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.
-------
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
-------
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
-------
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
-------
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
Chemistry." Vol. 8, D. Van Nostrand Co., Inc.,
Princeton, N. J., 1961, 306 pp.
2. Moeller, T. "Inorganic Chemistry." John Wiley
and Sons, Inc., New York, 1953, 966 pp.
3. Jacobs, M. B. "Methods for the Differentiation
of Sulfur-Bearing Components of Air Contami-
nants." In: Air Pollution, L. C. McCabe (ed.),
McGraw-Hill, New York, 1952, pp. 201-209.
4. Amdur, M. 0. "Report on Tentative Ambient
Air Standards for Sulfur Dioxide and Sulfuric
Acid." Ann. Occup. Hyg., Vol. 3, pp. 71-83.
5. Patty, F. A. (ed.) "Industrial Hygiene and
Toxicology. Vol. II. Toxicology." D. W. Fas-
sett and D. D. Irish (eds.), Interscience Pub.,
Inc., New York, 1963, pp. 831-2377.
6. McCord, C. P. and Witheridge, W. M. "Odors,
Physiology and Control." McGraw-Hill, New
York, 1949, 53 pp.
7. Bienstock, D., Brunn, L. W., Murphy, E. M., and
Benson, H. E. "Sulfur Dioxide—Its Chemis-
try and Removal from Industrial Waste Gases."
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-
pounds." Chem. Rev., Vol. 62, pp. 549-589, 1962.
9. Gerhard, E. R. and Johnstone, G. F. "Photo-
chemical Oxidation of Sulfur Dioxide in Air."
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.
89, pp. 271-275, April 1963.
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
-------
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
-------
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
-------
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
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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.
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61st Annual Meeting, Air Pollution Control As-
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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
-------
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
-------
-------
Chapter 3
ATMOSPHERIC CONCENTRATIONS OF SULFUR OXIDES
-------
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
-------
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
-------
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.
F. REFERENCES
1. Zimmer, C. E. and Larsen, R. I. "Calculating
Air Quality and its Control." J. Air Pollution
Control Assoc., Vol. 15, pp. 565-572, Dec. 1965.
2. Brasser, L. J., Joosting, P. E., and van Zuilen,
D. "Sulfur Dioxide—To What Level is it Ac-
ceptable?" Research Institute for Public Health
Engineering-, Report G-300, Delft, The Nether-
lands, July 1967.
3. Larsen, R. I. "A New Mathematical Model of
Air Pollution Concentration, Averaging Time,
and Frequency." (Presented at 61st Annual
Meeting of the Air Pollution Control Associa-
tion, St. Paul, Minnesota, June 23-27, 1968.)
4. "Concentrations of Volatile Sulfur Compounds
in Atmospheric Air." Air Industrial Hygiene
Foundation of America, Inc., Spec. Res. Bulls.
1 and 2, 1937, 1938.
5. Commins, B. T. and Waller, R. E. "Observations
for a Ten-Year Study of Pollution at a Site in
the City of London." Atmos. Environ., Vol. 1,
pp. 49-68, 1967.
6. "Report of the International Joint Commission,
United States and Canada, on the Pollution of
the Atmosphere in the Detroit River Area."
International Joint Commission (United States
and Canada), Washington, D.C./Ottawa, Can-
ada, p. 115.
7. Linzon, S. N. "Sulfur Dioxide Injury to Trees
in the Vicinity of Petroleum Refineries." Forest
Chronicle, Vol. 41, pp. 245-250, June 1965.
8. Katz, M. "Sulfur Dioxide in the Atmosphere of
Industrial Areas." In: Effect of Sulfur Dioxide
on Vegetation, National Research Council, Ot-
tawa, Canada, 1939, pp. 14-50.
9. Sullivan, J. L. "The Nature and Extent of Pol-
lution by Metallurgical Industries in Port Kem-
bla." In: Air Pollution by Metallurgical Indus-
tries, Div. Occupational Health N. S. W., Dept.
of Public Health, Sydney, Australia, Vol. 1, 1962,
pp. 1-59.
10. Linzon, S. N. "The Influence of Smelter Fumes
on the Growth of White Pine in the Sudbury
Region." Joint Pub. Ontario Dept. Lands and
Forests/Toronto Dept. Mines, 1958.
11. Martin, A. and Barber, F. R. "Investigations of
Sulfur Dioxide Pollution Around a Modern
Power Station." J. Inst. Fuel, Vol. 39, pp. 294-
307, July 1966.
12. McCaldin, R. O. and Bye, W. E. "Air Pollution
Appraisal, Seward and New Florence, Pennsyl-
vania." U.S. Public Health Service, Robert A.
Taft Sanitary Engineering Center, 1961.
13. Coste, J. H. "Investigation of Atmospheric Pol-
lution." Cong. Intern. Quim. Pura Aplicada (Ma-
drid), Vol. 6, pp. 274-287, 1934.
14. Coste, J. H. and Courtier, G. B. "Sulfuric Acid
as a Disperse Phase in Town Air." Trans.
Faraday Soc., Vol. 32, pp. 1198-1202, 1936.
15. Commins, B. T. "Determination of Particulate
Acid in Town Air." Analyst, Vol. 88, pp. 364-
367, May 1963.
47
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16. 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., August
1960, pp. 193-196.
17. Bushtueva, K. A. "The Determination of the
Limit of Allowable Concentrations of Sulfur
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.
18. 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.
19. 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.
20. 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.
21. "Air Quality Data (1962) National Air Sam-
pling Network." U.S. Dept. of Health, Educa-
tion, and Welfare, Public Health Service, 1964.
22. "Air Quality Data (1963) National Air Sam-
pling Network." U.S. Dept of Health, Educa-
tion, and Welfare, Public Health Service, 1965.
23. Perry, W. H. and Tabor, E. C. "National Air
Sampling Network Measurement of SO3 and
NO.." Arch. Environ. Health, Vol. 4, pp. 254-
264, March 1962.
24. Gorham, E. "Atmospheric Pollution by Hydro-
chloric Acid." Quart. J. Roy. Meteorol. Soc., Vol.
84, pp. 274-276, July 1958.
25. "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.
26. "Air Pollution Measurements of the National
Air Sampling Network. Vol. II. Analysis of Sus-
pended Particulates, 1957-1961." U.S. Dept. of
Health, Education, and Welfare, Public Health
Service, PHS-Pub-978, 1962.
27. "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.
28. Katz, M. "Some Aspects of the Physical and
Chemical Nature of Air Pollution." W.H.O.
Monograph Series 46, Columbia Univ. Press,
New York, 1961, pp. 97-158.
29. Junge, C. E. "Sulfur in the Atmosphere." J.
Geophys. Res., Vol. 65, pp. 227-237, Jan. 1960.
30. Lyon, T. L., Buckman, H 0., and Brady, N. 0.
"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
-------
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
-------
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
-------
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
-------
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
-------
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
Pollution on Materials and the Economy." In:
Air Pollution, 2nd edition, Vol. I, A. C. Stern
(ed.), Academic Press, New York, 1968, pp. 617-
654.
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.
1962.
4. Serada, P. J. "Atmospheric Factors Affecting
the Corrosion of Steel." Ind. Eng. Chem., Vol.
2, pp. 157-160, Feb. 1960.
5. Greenblatt, J. H. and Pearlman, K. "The Influ-
ence of Atmospheric Contaminants on the Cor-
rosion of Steel." Chem. Canada, Vol. 14, pp.
21-23, Nov. 1962.
6. Vernon, W. H. J. "The Corrosion of Metals, Lec-
ture I." J. Eoy. Soc. Arts, pp. 578-610, July 1,
1949.
7. Sanyal, B. and Bhardwar, D. V. "The Corrosion
of Metals in Synthetic Atmospheres Containing
Sulphur Dioxide." J. Sci. Ind. Res. (New Delhi),
Vol. ISA, pp. 69-74, Feb. 1959.
8. Preston, R. St. J. and Sanyal, B. "Atmospheric
Corrosion by Nuclei." J. Appl. Chem., Vol. 6, pp.
26-44, Jan. 1956.
9. Vernon, W. H. J. "A Laboratory Study of the
Atmospheric Corrosion of Metals, Parts II and
III." Trans. Faraday Soc., Vol. 31, pp. 1668-
1700, Dec. 1935.
10. Vernon, W. H. J. "The Atmospheric Corrosion
of Metals." Soc. Chem. Ind. (Chem. Eng.
Group), Prof., Vol. 19, pp. 14-22, 1937.
11. Tice, E. A. "Effects of Air Pollution on the
Atmospheric Corrosion Behavior of Some Metals
and Alloys." J. Air Pollution Control Assoc.,
Vol. 12, pp. 553-559, Dec. 1962.
12. "Symposium on Atmospheric Corrosion of Non-
Ferrous Metals." Spec. Tech. Pub. 175. (Pre-
sented at the 58th Annual Meeting, American
Society for Testing Materials, Atlantic City,
N. J., June 29, 1955.)
13. 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.
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
-------
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
-------
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
-------
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
-------
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
-------
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
-------
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
-------
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
-------
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
-------
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
-------
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
-------
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
-------
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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22. Mead, J. "Control of Respiratory Frequency."
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87
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Chapter 7
TOXICOLOGICAL EFFECTS OF SULFUR OXIDES
ON MAN
-------
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-
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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
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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
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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
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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
-------
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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102
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Chapter 8
COMBINED EFFECTS OF EXPERIMENTAL EXPOSURES TO
SULFUR OXIDES AND PARTICULATE MATTER ON MAN
AND ANIMALS
-------
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
-------
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
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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
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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
-------
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
-------
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
-------
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
-------
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
-------
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
-------
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
-------
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
-------
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.
: RESPIRATORY
> 1
'
1
1
J
: 1
: i 1
0 10 20 30 (
CARDIOVASCULAR
]
I
I
1
) 10 C
G ASTROI NTESTI N A L
j
I
I
I I
) 10 20 3
KAWASAKI
YOKOHAMA
FUJINO
KAINAN
DA I TO
0
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
-------
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
-------
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
-------
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
< 70
in
u.
o 60
40
CO
m 30
co
20
£10
D_
CO
£ 0
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
-------
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
-------
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
-------
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
-------
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.
153
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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-
154
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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
155
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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)
156
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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
157
-------
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
158
-------
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 \ -
-------
APPENDICES
-------
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
167
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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
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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
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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
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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
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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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