide or that  the  sulfur  dioxide was not
reaching the site of action. Experiments with
the rabbit trachea in vitro showed that con-
centrations of sulfur  dioxide of 7 ppm to 10
ppm (20 mg/m3 to 29 mg/m3) were suffici-
ent to produce cessation  of ciliary activity.
The absorption studies discussed below indi-
cate that these findings are  explicable on the
basis  of major absorption in the nasal cavity
and  pharynx of animals  exposed  via  this
route.
 E.  LIFETIME EXPOSURE OF ANIMALS
          TO SULFUR DIOXIDE

   There are two brief reports 52 53 of a study
 in which rats were exposed over most of their
 lifetime  to  concentrations of 1, 2,  4,  8, 16,
 and 32 ppm (about 3, 6, 11, 23, 46, and 92
 mg/m3)  sulfur dioxide. The life span of the
 rats appeared to be reduced by 0.08 months
 for  each  1  ppm increase of  sulfur dioxide
 concentration. Statistical analysis,54 however,
 fails to attach  significance to these changes.
 F.  ABSORPTION  AND DISTRIBUTION
          OF  SULFUR  DIOXIDE

  Balchum et  al.30 31  33 used labelled S3502 to
measure  the  absorption, distribution,  and
retention  of sulfur  dioxide  in  dogs.  The
effect of  nose  and mouth breathing as com-
pared with breathing the gas through a tra-
cheal cannula  was examined, as well  as the
uptake and distribution following exposure
of a segment of trachea only. Following in-
halation,  the sulfur  dioxide was widely dis-
tributed to the tissues with obviously greater
amounts  in the respiratory tract. A smaller
porportion of  the inhaled gas was found in
the trachea, lungs, hilar lymph nodes, liver,
and  spleen  when  the animals  breathed
through the nose and mouth  than when the
same amount was inhaled via a tracheal can-
nula. The labelled S3502 was  only slowly re-
moved from the  trachea and lungs, and its
presence in these tissues could be detected a
week after exposure. Ninety percent of in-
haled sulfur dioxide was removed from the
airstream and became localized in the respir-
atory tract including the pharynx. When a
tracheal  segment  alone was  exposed  to the
gas, S35 was detected in various tissues, indi-
cating that it  can be absorbed from the up-
per respiratory tract alone. S35 was detected
in the urine but not  in the f eces.
   Bystrova 55  found a  wide  distribution of
S35 throughout the tissues of rats following
inhalation of  high concentrations of sulfur
 (S3S) dioxide.  The amount of  S35 found in the
blood and tissues was related to the concen-
tration inhaled. The  S35 was attached to pro-
tein and  could still be found 11 days after ex-
posure. Traces, especially in the lungs, were
detectable 3 weeks aftr exposure.
   Frank  et al.™  exposed the surgically iso-
lated airways  of the head and upper neck of
anesthetized, paralyzed dogs to 22-ppm (63
mg/m3)  sulfur dioxide  labelled with S35 and
delivered at a rate of 3.5 1/min for 30 to 60
minutes. The  trachea was  cannulated below
this region, and the lungs were ventilated
with room air  by  a positive  displacement
pump. In  10  out of 12 measurements, over
95 percent of the sulfur dioxide administered
to the isolated upper airways was found to be
absorbed by the  mucosa. In two  of the ani-
       82

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mals, sampling was continued into the re-
covery period after the upper airways had
been returned to room air, and sulfur dioxide
was detected in one dog 5 to 37 minutes after
exposure. In the other dog sulfur dioxide was
present in  the  downstream sample 10 min-
utes after  exposure but not at  60  minutes.
The presence of sulfur dioxide was presum-
ably due to desorption from  the mucosa. In
all 5 animals, sulfur dioxide was found in one
or more expired gas samples collected either
at the carina or from a bronchus.  Since no
sulfur dioxide entered the lower airways in
inspired  air, the authors  conclude  that the
lungs were releasing the sulfur dioxide dur-
ing expiration, presumably from the pulmon-
ary  capillaries.  S35  appeared in the  blood
within 5 minutes of the start of exposure and
continued to increase throughout the expos-
ure. The radioactivity of the blood fell slowly
during the  2-hour observation period follow-
ing exposure; it was greater in the plasma
than in the  blood cells. Aeration of the venous
blood sample caused a loss of about 20 per-
cent of its radioactivity, but little or no radio-
activity was lost by aeration of arterial blood.
Radioactivity was also detected in the  urine
within minutes  after exposure.
  Dalhamn  and co-workers 48~30  studied the
absorptive  capacity  of the nasal cavity of
rabbits for sulfur dioxide.  Some  animals
breathed spontaneously  through the  nose
from  a chamber  containing  sulfur dioxide,
and samples were taken from cannula insert-
ed in the trachea immediately below the thy-
roid. In such animals, an initial exposure con-
centration of about  100 ppm (~290 mg/m3)
had been reduced to about 2 ppm (about 6
mg/m3) by the time it reached the tracheal
sampling tube. A concentration of about 240
ppm  (about 690 mg/m3) was  reduced to
about 2 ppm to 3 ppm by passage through the
nasal cavity. During  experiments in which
air was pulled through the animal's mouth,
the absorption was  less. A concentration of
190 ppm  (540  mg/m3) in the  inhaled air
reached the trachea at about 15 ppm (about
43 mg/m3). This observation fits with the
observation by Speizer and Frank " that the
increase in  pulmonary flow resistance in hu-
man  subjects was  greater during  mouth-
breathing than during nose-breathing at a
given concentration of sulfur dioxide in the
inhaled air. Somewhat lower absorption val-
ues  were  obtained  when air was sucked
through the nasal cavity  than had been ob-
tained with the animals breathing spontane-
ously through the nose.
  The overall conclusion is that at levels  of
100  ppm  to 300 ppm  (290  mg/m3 to 860
mg/m3), 90 percent or more of the inhaled
sulfur dioxide does not reach the lungs. This
offers a reasonable explanation for the high
levels that are needed in experimental ani-
mals to produce lung pathology and mortal-
ity.
  Standberg 2S studied the absorption of sul-
fur dioxide by rabbits breathing  spontane-
ously through the nose. A sampling device
was implanted in the trachea, and the sulfur
dioxide was tagged with S35 for  analytical
purposes. A concentration range of 0.05 ppm
to 700 ppm (145 /*g/m3 to 2,000 mg/m3)  in
the inhaled air was studied. There was  con-
siderable scatter in the data, but it was clear
that at concentrations of about  100 ppm
(~290  mg/m3)  there was an absorption  of
approximately 95 percent at inspiration and
approximately 98 percent at expiration. As
the concentration decreased,  the absorption
was  less efficient,  and at levels of 0.1 ppm
(285 /xg/m3) and below only about 40 percent
was absorbed during inspiration and about 80
percent at expiration, with some experiments
showing even lower absorption  efficiencies.
It was proposed that the higher  concentra-
tions cause excess secretion of mucus and in-
crease the absorption efficiency.
  Amdur 24 made use  of  Strandberg's data
to replot the dose-response curve relating re-
sistance increase to concentration  of sulfur
dioxide. The data on guinea pigs were avail-
able  over the range of 0.16 ppm to 835 ppm
(460 jug/m3 to 2,390 mg/m3), which was es-
sentially the same range covered by Strand-
berg's studies. If the nasal absorption was 95
percent or 98 percent for high concentrations
but only 40 percent or 50 percent  for low
concentrations as Strandberg observed, and
if the  response  observed  resulted  from the
concentration  reaching  the lung,  this could
perhaps explain the nonlinearity of the dose-
response curve. When the air concentrations
were calculated as effective "lung concentra-
                                                                             83

-------
tions"  using Strandberg's data, a straight
line  did result. At levels below 100  ppm
(~290 mg/m3), the experimental curve for
animals breathing  through a tracheal can-
nula gave values quite close to the hypotheti-
cal "lung" curve. Strandberg's finding  that,
at low  concentrations, sulfur dioxide pene-
trated  the upper respiratory tract probably
explains the similarity of response with and
without the cannula at concentrations of 0.4
ppm (1.1  mg/m3). Strandberg's data  obtain-
ed on rabbits appear to be applicable to gui-
nea pigs.

   G.   MISCELLANEOUS BIOCHEMICAL
     EFFECTS OF SULFUR DIOXIDE
   Since experiments have demonstrated the
wide distribution of S3S throughout the body
following  inhalation of sulfur dioxide, it is
reasonable to search for possible biochemical
effects. A  biochemical lesion often is the fun-
damental  basis for the response of an organ-
ism to  toxic  agents, and with many  com-
pounds the finding of such a biochemical le-
sion has provided the key to an understand-
ing of their toxic  action. There have been
a few biochemical studies,5*-61 of animals ex-
posed  to  sulfur dioxide,  but from these no
clear-cut picture of a biochemical lesion has
emerged.

              H.  SUMMARY
   This chapter describes  animal toxicology
of sulfur  oxides. Both sulfur dioxide and sul-
furic acid are considered in terms of dosage
required   to  produce  death,  pathological
change, and changes in pulmonary function.
   Both sulfur dioxide and sulfuric acid irri-
tate the respiratory system; they must, how-
ever, be employed  at high concentrations if
mortality  is chosen as the criterion of re-
sponse. Sulfuric acid is more toxic than sul-
fur dioxide, and its toxicity is dependent on
particle size. The guinea pig is apparently the
most susceptible laboratory animal studied to
date, although it can withstand concentra-
tions of sulfuric acid which would be  intol-
erable to. man.
   Compared to realistic air pollutant levels,
it requires relatively high concentrations of
sulfur  dioxide or  sulfuric acid to  produce
pathological lung change  or mortality in ani-
mals. The type of pathological change observ-
ed in the guinea pig depends on whether the
death was rapid  as a result  of bronchial
spasm or was delayed.
  Sulfur dioxide  is  capable of  producing
bronchoconstriction in experimental animals
such as the guinea pig, the dog, the cat, and
also  in man.  This bronchoconstrictive prop-
erty  is common to various respiratory irri-
tants. Receptors in the tracheobronchial tree
have  been  shown to be sensitive to sulfur
dioxide, and bronchoconstriction can be elic-
ited  by exposing only the  upper airways to
sulfur dioxide. The response is blocked by
atropine or by cooling  of the cervical vago-
sympathetic nerves.
  Dose-response curves have been establish-
ed for the guinea pig; they relate the  con-
centration  of sulfur dioxide to the observed
increase in pulmonary flow resistance  pro-
duced by one hour exposures. Slight increases
in resistance are detectable at 0.16 ppm (460
mg/m3)  and the changes are readily revers-
ible. The speed of onset (at least at high con-
centrations) and ready reversibility suggest
that changes in smooth muscle tone are the
cause of the observed bronchoconstriction.
  Sulfuric acid and  some,  but not all,  par-
ticulate  sulfates  also produce bronchocon-
striction in the guinea pig.  The response is
highly dependent  on particle size, with the
smallest particles  showing the greatest irri-
tant potency. Comparative data are available
only for the guinea pig; in this animal, sul-
furic acid  and irritant particulate sulfates
have a greater irritant potency at a given
concentration than sulfur dioxide alone.
  Data obtained on  guinea pigs suggest that
the  response to low concentrations is  simi-
lar in type to that produced by higher con-
centrations but that the response decreases
in magnitude with decreasing concentration.
The nature of the  experimental techniques
used on  guinea pigs may render the animals
especially  sensitive  to  irritant action.  In-
creases in flow-resistance  produced in  these
animals  are not considered as  indications of
major physiological change and are not suit-
able for direct extrapolation.
  The physiological response elicited in cats
by  small  particulate irritants is probably
caused  by reflex  action on airway  smooth
       84

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muscle.  Morphological studies show that the
principal sites of constriction are the aveolar
ducts and terminal bronchioles. Bronchi and
bronchioles larger than 400 /j. are unaffected.
The response to the particulate irritants dis-
appeared more slowly than did the response
to gaseous irritants.
   To summarize our knowledge of  the  ab-
sorption and distribution of  sulfur dioxide,
it has been shown  that sulfur dioxide is ab-
sorbed in the  upper airways, and nasal  ab-
sorption can account for as much as 95 per-
cent to 98 percent at high sulfur dioxide con-
centrations.  This absorption provides a pro-
tective effect to the remainder of the pulmon-
ary system  and  responses  are generally
greater  when  sulfur dioxide is breathed  via
tracheal cannulae.

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37.  Frank, N. R. and Speizer, F. E.  "S02 Effects on
    the Respiratory System in Dogs." Arch. Environ.
    Health, Vol. 11, pp. 624-634, 1965.
38.  Widdicombe, J.  G.  "Respiratory Reflexes  from
    the Trachea and Bronchi of the Cat." J. Physiol.,
    Vol. 123, pp. 55-70,  1954.
39.  Widdicombe, J.  G. "Receptors in the Trachea and
    Bronchi of the  Cat."  J.  Physiol.,  Vol. 123, pp.
    71-104,  1954.
40.  Nadel, J. A., Salem, H., Tamplin,  B., and Yoki-
    wa,  Y.   "Mechanism  of  Bronchoconstriction."
    Arch.  Environ.  Health, Vol. 10, pp. 175-178, Feb.
   1965.
41.  Widdicombe, J.  G., Kent,  D. C., and Nadel,  J. A.
    "Mechanism of  Bronchoconstriction during In-
    halation of Dust." J. Appl. Physiol., Vol. 17, pp.
    613-616,  1962.
42.  Amdur,  M. 0. "The  Respiratory   Response of
    Guinea  Pigs  to Sulfuric Acid  Mist."   A.M.A.
    Arch.  Ind. Health,  Vol.  18,  pp. 407-414,  Nov.
    1958.
43.  Hemeon,  W. C.  L.  "The  Estimation of  Health
    Hazards from Air Pollution." A.M.A. Arch. Ind.
    Health, Vol. 11, pp. 397-402,  1955.
44.  Nadel,  J.  A., Corn,  M., Zwi, S., Ferch,  J., and
    Graf,  P.  "Location and  Mechanism of Airway
    Constriction after Inhalation of Histamine Aero-
    sol and Inorganic Sulfate Aerosol." Proceedings,
    2nd International Symposium on Inhaled Parti-
    cles and Vapors, C.  N. Davies  (ed.),'Pergamon
    Press, Oxford, 1966, p. 55.
45.  Amdur,  M. O. and Underbill, D. "The Effect of
    Various Aerosols on  the Response of  Guinea
    Pigs to Sulfur Dioxide."  Arch. Environ.  Health,
    Vol. 16,  pp. 460-468, 1968.
46.  Cralley, L. V. "The Effect of Irritant Gases upon
    the Rate of Ciliary Activity." J. Ind Hyg. Toxi-
    col., Vol. 24, pp. 193-198, 1942.
47.  Dalhamn,  T. and Strandberg,  L.  "Acute Effect
    of  Sulfur Dioxide on the Rate  of Ciliary  Beat
    in the Trachea  of Rabbit, In Vivo  and In Vitro,
    with  Studies  on  the  Absorptional Capacity of
    the Nasal Cavity."  Int. J. Air  Water Pollution,
    Vol. 4, pp. 154-167, Sept. 1961.
48.  Dalhamn,  T.  "Studies on the Effect of  Sulfur
    Dioxide  on Ciliary  Activity in  Rabbit Trachea
    In  Vivo and In Vitro and on the Resorptional
    Capacity of the Nasal Cavity."  Am. Rev. Resp.
    Dis., Vol.  83, pp. 566-567, April 1961.
49.  Dalhamn,  T. and Sjoholm, J.  "Studies on SO-,,
    N02, and NH3: Effect on Ciliary  Activity  in Rab-
    bit Trachea of Single In Vitro  Exposure and Re-
    sorption in Rabbit Nasal  Cavity."  Acta Physiol.
    Scand., Vol. 58,  pp. 287-291, 1963.
50.  Dalhamn,  T. and Strandberg, L.  "Synergism be-
    tween  Sulphur   Dioxide  and  Carbon Particles.
    Studies on Adsorption and on Ciliary Movements
    in  the Rabbit  Trachea In Vivo."  Int.  J. Air
    Water Pollution, Vol. 7, pp. 517-529, 1963.
51.  Dalhamn,  T. and Rohdin,  J. "Mucous Flow and
    Ciliary Activity in the Trachea of  Rats Exposed
    to Pulmonary Irritant Gas."  Brit. J. Ind. Med.,
    Vol. 13, pp. 110-113, April 1956.
        86

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52.  Ball, C. O. T., Heyssel, R. M.,  and Balchum, O.
    J., Elliott, G. 0.,  and Meneely, G. R. "Survival
    of Rats Chronically Exposed to Sulfur Dioxide."
    Physiologist, Vol.  3, p. 15, Aug. 1960.
53.  "Air Pollution Conference Report." Pub. Health
    Reports, Vol. 75,  pp. 1173-1189,  Dec.  1960.
54.  Goldsmith, J. R.  Personal communication.
55.  Bystrova, T. A. "Effects of Sulfur Dioxide Stud-
    ied with the  Use  of Labeled Atoms."  Gig.  i
    Sanit.,  Vol.  20, pp. 30-37,  1957.  In:  U.S.S.R.
    Literature on  Air Pollution and  Related  Occu-
    pational Diseases. A Survey, Vol. 1, Translated
    by B. S. Levine, U.S. Dept. of  Commerce,  Office
    of Technical Services, Washington, D.C., pp. 89-
    97, Jan. 1960.
56.  Frank, N. R.,  Yoder, R. E., Yokoyama, E., and
    Speizer, F. E.  "The Diffusion of SO2 from Tissue
    Fluids  into  the  Lungs Following  Exposure of
    Dogs to S02."  Health Physics, Vol. 13, pp. 31-38,
    1967.
57.  Speizer, F. E.  and Frank, N. R. "A Comparison
    of Changes  in Pulmonary  Flow  Resistance in
    Healthy Volunteers  Acutely Exposed to SO2 by
    Mouth and by Nose." Brit. J.  Indust. Med., Vol.
    23, pp. 75-79, 1966.
58.  Thompson, J. R.  and Pace,  D.  M. "The Effects
    of Sulphur Dioxide upon  Established Cell  Lines
    Cultivated In Vitro."  Canad. J. Biochem. Phys-
    iol., Vol. 40, pp. 207-217, 1962.
59.  Navrotskii, V. K. "Effects of Chronic Low Con-
    centration Sulfur Dioxide Poisoning on the Im-
    muno-Biological  Reactivity of  Rabbits."  Gig.  i
    Sanit.,  Vol.  24,  pp.  21-25, 1959.  In:  U.S.S.R.
    Literature on Air Pollution  and Related Occu-
    pational Diseases.  A Survey, Vol. 6, Translated
    by B. S. Levine, U.S. Dept. of  Commerce, Office
    of Technical  Services,  Washington,  D.C., April
    1961, pp. 157-163.
60.  Prokhorov, Yu.  D. and  Rogov, A. A. "Histopath-
    ological  and  Histochemical Changes in the Or-
    gans  of  Rabbits after Prolonged Exposure  to
    Carbon  Monoxide,  Sulfur  Dioxide,  and  their
   Combination."  Gig.  i Sanit., Vol. 24, pp.  22-26,
   1959.  In:  U.S.S.R. Literature  on  Air Pollution
    and Related  Occupational  Diseases.  A Survey,
    Vol. 5,  Translated by  B.  S. Levine, U.S. Dept.
    of Commerce, Office of  Technical Services,  Wash-
    ington,  D.C., 1961, pp. 81-86.
61.  Lobova,  E. K.  "Effect of Low Sulfur Dioxide
    Concentrations  on the  Animal Organism." In:
    U.S.S.R.  Literature on Air Pollution  and Re-
    lated Occupational Diseases.  A Survey, Vol.  8,
    Translated by B. S. Levine, U.S. Dept. of Com-
    merce, Office  of Technical Services, Washington,
    D.C., 1963, pp. 79-89.
                                                                                             87

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               Chapter 7
TOXICOLOGICAL EFFECTS OF SULFUR OXIDES
               ON MAN

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                          Table of Contents
                                                                    Page
A. INTRODUCTION                                                   91

B. EVALUATION BY PULMONARY FUNCTION                        91
   1. Sulfur Dioxide                              .                     91
     a. Short-Term Exposures                                   .      91
     b. Repeated Exposures                                     .      93
   2. Sulfuric Acid Aerosol                                             94
C. NASAL ADSORPTION                                    .         95
D. EFFECT ON REMOVAL OF MUCUS FROM THE
   RESPIRATORY TRACT                                            96
E. SENSORY THRESHOLD CONCENTRATIONS                  .      96
   1. Odor Perception Threshold                                  .      96
   2. Sensitivity of the Dark-Adapted Eye                                97
   3. Interruption of  Alpha  Rhythm                              .  .     98
   4. Optical Chronaxie                                                98

F. SUMMARY                                                        99

G. REFERENCES                                                   100

                             List of Tables

Table
7-1 Threshold Concentrations  of Sulfur Dioxide, Sulfuric
    Acid and their Combinations for Various Reflex Responses          .     99
 90

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                                      Chapter 7

          TOXICOLOGICAL EFFECTS OF  SULFUR OXIDES ON  MAN
           A.  INTRODUCTION
   Reviews of the health effects of air pollu-
tion have  been made by  Heimann,1 Gold-
smith,'-  Lawther,3 Phair,4 Phillips,5 Catcott,6
Stokinger,7  and Anderson.8  In addition, a
number of shorter papers report the health
effects of polluted air which contains oxides
of  sulfur  along with  other  pollutants.9-27
These  papers reveal  the complexity of  the
problem of  assessing the effects of air pol-
lution. Anderson 8 states that although there
are  many  serious limitations  to  published
research on the health hazards of air pollu-
tion, both epidemiological and detailed clin-
ical, physiological, and animal experiments
confirm  that these hazards exist. He  em-
phasizes the importance of particulate  ma-
terial as a  major contributor  to  the noted
responses, or as an index of air pollution re-
lated to these effects.
  This  chapter  considers the  available  evi-
dence, reported in the literature, on the  tox-
icological  effects of the oxides  of  sulfur on
man. More  extensive reviews of the toxicol-
ogy of oxides of sulfur have been  presented
by Greenwald 2S and Amdur.29 The combined
effects of sulfur dioxide and particulate mat-
ter are discussed in Chapter 8.
  Much of the human toxicological research
has  been  oriented  towards   occupational
health.  Considerations affecting community
air pollution must take  account  of the  re-
actions of unusually sensitive individuals, so
that the published studies  are  generally of
limited applicability to the  establishment of
community air quality criteria.

   B.  EVALUATION BY PULMONARY
               FUNCTION
  Various investigators  have examined the
response of human subjects  exposed for brief
periods  to  known concentrations  of sulfur
dioxide or sulfuric acid mist, and measured
the effects on pulmonary function. The most
valuable of these studies are those dealing
with constriction of the airways as reflected
in measurements of pulmonary flow resist-
ance. Such experiments evaluate directly the
response of man, thus having the advantage
that extrapolation from the response of some
other species of  animal  is avoided.  On  the
other hand, the number  of individuals used
in these studies  is necessarily limited, and
a paper reporting  the response of 10 sub-
jects is considered a major contribution. It is
difficult to extend results obtained on so lim-
ited a  sample to define the response of any
species of animals, and no one seriously pro-
poses such extrapolations.
            1.   Sulfur Dioxide
a. Short-Term Exposures
  Sim  and Pattle 30 exposed healthy males
aged 18 to 45 to sulfur dioxide either by face
mask (264 exposures) for 10 minutes or in
a chamber (330 exposures)  for 60 minutes.
During the chamber exposures the men were
allowed to walk around or  smoke if they
wished. Mask exposures used concentrations
from about 1 ppm to 80 ppm (~3 mg/m3
to ~230 mg/m3), while concentrations in  the
chamber were from 1 ppm to 23 ppm (~3
mg/m3 to ~65 mg/m3). The subjects were ob-
served clinically, and increases in airway re-
sistance greater  than 20 percent were  re-
corded.
  From the wide range of  concentrations,
and  the large number of exposures, a dose-
response relationship  was found.  Unfortu-
nately, it  was not expressed  in  as  much
detail  as  the extensive  experimental  data
warranted on this occasion.  It was reported
that with  dosages below  800  mg-min/m3
(equivalent to  exposures  of  10 minutes to
                                                                             91

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30 ppm or 60 minutes to 5 ppm) little change
was  noted either clinically or  by measure-
ment of  lung  resistance to air flow.  Occa-
sionally,  there was an increase in lung  re-
sistance  sufficient to be  detected by the  in-
strument used. At the same time, there were
auscultatory signs of irritation in the chest
of some,  but not all, of the subjects.  When
dosages above 1330 mg-min/m3 (presumably
50 ppm for 10 minutes or 9 ppm for 60 min-
utes)  were used, the  lung  resistance  in-
creased significantly  above normal in 50 per-
cent of the people exposed. The authors  did
not  define "significantly above normal" in
this  context. Measurements made during ex-
posure showed that  the  increase of airway
resistance occurred within the first 10 min-
utes with little  further  change at the end
of an hour, which makes the  authors' choice
of the C  x t-relationship  to describe the pat-
tern of response seem at variance with their
findings.  Rhinorrhea and lachrymation were
common  symptoms  at higher  dosages,  but
the most frequent physical finding was  the
presence of high-pitched musical rales, with
a tendency to prolongation of the expiratory
phase of respiration. Moist rales were com-
monly heard in the more peripheral regions
of the lung after prolonged exposure, where-
as in those who received smaller dosages or
shorter exposures, rales were heard anteri-
orly over the large bronchi. Once again, this
result seems at  variance with the use of a
C X t-relationship  in connection  with  the
data.
   There  was no correlation between familial
history of allergy and symptomatology,  but
in isolated instances there was evidence of
increased flow resistance and considerable
discomfort in those who  had  previously been
sensitive to fog in the London area or who
had  definite personal histories  of  allergy.
The effect of the smoking habits of the sub-
jects,  or the  effect  of  smoking  during  ex-
posure, were not discussed.
   In 8 out of the 594 exposures there were
undefined  "significant   changes" in  pulse
rate, respiratory rate,  volumes  of tidal or
supplemental  air, vital  capacity,  maximum
breathing capacity,  or blood  pressure. Two
of these individuals had previous personal
histories of allergy  and 2 had experienced
previous discomfort from smog.  The other
4 were suffering from the onset of mild res-
piratory infections  on  the day of exposure.
One person developed  a unilateral, nonspe-
cific pleural effusion 1  week after exposure.
The investigators  themselves  were in  nor-
mal health at the start of the experiments,
which  extended over  a  10-month  period.
They both developed what  appeared to be
an increased sensitivity to sulfur dioxide and
sulfuric  acid mist.   One of  them, who was
entirely  free of chest symptoms at the out-
set,  developed  a moderately severe but ex-
tremely persistent bronchitis which was im-
mediately exacerbated into an  uncomfortable
period of coughing and wheezing on exposure
to either sulfur dioxide or sulfuric acid.
  Frank and co-workers 31~34 have examined
the response of human subjects to sulfur di-
oxide.   In the experiments  reported  ini-
tially,31  11 healthy adults were exposed on
separate occasions to average sulfur dioxide
concentrations  of  1 ppm (~3 mg/m3),  5
ppm  (~14  mg/m3),  and  13 ppm   (~37
mg/m3).   Exposures lasted 10 minutes to
30  minutes  and,  for  each  subject,  were
spaced at least 1 month apart. The subjects
were seated  in a  -body plethysmograph,
breathing  spontaneously by  mouth  while
measurements of respiratory mechanics were
made with an esophageal catheter. The meas-
urements did not necessitate the interruption
of  exposure to the gas. At  1  ppm, only one
of the 11 subjects showed a statistically sig-
nificant  increase in  flow resistance, and his
control  resistance was the  highest encoun-
tered.   One other subject showed a  statis-
tically significant decrease in resistance dur-
ing exposure to 1 ppm.  At the 5 ppm level,
9 out of the 11  subjects showed a statistically
significant increase  in  resistance over con-
trol values, and the average increase for the
group was 39  percent above control.  At 13
ppm all subjects showed an increase in re-
sistance, and 9 of these measurements were
statistically significant on an individual ba-
sis. The average increase for the group was
72  percent above control.
  The  data  obtained in  man  may be  com-
pared with data obtained by similar methods
in  guinea pigs exposed to the same concen-
trations.  Data for  guinea pigs were avail-
       92

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able for animals  breathing normally and
breathing through a tracheal cannula. The
human  subjects were  mouth-breathing.  It
was found that, except at the lowest gas con-
centration, the  human  subjects appeared to
be  slightly more sensitive than the  guinea
pigs.  The most comparable dose-response
relationships  were  for the tracheotomized
guinea pigs and the normal human subjects.
  The time course of the resistance changes
was examined.  Within  1 minute of exposure,
flow resistance had increased significantly.
The increase after 5 minutes  was greater
than the increase at 1 minute, but no fur-
ther significant  change occurred  between 5
minutes  and  10 minutes.  If  the 5-minute
and 10-minute values are averaged to  repre-
sent the "peak" response, then 45 percent
of  this  peak was  reached within the first
minute  of  exposure. Five exposures  to the
higher two concentrations  (5 ppm and  13
ppm) were extended to 30 minutes,  but  al-
though  the  resistance  remained elevated
throughout this exposure period,  the  resist-
ance tended  to  decrease  slightly from the
10-minute  values.  (In this  regard, the  re-
sponse of human subjects to sulfur dioxide
differed from that of guinea pigs, in  which
the resistance did not decline during  an  ex-
posure period of 1  hour 35-36 and continued
to increase in a limited number of animals
exposed for 3 hours.)  The extension  of the
exposure time to 30 minutes for  5 subjects
exposed  to 1 ppm  did not  produce  an  in-
crease in flow  resistance, suggesting that,
within the limited time intervals studied, the
response is related to  the concentration of
sulfur dioxide and not to a C X t-relationship.
This statement cannot obviously  be extrap-
olated to long-term exposures.
  The average  flow resistance for the group
still remained elevated 15 minutes after the
end of exposure to both  5 ppm and 13 ppm
sulfur dioxide.  At 5 ppm the difference was
statistically significant in 4 individual sub-
jects; at 13 ppm it was not significant for
any individual  subject.  In 5 subjects,  pe-
riodic measurements were made  within the
15-minute  period and it  was found that, at
times,  recovery may  be completed   within
less than 5 minutes after exposure  ceases.
This point should be  borne in mind when
using techniques  which involve a lapse of
time between exposure and measurement.
  A decrease in compliance was noted in only
one  single  instance during  an exposure to
13 ppm.  At the same time the increase in
flow resistance of this individual was below
the average of the group.  Once again the
response of human subjects appears to differ
from that of guinea pigs in  which slight de-
creases  in  compliance appeared to  accom-
pany the resistance increase.  There was a
slight increase in functional residual capac-
ity at 13 ppm, but the two lower concentra-
tions (1  ppm and  5  ppm)  produced  no
change.   Alterations in  maximum flow rate
(as  measured with the Wright peak flow-
meter) and in timed vital capacity were min-
imal when compared  to alterations  in  pul-
monary  flow  resistance.  Exposures which
increased the pulmonary flow resistance by
89 percent showed only a 7 percent decrease
in peak flow and, though the timed vital ca-
pacity  values  were  generally  lower,  the
changes expressed as percentages were mini-
mal. A  possible explanation for the relative
insensitivity  of these  measurements  is that
they are preceded by  a maximal inspiratory
effort  which  may temporarily obliterate
changes  of flow resistance of the magnitude
of those seen in  this study.  The smoking
habits of the  subjects did not appear to in-
fluence the response  to sulfur dioxide.

b. Repeated Exposures
   Frank et al.M also found that when sulfur
dioxide  (either with or without sodium chlo-
ride aerosol)  is  administered twice in the
course of one experiment  (with  a 15-minute
period of clean air between exposures), the
response to the second exposure is less than
the  response  to the first.  The  human  sub-
jects thus showed an  adaptation to repeated
exposure to the gas.
   Speizer and Frank 33  compared the effect
of sulfur dioxide  on human subjects breath-
ing  the  gas  by nose  and by mouth.  Eight
subjects  were studied.  Exposures  were to
either  15  ppm  (~43 mg/m3)  or  28 ppm
(~80 mg/m3) sulfur dioxide and  were of
10-minute  duration.  Pulmonary flow resist-
ance was measured during both types of ex-
posure.   The flow resistance of the nose was
                                                                             93

-------
measured during  the  nose  breathing  ex-
posures.  When sulfur dioxide was breathed
by mouth the pulmonary flow resistance in-
creased in 9 out of 12 experiments, and the
magnitude of the change  was on the aver-
age  greater  at the higher  concentration.
When the same concentrations of sulfur di-
oxide were administered by nose, pulmonary
flow resistance increased  in  only  3 out of
12 experiments and decreased in one experi-
ment.  During the 15 minutes following the
end of  exposure the resistance remained ele-
vated in 5 of the 12 experiments in which the
gas was  breathed by mouth.  Four  of these
exposures were to 28 ppm.  When the  gas
was  breathed  by nose the pulmonary flow
resistance was  often higher  during the re-
covery  period  than it had been during ex-
posure. In 3 experiments it rose significantly
for the first time during the recovery period,
and in  2 others the increase was greater dur-
ing recovery than it had  been during ex-
posure.
  The  response of nasal resistance to sulfur
dioxide was variable. In 8 of the 12 experi-
ments  it increased at some point during ex-
posure; in 3 experiments there was  a de-
crease; and 1 subject showed first a  decrease
and  then an  increase during the same ex-
posure.  The subjects  who  showed an in-
creased nasal resistance experienced no  dif-
ficulty  in breathing.
  When exposed by mouth, most of the sub-
jects coughed several times during  the first
few  minutes and had slight burning sensa-
tions of the throat and substernal area for
at least 5 minutes.  When exposed by nose,
there was little coughing and  no chest symp-
toms although some  subjects  did experience
irritation of the posterior pharynx which
lasted a few minutes.
  Nadel  et aL37 reported that airway resist-
ance, determined  with  a body plethysmo-
graph, was increased by exposure to 2 ppm
(~6 mg/m3) and 5 ppm (~14 mg/3)  sul-
fur dioxide for 3 to 10 minutes. One indi-
vidual  out of 7 exposed to 5 ppm for 10 min-
utes, showed a marked increase in airway
resistance which was reversible by isopro-
terenol inhalation. This subject had no pre-
vious history of pulmonary disease.  In later
studies 38 39 an examination was made of the
response of 7 subjects exposed by mouth for
10 minutes to from 4 ppm to 6  ppm sulfur
dioxide. Such exposures increased the air-
way resistance, and the onset of change va-
ried from  10  seconds to 4 minutes.  A maxi-
mum response was usually observed within
1 minute, but in 2 subjects the resistance in-
creased during continued  exposure,  and in
2 others the resistance decreased during ex-
posure. The subject who showed the greatest
change became dyspneic and wheezed during
the exposure.  After subcutaneous  injection
of 1.2 mg  to  1.8 mg atropine sulfate, sulfur
dioxide caused no  significant  change in air-
way resistance.  Most subjects coughed and
some experienced irritation of the pharynx
and  substernal area. These symptoms were
not affected by the atropine.
  Tomono 40 reported that the lowest level of
sulfur  dioxide which  could induce broncho-
constriction in 46 healthy male subjects was
1.6 ppm (~4.6 mg/m3). The changes were
relieved by isoproterenerol inhalation.
  Burton et al.*1 examined airway resistance
and dynamic lung compliance in 10 subjects
immediately following 30-minute exposures
to  1 ppm  (~3  mg/m3)  to 3 ppm  (~9
mg/m3) sulfur dioxide.  Comparison with in-
dividual or mean group controls did not re-
veal significant increases in resistance  or
compliance during quiet breathing or during
hyperventilation.

2. Sulfuric Acid Aerosol
  Amdur et al.*2 exposed subjects to sulfuric
acid mist  of  MMD Iju, at concentrations of
0.35 mg/m3 to 5 mg/m3 for 15 minutes. Res-
piration rate, tidal volume, and  minute vol-
ume were measured.  The subjects breathed
through a pneumotachograph which permit-
ted the measurement  of inspiratory and ex-
piratory flow rate. In  15 subjects exposed
to 0.35 mg/m3 to 0.5 mg/m3,  the respiration
rate increased  about  30 percent above con-
trol values, the maximum inspiratory and ex-
piratory flow rates decreased about 20 per-
cent, and  tidal volume decreased  about 28
percent. These changes occurred within the
first 3  minutes of exposure and were main-
tained  throughout  the  15-minute  exposure
period. When the exposure ended, lung func-
tion returned rapidly to preexposure levels.
       94

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The first minute after termination of the ex-
posure the tidal volume rose above control
values and then  returned  to preexposure
levels. Breathing  through the same appa-
ratus with omission of  the  acid  mist  was
done as a control and no such changes were
observed.  At the  highest level  (5 mg/md)
the acid mist was perceptible to all, and some
subjects showed a  marked response. The re-
sponse was much  more varied at this level,
the main  effect  being a  decrease in minute
volume and a prolongation of the expiratory
phase of the respiratory cycle. These experi-
ments do  not indicate  whether bronchocon-
striction  was the  response to sulfuric acid,
although they suggest  that this  may  be the
case.
  Sim and Pattle 3U studied  the  response of
healthy males, aged 18  to 46, to sulfuric acid
mist. They made  183 exposures of 10 min-
utes by mask and 316 60-minute chamber
exposures to  an acid mist at  a relative hu-
midity of 62  percent.  The droplet size  was
1/1 and the strength of the sulfuric acid drop-
lets was 10 N.  They also made a total of 40
exposures in  the chamber at  91 percent rela-
tive humidity. The droplet size was 1.5/j. and
the normality was 4 N,  and concentrations
of the dry mist were 3 mg/m1 to 39 mg/m3
and  of the wet mist were  11.5 mg/m3 to
38 mg/m3. The reporting of the results was
vague. The sulfuric acid was more irritant
at high  humidity,  when  exposure at 20.8
mg/m3 for  30  minutes  produced intense
coughing  which  did  not  cease  entirely
throughout the exposure  period.  The mist
was  described as "almost intolerable  at the
onset" but the men "were able  to continue
for a period  of 30  minutes."  No airway re-
sistance measurements could  be made dur-
ing the first 10 minutes. When the coughing
had  diminished enough to permit measure-
ment, the increases ranged from 43 percent
to 150 percent above normal.  When the ex-
posure was to dry mist at 39 mg/m3 for a
60-minute exposure, the  mist was well tol-
erated and there was minimal  coughing. All
12 men in the group showed an increase in
resistance with a range of changes from 35.5
percent  to 100 percent  above normal.   As
was  mentioned previously, the investigators
themselves became sensitive to both  sulfur
dioxide and sulfuric acid mist.  One of them
had his last exposure to 39.4 mg/m3 of the
dry mist,  and he then exhibited chest symp-
toms for the remainder of the exposure and
wheezed persistently for 4 days  thereafter.
Two subjects  exposed to sulfuric acid devel-
oped long-lasting bronchitic symptoms.
  Two points  of value from this study apply
to toxicological  evaluation. One is the  ob-
served effect of high humidity on the irri-
tant potency of sulfuric acid.  The other is
that, in terms of sulfur equivalent, sulfuric
acid is considerably more irritant to human
subjects than  is sulfur dioxide.
  Lawther 43 believes that experiments in the
laboratory in which normal subjects have in-
haled sulfuric acid  mists of various particle
sizes but of concentrations of approximately
1 mg/m3  have failed to produce significant
alterations in airway resistance.  He men-
tions that certain  individuals  show a  re-
sponse to  sulfur dioxide at concentrations at
which  the group tested as a whole did  not
respond and suggests that no  such hyper-
sensitivity to sulfuric acid has been recorded.
These opinions are presumably  based on  the
author's own unpublished data and are diffi-
cult to evaluate.

        C.  NASAL ADSORPTION
  Frank  and Speizer44 4~'  made  measure-
ments  of  the  uptake and  release of  sulfur
dioxide by  the  human  nose.  Subjects
breathed through a  face mask with special
ports for  sampling  tubes.   Samples could be
taken within the mask within the nose 1  cm
to 2 cm beyond the  alae nasi, and within  the
oropharynx as far  back as could be toler-
ated. The electrical  conductivity method was
used to determine the concentration of sul-
fur dioxide in samples taken during both in-
spiration and expiration. The concentration
within the mask averaged 16  ppm  (~46
mg/m3), and exposures were of 25-minutes
to 30-minutes duration. The average con-
centration  in the nose was  13.8  ppm  (~39.5
mg/m'), representing a decrease of 14 per-
cent.  The  concentration at the oropharynx
was too small to be measured accurately.
During exhalation, the sample from the nose
contained  an average of 2 ppm, suggesting
                                                                             95

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a desorption from the mucosa during exhala-
tion.

 D.  EFFECT ON REMOVAL  OF  MUCUS
   FROM THE RESPIRATORY TRACT
  In a study46 of the effect of sulfur dioxide
on the rate of removal of mucus from the
respiratory  tract of human  subjects,  expo-
sures to from 10 ppm to 15 ppm (~29 mg/m3
to ~43 mg/m3) for 1  hour  produced a 10-
percent to  15-percent decrease in the  clear-
ance rate, while a concentration of 25 ppm
to 30  ppm  (~72 mg/m3 to ~86 mg/m3)
caused a 45-percent to 50-percent decrease
and  50 ppm to 55 ppm  (~140 mg/m3  to
~160  mg/m3)  caused  a  65-percent to 70-
percent decrease. It was not reported wheth-
er or not the subjects were nose-breathing
during exposure.

       E.  SENSORY  THRESHOLD
            CONCENTRATIONS
  The kinds of response to sulfur dioxide dis-
cussed in this section,  although  not strictly
within the realm of toxicology, are appended
here because the data  are closely related to
the discussion in this Chapter.
  Many recent investigations in Russia have
been directed toward determining sulfur ox-
ides threshold concentrations  for various
sensory responses. These investigations have
included determination of odor thresholds
and the effects of sulfur  dioxide on optical
chronaxie, sensitivity of the dark-adapted eye
to light, interruption of the alpha («) rhythm
in electroencephalograms, and  interference
with cortical conditioned  reflexes as shown
by electroencephalograms. Most of these in-
vestigations have been summarized, and the
more recent methodology described, by Ry-
azanov.47

       1.  Odor Perception Threshold
  An odor threshold is typically determined
in  a well-ventilated chamber containing  2
orifices from which emerge 2 small streams
of gas, one very pure air and the other being
a stream of the test gas. The subject sits in
front of the apparatus, sniffs both orifices,
and points out the odorous one.  This ex-
periment is repeated with the same concen-
tration of  test gas over a period of several
days.  The experiment  is performed with in-
creasingly reduced concentrations until the
subject, in the majority of instances, denies
the presence  of an odor or gives erroneous
answers. The threshold concentration for the
most sensitive subject in a group of volun-
teers  is defined  as  the threshold for  odor
perception.47
  Using the  2-orifice  apparatus described
above, Dubrovskaya48  conducted sulfur di-
oxide odor  perception threshold  tests on 12
subjects. Sulfur  dioxide concentrations of
0.5 mg/m3  to 13 mg/m3 (0.17  ppm to 4.6
ppm) were used in 530 threshold determina-
tions.  Six test subjects sensed the odor of
sulfur dioxide in the range 2.6 mg/m3 to 3.0
mg/m3; four  subjects sensed the odor in the
range  1.6 mg/m3 to  2.0 mg/m3; one sensed
the odor in  the  range 2.1 mg/m3 to 2.5
mg/m3; and one sensed the odor in the range
3.1 mg/m3  to 3.6 mg/m3.  Thus, the aver-
age sulfur dioxide odor threshold concentra-
tion was 0.8  ppm to 1 ppm (~2.3 mg/m3
to ~2.9 mg/m3),  and for the more sensitive
of these persons it was 0.5^»ppm to  0.7/ppm
(~l,|omg/m3 to ~%0 mg/m3); it should be
noted, however,  that most of the  subjects
were of an age at which odor perception was
presumed to be most sensitive.
  Bushtueva49 reported that among 10 test
subjects the  minimum concentration of sul-
fur ic acid aerosol (particle  size not given)
which was  sensed by odor ranged from 0.6
mg/m3 to 0.85 mg/m3 (average 0.75 mg/m3).
In tests made on five subjects 50 a combina-
tion of sulfur dioxide at 1 mg/m3 (0.35 ppm)
and sulfuric  acid  mist at 0.4 mg/m3 was be-
low the odor  threshold.
   Popov et al.51 used an apparatus in which
the  sulfur  dioxide concentration  could be
changed rapidly and showed that the  odor
of  sulfur dioxide could be detected at con-
centrations of 4 mg/m3  (1.4 ppm). At 4.0
mg/m3 to 6.5 mg/m3 (1.4 ppm to 2.3 ppm),
the majority  of their test subjects perceived
the gas as a strong odor; a few perceived it as
a faint odor. Subjects described concentra-
tions of sulfur dioxide above 8.5  mg/m3 (3.0
ppm)  as having a very sharp odor. The  num-
ber of subjects involved in these studies was
not stated.
   Recent determination of sulfur dioxide
odor  thresholds52 conducted for the Manu-
       96

-------
 facturing Chemists' Association gave some-
 what lower values than  those  cited above.
 The concentrations  at which first  one-half
 and then all of the panel members could posi-
 tively recognize the odor were reported both
 to be 0.47 ppm (1.3 mg/m3). The details of
 the  test procedure are thoroughly discussed
 in the  report, but one important aspect is
 reiterated as a reminder that odor thresholds
 usually represent values derived under ideal-
 ly suited  conditions and  with  trained  indi-
 viduals. The investigators, who were highly
 qualified to judge on the basis of substantial
 experience  with  consumer evaluation  of
 known  flavor  and odor situations,  derived
 threshold values, in test rooms under  ideal
 conditions, lower than those which would be
 recognized by  the majority of a population
 under ordinary atmospheric conditions.  This
 does not mean that normal  individuals ex-
 posed to sulfur dioxide under ideal test con-
 ditions  could not perceive the 0.47 ppm level
 indicated, but  because of  background  odor
 and  lack of awareness or concern with am-
 bient odor  conditions, such individuals  in
 an everyday situation would probably be less
 responsive to this low concentration than are
 subjects undergoing a test.

  2.  Sensitivity of the Dark-Adapted Eye
  The  sensitivity  of the eye to  light  while
a subject is  in  darkness increases with time.
 Several investigations have been made of the
effects  of inhalation of sulfur oxides on this
sensitivity.  Typically,  measurements of a
subject's normal sensitivity are  taken  in a
dark, well-ventilated  chamber in complete
silence  (sudden stimuli, including noise, may
change  the sensitivity).   Each  subject  is
tested once daily following preliminary con-
ditioning- at a  high light  level. Light sensi-
tivity is measured at 5-minute or 10-minute
intervals, and  a normal curve of increasing
sensitivity to light is established from meas-
urements taken over a period of 7  days to
10 days.47
  Dubrovskaya "8  studied the effect of in-
haling sulfur dioxide in concentrations from
0.96  mg/m3 to 19.2  mg/m3 for 15  minutes
before   measuring light sensitivity during
dark adaptation.  She reported that light
sensitivity was increased by sulfur dioxide
 concentrations of 0.96 mg/m3 to 1.8 mg/m3
 (0.34 ppm to 0.63 ppm), that the increase in
 sensitivity reached  a maximum at concen-
 trations of 3.6 mg/m3 to 4.8 mg/m3 (1.3 ppm
 to 1.7 ppm), and that further increases in the
 sulfur dioxide concentration resulted in pro-
 gressive lowering of eye sensitivity to light
 until at 19.2 mg/m3 the sensitivity was iden-
 tical with that of the unexposed subject.
   In exposures  during light adaptation, sul-
 fur  dioxide concentrations  of 0.6 mg/m3 to
 7.2 mg/m3  (0.21  ppm  to 2.5 ppm)  caused
 slight increases  in eye sensitivity.  Maximum
 sensitivity was  attained at  1.5 mg/m3  (0.52
 ppm); at higher concentrations the increased
 sensitivity began to abate. Two human sub-
 jects were used in  these experiments. The
 odor threshold was  between 2.5 mg/m3 and
 3.0 mg/m3 for one subject  and between 3.0
 mg/m3 and 3.6 mg/m3 for the other, so that
 changes in sensitivity to light during dark
 adaptation were caused by sulfur dioxide con-
 centrations below the odor  threshold.
   Bushtueva 49 studied the effect of sulfuric
 acid mist on the sensitivity id light  of two
 test  subjects. The test periods were  60, 90,
 and  120 minutes. During the first half hour,
 sensitivity was  measured every  5 minutes,
 and  after  that  every 10 minutes. In each
 subject  a control  curve  was  established  by
 7 repeated tests, and then the effect on light
 sensitivity of sulfuric acid aerosol  exposure
 for 4 minutes and for 9 minutes at the 15th
 and  60th  minutes, respectively,  was  deter-
 mined.  With sulfuric acid mist of undeter-
 mined particle size at a concentration of 0.6
 mg/m3,  a just  detectable increase in  light
 sensitivity was found as a result of the ex-
 posure at  the 15th minute, but no detectable
 effect was observed  as a result of the ex-
 posure at the 60th  minute.  Concentrations
 in the range of 0.7  mg/m3 to 0.96 mg/m3
 brought about a  well-defined increase in light
 sensitivity. With 2.4 mg/m3, increased sensi-
 tivity to light was elicited by the exposures
 at both the 15th  and 60th minutes of the test;
normal sensitivity was restored in 40 to 50
minutes.
  Bushtueva 50  studied  the  effect of sulfur
 dioxide, sulfuric acid mist and combinations
 of the two on sensitivity of the eye to light
 in 3  subjects.  The combination of sulfur di-
                                                                              97

-------
oxide at 0.65 mg/m3 (0.23 ppm) with sul-
furic acid mist at 0.3 mg/m3  resulted in no
change in sensitivity of the eye to light.  An
increase of approximately 25 percent in light
sensitivity resulted from  exposure to either
sulfur  dioxide at 3 mg/m3 (~1.0 ppm) or
sulfuric acid mist at 0.7 mg/m3.  The combi-
nation of sulfur dioxide at 3 mg/m3 with sul-
furic acid mist at 0.7 mg/m3  resulted in an
increase of  approximately  60  percent  in
light sensitivity.  Exposures lasted  for 4%
minutes.
     3.   Interruption of Alpha Rhythm
  The  electroencephalogram is a composite
record of the electrical activity of the brain
recorded as the difference in electrical poten-
tial between 2 points  on the head.  In  the
adult, the electroencephalogram   character-
istically shows a fairly uniform frequency
from 8  cycles to 12 cycles per second in the
posterior  head  regions.   Variations  occur
with age, and the state of wakefulness and
attentiveness, or as  a result of incoming
sensory stimuli  from exteroceptive or in-
teroceptive  receptors.   The dominant fre-
quency is inhibited or attenuated by eye open-
ing and by mental activity.53
  Subjects with well-defined a-rhythms stud-
ied in a silent and electrically-shielded cham-
ber  show  a  temporary  attenuation of  the
a-rhythm  each time they are given a light
signal.  When  the  light  is  excluded,  the
a-rhythm  returns  to normal.  A  concentra-
tion of test gas is determined which is so low
that by itself it does not cause attenuation of
the a-rhythm. A subject breathes the gas at
this concentration,  and then he receives the
light signal.  After exposure to this sequence
 (gas then light) several times (5 to 30 times
in 1 day), a subject will show  attenuation
before he receives  the  light signal; that is,
he  responds to  the unperceived  odor. The
unperceived  odor thus becomes   the  condi-
tioning stimulus and  brings  about the so-
called conditioned electrocortical reflex.47
  Bushtueva et  al.54 reported  that 20-second
exposures of 6 human subjects to sulfur di-
oxide concentrations from 0.9 mg/m3 to  3
mg/m3  (~0.3 ppm to ~1.0 ppm) produced
attenuation of the a-wave lasting 2 to 6  sec-
onds; at concentrations of 3.0 mg/m3 to 5.0
mg/m3  (~1.0 ppm to 1.7 ppm)  attenuation
lasted  throughout the  20-second  exposure.
Exposures to 0.6 mg/m3 (~0.2 ppm) did not
cause attenuation of the a-wave.  Exposures
to sulfuric acid mist at 0.6 mg/m3 to 0.75
mg/m3  caused attenuation of the  a-wave,
whereas exposures  to  0.4  mg/m3  to  0.5
mg/m3  did  not.  For  both substances,  the
threshold for attenuation  of  the  a-wave is
the same as the odor threshold or the thresh-
old of irritation of the respiratory tract.  In
other experiments, Bushtueva demonstrated
that electrocortical conditioned reflexes could
be  developed with  sulfur dioxide  at  0.6
mg/m3  (~0.2 ppm)  or with sulfuric acid
mist at 0.4  mg/m3, but not with lesser con-
centrations  of  either  substance.   Finally,
Bushtueva 55 demonstrated that combinations
of sulfur dioxide at 0.50 mg/m3 (0.17 ppm)
with sulfuric acid mist at 0.15 mg/m3 or sul-
fur dioxide at 0.25 mg/m3  (0.087 ppm) with
sulfuric acid mist at 0.30 mg/m3  could pro-
duce electrocortical conditioned reflexes.

          4.  Optical Chronaxie
  Chronaxie is defined as the time required
for  excitation  of  a nervous  element by a
definite stimulus.  In the  determination of*
optical  chronaxie, a weak  electrical current
is applied to the eyeball to give  the sensa-
tion of  a light flash. For each subject there
is an intensity of stimulation (measured in
volts)  below  which no sensation  of  light
takes place. The time required for this mini-
mal voltage to produce the sensation of light
in a subject is the optical  chronaxie for the
subject. According to Pavlovian theory, the
excitation of one area of the cerebral cortex
may inhibit the excitation  of  other areas
through the rule of induction.47 It has there-
fore been postulated that  excitation of the
olfactory sensory area by  the oxides of sul-
fur  inhibits the light-sensing area of the
cerebral cortex and thus  increases optical
chronaxie.
  Bushtueva 50 studied  the effects of differ-
ent concentrations of sulfur dioxide, sulfuric
acid mist, and combinations  of the two on
the optical chronaxie of three subjects.  Op-
tical chronaxie was determined in each test
subject at 3-minute intervals as follows: at
the start and on the 3rd, 6th, 9th, 12th and
15th minutes. Between the 6th and 9th min-
       98

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utes the subjects inhaled sulfur dioxide, sul-
furic acid mist, or their  combination for 2
minutes.  In each subject the threshold con-
centrations  of sulfur  dioxide  and  sulfuric
acid mist were first determined  independ-
ently, and then threshold concentrations for
combinations of the two were determined.
  Results presented for one subject were:
     1. Neither sulfur dioxide at 900 /*g/m3
      nor sulfuric acid mist at 600 /ug/m3
      produced increased optical chronaxie,
      but the combination  of these concen-
      trations produced  a  16 percent in-
      crease in optical chronaxie;
     2. concentrations of  sulfur dioxide  at
      1200  /xg/m3 with sulfuric acid mist at
      400  /ig/m3  produced  no increase  in
      optical chronaxie; and
     3. concentrations of either  sulfur diox-
      ide at 1500 |ug/m3 or sulfuric acid mist
      at 750  /xg/m3 increased optical chro-
      naxie, and the effects of the combina-
      tion at these concentrations were ad-
      ditive.  Similar results were reported
      for the other subjects.
  The data  obtained  by Bushtueva55  are
summarized in Table 7-1.  Consideration of
the levels noted provides information which
may  be  relevant  to the establishment  of
"Level I" and  "Level II" of the World Health
Organization's  "guides  to  air  quality."56
These "guides," equivalent  in  usage to our
term "criteria," covers sets of concentrations
and exposure  times at which specified types
of effects are  noted or at which no effect is
 noted. The  definitions of these levels are as
 follows:
       Level  I  (Range I)  Concentrations
     and  exposure times at or below which,
     according to present knowledge, neither
     direct  nor indirect  effects  (including al-
     teration of reflexes  or of adaptive or pro-
     tective reactions)  have been observed.
       Level II  (Range II)  Concentrations
     and  exposure times at and above which
     there  is  likely to  be irritation  of  the
     sensory organs, harmful effects on vege-
     tation, visibility reductions, or other ad-
     verse effects on the environment.
       Level III  (Range III) Concentrations
           and exposure times at and above
     which  there is likely to be impairment
     of   vital  physiological  functions   or
     changes that may  lead to chronic  dis-
     eases or shortening of  life.
       Level IV  (Range IV) Concentrations
     and  exposure times at and above which
     there is likely to be acute illness or death
     in susceptible groups of the population.
   The practical ramifications of these neuro-
 physiological responses have  not been  ex-
 plored. In  addition, one should be cautioned
 in the interpretation of  these data since there
 have been no replicate studies to confirm the
 reported  neuro-physiological  responses  and
 information  concerning  the  experimental
 conditions was less than adequate.
               F.   SUMMARY
   Various  animal  species,  including man,
 respond to  sulfur dioxide by bronchoconstric-
       Table 7-1. THRESHOLD CONCENTRATIONS  OF SULFUR DIOXIDE, SULFURIC ACID,
                   AND THEIR COMBINATIONS FOR VARIOUS RESPONSES55
                                                         Threshold Concentration
               Procedure Used
H2S(X
SO,
H2SO,
S02
Threshold Concentration of Irritation
Effects and Odor Perception
Data Obtained by the Method of Eye
Adaptation to Darkness
Data Obtained by the Method of
Optical Chronaxie
Encephalographic Method
"Electrocortical" Conditioned Reflex


600-850

630-730

730
630
400


1600-2600

920

1500
900
600


>300

>300

600
>300
150
300

500

500

1200
500
500
250
                                                                               99

-------
tion,  which  may be assessed  in  terms of  a
slight increase in airway resistance. Normal
individuals,  exposed to sulfur dioxide via the
mouth,  exhibit small changes in airway re-
sistance which are often insufficient to  pro-
duce  any respiratory symptoms.  The effects
may  be  even   smaller  when  the  subject
breathes through his nose.
  Laboratory observations of respiratory ir-
ritations  suggest that most individuals will
show a response to sulfur dioxide at concen-
trations of 5 ppm (~14 mg/m3) and above.
At  concentrations of 1 ppm to 2 ppm  (~3
mg/m3  to ~6 mg/m3) an effect can be de-
tected only  in certain  sensitive individuals,
and on occasion, exposures to 5 ppm to 10
ppm  (~14 mg/m3 to ~30 mg/m3) have been
shown to cause severe bronchospasm in such
persons;  no  further special study at lower
concentrations  has  been  carried  out  with
these individuals.  The exposure of the more
sensitive  individuals to 1 ppm  (~3 mg/m3),
although  it does not produce severe broncho-
spasm,  does elicit a detectable response.
  Sulfuric acid  is a much more potent  irri-
tant to man than is sulfur dioxide, and its
effects are highly dependent on particle  size.
Insufficient  data are available for quantita-
tive assessment  of the health hazard. There
is inadequate information on the response
of human subjects to any of the  other  par-
ticulate sulfates.  Nasal  absorption and de-
sorption of  oxides  of  sulfur,  and the effect
of the oxides on the removal of mucus from
the respiratory  tract are  briefly considered.
  In  most of the studies  discussed, an in-
crease in pulmonary flow  resistance was the
indicator  of response  employed.  However,
the concentrations of oxides  of  sulfur  just
needed to elicit certain sensory responses are
presented, although the  practical ramifica-
tions of these  neurophysiological responses
have  not been  fully explored.  These values
may  ultimately  have significance for the es-
tablishment  of Levels  I and II of air quality
as promulgated  by the World Health Organi-
zation.

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    lia,  Vol. 44, pp. 897-921, June 15, 1957.
24.  Oswald, N. C. "Physiological Effects of Smog."
    Roy. Meteorol. Soc. J., Vol. 80, pp. 271-278, 1954.
25.  Anderson, R. J. "Epidemiologic Studies of  Air
    Pollution."  Diseases of the Chest, Vol. 42, pp.
    474-481, Nov.  1962.
26.  Cooper, W.  C. "Epidemiologic Studies on  Air
    Pollution."   Amer.   Med.  Assoc.,   Arch.  Ind.
    Health, Vol. 15, pp. 177-180,  1957.
27.  Wallace,  A. S.  "Mortality from  Asthma and
    Bronchitis in the Auckland 'Fumes Area'."  New
    Zealand Med. J., Vol. 56,  pp.  242-249,  1957.
28.  Greenwald, I. "Effects of Inhalation of Low Con-
    centrations of  Sulfur  Dioxide Upon Man and
    Other Mammals." Amer. Med.  Assoc., Arch, Ind.
    Hyg. and Occup. Med., Vol. 10, pp.  455-475, Dec.
    1954.
29.  Amdur, M. O.  "Report on Tentative Ambient Air
    Standards  for  Sulfur  Dioxide  and  Sulfuric
    Acid." Ann. Occup. Hyg.,  Vol. 3, pp. 71-83, Feb.
    1961.
30.  Sim, V. M. and Pattle, R. E. "Effect of Possible
    Smog Irritants on Human Subjects."  J. Amer.
    Med.  Assoc.,  Vol. 165,  pp. 1908-1913,  Dec. 14,
    1957.
31.  Frank, N. R.,  Amdur, M.  O., Worcester, J., and
    Whittenberger, J.  L.  "Effects of Acute  Con-
    trolled Exposure to  SO. on Respiratory  Mechan-
    ics in Healthy Male Adults." J. Appl.  Physiol,,
    Vol. 17, pp. 252-258, March 1962.
32.  Frank, N. R.  "Studies  on the Effects of Acute
    Exposure to Sulfur Dioxide in Human Subjects."
    Proc.  Roy.  Soc. Med.,   Vol. 57,  pp.  1029-1033,
    1964.
33.  Speizer, F.  E.  and Frank,  N. R. "A Comparison
    of  Changes  in Pulmonary Flow  Resistance  in
    Healthy Volunteers  Acutely Exposed to SO2 by
    Mouth and by  Nose." Brit. J. Ind.  Med., Vol. 23,
    pp.  75-79, 1966.
34.  Frank, N. R., Amdur, M. O., and Whittenberger,
    J.  L.  "A Comparison  of  the  Acute Effects of
    SO2 Administered Alone or in  Combination with
    NaCl  Particles on the Respiratory Mechanics of
    Healthy Adults." Int.  J.  Air Water Pollution,
    Vol. 8, pp. 125-133, 1964.
35.  Amdur, M. 0.  "The Effect of Aerosols on the
    Response  to Irritant Gases." In:  Inhaled Parti-
    cles and  Vapors. C. N. Davies (ed.), Proc. In-
    tern  Symposium,  Oxford,  March 29-April 1,
    1960,  Pergamon Press,  Oxford,  1961, pp.  281-
    292.
36.  Amdur, M. O.  "The Physiological Response of
    Guinea Pigs to Atmospheric Pollutants." Intern.
    J. Air Pollution, Vol. 1, pp. 170-183, Jan. 1959.
37. Nadel,  J. A., Tierney, D. F., and Comroe, J. H.
    "Pulmonary Responses  to  Aerosols." Proc. 3rd
    Air Pollution Med. Res. Conference, California
    State Dept. of Public Health, Los Angeles, Cali-
    fornia, Dec. 9, 1959, pp. 66-74.
38. Nadel, J. A., Salem, H., Tamplin, B., and Tokiwa,
    Y. "Mechanism  of Bronchoconstriction." Arch.
    Environ. Health, Vol. 10, pp. 175-178, Feb. 1965.
39. Nadel, J. A., Salem, H., Tamplin, B., and Tokiwa,
    Y. "Mechanism  of Bronchoconstriction  During,
    Inhalation of Sulfur Dioxide." J. Appl. Physiol.,
    Vol. 20, pp. 164-167, 1965.
40. Tomono, Y.  "Effects of  S02 on Human Pulmon-
    ary Functions." Japan J. Ind. Health, Vol. 3, pp.
    77-85, Feb. 1961.
41. Burton,  G. G., Corn, M., Gee, J. B.  L., Vassallo,
    D., and Thomas, A. "Absence of 'Synergistic Re-
    sponse' to  Inhaled Low  Concentration Gas-Aero-
    sol Mixtures in  Healthy Adult Males." (Present-
    ed at 9th Annual Air Pollution Medical Research
    Conference, Denver,  Colorado, July  1968.)
42. Amdur,  M.  O., Silverman,  L.,  and  Drinker, P.
    "Inhalation  of  Sulfuric  Aicd  Mist by  Human
    Subjects."  Amer. Med.  Assoc.  Arch. Ind.  Hyg.
    Occup.  Med., Vol.  6, pp. 306-313, Oct. 1952.
43. Lawther, P. J. "Compliance with the Clean Air
    Act. Medical Aspects." J. Inst. Fuel, Vol. 36, pp.
    341-344, Aug. 1963.
44. Frank,  N. R. and Speizer,  F.  E. "Uptake  and
    Release  of  S02 by the  Human  Nose." Physiol.,
    Vol. 7, p. 132, Aug. 1964.
45. Speizer, F. and  Frank, N.R. "The  Uptake and
    Release  of  S03 by  the Human Nose." Arch.
    Environ. Health, Vol. 12, pp. 725-728, 1966.
46. Cralley, L.  V.  "The Effect of Irritant Gases
    Upon the Rate of Ciliary Activity." J. Ind. Hyg.
    & Toxicol.,  Vol. 24, pp. 193-198, 1942.
47. Ryazanov,  V. A.  "Sensory Physiology as Basis
    For  Air Quality  Standards."  Arch. Environ.
    Health,  Vol. 5,  pp. 479-494, Nov. 1962.
48. Dubrovskaya, F. I. "Hygienic Evaluation of Pol-
    lution of Atmospheric Air of a Large City with
    Sulfur   Dioxide  Gas."  In:  Limits  of  Allow-
    able Concentrations  of  Atmospheric  Pollutants,
    Book 3, Translated by B. S. Levine, U.S. Dept.
    of Commerce. Office of Technical Services, Wash-
    ington, D.C., 1957, pp. 37-51.
49. Bushtueva,  K.  A.  "The Determination  of the
    Limit of Allowable Concentration   of Sulfuric
    Acid in  Atmospheric Air."  In: Limits of Allow-
    able Concentrations  of  Atmospheric  Pollutants,
    Book 3, Translated by B. S. Levine, U.S. Dept.
    of Commerce, Office of Technical Services, Wash-
    ington, D.C., 1957, pp. 20-36.
50. Bushtueva, K.  A. "Threshold  Reflex Effect of
    S02 and Sulfuric  Acid  Aerosol Simultaneously
    Present in  the Air." In:  Limits  of Allowable
    Concentrations of Atmospheric Pollutants, Book
    4,  Translated by  B. S. Levine, U.S. Dept. of
    Commerce, Office of Technical Services, Washing-
    ton, D.C., Jan. 1961, pp. 72-79.
                                                                                           101

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51. Popov, I. N., Cherkasov, Ye. F., and Trakhtman,
    O.  L.  "Determination of Sulfur Dioxide  Odor
    Threshold Concentration." Gig. i Sanit, Vol.  5,
    pp.  16-20, 1952.  In:  U.S.S.R. Literature on Air
    Pollution and Related Occupational Diseases.  A
    Survey, Vol. 3, Translated by B. S.  Levine, U.S.
    Dept. of Commerce, Office of Technical Services,
    Washington, D.C.,  May 1960, pp. 102-106.
52. "Determination  of  Odor Thresholds for 53  Com-
    mercially Important Organic  Compounds." Re-
    port by Arthur D.  Little, Inc. to the  Manufactur-
    ing  Chemists' Association, Jan. 11,  1968, 21 pp.
53. Grollman,  A. (ed.) "The Functional  Pathology
    of  Disease;  The Physiologic Basis of Clinical
    Medicine." 2nd edition, McGraw-Hill, New York,
    1963, 979 pp.
54. Bushtueva, K.  A.,  Polezhaev, E. F., and Semen-
    enko, A. D. "Electroencephalographic Determina-
   tion of Threshold Reflex Effect  of Atmospheric
   Pollutants."  Gig. i  Sanit., Vol. 25, pp.  54-61,
   1960. In:  U.S.S.R.  Literature on Air Pollution
   and Related  Occupational  Diseases. A Survey,
   Vol. 7, Translated by B. S.  Levine, U.S. Dept. of
   Commerce, Office of  Technical Services, Washing-
   ton, D.C., 1962, pp. 137-142.
55. Bushtueva, D. A. "New Studies of the Effect of
   Sulfur Dioxide and  of  Sulfuric Acid Aerosol on
   Reflex Activity of Man." In: Limits  of Allow-
   able Concentrations of  Atmospheric Pollutants.
   Book 5, Translated by B. S. Levine, U.S. Dept. of
   Commerce, Office of Technical Services, Washing-
   ton, D.C., March 1962,  pp.  86-92.

56. "Atmospheric Pollutants." World Health Organ-
   ization,  Technical  Report  Series  271, Geneva,
   1964.
        102

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                   Chapter 8
COMBINED EFFECTS OF EXPERIMENTAL EXPOSURES TO
 SULFUR OXIDES AND PARTICULATE MATTER ON MAN
                 AND ANIMALS

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                          Table of Contents
                                                                Page
A. INTRODUCTION                                              105
B. EVALUATION BY MORTALITY AND PATHOLOGY
   IN ANIMALS                                               .   105
   1.  Sulfur Dioxide, Sulfuric Acid, and Particles                       105
   2.  Sulfur Dioxide and Sulfuric Acid                            .    106
C. EVALUATION BY PULMONARY FUNCTION IN ANIMALS         107
D. EVALUATION BY PULMONARY FUNCTION IN MAN . ...          109
E. SUMMARY                  .                        	    Ill
F. REFERENCES                                                 111
 104

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                                    Chapter 8

         COMBINED EFFECTS OF  EXPERIMENTAL  EXPOSURES TO
  SULFUR OXIDES AND PARTICULATE MATTER  ON MAN AND ANIMALS
          A.  INTRODUCTION
  The  problem of interactions of irritant
gases and  particulate  material  is one of
greatest interest in air pollution toxicology.
Its implications are far broader than the pre-
sent  specific discussion  of the effect of par-
ticulate material on the response to sulfur
dioxide. For a treatment of the broader as-
pects of the problem, see Chapters 9 and 10
in the companion document, Air Quality Cri-
teria for Particulate Matter.

   B.  EVALUATION BY MORTALITY
     AND PATHOLOGY IN ANIMALS

   1.  Sulfur Dioxide, Sulfuric Acid, and
                Particles
  Schnurer1 exposed rabbits  and rats (23
hours per day for 80 days) and  mice (17
days) to  atmospheres produced from burn-
ing equal amounts of anthracite coal, of coke,
and of bituminous coal. The resulting sulfur
dioxide concentrations were 1.91 ppm  (5.46
mg/m3) for anthracite  coal, 9.12  ppm  (26.1
mg/m3)  for coke,   and   7.51 ppm   (21.5
mg/m3) for bituminous coal. The correspond-
ing particle concentrations were  312,  370,
and 4,410 particles per cc.  The control atmos-
phere contained 125  particles per cc. Taking
the weight gain of control animals as 100 per-
cent, the rats  exposed  to  anthracite smoke
gained 105  percent, the rats exposed to coke
smoke gained 114 percent, and the rats ex-
posed to  bituminous coal  smoke gained 75
percent. With the rabbits these values were
84 percent,  77 percent, and 9 percent respec-
tively.  The hemaglobin percentage and the
red and  white blood cell  counts rose in all
groups, but this rise was less pronounced in
the rabbits exposed to anthracite smoke. The
greatest changes in the above measurements,
the greatest number of uncomplicated pneu-
monias, and the greatest incidence of bron-
chitis were observed in the animals exposed
to bituminous  coal smoke.  No  significant
pathological change could be detected in the
lungs of animals exposed to coke or anthra-
cite smoke 21/2 months or 14 months after
exposure.  Animals exposed  to  bituminous
coal  smoke  developed evidence  of fibrosis,
proliferation of the bronchial epithelium, and
marked peribronchial lymphoid hyperplasia.
  The exposures  to anthracite  coal smoke
and coke smoke were  essentially equivalent
in terms of particle concentration, but the
smoke from the coke contained about 9 ppm
(~26 mg/m3) sulfur  dioxide as  opposed to
about 2 ppm (~6  mg/m3) for the anthracite
coal smoke. Neither of these exposures pro-
duced pathological alterations in the lungs.
The  smoke from  coke and bituminous coal
contained about 9 ppm (~26 mg/m3) and 8
ppm  (~23 mg/m3) sulfur dioxide, but the
particle concentration of the bituminous coal
smoke was over 10 times that of the smoke
from  the coke. The bituminous  smoke pro-
duced  pathological alterations which  were
not observed in animals exposed to the smoke
from  the coke. The pathological  alterations
observed in the animals  exposed to bitumin-
ous coal smoke may possibly be associated
with the simultaneous presence of high levels
of sulfur dioxide and smoke. Unfortunately,
however, the  experiments  do not allow a
simple interpretation.
  Susceptibility to infection by pneumococci
of rats exposed to coal dust or  smoke has
been studied.2  Sulfur dioxide concentrations
in the coal smoke ranged between 0.7 ppm
(2.0 mg/m3) and  1.6 ppm (4.6 mg/m3), and
                                                                          105

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smoke concentrations would have been con-
sidered as  "dense"  on  visual  inspection
(equivalent to about a No. 3 reading on the
Ringelmann chart). Exposures ranged from
2 to 154 days,  and no difference was noted
between the control animals and exposed ani-
mals in regard  to mortality or  susceptibility
to infection. On the other hand, the strain of
rats used normally  are known to  develop
areas in the lung which are filled with mucus
or pus, and the incidence  of this condition
was 20 percent in the control animals and 40
percent in animals  exposed to smoke for
more than 20 weeks.
    Pattle and  Burgess 3 studied the effect of
mixtures of sulfur dioxide and smoke on mice
and guinea pigs. The concentrations of sulfur
dioxide used were in the range of  2,700
mg/m3 to 12,000  mg/m3 (940  ppm to  4,200
ppm)  and the smoke concentrations  were in
the range of 50 mg/m3 to 135 mg/m3. The
end point was the dosage required to produce
death. With concentrations of this magnitude,
the results obtained have little applicability
to air pollution criteria. Although they found
that the lethality of  mixtures  of sulfur di-
oxide and smoke was  greater than the lethal-
ity of the sulfur  dioxide alone, they consid-
ered the effect to  be a simple additive one re-
sulting from  the action of smoke in blocking
the bronchi and alveoli.
   Salem and Cullumbine 4 studied the effects
of  kerosene smoke on the acute toxicity to
guinea pigs  and  mice of  various irritants,
among them sulfur dioxide and sulfuric acid.
As in the work of Pattle and  Burgess,3 the
concentrations  were orders  of  magnitude
greater than those found in polluted atmos-
pheres. Sulfur dioxide concentrations were
between 1, 200  ppm (3,400 mg/m3) and 2,700
ppm, (7,700 mg/m3) while sulfuric acid con-
centrations  were  in  the range 55/ig/m3  to
174 ju.g/m3.  The  smoke concentrations were
presumably about 600 mg/m3,  although it is
not clearly stated whether this was the con-
centration used in the combinations. The end
point was the mean fatal dose. The adminis-
tration, of smoke prior to exposure to the ir-
ritant substances did not alter the toxicity in
contrast with  a  report by Pattle and Bur-
gess 3 of  a protective effect.  The  effect  of
smoke on the toxicity of the various irritants
was  highly  variable  when  the  two agents
were given simultaneously. In guinea pigs the
toxicity of sulfur dioxide was decreased by
the smoke and in mice it was increased; the
toxicity of sulfuric acid was increased by the
smoke.
  Gross et als reported the typical lesions of
pneumontis  in the  lungs of hamsters,  rats,
and  guinea  pigs exposed to "a sufficiently
large number of carbon particles with either
adsorbed sulfur dioxide or nitrogen dioxide."
Exposure was 8 hours per day, 5 days a week,
for 4 weeks. The histological sections from
animals killed about a month after the end of
exposure, indicated  that the  lesions were per-
sistent. The lesions  were concentrated in the
regions of the respiratory  bronchioles and
alveolar ducts and  consisted of cellular wall
thickening. Data were not provided about the
amount of irritant absorbed by the activated
carbon particles, or the  particle size of the
carbon, nor  on the meaning of "a sufficiently
large number of carbon  particles." It was
concluded that under certain experimental
conditions the irritant gases were  capable of
rendering normally inert particles irritant,
but these conditions were not defined.

    2.   Sulfur Dioxide and Sulfuric Acid
  The effect of a combination of sulfur diox-
ide and sulfuric acid on guinea pigs has been
reported.6 Only  one combination of concen-
trations  was  used, 89 ppm  (255 mg/m3)
sulfur dioxide and 8 mg/m3 sulfuric acid
(l-/i MMD).  Eight  animals were exposed
to this combination for 8 hours and 2 of these
animals were reexposed 4 days  later to the
same combination.  Since only one combina-
tion of concentrations was used in these ex-
periments, they do not provide  evidence for
synergism,  and the  author concludes that
further studies are needed before the results
can be interpreted.
  Bushtueva"8  reported that  exposure  of
guinea pigs to 0.5  mg/m3 sulfuric acid pro-
duced  only  slight lung irritation. When the
sulfuric acid  was  combined with 0.3  ppm
(~0.9 mg/m3)  sulfur dioxide,  considerable
changes in  lung pathology  were observed  2
months  after  a  2-week   exposure. These
changes included thickening of  the  inter-
       106

-------
alveolar septa, formation of lympathic folli-
culi,  and perivascular and  peribronchiolar
fibrosis. Histamine content of the  lungs in-
creased concomitantly with the pathology. It
is difficult to draw any unified conclusions of
practical value from these experiments, since
none was designed  so that  the joint  toxic
action could be satisfactorily assessed.

   C.   EVALUATION BY  PULMONARY
         FUNCTION  IN ANIMALS
   The increase in pulmonary flow resistance
has been used by Amdur et al.9'11 to study the
effect  of  simultaneous exposure of  guinea
pigs to irritant gas and to  an aerosol. Three
experiments deal  with the situation in which
both the gas and the aerosol are irritant. Two
of these use sulfur dioxide and sulfuric acid
mist,10 and  one uses sulfur dioxide and zinc
ammonium  sulfate.11
   In the sulfur dioxide-sulfuric acid  experi-
ments  the  concentrations  employed  were
high  (about 100  ppm sulfur dioxide and  8
mg/m3 to 15 mg/m3 sulfuric acid). When the
sulfuric  acid  had a  particle size of  0.8-/x
MMD, the joint toxic action was synergistic.
When the acid particles were larger, with an
MMD  of  2.5,u, the response  to  the mixture
was  slightly less than the response  to the
higher level of sulfur dioxide alone.
   The concentrations used in the experiment
with zinc ammonium sulfate and  sulfur di-
oxide were  at about the concentrations at
which these substances were  estimated  to
have been present during the Donora episode.
Zinc ammonium  sulfate, 0.29-/X MMD, was
used at 0.25 mg/m3,  and the sulfur dioxide
was at 2 ppm  (~6 mg/m3). The effect of the
combination demonstrated synergism  as had
been observed with the smaller-sized sulfuric
acid. An explanation for these results may go
beyond the simple hypothesis that adsorption
of sulfur dioxide by the  smaller-size acid
particles, which penetrated the deeper areas
of the lung, increased the amount  of sulfur
dioxide reaching the alveoli.
  Other experiments  have  studied  the  com-
bined effects of sulfur dioxide  and "inert"
aerosols  (in the sense that they do not pro-
duce a  statistically significant alteration in
the flow-resistance of  guinea pigs exposed for
the  standard  1-hour  test  period  of  this
work).1" The initial "inert" aerosol used as a
standard  was sodium chloride at a concen-
tration of about 10  mg/m1  in  combination
with  a variety of irritant gases. This  con-
centration of  sodium chloride as an aerosol
of 2.5-^ MMD did not  alter  the response to
sulfur dioxide. In all subsequent experiments
a 1-percent sodium chloride solution was dis-
persed as an aerosol  with a count mean size
of about  QMfjL  (,rg- = 3.3). This aerosol did
potentiate the response to the sulfur dioxide
when  tested  over the  concentration  range
2 ppm to 200 ppm (~6 mg/m3 to 570 mg/
m'1).'" The data were examined by comparing
the concentration of gas plus aerosol with the
concentration  of  gas  alone required to pro-
duce the same percentage increase in resist-
ance. Over the concentration range of 25 ppm
to 250  ppm   (72 mg/m3  to  715 mg/m3)  a
given  concentration   of sulfur dioxide plus
aerosol produced about  the same response as
was produced by 2.5  to 3 times that concen-
tration of the gas alone.
  At lower concentrations the  relationship
changed, and  at 2 ppm the gas  plus aerosol
produced the same response as 30 times that
concentration  of gas alone. A comparison of
the dose-response curves  for sulfur dioxide
and  sulfuric  acid  (0.8/x)  gave a  similar
picture.
  At the  higher concentration  ranges, the
response to sulfuric acid was uniformly 15
to 20  times the  response to an equivalent
concentration  of  sulfur dioxide, but at 0.5
ppm (1.4  mg/m3) sulfuric acid the response
is equivalent to the response  to 60 ppm (170
mg/m3) sulfur dioxide rather than to 8 ppm
to 10 ppm (23 mg/m3 to 29 mg/m3) as would
have been predicted. However, for the entire
concentration  range  tested, response to sul-
furic acid was about 3 times  the response to
an equivalent amount of sulfur dioxide in the
presence of the aerosol,  which suggested that
the gas-aerosol mixture had the same  bio-
logical effect as sulfuric acid.  The implication
is that the sulfur  dioxide had become at-
tached to  the  particles  in some manner and
created an irritant aerosol.
  Decreasing the concentration of the sodium
chloride aerosol to about 4 mg/m3 decreased
the potentiating  effect.12  The dose-response
                                                                             107

-------
curve is parallel to that  obtained with the
higher concentration, but only 1  point, that
at 20 ppm (57 mg/m3), is greater than the
corresponding point for sulfur dioxide alone.
This  decrease  in  potentiating effect  with
decreased aerosol concentration  again  sug-
gested  that  the  response  was mediated
through the formation of an irritant aerosol.
It also  suggested that the irritant aerosol
formed  by sodium chloride with sulfur di-
oxide was not a very potent irritant, since the
effects had essentially vanished at an aerosol
level of 4 mg/m3.
  Another factor suggesting  the formation
of an irritant aerosol  comes from examina-
tion  of  the postexposure data. After expo-
sures to gas-aerosol combinations were ter-
minated,  the   resistance  values  remained
above control values rather than returning to
the preexposure level within an hour as had
occurred after exposure to these levels of ir-
ritant gas alone.13 As was pointed out at the
end of Section D of Chapter 6, the return to
control  values  was much  slower when the
irritant had  been  particulate matter  than
when it had been gaseous. The response to
113 ppm  (323  mg/m3) sulfur dioxide alone
and to 26  ppm (74 mg/m3)  sulfur dioxide
plus 10  mg/m3 of NaCl aerosol was similar
during the 1-hour exposure period. The ani-
mals  exposed  to the  higher level of sulfur
dioxide  alone had shown a complete return
to preexposure resistance values  by  45  min-
utes after the exposure ended. Those exposed
to the lower concentration plus aerosol still
showed  elevated resistance values  2 hours
after the end of the exposure.
  There is also  evidence  that the  level of
elevated  resistance during the postexposure
period is related to the concentration of the
particulate material present. First of all, the
time course of the response to various sulfur
dioxide  concentrations in the presence of  a
fixed  sodium chloride aerosol  concentration
(10 mg/m3) was examined. At the end of the
exposure period  the resistance values  were
higher at higher sulfur dioxide concentra-
tions. One hour after the exposure ended they
were  all above control values but were all of
the same  order of  magnitude, regardless of
sulfur dioxide concentration. Two hours  after
the end  of the exposure, the resistance values
of the animals exposed to sulfur dioxide con-
centrations of 25 ppm (72 mg/m3)  or above
had increased slightly. The animals exposed
to 2 ppm  (~6 mg/m3) had returned to pre-
exposure levels by 2 hours after the  end of
exposure.
  Next, the total amount of aerosol was re-
duced in 2 ways: by reducing the concentra-
tion to 4 mg/m3 for 1 hour, and by exposing
animals for only half an hour to 10 mg/m3.9
The sulfur  dioxide concentration  was fixed
at about 20 ppm (~60 mg/m3). The  results
were entirely consistent with the hypothesis
that there was a residual effect from an ir-
ritant aerosol which had been formed. An in-
crease  in  resistance was observed between
the first and second postexposure hours when
the exposure had been for half an hour,  and
the resistance continued at about this level
for the  5-hour postexposure  observation
period.
  It has also been found that the potentiation
of the response to sulfur dioxide by aerosols
of sodium  chloride  is slow  to develop.912
When the responses  to gas alone, and to gas
plus aerosol,  are  compared  at 10 minutes
there is no apparent difference. In this aspect
the response is different from that produced
by formaldehyde with sodium chloride12 or
that produced by aerosols of soluble metal
salts known to catalyze the oxidation of  sul-
fur dioxide to sulfuric acid.9
  The solubility of sulfur dioxide in a liquid
droplet  appears to play some  role in  its po-
tentiation by  inert aerosols. This  has been
suggested 9 by the way in which the potenti-
ating ability of  aerosols of soduim chloride,
potassium chloride, and ammonium thiocyan-
ate is related to the  solubility of sulfur di-
oxide in solutions of these salts. At the humi-
dities prevailing in  the exposure  chamber,
these substances would have been present as
solid particles which, upon entering the moist
respiratory tract,  would take up water  and
become  droplets.
  Most  solid aerosols tested * have not poten-
tiated the response to sulfur dioxide, which'
suggests a role of solubility in potentiation.
Thus, spectrographic carbon, activated coco-
nut charcoal, iron oxide fume, triphenylphos-
phate,  fly ash,  and  manganese dioxide at
levels of 8 mg/m3 or above, produced no de-
       108

-------
tectable effect on the resistance nor did they
potentiate the response to levels of sulfur di-
oxide ranging between 1 ppm and  100 ppm
 (3 ~mg/m3 and ~290 mg/mO. In several of
the 19 groups of animals exposed to sulfur
dioxide plus solid aerosols, the response was
apparently less than that observed with a cor-
responding concentration of sulfur dioxide
alone. The attenuations were not statistically
significant  for either group of animals ex-
posed to what was termed only "fly ash from
an  oil-fired  burner,"  one  exposure  being
about  10 ppm (~30 mg/m3)  and  another
being at about 20 ppm (~60 mg/m1) sulfur
dioxide. When the response data from the
two individual experiments were compared
with those  from  response to 20 ppm sulfur
dioxide alone, the attenuating effect was sta-
tistically significant. It is  also mentioned that
while triphenylphosphate aerosols of 0.3/x  or
1/x, failed to alter the response to sulfur diox-
ide even  when present in concentrations  off
50 mg/m3,  aerosols of 2/t had  a striking at-
tenuating effect  when given with sulfur di-
oxide, and they also protected against the gas
when   given  prior to exposure  to  sulfur
dioxide.

  The aerosols which appeared to have im-
portance in the potentiation of  sulfur dioxide
were the aerosols of soluble salts which might
catalyze the oxidation to sulfuric acid.9 Aero-
sols of ferrous iron, manganese, or vanadium,
when  used at concentrations of  0.7 mg/m3
to 1 mg/m3 produced a  potentiation of the
response. A sulfur dioxide concentration  of
0.2 ppm (~0.6mg/m3) produced a resistance
increase  of about  10 percent when  given
alone  and an increase of about  35  percent
when  given in the presence of these  aerosols.
The potentiation  was already  observable  at
10 minutes. It could be demonstrated by qual-
itative tests for sulfate that there was sulfate
present on the  aerosol  collected from the
chamber, which was not the case with sodium
chloride aerosols.
  These experiments suggest that the nature
of the particulate material, as well as its size
range  are key factors. The aerosols of im-
portance are  those capable of dissolving sul-
fur dioxide and possibly  of oxidizing it  to
sulfuric acid mist.
   D.  EVALUATION  BY  PULMONARY
           FUNCTION IN MAN

  Frank et af.11  examined the response of
human  subjects  to levels  of  sulfur diox-
ide of about  1  ppm  (~3 mg/m3),  5  ppm
(~15 mg/m3), and 15 ppm  (~43 mg/m3),
with  and without  the addition  of sodium
chloride  aerosol.  In the initial  experiments,
the agents were administered for 10-minute
periods in sequence with a 15 to 20 minute
recovery period between exposures. In a sec-
ond series, the gas and gas plus  aerosol ex-
posures of each subject were made at least
a month apart and were extended to 30 min-
utes. In the experiments in which the gas and
the gas plus aerosol were given in sequence,
the response to the second exposure was con-
sistently lower than the response  to the first
exposure, no  matter in which order the  gas
alone and gas plus aerosol were given. In the
second series, when the exposures were a
month or more apart,  no difference was de-
tected between the response to the gas alone
and the response  to the gas plus aerosol.
  When  the data for the control  values and
the resistance response for  the  same indi-
vidual to the  same level of sulfur dioxide on
different occasions  are examined, it is seen
that a very dramatic potentiation would have
been needed to yield positive results  in this
study. On one subject studied  on seven oc-
casions, the control resistance values ranged
from  0.65 to  1.48 cm ELO/l-sec, a difference
of about 128  percent.  The alterations  pro-
duced by exposure on 3 different occasions to
15 ppm  sulfur dioxide were 86 percent, 58
percent, and  156  percent increases in  resist-
ance.  Two exposures to 15 ppm sulfur diox-
ide plus aerosol produced on one occasion an
increase of 220 percent and on  the other oc-
casion an increase of 42 percent. The subject
who showed  the  most  extreme  variation on
three occasions had control resistance  of 1.13
cm, and 1.46 cm ELO/1-sec and corresponding
resistance increases were  130 percent, 93
percent, and 410 percent during exposures to
15 ppm sulfur dioxide  alone. The  differences
in response on the various occasions were not
related to absolute level of control resistance,
to functional  residual  capacity,  to time of
year,  or  to the previous total number of ex-
                                                                             109

-------
posures. The variations on exposures to gas
alone on different occasions were as great as
the differences between the response to gas
alone and to gas  plus aerosol.  The  study
makes apparent the difficulties of studies on
humans.
  The potentiating effects on guinea pigs
are observed  by establishing dose-response
curves for a large  sample of  animals:  such
studies with humans are virtually impossible.
The study of Frank et al.14 does, however,
present two important conclusions. The first
is the demonstration  of  variability  of re-
sponse to sulfur dioxide  on different occa-
sions. The second relates to the data on con-
trol resistance values for the same individual
on  different  occasions. The  comparison  of
this variation with  the magnitude of change
produced by sulfur dioxide exposures serves
to set the latter in  proper physiological per-
spective.
  Toyama 15 studied the flow  resistance re-
sponse of 13 subjects to sulfur dioxide with
and without sodium chloride aerosol.  Control
measurements were made, and the subjects
were then exposed in sequence for 5 minutes
to sodium chloride,  sulfur dioxide alone, and
sulfur dioxide plus  sodium chloride. The sul-
fur dioxide  concentrations ranged from 1.6
ppm to  56 ppm  (4.6 mg/m3 to 160 mg/m3).
The sodium  chloride  aerosol  produced  no
change in resistance. The sulfur dioxide pro-
duced an increase in resistance and the sulfur
dioxide  plus  sodium  chloride produced  a
greater increase than the gas alone  in  all
subjects. Dose-response curves were plotted
for the  gas alone and for the  gas plus aero-
sol. There was striking overall resemblance
to the dose-response curves for the guinea
pig experiments of Amdur.10
  A comparison of equal response concentra-
tions  of  gas alone  and of gas plus  aerosol
shows similarity to the animal data in that
the ratio  is greater at the lower concentra-
tions. The sodium  chloride  used in  these
studies  had a CMD  of 0.22M. Nakamura 16
studied  in a  similar manner the effect  of
sodium chloride  with a CMD of 0.95/* on the
response  of  10  subjects  to sulfur dioxide.
Again, in every case the response was greater
when the sodium chloride aerosol was com-
bined with the sulfur dioxide.
  It is tempting to conclude that these stud-
ies 1516 have demonstrated that the human
subjects had behaved as did Amdur's guinea
pigs. However, this conclusion is not neces-
sarily valid. The  exposures of human  sub-
jects were for 5 minutes, and it has been in-
dicated " 12 that in the guinea pig the poten-
tiating effect of  sodium chloride on sulfur
dioxide is not apparent at 10 minutes. If the
2 species had  been behaving  in the  same
manner, a potentiation would not have been
observed in  these experiments.
  When  the exposures were  given  in  se-
quence, the  response to the second exposure
(always the combination exposure)  was in-
variably greater than the response to the first
exposure. The results of sequential exposures
to gas and  to gas plus aerosol could be in-
terpreted if  data  were given for a similar
number of  subjects exposed  twice  in  this
manner to  the gas alone. In the 10-minute
exposures reported by Frank et al.1* the se-
quence of gas and of mixture was varied, but
the response to the second exposure was less
than the  response to the first. As stated
earlier, sequential exposures  in experiments
of this type are understandable as a practical
procedure, but they constitute a "toxicologi-
cal trap" for the unwary which unfortunately
is not evaded  merely by  randomizing  the
sequence.
  Burton et al.17 found that the presence of 2
mg/m3 to 2.7 mg/m3 of sodium chloride aer-
osol below Iju. did not affect the response of 10
subjects to from 1 ppm to 3 ppm  (~3mg/m3
to ~9mg/m3) sulfur  dioxide.  There was no
evidence  of  alteration of  pulmonary  me-
chanics  immediately following exposures to
this gas concentration, either with or without
the added  aerosol. This  lack of response
would have  been predicted on the basis  of
animal experiments with 4 mg/m3 sodium
chloride.12
  Toyama  and  Nakamura1S  examined  the
effect of aerosols of hydrogen peroxide with
CMD values of 4.6/x and 1.8/x on the response
to sulfur dioxde. They give CMD values of
4.6/i and 1.8/t for  the aerosols, measured in
a manner which does  not necessarily relate
to the airborne size. The hydrogen peroxide
concentrations  were  of the  order of  0.3
mg/m3. Sulfur dioxide concentrations ranged
       110

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from 1.5 ppm to 60 ppm  (4.3 mg/m3 to 170
mg/m3).  The sulfuric  acid concentrations
produced  by the oxidation of sulfur dioxide
were 0.8 mg/m3 to 1.4 mg/m3 for the larger
aerosol and  0.01  mg/m3  to  0.1  mg/m3 for
the smaller aerosol, but the  reasons for the
differences in acid concentration are not dis-
cussed.
  The response to the mixture was greater
than  the  response to sulfur dioxide alone.
The response was greater  with the larger
aerosol than with the smaller aerosol and is
in accord with the particle size  effect dis-
cussed earlier. It  is likely that it is also  re-
lated to the  concentration  of sulfuric acid
formed, since this was reported to be at least
10 times greater when the larger aerosol was
used.  When  the  sulfur  dioxide  exposures
were grouped at 1 ppm to 10 ppm, 10 ppm
to 30 ppm,  and 30 ppm to 60  ppm, the  re-
sponse was graded with concentration in the
presence of the smaller aerosol  (lower acid
concentration) but was  uniformly about the
same, an increase of 35 percent to 40 percent
in resistance,  for the 3 levels of gas when the
larger particles (higher acid concentration)
were present. These experiments  present the
same problem of sequential exposures  dis-
cussed above and  do not demonstrate syner-
gism.
  The data on the effect of  particulate ma-
terial  on  the  response  of  human subjects
does not consistently demonstrate a potentia-
tion by sodium chloride aerosol or a syner-
gism with sulfuric acid  mist. There is  some
suggestion of such effects in three papers,
but lack of adequate control data on repeated
exposure  to  sulfur  dioxide alone precludes
proper interpretation  of these data.

              E.  SUMMARY
  The experiments reviewed use changes in
pulmonary function,  changes in pathology,
and mortality to evaluate possible potentiat-
ing or synergistic effects of particulate mat-
ter on  the toxicity  of sulfur dioxide.  Only
changes in  pulmonary  function  may  be
studied in experiments  on man. Synergism
by both irritant and "inert" particles is con-
sidered.
  Sulfur dioxide in the atmosphere may be
partly converted into  the more irritant sul-
furic acid,  especially at high humidity and
in the presence of particulate material. The
irritant potency of sulfuric  acid  aerosol in
itself is dependent on size and relative humid-
ity.
  The potentiation by particulate matter of
toxic responses to sulfur dioxide (synergism)
has  been observed  under  conditions  which
would promote  the  conversion of sulfur di-
oxide to sulfuric acid. The degree of potentia-
tion is related to the concentration of partic-
ulate matter. A threefold to  fourfold  poten-
tiation of the irritant response to sulfur di-
oxide is observed in the presence of particu-
late matter capable of oxidizing sulfur diox-
ide to sulfuric acid. Aerosols of soluble salts
of ferrous  iron, manganese, and vanadium
have been observed to produce this potentia-
tion, although  the concentrations used  (0.7
mg/m3  to  1.0  mg/m3)  were considerably
greater than any reported  levels of the met-
als  in urban air.
  Experiments  with  normal human subjects-
have failed to  demonstrate  any  consistent
potentiation of response to sulfur  dioxide by
sodium  chloride particles. In  the guinea pig,
sodium  chloride is the least  effective  of the
various soluble aerosols that produce  any
potentiation.
            F.   REFERENCES
 1.  Schnurer, L.  "Effects of Inhalation of Smoke
   from Common  Fuels."  Am. J. Pub.  Health, Vol.
   27, pp. 1010-1022, 1937.
 2. Vintinner, F. J. and Baetjer,  A. M. "Effect of
    Bituminous Coal Dust and Smoke on the Lungs—
   Animal Experiments. I.  Effects on Susceptibil-
   ity to Pneumonia."  Ind. Hyg. &  Occup. Med.,
    Vol. 4, pp. 206-216, 1951.
 3.  Pattle, R. E. and Burgess, F.  "Toxic Effects of
   Mixtures  of  Sulfur  Dioxide  and   Smoke  with
    Air."  J. Pathol. Bacteriol.,  Vol. 73,  pp. 411-419,
    April 1957.
 4.  Salem, H. and Cullumbine, H. "Kerosene Smoke
   and Atmospheric  Pollutants." Arch. Environ.
   Health, Vol. 2, pp. 641-647, June 1961.
 5.  Gross, P., Rinehart,  W. E., and deTreville, R. T.
   "The Pulmonary Reactions to Toxic Gases." Am.
   Indust. Hyg.  Assoc. J.,  Vol. 27,  pp.  315-321,
    1967.
 6. Amdur, M. O.  "Effect of a  Combination of SO,
   and H2S04 on Guinea Pigs."  Pub. Health Re~-
   ports, Vol. 69, pp.  503-506, May 1954.
 7.  Bushtueva, K.  A.  "Toxicity of HQSO4 Aerosol."
    Gig.  i  Sanit., Vol.  22, pp  17-22, 1957.  In:
    U.S.S.E.  Literature on Air Pollution and  Re-
   lated Occupational  Diseases.  A Survey, Vol. 1,
                                                                                111

-------
   Translated  by  B.  S.  Levine,  U.S.  Dept.  of
   Commerce, Office  of  Technical  Services,  Wash-
   ington, D.C., Jan. 1960, pp. 63-66.
 8. Bushtueva, K. A.  "Experimental Studies  on the
   Effect of Low  Oxides of Sulfur Concentrations
   on  the Animal  Organism."  In: Limits  of  Al-
   lowable  Concentrations of  Atmospheric  Pollut-
   ants, Book 5,  Translated by B. S.  Levine,  U.S.
   Dept.  of Commerce, Office  of  Technical  Ser-
   vices, Washington, D.C., March 1962, pp. 92-102.
 9. Amdur,  M. O. and Underbill, D. "The Effect of
   Various  Aerosols on the Response of Guinea Pigs
   to Sulfur Dioxide."  Arch. Environ. Health, Vol.
   16, pp. 460-468, 1968.
10. Amdur,  M. O.  "The  influence of Aerosols Upon
   the  Respiratory Response  of  Guinea  Pigs  to
   Sulfur Dioxide."  Am. Ind. Hyg. Assoc. Quart.,
   Vol. 18,  pp. 149-155, June 1957.
11. Amdur,  M. 0.  and Corn, M. "The Irritant Po-
   tency  of Zinc  Ammonium Sulfate of Different
   Particle  Sizes."  Am.  Ind.  Hyg. Assoc, J., Vol. 24,
   pp. 326-333, July-Aug. 1963.
12. Amdur,  M. 0.   "The Effect  of Aerosols  on the
   Response to  Irritant Gasss."  In:  Inhaled  Par-
   ticles and Vapors, C. N. Davies  (ed.), Proc. In-
   tern.  Symposium,  Oxford,  March 29-April 1,
   1960,  Pergamon Press,  Oxford, 1961, pp.  281-
   292.
13. Amdur,  M. O.  "The Physiological Response  of
   Guinea Pigs to Atmospheric Pollutants." Intern.
   J. Air Pollution, Vol. 1, pp.  170-183, Jan. 1959.
14. Frank, N. R., Amdur, M. O., and Wittenberger,
   J. L.  "A Comparison  of  the Acute Effects  of
   SO,  Administered Alone or in Combination with
   NaCl Particles on the Respiratory Mechanics of
   Healthy Adults." Intern.  J. Air  Water  Pollu-
   tion,  Vol.  8, pp. 125-133,  1964.
15. Toyama,  T.  "Studies on Aerosol. I. Synergistic
   Response of the Pulmonary Airway Resistance
   on Inhaling Sodium Chloride Aerosols and SO,,
   in Man." Japan J. Ind. Health, Vol. 4, pp. 86-92,
   1962.
16. Nakamura, K. "Response of Pulmonary Airway
   Resistance by Interaction of Aerosols and  Gases
   of  Different  Physical  and  Chemical  Nature."
   Japan J. Hyg., Vol. 19, pp.  322-333, Dec. 1964.
17. Burton, G. G., Corn, M., Gee, J. B. L., Vassallo,
   C., and Thomas, A.  "Absence of 'Synergistic Re-
   sponse' to Inhaled Low Concentration Gas-Aero-
   sol Mixtures  in Healthy  Adult  Males."  (Pre-
   sented at 9th Annual Air  Pollution Medical Re-
   Search Conference.) Arch. Environ. Health, Vol.
   18, pp. 681-692, 1969.
18. Toyama, T. and Nakamura,  K.  "Synergistic Re-
   sponse of Hydrogen Peroxide Aerosols and Sul-
   fur  Dioxide to  Pulmonary Airway Resistance."
   Ind.  Health, Vol. 2, pp. 34-45,  March 1964.
        112

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                 Chapter 9
EPIDEMIOLOGICAL APPRAISAL OF SULFUR OXIDES

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                            Table of Contents
                                                                      Page
A. INTRODUCTION                                                   117
B. APPLICATION OF EPIDEMIOLOGY TO AIR POLLUTION
   STUDIES                                                          117
   1.  Indices                                                          117
   2.  Cautions                                     .                    118
C. INDICES OF HUMAN RESPONSE: THE EPIDEMIOLOGIC
   STUDIES                                                          119
   1.  Acute Episodes               .                .                    119
      a. Mortality                                 .                    119
      b. Morbidity                 .                .                    125
   2.  Chronic  (Long-Term) Air Pollution                                126
      a. Day-to-Day Variations in Mortality and Morbidity             .    126
      b. Geographical Variations in Mortality                        .    127
        1. Studies Based on Available Data                          .    127
        2. Special Studies Involving the Collection of New Data        .    128
      c. Geographical Variations in Morbidity—Special Studies         .    130
      d. Morbidity—Incapacity for Work                             .    135
   3.  Studies of Children                                   .      ...    137
   4.  Studies of Pulmonary Function                                    139
   5.  Studies of Panels of Bronchitic Patients                            140
   6.  Miscellaneous Studies                                             142
D. EFFECTS OF INDUSTRIAL EXPOSURE                            142
E. SUMMARY                                                       .144
F. REFERENCES                                                     147
                              List of Figures
Figure
9-1  Mortality  Figures for the January 1956 and December 1957 Smog
     "Episodes" in London.                               .              121
9-2  Death Rate  and Air Pollution Levels in Dublin, Ireland, for 1938-
     1949.                                                            124
9-3  Age-Standardized Morbidity  Rate per 1,000  for Three Diseases in
     Japan.                                                	    132
9-4  Incidence  of Respiratory Disease Lasting More Than Seven Days in
    ''Women Versus Concentration  of Sulfates in the City Air at Test
     Sites.         .                                .       	    135

 114

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                                                                        Page
9-5  Effect on Bronchitic Patients  of  High Pollution  Levels  (January
     1954).                                                             140
9-6  Comparison of Person-Days  of Acute Illness with Seven Levels  of
     Sulfur  Dioxide Exposure in  Chicago for Patients With Severe
     Chronic Bronchitis (Age 55 or More) for October-November 1967.       141


                            List of Tables
Table
9-1  Survey of Selected Acute Air Pollution Episodes in  Greater London.     125
9-2  Pollution Levels in Salford.                                    .      129
9-3  Industrial Exposures.                                           .    144
                                                                      115

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                                      Chapter  9

             EPIDEMIOLOGICAL APPRAISAL  OF SULFUR OXIDES
           A.  INTRODUCTION

  Health  effects produced  by  atmospheric
sulfur oxides are discussed in this chapter in
terms of epidemiologic studies.  Because sul-
fur oxides tend to occur in the same kinds of
polluted atmosphere as  particulate matter,
few  epidemiologic  studies  have been  able
adequately to differentiate the effects of the
two pollutants.  It follows, therefore, that the
studies  presented  in this chapter  are fre-
quently identical with those described in the
companion document,  Air Quality Criteria
for Particulate Matter.
  Epidemiologic  studies, as  distinguished
from  toxicologic or experimental  studies,
analyze the effects of pollution from ambient
exposure on  groups of  people  living  in  a
community. Such studies have the advantage
of examining1 illness where  it occurs natur-
ally, rather than in a  laboratory, but carry
the disadvantage of not being able to control
precisely  all the  factors of  possible  im-
portance.  Nevertheless,  the preparation of
air quality criteria must rest on  epidemio-
logic studies because of the very severe limi-
tations of toxicologic and industrial studies
for this purpose.  Other countries, notably
the Netherlands and  Sweden,  have based
their  air quality criteria solely on epidemio-
logic  studies.
  In  determining  whether or not  an asso-
ciation is causal, consideration must be given
to several aspects of association which in-
clude  strength,  consistency,  specificity,  tem-
porality, biological gradient, plausibility, co-
herence, and analogy.1  A judgment  of the
value  of an epidemiologic study requires an
understanding of these aspects.
  Many types of epidemiologic evidence sug-
gest that air pollution may exert consider-
able influence on the health, as well as on
the "satisfaction with  life," of major seg-
ments of the world population.
  Several health indices are described in Sec-
tion B-l; certain precautions which should
be observed in the application of epidemio-
logic methods  to air quality criteria are sug-
gested  in Section B-2.  The studies them-
selves are listed in  Section C, according to
the index employed.  Several industrial ex-
posures to the oxides of sulfur are mentioned
in Section  D.  discussing  their relevance to
the epidemiologic studies.

 B.  APPLICATION OF  EPIDEMIOLOGY
     TO AIR POLLUTION  STUDIES

                1.   Indices

  Various indices of health may be used for
correlation with air pollution by the oxides
of sulfur. Among the possible indices are:
    1. Mortality (greater than expected):
       (i)  Deaths from all causes
       (ii)  Deaths from specific causes
       (iii) Deaths among the different age
           and sex groups
    2. Morbidity:
       (i)  Incidence  of  disease — chronic
           bronchitis,  pulmonary  emphy-
           sema,  diffuse  interstitial pneu-
           monitis,  cancer of respiratory
           tract,  disease  of remote organ
            (e.g., gastro-intestinal, ophthal-
           mic,  and  cardiovascular  sys-
           tems)
       (ii)  Prevalence of diseases—same
           examples as for "incidence"
       (iii) Prevalence of respiratory symp-
           toms  (e.g., changes in quality
           and/or quantity of sputum pro-
           duction)
                                                                             117

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       (iv) Exacerbation of  diseases—-rhi-
           norrhea,  asthma,  tracheobron-
           chitis, and chronic illness and
           enhancement of infection:  pneu-
           monia,  sinusitis,  otitis,  mas-
           toiditis
       (v)  Changes  in clinical conditions
            (e.g.,  bronchitic patients)
    3. Changes in various  aspects of  lung
      function:
       (i)  Ventilatory  function—decrease
           in  peak flow rate,  decrease  in
           spirometric  volumes,   impair-
           ment  of flow-volume  relation-
           ships, and increased airways re-
           sistance
       (ii)  Blood/gas distribution—impair-
           ment of lung-gas distribution
       (iii) Blood/gas  exchange — impair-
           ment of pulmonary blood-gas ex-
           change
       (iv) Increased work of breathing
  Definitions of the  various  disease  states
are to be found in the glossary; most of the
pulmonary function methods have been men-
tioned in Chapters 9 and 10 of the compan-
ion document, Air Quality  Criteria for Par-
ticulate Matter.
  The manner of presentation of the state
of epidemiological  knowledge  of  effects  of
sulfur dioxide  in the ambient atmosphere
when accompanied by particulate matter is
outlined in the Table of Contents.

               2.   Cautions
  In the first place,  as discussed in Chapter
2, methods of measurement vary from coun-
try to country and  place to place.  Results
from the  various  methods  of measurement
are frequently very dissimilar.
  Secondly, pollution and health indices are
not always measured over the same time pe-
riods.  It is to be hoped that the pollution lev-
els  cited bear some  relation to those extant
during  the time  when the chronic disease
states were developing.  Further, acute ef-
fects  require frequent  short-term  pollution
measurements  to  enhance  detection,  while
long-term  chronic processes  may be ade-
quately related to long-term sampling inter-
vals.  Air pollution measurements useful in
studies of acute health  effects are becoming
available; a less satisfactory situation exists
for the long-term effects studied.
  Thirdly, in many  instances the  possible
role of cigarette smoking has not been con-
sidered.  It is expected that future epidemio-
logic studies involving  adults will routinely
collect data on smoking habits of the study
group. Other factors are significantly related
to respiratory  disease.  These include occu-
pational and other past exposures; infections,
past and present; and allergy and heredity.
  Few or no epidemiologic studies have been
possible  where the pollution challenge has
been limited to oxides of sulfur, unaccom-
panied by  significant amounts of other pol-
lutant substances.  Indeed, most of the avail-
able conclusions  link sulfur dioxide levels
with those of concurrently measured particu-
late matter; some studies attempt statistical
separation of the culpability of one factor
from the other in the effects cited.
  In seeking the possible effects on  popula-
tions resident in areas of differing air pol-
lution, factors such  as smoking, type  and
conditions  of employment, ethnic group, and
mobility  in response to experienced  irrita-
tion or disease have sometimes  been consid-
ered. There has,  however, been a minimum
of attention paid to the indoor or domestic
environments  and their potential contribu-
tion. Measurement of such indoor exposures
might be difficult, but omission of the infor-
mation could  well modify the appraisal of
the importance of pollution by the oxides of
sulfur.
  Toxicologic studies indicate a  specific po-
tential of some oxides  of sulfur to  produce
human responses.  The levels used  in  tox-
icologic  studies are far  higher  than those
found  in the  communities in the epidemio-
logic studies under review.   Thus the actual
responsibility of oxides  of sulfur for  the com-
munity responses is uncertain, and it is some-
times necessary  to  invoke  additional  con-
cepts;  for example, the  idea of synergism
with other known or unknown ambient pol-
lutants, or the idea that sulfur dioxide is but
an  index of availability of  some other  sub-
stance (s) which are fully responsible for the
effects reported.
  Over a short period of time, mortality fluc-
       118

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tuates  considerably, and only a systematic,
long-term approach will allow a valid deter-
mination  of the  real role of air pollution.
Cassell et al.-  have reviewed the problem of
detecting  peaks  in  mortality  and relating
them to any single variable.  The danger with
episodic studies is  that short-term  fluctua-
tion in the death rate, when picked to coin-
cide with  an air  pollution incident, may ap-
pear to be causally related; in the long term,
however, numerous other unassociated peaks
are found in both the death rates and the air
pollution levels.
  The  concept of  "susceptible population"
demands consideration.  Human responses to
toxicants, and to community air pollution,
show wide variations, which contribute in no
small way to the difficulty in assessing in a
general manner  the effects of  pollutants.
Since air  quality  criteria must,  unless other-
wise  specified,  consider   "all"  population
rather  than just major segments of it, stud-
ies  must  consider especially the impact of
air  pollution on the "most sensitive" respond-
ers. Many factors seem to enhance suscepti-
bility or sensitivity to air pollution. These in-
clude being at the extremes of  age, (i.e., in-
fants and the  very old); having pre-existing
chronic respiratory disease  (e.g.,  pulmonary
emphysema  or chronic  bronchitis); having
preexisting  cardiovascular   disease  (func-
tional capacity not defined); regularly smok-
ing cigarettes; or living in overcrowded or
depressed socioeconomic  strata.  Some  of
these factors have been singled out for atten-
tion in the references to be cited, and  the
level of pollutant said  to  have an  "effect"
may take cognizance of such special sensi-
tivity.
  The  effects  discussed are related insofar
as possible to  specific pollution over specific
time intervals; it must be  emphasized that
lower values by no means imply a "no effect"
level of the pollutants.

  C.  INDICES OF HUMAN RESPONSE:
     THE EPIDEMIOLOGIC STUDIES

            1.  Acute Episodes
a. Mortality
  The first well studied air pollution episode
occurred  between December 1  and 5, 1930,
in the Meuse Valley, Belgium, when a heavy
fog covered the entire valley.  Several  hun-
dred people were severely ill with respiratory
symptoms, and 63  died.  Although no precise
measurements  were made  during  the epi-
sode, Firket estimated that a number of pol-
lutants  rose to high  levels  and that sulfur
dioxide  and sulfuric acid,  which may  have
reached a  total of 25,000  /*g/m3 or higher
(~9 ppm), were  probably the chief  cause
of the illness.3-4
  During late October 1948, Donora, Penn-
sylvania was blanketed by a dense  fog, and
43 percent of the population was affected to
some  degree.  Twenty persons  died during
or shortly after the smog, and 10 percent of
the population  was classified as severely af-
fected.  No measurements  were taken  dur-
ing the  episode, but a detailed  study after-
wards 4  concluded  that no  single agent was
responsible, and that the  observed effects
were due to a chemical agent together  with
particulate matter.  Sulfur dioxide and its
oxidation products were  undoubtedly signifi-
cant contaminants.  During subsequent in-
version  periods, presumably not as severe as
the one in October 1948, daily  averages of
sulfur dioxide  as high as 0.4 ppm (~1140
fug/ra3)  were recorded/'
  In writing about the Meuse Valley episode
in 1936, Firket stated that if there were a
similar  phenomenon in  London, some  3200
deaths might  occur.  Unfortunately he was
quite  accurate  in his estimate  since, in De-
cember  1952,  the world's  most disastrous
smog  incident  occurred  in  London, causing
about 4000 excess  deaths  throughout the
Greater London area.  Marked increases were
noted in both respiratory and cardiovascular
deaths  (and for almost  every  cause except
traffic accidents; presumably the smog was
too thick  for  people to  drive).  Since some
of the diseases such as lung cancer and tu-
berculosis were obviously existent before the
pollution episode, much  of the  effect of the
fog was clearly to hasten the death of people
who were already ill.  Detailed investigations
were made of 1,280 post-mortem reports of
persons  who  had  died  before, during,  or
shortly  after the episode. No fatalities were
found which could not have been explained
by previous respiratory or cardiovascular le-
                                                                             119

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sions. In this episode as in others, the elderly
and persons with pre-existing pulmonary and
cardiac  disease  were most susceptible.
  The maximum daily concentration of sul-
fur dioxide recorded during the 1952 Lon-
don  smog  was  1.34  ppm  (about   4,000
^ig/m3)* which  appeared  on the third and
fourth day of the fog. Corresponding  smoke
levels were  4.46  mg/m3  (~4500  /ig/m3).
These figures are from County Hall,  where
only volumetric  (hydrogen peroxide)  meas-
urements of SOj were made.6
  Greater London has had several air pollu-
tion  episodes before and since the large one
of December 1952, but none has come close
to causing 4,000 excess deaths.
  A number of  investigations have analyzed
and  compared the various London episodes.
The report by Brasser et al.1  appears to cover
all the  episodes and  to present  a relatively
detailed analysis of each of these episodes,
pointing out the importance of the duration
of the  maximum  values.   More  recently,
Joosting * has examined the  relationship be-
tween the duration of maximum values of
sulfur dioxide and smoke during air pollu-
tion  episodes, as well as the differential re-
lationship between sulfur dioxide and  smoke
levels and the resulting mortality.
  In  conurbations,  such  as London,  New
York, Chicago, and Detroit,  it  has been pos-
sible to  observe deviations from  the moving
averages  of  deaths during various  seasons,
and  to  relate such deviations  to the coinci-
dent period  levels of air pollutants.9
  Gore  and Shaddick10  and  Burgess and
Shaddick"  reviewed acute  "fog" episodes
which occurred in London in  1954, 1955, 1956
(January and December), and  1957 (Decem-
ber), in terms of excess  mortality  above a
moving  average, related to the  mean of daily
readings at seven stations for smoke and SCv
Figure  9-1  shows mortality figures for the
January 1956 and  December 1957 episodes.
Somewhat differing patterns of onset of mor-
tality rise,  of  age of  population  suffering
most heavily, of deaths related to bronchitis
and to other respiratory diseases, and of total
deaths, were noted in these acute episodes.
Common to them, however,  were elevations
of mean daily levels of S02 and smoke meas-
ured at seven different stations from two to
four times the winter average levels; "ef-
fects"  were estimated at 2,000 jug/m3  black
suspended matter together with 1145 /*g/m3
(0.4 ppm)* of sulfur dioxide  (representing
all acidic  gases). Deaths ascribed  to  bron-
chitis  were materially affected, but deaths
due to other causes also increased.  Deaths
appeared to begin to  increase before the on-
set of  the episodes; during  the  episodes, of
course, they increased substantially.  Scott12
observed a similar relationship, for similar
periods of "fog," with "effective pollutant"
levels at seven different  stations in  London
of 2,000 jug/m'^ for smoke and 0.4 ppm for
SO,  (reported  by Scott as 1,140 /ig/m3).**
There  was a sharp impact on the elderly and
the greatest proportionate rise, for cause of
death,  in bronchitics.
  Martin  and  Bradley13  correlated  daily
mortality  (all  causes)  and  daily bronchitis
mortality  with mean daily black suspended
matter for the winter of 1958-1959, and also
found  a significant positive association be-
tween  mean  daily sulfur dioxide levels and
deaths  (all   causes).    Bronchitis  deaths
showed a lower correlation with the pollution
level,  and the authors suggest  the need for
consideration  of effects  of air pollution  on
patients with cardiovascular disease.  In ad-
diton, excess deaths have been related  to in-
creases (on  the  day preceding death)  of
mean daily black suspended  matter by more
than 200 /ig/m3, and rises in mean daily S02
of more than about 75 /tg/m3 (2.5 parts per
hundred million).* In a  later paper14, data
are shown to suggest an increase in mortality
* Unless otherwise stated, British measurements of
 S02 concentrations  are obtianed by the hydrogen
 peroxide titrimetric method  and may be higher
 than the actual SO, concentration due to the pres-
 ence of other acidic gases  (see Chapter 2).
* SO, values in this study were originally reported
  in ppm.
** SO-, is converted from ppm to /ig/m3 in Scott's
  report  by using an equivalency 2,850 jltg/ma=l
  ppm.  This report uses 2,860 Jltg/m1)=l ppm, and
  for consistency attempts  to express  the value
  (0°C,  760 mm Hg)  in Mg/m3 first.  Most of the
  American SO2  values are measured at 25 °C, 760
  mm Hg; the  equivalency under these circum-
  stances is 2,610 jug/m3=l ppm.
* S0: values in this study were originally reported
  in parts per billion (ppb).
       120

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from all causes, and of respiratory and car-
diac morbidity,  associated  with  levels  of
smoke about 1,000 pg/m3, and SO2 concentra-
tions of 715 pg/m3 (25 pphm). This "effect"
is properly related to abrupt rises in the con-
centrations  of smoke and/or SO2, with per-
haps a continuum of effects at lower levels.
Since these measurements were  obtained at
a single point in  Central London, it  should
be presumed that a relatively wide range of
                              values around  these  levels actually contrib-
                              uted to the mortality statistics which were
                              correlated.  A  re-analysis by  Lawther15  of
                              these mortality studies places the mortality
                              "effect" at about  750 /xg/m3 for smoke and
                              715  /ig/m3  (0.25  ppm)  for S02.  Joosting8
                              states that the maximum sulfur dioxide con-
                              centration above  which  significant  correla-
                              tions occur with  death  and  disease is 400
                                      to  500  /xg/m3  (0.15  ppm  to  0.19
                      JANUARY, 1956
                                          DECEMBER, 1957
             <
                200r
                180-
                160-
                14C-
             O  120-
             GC
             HI
             CD

             D
             Z
IOC -
                                            ALL AGES
                            70+YEARS
                                           0-69 YEARS
                       31  5  10  15  20 25
                                                          25  30
                                                    10 15
                       DEC.  JAN.
                                                             NOV.  DEC.
          Figure 9-1.   Mortality Figures for the January 1956 and December 1957 Smog
                      "Episodes" in London. *

           The figure shows the increase in numbers of deaths during smog "episodes"
           (shaded periods), especially in the older age group.
                                                                               121

-------
ppm) ** when there is a high soot content.
  The Dutch report on sulfur dioxide,7 which
discusses in  detail  seven air  pollution  epi-
sodes in London, states that in the December
1956 episode, 400 excess deaths, or 25  per-
cent above  expected,  were  observed in
Greater London at maximum 24-hour levels
of 1,200  /xg/m3 for smoke and 1,100  /*g/m3
for SOo (0.4 ppm).** The report also notes
that in January 1959, 200 excess deaths were
observed in Greater London, or 10 percent
above the expected mortality, at a level of
1,200 yug/m-1 for smoke and 800 ,ug/m3 (0.30
ppm) ** for SO-.7 The episodes all took place
during winter;  cold weather seems to be an
important  factor  in London  air pollution
mortality.
  In Martin's review 14 in 1964 of daily mor-
tality in London during the winters of 1958-
1959 and 1959-1960, he concluded:  "From
the data it would be difficult to fix any thresh-
old value below which levels of air pollu-
tion might be regarded as safe." However,
his review  included data with  sulfur dioxide
concentrations  ranging upward  from about
400 /*g/m3  (0.14 ppm), and accompanied by
smoke  concentrations  of  500  ^g/m3  and
above.
  As a result of smoke control  regulations,
the particle content of London air has stead-
ily  decreased since the 1950's but the sulfur
dioxide concentrations  have not decreased
proportionately.  At the same  measuring
sites as in  1952, sulfur dioxide was actually
slightly higher in the 1962  episode than in
that of 1952, but smoke levels were consider-
ably lower.  Also,  as  Brasser  et al.  have
noted,  there was only one day of maximum
pollution values in 1962 as contrasted  with
the two  days of maximum  pollution  in De-
cember 1952."  Since 1952,  a great  deal of
publicity has been given to the  harmful ef-
fects of smog, and more susceptible individ-
uals have been  encouraged to use masks and
niters  and stay indoors.  In addition, when
episodes come  close together, a large num-
ber  of susceptible individuals might not ac-
SO3 is converted from ppm to ^g/m3 in the Dutch
reports by using the equivalency, 2700 ^g/rrfcl
ppm. This report uses 2,860 p,g/m3=l ppm when-
ever possible.
                                          cumulate, since some are killed off each time.
                                          An effect as large as that seen in the first
                                          incident  would not,  therefore,  be expected.
                                            The number of deaths in New York City
                                          was reviewed for excess mortality in rela-
                                          tion to the air pollution episode of Novem-
                                          ber 1953 by Greenburg et a/.16 Excess deaths
                                          were related to elevations of concentrations
                                          of  sulfur dioxide and  suspended particles.
                                          Average daily smoke shade measured in Cen-
                                          tral Park  was in excess of 5.0 coh  units,
                                          while the SO... rose from the New York City
                                          average  ranges of 430  /*g/m3 to 570 /ig/m3
                                          (0.15 to 0.20 ppm)* to a maximum level of
                                          2,460 jug/m3 (0.86  ppm),  probably a half-
                                          hour value.  For this  episode,  there was  a
                                          "lag effect," and distribution of  excess deaths
                                          among all age  groups was noted.  The num-
                                          ber of deaths, although not  showing  the
                                          marked rise seen in some of the London epi-
                                          sodes, was  above average for comparable pe-
                                          riods in other years  during and immediately
                                          after the incident.  For the November 15 to
                                          24,  1953,  period, the  average number  of
                                          deaths per day was 244, whereas during the
                                          3  years  preceding  and following 1953, the
                                          average was 224 deaths per day for the same
                                          calendar period.
                                             A later  episode  (1962)  was studied,  but
                                          Greenburg et al." did  not discern an excess
                                          mortality.  However, McCarroll  and  Brad-
                                          ley,lv reviewing episodes in New York City
                                          in  November and December of  1962, Jan-
                                          uary and February of 1963, and February
                                          and March of 1964,  compared 24-hour aver-
                                          age levels  of various  pollutants with New
                                          York City mortality figures, employing daily
                                          deviations  from 15-day moving average; the
                                          measurements  were performed at a  single
                                          station in lower Manhattan, and fluctuations
                                          in  the values at this station were known to
                                          correlate well with those at another  station
                                          6.5 miles away. Excess deaths  on December
                                          1,  1962,  followed a  daily  average sulfur di-
                                          oxide  concentration of  2,600  /ig/m3 (0.72
                                          ppm) * and smoke shade in excess of 6 coh
                                          units, during a period of atmospheric inver-
                                          sion  and low  ground-wind speed. The in-
                                          creased  death  rates were shared  by the 45
                                               SO» values in this study were originally reported
                                               in ppm.
       122

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to 64 age group, as well as by the age group
over 65.  In a later episode, January 7, 1963,
associated  with  an  SO2  concentration  of
about 1,715 /ig/m3 (0.6 ppm) * and a smoke
shade value of 6 coh units, there was a peak
death rate apparently superimposed  upon
an elevated  death rate average due  to  the
presence of influenza virus in the community.
  Another severe episode of air pollution en-
compassed the New York  City area during
the Thanksgiving weekend, November 23 to
25, 1966. The maximum 24-hour average of
hourly S02  values  was  1,460 /*g/m3  (0.51
ppm) *  (electroconductivity)  on November
23, and 1,344 and 1,175 /.g/m3  (0.47 and 0.41
ppm) on the 24th and 25th. The maximum
hourly concentration was 2,915 /*g/m3 (1.02
ppm).  Smoke  shade  values were  above 5
cohs on the 3 days. The average number of
daily deaths  during the 7  days of the air
pollution episode was 261  compared  to the
expected value of 237  for control periods in
6 surrounding years.19
  An example of the  inherent danger of re-
lating  mortality  peaks to  air pollution is
shown by  Leonard  et al.20 in the Dublin
studies.   During the war and post-war years
of 1941 to 1947, peat was burned as  the main
fuel  rather than coal,  and  air pollution  (as
measured by particle concentrations)  was
markedly decreased.   Sulfur  dioxide levels
varied in a manner similar to those of sus-
pended particulate matter.  The winter peaks
in death, however, were unaffected,  and thus
do not seem  to  be  related  to air  pollution.
When coal  again became available in  1948,
the air pollution levels rose with no apparent
effect on the death rate (see Figure  9-2).
Unfortunately, it is not possible to assess the
effect of  changing medical  practices and the
advent of antibiotics for use in treating res-
piratory diseases on these data.
  In Detroit21 a rise in infant mortality and
deaths in cancer patients occurred over a 3-
day period accompanied by a rise in the 3-day
mean suspended particulate matter for the
same period  above 200 /*g/m3  and accom-
panied by an instantaneous SO2 maximum
of 2,860  fig/m5  (1.0  ppm)*  (September
1952). This is not believed to be related to
the cold temperatures which have character-
ized the London episodes.
  In Osaka, Japan, Watanabe22 reported on
excess deaths in a December 1962 smog epi-
sode.  There were 60 excess deaths related
to mean daily  concentrations of suspended
matter greater than  1,000  /tg/m3,  with ac-
companying sulfur dioxide greater  than  285
fi.g/m3 (0.1  ppm)*; the measurements were
made at a single  station in  the central com-
mercial area of the city.
  In  an  effort to include all the  available
relevant data, we must mention the discus-
sion by Brasser et alJ, calling attention to the
availability  of data for Rotterdam. He says:
       "From investigations at Rotterdam in-
    dications have been obtained that there
    exists  a positive  association with  the
    total mortality if the value of 500 pg/m3
     [0.19 ppm]* per 24 hours is surpassed
    for a few days. Perhaps this effect be-
    gins to  be active at lower concentrations
    already present.  There is a faint indi-
    cation that this will happen somewhere
    between 300  and  500  pg S02 per m*
     [0.11 to 0.19] * per 24 hours."
  The Rotterdam episodes of January-Feb-
ruary  1959  and  December 1962 have  also
been discussed  by Joosting.8 What is espe-
cially significant is that particulate levels are
generally low in  Rotterdam. On comparing
particulate and SO2 concentrations, Joosting
has characterized the ratio of particulates to
S02as 1:1, 1:1.5 to 1:2, and 1:3 to 1:4. Rot-
terdam is in the last category, whereas Lon-
don is in the first. Measurements in Rotter-
dam are made  with the hydrogen  peroxide
titrimetric method.
  When a marked increase in air  pollution
is associated with a sudden dramatic rise in
the death rate  or illness rate lasting for a
few days and both return to normal shortly
thereafter, a causal relationship is strongly
suggested. Sudden changes in weather, how-
ever,  which may have caused the air pollu-
tion incident, must be considered as another
possible cause  of the death rate  increase.
Over the years, a number of such acute epi-
 • SO5 values in this study were originally reported
  in ppm.
 : The numbers in brackets are the editor's; an equiv-
  alency of 2,700 ^tg/m'-l ppm SO, was used to
  assure consistency with any conversions made by
  the authors.
                                                                             123

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socles have been reported, and  there seems
little doubt that air pollution was the cause.
  Table 9-1 is an attempt by Brasser et al.~
to summarize some of the recent major air
pollution episodes in Greater London.
  The British  studies presented  in this sec-
tion suggest that excess  mortality, a small
rise in  the  daily death rate, is  detectable in
large populations  if  the  concentrations  of
sulfur dioxide  rise abruptly  to  levels at or
about 715 /xg/m3 (about  0.25 ppm) in the
presence of smoke at 750  /xg/m3.  The major
targets   are the aged population,  patients
with chronic obstructive pulmonary disease,
and patients with  cardiac disease.  A more
distinct rise in deaths is noted generally when
sulfur  dioxide exceeds 1,000 /xg/m3 (about
0.35 ppm) for 1 day and  particulate matter
reaches  about  1,200 /ug/m3.  Daily concen-
trations of  sulfur dioxide  in excess  of 1,500
ng/m3 for 1 day (~0.5 ppm) in conjunction
with levels  of suspended particles exceeding
2,000 /*g/m3 appear to be  associated with an
increase in the death rate of 20 percent or
more over base line levels. This  same effect
is observed at  lower  sulfur dioxide  levels if
the  maximum  pollution   levels   last for  a
longer period.
b. Morbidity
  The acute episodes have  resulted in sub-
stantial increases in illness.  Thus a survey 2S
of  emergency  clinics at major New York
City hospitals in November  1953 indicated a
rise in visits for upper respiratory infections
and cardiac diseases in both  children  and
adults in all of  the  four hospitals  studied.
Sulfur  dioxide  ranged  between 200 ^g/m3
and 2,460  /xg/m3  (0.07  ppm to 0.86 ppm)*
during the period from November 12 to 24,
and hospital  admissions  were clearly  ele-
vated by November  16, at which  time con-
centrations had not yet exceeded 715 itg/m3
(0.25 ppm); "smoke shade"  at this time was
clcse to 3 coh units.
  Again, the number of emergency clinic
visits for  bronchitis  and asthma at seven
large New  York City hospitals was examined
during the Thanksgiving 1966  air pollution
episode.24 There  was  a  rise  in the  number
of such visits on the third day of the  episode,
among the patients age 45 and over,  at three
of the seven hospitals investigated.   Unfor-
tunately, the Thanksgiving holiday greatly
* S02 values in this study were originally reported
  in ppm.
                 Table 9-1.—SURVEY OF SELECTED ACUTE AIR POLLUTION
                            EPISODES IN  GREATER  LONDON.7
                           Dec. 1952  Jan. 1956 Dec. 1962  Dec. 1957  Dec. 1956  Jan. 1955  Jan. 1959

Duration  of  the  cumulation
  period in days                  5        5         5        5        10       11        5
Number of days with maxi-
  mum pollution                   22115       1x3 a       1
SO2 level  preceding episode        500      300       400       300       300       300       300
S02 maximum                  4000      1500      3300      1600      1100      1200       800
SO. increase per day             1200      500      1000       325       400       450       250
Soot level preceding episode        400      500       200       400       400       500       400
Soot maximum                  4000      3250      2000      2300      1200      1750      1200
Soot increase per day            1200      1300       600       500       400       600       400
Number of excess deaths         3900      1000       850       800       400       240       200
Number of days with  excess
  mortality                      18       10       13        10        6        6        6
Daily  mortality expected un-
  der normal circumstances        300      330       310       300       270       320       325
Average  daily  mortality  in
  the  period  (excess  mortal-
  ity  as  a  percent of nor-
  mal) .                .        170      130       120       125       125       112       110

  Remark: The SO2 and soot concentrations mentioned are average values over 24 hours expressed in
  a Maximum pollution values of one day's duration occurred three times.
                                                                                125

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complicated  evaluation  of the  emergency
clinic visits over the holiday period.'^
  In the investigation of the London episode
of December 1952, information on illness was
collected from  as  many sources as possible
including sickness  claims,  applications for
hospital  admission, pneumonia notifications,
and records of physicians. The analysis dem-
onstrated a real and important increase in
morbidity, though  there was some indication
that the  increase in illness was not as large
proportionately as the increase in deaths and
the effects were not so  sudden in  producing
a marked rise  in the early days  of the epi-
sode.  In a  number of other severe London
episodes  the increase in morbidity put a con-
siderable strain on the health services.
  These  episodes  reflect  results  which fall
into Level IV of the World Health Organi-
zation's  "guides  to air quality."2S   These
"guides," equivalent in  usage to our  term
"criteria," cover sets of concentrations and
exposure times at  which specified types of
effects are  noted  or at which no effect is
noted. Level IV includes "concentrations and
exposure times at and above which there is
likely to be acute illness or  death in sus-
ceptible groups of the population."

  2.  Chronic  (Long-Term) Air Pollution
  Kurland 26 has called to our attention the
fact that the air pollution episodes represent,
by  definition,  episodes  of massive,  over-
whelming,  and unusual exposure, and thus
the most significant pathologic effects. There
is an "iceberg"  effect in that such data repre-
sent the  obvious, while the greater share of
the problem remains  submerged. We are
dealing with an essential dose-response sit-
uation, the  upper limits of which  are repre-
sented by these episodes.
a. Day-to-Day  Variations in  Mortality and
   Morbidity
  In a systematic approach to analyzing res-
piratory and cardiac morbidity daily in Lon-
don, Martin 14  examined deviations in  mor-
bidity from a 15-day moving average in Lon-
don  during the winters  of 1958-1959 and
1959-1960.  Both smoke and  sulfur dioxide
concentrations  appear to  be  about equally
related to morbidity rates, and a definite ex-
cess in morbidity seemed to exist as  it did
for mortality, though there was a somewhat
greater degree of irregularity.
  An approach similar to Martin's, but lim-
ited to observations on mortality, was used
by  McCarroll and  Bradley 18  in New York
City. Covering a 3-year period (1962-1964)
they examined a number  of peaks in New
York City mortality associated with periods
of high air pollution. There are examples
given where sulfur dioxide and smoke shade
appear to be  related to mortality. The au-
thors present other episodes, however,  where
the relationship to air pollution is not nearly
as clear, although the death rate fluctuates
to  even  higher  peaks.  Reference  to this
analysis has  already been made in our dis-
cussion of  the data on episodes in Section
B-l.
  The rate of hospital admissions, obtained
from data  collected by a  medical insurance
group, was used by Sterling et al.27 to study
the effects of air pollution on hospitalization
of about 10,000 individuals in Los Angeles.
Certain diseases considered to be relevant to
air pollution,  such  as allergic disorders, in-
flammatory disease of the eye,  acute  upper
respiratory  infections, influenza, and bron-
chitis, were found to be related to daily con-
centrations (measured as daily average mini-
mum and maximum values) of oxidants, car-
bon monoxide,  sulfur dioxide,  oxides  of
nitrogen, ozone, oxidant precursor, and par-
ticulate matter.  Measurements were  taken
at eight different stations five to ten miles
apart from March to October.  The analyses
showed significantly larger admission rates
on those days among the highest third of sul-
fur  dioxide  pollution than  on  those days
among the lowest third. Sulfur dioxide con-
centrations  during the period of the study
averaged less  than 0.015 ppm (~45 /tg/m3).
Concentrations on days of highest pollution
were not reported.  The method of analysis
generally is new and complex, and the author
noted the need  for  additional time periods
to be studied to  take into account the pos-
sibility of seasonal variations. The analysis
must also be extended to  other cities.
  McCarroll  et  al.2t  studied residents of  a
New York City housing project, using week-
ly questionnaires. Exact levels of sulfur di-
oxide which could be used for establishment
       126

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of air quality criteria were not given; how-
ever, the data indicate  that  sulfur  dioxide
rather than  particulate  matter was associ-
ated with eye irritation.  Symptoms of cough
were also shown to be related to air pollu-
tion but were not well differentiated between
association with particles and sulfur dioxide.
The particular time-series analysis used with
these data is not well known, and the biases
inherent in its use have not been fully de-
termined.
  Results also obtained  at Rotterdam have
shown that when the S02 concentration rose
for 3 to 4 days from about 300 /ug/m3 to 500
/ig/m3  (0.11 ppm to 0.19 ppm),* the number
of admissions into  hospitals for respiratory
tract  "irritation" rose,  especially in  older
individuals.7

b. Geographical Variations in Mortality
  1. Studies  Based  on Available  Data.—
Mortality and morbidity statistics each have
advantages as  well  as  disadvantages. Rec-
ords of  illness  should  be more  fruitful in
defining  subtle effects, since illness precedes
death and since all illness  does not result in
death.  Mortality statistics are collected in
every country and are  available for quick
tabulation.   Unfortunately,  the  quality of
mortality statistics varies. One of the prob-
lems is that, with the present system of tabu-
lating mortality data, a single cause of death
must be selected and coded, even though more
than one cause may be involved in the death.
The single cause of death designated (e.g.,
specific chronic respiratory disease)  depends
largely  on the  judgment  of the attending
physician and  has  little, if any, relation to
epidemiologic use. While contributing causes
of death  appear on the death certificate, they
are not  reflected in summary tabulations.
The coding of only the "underlying" cause
of death  minimizes the  importance of such
diseases  as emphysema  which often appear
on  the death certificate as contributory or
associated causes of death.28
  Almost all studies of  the effects  of long-
term exposure on  death rates compare the
 * SOj is converted from ppm to ^g/m3 in the Dutch
   reports by using the equivalency, 2,700 pg/m*=l
                                           rate in one area with that in another.  Mor-
                                           tality as well as morbidity studies are ham-
                                           pered by the possibility of differences other
                                           than air pollution existing between the areas,
                                           such as social class, occupation, age, and sex
                                           composition of the population, and cigarette
                                           smoking.  Assuming that almost all deaths
                                           are  recorded and  tabulated, comparison of
                                           total mortality  rates (i.e.,  deaths  from all
                                           causes) obviates the bias of diagnostic  selec-
                                           tion, but does not lessen the chances of other
                                           associated  factors   having  caused  the dif-
                                           ference.
                                              Buck  and Brown 29 reported in  1964 the
                                           relation of standardized mortality ratios for
                                           the  5-year period  1955-1959 to  four vari-
                                           ables:  daily smoke and  S02 concentrations
                                           for March 1962 (presumed representative of
                                           the study period), population density in 1961,
                                           and a social index  of 1951. The studies in-
                                           volved populations  in 214 areas of the United
                                           Kingdom  (19 London boroughs, 40 county
                                           boroughs,  70 other boroughs, 61  urban  dis-
                                           tricts, and 15 rural districts).
                                              Statistical  analysis  indicated  that  bron-
                                           chitis mortality had a significant positive as-
                                           sociation with both the smoke and S02 con-
                                           centrations encountered in these residential
                                           areas, and also with social index.  The stand-
                                           ardized mortality rates for lung cancer were
                                           not, in general, significantly associated  with
                                           smoke or SOo concentrations in the residen-
                                           tial  areas.  Examination of the tables  given
                                           by Buck and Brown suggests that the excess
                                           of bronchitis mortality  occurred  for classes
                                           of area where the average  daily smoke and
                                           SO2  concentrations  both   exceeded   200
                                           /*g/m3.* Although  smoking habits were re-
                                           viewed and were apparently  uniform from
                                           area to  area, occupational and domestic in-
                                           door environmental exposures were not con-
                                           sidered.  The pollutant values selected for
                                           the  correlations did not cover the same time
                                           periods  as the mortality figures.  The asso-
                                           ciations of bronchitis mortality with smoke
                                           and sulfur dioxide  were about equal, and the
                                           effects of the two pollutants cannot be sepa-
                                           rated.  Variations in smoking habits did not
                                           seem to account for much  of the mortality
                                           variation.
ppm. This report uses 2,860
ever possible.
                              '^l ppm when-
                                               : 2°0 jug/m3 of SOZ is equivalent to 0.070 ppm.

                                                                               127

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  In addition to studies of acute variations
in mortality in relation to  air pollution in-
dices, Burgess and Shaddick11 studied mor-
tality rates in London and their relationship
to smoke, sulfur  dioxide, social class, and
place of birth (in  or out of London). Aver-
age  levels  of sulfur dioxide did not vary
much among  the  areas,  ranging  from 190
,ug/m3 to 315 yug/m3 (0.07 ppm to 0.11 ppm);
sampling  was performed at seven  widely
scattered points every 24 hours during nor-
mal winter weather and every 4 hours dur-
ing fog periods.   A significant relationship
between lung cancer or bronchitis mortality
and  smoke or sulfur dioxide was not dem-
onstrated.  Births  in London and  low social
class  (occupational stratification)  were both
associated with higher rates. The differences
in sulfur dioxide levels are small among the
different areas, and it  is difficult to  believe
that,  even if sulfur  dioxide  were a fairly
strong causal factor, any significant differ-
ences could  be shown by this method. What
appear  to be the  same data, slightly rear-
ranged, are reported by Gore and Shaddick 9
with  the same basic conclusions.
  In a similar study carried out a few years
prior to the above,  Pemberton and Gold-
berg 30  compared  bronchitis death rates  in
persons over  age  45 in 33  county boroughs
of England and Wales for which air pollu-
tion data were available.  Two indices of so-
cial  conditions were used:  (1) the number
of persons per room, and (2) an estimated
percentage  of households with income ex-
ceeding a certain level.  Counties from urban
and industrial areas were included.  Signifi-
cant correlations were found with bronchitis
death rates  and sulfur  dioxide pollution, but
not with "total solids." The association was
true for male but not for female bronchitis
rates. No significant correlation was found
between the two indices  of social class and
sulfur dioxide pollution.  No  evidence was
given for smoking differences, and  no spe-
cific  sulfur  dioxide levels  were given that
would allow  establishment  of  ambient air
quality.
   Gorham 31 found a correlation between the
crude pneumonia death rate and atmospheric
sulfate  deposits in the 53  counties of Eng-
land  and Wales. The original data were not
given,  and the rates were not corrected for
age differences or social class; the study can
therefore  only be suggested until confirmed
by more accurate methods.
  Other studies 32-33 have  confirmed an asso-
ciation in Great Britain of bronchitis death
rates with general indices of air pollution,
and an equally strong association in general
holds up  when various measures of social
class are held constant by statistical  means.
Lung cancer mortality is consistently asso-
ciated  with measures of  population  density
and cigarette smoking, but not with general
indices of air pollution.
  2.  Special Studies  Involving  the  Collec-
tion  of New  Data.—In  1964,  also,  Wicken
and Buck 34 reported on a  study of bronchitis
and  lung cancer mortality in six areas of
Northeast England, one  in  Eston,  another
in Stockton and four in rural districts.  The
deaths covered the  period 1952 to 1962.  The
survey of decedents with cause of death from
bronchitis  or lung  cancer  was  matched
against the survey of decedents with cause
of death  from nonrespiratory  disease  con-
trolled  for  age and sex; the basis for the
diagnostic classifications  was not stated in
the report.  Personal interviews were carried
out with  next of kin.  Personal interviews
of a random sample of households were also
conducted to obtain sex, age, smoking habits
and occupation of the population at risk, the
living  population.  The survey  of decedents
was  carried out between January and Oc-
tober 1963; the survey of the living  popula-
tion  was carried  out between December 1963
and  March 1964. Smoke  and sulfur  dioxide
concentrations were measured in the Eston
urban district.  One year's aerometric  data
were obtained.  The study was  excellent in
principle  though,  unfortunately, sulfur di-
oxide  and particulate values were available
only for the Eston urban district.
   Eston,  itself, as a sub-study, was subdi-
vided  into  North  Eston  and  South Eston.
North Eston contains or  lies near heavy in-
dustrial plants,  whereas  South Eston  is a
residential  area.  During the  period  May
1963 to April 1964,  mean weekly observa-
tions of the sulfur dioxide and smoke  con-
centrations were carried  out in two  sites in
North Eston and one station in  South Eston.
       128

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The sulfur dioxide value in North Eston on
the yearly average was  115 /xg/m3 (0.040
ppm) and for South Eston it was 74
(0.026 ppm).  Smoke values were 160
and 80 jug/m3 for North and South Eston re-
spectively.  The deaths studied occurred  be-
tween  1952 and  1962.  Adjustments  were
made for  differences in  age composition,
smoking habits  and  social  class, and  these
were  insufficient to explain the  differences
in lung cancer and bronchitis mortality  rates
between  the two localities. Occupational  ex-
posure to pollution was then  taken into  ac-
count in the analysis.  The  conclusion was
that there is an association between the  de-
gree of  air pollution and the incidence of
lung cancer and bronchitis mortality in the
two areas  of  the  Eston urban  district.
Though both sulfur dioxide and smoke values
and concentrations are furnished in the  re-
port and the effects apparently cannot be
separated,  Brasser  et al.7 apparently  have
used the sulfur  dioxide concentration as the
more relevant measure of  this study.
  In a later study by Burn and Pemberton 35
the community of Salford was classified into
three pollution areas according to Table 9-2.
Five sampling stations in the area were em-
ployed.  Despite the closeness of the ranges
of values, a high rate of bronchitis mortality,
of lung cancer mortality, and of deaths  from
all  causes,  was  observed  in the  high,  com-
pared to the lower pollution  wards. It ap-
pears (see Section  C-4)  that  there was also
                                          an increased rate of bronchitis morbidity in
                                          the highly polluted wards.
                                            Winkelstein et aL36~3s divided  the  city of
                                          Buffalo into three zones based on a network
                                          of 21 air sampling  stations operated for a
                                          2-year period. The city was also divided by
                                          census tracts into  five economic levels based
                                          on median  family  income reported from the
                                          U.S.  Census. Although the method by which
                                          the air pollution zones  were determined is
                                          not clearly  described,  in the high zone  sul-
                                          fation  levels  were  greater than  approxi-
                                          mately 0.45, in the intermediate zone, 0.30 to
                                          0.45, and the low zone less than 0.30  (all
                                          units mg/cm2/30  days).   Total mortality
                                          from all causes  for  men aged 50 and over
                                          showed no  association with sulfation within
                                          each economic stratum. Deaths from chronic
                                          respiratory diseases, including asthma, bron-
                                          chitis,  chronic interstitial pneumonia, bron-
                                          chiectasis,  and emphysema, could be exam-
                                          ined  only for white  males aged 50 to 69 be-
                                          cause of insufficient numbers.  Only in the
                                          second  economic  level  (income $5,175  to
                                          $6,004)  were there  more  than  five  deaths
                                          in each air pollution level.  Within  this in-
                                          come group  a clear gradient  in mortality
                                          for  chronic  respiratory  disease was  seen
                                          from low to high air pollution, with the big-
                                          gest  difference being that between the mod-
                                          erate and high pollution areas.  In the first
                                          (i.e., lowest) economic level (income $3,005
                                          to $5,007), mortality for chronic  respiratory
                                          disease  was higher in the "high" oxides of
                        Table 9^2. POLLUTION LEVELS IN SALFORD.
                             (SEASONAL DAILY AVERAGES) ffi
Pollution area
 classification
                     Smoke,
    SO,,

(ppm in parentheses)
   Deaths
observed
	x 100
expected
                   Winter   Summer    Winter
                                                            All                 Lung
                                               Summer      Causes   Bronchitis   Cancer
High

Intermediate

Low

680

490

450

270

170

170

715
(0.25)
460
(0.16)
340
(0.12)
255
(0.09)
200
(0.07)
145
(0.05)
106

100

90

128

97

52

124

84

79

Note:  The data in the original  report show SO«  concentrations in parts per hundred million (pphm).

                                                                              129

-------
sulfur area than in the  "intermediate" pol-
lution  area.  No  consistent  gradient was
found for lung cancer deaths.
  As the authors point  out, since the only
association  between sulfation  and  respira-
tory disease mortality was in the lowest eco-
nomic classes  (first and second classes), and
these classes were likely to have increased
occupational exposures  to air pollution, the
relationship might be due to an intervening
occupational variable.  However, Reid has
called  attention to the likelihood of air pol-
lution  affecting  the lowest  socioeconomic
group most.39  This may be ascertained  by
a study  which  can measure  effects on the
lowest socioeconomic group in  low, moder-
ate,  and high  pollution  areas.  As  in most
community studies the effect of differences
in smoking habits  was  not  known in the
Buffalo study.  Also, the study  did  not take
account  of the  ethnic  background of the
decedents,  although Winkelstein's  analysis
of mortality from gastric cancer as related
to particulate levels attempted to do this.
  From  an aerometric  standpoint, one  of
the  most extensive studies of variations in
mortality and  morbidity within a city was
the work of Zeidberg et al. in Nashville, Ten-
nessee.40' 41  Aerometric  data  were  collected
at 123 sampling stations in a grid across the
city. An area of  "high" SO^ concentrations
was denned which had a geometric mean an-
nual 24-hour level of 0.01 ppm (~30 ^g/m3)
or more. The "low" S02 area had 0.005 ppm
 (~15 ,ttg/m3)  or  less.  The  high sulfation
area had 0.351 mg SO3/100 cm2-day or more
as an annual geometric mean. Areas of high,
moderate,  and  low pollution were  also  de-
fined by soiling index, annual dustfall, and
suspended  particulate matter.  All  codable
deaths registered  between  1949 and 1960
 (32,067)  were then distributed among cen-
sus  tracts  rated according to high, moderate,
and low pollution levels, and upper, middle,
and lower  economic classes, and then further
coded by  age, sex, race, and underlying
cause of death.  In the study,  account was
not  taken of smoking habits of the deceased;
also, the "middle class" group covered a rela-
tively large segment of the decedents.  Stand-
ardized  mortality  ratios (for total respira-
tory disease,  and for pneumonia, influenza,
bronchitis,  emphysema,  tuberculosis,  and
lung and bronchial cancer) were then re-
lated to  the  pollution  indices obtained dur-
ing 1959.  The statistically significant  mor-
tality increases were those for all respiratory
diseases related to sulfation and soiling; lung
and  bronchial  cancer  mortality,  and bron-
chitis  and emphysema mortality were not
clearly related.  "High"  pollution in these
studies for soiling referred to more than 1.1
coh unit/1,000 linear  feet.  A  later paper42
derived from the same study period analyzed
infant  and fetal death rates between  1955
and  1960.  For white  infant mortality, sig-
nificant  regressions were obtained  for sul-
fation; dustfall (alone, or as an interaction
variable) was the most  frequently  related
variable.
   In summary, the results of this  analysis
of long-term exposure studies indicate  ef-
fects which  would  coincide with Level  III
of the World Health Organization's  "guides
to air  quality."25  Level  III'is  defined as
"concentrations and exposure times at and
above  which there is likely to be impairment
of vital physiologic functions or changes that
may lead to chronic diseases  or  shortening
of life."

c. Geographic  Variations in Morbidity—Spe-
   cial Studies
   It has  been postulated  that  the study  of
records  of  illness  rather  than  mortality
should be more fruitful in defining subtle
effects, since  morbidity  is an earlier and
more sensitive index of deviation from nor-
mal health.  A much larger insult must pre-
sumably be given to the body to cause  death
than to  cause illness.  Routinely  collected
morbidity data are, however, not generally
available.  Data may occasionally be obtained
from  group  insurance plans,  hospital  ad-
mission  records, or existing school  records.
Since  such data are usually not collected in
a uniform, precise manner, most morbidity
studies require expensive and time-consum-
ing  field  surveys  with  questionnaires  or
actual medical examinations of the subjects.
   Morbidity studies of adults involving long-
term exposures are frequently not as useful
as desired, due to  the presence  of compli-
cating factors such as occupation and smok-
       130

-------
ing.  Accordingly,  Anderson  has  recom-
mended 43 that children and  housewives be
used  to determine the  health effects of air
pollution.
  A study was conducted by  Petrilli et  al."
in Genoa, Italy, which followed Anderson's
recommendation.  This intensive survey of
community respiratory morbidity was actu-
ally a set of epidemiologic studies to deter-
mine  the air pollution effects in Genoa.  The
subjects studied in one  of the research proj-
ects were women of 65 years of age,  non-
smokers who lived for  a long- period in the
same  area and  who had no  industrial ex-
perience.  Economic and social conditions in
the areas of residence were  considered as
well as the levels of pollution in these areas
of residence.  Air  pollution was  monitored
in Genoa for 10  years  (1954-1964) at 19
sites  covering the  suburban area, the  resi-
dential  center,  and the industrialized area.
Sulfur dioxide was measured by a technique
analogous to the volumetric method of the
English Department of Scientific and Indus-
trial  Research.  Carbon monoxide was also
monitored. A retrospective  survey was car-
ried out using the M.R.C. questionnaire with
slight modifications. As has been noted, sev-
eral different epidemiologic studies appeared
to have been conducted. Consideration was
taken in the  sample selection  of age, length
of residence  in the same area,  presence of
cardiovascular  disease, living habits,  pre-
vious  working habits, etc., in the design of
the study. Morbidity indices were calculated
for 1961 and 1962 for the population which
received free medical care from the munic-
ipality and therefore was under continuous
medical observation. Prevalence and inci-
dence rates were calculated for  symptoms
such as cough, sputum, dyspnea, rhinitis,  and
recent and past  respiratory  diseases.  The
frequency of these respiratory symptoms was
much greater in the central residential area
than in the  suburban residential area, even
though the annual means of  sulfur dioxide
in the two areas were  relatively close;  the
pattern for rhinitis was somewhat erratic.
  Sulfur dioxide measurement in the clean-
* SOa values in this study were originally reported in
  ppm.
est area, that is, the suburban residential dis-
trict, was 80 /xg/m3 (0.028 ppm) * with the
winter  value being  85 jig/m3  (0.030  ppm)
and the summer value 55 ju.g/m3 (0.019 ppm).
The residential center area had an annual
average value  of 105 /xg/m3 (0.037 ppm),
with a  winter  average of  115 /xg/m3 (0.040
ppm) and a summer  average of 85 ><.g/m3
(0.030 ppm).   The industrial area averaged
265 /xg/m3 (0.093 ppm) for its annual mean
with a  winter  average of 315 /xg/m3  (0.11
ppm) and a summer average of 230 /xg/m3
(0.080 ppm).
  The study showed a striking correlation be-
tween frequency of  symptoms and the  dis-
eases of the respiratory tract and air  pollu-
tion levels. In the suburban residential area,
the indices were almost always significantly
lower for the data collected and particularly
for the frequency of cough, sputum, dyspnea,
rhinitis, and recent  respiratory disease, es-
pecially  bronchitis.  There  was usually  a
gradient between the suburban area and the
industrial area.  What was especially  sig-
nificant was the finding of differences gen-
erally in the prevalence of respiratory  dis-
eases during the summer  in the  industrial
area as  compared with the  moderate and low
pollution areas.  This  should contribute to
our knowledge regarding the relationship be-
tween different climatic conditions and the
health effects of air pollution. It has  been
postulated that it is usually in the winter
that air pollution of the reducing type exerts
the most deleterious effects.
  The study also examined a number of areas
in the city.  Data for  the  seven districts in
the town of Genoa showed  a very significant
correlation (r = 0.98) between the frequency
of bronchitis and the  annual mean of sul-
fur dioxide levels. A nonsignificant correla-
tion between the frequency of bronchitis and
suspended matter and  dustfall was observed
in the study.  There was a  suggested  rela-
tionship between  winter  temperature and
bronchitis, but this  was  further reduced
when adjustment was made for air pollution.
  What is particularly significant about this
study is that the differences in respiratory
disease  were found  between areas with an
annual mean of 105 /xg/m3  (0.037 ppm) and
one of  80 /xg/m3 (about 0.028 ppm).   Also
                                                                             131

-------
highly significant was the  observation that
effects of  air pollution  were  found in the
summer  prevalence of respiratory disease.
Very sharp  differences  were  found within
a communi^ which is characterized by maxi-
mum sulfur  dioxide levels  below an annual
average of 300 /^g/m3 (0.10 ppm). Finally,
the  very  striking differences between the
area with IQW levels of pollution and the in-
dustrialized  areas were  noted  and should
lend support to the results of studies in other
areas.
  Toyama,45  in a comprehensive study of air
pollution  and its health effects  in Japan,
charted the age-standardized morbidity rates
(per thousand)  secured  by interview  sur-
vey in 1961,  and described a gradient of res-
piratory disease  morbidity from  the highly
industrialized  (and  presumably  polluted)
areas to the  rural areas of Japan.  Further,
the pulmonary disease morbidity  ratio was
higher in the industrialized, polluted areas
than were the ratios for other disease group-
ings. This gradient was not noted for cardio-
vascular  diseases  nor for gastrointestinal
diseases.  Unfortunately,  specific pollutant
concentrations were not clearly indicated  to
accompany  these data on  morbidity.   The
age-standardized morbidity rates  per  thou-
sand for  several cities in Japan are shown
in Figure 9-3.45
  Pulmonary function and respiratory symp-
toms were compared in  population areas  of
high (95  /*g/m3)  and low  (25 yug/m3)  S02
pollution  (annual means of 0.034 ppm and
0.009 ppm respectively)* (measured by H2O2
absorption,  H^S04 titration)  in Port Kem-
bla, Australia.4fi Coh values in the more pol-
luted and in the cleaner area, averaged over
one year, were 2.7 and 1.3 respectively. Since
the pollution in this area was due to a single
large source, pollutant levels fluctuated wide-
ly.  One peak reading  of over  13 ppm was
observed, and daily averages  ranged up to
17 times  the annual mean.  Chronic bron-
chitis rates  for  men over 55  were higher
in the polluted area, but rate differences for
other age groups and  for  women were  not
statistically  significant  between  the areas.
A higher incidence in the polluted area was
also found for a variety of respiratory symp-
toms such  as  head colds, wheezing,  and
chronic cough.  The effects were said to have
disappeared when pollution was reduced  by
using a higher stack at a smelter.47  Adjust-
ments were not made for differences, which
were known to  exist,  in age and smoking
between the two  areas.   In  addition,  the
heavily polluted area  was of  lower socio-
economic class:  only 3.2 percent of its popu-
lation was in professional and administrative
occupations, and 10.2 percent were laborers
as compared  to 10.2 percent  professionals
and  2.4 percent laborers in the clean area.
A difference of over  one  inch in average
 ! SO2 values in this study were originally reported in
  ppm.
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KAWASAKI

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                                   RATE PER THOUSAND
   Figure 9-3. Age-Standardized Morbidity Rate per 1,000 for Three Diseases in Japan.
                                                  A
  The mortality rate for respiratory diseases shows a clear correlation with pollution levels. There is no such clear
  correlation for cardiovascular or gastrointestinal disorders.
       132

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 height of the population  in  the  two areas
 also indicates the two populations were not
 completely  comparable.  No significant  dif-
 ferences  that could be related to air pollu-
 tion  were  found  in respiratory function
 measured as  FEVi.0. In Port Kembla,  S02
 concentrations are highest during the sum-
 mer, rather than winter, so that  this study
 is not biased by the question of whether the
 effects are  due to  pollution or low temper-
 ature, as has been the case in many of the
 British and American epidemiologic studies.
 Notwithstanding the stated deficiencies of the
 study, the finding that respiratory symptoms
 disappeared when  pollution  was  reduced
 would appear to  confirm an effect of sulfur
 dioxide at the level found  originally in  the
 old high  pollution  area  of  Port Kembla, if
 no other  change  took place which could ac-
 count for the reduction.
   In 1965, Holland et al.4"-49  reported on their
 study  of  the prevalence of chronic respira-
 tory disease symptoms and performance of
 pulmonary  function  tests  of outdoor tele-
 phone workmen in London, in rural England,
 and on the east and west coasts of the United
 States. Types of occupational exposure,  use
 of  cigarettes, and socioeconomic  matching
 were considered.  The annual mean concen-
 tration of suspended particulate  matter in
 the British exposures, both rural and in Lon-
 don, was approximately 200 /xg/nv1. For sul-
 fur dioxide, the mean concentrations were:
 285  /ig/m3  (0.1  ppm)*  in London and  in
 rural  areas  of England,  55 /*g/m3  (0.02
 ppm).  Persistent  cough and phlegm and
 chest illness episodes were 1.4 times as fre-
 quent  in men aged 40 to 49,  and  2.2  times
 as frequent in men aged 50 to 59, in the Lon-
 don  area as  in  rural England.   Increased
 sputum volume was more frequent and pul-
 monary function was  poorer in London than
 in the rural areas.  These  differences held,
 even when the data  were  standardized  for
 smoking.
  In an earlier study, conducted in 1960 and
 1961 following a  number of related studies
yielding  consistent   results,  Holland  and
Reid 50 reviewed respiratory symptoms, spu-
 tum production, and lung function levels in
 mail van  drivers and vehicle  maintenance
 men in central London and mail van  drivers
 and engineering workers  also driving vans
 in and around three county towns in South-
 ern England. The conduct of the study was
 exemplary.  A   standardized  questionnaire
 was used as were trained  interviewers. Be-
 cause  of the design of the study, socioeco-
 nomic factors were the same, the  occupa-
 tional exposures were homogeneous, and cor-
 rections were applied  for smoking.   There
 were some physique differences in the  rural
 areas, and allowances were made for  these
 in the statistical evaluation. Unfortunately,
 no comprehensive indices  of  air pollution
 were available  for  the three towns.  How-
 ever, mean sulfur dioxide readings expressed
 as sulfate per 100 cm2 lead oxide were avail-
 able for two  stations in St. Pancras near the
 London  survey  center  and two stations  in
 Gloucester, one  of the three towns. Brasser
 et al.~  have furnished the following SO., val-
 ues: London (St. Pancras)  summer average
 100 /<,g/m3 (0.035 ppm), winter average 500
 ,ug/m3   (0.17  ppm)  and Gloucester,  Peter-
 borough and  Norwich 75 /xg/ni3 (0.026 ppm)
 and 200 ju,g/m3 (0.070 ppm) respectively for
 summer and winter averages.
   Between the age of 50 and 59, the London
 men had more  frequent  and  more  severe
 respiratory symptoms,  produced more spu-
 tum, and had significantly poorer perform-
 ance  on lung function tests.   Dyspnea  of
 grade 3* or more was more than four times
 as frequent in London as in the county towns
 among men 50 to 59 years  of age; this is a
 highly significant difference.   The authors
 concluded  that the  relatively high level of
 pollution in London was  the  major  reason
 for the  excessive frequency or severity of
 chronic bronchitis in London.
   In a group of Canadian  veterans studies
by Bates et ol,31 a relationship between air
pollution and both bronchitis and pulmonary
function measurements has been  reported.
There  are, unfortunately,   inadequate  data
 ' SO2 values in this study were originally reported
 in ppm.
  ' The author  grades dyspnea1B according to  five
  levels; grade 3 represents dyspnea when walking
  even at a slow pace on level ground, but not to
  the extent that it is necessary to stop for breath.
                                                                            133

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on the levels of smoke, sulfur dioxide, and
other pollutants, in the four Canadian cities
compared, to derive specific relationships be-
tween the levels of these pollutants and the
prevalence or exacerbation of disease or the
deterioration of pulmonary function. How-
ever, there is an association in the  "dirty"
cities (Montreal and Toronto) versus the
"clean" cities (Halifax and Winnipeg) of in-
creased prevalence and severity of bronchitis,
and poorer pulmonary function performance.
  One of the most detailed and carefully de-
signed American studies was carried out by
Anderson and Ferris in Berlin, New Hamp-
shire, and Chilliwack, British Columbia.52-54
In each town a carefully drawn, random sam-
ple of the population was given standard pul-
monary function tests and a  standard ques-
tionnaire  for  respiratory  symptoms.  In
Berlin, the  sulfation  rate for August and
September 1960 averaged  426.0 /tg/100 cm2-
day while in  Chilliwack the  sulfation con-
centration for  August and September 1963
averaged 50.3 jug/100 cm2-day. This was con-
verted to an  equivalent  sulfur dioxide value
for Berlin of 35 /*g/m3  (0.012 ppm) * based
on readings for one station.  No information
is  provided to show how the  Chilliwack sul-
fation  values  were converted  to an  S02
equivalent of 2.85 jug/m3  (0.001).*  Soiling
values were  virtually identical; coh values
averaged  0.5 for  Berlin  and greater than
0.5 for Chilliwack. The prevalence of chronic
respiratory disease was initially greater in
Berlin, but  adjustments for  differences in
age and in cigarette smoking eliminated all
the differences in prevalence.  However, even
after  correction  for age, height,  sex,  and
smoking  habits,  the  Berlin   residents  had
slightly  lower  results  on pulmonary  func-
tion tests (FEVn, and Peak Expiratory Flow
Rate). This  difference might be due to the
different climates, or to a slightly lower so-
cioeconomic  class in Berlin, or to ethnic dif-
ferences between the two  towns, or to occu-
pational exposures. There were also studies
comparing areas within Berlin, and no dif-
ference  in respiratory symptoms or pulmo-
nary  function  could be found between an
area where the sulfation rate averaged 610
/Ag/100  cm2-day  (2-month  period)  and an-
other area of the town averaging 255 /jg/100
cm2-day for the same period.52-53- °5.  As in
the two-town study, the disease  rates in the
two areas of the town were strongly affected
by differences in the proportions  of the popu-
lations  who  were cigarette  smokers.  The
authors correctly note the limited possibility
of ascertaining effects, due to the very low
pollution values and the movement of people
with respiratory disease to the even less pol-
luted areas of Berlin.
  A study56 comparing  two areas exposed
to pollution from a single source was  under-
taken in the Seward-New  Florence area of
Pennsylvania. The sulfation rate was  6.2
times greater in  Seward (3.7  mg S03/100
cm2-day) than in neighboring New Florence,
while suspended particulate  matter concen-
trations were 1.4 times greater. These were
151 /*g/m3 and 109 /ug/m3 respectively. Dur-
ing the study period  from October 1959 to
April 1960, the average  24-hour S02 meas-
urement was 255 /ig/m3  (0.09 ppm) * in
Seward,  compared to less  than  30  /ig/m3
(0.01 ppm) in New  Florence, both  by the
West-Gaeke method.  Slightly higher  values
for airway resistance were found in Seward
even  after correcting for  differences in
height and  age. No  adjustment was made
for other factors  which may have affected
airway  resistance, such as smoking and oc-
cupation.  The difference in  body height is
also difficult to interpret.
  The Nashville air pollution study reviewed
total morbidity in  relation  to air pollution.40
The morbidity data were obtained by trained
interviewers in  a questionnaire survey of
sample households  in the city. The aerometric
data used for the  survey were the same as
those used  for the  morbidity study. An area
of "high" SOo concentration  was denned as
one which had a geometric mean annual 24-
hour level of 30 /tg/m3 (0.01 ppm)* or more.
The  "low"  SO;, area  had  15 jug/m3  (0.005
ppm) or less. The high  sulfation area had
0.351 mg S03/100 cm2-day or  more as an
annual geometric mean. Areas of high, mod-
** SO2 values in this study were originally reported
  in parts per billion (ppb).
* SO2 values in this study were originally reported
  in ppm.
       134

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erate, and low pollution were also defifined by
soiling index, annual dustfall, and suspended
particulate matter.  As  expected,  when the
data were  analyzed by  socioeconomic class,
higher illness rates  were reported from the
lower  class  households, and  there  was  a
strong tendency for persons of lower social
class to be resident in areas of high air pollu-
tion.
  Since  only  the large  middle class were
present in  all pollution  zones, analyses con-
trolled for  socioeconomic status were  limited
to it.  A direct correlation between  illness
rates  from all causes and pollution could not
be shown  with any consistency  except for
persons 55 years and older (both sexes). A
decline in morbidity rates from high to low
pollution areas could be shown for this group
with the soiling index and SOo concentrations
as pollutant variables, but  no consistent de-
cline  with  sulfation, dustfall,  or suspended
particle concentrations was seen. There was
no correlation between pollution indices and
morbidity  rates for  cancer, respiratory, or
gastrointestinal  diseases.  Attempts  were
made to  minimize the effect of occupational
exposure by studying females keeping house.
In this group, a small but consistent gradient
in illness from all causes correlated with air
pollution indices. No consistent findings could
be found for working females from all social
classes  combined. Because  of  the possible
wide variations within the large group called
"middle class," the study may not have taken
socioeconomic status wholly into account. The
lack of information on  cigarette smoking  is
another deficiency. The morbidity differences
that are shown are most striking between the
"high" pollution group versus the "moderate"
and "low."
  d. Morbidity—-Incapacity for Work
  Dohan " r>s compared  respiratory morbid-
ity in hourly employees  in five United States
cities by use of insurance and personnel sta-
tistics of a large electronics company.  Hourly
employees received insurance payments after
the seventh  day of  illness  provided  that a
physician's certificate was received. For the 3
study  years, the respiratory absentee rates
showed a  direct  relationship to suspended
particulate  sulfates. The  latter concentra-
tions  ranged from a low of 7 /ig/m3  in Cin-
cinnati  to about 14  fig/m3  in  Camden and
Woodbridge, New Jersey, and in Indianapo-
lis, to a high of 20 /tg/m3 in Harrison, New
Jersey. A breakdown by type of respiratory
disease showed miscellaneous respiratory in-
fections, influenza, and bronchitis to be most
directly related to the sulfate levels ( see Fig-
ure 9-4). Pneumonia, asthma, and sinus dis-
ease were not significantly correlated. The
incidences of gynecologic problems, urinary
tract disease, and appendicitis were not re-
lated to  several indices of air  pollution, in-
cluding  sulfate;  nonoccupational  accidents
did,  however,  increase  progressively  with
sulfate, as  did the  respiratory diseases.  In
addition,   neuropsychiatric   diseases   were
highest in the three  cities with highest pollu-
tion indices. The correlation between all in-
dices of air pollution and accidents  and men-
tal illness may indicate that secondary ef-
  80h
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                           HARRISON
             WOODBRIDGE
                                CAMDEN
                          INDIANAPOLIS
     CINCINNATI
                    1, i
                                  .ill
                   10
                           15
                                   20
                                           25
                SULFATES ^g
Figure 9-4.  Incidence of Respiratory Disease Lasting
          More than Seven Days in Women Versus
          Concentration of Sulfates in the City Air
          at Test Sites**4" $®
The incidence of respiratory disease lasting more than
seven days in this group is directly related to concen-
trations of suspended sulfates in the cities shown.
                                                                                135

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fects of air pollution, such as reduced visibil-
ity and gloomy weather, have a measurable
effect on health and welfare, or that the re-
sults  are too nonspecific to  attach  causal
significance.
  Age differences were rather marked among
the cities, yet age standardized rates were not
calculated. Without detailed  calculations it is
not possible to state whether differences such
as only 0.2 percent of the Cincinnati women
being over age 45 compared to 35 percent of
Camden, New Jersey,  women would signifi-
cantly affect  the rates. Differences in social
class and standard of  living were probably
not great, since all subjects were hourly em-
ployees of the same company. Differences in
patterns of illness reporting and acceptabil-
ity of different diagnoses within each city are
difficult to assess, but presumably were mini-
mized by limiting the study  to absences of 8
days and more. Other possible differences,
such as  weather and  climate in the cities,
exposure to toxic materials, plant morale, and
air conditioning were  discussed by the au-
thors and judged by them not  to be of major
importance. No data are available on  differ-
ences in  cigarette smoking, or plant rules re-
garding  smoking at work,  in the different
locations. A unique and strong factor of this
study is that other pollutants such as total
suspended particlate matter, benzene-soluble
organics, and certain trace metal concentra-
tions  did not correlate with the respiratory
disease rates. The findings of this study need
to be confirmed.
  During 1961-1962 a study of the incidence
of incapacity for work was conducted  by the
British Ministry  of Pensions and National
Insurance.09 The population covered was rep-
resentative of  the working  population of
England and Wales. Rates  of sickness ab-
sence for bronchitis, influenza, arthritis, and
rheumatism were related to  indices of pollu-
tion. There was a  significant correlation be-
tween  bronchitis  incapacity in middle-aged
men  (35 to 54) and the average seasonal (Oc-
tober through March) levels  of smoke and
sulfur dioxide in high-density residential dis-
tricts, based on 24-hour measurements. For
Greater London, there  was a significant cor-
relation  between bronchitis incapacity and
both smoke and sulfur dioxide for  all ago
groups taken together, and for men aged 35
to 54 and 55 to 59. It is interesting that there
was also more incapacity from arthritis and
rheumatism in areas having heavy smoke pol-
lution. Influenza  incapacity was greater in
those  areas with higher pollution levels over
Great Britain as a whole but not within the
Greater London conurbation, nor was there
in this latter  area  any association between
pollution and psychosis or psychoneurosis.
The lowest bronchitis inception rates related
to smoke levels between 100 /*g/m3 and 200
/*g/m3 and to sulfur  dioxide concentrations
between 150 /*g/m3 and 250 /xg/m3  (0.053
ppm and 0.081 ppm). The highest values re-
lated  to concentrations  of 400  /*g/m3 smoke
and 400 /x.g/m3 (0.14 ppm)  sulfur dioxide.
  Burn  and Pemberton 31 compared areas of
high and low  pollution  in Salford, England.
Pollution data were obtained from five stand-
ard D.S.I.R.  instruments  operating for 2
years, 1958 and 1959. The  aerometric data
were  obtained for 24-hour  periods. Average
daily sulfur dioxide concentrations during the
winter months in the  more polluted  areas
were approximately 715 /*g/m3 (0.25 ppm) *
compared  to  285 /tg/rn3 (0.10  ppm)  in the
cleaner  areas  (measurement  method not
clear). Smoke pollution was also considerably
higher in the polluted areas. Bronchitis mor-
bidity, as measured by incapacity certificates
from  the  Ministry of  National Insurance,
was higher for the study group  (men aged
45 to 64) in the polluted areas.
  Brasser et al.7 have reanalyzed the Salford
data without indicating why this reanalysis
was necessary. They prepared new isopleths
and concluded that  the  correlations between
absenteeism  for  bronchitis and pollution
levels are considerably higher than originally
was  presumed by  the  investigators them-
selves. The population 45 to 64 used for de-
nominators of the rates had to be estimated
by assuming that each district  had the same
proportion in that age group as the town as
a whole.  In  addition,  large  differences in
socioeconomic class probably existed between
the areas, but no adjustments were possible.
Differences in occupation may  also have af-
 SO2 values in this study were originally reported
 in pphm.
       136

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fected incapacity rates. No data on cigarette
smoking were available.
  Results  obtained in The Netherlands have
also shown that when the SCX- concentration
rose for 3 to 4 days from about 300 jug/nr1 to
500 /ig'/m1 [0.11 ppm to  0.19 ppm]*, absen-
teeism at  both Rotterdam  and Vlaardingen
increased  by  at least 30  percent;  in certain
groups (e.g.,  those over 45 years of age)  the
increase was as large as 50 percent to  100
percent.7
  Verma ft al.'w presented information on ill-
ness absences in relation to air pollution. Ill-
ness data  for the employees (males and fe-
males, ages 16 through 64)  of a metropolitan
New York insurance company were obtained
through the records of the personnel depart-
ment. They included medical history,  X-ray
information,  and laboratory results obtained
by the medical department  of the company,
and were  classified by absences due to respi-
ratory illness and to nonrespiratory illness.
Mean daily concentrations of air  pollutants
and meteorologic data were secured from the
monitoring  system  of  metropolitan New
York: smoke shade, sulfur dioxide, and car-
bon monoxide content were  reported. The
data for the 2  years,  1965 and 1966, were
examined  statistically and several  conclu-
sions were reached. There was a strong time
dependence and a yearly cyclical behavior;
when these factors were removed there re-
mained  no strong  positive  relationship  be-
tween respiratory absence  and the pollution
variables studied. Respiratory illness absence
rates were at their highest  level when sulfur
dioxide  and  smoke  shade  levels were both
high on cool days; and a lag effect for respira-
tory absences was not noted.

          3.   Studies  of Children
  Comparisons of the prevalence of respira-
tory disease  in areas of varying pollution
levels have been made to delineate the roll of
air pollution  and specific pollutants. A prob-
lem common  to all the studies is the difficulty
in guaranteeing that the areas are  similar
 : The numbers in brackets are the editor's; an equiv-
  alency of 2,700 yug/m3=l  ppm SO. was used  to
  assure consistency with any conversions made by
  the authors.
(except for air pollution) in all factors that
might affect the prevalence of disease.
  Because studies on adults tend to be com-
plicated by smoking habits, changes  of oc-
cupation,  and changes in address over a per-
iod of years, several studies have been di-
rected  at  effects  of air pollution on  school
children.  The advantages of using children
for research on the primary etiologic effects
of air pollution was  first noted several years
ago;"1 Anderson has  most recently reaffirmed
this  view." A major element of concern is
that deleterious  effects  on the  respiratory
system of very young children may have an
effect on  the subsequent  evolution  of  the
chronic bronchitis syndrome  in  the adult
population.
  The relationships of respiratory infections
in children to long-term residence in specific
localities  have  been studied in England by
Dcuglas and Waller."J Levels of air pollution,
in terms  of domestic coal  consumption rec-
ords, were used to classify  four groups; the
authors include an evaluation of the validity
of this method at the end of their report. The
histories  of 3,866 children  born during the
first week of March 1946 were followed until
1961, when the children were 15 years of age.
Social class composition of these children did
not  differ significantly from area to area.
Measured concentrations for smoke and for
SO-  in 1962 and  1963  were compared with
the earlier  prediction of pollution  intensity
based on  the coal consumption data, and in-
dicated an overlap for  greater London area
of low  and moderate groupings; for other
areas,  the predicted gradient  of concentra-
tions was affirmed.  Sulfur dioxide  varied
from about 90 /xg/m3  (0.031  ppm)   in the
"very low" group to about 250 /xg/m3  (0.087
ppm) in the "high" pollution group. Because
of the age of the subjects, smoking was ap-
parently  not considered in this evaluation.
In 1965, 19 percent of the boys and 5 percent
of the girls, aged 11 to 13, smoked at least
one  cigarette a week regularly.03
   In the Douglas  and Waller study, the gen-
eration of pollutants in the indoor home en-
vironment (e.g., by heating and cooking) was
not  considered. Interviews were conducted
with the  mothers when the  children were 2
and 4 years of age; information was obtained
                                                                              137

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about upper and lower respiratory illness and
recorded hospital admissions for these and
other causes. Data about colds, coughs, and
hospital admissions  were also  gathered by
school doctors at medical examinations when
the children were 6, 7, 11 and 15 years of age.
Between the  ages of 6-V£ and 10-1/2, special
records  for causes of school absence exceed-
ing one week were reviewed with the moth-
ers.  Families numbering 3,131 remained  in
the same pollution area throughout the first
11 years of this study. The conclusions of the
study were that upper  respiratory  tract in-
fections were not related to the amount  of
air pollution, but that lower respiratory tract
infections were. Frequency and  severity  of
lower respiratory tract infections increased
with  the amount of air pollution exposure,
affecting both boys and girls, and with no dif-
ferences detectable between children of mid-
dle class and working class families. This as-
sociation was found  at each of  the  examina-
tion ages, including  age 15. At age 15, per-
sistence of rales  and rhonchi  (chest noise),
possibly the prodrome of adult chronic respir-
atory disease, was some 10-fold  less in the
very low pollution area, and a factor of 2 less
in the low pollution area  than that in the
high  pollution area.  If  the  1962-1963 meas-
ured  concentrations  for smoke and SO;, can
truly be extrapolated to the 15-year respira-
tory illness survey, then these British school
children experienced increased frequency and
severity of lower respiratory diseases in as-
sociation with annual mean smoke concentra-
tions ranging above  130  jug/m3  and SO2
above 130 /*g/m3  (0.046 ppm).
   The  lower respiratory  tract  findings  of
Douglas and Waller were confirmed  in  a
study by Lunn et al.R4 The patterns of respi-
ratory  illness in school children of the age
group 5 to 6 were studied by them with refer-
ence to residence in four areas of  Sheffield.
The data  were collected during the summers
of 1963, 1964, and 1965 in order to  minimize
effects of winter  respiratory illness upon the
pulmonary function  tests. Mean daily smoke
levels measured in each of four areas ranged
from 97 /*g/m3 in the "low" area to 301 /u.g/m3
in the "high" area.  S02 concentrations were
respectively  123 //.g/m3 (0.043  ppm),  181
      3 (0.063 ppm), 219 Atg/m3 (0.077 ppm),
and 275 /*g/m3 (0.096 ppm) in the four areas,
during  1963-1964.  Somewhat lower  smoke
levels  were noted  the  following  year,  al-
though  the  gradient  between the  districts
was  preserved. However,  the sulfur dioxide
values were obtained at five schools between
October 1965  and May 1966 inclusive. The
values were 109 /xg/m3 (0.038 ppm) and 134
/ig/m3  (0.047  ppm)  corresponding to the
"low"  pollution area, and then 194 jug/m3
(0.068 ppm),  241 ^g/m1  (0.085 ppm), and
304 jug/m3 (0.11 ppm) respectively. Question-
naire of the parents, physical examination,
observation  for the presence of nasal dis-
charge, examination of the  eardrums, and
recording of both the forced expiratory vol-
ume in 0.75 seconds (FEVo.7.-,) and the forced
vital capacity  (FVC), were completed during
each of the summer terms of 1963, 1964, and
1965.  Several socioeconomic  factors were
compared for the various districts; smoking
was appropriately disregarded for this age
group; internal home environments, or differ-
ences in home heating systems, were not re-
ported. The authors conclude that there is an
association between the levels of  atmospheric
pollution and chronic upper respiratory infec-
tions (as indicated by mucopurulent nasal dis-
charge, history of three or more colds yearly,
or scarred or  perforated eardrum). Further,
lower respiratory tract illness (measured by
history of frequent chest colds or episodes of
bronchitis or  pneumonia)  was similarly as-
sociated. Functional changes, in the form of
reduced FEVo.y.-,  ratios emerged  where there
was a  past history of  pneumonia or bron-
chitis, of persistent or frequent coughs, or of
colds going to the chest. There  appeared,
therefore, to be a persistence of respiratory
dysfunction, even in the absence of high-
pollution extant  at the time of the function
testing.  This  study clearly demonstrated the
association between respiratory  illness in in-
fant  school children and  atmospheric pollu-
tion. The lowest "effect" level for smoke and
S02 was not clearly indicated by this study,
but the increased association of  "respiratory
infections"  in school children was detected
in areas whose mean daily figures exceeded
about 100 /ug/m3 for smoke and 120 /xg/m3
 (0.042 ppm) for S02.
   A  study for Manzhenko 65 of  upper respi-
       138

-------
ratory tract conditions in school children in
Irkutsk is  difficult to relate to the Sheffield
study. However, the higher incidence of res-
piratory tract conditions  and the undefined
abnormal X-ray findings  in these children's
lungs are disturbing evidence  of the  possi-
bility of an association between serious res-
piratory disease and residence in a polluted
community.
  Toyama4r>  studied  two groups of school
children, 10  to 11 years  old, in Kawasaki,
Japan.  Sulfation rates at the  school in the
more polluted area  varied from  0.5 to 1.9
and averaged 0.9 mg/100 cm--day Pb02; no
sulfation rates were  given for area of lower
pollution. The children from the more pol-
luted area had a higher  frequency  of non-
productive cough, irritation of the upper res-
piratory tract, and  increased mucus  secre-
tion.  The dustfall  rate  was  considerably
lower in the less polluted  area except for an
occasional  month when the  dustfall  in the
two areas  was almost equal.  Whether the
effect was due to oxides of sulfur or particu-
late matter cannot be determined from this
study.

     4.   Studies of Pulmonary Function

  Spicer et «L66 studied a group of patients
with chronic obstructive airway disease who
resided  in  a  small area of downtown  Balti-
more. Air samplers  were placed at the resi-
dential  area  and at the  University, where
extensive pulmonary function tests were per-
formed.  The patients became better or worse
in their pulmonary function as a group, sug-
gesting  that  they were influenced by a fac-
tor  in their  common environment.  It was
not, however, possible to determine a simple
cause and  effect relationship  with any one
pollutant.  Subtle changes in the pollutant
concentrations and weather conditions may
have been responsible.
  Shephard et al.K1  studied  a  group  of 10
cardiac  cripples who were confined to  their
homes.   Air  pollution measurements  were
carried  out by sampling equipment  placed
inside the homes. Pulmonary function tests
were repeated at the same hour of the day,
3 times weekly,  for 2  months.  Although
a response to suspended particulate pollution
was demonstrated, no consistent changes in
pulmonary function were noted with sulfur
dioxide levels, measured  as  total  gaseous
acid (sic).  During one  inversion period,  a
6-hour average of sulfur dioxide concentra-
tions  (hydrogen peroxide  titremetric meth-
od) reached 460 fig/m3  (0.16 ppm)*.  The
indoor readings were considerably lower, the
highest indoor concentration being sustained
for 6 hours.
  Holland et a?.49 report decreased perform-
ance of the FEVi.« test in London and British
rural  outside telephone  workers  compared
with their American counterparts. For both
groups  the  FEV was further decreased in
relation to  smoking intensity.  FEV differ-
ences  within  the United Kingdom workers
(i.e., London  versus rural), may be related
to an  appreciable  extent  to  the  sulfur di-
oxide  concentrations accompanying the par-
ticulate levels. A more detailed  discussion
of the study appears in Section C.
  Toyama 4r> reported measurements of  peak
flow rate  and total  vital capacity perform-
ance in Japanese school children in  areas
of differing air pollution measured monthly;
fluctuations were observed in the mean  peak
flow rates of children  attending schools and
living  in polluted industrial areas, and the
variations   were  smaller  for  children  in
cleaner areas. Total vital capacity was not
significantly different  among pupils of the
various schools. There was a substantial dif-
ference in  peak  flow rates between  the two
school districts at times of highest pollution.
When pollution values were lowest,  the dif-
ferences were less.  Monthly dustfall was
15 to  70 tons/km2-mo* in  the more  polluted
areas;  lead  peroxide candle sulfation rates
from month to month ranged from  0.5 to 2
mg S03/100 cm2-day in  the higher  polluted
area.
  In Osaka, Watanabe2-  studied the  peak
flow rate and  vital capacity performances of
children in schools enduring differing air
pollutant concentrations.  It was noted that
individual peak flow rates were more mark-
edly decreased in the winter months  (Sep-
tember  to  December  1963)  for the school
* S02 values in this study were originally reported
  in ppm.
* In the United  States, dustfall  is measured in
  tons/mi2-mo.
                                                                              139

-------
in the highly polluted area than for the school
in the low pollution area.  Daily mean  con-
centrations  of both dustfall  and sulfur di-
oxide concentrations were twice as great in
the polluted area as in the unpolluted area.
  In  the paper  by Lunn  et  al.ai  Sheffield
school children were shown to have reduced
FEV 0.7r) and FVC ratios in the area of high-
est  pollution.  The measurements were made
during  the  summer, when pollution levels
were low and apparent  incidence  of acute
respiratory  infection was  diminished,  sug-
gesting,  in contrast to  the  Japanese studies
referred to  above, that there may be  per-
sistence  of the respiratory  function deterio-
ration in relation  to residence  in the  area
of high pollution. Mean daily averages meas-
ured at  a single station were:  smoke, 300
jug/m3; SO,, 275  ^g/m' (0.096 ppm).  In the
Port Kembla  study46  mentioned in Section
C-2c of this  chapter,  no  significant  differ-
ences  in pulmonary  function  were noted
which could be attributed to air pollution.
  The studies relating morbidity and deteri-
oration in pulmonary function to particulate
levels cover effects which are also included
in Level III of the World Health Organiza-
tion's "guides to air quality.'""

 5.   Studies of Panels of Bronchitic Patients
  Lawther 6X related several episodes of acute
urban pollution to  a worsening  of condition
in a group of bronchitic patients, well studied
in a registry  at  St. Bartholomew's hospital
in London. Changes in their symptomatology
were recorded in a daily  diary, and acute
worsening  in  significant  numbers  of  the
group was associated with  daily rises in air
pollution above 300 /ug/m3 of smoke and 600
jug/m3 (0.21  ppm)* of sulfur dioxide.  Fig-
ure  9-5 shows graphically the  effects ob-
served on 29 bronchitic patients of high pol-
lution levels in January 1954.
  Angel et  al.70 reviewed the occurrence of
new respiratory  symptoms in men working
in factories  and in  offices, most of  whom
had  prior  evidence  of chronic  bronchitis.
The study group of 85 men, observed through
the winter of 1962-1963, was selected from
a group of 1,000 men, age 30  through 59,
without  apparent  classification of  either
smoking patterns or possible occupational or
          16  17  18  19 20  21  22
  MEAN  45!
 TEMP°F 40|
        35i
                                      S02
                                      ppm
  BETTER
                JANUARY 1954
 Figure 9-5.  Effect on Bronchitic Patients of High A
          Pollution Levels (January 1954).es?681 "1

 The figure represents the effect on bronchitic patients of
 increased pollution levels; patients stated whether they
 regarded their condition as "worse" or "better".
residential exposure differences.  Increased
sputum production, deterioration of pulmo-
nary  function performance  (FEVi.0), and
the more frequent  occurrence of respiratory
symptoms classified as "upper"  (coryza, in-
fluenza, and  acute  respiratory disease), and
"lower" (chest colds,  bronchitis, wheezy at-
tacks,  pneumonia), were all associated with
increases  in  both smoke and sulfur dioxide
concentrations.  There was frequently diffi-
culty  in defining an exacerbation of disease
in those  individuals  already  experiencing
chronic bronchitis.  During  this period, ill-
ness peaks (attack rate) may have occurred
with weekly mean concentrations  of smoke
exceeding 400 //.g/m3  and of sulfur dioxide
exceeding 460 /ug/m3  (0.16  ppm)*; weekly
mean  concentrations  were calculated  using
the highest  daily mean occurring each week
at each of 13 locations in the area.
    Carnow et al." studied over 500 patients
with respiratory disease in  Chicago during
* SOi values in this study were originally reported
  in ppm.
       140

-------

O
(/>
cr

25
20
5
n
697
970
908
607
360
158
98
TOTAL PERSON - DAYS

13.6%

17.1%

18.7%

18.2%

18.6%

22.1%

26.5%
      0.05  0.10  0.15   0.20   0.25   0.30
               CONCENTRATION, ppm
                                    0.30 +
 Figure 9-6. Comparison of Person-Days of Acute Illness
         with Seven Levels of Sulfur Dioxide Exposure
         in Chicago, in Patients with Severe Chronic
         Bronchitis (Age 55 or More), for October-
         November, 1967.

  There is an increase in illness for bronchitics over age 55
  with increase in sulfur dioxide concentrations. The re-
  lationship is with 24-hour SC>2 levels on the day prior
  to illness.
the winter of 1966-1967.  Semidaily aver-
ages of sulfur dioxide (West-Gaeke Method)
were computed from eight continuous moni-
toring stations in Chicago  for the hours of
6 a.m.  to  6 p.m., and for  6  p.m. to 6 a.m.
Pollution   by  particulate  matter was  also
present but not analyzed in this  report; the
geometric  mean for particulates  in  Chicago
during  1964-1965 was 148 jug/m3, according
to the  National  Air  Surveillance  Network
 (NASN)   data.72  The  semidaily  averages
were  used to  estimate the 24-hour  average
concentrations of sulfur dioxide to which
the patient was exposed at work and at home.
The chronic bronchitics were divided  into
two groups according to the severity of their
disease, and the analyses were kept separate
for the two groups. For patients age 55 and
over  with  severe bronchitis,  a significant
association  was  demonstrable between the
level  of sulfur dioxide and  person-days of
illness. The differences  in illness rates in
this group  for different levels of  exposure
was most marked  for disease on the day
following exposure. A marked rise in illness
rate was noted for patients  exposed to 715
/xg/m3  (0.25  ppm)*  of sulfur  dioxide or
more.  (See Figure 9-6.)
  For patients under  55,  no differences in
illness were noted with exposure, except for
the group exposed to 860 /xg/m3 (0.30 ppm)
or more of sulfur dioxide.
  For the patients with mild bronchitis, ill-
ness was not related to air pollution in those
age  55 or more,  while those under age 55
seem to be worse when exposed to more than
860 /*g/m3  (0.30 ppm)  S02.  These analyses
indicate that  groups of  persons exposed to
higher levels of sulfur dioxide tend to experi-
ence higher rates of  acute respiratory dis-
eases.  However, the group with higher res-
piratory illness rates could merely happen to
live  in the  more  polluted areas.  The  situa-
tion is similar to the findings of most epi-
demiologic  studies which indicate that  per-
sons of  low social  class tend to have high
illness rates and also  tend to live in more
polluted areas.  In an  attempt to eliminate
this  class-site factor, further analyses  were
therefore carried out for  the same groups
of patients, but this time for single months,
using each patient as a control against him-
self. For each patient, the difference between
his mean exposure to  SOn on days of illness
and on days of no illness was computed.  The
only significant  differences were for those
age 55 and over with  severe bronchitis; no
statistically significant differences  were de-
monstrable  for the other groups. This tends
to show that the association for mild bron-
chitic  in  the younger age  group mentioned
above was more likely due to another factor.
  An association between sulfur dioxide con-
centration and illness ratio in only one age
group  could be regarded as a chance happen-
ing.  Yet the  elderly  patient with  severe
* SO3 values in this study were originally reported
  in ppm.
                                                                                141

-------
chronic bronchitis would appear to be espe-
cially susceptible, since this  group is also
heavily involved in the excess deaths of acute
pollution episodes in London and New York.
Accordingly, it seems reasonable to infer, as
the author did, that there is in all likelihood
an effect of high daily levels of sulfur diox-
ide on  older patients with advanced bron-
chitis; this effect is one of  precipitating ill-
ness  and of exacerbating  symptoms.  The
technique used in this study of developing a
personal pollution index estimated for each
patient  with regard to his place of employ-
ment and residence adds confidence  to the
authors' analysis.
  An increase in respiratory symptoms was
noted among elderly  emphysematous  indi-
viduals  in a rest home in the Ruhr area dur-
ing December  9-13,  1959.  The complaints
included breathlessness,  throat and eye irri-
tation, and depression and apathy  (without
further specification).  The estimated mean
indoor sulfur dioxide concentration was 540
fig/m3 [0.20  ppm]* for 24 hours. Although
the method  of  measurement was not speci-
fied, it probably was  the Woesthoff method.
For the same period, at an estimated 24-hour
indoor sulfur dioxide concentration of 270
/ig/m3 [0.10 ppm] * for 4 days, there was an
increase in functional disturbance.7-8-73
  Patients with preexisting chronic respira-
tory disease in  general seem to have an exa-
cerbation of their symptoms when the sulfur
dioxide  level exceeds  600  ^g/m3 (approxi-
mately 0.2 ppm) for 24 hours or more in the
presence of a substantial amount of unmeas-
ured particulate pollution.
         6.   Miscellaneous Studies
  Although  the major  action of sulfur ox-
ides has been assumed to be by surface con-
tact  on the  mucous membranes  of the res-
piratory system, the possibility of effects on
the total body system (systemic effects)
must  be considered.  Sulfur dioxide  is ab-
sorbed into  the blood  stream  and may pro-
duce subtle  effects  on other organs.  A few
of the studies mentioned previously have sug-
 ' The numbers in brackets are the editor's; an equiv-
 alency of 2,700 fng/m3=l ppm S02 was used to as-
 sure consistency with any conversions made by the
 authors.
gested that sulfur oxides are a cause of sev-
eral kinds of illness, rather than respiratory
illnesses alone.  Even if it is assumed that
sulfur oxides are a cause of these results,
the effect observed may be secondary to res-
piratory tract irritation, or indeed, to er-
rors in diagnostic classifications.
  Reports from Czechoslovakia 74 75 suggest
that sulfur oxides may have  an influence
on blood formation in children.  However, no
details or supporting data for their  conclu-
sions are given.
  Elfimova et al.76 77 compared "biochemical
blood tests"  in areas enduring an average
of 2,000 /xg/m3 (0.70 ppm)  SO. with an area
having an average of 830 ^g/m3 (0.29 ppm).
Sulfur dioxide could be detected in a much
larger proportion of blood samples from sub-
jects in  the polluted districts than in those
from subjects in the clean district. Ascorbic
acid levels  were also measured and presum-
ably were lower in the polluted area, but the
two published versions seem to  have con-
flicting values.  At best, these studies indicate
a need for further research, probably in the
laboratory, and are not yet sufficiently de-
scribed to  warrant  their utilization in air
quality criteria.
  Yanysheva 7S found an  excess of respira-
tory disease, anemia, and rickets among Rus-
sian children living in a highly polluted area
(13,300 jug/m3 to  33,000 /xg/m3, or 4.6 ppm
to 11.5 ppm) * compared  to a  control area.
Epidemiologic methods and bias factors such
as  social class  are  not  well  described, al-
though the types of anemia reported are the
same  as mentioned above.  Sulfur dioxide
levels  in these three studies are  extremely
high even in  the "clean" areas, and possibly
some error has been made in reporting  (or
analysis  of  S02), although Yanysheva  de-
scribes symptoms  of  respiratory  disturb-
ances  and  material  damage  that would, in
fact, indicate very high levels.

     D.  EFFECTS  OF INDUSTRIAL
               EXPOSURE
  Studies of workers occupationally exposed
to pollutants provide a unique opportunity to
* SO2 values in this study were originally reported
 in mg/m3.
       142

-------
isolate the  effects of various chemicals.  By
carefully choosing industrial situations, pop-
ulations can be found  which have been  ex-
posed to rather high levels of specific  pol-
lutants  for a  long period  of  time.   An
extremely serious disadvantage of this type
of study for the preparation of air quality
criteria is that the exposed workers are gain-
fully employed, and lack of disease in them
may not indicate safety of the concentrations
to a general population  which includes  the
elderly  and infirm.  Sensitive  people   are
either  not  selected  for employment, or  are
soon lost to employment.
  In conjunction with previously described
Berlin, New Hampshire, studies,  Ferris et
al.79 compared  samples of  workers  from a
pulp mill and  from an adjacent paper mill.
Air concentrations of sulfur dioxide in areas
of the pulp mill averaged from 5,720 /*g/m3
to 37,180 ^g/m3  (2 ppm to  13 ppm)*. Occu-
pational  exposure at the paper mill  was al-
most  nonexistent, and  most of the workers
had been at the same job in each of  the
plants for a number of  years. Some of  the
men in the pulp mill were exposed  to chlo-
rine as well as sulfur dioxide, and some only
to sulfur dioxide. No significant  differences
were  found in respiratory symptoms or in
simple tests of pulmonary  function between
workers  in the two mills, but men working
with chlorine  had slightly  lowered respira-
tory function compared to  those  exposed to
sulfur dioxide  alone.  A unique  feature of
this industrial report is that cigarette smok-
ing was allowed for in the analysis.  The
working men of both mills had a lower preva-
lence  of respiratory disease than the male
population  of Berlin, New  Hampshire, sug-
gesting that working  populations may  not
be representative of the  general population.
  Skalpe 80 also compared workers from pulp
and paper  industries in Norway.  Sulfur di-
oxide concentrations at the pulp mill varied
between  5,720 pg/m3 and 102,960 /xg/m3 (2
ppm to 36  ppm) *.  No significant difference
in age or smoking habits was found between
the groups, but exact comparisons  similar
to those of Ferris were not made.  A signifi-
cantly higher frequency of cough, expectora-
tion, and shortness of breath on exertion was
found in the exposed pulp mill workers,  the
difference being greater in age groups under
50 years. In these younger workers the maxi-
mal  expiratory flow  rate was also signifi-
cantly lower,  but  no difference was found
in the older men.  The  older workers had
been  employed for a longer  time, and pos-
sibly those most susceptible had already been
eliminated  from   the  working  population.
Even the younger workers, however, had
all been employed for over 1 year.
  Andersonsl compared oil  refinery work-
ers in South Persia with similar workers not
exposed to sulfur dioxide. Exposure periods
ranged  from 1 to 19 years,  and daily con-
centrations of sulfur dioxide  varied between
zero   /xg/m3  and  71,500  /*g/m3  (25 ppm)*
with  occasional figures  of  286,000  ju,g/m3
(100  ppm)  recorded.  No differences were
found between the  two groups  in several
measures of  health, including pulmonary
function, chest X-rays, or clinical examina-
tion.
  Kehoe et al.b-  studied 100 refrigeration
plant workers  who, for  periods of 4  to 12
years, had  been  exposed to concentrations
exceeding 28,600 /xg/m3  (10 ppm)* of sul-
fur dioxide.  Compared to workers in  other
areas of the plant where no significant ex-
posure to sulfur dioxide was experienced, the
exposed  workers  were found to have a sig-
nificantly higher incidence of nasal pharyn-
gitis, alterations in sense of smell  and taste,
and  an  increased sensitivity to other irri-
tants.  In  addition, a higher  incidence of
shortness of breath,  increased fatigue, and
abnormal reflexes  was found in the exposed
groups.  The  incidence of "colds" was not
different between  the two  groups, but the
duration of respiratory illnesses was longer
in the exposed group. This  study was per-
formed shortly after the limitation  of ex-
posures  by  control measures,  and concen-
trations in prior years may have ranged from
228,800 jug/m3 to 286,000 /xg/m3 (80 ppm to
100  ppm).  The data presented are insuffi-
cient to determine whether the severe effects
noted were  limited to the workers who had
been  exposed to the higher concentrations of
previous years.
* S02 values in this study were originally reported
  in ppm.
                                                                            143

-------
  Thus the industrial exposures suggest that
no significant effect on health or pulmonary
function can  be noted  at exposures up to
about 5,700 /ig/m3  (2 ppm)  for the working
hours  of the  day  over  a period of several
years.  In these situations there is a lack of
a demonstrable effect of exposure to rela-
tively pure sulfur  dioxide at concentrations
that are well  above those implicated in am-
bient exposures. However,  as noted previ-
ously, studies of occupational exposure have
severely limited value for  the  preparation
of ambient air quality criteria.
  The effects  on both morbidity and mortal-
ity  demonstrated for community exposures
are probably a result of the synergism of the
sulfur dioxide and the suspended particulates
found in the ambient atmosphere rather than
the effects of either pollutant alone. The data
regarding the industrial  exposures are sum-
marized in Table 9-3.

              E.   SUMMARY
  This chapter reviews epidemiologic studies
of the  relationship between pollutant  con-
centrations  and their effects on health.  In-
dices varying  from disturbance of lung func-
tion to death are considered.
  In considering levels of pollution at which
                   health effects occur, concentrations are given
                   in the original units employed since conver-
                   sion from one method to another is not recom-
                   mended.  Attention must also be given to the
                   averaging time employed in the original ob-
                   servation; because of the typical log-normal
                   distribution of sulfur oxide concentrations,
                   long-term averages  are considerably lower
                   than  short-term  averages in  the same lo-
                   cations.
                     Short-term exposure to sulfur oxides  may
                   produce symptoms and illness in otherwise
                   healthy people, but the magnitude of the ef-
                   fects  and concentrations necessary to  pro-
                   duce the  effects is not well defined, and ex-
                   posures  are generally  substantially higher
                   than  the  levels cited  in the  epidemiologic
                   studies.
                     Over the years, a number of acute air
                   pollution  episodes  have  been  reported  in
                   the United States and abroad.  Both  oxides
                   of sulfur  and particulate matter have  con-
                   tributed  significantly to  the  health  effects
                   associated with these episodes.
                     In London,  a rise in  the  daily  death  rate
                   has been  detected when the  concentrations
                   of sulfur  dioxide rose abruptly to levels  at
                   or about  715  jug/m3 (0.25  ppm)  as  meas-
                   ured  by  the  hydrogen  peroxide  titrimetric
                            Table 9-3.—INDUSTRIAL EXPOSURES
                            Level of Exposure,
                                                                            Reference

Pulp versus paper mill workers
Berlin, New Hampshire
Pulp versus paper mill workers
Norway
^g/m3 S02
5,700 to 37,000
5,700 to 103,000;
many over 30,000
No.
No difference in pulmonary 79
function or respiratory disease
prevalence rates after control
for cigarette smoking
Excess cough, sputum, and 80
expectoration under age 50.
No effect over age 50.
Author
Ferris
et al.
Skalpe
Exposed versus non-exposed oil
refinery workers, South Persia
0 to 71,500; over    No effect on pulmonary function,
286,000 occasionally chest X-ray or clinical examina-
                 tion
                                              81
                                    Anderson
Exposed versus non-exposed
refrigeration plant workers,
United  States
over 28,000;
286,000 at times
Increased shortness of breath
and fatigue and abnormal re-
flexes. Longer duration of
"colds." No effect on respiratory
disease incidence.
                                              82
Kehoe
etal.
       144

-------
 method)  in  the  presence of smoke at 750
 /ig/m3.  The  elderly and patients with heart
 or lung disease were predominantly affected,
 but others have also been involved, particu-
 larly when pollution reached higher levels.
 Daily concentrations of sulfur dioxide in ex-
 cess  of 1,500 /xg/m3 for  1  day (0.52 ppm)
 in conjunction with levels of suspended par-
 ticles exceeding  2,000 /xg/m3 have resulted
 in an increase in the  death rate of 20 per-
 cent or more over base line levels.
  In  New York City, sulfur dioxide concen-
 trations  of  1,500  /xg/m3 (0.52 ppm)  (as
 measured  by the hydrogen peroxide  titri-
 metric method)  and suspended particulate
 matter, measured as  a  soiling index  of  6
 cohs  or greater,  have  led to increased  mor-
 tality.
  In  Rotterdam,  a 24-hour mean concentra-
 tion of 500 /tg/m3 S03 (0.19 ppm) (hydro-
 gen peroxide titrimetric method) lasting for
 3 to 4 days has led to an increased  mortality
 rate.  This observation is especially signifi-
 cant  because particulate levels are very low
 in Rotterdam. Even lower  levels  of pollu-
 tion from 300 /xg/m3 to 500 /xg/m3 SOU (0.11
 ppm  to 0.19 ppm) for 24 hours, are thought
 possibly to increase mortality.
  Morbidity  rates have been increased in all
 episodes which have resulted in an  increased
 mortality.  Thus, in London, an increase in
 emergency admissions to hospitals, calls to
 general practitioners, and certified sickness
 absence from work has been noted. In  Rot-
 terdam increased hospital admissions for res-
 piratory  disease,  particularly in older  per-
 sons,  has occurred when SOL, levels have risen
 to 300 «g/m3 to. 500 /xg/m3 (0.11 ppm to 0.19
    (w^^^WuXfiTx t£*U/Lt*S     .
 ppm); there Was also oeen  an increase  in
 absenteeism  from work  which reached 30
 percent for all ages and  50 percent to 100
 percent in persons age 45 and  over.
  A survey of emergency clinic visits to ma-
 jor  New York City hospitals in November
 1953 revealed an increase in visits for upper
 respiratory infections  and cardiac  diseases
 in both children and adults in all of the  four
hospitals  studied.   Sulfur  dioxide levels
ranged between 200 /xg/m3 and 2,460 /xg/m3
 (0.07 ppm to 0.86 ppm)  during the period
from  November 12  to 24, and hospital ad-
missions had clearly increased by November
 16, at which time concentrations had not yet
 exceeded 715 /xg/m3 (0.25 ppm); smoke shade
 at this time was close to 3 coh units.
   The most striking  effects have been ob-
 served in  association with exceptional epi-
 sodes  of air pollution. However, lower and
 more persistent concentrations are also cor-
 related with mortality and morbidity. British
 studies have indicated an association of bron-
 chitis  death rates with air pollution concen-
 trations  that is  apparently  independent of
 social  class  differences, but which also do
 not specify the role played by sulfur oxides.
 Instead,  these studies treat of a combination
 of  sulfur  oxides  and particulates.   In one
 major study of Eston, sulfur dioxide values
 for a year averaged 115 /xg/m3 (0.040 ppm)
 in the dirty area and 74 /xg/m3 (0.026 ppm)
 in the cleaner area. Smoke values were 160
 /xg/m3 and 80 /xg/m3 respectively.
  In the United States, the Buffalo study in-
 dicated an effect on chronic bronchitis disease
 mortality for men aged 50 to 59 in the low
 social  classes. This finding of air pollution
 exerting a  special effect on the low social
 classes appears to be consistent with the
 British findings.
  A study in Genoa, Italy, made use of house-
 wives. One of the groups surveyed included
 women all 65 or more years of age who were
 nonsmokers, who had lived for a long period
 in the same area and who had no industrial
 exposure.
  There was a finding of increased frequency
 of cough,  sputum, dyspnea,  and bronchitis
 in the moderate-pollution area over the clean-
 est area.  A much sharper difference in fre-
 quency between the cleanest and the dirtiest
 area was found.   The cleanest area had an
 annual mean of  80 /xg/m3 (0.028 ppm)  of
 sulfur  dioxide, the mean of  the moderately
 clean area was 105 /xg/m3 (0.037 ppm), and
the dirty area averaged 265 /xg/m3  (0.093
ppm).  The measurement of sulfur dioxide
was recorded by a technique analogous to the
volumetric method of the British.
  This study also showed a  correlation be-
tween  the  frequency  of bronchitis and the
annual mean of sulfur dioxide levels for the
seven districts of  Genoa whereas the corre-
lation  between  the frequency of bronchitis
                                                                             145

-------
and  suspended matter and dustfall was  not
statistically significant.
  In Berlin, New Hampshire, no effect was
observed  for  long-term exposure in  areas
with sulfation levels  averaging 610 /»g/100
cm2-day.  The  authors  recognized that  the
lack  of results may have been influenced by
the narrow differences in air quality between
the areas  compared, and they also noted that
there probably had been a selected migration
of diseased persons to the less polluted areas,
which  could have affected the results.
  Another morbidity study which  included
housewives was that conducted in Nashville.
This showed  a direct  correlation  between
illnesses  for  all  causes  for  housekeeping
white  females, 15 to 64 years of age, and
sulfur  dioxide levels.  It  also  showed  that
morbidity from cardiovascular disease in the
55 and older age group, for both sexes, was
twice as high in the most polluted area as
compared with the least. However, cigarette
smoking was not taken into account and the
adjustment  made for socioeconomic  status
may  not have been adequate.
  The  study of Port Kembla, Australia, had
shown  differences in  respiratory symptoms
for areas  which had long-term values  of 95
Atg/m3  SO, (0.034 ppm)  and 25 /.g/m3  (0.009
ppm)  measured by absorption  in a sulfuric
acid  solution containing hydrogen peroxide.
The  study is  unusual in that the source of
pollution  was the single stack  of a smelter
and  daily averages were up to  17 times  the
annual mean.  However,  the  findings  that
respiratory symptoms disappeared when pol-
lution  was reduced through installation of a
higher stack, would  appear to confirm an
effect of sulfur dioxide at the concentrations
originally measured, provided that no  other
change took place which  could account  for
the disappearance of symptoms.
  The  study of school children in Great Brit-
ain indicated that they experienced increased
frequency and severity of respiratory dis-
eases  when  the  long-term levels exceeded
about  120 /.g/m3 (0.046 ppm)  S02  and  100
/ng/m3  for smoke.
  Several studies  have  been noted  relating
daily variations in air pollution with changes
in the  clinical  condition of patients  with
chronic lung disease.  A good deal of infor-
mation  exists on the effects of exposure to
moderately elevated levels of S02 lasting a
day to 3 or 4 days. A daily average level of
about  600 |ug/m3  of S02 (0.21 ppm)  has
caused accentuation of symptoms in persons
with chronic respiratory disease on the  day
following the high S02  level if particulate
matter  at a similar concentration was also
present.
  This finding by Lawther was also observed
by Carnow in Chicago. He too noticed a sharp
rise in illness rates on the day following expo-
sure to  715 jug/m3  (0.25 ppm)  of sulfur diox-
ide (West-Gaeke method) or more for  pa-
tients 55 and over with severe bronchitis.
Particulate matter was also present in  the
atmosphere.
  The study of an elderly emphysematous
population in a rest home in the Ruhr area of
Germany demonstrated that complaints in-
cluding breathlessness, throat and eye irrita-
tion,  and "depression and  apathy  without
further specification" increased at estimated
indoor sulfur  dioxide concentrations of  540
/ig/m3 (0.20 ppm) for 24 hours. There was an
increase in functional disturbance at an aver-
age daily level of 270 /*g/m3  (0.10 ppm)  for
4 days,  again an estimated indoor level, mea-
surement presumably being  made by  the
Woesthoff method.
  The analyses  of the numerous  epidemio-
logical studies discussed  clearly indicate an
association between air pollution, as measur-
ed by particulate matter accompanied by sul-
fur dioxide, and health effects of varying se-
verity. This association is most'firm for  the
short-term air pollution episodes.
  There are probably no  communities which
do not contain a reservoir of individuals with
impaired health who  are prime targets  for
the effects of elevated levels  of particulate
matter and sulfur oxides. However, to show
small changes in deaths associated with coin-
cident higher levels of air pollutants require
extremely large  populations.  In small  cities,
these small changes cannot be detected sta-
tistically.
  The epidemiologic studies concerned with
increased mortality also show increased mor-
bidity. Again, increases in morbidity as mea-
sured, for example, by increases in hospital
admissions or emergency  clinic visits,  are
       146

-------
most easily detected in major urban areas.
   It  is  believed  that,  for the large  urban
communities which are  routinely exposed to
relatively high levels of pollution, sound sta-
tistical analysis  can  detect with confidence
the small changes  in daily mortality  which
are  associated  with  functions in  pollution
concentrations.  Unfortunately, only limited
analysis has thus  far been made, and this has
been  attempted only in  London and in New
York.
   The association between longer-term com-
munity exposures to particulate matter  for
respiratory disease incidence and prevalence
rates is conservatively believed to  be  inter-
mediate in its reliability.  Because  of the re-
enforcing nature  of the studies conducted to
date, the conclusions to be drawn  from this
type  of study can be characterized as prob-
able.
   The  association  between  long-term resi-
dence in  a polluted area and chronic disease
morbidity and mortality is somewhat  more
conjectural. However, in the absence of other
explanations, the findings of increased mor-
bidity and of increased death rates for select-
ed causes, independent  of economic status,
must still be considered consequential.

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                                                                                           149

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         Chapter 10
SUMMARY AND CONCLUSIONS

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                              Table of Contents
                                                                         Page
A. SUMMARY                                                           153
   1. General                                                            153
   2. Relationship of Maximum Concentrations to Average Concentrations    154
   3. Effects on Health                                                   155
   4. Effects on Visibility                                                158
   5. Effects on Materials                                                159
   6. Effects on Vegetation                                               160
B. CONCLUSIONS                                                       161
   1. Effects on Health                                                   161
   2. Effects on Visibility                                                162
   3. Effects on Materials                                                162
   4. Effects on Vegetation                                     .          162
C. RESUME                                                             162
 152

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                                      Chapter  10

                          SUMMARY AND CONCLUSIONS
              A.  SUMMARY

                1.   General

   This document  presents  criteria of air
 quality in terms of the effects empirically ob-
 tained and published for various  concentra-
 tions of one family of pollutants,  the sulfur
 oxides, their acids and acid salts. These ef-
 fects do not, for the most part, derive solely
 from the presence of sulfur oxides in the at-
 mosphere. They are the effects that have been
 observed when various concentrations of sul-
 fur oxides, along with other pollutants, have
 been present  in the atmosphere.  Many of
 these effects are produced by a combination
 of sulfur oxides pollution and undifferentiat-
 ed particulate matter;  the contributions of
 each  class are difficult to distinguish. More-
 over, laboratory studies have shown that  a
 combination of sulfur oxides and particulates
 may  produce  an effect that is  greater  than
 the sum of the effects caused by these pollu-
 tant classes individually. Because  of the in-
 ceractions between pollutants, and the reac-
 tions of pollutants with oxygen and with wa-
 ter in the atmosphere, and because of the in-
 fluence of sunlight and temperature  on these
 reactions, the  criteria for  sulfur oxides can
 not  be presented  as  exact expressions of
 cause  and  effect that have been  replicated
 from laboratory to laboratory. They are pre-
 sented as useful  statements of the effects that
 can be predicted when sulfur oxides are pres-
 ent in the atmosphere; they are derived from
 a careful evaluation of what has so far been
 reported.
  The sulfur oxides are common atmospheric
 pollutants which arise mainly from the com-
 bustion of fuels. Solid and liquid fossil fuels
 contain sulfur, usually in the form  of inor-
ganic sulfides  or  sulfur-containing  organic
 compounds.  Combustion of the fuel forms
about  25 to 30  parts of sulfur dioxide to 1
part of sulfur trioxide.
   Sulfur dioxide  is a  non-flammable, non-
explosive colorless gas that most people can
taste at concentrations  from 0.3 ppm to 1
ppm (about 0.9 mg/m3 to 3 mg/m3) in air.
At concentrations above 3 ppm (about 8.6
mg/m3),  the gas  has  a pungent, irritating
odor. In  the atmosphere, sulfur dioxide  is
partly converted to sulfur trioxide or to sul-
furic acid and its salts by photochemical or
catalytic processes. Sulfur trioxide is imme-
diately converted to sulfuric acid in the pres-
ence of moisture. The degree of oxidation of
sulfur  dioxide in the atmosphere is depend-
ent on a  number of factors, including resi-
dence time, amount of moisture present, and
the intensity and duration of sunlight and its
spectral  distribution. The amounts  of cata-
lytic material,  hydrocarbons and  nitrogen
oxides, and the amounts of sorptive and alka-
line materials present, also affect the oxida-
tion process.
   In the United  States, sulfur dioxide is most
commonly measured  by  the  colorimetric
West-Gaeke (pararosaniline)  and  the con-
ductometric methods. The West-Gaeke  meth-
od is specific for  sulfur dioxide and sulfite
salts. The method has been modified to com-
pensate for interferences  produced by  the
presence of nitrogen oxides, ozone,  or heavy
metal salts in the sample, and the modified
method is the method of choice of  the Na-
tional Air Pollution Control Administration.
Conductometric  methods measure sulfur di-
oxide concentrations as a function of change
in the electroconductivity of a solution. These
methods  are  general, in that they react to
changes in electroconductivity brought  on by
other soluble gases, as well as by sulfur di-
oxide, and the indicated values for sulfur are
sometimes very approximate.
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  The technique most frequently used in Eu-
rope to measure sulfur dioxide is the hydro-
gen  peroxide  acid  titration  method, or an
automated  conductometric  version  of the
same technique.  The presence of other acidic
or alkaline gases in the sample may affect the
results.
  The lead peroxide candle is a  widely used
technique which determines a "sulfation
rate." The method gives integrated values for
relatively long periods, but provides  no indi-
cation of short-term fluctuations. It provides
only a rough indication  of sulfur  dioxide
concentrations.
  Recently, two long-path spectroscopic tech-
niques have been introduced that sense sulfur
dioxide  concentrations  remotely. Although
these techniques are complex and expensive,
they may eventually be developed to  provide
a sulfur dioxide  "pollution contour" for large
areas of a city,  as  well as pollution  concen-
trations at different elevations.
   Sulfuric acid aerosol in suspended  particu-
late material  may be measured  by titration
or by controlled  decomposition to sulfur di-
oxide. The sulfur dioxide can be measured by
a number of methods, including  spectropho-
tometry, coulometry, and flame  photometry.
Particulate sulfate may be analyzed by spec-
trophotometric or turbidimetric  methods.
   Each method  of  measuring sulfur oxides
pollution is unique  in terms of measuring
time  resolution,  operating costs and skills,
time required for analysis, and the specificity
of the technique. A single program may make
use of both general and specific methods. In
selecting the methods to be used in a sampling
program, it is especially important  to con-
sider the degree to which  data obtained from
one method can be compared to data obtained
from another.
   An estimated  28.6 million tons of sulfur
dioxide were  emitted to  the atmosphere  of
the United States in 1966, as compared with
an estimated 23.4  million  tons emitted  in
1963. The principal share,  58.2  percent,  of
the 1966 tonnage came from the combustion
of coal, primarily for the generation of elec-
tric power and  for space heating. The  com-
bustion of residual fuel oil  and  other petro-
leum products, also primarily for power gen-
eration and space heating, accounted for 19.6
percent of the total,  while  the remainder
came from the  refining of petroleum  (5.5
percent),  the  smelting of  sulfur-containing
ores (12.2 percent),  the manufacturing  of
sulfuric acid  (1.9 percent), the burning  of
refuse (0.4 percent), and the burning of coal
refuse banks  (0.4  percent).  Paper-making
and other industrial operations also contrib-
uted minor amounts to the total.
  The National Air Pollution Control Admin-
istration operates two nationwide programs
for surveying sulfur  oxides pollution levels
in the United  States.  The National Air  Sur-
veillance  Network  (NASN)   takes  24-hour
samples of sulfur  dioxide from about 100
sites 26 times a year, and the Continuous Air
Monitoring Project (CAMP)  records 5-min-
ute average concentrations of sulfur dioxide
continuously in six large cities—Washington,
Philadelphia, Cincinnati, Chicago, St. Louis,
and Denver. The NASN program employs the
colorimetric, West-Gaeke method of analysis,
while the CAMP program uses the  electro-
conductivity technique. Recently, continuous,
colorimetric West-Gaeke monitoring devices
were installed at  the six CAMP locations.
  Levels recorded in the CAMP cities over a
6-year period  show mean annual concentra-
tions ranging  from 0.01 ppm, in San Fran-
cisco, to 0.18 ppm, in Chicago, with the ave-
rages exceeding, for 1 percent of the time, a
concentration  between 0.09  ppm and  0.68
ppm. The NASN annual average concentra-
tions ranged from 0.002 ppm, in Kansas City,
Missouri,  to  0.17 ppm, in New York City.
The highest 24-hour average concentration
was 0.38 ppm, also in New York City, while
the lowest 24-hour averages  were below the
minimum detectable   range  of the  instru-
ments—below  approximately  0.001  ppm.
Geographically, the highest values were re-
corded in  the northeastern part of the United
States, especially east of the Mississippi Riv-
er and north of the Ohio River, where large
quantities of  sulfur-bearing  fossil fuels are
burned.

2.  Relationship of Maximum Concentrations
        to Average Concentrations

  Although it is convenient  to discuss the
various effects of sulfur dioxide in connec-
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tion with the average concentrations of the
gas over a long period, such as a year, some
effects are thought to be associated with the
peak  concentrations that may  occur during
the period and to  better define the kind and
extent of effects that may be occurring in a
given community,  it is useful to know what
these peak values may be.
  For a given averaging time, measurements
of sulfur dioxide concentrations follow a log-
normal frequency  distribution.  The two sta-
tistical parameters used to describe this dis-
tribution  are the  geometric mean and  the
standard  geometric deviation,  which is  an
index of the deviation  of the samples from
the mean.
  Once  sufficient  sampling  data have been
gathered, the geometric mean and  the stand-
ard geometric deviation can be used to calcu-
late  the  expected   maximum concentration,
the minimum concentration, and the concen-
tration at any percentile, provided that the
averaging time is 1 hour or greater. Further,
it  is possible to calculate expected maxima
for one averaging  time from data obtained
at another averaging time.
  For a given typical,  multiple source urban
area,  a  fairly good  approximation  of  the
frequency  distribution  of  hourly average
concentrations for a year at a  given  station
can be obtained from  measurements taken
for 24-hour  periods on about  26  randomly
selected days. The accuracy of the approxi-
mation will depend on the number of samples
taken, compared to the total number of sam-
ples that  could have been taken if air sam-
pling had been continuous.
  The CAMP data for various years in the
period 1962 to 1967 appear to be fairly rep-
resentative of the  distribution  of  sulfur di-
oxide concentrations  for large U.S.  metro-
politan areas.  The range of standard  geo-
metric deviations  for  the CAMP cities is
roughly from 2 to 2.5. These  values corre-
spond to hourly maxima that range from 10
to 20 times  the annual mean, respectively.
Similarly, the 8-hour maximum ranges from
about 6 to 10 times the annual mean, and
the 1-day maximum is between 4 and 7 times
the annual mean.
  The ratio of the maximum sulfur dioxide
concentration to the average values may be
greater for measurements made near a sin-
gle point source than for a city as a whole.
For averaging periods from 4 to 54 minutes,
for example, the  maximum  concentrations
encountered near  a point source were, re-
spectively,  30 to 160 times the 6-month aver-
age value.
           3.   Effects on Health
  The current  scientific literature indicates
that, for the most  part, the effects of the ox-
ides of sulfur on  health are related  to irri-
tation  of the respiratory system.  Such in-
j ury may be temporary or permanent.
  Laboratory  studies  show  that  sulfur di-
oxide can produce  bronchoconstriction in ex-
perimental animals such  as the guinea pig,
the dog, and the cat.  Dose-response curves
have been established for the guinea pig, the
most  susceptible laboratory  animal  studied
to  date. They relate the concentration  of
sulfur dioxide  to  the observed increase  in
pulmonary  flow resistance  produced by  1-
hour  exposures.  Slight increases in resist-
ance are detectable at 0.16 ppm  (460 ,ug/m3)
and the changes are readily reversible.
  Sulfuric  acid  and some, but not all,  par-
ticulate sulfates  also  produce  bronchocon-
striction in the guinea  pig.  The response is
highly dependent  on  particle size, with the
smallest particles  showing  the greatest ir-
ritant  potency.  In this animal, as in man,
sulfuric acid and irritant particulate sulfates
have a greater  irritant potency at a given
concentration than does sulfur dioxide alone.
  The potentiation by particulate matter of
toxic responses to sulfur dioxide (synergism)
has been  observed under conditions which
would  promote the conversion of sulfur di-
oxide to sulfuric  acid.  The  degree of  po-
tentiation is related to the concentration of
particulate matter. A threefold to fourfold
potentiation of the irritant response to sul-
fur dioxide is  observed in  the presence  of
particulate matter capable of oxidizing sul-
fur dioxide to sulfuric acid. Aerosols of solu-
ble salts of ferrous  iron, manganese, and
vanadium have been observed to produce this
potentiation, although  the   concentrations
used  (0.7 mg/m3  to 1.0 mg/m3)  were con-
siderably greater than any levels of the met-
als reported in urban air.
  Generally speaking,  the laboratory work
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that has been performed to date with ani-
mals has only partial relevance for air qual-
ity  criteria. In most of the studies, the lab-
oratory environment has not simulated very
closely the actual environment.  Exposures
have been  to  high and constant concentra-
tions, rather than to the low and fluctuating
levels commonly  found in  the  atmosphere.
Other normally  occurring stresses, such  as
fluctuating temperature,  have not, in gen-
eral, been  applied. These studies  do, how-
ever, provide  valuable information on some
of  the bioenvironmental  relationships that
may be involved  in the effects of the sulfur
oxides on health.  The data they provide  on
synergistic effects show very clearly that in-
formation derived from single substance ex-
posures should be applied to ambient air sit-
uations only with great caution.
  The response  of bronchoconstriction  in
man may be  assessed in terms of a  slight
increase in airway  resistance.  Normal in-
dividuals, exposed to sulfur dioxide via the
mouth, exhibit small changes in airway re-
sistance, which are often insufficient to pro-
duce any respiratory symptoms. The effects
may  be  even smaller  when  the subject
breathes through his  nose.  As  in animals,
sulfuric acid is a much more potent irritant
in  man than  is sulfur dioxide.  Ag-ain, the
irritant effect is highly dependent on particle
size.
  Laboratory observations of respiratory ir-
ritations suggest that most individuals will
show a response  to sulfur dioxide when ex-
posed for 30 minutes to concentrations of 5
ppm (about 14 mg/m3) and above. Exposure
of  certain sensitive  individuals to 1 ppm
 (about  3  mg/m3) can produce detectable
changes in pulmonary function.  Similar ex-
posure of these same individuals has, in some
instances,  produced  severe  bronchospasm.
In  most of the studies discussed, an increase
in  pulmonary flow resistance was the indi-
cator of response employed.
  Epidemiologic studies do  not have the pre-
cision  of laboratory  studies,  but they have
the advantage of being  carried out  under
ambient air  conditions.  In most epidemic-
logic studies, indices of air pollution level are
obtained by  measuring selected pollutants,
most  commonly particulates and sulfur com-
pounds. To use these same studies to estab-
lish criteria for individual pollutants is jus-
tified by the experimental data on interaction
of pollutants.  However, in reviewing the re-
sults of epidemiologic investigations it should
always be remembered that the specific pol-
lutant  under discussion is being used as an
index of pollution, not as a physicochemical
entity.
  It has been  suggested that industrial ex-
perience with  sulfur oxides  exposures  may
be relevant to ambient air  quality  criteria.
In the  absence of epidemiologic evidence, one
might, as a rough approximation, select some
fraction  of  the concentrations reported for
industrial  exposures.  In selecting such  a
fraction, several factors should be taken into
consideration.  Industrial exposure, for ex-
ample, is not continuous, and it may  not
include the synergistic effects which result
from the presence of more than one class of
pollutant.  Further,  the  exposed  population
may not include the  segments most suscepti-
ble to the effects.
  From the epidemiologic studies available,
it is easy to conclude that there is an effect
of the oxides  of sulfur  in  the ambient at-
mosphere on  the health  of  the population,
and that the degree of effect  is related to the
degree of pollution.  Episodes of acute ele-
vation of oxides of sulfur and other pollutant
concentrations have been associated with a
larger  number  of  deaths  than  expected.
Those  predominantly affected  were individ-
uals with chronic pulmonary disease or car-
diac disorders, or very young or old individ-
uals.  However, the general population has
also been involved.
   Studies of  episodes occurring  in London
suggest that  a rise  in the daily  death rate
occurred when the concentrations of sulfur
dioxide rose abruptly to levels at or about
715 /xg/m3  (0.25  ppm)  (as measured by the
hydrogen peroxide  titrimetric method)  in
the presence of smoke at 750 /*g/m3. A more
distinct rise in deaths has been  noted gen-
erally  when  sulfur dioxide exceeded  1000
jug/m3 (0.35 ppm) for one day, and particu-
late matter reached about 1200 /*g/m3 (meas-
ured by the British reflectometer method).
Daily concentrations of sulfur dioxide in ex-
cess of 1500 /xg/m3 for one day  (0.52 ppm)
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 in conjunction with levels of suspended par-
 ticles exceeding 2000 /xg/m3 appear to have
 been associated with an increase in the death
 rate of 20  percent  or  more over base  line
 levels.  This same effect  has been observed
 at lower sulfur dioxide levels when the maxi-
 mum pollution levels  lasted for  a longer
 period.
   Air pollution episodes  in New  York City
 have been  associated  with exposures simi-
 lar to those of the London  episodes. In one
 case, for example,  excess  deaths  were de-
 tected in New York following a 24-hour pe-
 riod during which sulfur dioxide  concentra-
 tions exceeded 1500 ^g/m1  (>0.5 ppm)  (as
 measured by the hydrogen peroxide titri-
 metric  method)  and suspended  particulate
 matter  was measured  as a soiling index of
 6 cohs or greater.
   For Rotterdam,  there  have been  indica-
 tions of a positive association between total
 mortality and exposure for a few days to 24-
 hour mean concentrations of 500 /tg/m3 (0.19
 ppm)  sulfur  dioxide.  Further, it has been
 reported that: "There  is a faint  indication
 that this  will  happen  somewhere  between
 300  and 500 p.g  SO,, per m3 per  24 hours"
 (0.11 ppm and 0.19 ppm).
  A survey of emergency  clinics  at major
 New York City hospitals revealed a rise in
 visits for upper  respiratory infections and
 cardiac diseases in both children and adults
 in all 4 hospital studies during a 10-day pe-
 riod of  elevated pollution levels.   Sulfur di-
 oxide ranged  between 200  /*g/m3 and 2460
 /xg/m3 (0.07 ppm to 0.86 ppm) during the pe-
 riod studied; hospital admissions were clear-
 ly elevated  at a  time  when concentrations
 had not yet  exceeded 715 /tg/m3 (0.25 ppm).
 Smoke shade was close to  3  coh units.
  In London,  a one-day exposure  to a daily
 average level of 600 /ig/m3 of sulfur dioxide
 (0.20 ppm) caused accentuation of  symptoms
 in persons with chronic respiratory disease
 on the day following the high sulfur dioxide
 level if particulate matter  at a substantial
concentration  was also a pollutant.
  This finding in London  was also observed
in a Chicago study.  The Chicago study noted
a sharp rise in illness  rates on the day fol-
 lowing  a  one-day  exposure to 715 /*g/m3
 (0.25 ppm)  of sulfur dioxide  or  more  for
 patients 55 years of age and  over with se-
 vere bronchitis. Particulate matter was also
 present.
   Effects at lower levels of sulfur dioxides
 have also been noted.  In Rotterdam, during
 a  few days in which sulfur dioxide concen-
 trations rose  from about 300  to 500  /*g/m3
 (0.11 ppm to  0.19 ppm), the number of hos-
 pital admissions for irritations of the respi-
 ratory  system rose,  particularly for  older
 persons. Absenteeism from work under such
 conditions increased substantially, especially
 for those 45 years old and over.
   The lowest  levels at which effects are re-
 ported  for short-time  periods  are those re-
 ported  for  the  Ruhr  area.  An effect  was
 noted on "functional disturbance" at an esti-
 mated daily indoor mean of 270 /*g/m3  (0.10
 ppm) for 4 days and an increase in "symp-
 toms, illnesses, or diseases" (breathlessness,
 throat  and eye irritation,  and "depression
 and  apathy without further specification")
 was noted at  a daily indoor mean of about
 540 jug/m1 (0.20 ppm).
   Longer term exposure to lower levels than
 those found during an air pollution episode
 has also been associated with  demonstrable
 health effects.  It is for this reason that it
 must be emphasized that the levels of  a pol-
 lutant  at which effects are  detected are not
 the concentrations at which  the pollutant
 may begin to  have an effect on health.  The
 initiation of the  deleterious effects presum-
 ably must take place before, and at a lower
 concentration, than that at  which the exist-
 ence of a strong association is accepted for
 statistical reasons.  Repeated respiratory in-
 fections  in early  childhood,   for  example,
 which in one study appeared to be related to
 air pollution,  may have contributed  to the
 later development of the chronic bronchitis
 syndrome in the adult.
  A major British study has found an asso-
 ciation  between mortality from bronchitis
and lung cancer and levels  of  air pollution,
after  taking into consideration  differences
in  age,  smoking habits, social class, and oc-
cupational exposure. The sulfur dioxide val-
ues for a year averaged 116 /ig/m3  (0.040
ppm)  for the polluted area, and 75 jug/m3
 (0.026  ppm)  for  the  cleaner  area.  Corre-
sponding smoke values were 160 /*g/m3  and
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80 jug/m3, respectively. It was not possible
to separate the effects of sulfur dioxide from
the effects of comparable  amounts of smoke
which were  present. This is consistent with
other British studies, which indicate an asso-
ciation  of bronchitis  death rates with  air
pollution concentrations that is  apparently
independent of social  class differences,  but
which can not specify the specific role played
by sulfur oxides.
  Children and housewives  appear to repre-
sent the most suitable subjects for determin-
ing the  health effects of long-term exposures
to routine levels of air pollution.  A study in
Genoa, Italy, included housewives 65 or more
years of age, who were  non-smokers, and
who had lived for a long period in the same
area without having  any industrial experi-
ence. Sulfur dioxide was monitored for 10
years at 19 sites  by  a technique analagous
to the volumetric method of the British.  An
increased frequency of cough, sputum, dysp-
nea, and bronchitis was noted in the mod-
erately polluted area as compared to the rela-
tively clean  area.  Differences were noted in
the  summer prevalence of respiratory  dis-
eases in the industrial area, with an annual
mean of 265 /xg/m3 S02 (0.093 ppm) when
compared to the middle [annual mean of 105
/xg/m3  SO2  (0.037 ppm)]  and low  [annual
mean of 80 /xg/m3 S02 (0.028  ppm)] pollu-
tion areas.  The study also showed  a very
significant correlation between the frequency
of bronchitis and  the annual mean of sulfur
dioxide levels for the  seven districts of the
city, whereas  the correlation between  the
frequency of bronchitis and suspended mat-
ter and dustfall was not significant.
  Another  morbidity  study which  has  in-
cluded housewives is that conducted in Nash-
ville. This  showed a  direct correlation be-
tween illnesses for all causes for housekeep-
ing white females, 15 to 64 years of age,  and
sulfur  dioxide levels.   It also showed  that
the  cardiovascular morbidity in  the  55  and
older age group,  for both  sexes, was twice
as high in the most polluted area as compared
with the least.  Cigarette smoking was  not
taken into account, and the adjustment made
for socioeconomic status may not have been
wholly adequate.
  Differences in respiratory symptoms have
also  been found  in areas which  had long-
term values of 95 yug/m3 sulfur dioxide (0.034
ppm) and 25 /xg/m3 (0.009 ppm)  measured
by hydrogen  peroxide  absorption,  sulfuric
acid titrations. The study is unusual in that
the source of pollution was the single stack
of a  smelter, and daily averages were up to
17 times the  annual mean.  However,  the
findings  that  respiratory  symptoms disap-
peared when  pollution  was locally  reduced
through installation of a higher stack, would
appear to confirm an effect of sulfur dioxide
at the concentrations originally  measured,
provided that  no  other change took place
which could account  for the  disappearance
of symptoms.
  Studies of schoolchildren in Great Britain
have indicated that increased  frequency and
severity  of respiratory  diseases  occurred
when  long-term  pollution  levels  exceeded
averages of about  120 /xg/m3 (0.046  ppm)
sulfur dioxide and  100 /xg/m3  for  smoke.

         4.   Effects on Visibility
  Particles suspended in the air reduce visi-
bility, or visual range, by scattering and ab-
sorbing light  coming  from both  an object
and  its  background,  thereby  reducing the
contrast between them.  Moreover, suspended
particles scatter light into the line of sight,
illuminating the air between,  to further de-
grade the contrast between an object  and
its  background.  This  phenomenon is de-
scribed in detail in a companion document
Air Quality Criteria for Particulate Matter.
  The scattering of light into  and out of the
line  of viewing by particles in the narrow
range of 0.1 /* to 1 /x in radius has the greatest
effect on visibility.  Of  the total  suspended
particulate matter  in  urban  air,  commonly
from 5 percent to 20 percent consists of sul-
furic acid and other  sulfates,  and of these,
80 percent or  more by  weight are smaller
than  1 fi in radius.  Consequently,  suspended
sulfates  in  the air can contribute signifi-
cantly to reduction  in visibility.
  Characteristic behavior of suspended  par-
ticles in  the size range  mentioned makes it
possible to relate visual range to  concentra-
tions of overall  particulate  matter.  Since
sulfur dioxide levels,  in general, correlate
with  levels of  overall  suspended particulate
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matter, and since the ratio of sulfur dioxide
to suspended sulfate can be estimated, given
the relative humidity, it  is possible to esti-
mate visibility for various relative humidities
from  sulfur  dioxide  concentration.  Using
such data  as appear in  Chapter 1, Figure
1-5, we can estimate that at a concentration
of 285 /xg/m3 (0.10 ppm) of sulfur dioxide
and with  a relative  humidity  of  50 per-
cent, visibility in New York City would typi-
cally be reduced to about 5 miles. At a visual
range  of  less than  5  miles, operations are
slowed  at  airports  because  of the need  to
maintain larger distances  between aircraft.
Federal Aviation Administration restrictions
on  aircraft operations  become increasingly
severe as the visual range decreases below
5 miles.
          5.  Effects on Materials
  Laboratory and  field studies underscore
the importance of  the  combination  of par-
ticulate and sulfur oxides pollution in a wide
range  of damage to materials.  On the basis
of present knowledge, it is difficult to evalu-
ate precisely the relative contribution of each
of the two classes of pollution; however, some
general conclusions may be drawn.
  Steel test panels, dusted with a number  of
active  hygroscopic particles commonly found
in polluted atmospheres,  corroded at a low
rate in clean air at relative humidities below
70  percent. The corrosion rate was higher
at relative humidities above 70 percent.  It
greatly increased when traces of sulfur di-
oxide were added to the laboratory  air.
  It is apparent that corrosion rates of vari-
ous metals are higher  in  urban and indus-
trial atmospheres with  relatively high levels
of  both particulate and sulfur  oxides than
they are in rural and other areas of low pol-
lution. High humidity and temperature also
play an important synergistic  part in  this
corrosion  reaction.  Studies  show increased
corrosion  rates in industrial areas where air
pollution levels, including sulfur oxides and
particulates, are higher.  Further, corrosion
rates are  higher during the  fall and winter
seasons when particulate and sulfur oxides
pollution is more severe, due to a greater con-
sumption of fuel for heating. Depending on
the kind of metal  exposed as well  as loca-
tion and duration  of exposure,  corrosion
rates were l]/£ to 5 times greater in polluted
atmospheres than in rural environments.
  In Chicago and St. Louis, where steel pan-
els  were exposed at a  number of sites, high
correlations were found in each city between
corrosion rates, as measured by weight loss,
and sulfur dioxide concentrations,  as meas-
ured  by  the  West-Gaeke  method.  In  St.
Louis,  except  for one  exceptionally polluted
site, corrosion losses were 30  percent to 80
percent higher than losses measured in non-
urban   locations.   Sulfation   rates  in   St.
Louis,  measured by lead peroxide candle,  also
correlated well with weight loss due to  cor-
rosion.   Measurements  of dustfall  in   St.
Louis,  however, did  not correlate  signifi-
cantly with corrosion rates. Over a  12-month
period in Chicago,  the corrosion rate at the
most corrosive site  (mean S0a level of  0.12
ppm) was about 50 percent higher than at
the least  corrosive site  (mean SO- level of
0.03 ppm).  Although  suspended particulate
levels measured in Chicago with high-volume
samplers also correlated with corrosion rates,
a co-variance  analysis indicated that sulfur
dioxide concentrations were  the  dominant
influence on corrosion.  Based on these data,
it appears that considerable  corrosion may
take place (i.e., from  11 percent to  17 per-
cent weight loss in steel panels) at annual
average sulfur dioxide concentrations in the
range of 0.03 ppm to 0.12 ppm, and although
high particulate levels tend  to accompany
high sulfur dioxide levels, the sulfur dioxide
concentration  appears  to have the  more im-
portant influence.
  Sulfur oxides pollution contributes to the
damage of electrical equipment of  all kinds.
Studies have reported a one-third  reduction
in the  life of overhead power line hardware
and guy wires in heavily polluted areas. In
some areas  it has  been  found  necessary to
use more expensive, less corrodible  metals,
such as gold, for electrical contacts.
  Sulfur oxides pollution attacks a wide va-
riety of building materials—limestone, mar-
ble,  roofing slate,  and mortar—as well as
statuary and other works of art, causing dis-
coloration and deterioration.  Certain textile
fibers—such as cotton, rayon,  and nylon—
are  harmed by atmospheric  sulfur oxides.
                                                                              159

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Dyed fabrics may fade in atmospheres con-
taining  sulfur oxides  and  other  pollutants.
Severe fading was noted for some dyes  in
fabrics  exposed in Chicago, where annual
average sulfur dioxide levels were 0.09 ppm.
Leather exposed  to sulfur  oxides may lose
much of its strength, and paper may become
discolored and brittle.
  Concentrations of  1 ppm sulfur dioxide
can  increase the drying time  of some oil-
based paints by 50 percent to 100 percent.
Some films  become softer  and others more
brittle, both  developments  adversely  affect-
ing durability.  Sulfur dioxide  also appears
to render some paint  films water sensitive,
consequently reducing the film gloss.  Under
certain  conditions sulfur  dioxide levels  of
0.1  ppm to 0.2 ppm  cause the  blueing  of
Brunswick green, and in the presence  of am-
monia produce a troublesome  defect called
crystalline bloom brought about by the for-
mation  of  very  small  ammonium  sulfate
crystals.
         6.  Effects on Vegetation
  Sulfur dioxide may cause acute or chronic
leaf  injury to plants.  Acute  injury,  pro-
duced by  high  concentrations for relatively
short periods, usually  results in injured tis-
sue drying to an ivory  color;  it sometimes
results in  a darkening  of  the  tissue to a
reddish-brown.  Chronic injury,  which re-
sults from lower concentrations over a num-
ber of days or weeks,  leads to pigmentation
of leaf tissue, or leads to a gradual yellowing,
or chlorosis, in which the chlorophyll-making
mechanism  is  impeded.   Both  acute  and
chronic  injury may be accompanied  by the
suppression of growth and yield.
  Acute injury apparently affects the plant's
ability to  transform absorbed sulfur dioxide
into  sulfuric acid,  and  then into  sulfates.
At high rates of absorption, sulfite is thought
to accumulate, resulting  in the formation  of
sulfurous  acid, which attacks the cells.  The
amount of acute  injury  depends  on the ab-
sorption rate, which is a  function of the con-
centration. A given amount of gas at  a high
concentration will be absorbed in a shorter
period and will cause  more leaf destruction
than the same amount of gas at a lower con-
centration.  Mathematical  expressions have
been worked out which,  for some plant spe-
cies, relate concentration, time of exposure,
and amount of damage.
  Different varieties of  plants vary widely
in their susceptibility to acute sulfur dioxide
injury.  The threshold response of alfalfa to
acute injury is 1.25 ppm  over 1 hour, where-
as privet  requires 15 times this concentra-
tion for the same amount of injury to de-
velop.  Some species of trees and shrubs have
shown injury  at exposures of 0.5  ppm for
7 hours, while injury has been  produced in
other species  at 3-hour  sulfur dioxide ex-
posures of 0.54  ppm and, in still others, at
8-hour  exposures  of 0.3 ppm.  From  such
studies, it appears that acute symptoms will
not occur if the 8-hour  average concentra-
tion does  not  exceed 0.3 ppm.   (From the
data on the CAMP cities, a maximum 8-hour
concentration of 0.3 ppm would correspond
to a yearly average concentration of between
0.03 ppm  and 0.05 ppm).  However, sulfur
dioxide concentrations from 0.05 to 0.25  ppm
may react synergistically with either ozone
or nitrogen dioxide in short-term exposures
(e.g., 4 hours) to produce moderate-to-severe
injury to certain sensitive plants.
  Chronic plant  injury results from  the
gradual accumulation of excessive amounts
of sulfate in  leaf  tissue. Sulfate formed in
the  leaf  is  additive  to  sulfate  absorbed
through the roots, and when sufficiently  high
levels accumulate, chronic symptoms, accom-
panied  by leaf  drop, may occur.  Chronic
symptoms and excessive  leaf drop have  been
reported in locations where  the mean  an-
nual concentration is below  approximately
0.03 ppm.
  It has been suggested  that  sulfur dioxide
might  suppress  growth  and  yield without
causing visible injury. One investigator re-
ported that yields of rye  grass grown in un-
filtered air were significantly  lower  than
similar yields of plants grown in filtered air.
No  visible symptoms  of  injury were  ob-
served.  Sulfur  dioxide  levels in the unfil-
tered air ranged from 0.01  ppm to 0.06 ppm,
with exposure periods ranging from 46 to
81 days; other gaseous pollutants may have
also been  present. Usually, the suppression
of growth and yield is accompanied by visible
symptoms of injury—a  linear  relationship
has been  derived, for example, between the
       160

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yield of alfalfa and the total area destroyed
by acute symptoms, or the  area covered  by
chlorosis.
  Sulfuric acid mist,  which  may occur  in
polluted fogs and mists, also damages leaves.
The  acid  droplets may cause a spotted in-
jury to wet  leaves at  concentrations of 0.1
mg/m3.
            B.  CONCLUSION
  The  conclusions which follow are derived
from a careful evaluation by the National
Air Pollution Control Administration of the
foreign and  American studies cited in pre-
vious chapters of this document.  They repre-
sent  the Administration's best judgment  of
the effects that may occur when various lev-
els of  pollution are reached  in the  atmos-
phere.  The data from which the conclusions
were derived, and qualifications which should
be considered in using the data, are identified
by chapter reference in each case.

           1.  Effects on Health
  Analyses   of numerous  epidemiological
studies  clearly  indicate  an association be-
tween  air pollution, as measured by sulfur
dioxide, accompanied by particulate matter,
and health effects of varying  severity.  This
association is most firm for the short-term
air pollution episodes.
  There are probably no communities which
do not contain individuals with impaired
health  who  are particularly  susceptible  to
the adverse effects of elevated levels of sulfur
oxides  and particulate matter.  However,  to
show small changes in deaths associated with
coincident higher levels of air pollutants re-
quires  extremely large populations. In small
cities,  these  changes are difficult to detect
statistically.
  The  epidemiologic studies concerned  with
increased mortality also show increased  mor-
bidity. Again, increases in morbidity as meas-
ured, for  example, by increases in hospital
admissions or  emergency  clinic visits, are
most easily  detected in major urban areas.
  It  is  believed that,  for  the  large urban
communities  which are routinely exposed  to
relatively high  levels of pollution, sound sta-
tistical analysis can detect  with confidence
the small  changes in daily  mortality which
are associated  with fluctuation  in pollution
concentrations. Such analysis has  thus far
been attempted only in London  and in New
York.
  The association between long-term  com-
munity exposures to  air pollution and respir-
atory disease incidence and prevalence rates
is conservatively believed to be intermediate
in its reliability. Because of the reenforcing
nature of the  studies conducted to  date, the
conclusions to be  drawn from this type of
study can be characterized as probable.
  The association between long-term  resi-
dence in  a polluted area  and chronic disease
morbidity and mortality  is somewhat more
conjectural. However, in  the absence of other
explanations, the findings of increased mor-
bidity  and of  increased  death rates for se-
lected causes, independent of economic status
must still be considered  consequential.
  Based  on the above  guidelines the follow-
ing conclusions are  listed in order of relia-
bility,  with the  more reliable conclusions
first.
  As  discussed in Chapter 2, the sulfur ox-
ides measurement systems used by American
and  foreign  agencies  are  not  always  the
same. However,  for  the most part, data de-
rived  from one measurement system  can be
converted to other systems.
  a. AT  CONCENTRATIONS OF ABOUT
1500 fj-g/m* (0.52 ppm) of sulfur dioxide (24-
hour  average) ,  and  suspended particulate
matter measured as a soiling index  of 6 cohs
or greater, increased  mortality may occur.
(American data;  see Chapter 9, Section  C-
la.)
  b. AT  CONCENTRATIONS OF ABOUT
715 pg/m3 (0.25 ppm)  of sulfur dioxide and
higher  (24-hour  mean),  accompanied  by
smoke at a concentration of 750 /*g/m3, in-
creased daily death rate may occur. (British
data; see Chapter 9, Section C-la.)
  c. AT  CONCENTRATIONS OF ABOUT
500 p.g/m3 (0.19 ppm)  of sulfur  dioxide (24-
v         \   tv     -  tutt   iii   i
hour mean) j  with low particulate levels, in-
creased mortality  rates may  occur. (Dutch
data; see Chapter  9, Section C-la.)
  d. AT CONCENTRATIONS RANGING
FROM 300 Atgr/m3 to 500 ^g/m3 (0.11 ppm to
0.19 ppm) of sulfur dioxide (24-hour mean),
with low particulate levels, increased hospital
admissions of older  persons for respiratory
                                                                             161

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disease may occur; absenteeism from work,
particularly with older persons, may also oc-
cur. (Dutch data; see Chapter 9, Section C-
**»•)
  e. AT CONCENTRATIONS OF ABOUT
715 i*.g/m3 (0.25 ppm)  of sulfur dioxide  (24-
hour  mean),  accompanied by  particulate
matter, a sharp rise in illness  rates for pa-
tients over age 54 with severe bronchitis  may
occur.  (American data; see Chapter 9,  Sec-
tion C-5.)
  f. AT CONCENTRATIONS OF ABOUT
600 p.g/m3 (about 0.21 ppm) of sulfur diox-
ide (24-hour mean), with smoke concentra-
tions  of  about   300  /xg/m3, patients with
chronic lung disease may experience  accen-
tuation  of  symptoms.  (British data;  see
Chapter 9, Section C-5.)
  g. AT CONCENTRATIONS RANGING
FROM  105 pg/m* to 265 /^g/m3 (0.037  ppm
to  0.092  ppm)  of sulfur dioxide  (annual
mean),  accompanied  by  smoke  concentra-
tions of about 185 /*g/m3, increased frequen-
cy of respiratory symptoms and lung disease
may occur. (Italian data; see Chapter 9,  Sec-
tion C-2c)
  h. AT CONCENTRATIONS OF ABOUT
120 M/m3  (0.046  ppm)  of sulfur dioxide
 (annual mean), accompanied by smoke  con-
centrations  of about 100 jug/m3, increased
frequency  and severity of  respiratory  dis-
eases in schoolchildren may occur.  (British
data;  see Chapter 9, Section C-3.)
  i. AT CONCENTRATIONS OF  ABOUT
115 fng/ms  (0.040  ppm)  of sulfur dioxide
 (annual mean), accompanied by smoke  con-
centrations of about 160 yug/m3, increase in
mortality from bronchitis and from lung  can-
cer may occur. (British data; see Chapter 9,
Section C-2.)

          2.   Effects on Visibility
  AT A CONCENTRATION OF 285 pg/m*
 (0.10 ppm) of sulfur dioxide, with compara-
ble concentration of particulate matter  and
relative  humidity of 50  percent,  visibility
may be reduced to about five miles. (Ameri-
can data; see Chapter 1, Figure ±=00  \ -
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APPENDICES

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                             APPENDIX  A—SYMBOLS
    the cross sectional area of a particle for
      light attenuation

    the cross sectional area of an i particle
       (see i and j, below)
 t
    the sulfur dioxide concentration (ppm
      or f*g/m3) in air or the weight (per-
      cent) HoSOi in acid droplets
 i
    the minimum concentration which  will
      damage a particular plant in a given
      time

    the particle-scattering ratio

    the scattering ratio of an  i particle
E

E

K
M
N
S35
    a  constant

    visual range
    geometric mean.  For sample values x1(
      x2, . . . xn, the geometric mean is
       V Xi, x2, . . . xn  or
    the number of particles per unit volume
      of atmosphere

    the number of ij particles per unit vol-
      ume
    probability

    the radioactive isotope of sulfur having
      a mass number 35

    a constant related to damage to a par-
      ticular plant species by sulfur dioxide

    the diameter of a spherical particle

    Napierian  log  base  (=2.718281)

    the fraction of pollutant gases replaced
      per unit time with diluting air
the acceleration of gravity, cm/sec2

(subscript)  identifies  a  particle  of a
  given diameter and  a given index of
  refraction

identifies a particle of a given refractive
  index

the fraction of S02  loss  per unit time
  due to oxidation to S03

the index of refraction

the coefficient for converting  LT to  de-
  sired units

a constant related to the  minimum S02
  concentration that damages a particu-
  lar species of plant

correlation coefficient

the exposure time

"standard normal exceedance deviate".
  The  number of standard deviations
  an observed value  is from the median
  when the underlying distribution  is
  normal.

the wavelength of light in Angstroms,
  microns, or nanometers

the density  of  a  particle  or droplet

the attenuation coefficient  per unit path
  length

standard geometric  deviation

probability function, usually expressed
  asz2 ("CHI SQUARE")

summation,  or  sum of a series
      164

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                        APPENDIX B—ABBREVIATIONS
A       Angstrom, 1 A = 1(H cm
CAMP  Continuous Air Monitoring Project
coh     coefficient of haze
cm     centimeter, 1 cm = 1(H m
CMD   count median diameter
cm2     square  centimeter
DSIR   Department of Scientific and Indus-
          trial Research (England)
FEV   forced expiratory volume
FVC   forced vital capacity
g       mass, grams
hr      hour
LC50    concentration of toxicant lethal to
          50% of subjects
1       volume, liters
MMD   mass median diameter
m      length, meters
m3      cubic meter
mi      mile
mi2     square mile
min     minutes
n       micron,  lfi~W~4 cm = 10-s m
n*g      microgram, 1 ,ug=10"6 g
mg     milligram, 1 mg = 10~3 g
MRC    Medical Research Council
m/*     millimicron, 1 nv = 10-9 m = lnm
NASN  National Air Surveillance Network
nm     nanometer, lnm = 10-9 m = lmju.
mo     months
ppb     parts per billion
ppm    parts per million
pphm   parts per hundred million
RH     relative humidity
sec     seconds
yr      year
                                                                         165

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                  APPENDIX  C—CONVERSION FACTORS

  To Convert                       To                            Multiply By
mg/m3                         Aig/m3                             1000
mg/100m3                      /*g/m3                               10
,ug SCX/m3 (0° C, 760mm Hg)       ppm S02 (vol)                      3.5 XlO-4
ILK S02/m3 (0° C, 760mm Hg)       ppm SO* (wgt)                      7.7 X10-"
ppm S02 (vol)                   fig SO2/m3 (0° C, 760 mm Hg)          2860
ppm S02 (wgt)                  Mg SOo/m3 (0° C, 760 mm Hg)          1290   „
                                  em   iP                        10-
m                                m-^  r^                      -16-*-
Ib                                A-
      166

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                             APPENDIX  D—GLOSSARY
Abscission—the natural separation  of  flow-
  ers,  fruit, and leaves from plants by the
  development and subsequent disorganiza-
  tion of a separation layer
Aerosol—a cloud  of  solid particles  and/or
  liquid  droplets  smaller  than  100/w in di-
  ameter, suspended in a gas
Ainvay—any  part of the  respiratory tract
  through which air passes during breathing
Airway resistance—resistance to  the flow of
  air in the passages to the lungs
Ala  (pi. alae) nasi—the  outer part of the
  nostril
Alpha  rhythm,—a uniform set of electroen-
  cephalographic waves with a frequency of
  approximately ten per second
Alveolus (pi. alveoli)—a small, sac-like  dila-
  tion  at the inner most end of the  airway,
  through  whose walls gaseous exchange
  takes place
Anemia—a condition in which the  number
  of red blood cells per cubic centimeter of
  blood is below normal;  can  be  further
  characterized by descriptions of the alter-
  ations in the red blood  cells  (e.g., hypo-
  chromic, microcytic)  or of the  clinical
  state it is associated with
Anhydride—a  chemical  compound  derived
  by the extraction of a molecule of water
  from the original molecule
Anoxia—a deficiency of the amount of  oxy-
  gen reaching the body tissues
Arrest, cardiac—the cessation of heartbeat
Atelectasis—the collapse of  all  or  part  of
  a lung,  with resultant loss of functioning
  tissue
Atr'opine—a parasympatholytic drug which
  in general  tends to relax smooth  muscle,
  slow the heart rate, and dilate the pupils
Attenuation—in  physics,   any   process  in
  which the flux density  (or power, ampli-
  tude, intensity,  illuminance,   etc.)  of a
  "parallel beam" of  energy decreases with
  increasing   distance  from  the   energy
  source.  A more general usage of this word
  is  also found  in this  publication:  any re-
  duction  in  strength,  density,  effect,  or
  amplitude.
Auscultation (adj. auscultatory)—the act of
  listening for sounds within the body, usu-
  ally with the use of a stethoscope
Bloom,  crystalline—the  formation of  very
  small crystals  on the surface  of organic
  films, resulting in noticeable bloom caused
  by the efficient scattering of light
Bradycardia—an  abnormal slowness of the
  heartbeat
Bronchiectasis—a  chronic  dilatation of  a
  bronchial passage
Bronchiole—one of the finer subdivisions of
  the bronchial tree
Bronchitis—an inflammation of the bronchi,
  usually manifested clinically by cough and
  the production of sputum
Bronchitis, chronic—a long-standing  inflam-
  mation  of the bronchi  characterized by
  excessive mucus secretion in the bronchial
  tree and  manifested by a  persistent  or
  recurrent productive cough.  For the pur-
  poses of definition, these symptoms must
  be present on most days for a minimum
  of 3  months of  the year for at  least  2
  successive years  (American Thoracic So-
  ciety)
Bronchoconstriction—a diminution  in  the
  size of the lumen of a bronchus
Bronchodilatation—an increase in the size
  of the lumen of a bronchus
Bronchus (pi.  bronchi)—one of  the larger
  air  passages in the lung
Buffer—a substance capable  of  enabling  a
  system  to resist changes in condition;  a
  solution whose pH is changed only slightly
  by the  addition, within limits,  of an acid
  or a base
Cannula—a small tube for insertion into  a
  body cavity  or into a duct or vessel
Capacity,  forced  vital  (FVC)—the  largest
  amount of gas  which can be forcibly ex-
  pired from the  lungs following a maximal
  inspiration
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Capacity,  functional  residual  (FRC)—the
  volume  of  gas  remaining in the lungs as
  the resting end-expiratory level
Capacity,  vital—the maximum volume of gas
  which can  be expired from the lungs fol-
  lowing a maximum inspiration
Carcinogenesis—the production of cancer
Carina—a ridgelike structure; in anatomy
  of the respiratory tract, it is a prominence
  on the lowest tracheal cartilage and is sit-
  uated between the orifices of the two main-
  stem bronchi
Catalyst (adj. catalytic)—a substance  capa-
  ble of increasing the velocity of a reaction
  without chemically  or  physically chang-
  ing itself
Catheter—a  tubular device inserted into a
  canal, vessel, or body cavity for either the
  introduction or extraction of  some ma-
  terial
Chloroplast—a specialized body  (a plastid)
  containing chlorophyll in the cytoplasm of
  plants;  the  site of photosynthesis   and
  starch formation in plants
Chlorosis—a   disease  condition   in  green
  plants,  marked by yellowing or blanching
Chronaxie (chronaxy)—the  minimum  time
  required for the excitation of  a nervous
  element by a specified stimulus
Cilium (pi. cilia)—small, hairlike process at-
  tached to a free surface of a cell, capable
  of rhythmic movement
Clearance—the removal of material from the
  body or from an organ
Concentration—the total  mass  (usually in
  micrograms) of  the suspended particles
  contained in a unit volume  (usually one
  cubic meter) at a given temperature and
  pressure;  sometimes,   the  concentration
  may be expressed in  terms of total number
  of particles in  a unit volume  (e.g.,  parts
  per million); concentration  may also be
  called the  "loading" or the "level"  of a
  substance;  concentration may also pertain
  to the strength of a solution
Conductometric—a method of analysis based
  on the conductivity of a sample
Conifer—belonging to the  coniferales or-
  der,  consisting primarily  of  evergreen
  trees  and shrubs
Conjunctiva—the delicate membrane lining
  the eyelids and covering the exposed sur-
  face of the eyeball
Conjunctivitis—an inflammation of the con-
  junctiva
Consolidation—the process by which a dis-
  eased lung  passes  from  an  aerated col-
  lapsible state to one of an airless solid con-
  sistency because of  accumulation of exu-
  date
Criteria, air quality—a compilation  of the
  scientific knowledge of the relationship be-
  tween various concentrations of pollutants
  in the air and their  adverse effects
Deciduous—falling  off  or shed at the end
  of a growing period or season
Deliquesce—to dissolve gradually  and be-
  come liquid by  absorbing moisture from
  the air
Desorption—the release of a substance which
  has  been taken into another substance  by
  a physical process or held in concentrated
  form upon  the surface of  another sub-
  stance;  the reverse  of absorption  or ad-
  sorption
Desquamate—to cast off epidermis in shreds
  or scales;  to peel off in sheets or scales
Diameter, count  median  (CMD)—the geo-
  metric median size  of a  distribution  of
  particles,  based on a numerical count
Diameter, mass median  (MMD)—the geo-
  metric median size  of a  distribution  of
  particles,  based upon a weight  (usually
  derived from a Stokes' Diameter)
Dichotomous—dividing in  succession  into
  pairs; showing a dual  arrangement
Distal—furthest or most remote from the
  median line of the  body, from the point
  of attachment, or from the origin; periph-
  eral (cf. proximal)
Dolomite—a limestone or  marble  rich  in
  magnesium carbonate
Dyspnea—difficult or  labored breathing
Edema—a condition due  to the presence of
  abnormally large amounts of fluid in the
  intercellular tissue spaces of  the body
Effusion—the escape of fluid into a tissue or
  part, usually by the rupture of a vessel
  or extravasation through its walls
Electroencephalogram   (EEG)—a   graphic
  recording of electric currents  developed
  in the brain, obtained with the use of elec-
       168

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  trodes which are usually applied to the
  scalp
Emphysema—a swelling due to the presence
  of  air, usually  excess or additional  air.
  The term is usually used to refer to pul-
  monary emphysema
Emphysema,  pulmonary—a  condition  in
  which there is overdistension of air spaces
  and resultant destruction of alveoli and
  loss of functioning lung tissue
Epidemiology—a  science dealing with the
  factors involved in the distribution and
  frequency of a disease process in a popu-
  lation
Epidermis—the outermost layer of skin in
  animals; any integument
Epithelium—a closely packed sheet of cells
  arranged  in one or more layers, covering
  the surface of the body and lining hollov/
  organs
Exacerbation—an  increase in the severity of
  any symptoms or of a disease
Exteroceptive—activated by or relating to
  any stimulus impinging on an organism
  from the outside
Fibrosis—the  development of fibrous tissue;
  sclerosis
Filiform—having  the shape  of  a  thread or
  filament
Follicle (follicule)—a  very small  excretory
  or secretory sac  or a small gland
Gallamine—a  drug used to  relax  skeletal
  muscles
Gneiss—a laminated  or  foliated  metamor-
  phic rock
Goblet cell—a type of epithelial cell contain-
  ing mucus and having the shape of a flask
  or goblet
Halide—any binary compound of  a halogen
Halogen—any one of the chemically related
  elements fluorine, chlorine,  bromine, io-
  dine,  and astatine
Hemoglobin—a protein found in  red blood
  cells,  responsible for  oxygen transport to
  all parts of the body
Hilutn (hilus)—a  depression  or pit at that
  part  of an  organ where the vessels and
  nerves enter
Histamine—a substance which produces dila-
  tation of capillaries and stimulates gastric
  secretion, occurring  in  both  animal and
  vegetable  tissues; /J-imidazol-ethylamine
Histology—the study of the anatomy of tis-
  sues and their microscopic cellular struc-
  ture
Hydrocarbon—a  compound containing  only
  hydrogen and carbon. This group is sub-
  divided into ali cyclic, aliphatic,  and aro-
  matic  hydrocarbons according to the ar-
  rangement of the atoms and the chemical
  properties  of the compounds
Hygroscopic—readily absorbing and retain-
  ing moisture
Hypertrophy—an  enlargement   or  over-
  growth of an  organ  or tissue due to an
  increase in the size of its constituent cells
Impactor,  cascade—an  instrument which
  employs several  impactions in series to
  collect successively smaller sizes  of  par-
  ticles
Incidence—the rate at which a certain event
  or disease occurs
Intercostal—situated between ribs
Interoceptive—of or relating to any stimulus
  arising from within the body
Interstitial—pertaining to or situated in the
  space between cells
Isopleth—a line on a map connecting points
  at which a  given variable has a specified
  constant value
Isoproterenol—a  sympathomimetic drug
  which  is used  to  relieve bronchoconstric-
  tion and which also can function as a car-
  diac stimulant
Lacrimation   (lachrymation)—tear  forma-
  tion, especially in excess
Lamina  propria—a connective tissue layer
  located just beneath the epithelial cells and
  basement membrane  of many organs
Larch—a tree of the genus Larix or of the
  family Pinaceae
Larynx—the organ concerned with the pro-
  duction of the voice, situated at the upper
  end of the trachea
Leach—to dissolve out  by  the  action  of  a
  percolating liquid
Lesion—an  injury  or  other  circumscribed
  pathologic  change in a tissue
Lumen—the inner  space of a hollow organ
  or tube
Lymphocyte—a variety  of white blood cells
  which  arises in  the  reticular tissue of
  lymph glands
                                                                              169

-------
Lymphoid  cell—a mononuclear cell  found
  in lymphoid tissue  (such  as the spleen,
  tonsil, lymph nodes), ultimately concerned
  with immunologic function
Mean,  geometric (Mg)—a measure of  cen-
  tral  tendency for  a log-normal  distribu-
  tion; the value of  a given  set of samples
  above which 50 percent of the values lie
Monochromatic light—a  beam of light hav-
  ing some desired, narrow range of wave-
  lengths
Monodisperse—characterized by particles of
  uniform  size in a dispersed  phase
Morbidity—the occurrence of a disease state
Morphology—a  branch  of biology dealing
  with  the  structure and form  of  living
  organisms
Mortally—the ratio  of the total number of
  deaths to the total population, or  the ratio
  of the number of deaths from a given dis-
  ease to the total number of people having
  that disease
Mucosa—a mucous membrane
Mucus (adj.  mucous)—the clear viscid se-
  cretion  of  a mucous membrane
Mural—pertaining to  the wall of  a  cavity
Nasopharynx—the   part  of  the  pharynx
   (throat) lying above the level of the soft
  palate
Nebulize—to reduce to a fine spray
Necrosis—localized death  of cells
Nembutal—a barbiturate drug used  as a hyp-
  notic and  a sedative;  pentobarbital
Node—a circumscribed  swelling
Node, lymph—one of many accumulations of
  lymphatic  tissue situated  throughout the
  body
Nucleus  (condensation nucleus)—a particle
  in the size range from 0.1/x to 1/x which
  serves as a nidus on which water or other
  vapors  in  the air  can condense to form
  liquid droplets
Olefin—a class of unsaturated hydrocarbons
   of the general formula Cn H2n
Olfactory—pertaining to the sense of smell
Optical—pertaining to vision
Oro pharynx—that  part   of  the  pharynx
   (throat) lying between the level  of the
  soft palate and the epiglottis
Paraffin—a purified  mixture of solid  hydro-
  carbons  obtained  from  petroleum,  occur-
  ring as an odorless, tasteless, colorless or
  white,  relatively translucent  mass
Parenchyma—the specific or functional tis-
  sue of  a gland or organ, as opposed to its
  supporting framework
Pathogen—any disease-producing organism
  or material
Pathogenesis—the production  or  the mode
  of origin and  development  of  a disease
  condition
Pathology—the study of the essential nature
  of disease,  particularly with  respect to
  the structural and functional changes in
  organs and tissues
Pharynx—the upper expanded portion of the
  alimentary canal lying between the mouth,
  the nasal cavities, and  the  beginning of
  the esophagus; the throat
Photochemistry—a branch of chemistry deal-
  ing with the effect of radiant energy  (as
  light)  in producing chemical changes
Photosynthesis—the formation of carbohy-
  drate  from carbon dioxide and  water in
  the presence of chlorophyll  and light, in
  plant tissues
Physiology—a  science which studies  the
  function of a living organism or its parts
Phytotoxic—harmful to plant  materials
Plethysmograph—an apparatus for the de-
  termination and  recording  of  a  change
  in the  size of an organ or limb or body
Pneumonitis—a general term for inflamma-
  tion of the lung
Pneumotachygraph—an instrument used to
  determine  the  force and  velocity of re-
  spired air
Potentiation—synergism,  as  between two
  agents which together  have  a  greater ef-
  fect than the sum of  their effects when
  acting separately
Prevalence—the number  of  cases  of a dis-
  ease at a given time
Privet—any  one of  various plants of  the
  genus  Ligustrum, used extentively as or-
  namental shrubs
Procaine—a  drug which is  used primarily
  as a local anesthetic
Proximal—nearest to the center of the body
  or the point of origin  (cf. distal)
Rale—an abnormal respiratory sound heard
  in auscultation of the chest
       170

-------
Ratio, standardized  mortality—the ratio  of
  the number of deaths observed in a given
  population over a given period of time to
  the number of deaths expected to occur in
  the given population over the same period
  of time if the given population behaved as
  any other group  of  similar  composition
  would during that same period
Rhinitis—an inflammation of the nasal mu-
  cous membrane
Rhinorrhea—"runny nose"
Rhonchus (pi. rhonchi)—a dry, coarse sound
  usually originating from partial obstruc-
  tion in a bronchial tube
Spasm—an involuntary and  abnormal mus-
  cular  contraction, usually  sudden  and
  forceful, and often accompanied by pain
  and/or loss of function
Spectroscopy—the branch of physical sci-
  ence dealing with the theory and interpre-
  tation of bands of light
Spirometer—an instrument for the measure-
  ment of  the volume of gas  respired by the
  lungs
Squamous—resembling  or  covered  with
  scales
Standards, air  quality—levels of air  pollut-
  ants which can not legally be exceeded
  during a specific  time  in  a specific geo-
  graphical area
Subcutaneous—beneath the skin
Sympathetic—referring  to the sympathetic
  trunk  or the entire sympathetic nervous
  system,  concerned  with the involuntary
  regulation of cardiac muscle, smooth mus-
  cles, and glands
Synergism—a situation  in which  the com-
  bined  action  of two or more agents act-
  ing together is greater  than the sum  of
  the action  of these agents  separately
Systemic—relating to the body as a  whole,
  rather than to its individual parts
Toxicology—the study of  poisons,  including
  their preparation,  identification,  physio-
  logic action, and antidotes
Trachea—windpipe; the  airway extending
  from the larynx to the origin  of the two
  mainstem bronchi
Tracheotomy—a  surgical opening  through
  the skin and muscles of the neck into the
  trachea
Transpiration—the emission of water vapor
  from the surface of plant leaves
Vagosympathetic—referring to the parts of
  the nervous  system with innervation by
  the vagus nerve and  innervation through
  the  sympathetic  nervous system
Vagus—pertaining  to either  of the  pair of
  tenth (X) cranial  nerves,  which supply
  parasympathetic, visceral afferent, motor,
  and  general sensory  innervation
Valence—an integer representing the  num-
  ber of hydrogen or chlorine atoms which
  one atom of an element is capable of com-
  bining with
Ventilation, minute—the total  volume of gas
  respired in one minute, i.e., the tidal vol-
  ume multiplied by breaths per minute.
Viscus  (pi.  viscera)—any  internal  organ
  within a body cavity
Visual range—the distance, under daylight
  conditions, at which the apparent contrast
  between  the specified type of target and
  its background becomes just equal to the
  threshold contrast of  an observer, i.e., the
  distance  at which it is just possible to see
  a dark  object against  the  sky near the
  horizon
Volume, forced expiratory (FEV)—the vol-
  ume of  gas forcibly exhaled over a given
  time interval  (usually  measured  in  sec-
  onds) after  maximum inspiration,  e.g.,
  FEVi.o for this  measurement over a one
  second period
Volume, minute—same as minute ventilation
Volume, tidal—the volume of gas inspired or
  expired  during each respiratory cycle
                                                                            171

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                                         AUTHOR  INDEX
Adams, D. F., 61, 66
Agnese, G., 129
Ahlquist, N. C., 13
Ajax, R. J., 55
Alekseeva, M. V.,  23
Altman, P. L., 61
Alshuller,  A. P., 8
Amdur, M. O., 5, 75, 76, 77, 78, 79,
  80, 81, 83, 91, 92, 93, 94, 107, 108,
  109, 110
Andelman S. L., 91
Anderson, A., 143,  144
Anderson, D. M., 25, 52, 53
Anderson,  D.  0., 91, 120, 131, 134,
  137
Anderson, R. J. 91
Angel, J.  H.,  140
Ascher, L., 91
Aviado, D. M., 78
Axt, C. J., 9

Baetjer, A. M., 107
Ball, C. O. T., 82
Barber, F. R., 42
Baines, F., 53, 54
Balchum,  0. J., 78, 82
Barkley, J. F., 51,  53, 55
Barnes, J. M., 91
Barrett, C. F., 19
Barringer, A. R.,  22
Bates, D.  V-,  134
Battista, S. P., 77
Becker, W. H., 137
Bell, A., 91, 132, 140
Bellin, A., 24, 25 43
Belton, J., 122, 123
Benner, R. C., 53
Benson, F. B., 23
Benson, H. E., 5
Berry, C.  R.,  65
Bertramson, B. R., 45
Bhardwar, D. V., 51
Bienstock, D., 5
Bleasdale, J. K. A., 62,  65
Bokhoven, C., 22
Boone,  R. E., 25
Booras, S. G., 24
Bracewell, J.  M., 7
Bradley, W.,  120, 122
Brady, N. O., 45
Brandt, C. S., 61, 62, 63
Brasser, L. J., 33, 40, 120, 122, 123,
  125,  127, 129, 133, 136, 137, 139
Brasted, R. C., 5
Braverman, M. M., 125
Brennan, L., 61
Brewer, R. F., 61, 66
Brice,  R. M., 25
Brooks, A. G. F., 11
Brown, D. A., 127
Brunn, L. W., 5
Buck,  S. F., 127, 128
Buckman, H.  0., 45
Buffalini, J. J., 8
Burdick, L. R., 51, 53, 55
Burgess, F. 75, 76, 106
Burgess S. G., 120, 128
Burgess, W. A., 143, 144
Burn,  J. L., 129, 144, 136
Burton, G. G., 94, 110
Bushtueva K. A., 13, 23, 43, 76, 96,
  97, 98, 99, 107
Bye, W. E., 19, 23, 42
Bystrova, T. A., 82

Calvert, J. G., x, 8
Cappel, J.,  75
Carey, G. C. R.,  139
Carnow, B. W., 140
Carpenter, S. B., 8, 9
Cartwright, J., 11
Cassell, E. G., 119, 125, 126
Catcott, E.  J., 91
Catteral, M., 91
Chaney, A. L., 25, 43, 45
Charlson, R. J., 13
Cherkasov, YE. F., 96
Clancy, F. K., 22
Coffin, D. L.,  91
Collier, C.,  78
Comichi, S., 23
Commins, B. T., 9, 11, 24, 38, 43
Comroe, J.  H., 94
Conlee, C.  J., 55
Cooper, P., 74
Cooper, W. C, 91
Corn,  M., 77, 80, 81, 94,107,110
Coste, J. H., 13, 42
Coughanowr,  D.  R.,  7
Could, R. A., 61, 63
Courtier, G. B., 13, 42
Couy,  C. J., 53
Cralley, L. V., 81, 96
Critchlow, J., 76
Crowley, D. 122, 123
Cuffe, S. T., 19
Cullumbine, H., 75, 76, 106

Daines, R.  H., 61, 63
Dainton, F. S., 8
Dalhamn, T., 75, 81, 83
Daly, C., 128
Darley, E. F., 61,  66
Davis, T. R. A., 77
De Groot,  I., 126
De Treville, R. T., 106
Devitofrancesco, G., 7
Dev Jain,  K., 8
Diamond, J. R., 119, 125, 126
Dickerson, R. C., 23
Dittner, D. S., 61
Dohan, F.  C., 135
Dorries, W., 63
Douglas, J. W. B., 137
Doyle, G. J., 7, 8
Drinker, P., 75, 76, 91, 94
Drolette, B. M., 125
Dubrovskaya, F. I., 96, 97
Dutra,  F.  R., 75
Dybicki, J., 78, 82

Elfers, L. A., 22
Elfimova, E. V., 142
Elliott, A., 138
Elliott, G. O., 82
Endow,  N., 8
Engdahl, R. B., 19
Erhardt, C. L., 125

Fairbairn, A. S., 128
Farber,  S. M., 91
Farmer, J. R., 23
Ferris, B. G., Jr.,  134,143,144
Fesch, J.,  81
Field, F.,  123, 125
Firket, J., 119
Fish, B. R., 7
Fletcher, C. M., 140
Foran, M. R., 52
Forker, G. M., 10
Frank,  N. R.,  78, 82, 83, 92, 93,
   95, 109,  110
Franklin, E. C., 61, 63
        172

-------
Frey, S. A., 21
Fried, M.,  45

Gall, D., 7
Gartrell, F. E., 8, 9
Gee, J. B. L., 94, 110
Gerhard, E. R., 7
Gerstle, R.  W., 19
Gibbons, E. V., 52
Gilbert, E.  E., 7
Gilbert, P.  T., 53
Glasser, M., 123, 125
Goetz, A., 8
Goldberg, C., 128
Goldring, I. P., 74
Golden, C. C., 23
Goldsmith,  J. R., 82, 91, 133
Gore,  A. T., 120, 128
Gorham  E., 23, 45, 128
Graesser, F. E., 74
Graf, P., 81
Greenburg, L., 23, 74, 122, 125
Greenblatt J.  H., 51
Greenwald, L, 91
Grollman,  A., 98
Gross, P.,  106
Gruber, C.  W., 19
Gunn, F. D., 76

Hagstrom,  R.  M.,  130
Hamming,  W. J., 24, 25, 43
Handyside, A. J., 138,  139
Hangebrauck, R.  P., 19
Hartzell, A., 73, 74
Haselhoff,  E., 63
Heck, W. W., 61, 62, 63, 66
Hedgcock, G. G., 61 64
Heggestad, H. E., 66
Heimann, H.,  91
Hemeon, W. C. L.,  80
Hendricks,  R. H., 61, 62, 63, 66, 76
Hendrickson, E. R., 19
Hepting, G. H., 65
Heyssel,  R. M., 82
High, M. D., 19
Hill, A. B., 117
Hill, G. R., 61, 62, 63, 64, 66
Hill, J. D.,  140
Hindawi, I. J., 66
Hochheiser, S., 23
Hodgman,  C. D.,  10
Holbrow, G. L., 51
Holland, W. W., 133, 138, 139
Holmes, J.  A., 61, 62, 63
Horada,  M., 62, 65
Horton, R.  J. M., 130
Horvath, H., 13
Huey, N. A., 24
Huschke, R. E., 10

Ishikawa, K., 78
Ivin, K. J.,  8
Jacobs, M. B., 5, 23, 125
Johnson, A. B.,  62
Johnston, H. S.,  8
Johnstone, G. F., 7
Johnstone, H. F., 7
Jones, J. L., 8
Joosting,  P. E., 33,  40,  120,  122;
  123, 125,  127,  129,  133, 136,  137,
  142,
Junge C. E., 7, 45            «

Kanitz, S., 129
Kapalm, V., 142
Katz, M., 8, 19, 23,  42, 45, 61, 64,
  65
Kopezynski, S. L., 8
Kramer, G. D., 23
Kuczynski, E. R., 22
Kurland, L. T., 126
Kehoe, R. A.,  143, 144
Kenline, Pa. A.,  25
Kensler, C. J. 77
Kent, D. C., 79
Kerr, H. P., 139
Kitzmiller, K., 143, 144
Knowelden, J., 138, 140

Liadlaw, S, A., 91
Landeau, E., 91, 130
Lange, N. A., 10
Larsen, R. I., 33, 38,  40, 46
Lawther, P. J., 91, 95, 122, 140
Leblanc, T. J., 143, 144
Lee, R. E., Jr., 9
Leighton, P. A.,  8, 10
Leonard, A. G., 122, 123
Leong, K. J., 74, 75
Lepper, M. H., 140
Liberti, A., 7
Lieben, J., 25, 52, 53
Lindau, G., 63
Linzon, S. N., 42, 65
Lobova, E. K., 84
Law, M. J. D., 23
Lucas, D. H., 19
Ludman, W. F.,  23
Ludwig, F. L., 9
Ludwig, J. H., 19, 20
Lunn, J. E., 138, 140
Lutsep, H., 7
Lyon, T. L., 45
Lyons C. J., 91
Lyubimov, N. A., 23

MacFarland, H.  A., 74, 75
Machle, W. F., 143, 144
Mader, P. P., 24, 25, 43
Maeller T., 5
Manzhenko, E. G., 138
Markush, R. E.,  127
Martin, A., 42
Martin, A. E., 91, 120, 122, 126
Mason, B. J., 7
Massey, L. M., 61
Mathur, K., 75
Matushima, J., 62, 65
McBurney, J.  W., 53
McCaldin, R. O., 23, 42, 51
McCallan, W. E., 74
McCallum, A. W., 61, 62, 64
McCarroll, J.  R., 119, 122, 125, 126
McCord, C. P., 5
McPhee, R. D., 23
Mead, J., 77, 78
Meeker, J.  E., 19
Meneely, G. R., 78, 82
Menser, H. A., 66
Middleton,  J. T., 61, 66
Middleton,  W. E. K.,  9
Moore, D. J., 19
Morgan, W. K. C., 139
Morgenson, A., 65
Mountain,  I. M., 119,  125, 126
Mountain, J. D., 119,  125, 126
Murphy, E. M., 5
Murphy, S. D., 77

Nadel, J. A., 79, 81, 94
Nader, J. S., 9
Nakamura, K., 110
Navrotskii, V. K., 84
Negherbon, W. 0., 73
Nelson, H.  W., 91
Newberry,  B.  C., 22
Newill, V. A., 23
Newstein, H.,  20
Niessen, H. G. L., 22
Noack, K.,  63, 64
Norris, C. H., 22
Noyes, C. M.,  7

O'Donoghue, J. G., 74
O'Gara, P.  J., 63
O'Keeffe, A. E., 23
Olmstead, P.,  75
Orning, A.  A., 19
Ortman, G. C., 23
Oswald, N. C., 91

Pace, D. M., 84
Palmer, H. F., 22
Parcher, J. P., 7
Parker, A.  53, 54, 55
Pattle, R. E., 75, 76
Patty, F. A., 5
Perlman, R., 51
Pemberton, J., 128, 129,136
Perry, W. H., 45
Petr, B., 142
Petrie, T. C., 54
Petrilli, R.  L., 131
Phair, J. J., 91, 126, 139
Phillips, P. H., 91
Pitts, J. N., Jr., 8
                                                                                              173

-------
Polezhaev, E. F., 98
Pollack, S. V., 126
Popov, I. N., 96
Prager, M. J., 8
Preston, R. St. J., 52
Prindle, R. A., 91, 130, 134
Prokhorov, Yu. D., 84
Pueschel, R.  P.,  8
Pushkina, N. N., 142

Ratner, I. M., 74
Reed, J. I., 125
Regan, C. J., 54
Rehme, K. A., 24
Reid, D. D., 128,  130, 132, 133,  137,
    139
Reid, L., 74, 76
Renzetti, N. A., 7, 8
Rinehart, W. E., 106
Roberts, A., 91
Robinson, E., 9,  10, 12
Rodes, C. F., 22
Roesler, J. F., 9
Rogov, A. A., 84
Rohdin, J., 81
Rohrman, F. A.,  19, 20
Ryan, T., 7
Ryazanov, V. A., 96, 97, 98

Salem, H., 78, 79, 94, 106
Saltzman, B. E., 21
Salvin, V. S., 55
Samorodiva,  R. Ya. S., 23
Santner, J. T., 23
Sanyal, B., 51, 52
Scaringelli, F. P., 21, 24
Schikorr,  G., 52
Schilling, F.  J., 137
Schmidt, P., 142
Schnurer, L., 105, 108
Schueneman, J. J., 19
Schulz, R. Z., 75, 76
Schulze, F., 23
Schumsky, D. A., 126
Schwartz, C. H., 19
Scorer, R. S., 19
Scott, J. A., 120
Scott, W. E., 8
Selby, S. M., 10
Sellers, E. A., 74, 76
Seltser, R., 139
Semenenko, A. D., 98
Sereda, P. J., 51
Setterstrom, C., 62, 65, 66, 73, 74
Shaddick, C. W., 120, 128
Shashkov, V. S.,  142
Sheffer, T. C., 61, 64, 65
Shekelle, R.  B., 140
Shephard, R. J., 139
Shikiya, J. M., 24
Shock, J. M., 22
Shuck, E. A., 8
Sigmon, H.,  75
Silverman, L., 94
Sim, V. M., 91, 95
Sjoholm, J.,  81, 82
Skalpe, T. O., 143, 144
Smith, B. M., 7
Smith, W. S.,  19
Solberg, R. A., 61, 66
Speizer, F. E., 28, 82,  83, 92, 93, 95
Spicer, W. S., Jr., 139
Spierings, F., 64
Sprague, H. A., 129
Spurr, G., 19
Stahl, R. W., 19
Stalker, W. W., 23
Stamler, J., 140
Standiford, N. E., 139
Steffens, C., 9
Sterling, T.  D., 126
Stern, A. C., 8, 91
Stevens, E. R., 8
Stevens, R. K., 23
Stevens, W., 20
Stevenson, H. J. R., 9
Stokinger, H. E., 91
Stoklasa, J., 62
Stone, R. W., 133, 139
Storey,  P. B., 139
Standberg, L. G., 77, 81, 82
Sullivan, J. L., 42, 65
Sussman V.  H., 25, 52, 53
Swain, R. E., 62, 65

Tabor, E. C., 23, 27
Tamplin, B., 79, 94
Taylor, E. W., 139
Tendorf, R.  B., 11
Terabe, M., 23
Thomas, A., 94, 110
Thomas, F. W., 8, 9
Thomas, M.  D., 13, 25, 44, 45, 61,
  62, 63, 64, 66, 76
Thompson, J. E., 24
Thompson, J. R., 84
Tice, E. H.,  52
Tierney, D. F., 94
Tinker, C. M., 140
Tisdale, S. L., 45
Tomono, Y., 94
Toyama, T., 132,  139
Trakhtman, 0. L., 96
Treon, J. F., 75
Trieff, N. M., 20
Turner, M. E., 139
Turner, T. H., 53
Tyler, R. G., 25

Underbill, D., 81, 107, 108, 109
Upham, J. B., 52, 55
Urone, P., 7

Van Den Heuvel, A. P., 7
Van Zuilen, D., 120, 122, 123,  125,
    127, 129, 133, 136, 137, 142
Vassallo, C., 94, 110
Verma, M. P., 137
Vernon, W. H. J., 51, 52
Vintinner, F. J., 105
Von Lehmden, D. J., 19

Wagman, J., 7, 9
Wallace, A.  S., 91
Waller, R. E., 11, 38, 54, 137
Walter, E. W., 119, 125, 126
Watanabe, H., 123, 126, 139
Weast, R. C., 10
Weaver, J. E., 61, 62, 65
Weedon, F.  R., 73, 74
Wellington,  J. R., 52
Wells, A. E., 61, 62, 63, 65, 66
Whitby, G. S., 61, 62
Whittenberger, J. L., 92, 93, 109,
    110
Wicken, A. J., 128
Widdicombe, J. G.,  79
Wilkins, E.  T., 91, 120
Williams, J. D., 23
Wilson, R. H. L., 91
Winkelstein, W., 129
Witheridge, W. M., 5
Wohlers, H. C., 20
Wood, F. A., 61
Worcester, J., 92, 143, 144

Yanysheva, N. Ya.,  142
Yocum, J. E., 51, 53
Yoder, R. E., 82
Yokiwa, Y., 79, 94
Yokoyama, E., 78, 82
Younker, W.,  75

Zeidberg, L. D., 130, 134
Zickmantel, R., 134
Zimmer, C. E., 23, 33, 40
Zimmerman, P. W., 62, 66, 73
Zwi, S., 80
        174

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                                          SUBJECT  INDEX
Absorption
  of S02 in animals, 82-83
  nasal, 95
Acid titration method, 22, 23-24,
  26-27
Acidity
  of rainfall and dustfall, 45
Age
  effect on animal exposure to
    H:S04 mist, 75-76, 80-81
  effect on plant resistance to
    SO:, 66
Air pollution episodes
  mortality figures during, 119-125
Air quality  data
  SO,, 33-47
Alfalfa
  effect of SO, on, 53-64, 67
Alpha rhythm, 96, 98
Aluminum
  effect of SOX  on, 52
Anemia
  Occurrence in highly polluted
    areas, 142
Asthma
  during air pollution episodes, 125
Atmospheric reactions of SOX, 7-9
Australia
  concentrations of  S02, 42
  effects of  SO 2 on vegetation, 65
  morbidity studies, 132

               B

Baltimore, Maryland
  morbidity study, 139
Barley
  effect of SO2 on, 61
Blood formation
  effect of S02 on, 142
Blood pressure
  effect of SO: on, 92
Bronchitis
  correlation with SO2 levels,  119-
    139, 140-142
  during air pollution episodes,
    119-126
  mortality, 119-130
Bronchoconstriction
  effect of SO, on, 94
  mechanism in cats caused by
    SO., 79, 84, 85
Buffalo, New York
  mortality study, 129
Building materials
  effects of SOX on, 54-56
CAMP  (Continuous Air  Monitor-
  ing Program) data, 33-47
Canada
  morbidity study, 134
Cancer
  mortality, 130
Catalytic oxidation of S0:, 7
Chicago, Illinois
  effect of S02 on materials, 53-56
  morbidity study, 140, 141
Children
  epidemiologic studies of, 137-139
Chilliwack, British Columbia
  morbidity study, 134
Ciliary  action
  effect of SO. on, 81-82
Citrus trees
  effect of SO: on, 62
Clinical visits during episodes, 125
Coal combustion gases
  mortality of animals from
    inhalation of, 105-106
Coal refuse  burning
  emissions of SO: from, 19-20, 25
Coke processing
  emissions of SO: from, 20
Colorimetric (West-Gaeke)
  method, 21,  24-26, 33
Combined effects of SO: and
  H2SO,, 105-107
Combustion sources of SOX, 5, 19-
  20, 25
Compliance  (lung)
  effect of SO: on, 93
Conductometric methods, 21-22, 23-
  24, 25-26
Copper
  effect of SOX on, 52
Corrosion of metals
  effect of SOZ on, 51-53, 55-56
Corrosion rate, 51-53, 55-56
Cough reflex, 79-80
Coulometry, 23-24, 26
Czechoslovakia
  morbidity studies,  142
                                                                                       D
Detroit, Michigan
  mortality study, 123
Distribution of SO: in animals, 82-
  84
Dolomites
  effect of SO: on, 53-54, 56
Donora, Pennsylvania
  mortality study, 119
Dose-response curve, 83, 84-85, 110
Dublin, Ireland
  mortality study, 123
Dyed fabrics
  effect of sulfur compounds on,
    55, 56
                E

Economic Loss
  metal' corrosion, 53
Electroconductivity
  measurement of SO2, 33
England (see United Kingdom)
Epidemiologic studies, 119-142
Eston, England
  mortality study, 128, 129
Fading of fabrics
  effect of SO2 on, 54, 56
Flame photometry measurement of
  sulfur compounds, 24, 26
Fog episodes
  mortality figures during, 119
Fuchsin-formaldehyde method, 23
Fumigation experiments, 63, 65

                G
Genoa, Italy
  morbidity study,  131
Grasses
  effect of SO: on, 61, 62

                H

Hospital admissions during
  episodes, 125
Humidity
  effect on irritant potency of
    H:S04, 95
  effect on plant resistance
    to SO2, 65
                                                                                             175

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Humidity effect on atmospheric
    H..SO, formation, 43-45
Hydrogen peroxide measurement
  method of SO,, 21-22, 23, 26

                I

Industrial exposure studies, 142-
  144
Irradiation of SO2, 7
Japan
  mortality study, 123
  morbidity studies, 132, 139-140

                K

Kerosene smoke, 106
Laboratory animals
  effect of SOX on, 73-75, 76-80,
    81-85
  effect of H2SO4 mist on, 75-76,
    80-81, 84-85
  effect of zinc ammonium
    sulfate on, 81
Lead peroxide candles, 24-25, 26
Leaf tissue
  effect of SO. on, 61-65, 66-68
Leather
  effect of S02 up, 55, 56
Lifetime exposure of animals
  to SO,, 82
Light intensity
  effect on plant resistance to  SO2,
    66
Light scattering
  by H2SO, particles, 9-10
  by sulfate particles, 9-10
Limestone
  effect of SO2 on, 53-54, 56
London, England
  mortality studies,  119-125
  morbidity studies,  125-126
Los Angeles, California
  morbidity study, 126
Lungs
  reaction to S02, 76-80
  reaction to H,S04  mist, 80-81
Lung resistance
  effect of SO. on, 91-94
  effect of H2SO4 mist on, 94-95

                M
Marble
  effect of SO, on, 56
Measurement  methods
  of S02, 20-23, 24-25, 25-26
  of H,S04, 24, 25, 26
  of sulfates,  24, 25, 26
Mechanism of SO., injury to
  vegetation,  63
Meuse Valley, Belgium
  mortality studies, 119, 120
Minute volume
  effect of H,SO4 mist on, 94-95
Monitoring programs, 33-47
Morbidity
  as an index of health, 117
  during air  pollution episodes,
    125-126
Morbidity studies, 130-142
Mortality
  index of health, 117
  due to combined effect of SO2,
    H,SO4, and particles, 105-107
  due to S0;  exposure, 73-75
Mortar
  effect of SO2 on, 53-54, 56
Mucus
  effect of SO: on removal of, 95
               N

Nasal resistance
  effect of SO2 on, 94
Nashville, Tennessee
  mortality studies, 130
  morbidity studies, 134
National Air Surveillance
  Network (NASN), 33-47
New Hampshire (Berlin)
  morbidity studies, 134, 143
New York  City
  mortality studies, 122, 123
  morbidity studies, 125-127, 137
Norway
  morbidity study, 143
Nutrient supply
  effect on plant resistance to
    SO2, 66

                O

Occurrence of SOX in the
  atmosphere, 5
Oil refineries
  morbidity studies in the
    vicinity of, 143
Optical chronaxie,  98-99
Oxidation of SO2
  in power plant plumes, 8
  in nickel-smelting plumes, 8-9
Painted surfaces
   effect of SO2 on drying time,
     51, 56
   effect of SO2 on glossiness, 51, 56
   general effect of SO2 on, 51, 56
Paper
   effect of SO2 on, 55, 56
Particle size
  effects on animal response to
    pollutants, 79-81
  distribution of sulfates, 9
Pennsylvania (Seward-New
    Florence)
  morbidity study, 134
Persia (southern)
  morbidity study, 143
Petroleum refineries
  emissions of SO2 from the
    vicinity of, 19-20, 25, 42, 47
pH (see acidity)
Photochemical oxidation  of S02, 7-
  8
Photooxidation rate of SO2 7
Pine trees
  effect of S02 on, 61, 62, 64-65,
    67-68
Pittsburgh, Pennsylvania
  effect of SO2 on materials, 52
Plants
  effect of SO. on, 61-65, 66, 68
  effect of H2S04 mist on, 67-68
Pneumonia death rate, 128
Potentiation of SO2, 108, 109
Power plants
  S02 in the vicinity of, 42, 47
Pulmonary function
  as an index of health, 117-118
  effect of simultaneous
    exposure to S02 and  NaCl, 108,
      110
  effect of  simultaneous
    exposure to SO2 and  H2SO4,
      107-108
  effect of  SO2 and H2SO4 mist on,
    91-95
Pulp  mills
  morbidity studies in the vicinity
    of, 143
Pulse rate
  effect of SO2 exposure  on, 92

               R

Refuse  Incineration
  emissions of SO, from, 19-20, 25
Respiratory rate
  effect of S02 exposure  on, 92
  effect of H2S04 mist on, 94-95
Respiratory response, 76-79
Rotterdam, The Netherlands
  mortality studies, 123
  morbidity studies, 127, 137
St. Louis, Missouri
   effect of S02 on materials, 52-54
Salford,  England
   mortality study, 129
   morbidity study, 136
        176

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Sampling techniques for SO2, 20-27
Slate
  effect of S02 on, 56
Smelters
  emissions of S02 from the
    vicinity of, 19-20, 25, 42
Soil moisture
  effect on plant resistance to S(X,
    66
Soiling index relationship to
  morbidity, 145
Sources of atmospheric SOX, 19-20,
  25
Spectroscopic  measurement
  methods of SO,, 22, 24, 26
Steel
  effect of SOX on, 51-54, 55-56
Sulfation plate, 24
Sulfation rates, 20-27, 55-56, 144-
  147
Sulfur oxides
  effect of sunlight on, 9-14
Sulfuric acid
  relationship to SO,, 42-45
  formation during photo chemical
     reactions, 7
  emissions of SO,
     manufacture of, 19-20, 25
Sulfuric acid  mist
  effect on laboratory animals,  75-
     76, 80-81
  effect on man,  94-95
  effect oft materials, 55-56
  effect on plants, 66, 68
  measurements  of, 25, 27
Susceptibility of vegetation to SO2,
  61-68
"Susceptible population," 119
Suspended sulfates
  concentrations, distribution, and
    measurement of, 25, 26
Synergism of SO, and NaCl, 111
Synergistic effects
  S02 and 03 effects on tobacco, 66
  NO2 and SO3 effects on tobacco,
    66
Temperature
  effect on plant resistance to SO;,
    65
Tennessee  (eastern)
  effect of SOS on vegetation, 64
Textiles
  effect of sulfur compounds on,
    55-56
Threshold  concentrations of sulfur
  compounds brain sensitivity, 96,
    98, 99
  eye sensitivity, 96, 97, 98-99
  odor perception, 96-97, 99
Tidal volume
  effect on H=SO4 mist on, 94
Tobacco plants
  effects of SO, and O3 on, 66
  effects of NO2 and S02 on, 66
Trail, British  Columbia
  concentrations of SO., 42
  effects of S02 on vegetation, 64
Trees (see also Pine and Citrus
    trees)
  susceptibility to S02, 63-65

               U
U.S.S.R.
  morbidity studies, 138, 139, 142
United Kingdom
  mortality studies, 127, 128
  morbidity studies, 136, 137, 138
Visibility reduction
  by SO^ and H2SO, mist, 9-14

Vital capacity
  effect of SO, on, 91, 99
                W

West-Gaeke method (see also
  Colorimetric method), 21, 22, 24-
    25, 25-26
Wind speed effect on atmospheric
  H2SO, formation, 43
Zinc
  effect of SO2 on, 52
Zinc ammonium sulfate
  effect on laboratory animals, 81
                                                                                               177

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                              ACKNOWLEDGEMENTS

    The following sources, in most instances the copyright holders, have granted permission
to the National Air Pollution Control Administration to include the following figures and
tables in Air Quality Criteria for Sulfur Oxides:
Table 1-2.—McGraw  Hill, Inc., New York
  and Chemical Rubber Company

Page  20—American Institute  of  Chemical
  Engineering, New  York; and Electrical
  World Copyright 1967, all rights reserved
  by McGraw Hill, Inc.

Page 42—National Research Council Ottawa,
  Canada

Table 3-4.—Pergamon Press, Inc., New York
  City

Table 9-1.—Research  Institute for Public
  Health  Engineering.  Delft,  The Nether-
  lands
Figure 5-1.—American Society of Plant Phy-
  siologists, Washington, D. C.
Figure 9-1.—Royal Society of Health
Figure 9-2.—Royal Dublin Society, Dublin,
  Ireland
Figure 9-3.—American Medical Association,
  Chicago, 111.
Figure 9-4.—Lea and Febiger, Philadelphia,
  Pa.
Figure 9-5.—British  Medical Journal, Lon-
  don
Figure 9-6.—Air Pollution Control Associa-
  tion, Pittsburgh, Pa.
                                                  * U. S. GOVERNMENT PRINTtNG OFFICE : 1969 — 347-411/31
       178

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