External Review Draft No. 1
                                              April 1980
Draft
Do Not Quote or Cite
            Air Quality Criteria
          for Particulate Matter
             and Sulfur Oxides
                      Volume  I
           Summary and Conclusions
                          NOTICE

This document is a preliminary draft. It has not been formally released by EPA and should not at this stage be
cons oied to represent Agency policy. It is being circulated for comment on its technical accuracy and
polity implications.
              Environmental Criteria and Assessment Office
             Office of Health and Environmental Assessment
                 Office of Research and Development
                 U.S. Environmental Protection Agency
                 Research Triangle Park, N.C. 27711

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Draft
Do Not Quote or Cite
                                External Review Draft No. 1
                                                April 1980
             Air  Quality Criteria
           for Participate  Matter
              and Sulfur Oxides
                       Volume I
            Summary and Conclusions
                           NOTICE

This document is a preliminary draft. It has not been formally released by EPA and should not at this stage be
construed to represent Agency policy. It is being circulated for comment on its technical accuracy and policy
implications.
                Environmental Criteria and Assessment Office
                Office of Health and Environmental Assessment
                   Office of Research and Development
                  U.S. Environmental Protection Agency
                   Research Triangle Park, N.C. 27711

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                               PREFACE

          AIR QUALITY CRITERIA FOR PARTICIPATE MATTER AND SULFUR OXIDES



     This criteria document has been prepared in response to Sections

108 and 109 of the 1977 Clean Air Act Amendments.   The 1977 Amendments

modified Section 109 of the 1970 Clean Air Act by adding the following

subsection:

          "Not later than December 31, 1980, and at five-year intervals
          thereafter, the Administrator shall complete a thorough review
          of the criteria published under section 108 and the national
          ambient air quality standards promulgated under this section
          and shall make such revisions in such criteria and standards
          and promulgate such new standards as may be appropriate in
          accordance with section 108 and subsection (b) of this section...."

     The goal of the Clean Air Act is to protect public health and

welfare and enhance the quality of the nation's air.  Under the Clean

Air Act, the Environmental Protection Agency is responsible for reviewing

air quality criteria and establishing, on a nationwide basis, ambient

air quality standards protective of health  (national primary ambient air

quality standards) and welfare (national secondary ambient air quality

standards).  To meet the national ambient air quality standards, the

States and Territories are responsible for developing pollutant emission

limiting regulations and strategies for controlling particular sources.

     The first step in carrying out the nation's air quality management

program is to identify specific pollutants which, in the words of the

Clean Air Act, "may reasonably be anticipated to endanger the public

health or welfare." Particulate matter and sulfur oxides have been

identified as such pollutants since 1971.  Once a pollutant is  "listed"

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under Section 108(a) of the Clean Air Act, EPA publishes an air quality
criteria document which forms the scientific basis for the national
ambient air quality standard.  The Act requires the criteria document to
contain the "latest scientific knowledge useful in indicating the kind
and extent of all identifiable effects on public health or welfare."
     Separate criteria documents for sulfur oxides and particulate
matter were published in 1969.  These documents, Air Quality Criteria
for Sulfur Oxides (AP-50) and Air Quality Criteria for Particulate
Matter (AP-49), were the bases for the national ambient air quality
standards for sulfur oxides (SO ) and total suspended particulate matter
                               /\
(TSP) promulgated in 1971.  In this present review of criteria, EPA has
combined information on sulfur oxides and particulate matter into a
single document.  Sulfur oxides and particulate matter have many common
sources, such as combustion of fossil fuels, and they often exert a
combined action which adversely affects man and his environment.
     Manmade emissions of sulfur oxides come primarily from burning oil
and coal, while airborne particulate matter emanates from virtually all
of man's industrial  activities. Sulfur oxides exist in the atmosphere as
gaseous sulfur dioxide (S02) and as other sulfur compounds.  Much of the
sulfur from the combustion of fossil fuels enters the atmosphere as SOp.
About two-thirds of these emissions are deposited in the region of their
origin.  Of the S02 which enters the atmosphere, it has been suggested
that approximately one-third of it is converted to sulfates.
     The primary objective of this air quality criteria document is to
identify the effects of particulate matter and sulfur oxides on the
public health and welfare and provide a sound scientific basis for the
                                        IV

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consideration of National Ambient Air Quality Standards for these pollutants.
In addition to updating and reviewing the scientific evidence for health
and welfare effects, the document discusses sources, emissions and exposures
for these pollutants.
     This document is presented in four volumes.   Volume I, "Summary and
Conclusions" provides an overview of the document and its major findings.
Volume II focuses on measurement methods; sources and emissions; concentrations
and exposures, and transport, transformation, and removal mechanisms.  Volume
III examines the impact on the public welfare, covering effects on ecosystems
and vegetation, acidic precipitation, visibility impairment, climatological
effects, and effects in materials.  This information is intended to identify
criteria for development of National Secondary Ambient Air Quality Standards.
Volume IV presents the effects on human health by examing deposition, animal
and human experimental studies and epidemiological studies.  This volume
provides EPA's Administrator with information to propose and promulgate
National Primary Ambient Air Quality Standards.
     EPA gratefully  acknowledges the efforts and contributions of all
persons and groups who have participated in the preparation of this
document. The Environmental Protection Agency assumes full responsibility
for its content.

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                              CONTENTS
INTRODUCTION, EXECUTIVE SUMMARY,  AND CONCLUSIONS	   1-1
1.1  INTRODUCTION	   1-1
1. 2  HISTORICAL PERSPECTIVE	   1-3
1.3  SO  AND PM AIR QUALITY ASPECTS	  1-16
     1.5.1  Chemistry and Analytical Methods	  1-17
     1.3.2  Air Quality Measurement Applications	  1-19
            1.3.2.1  British Approaches	  1-20
            1. 3. 2. 2  American Approaches	  1-30
            1.3.2.3  BS-TSP Comparison Studies	  1-39
     1.3.3  Sources and Emissions	  1-43
     1.3.4  Environmental Concentrations and Exposure	  1-45
     1.3.5  Transmission Through  the Atmosphere	  1-47
1.4  WELFARE EFFECTS ASPECTS	  1-49
     1.4.1  Effects on Vegetation	  1^49
     1.4.2  Acidic Precipitation	  1-77
     1.4.3  Effects on Visibility and Climate	  1-84
     1.4.4  Materials Damage and  Soiling Effects	  1-87
1.5  HEALTH EFFECTS ASPECTS	  1-90
     1.5.1  Respiratory Tract Deposition and Biological Fate	  1-91
     1. 5. 2  Animal  Toxicology Studies	  1-93
            1.5.2.1  Effects of Acute and Chronic Exposure to
                     Particles or SOp	   1-95
            1.5.2.2  Effects of Exposures to Combinations of SO
                     and Particles	....   1-103
     1.5.3  Studies on the Oncogenic Properties of SO  and PM	   1-107
     1.5.4  Experimental Investigations of Human Subjects	   1-108
     1.5.5  Community Health Observational Studies	   1-113
            1.5.5.1  Overview Summary of Chapter 14 Contents	   1-115
            1.5.5.2  Methodological Factors Impacting
                     Interpretation of Results	   1-133
            1.5.5.3  Quantitative Dose-Response Relationships
                     Defined by Community Health Studies	    1-136

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                             LIST OF TABLES

Jable                                                                      Page

1-1  Summary of evaluation of sources, magnitudes, and directional
     biases of errors associated with British SCL measurements	      1-22

1-2  Summary  of evaluation of sources, magnitudes, and directional
     biases of errors associated with American S0? measurements	      1-27

1-3  Summary of evaluation of sources, magnitudes, and directional
     biases of errors associated with British smoke (particulate)
     measurements	      1-32

1-4  Summary of evaluation of sources, magnitudes, and directional
     biases of errors associated with American total suspended
     particulate (TSP) measurements	      1-36

1-5  Dose-response information summarized from literature pertaining
     to cultivated agronomic crops  as related to folilar, yield, and
     specific effects induced by increasing S09 dose	      1-52
                                              c.
1-6  Dose-response  information summarized from literature pertaining
     to forest tree species as related to foliar, yield, and specific
     effects induced by increasing S0? dose	      1-63

1-7  Dose-response  information summarized from literature
     pertaining to  native plants as related to foliar, yield
     and specific effects induced by increasing S02 dose	      1-69

1-8  Summary of effects of acute exposure to < mg/m  particles3
     in animals	      1-96

1-9  Summary of effects of chronic exposure to < mg/m  particles3
     in animals	      1-98
                                                  3
1-10 Summary of effects of exposure to < 13.1 mg/m  (5 ppm)
     sulfur dioxide in animals	      1-99

1-11 Summary of effects of combinations of particles3 (< mg/m ) and
     sulfur dioxide (13.1 mg/m  , 5 ppm) in animals	     1-104

1-12 Pulmonary effects of aerosols	     1-109

1-13 Effects of S02	     1-110

1-14 Pulmonary effects of SO,, and other air pollutants	     1-111
                                      VII

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l-14a  Qualitative association of geographic differences in mortality
       with residence in areas of heavy air pollution	  1-117

1-15   Qualitative studies of air pollution and acute respiratory
       disease	  1-120

1-16   Summary table - acute exposure effects	  1-123

1-17   Qualitative studies of air pollution and prevalence of chronic
       respiratory symptoms and pulmonary function declines	  1-127

1-18   Summary table - chronic exposure effects	  1-131

1-19   Summary of various reviewers'  evaluations of quantitative
       dose-response relationships derived from studies of
       mortality effects associated with acute exposures to
       S0? and parti culate matter	  1-140

1-20   Summary of various reviewers'  evaluations of quantitative
       dose-response relationships derived from studies of
       morbidity effects associated with acute exposures to
       SO™ and parti cul ate matter	  1-141

1-21   Summary of various reviewers'  evaluations of quantitative
       dose-response relationships derived from studies of
       morbidity effects associated with chronic exposures to
       S02 and particulate matter	  1-142

1-22   Expected effects of air pollutants on health in selected
       segments of the population:  effects of short-term exposures	  1-150

1-23   Expected effects of air pollutants on health in selected
       segments of the population:  effects of long-term exposures	  1-151

1-24   World Health Organization Guidelines for exposure limits
       consistent with the protection of public health	  1-152

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                               LIST OF FIGURES

Number                                                                     Page

1-1   Comparison of smoke calibration curves for Eel  reflectometer,
      Whatman No. 1 paper and a 1-in diameter filter.   From WSL (1967).
      The computer followed curve D during 1961-64 instead of the
      correct curve(s) B and C	   1-29

1-2   Representative examples of BS/TSP relationships defined by linear
      regression analyses employed to fit BS/TSP comparison data points
      as described in published reports	   1-40

1-3   Measurements of British Smoke vs Hi-vol TSP, showing a consistent
      relation between these measures over the entire range of reported
      observations.  Most points shown are annual mean values; see text
      for discussion	   1-42

1-4   Comparison of interpretations of studies evaluated by Holland
      et al. (1979), WHO (1979), and other reviews such as those
      in the NRC/NAS documents and the present chapter	  1-149
                                      IX

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                                   CONTENTS
                          VOLUMES I,  II,  III,  AND IV
Volume I.     Summary and Conclusions
     Chapter 1.   Introduction,  Executive Summary, and Conclusions	   1-1

Volume II.    Air Quality
     Chapter 2.   Physical and Chemical  Properties of Sulfur Oxides and
                 Particulate Matter and Analytical Techniques for Their
                 Measurement	 .   2-1
     Chapter 3.   Critical Assessment of Practical Applications of Sulfur
                 Oxides and Particulate Matter Measurement Techniques...   3-1
     Chapter 4.   Sources and Emissions	   4-1
     Chapter 5.   Environmental  Concentration and Exposure	   5-1
     Chapter 6.   Transmission Through the Atmosphere	   6-1

Volume III.  Welfare Effects
     Chapter 7.   Effects on Vegetation	   7-1
     Chapter 8.   Acidic Precipitation	   8-1
     Chapter 9.   Effects on Visibility  and Climate	   9-1
     Chapter 10. Effects on Materials	  10-1

Volume IV.    Health Effects
     Chapter 11. Respiratory Deposition and Biological Fate of Inhaled
                 Aerosol s and SO-	  11-1
     Chapter 12. Toxicological  Studies	  12-1
     Chapter 13. Controlled Human Studies	  13-1
     Chapter 14. Epidemiological Studies of the Effects of Atmospheric
                 Concentrations of Sulfur Dioxide and Particulate Matter
                 on Human Health	  14-1

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                        CONTRIBUTORS AND  REVIEWERS
Mr. John Acquavella
Health Effects Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Roy E. Albert
Institute of Environmental Medicine
New York University Medical Center
New York, New York  10016

Dr. Martin Alexander
Department of Agronomy
Cornell University
Ithaca, New York  14850

Dr. A. P. Altshuller
Environmental Sciences Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. David S. Anthony
Department of Botany
University of Florida
Gainesville, Florida  32611

Mr. John D. Bachmann
Strategies and Air Standards Division
Office of Air Quality Planning and Standards
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Mr. Allen C. Basala
Strategies and Air Standards Division
Office of Air Quality Planning and Standards
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Mr. Neil Berg
Monitoring and Data Analysis Division
Office of Air Quality Planning and Standards
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Mr. Michael A. Berry
Environmental Criteria and Assessment Office
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711
                                       XI

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Mr. Francis M.  Black
Environmental  Sciences Research Laboratory
U.S. Environmental  Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Joseph Blair
Environmental  Division
U. S. Department of Energy
Washington, D.C.  20545

Dr. Edward Bobalek
Industrial Environmental Research Laboratory
U.S. Environmental  Protection Agency
Research Triangle Park, North Carolina  27711

Ms. F. Vandiver P.  Bradow
Environmental  Criteria and Assessment Office
U.S. Environmental  Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Ronald L.  Bradow
Environmental  Sciences Research Laboratory
U.S. Environmental  Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Robert Bruce
Environmental  Criteria and Assessment Office
U.S. Environmental  Protection Agency
Research Triangle Park, North Carolina  27711

Mr. Angelo Capparella
Environmental  Criteria and Assessment Office
U.S. Environmental  Protection Agency
Research Triangle Park, North'Carolina  27711

Dr. Robert Chapman
Health Effects  Research Laboratory
U.S. Environmental  Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Robert J.  Charlson
Department of  Environmental Medicine
University of Washington
Seattle, Washington 98195

Dr. Peter Coffey
New York State  Department of Environmental Conservation
Division of Air Resources
Albany, New York 12233

Mr. Chatten Cowherd
Midwest Research Institute
425 Volker Boulevard
Kansas City, Missouri  64110

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Dr. Ellis B.  Cowling
School of Forest  Resources
North Carolina  State  University
Raleigh, North  Carolina  27650

Mr. William M.  Cox
Monitoring and  Data Analysis Division
Office of Air Quality Planning and Standards
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. T. Timothy  Crocker
Department of Community and Environmental Medicine
Irvine, California  92664

Mr. Stanley T.  Cuffe
Emission Standards and Engineering Division
Office of Air Quality Planning and Standards
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Thomas C. Curran
Monitoring and  Data Analysis Division
Office of Air Quality Planning and Standards
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Michael Davis
Environmental Criteria and Assessment Office
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Gerrold A.  Demarrais
National Oceanic  and  Atmospheric Administration
U. S. Department  Of Commerce

Dr. Jerrold L.  Dodd
Natural Resources Ecology Laboratory
Colorado State  University
Fort Collins, Colorado 80523

Dr. Thomas G. Dzubay
Environmental Sciences Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Mr. Thomas G. Ellestad
Environmental Sciences Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. John Evans
School  of Public  Health
Harvard University
Boston, Massachusetts  02115

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Dr. Lance Evans
Department of Energy and Environment
Brookhaven National Laboratory
Upton, New York  11973

Mr. Douglas Fennel!
Environmental Criteria and Assessment Office
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina 27711

Dr. Benjamin G.  Ferris, Jr.
School of Public Health
Harvard University
Boston, Massachusetts  02115

Mr. Patrick Festa
New York Department of Environmental Conservation
Division of Fish and Wildlife
Albany, New York  12233

Mr. Terrence Fitz-Simmons
Environmental Monitoring Systems Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Mr. Christopher R. Fortune
Northrop Services, Inc.-Environmental Sciences
P. 0.  Box 12313
Research Triangle Park, North Carolina  27709

Dr. Robert Frank
Department of Environmental Health
University of Washington
Seattle, Washington  98195

Dr. Warren Galke
Environmental Criteria and Assessment Office
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Mr. Phil Galvin
New York Department of Environmental Conservation
Division of Air Resources
Albany, New York  12233

Dr. Donald Gardner
Health Effects Research Laboratory
U.S.  Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. J.H.B.  Garner
Environmental  Criteria and Assessment Office
U.S.  Environmental Protection Agency
Research Triangle Park, North Carolina  27711
                                      xiv

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Dr. Donald Gillette
Health Effects Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Judy Graham
Health Effects Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Lester D. Grant
Environmental Criteria and Assessment Office
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Armin Gropp
Department of Chemistry
University of Miami
Miami, Florida  33124

Dr. Jack Hackney
Rancho Los Amigos Hospital
Downey. California  90242

Mr. Bertil Hagerhall
Ministry of  Agriculture
Pack
S-163 20 Stockholm
Sweden

Dr. Douglas  Hammer
2910 Wycliff Road
Raleigh, North Carolina  27607

Mr. R. P. Hangebrauck
Industrial Environmental Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Mr. Thomas A. Hartlage
Environmental Monitoring Systems Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Victor Hasselblad
Health Effects Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Thomas R. Hauser
Environmental Monitoring Systems Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711
                                      xv

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Dr. Car] Hayes
Health Effects Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Fred H. Haynie
Environmental Sciences Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Walter Heck
Department of Botany
North Carolina State University
Raleigh, North Carolina  27650

Dr. Howard Heggestad
USDA-SAE
The Plant Stress Laboratory
Plant Physiology Institute
BeltsviTle, Maryland  20705

Dr. George R. Hendrey
Department of Energy and Environment
Brookhaven National Laboratory
Upton, New York  11973

Dr. Ian Higgins
Department of Epidemiology
School of Public Health
University of Michigan
Ann Arbor, Michigan  48109

Mrs. Patricia Hodgson
Editorial Associates
Chapel Hill, North Carolina  27514

Mr. George C. Holzworth
Environmental Sciences Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Robert Horton
Health Effects Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Steven M. Horvath
Institute of Environmental Stress
University of California
Santa Barbara, California  93106
                                        XV7

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Dr. F. Gordon Hueter
Health Effects Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Janja Husar
CAPITA
Washington University
St. Louis, Missouri  63130

Dr. Rudolf Husar
Department of Mechanical Engineering
Washington University
St. Louis, Missouri  63130

Dr. William T. Ingram
Consulting Engineer
7 North Drive
Whitestone, New York 11357

Dr. Patricia M. Irving
Argonne National Laboratory
9700 South Cass Avenue
Argonne, Illinois  60439

Dr. Jay Jacobson
Boyce Thompson Institute
Cornell University
Ithaca, New York  14850

Mr. James Kawecki
Biospherics, Inc.
4928 Wyaconda Road
Rockville, Maryland  20852

Dr. Sagar V. Krupa
Department of Plant Pathology
University of Minnesota
St. Paul, Minnesota  55108

Dr. Edmund J. LaVoie
Section of Metabolic Biochemistry
American Health Foundation
Dana Road
Valhalla, New York  10592

Dr. Michael D. Lebowitz
Arizona Health Sciences Center
1501 North Campbell
Tucson, Arizona  85724
                                         xvii

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Dr. Robert E. Lee
Health Effects Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Allan H.  Legge
Environmental Science Center
University of Calgary
Calgary, Alberta, Canada  T2N 1N4

Ms. Peggy Le Sueur
Atmospheric Environment Service
Downsview, Ontario, Canada  M3H5T4

Dr. Morton Lippmann
Institute of Environmental Medicine
New York University
New York, New York  10016

Dr. James P.  Lodge
385 Broadway
Boulder, Colorado  80903

Dr. Gory J. Love
Institute of Environmental Studies
University of North Carolina
Chapel Hill, North Carolina  27514

Dr. David T.  Mage
Environmental Monitoring Systems Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Delbert McCune
Boyce Thompson Institute
Cornell University
Ithaca, New York  14850

Mr. Frank F.  McElroy
Environmental Monitoring Systems Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. David J.  McKee
Environmental Criteria and Assessment Office
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Mr. Thomas McMullen
Environmental Criteria and Assessment Office
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711
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Dr.  Daniel B. Menzel
Department of Pharmacology
Duke University Medical Center
Durham, North Carolina  27710

Dr.  Edwin L. Meyer
Monitoring and Data Analysis Division
Office of Air Quality Planning and Standards
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr.  Fred Miller
Health Effects Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr.  John 0. Mil liken
Industrial Environmental Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr.  Jarvis Moyers
Department of Chemistry
University of Arizona
Tucson, Arizona 85721

Dr.  Thaddeus J. Murawski
New York State Department of Health
Empire State Plaza
Albany New York  12337

Dr.  David S. Natusch
Department of Chemistry
Colorado State University
Fort Collins, Colorado  80523

Dr.  Stephen  A. Nielsen
Environmental Affairs
Joyce  Environmental Consultants
414 Live Oak Boulevard
Casselberry, Florida   32707

Dr.  Kenneth  Noll
Department of Environmental Engineering
Illinois  Institute  of  Technology
Chicago,  Illinois 60616

Mr.  John  R.  O'Connor
Strategies and Air  Standards Division
Office of Air Quality  Planning and  Standards
U.S. Environmental  Protection Agency
Research Triangle Park, North Carolina  27711
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Mr. Thompson G. Pace
Monitoring and Data Analysis Division
Office of Air Quality Planning and Standards
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Jean Parker
Environmental Criteria and Assessment Office
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Nancy Pate
Strategies and Air Standards Division
Office of Air Quality Planning and Standards
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Thomas W. Peterson
Department of Chemical Engineering
University of Arizona
Tucson, Arizona  85721

Mr. Martin Pfeiffer
New York State Department of Environmental Conservation
Bureau of Fisheries
Raybrook, New York  12977

Dr. Marlene Phillips
Atmospheric Chemistry Division
Environment Canada
Downsview, Ontario, Canada  M3H5T4

Dr. Charles Powers
Environmental Research Laboratory
U.S. Environmental Protection Agency
Corvallis, Oregon 97330

Mr. Larry J. Purdue
Environmental Monitoring Systems Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Mr. John C. Puzak
Environmental Monitoring Systems Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711
                                        xx

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Dr. Otto Raabe
Radiobiology Laboratory
University of California
Davis, California  95616

Mr. Danny Rambo
Environmental Research Laboratory
U.S. Environmental Protection Agency
Corvallis, Oregon  97330

Mr. Kenneth A. Rehme
Environmental Monitoring Systems Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Elmer Robinson
Department of Chemical Engineering
Washington State University
Pullman, Washington  99163

Mr. Charles E. Rodes
Environmental Monitoring Systems Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Mr. Douglas R. Roeck
GCA Corporation
Technology Division
Burlington Road
Bedford, Massachusetts  01730

Mr. J. C. Romanovsky
Environmental Sciences Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. August Rossano
University of Washington
Seattle, Washington  98195

Mr. Joseph D. Sableski
Control Programs Development Division
Office of Air Quality  Planning and Standards
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Mr. Dallas Safriet
Monitoring and Data Analysis Division
Office of Air Quality  Planning and Standards
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711
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Dr. Victor S. Salvin
University of North Carolina at Greensboro
Greensboro, North Carolina 27408

Dr. Shahbeg Sandhu
Health Effects Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Mr. Joseph P. Santodonato
Life and Material Sciences Division
Syracuse Research Corporation
Merrill Lane
Syracuse, New York  13210

Dr. Herbert Schimmel
Neurology Department
Albert Einstein Medical College
26 Usonia Road
Pleasantville, New York 10570

Dr. Carl L. Schofield
Department of Natural Resources
Cornell University
Ithaca, New York  14850

Dr. David Shriner
Environmental Sciences Division
Oak Ridge National Laboratory

Ms. Donna Sivulka
Environmental Criteria and Assessment Office
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. John M. Skelly
Department of Plant Pathology and Physiology
Virginia Polytechnic Institute
Blacksburg, Virginia  24061

Mr. Scott Smith
Biospherics, Inc.
4928 Wyaconda Road
Rockviell. Maryland  20852

Ms. Elaine Smolko
Department of Pharmacology
Duke University Medical Center
Durham, North Carolina
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Dr. Frank Speizer
School of Public Health
Harvard University
Boston, Massachusetts  02115

Dr. John D. Spengler
School of Public Health
Harvard University
Boston, Massachusetts  02115

Mr. Robert K. Stevens
Environmental Sciences Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. George E. Taylor, Jr.
Environmental Sciences Division
Oak Ridge National Laboratory
Oak Ridge, Tennessee  37830

Dr. Larry Thibodeau
School of Public Health
Harvard University
Boston, Massachusetts  02115

Dr. W. Gene Tucker
Industrial Environmental Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Mr. D. Bruce Turner
Environmental Sciences Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Mr. James B. Upham
Environmental Sciences Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. Robert Waller
Toxicology Unit
St. Bartholomew's Hospital
London, England

Mr. Stanley Wall in
Warren Spring Laboratory
Department of Industry
Stevenage, Hertfordshire SGI 2BX
England
                                   xxm

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Dr. Joseph F. Walling
Environmental Sciences Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. James Ware
School of Public Health
Harvard University
Boston, Massachusetts  02115

Dr. David Weber
Office of Air, Land, and Water Use
U.S. Environmental Protection Agency
Washington, D. C. 20460

Dr. Jean Weister
Health Effects Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Mr. R. Murray Wells
Radian Corporation
8500 Shaol Creek Boulevard
Austin, Texas  78766

Dr. Kenneth T. Whitby
Mechanical Engineering Department
University of Minnesota
Minneapolis, Minnesota  55455

Dr. Warren White
CAPITA
Washington, University
St. Louis, Missouri  63130

Dr. Raymond Wilhour
Environmental Research Laboratory
U.S. Environmental Protection Agency
Corvallis, Oregon  97330

Dr. William E. Wilson
Environmental Sciences Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr. John W.  Winchester
Department of Oceanography
Florida State University
Tallahassee, Florida  32306
                                    XXIV

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Mr.  Larry Zaragoza
Strategies and Air Standards Division
Office of Air Quality Planning and Standards
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina  27711

Dr.  William H. Zoller
Chemistry Department
University of Maryland
College Park, Maryland  20742
We wish to thank everyone who contributed their efforts  to  the preparation of
this document,  including the following staff members of  the Environmental
Criteria and Assessment Office, U.S. Environmental  Protection Agency,  Research
Triangle Park,  North Carolina:
Mrs. Dela Bates
Ms. Hope Brown
Ms. Diane Chappell
Ms. Deborah  Doerr
Ms. Mary El ing
Ms. Bettie  Haley
Mr. Allen Hoyt
Ms. Susan Nobs
Ms. Evelynne Rash
Ms. Connie  van Oosten
Ms. Donna Wicker
The  final  draft  of  this  document will cite the many persons outside of the
Environmental  Criteria and Assessment Office who have assisted in its pre-
paration.
                                      xxv

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              1.   INTRODUCTION, EXECUTIVE SUMMARY,  AND  CONCLUSIONS







1.1  INTRODUCTION



     Section 109(d) of the Clean Air Act as amended in  1977 requires  the



Environmental Protection Agency (EPA) to review the air quality criteria  for



sulfur oxides (S0x) and particulate matter (PM) and to  revise related standards,



as appropriate, by December 31, 1980, and at 5-year intervals thereafter.   In



addition, the Administrator may from time to time review and, where appropriate,



modify pertinent criteria under the authority of Section 108(c) of the Clean



Air Act.  Pursuant to the above provisions of the Clean Air Act, the present



document represents an important step in the preparation of the revised



criteria documents for SO  and PM.
                         /\


     The decision to issue a single document for these  two pollutants was



based on several considerations.  These include primarily the recognition



that:  (1) both SO  and PM originate from many common emission sources such



as the burning of fossil fuels; (2)  SO  and PM levels  frequently covary in



ambient air; (3) SO  and PM appear to likely act together to adversely affect
                   /^


both man and his environment;  (4), in community health studies and other



types of studies where combined exposure to SO  and PM is a factor, it is



difficult to isolate the effects of one pollutant  from those of the other;



and (5) the combination of sulfur oxides and particulate matter has been



linked with acidic precipitation, which damages aquatic and terrestrial



ecosystems.



     This document critically  reviews scientific information bearing  on



health and welfare criteria that will form  the bases for National  Ambient  Air



Quality Standards (NAAQS) for  S0x and PM.
                                    1-1

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     The information reviewed concerns:   (1)  pertinent air quality Information;



(2) welfare effects associated with S0x and PM;  and (3) health effects associated



with exposure to those air pollutants.   The present volume (Volume I) includes



the general introduction, executive summary and  conclusions for the entire



document.  The second volume (Volume II) on air  quality aspects, Includes



chapters discussing:  physical properties of SOX and PM and air quality



measurement techniques for each; critical appraisal of practical applications



of such measurement methods;  sources of SO  and PM emissions;  related
                                           /\


atmsopheric transport and transformation processes;  and ambient air



concentrations and exposure levels.  Volume III, concerning welfare effects,



contains document chapters on:  SO  and PM effects on vegetation and natural



ecosystems;  acidic precipitation formation and  effects;  effects on visibility



and climate;  and materials damage effects.  The last volume (Volume IV),



dealing with health effects of SO  and PM contains chapters on:  the uptake,
                                 )\.


deposition, and absorption of SO  and PM health  effects; human clinical



(experimental) studies of SO  and PM health effects; and pertinent community
                            f\


health (epidemiology) studies.



     In the present volume, there is first provided a brief historical review



of important events which have (1) contributed to concern about the health



and welfare effects of SO  and PM;  (2) stimulated extensive and highly



varied related research efforts;  and (3) helped to shape social/  legal



actions taken to eliminate or ameliorate such effects as major public  health



and welfare problems.  It is hoped that such a historical review will  provide



background material useful in assisting readers, especially those  not  well



familiar with the present subject matter, to develop a better Informed vantage



point or perspective from which to view the information  subsequently  presented



in this document.  The major points addressed by such information  and  important
                                   1-2

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conclusions regarding them, as discussed in each of the remaining three



volumes of the document, are then summarized following the historical



perspective discussion presented below.




     Before proceeding with the historical review, it should be mentioned



that a number of other important reviews and commentaries concerning the



health and welfare effects of SO  and PM have appeared during the past decade.



In that regard, the reader is referred to certain review articles and documents



appearing in the mid-to late 1970s for additional information on the present



subject matter.  Such materials include critical reviews and commentaries



written  by Rail (1974), Higgins et al.  (1974), Goldsmith and Friberg (1977),



Ferris (1978), and Waller (1978).  They also include the following evaluative



documents appearing in 1978:  an American Thoraic Society (ATS) review of



Health Effects of Air Pollution (1978); a National Research Council/National



Academy of Science (NRS/NAS) document on Airborne Particles (1978); and an



NRC/NAS document on Sulfur Oxides (1978).  More recent such reviews and



commentary appearing in 1979 include:  the 1979 World Health Organization



(WHO) document, Environmental Health (8): Sulfur Oxides and Suspended



Particulate Matter;  a report by Holland et al.  (1979) written for the



American Iron and Steel Institute and appearing in the American Journal  of



Epidemiology; and a reply to that report in the same journal by Shy (1979).



1.2  HISTORICAL PERSPECTIVE



     There is little question that severe air pollution generated by anthro-



pogenic activities has long exerted significant, even lethal, adverse effects



on the health and welfare of many industrial societies.   It has only been
                                   1-3

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within the past 50 years or so, however, that sufficient recognition of suet


effects as major public problems has stimulated both (1) extensive research to


better understand such problems and (2) strong governmental  and private


sector actions to control or eliminate them.


     It is not surprising that the air pollution incidents most often cited


as signal events precipitating great concern about air pollution problems and


strong actions in response to them occurred among the most heavily industrialized


societies then extant, i.e., in Western Europe, Great Britain and the United


States.  It is also easy to understand the urgency associated with taking


strong actions to control such problems in light of the magnitude and seriousness


of the effects experienced during those incidents.


     For example, in describing the effects of a thick fog that covered the


industrial Meuse Valley in Belgium during early December 1930, Firket (1931)


noted that several hundred people were afflicted by suddenly appearing acute


respiratory symptoms, complicated in many instances by serious cardiovascular


failure.   Firket (1931) further noted:  "More than sixty died on the 4th and


5th of December after only a few hours of sickness.  A sizeable number of


livestock had to be slaughtered."  Also, taking into account that mortality


rates were more than 10 times normal, Firket projected that over 3,000 deaths


would occur if a similar fog were to occur in a city the size of London.


     Twenty-two years later, such an event did occur in London and more than


4,000 deaths appeared to be attributable to the four-day London Fog of December


1952, according to Logan (1953).  Logan further noted:  "The incident was a


catastrophe of the first magnitude in which, for a few days, death rates
 £.

attained  a level  that has been exceeded only rarely during the past hundred
                                   1-4

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years - for example, at the height of the cholera epidemic  of  1854  and  of the
influenza epidemic of 1918-19."  Indeed, the death rate rivaled  or  exceeded
that on many of the worst days of other catastrophic events afflicting  London
injts more recent past, e.g., the Battle of Britain during World War II.
     Similar catastrophic air pollution incidents also occurred  around  the
same time in the United States.  Almost half of the residents  of Donora,
Pennsylvania, for example, were afflicted with respiratory  symptoms as  the
result of a "smog" covering the coke- and steel-producing Monongahela River
Valley during October, 1948 (Schrenk et al., 1949).  Twenty people  in the
small town of about 10,000 population died during the final week of the
"Donora Smog Episode," in comparison to the 2 or 3 deaths normally  expected
for the same period.  Over the next few years, catastrophic air  pollution
incidents also affected other United States communities.  One  such  case was  a
dramatic increase in infant mortality in Detroit, Mich., attributed to  a
"pollution incident" in September 1952 (Int. Joint Commission, 1960).   This
was followed by marked increases in respiratory distress cases and  fatalities
attributable (Greenburg et al., 1962) to air pollution occuring  on  an  even
larger scale during a "Thanksgiving Day" pollution episode  in  New  York City
in November, 1953—an experience later to be repeated several  more  times in
New York City during the early 1960s.
     It was clear from the above incidents and others occurring elsewhere in
the industrialized world that air pollution, especially under  certain weather
conditions leading to stagnant masses of pollutant-laden "fog" or "smog", was
capable of causing incidents rivaling natural disease epidemics or man-made
                                   1-5

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wartime disasters that constituted national  emergencies for the affected
societies.  Equally clear was the urgent need to take immediate action to
avert or reduce in severity future air pollution disasters.   Among the first
to_act were two of the most severely affected countries, Great Britain and
the United States.
     Many parallel historical threads can be discerned regarding the paths
taken by the two nations in trying to cope with air pollution problems,
including a number of similar mistakes as well as successes. In each country,
for example,, there occurred extensive expansion of epidemiological and
toxicological research aimed at identifying components of the killer smogs or
fogs responsible for the observed lethal effects and increased morbidity.
Also, in each country, although occurring within different specific time
frames and at different specific paces or rates, there ensued the upgrading
and expansion of air quality monitoring networks.  This included the expansion
of monitoring networks capable of indexing high levels of various industrial
pollutants implicated by the historical data as being associated with increased
incidences of both morbidity and mortality.   The latter invariably included
oxides of sulfur and particulate matter present in the killer fogs or smogs
of the 1940s and 1950s, although the relative contributions of each could not
be precisely linked to observed health effects.
     It is important to note in regard to the air quality data that very
precise accuracy and specificity were not then demanded; rather, "benchmark"
ranges of estimates of air pollutant concentrations were acceptable, especially
for indexing the rather high levels of pollution associated with severe
                                   1-6

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morbidity or mortality effects.  It mattered little if the exact amounts  of

S02, for example, were 143 or 781 or 1408 ug/m  plus or minus 5 or 10 percent,

when one was concerned that people would begin to experience severe morbidity

or_even die when S02 or particulate matter exceeded several hundred ug/m  .

Being able to establish that increased mortality or severe morbidity occurred

at, say, a range of 550 to 600 or even 500 to 1000 ug/m  of SOp or particulate

matter in comparison to the incidence of such effects observed at, say, 70 to
                          3
100 or even 50 to 200 ug/m  of the same pollutants was, understandably,

sufficient scientific evidence to support political and social measures

needed to avert  the worst air  pollution episodes.

     Nor was  it  particularly important whether or not SOp, specifically,  or

particulate matter of whatever specific size-range or chemical composition

could be precisely implicated  as the "culprit" causing one or another very

specific health  effect. Rather, it was sufficient to recognize that those

substances might not be any more than representative indicators of the total

mix or  some other potentially  lethal subfraction of pollutants typically

present during the dangerous past pollution  episodes.  Basically, the main

objective, regardless of  specific fine details associated  with various pollution

situations, was  to obtain sufficient information:   (1) to  allow for  reasonable

conclusions to be drawn regarding ranges  of  air  levels of  various pollutants

(or indices)  empirically  linked to  the occurrence  of  severe  health  effects

and (2) to help  serve as  a  guide  in directing pollution  control efforts

toward  sources emitting such pollutants  (or  mixes  containing them).

     In addition to the above  developments,  certain regulatory actions were
  L
taken in response to the  severe air pollution situations in  Britain and  the
                                    1-7

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 United States in the 1950s.  The British acted strongly on a national  scale
 by  passing the Clean Air Act of 1956 which forced implementation of very
 stringent controls on emissions from coal-fired combustion sources, essentially
 eliminating the use of coal for home-heating and many industrial purposes in
 heavily  industrialized and congested urban areas.   The effectiveness of those
 measures was reflected in the resulting declines seen by the early 1960s in
 both atmospheric sulfur oxides and particulate matter and associated mortality
 effects  (WSL, 1967).
     As  for the United States, action initially tended to be taken mostly on
 more restricted geographic bases and consisted mainly of local or state air
 pollution control ordinances being passed, often with the cooperation of
 local industrial leaders, to reduce air pollution.   Among the more notable
 examples were early actions taken to control air pollution in one of the most
 heavily  industrialized regions of the country, the Pittsburgh area.  There,
 and in other areas of Pennsylvania, extensive steel-making and coking operations
 and the burning of locally produced high-sulfur coal contributed to widespread
 elevations in both particuate matter and sulfur dioxide air concentrations.
 Notable improvements in air quality in various American regions were attained
 as the result of such initial actions.  However, simultaneous deterioration
 in air quality in many other communities or states lacking effective pollution
 control  laws, and the growing recognition of air pollution as a multi-state,
 regional  or national problem eventually led to the passage in the  United
 States of the Clean Air Act of 1970 and consequent promulgation of National
Ambient Air Quality Standards for sulfur oxides, particulate matter, and
other air pollutants of widespread concern.
     Subsequent to many of the above actions taken in the 1950s and early
1960s,  questions began to be raised regarding what less severe, but important,
                                   1-8

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effects on human health and welfare might be caused by lower  air  levels  of



oxides of sulfur, particulate matter, and other air pollutants, especially



Under conditions of prolonged periods (months or years) of exposure.   This



included increased recognition of and research on such problems as  SO  and  PM
   _ „                                                                A


effects on vegetation, visibility, and climate, as well as related  materials



damage effects and acidic precipitation formation and effects.  Again, fairly



similar paths were followed in both Great Britain and the United  States  in



trying to deal with such questions.



     In both countries, epidemiologists began to design studies to  either



retrospectively or prospectively define in more precise terms both  qualitative



and quantitative relationships between elevations of various  pollutants  in



the ambient air and specific sublethal health effects, such as acute or



chronic bronchitis, respiratory infections, temporary decrements  in pulmonary



function, and asthma  attacks.  Air quality monitoring networks set  up or



expanded earlier to provide at least representative, but not necessarily



thorough, coverage of geographic areas having varying pollution levels were



often looked to by the epidemiologists to provide requisite,  albeit less than



perfect, quantitative estimates of air quality to help define quantitative



air pollution-effect  relationships.  Only in relatively rare circumstances



were sufficient funds or other resources available to  allow for more  thorough



monitoring coverage to be arranged specifically  for collection of community



air quality data to be coupled with  health endpoint measurements.  Similarly,



expanded demands were placed on air  monitoring capabilities in terms  of  their



being needed to provide requisite  air quality  data for use in evaluating

 t

various welfare effects and related  atmospheric  transport  and transformation



phenomena.
                                    1-9

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     At the same time as the above expansion of research  efforts,  more  precise

estimates of air pollutant levels were being demanded or  expected  from  existing

or expanding air monitoring networks to help index progress  in reductions of

air pollutants in Britain and the United States.   Bearing on this  point,  the

following was later noted in Her Majesty's Report on the  Investigation  of

Atmospheric Pollution 1958-1966 (Warren Spring Laboratory, 1967):

         The industrial provisions of the Clean Air Act 1956 had come
    into force by June 1958, and the first smoke control  areas were
    declared under the domestic provisions in April 1958.  This timetable
    added urgency to the view that the existing survey of air pollution
    throughout the United Kingdom was too blunt an instrument either to
    assess the benefits accruing from the Act or to guide its future
    application, and that a scientifically planned National  Survey was
    necessary.  Such a survey was designed and the co-operation of the
    local authorities concerned was obtained where measurements were
    required in addition to those already being made.  Observations were
    started in the winter of 1962-63.  Not only has the whole pattern of
    co-operative observations been transformed in this way,  but so also
    has the basis of the co-operation:  the local authorities and other
    organizations are now making measurements as required to conform to
    an overall statistical plan.


A growing need was also felt for establishing or maintaining monitoring

systems using sufficiently uniform and reliable measurement approaches to

allow for comparability of air quality data from disparate geographic sites.

This need became perhaps most acutely felt in the United States in the late

1960s in light of the growing prospect of having to attain national ambient

air quality standards at lower air concentrations than were earlier

envisaged.   Pressure to meet such needs and demonstrate the benefits of air

pollution control in the United States intensified greatly with the passage

of the Clean Air Act of 1970.

 f.   Both the above needs and the anticipated use of air quality data in

future epidemiology and welfare effects studies increased the necessity for
                                   1-10

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better air quality data in terms of their specificity,  sensitivity,  accuracy,
precision, and reliability.  Thus, it became increasingly more  important  to
be able to distinguish with confidence between much closer absolute  levels of
afr pollutants even at relatively low ambient air concentrations  (e.g., at
levels around or lower than 100 to 200 pg/m3 of either  S02 or particulate
matter).  In other words, the emerging demands required practical  applications
of available or newly developed measurement techniques  to meet  previously
unheard-of levels of accuracy.  At times expectations may have  exceeded what
could realistically be achieved with field applications of available technology,
especially in comparison to theoretical limits of what  could be achieved  with
particular measurement techniques under ideal laboratory conditions.
     In responding to the above demands, several similar historical  parallels
can again be discerned between the British and American experiences, as well
as some quite significant differences.  In Britain, steps were  taken to
assure that a high degree of uniformity in measurements of pollutants was
maintained or further enhanced; this included the establishment of the National
Air Pollution Survey alluded to above.  As part of this effort, the British
Smoke (BS) filter method, widely used in Britain since  the early 1900s for
the measurement of black suspended particulate matter,  was officially adopted
to monitor air quality across the United Kingdom.  The daily smoke filter has
since been the standard air particulate matter measurement instrument used in
the United Kingdom, and responsibility for quality assurance for the use of
the instrument throughout the entire United  Kingdom was assigned to the
Warren Spring Laboratory (WSL) of the Department of Industry, where central
coordination and evaluation of uniformity, accuracy, and  reliability of  all
National Survey air quality measurement have been carried out since the  late
                                   1-11

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1950s.   Based largely on  WSL  evaluations, the daily smoke filter was later
adopted as a standard also  by the British Standards Institute and became one
of OECD's recommended procedures for measuring  suspended particulate matter.
     The WSL was also instrumental  in  selecting S02 measurement methods for
the British National  Survey air monitoring program.  Under WSL guidance, the
hydrogen peroxide method  was  adopted in  the  early  1960s as the standard
approach for measuring SOp.   This replaced the  lead dioxide  gauge still in
use at many sites in  Britain  (in 1962  there  were about 1200  gauges  in  operation)
The decision to adopt the hydrogen  peroxide  method was based on recommendations
of a WSL-organized "Work  Party" that considered both the deliberations of an
OECD Working Party and detailed comparisons  of  the two methods under field
conditions by WSL.
     Turning to concomitant developments in  the United States  during the past
twenty years, one can discern a  lage in  the  development  of  a standardized
nationwide approach to air  pollution monitoring and control.  During the
1950s and early 1960s numerous air  monitoring  systems established by different
governmental units sprang up  around the  country, often to meet needs associated
with enforcement of newly enacted  air  pollution control  ordinances.  It was
not until the mid-to-late 1960s  that effective procedures were implemented to
feed data obtained from the multiplicity of  air monitoring  sites  operated by
city, county, state,  and  federal  agencies into a central  data bank as  part of
a National Air Survey Network (NASN).   Even  then,  those  data were still often
derived from different measurement methods  used by various  agencies for
monitoring of a given pollutant.   Generally, the high-volume TSP measurement
method developed in the United States  in the 1950s was  used for assessing
airborne particulate  levels;  but,  at  times,  other methods  such as coefficient
of haze (CoH) measurements  were  also  employed to assess  particulate levels.
                                   1-12

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Similarly, several approaches, e.g., the West-Gaeke or sulfation methods,

were used to measure SOp.


     Considerably greater uniformity in monitoring approaches has,  however,


beeii achieved over the past decade or so through the publication of "Federal


Reference Methods."  Additional efforts were undertaken in the late 1960s  and


early 1970s by EPA and its predecessor Federal agencies to establish a new


nationwide air monitoring network using uniform measurement methods.   That


network was established as part of what became known as EPA's Community


Health and Environment Surveillance System (CHESS) Program.   The "CHESS"


monitoring network, set up in addition to other Federal air sampling stations


used for monitoring compliance with air regulations, included monitoring


sites dispersed in widespread urban and semi-rural areas of the United States


to provide air quality data representative of pollutant exposures experienced


by surrounding population groups.  Various health endpoints were evaluated


for those population groups as part of CHESS Program epidemiology studies.


Thus, the CHESS monitoring network, including sampling sites often situated


near or along side local or state monitoring sites, was designed to provide


air quality data  from a nationwide network using uniform measuring methods


that supplemented other data entered into the NASN data bank.  The hi-volume


TSP sampling procedure was usually employed in the CHESS Program to monitor


atmospheric particulate matter levels and the West-Gaeke method was generally


employed for SO,, measurements, along with additional procedures for estimating


suspended sulfates discussed  later.  The series of major air pollution/health


effects studies carried out between 1969 and 1975 as part of the CHESS Program,
 «.

and coupling such aerometric measurements with community health surveys,  have


been considered by many experts as the most comprehensive of their kind.
                                   1-13

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      It should be noted, however,  that a number of methodological  problems

 were engendered by attempts to rapidly deploy air monitoring stations at

 widespread sites across the United States and to bring them up to  full operational

 status in time to collect air quality data to be coupled with health surveys

 as part of the CHESS Program.   Of  particular concern are problems  which were

 detected regarding the collection  of health endpoint data and certain errors

 in air quality data generated from CHESS network sampling sites—several

 types of errors which were either  not detected at all during the CHESS health

 endpoint data collection period (1969-75) or were only detected and corrected

 through improved quality control procedures implemented and applied in the

 last few years of the Program (i.e.  1972 or 1973 onward).*  Improvements in

 the air quality data obtained during the last few years of the CHESS Program

 and, also, in other EPA air monitoring efforts,, were accomplished via a

 substantially expanded in-house EPA quality assurance program.  That program,

 conducted by EPA's Environmental Monitoring Systems Laboratory in Research

 Triangle Park, N.C., has since provided quality assurance backup for all of

 EPA's research and nationwide enforcement air monitoring activities.
 : s discussed in more detail later in Chapters 3 and 14, the matter of errors
 in air quality data collected as part of the CHESS Program (together with
other concerns regarding the collection of health endpoint data in CHESS
; jdies) contributed to considerable controversy regarding the validity and
accuracy of results of early CHESS studies, as interpreted and reported in a
1974 EPA monograph entitled "Health Consequences of Sulfur Oxides:  A Report
from CHESS" 1970-71, U.S.EPA Document No.  EPA-650/1-74-004 (May 1974).  The
controversy eventually led to the 1974 "CHESS Monograph" becoming the subject
of U.S.  Congressional oversight hearings in 1976.  Subcommittees of the U.S.
Ho&se of Representatives Committee on Science and Technology produced a report
on the Monograph,  other aspects of the CHESS Program, and EPA's air pollution
research programs  generally--a report entitled "The Environmental Protection
Agency's Research  Program with Primary Emphasis on the Community Health and
Surveillance System (CHESS):  An Investigative Report."  Of primary importance
for the present discussion, that report, widely referred to either as the
                                    1-14

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      From the foregoing,  it can be seen that  similar  needs and demands as

 those felt by the British in conjunction with the passage of their Clean Air

 Act of 1956 were later experienced by the Americans with the passage of their

 Clean Air Act of 1970.  Remarkably similar paths were also followed in both

 countries in responding to those needs; that  is, in both cases intensive

 efforts were carried out to rapidly expand and improve air monitoring

 capabilities, including introduction of more  uniformity in measurement

 approaches across geographic regions along with increased quality control

 efforts to help assure the validity of the aerometry  data collected.  Also,

 in each case it was contemplated that such improved and uniformly obtained

 aerometry data from throughout the two nations could  serve as  useful data

 pools to be coupled with welfare effects studies and  community health

 epidemiology studies aimed at both (1) improving knowledge of  quantitative

 air pollution/effects relationships and (2) demonstrating the  benefits to
*(continued)

"Brown Committee Report" or the "Investigative Report" (IR),  contained various
comments regarding sources of error in CHESS Program air quality and health
data and
quality control problems associated with the data collection  and analysis.
The I.R. also contained various recommendations to be implemented by the
Administrator of EPA pursuant to Section 10 of the Environmental Research,
Development, and Demonstration Authorization Act of 1978 ("ERDDAA," P.L.
95-155, 91 Stat. 1257, November 8, 1977). ERDDAA also requires that EPA and
the Agency's Science Advisory Board report to Congress on the implementation
of the IR recommendations.

     One recommendation of the IR was that an addendum to the sulfur oxides
monograph be published, to be used in part to qualify the usefulness of the
CHESS studies, and to apprise the public of the controversy surrounding
CHESS.  An addendum has been published, and is available from EPA, as
announced in the Federal Register of April 2, 1980, 45 F.R. 21702.  The addendum
isHncorporated by reference in this document in partial qualification of the
CHESS studies cited herein, and is part of the public file (or docket) established
for revision of this criteria document.  The addendum contains the full text of
the IR, reports to Congress by EPA on its implementation of the IR recommendations,
and a report to Congress by EPA's Science Advisory Board on the same subject.
See also Appendix A of of Chapter 14 of the present draft criteria document.
                                    1-15

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be accrued from implementation of the respective  Clean Air Acts.   In addition,



as will become apparent below, remarkably similar problems were encountered



and responded to with roughly comparable degrees  of success in the course of



practical applications of air pollution measurement techniques undertaken to



achieve the above objectives.



     In addition to the above developments in the United Kingdom and the



United States, many analogous steps have been taken by numerous other



industrialized countries over the past 30-40 years to cope with air pollution



problems.  In that regard, again many parallels (and dissimilarities) in the



historical evolution of their air monitoring programs, epidemiologic research



efforts, and political/legal regulatory control activities could be noted in



comparison to developments in Britain and the United States.   However, a



historical review of the evolution of such activities or analysis below of



results obtained with practical applications of sulfur oxides or particulate



matter measurement approaches or with community health studies outside



Britain and the United States is beyond the scope of present purposes.



1.3  SO  AND PM AIR QUALITY ASPECTS
       /\


     Turning now to the major points addressed in the remainder of this



document, much of the key information contained in Volume II, on air quality



aspects, is summarized below under Subsections 1.3.1 to 1.3.7.  Particular



emphasis is placed here on the critical assessment of practical applications



of air quality measurement techniques of crucial  later importance in



evaluating community health studies.  Of additional special interest below



are the discussions on transport and transformation phenomena and ambient air

 <.

concentration and human exposure data.
                                   1-16

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1.3.1  Chemistry and Analytical Methods



     The chemical and physical properties of SO  and PM determine  their
                                               A


behavior in the atmosphere and biologic toxicologic activity.   Increasing



sophistication of analytical instrumentation and methodology has enhanced  the



understanding of the relationship between atmospheric processes and sulfur



oxides and particulate matter.



     Sulfur dioxide dissolves readily in water, such as atmospheric moisture,



to form sulfurous acid which oxidizes to sulfuric acid and subsequently  to a



variety of particulate sulfates.  Metallic oxides such as manganese or iron



catalyze the reaction.  Particles may vary in size, shape, molecular composition,



and optical properties.  Thus, analytical methods for particulate  matter vary



according to the specific parameters measured.



     Methods used to measure sulfur dioxide can be classified as  integrated



or continuous.  Most of the methods are based on techniques involving absorption



and stabilization on a substrate.  The analysis of the collected  sample is



commonly based on colorimetric, titrimetric, turbidimetric, gravimetric, and



ion chromatographic measurement principles.  The most widely used  integrated



method to determine atmospheric sulfur dioxide is an improved version of the



colorimetric method developed by West and Gaeke and adopted as the EPA reference



method in 1971.  Sulfation methods, based on the reaction of SO  with lead
                                                               J\


peroxide paste to form lead sulfate, have commonly been used to estimate



ambient SO  concentration over extended time periods.  Continuous methods for
          /\


the measurement of ambient levels of sulfur dioxide have gained widespread



use in the air monitoring community.  Continuous sulfur dioxide analyzers

 «.

using the techniques of flame photometric detection, fluorescence, and second

-------
derivative spectrometry have been developed over the past 10 years and are
commercially available.
     Methods for determining soluble sulfates,  total sulfates, and specific
sulfate species involve the collection of participate matter and its subsequent
analysis by direct or indirect methods.   For trace soluble sulfate determinations,
a commercial method based on ion exchange chromatography is specific, exceptionally
accurate, and sensitive.   Methods of analysis for total  sulfur include x-ray
fluorescence, electron spectroscopy, and flame  photometry.  X-ray fluorescence
methods are nondestructive and applicable to large numbers of ambient aerosol
samples.  Procedures for determining specific sulfate species include thermal
volatilization and solvent extraction techniques, gas phase ammonia titration,
infrared and visible spectrometry, flame photometry, and electron microscopy.
Sulfate species may be estimated quantitatively by gas phase ammonia titration
methods and infrared spectroscopy.
     The majority of atmospheric particle samples are collected by either
filtration or impaction devices.   The collected samples are usually analyzed
gravimetrically to provide a direct measure of mass concentration.  The most
sidely used method for gravimetric analysis of mass concentrations is the
high volume sampler, the current EPA reference method for particles.  Other
methods include the British Smoke Shade and AISI tape samplers, multi-stage
cascade impactors, cy&lone samplers, and the dichotomous  sampler.  Chemical
analyses consist of manual wet-chemistry, atomic absorption, x-ray fluorescence,
optical emission spectrometry„ spark source mass spectrometry, neutron activation
analysis, and thin-layer chromatography with fluorescence detection.  Methods
 i.
for continuous or HI situ monitoring or atmospheric particles are also available.
They are not as closely related to mass concentration as are the integrated
                                   1-18

-------
methods, but they provide useful  information for studying particulate  sources,



transport, episodes, and effects  such as visibility.   The integrating  nephelometer



measures light scattering by atmospheric particles and is commonly used as  an



indicator of visibility.



     It should be noted that the  most widely used particulate matter measurement



device in the United States, the  high-volume sampler,  usually has  a relatively



high cut point, so that not only  fine particles (^2.5  urn MMD) but  also coarse



mode (2.5 to 15.0 urn) and large particles (mainly up to 30 urn MMD) are sampled.



In contrast, the other most frequently used method, the British smoke  (BS)



instrument tends to sample a much more restricted range of particles sizes,



these typically being less than 5.0 ug/m (mainly <3.0  urn MMD) and  chiefly in



the fine mode particle range.



 1.3.2  Air Quality Measurement Applications



     The critical assessment contained in Chapter 3 regarding practical



applications of measurement approaches employed in Great Britain and the



United States for determinations  of air concentrations of suflur oxides (SO )
                                                                           x\


and particulate matter (PM) is concisely summarized here.  Information presented



concerns published evaluations of the relative specificity, sensitivity,



accuracy, precision, and reliability of the methods when used under optimum



conditions in the hands of technically-expert analysts.  Much more emphasis,



however, is placed on evaluation of results obtained with practical applica-



tions of the measurement methods, often by  less technically-skilled personnel.



That evaluation draws mainly upon published commentary on quality control



assessments for the different applications.  Also, the major focus  here  is  on



British and American air measurement approaches most widely  used  in acquiring



S02 and particulate matter data utilized in quantitative community  health



studies discussed later.
                                   1-19

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1.3.2.1  British Approaches

British S0p Measurements—As  noted earlier,  the  lead  dioxide  gauge  was  used

extensively in Britain during the  years  prior  to 1960.   However,  use  of the

hydrogen peroxide method was  gradually interspersed with the  lead dioxide

gauge during the course of the 1950s,  often  being coupled in  tandem,  as it

were, with the apparatus for  smoke measurements.   Much  of the early (1950s)

British epidemiology data discussed later has  been related to SO,, measure-

ments obtained either by the  hydrogen  peroxide method,  especially where 24-hr

S02 values are used, or the lead dioxide sulfation rate method in some

cases where long-term (days to a month)  data were acquired.

     In 1962, as part of the   establishment  of the British National  Air

Pollution Survey, a working party was  set up to  compare the lead  dioxide

gauge with the hydrogen peroxide method, which was then chosen as the standard

method for use in the Survey.  As quoted in  Atmospheric Pollution,  1958-1966

(WSL, 1967):

         The hydrogen peroxide method  is subject to the limitation  that
    its reaction is not confined to sulphur  compounds;  the lead dioxide
    method has the limitation that the extent  of the  reaction can be
    substantially influenced by weather conditions.   Despite  limitations,
    both methods estimate pollution by sulphur compounds; the hydrogen
    peroxide method is somewhat more complicated, but has the outstanding
    advantage that it can measure concentrations of pollution over  short
    periods; the lead dioxide method is simple in operation,  but it is
    incapable of measuring concentrations over short  periods.

         Even so, it was considered desirable  to compare the results
    from the two types of instrument under controlled conditions.  A
    statistical analysis was made by Warren  Spring Laboratory of results
    from a group of 20 sites  at which both lead dioxide and hydrogen
    peroxide instruments had been operated over a period of 48 months.
    The 20 sites selected were those with a  reasonably complete set of
    results from March 1957 to February 1961 at which the two instruments
    were not more than 100 feet apart.

         The correlation between 829 pairs of  results from  the 20 sites
    over a period of four years was highly significant, showing that
    both instruments were predominantly affected by the same pollutant,
    sulphur dioxide.
                                   1-20

-------
The WSL (1967) report presented a plot of the comparison data  showing  that
                                                            o
the ± 2o confidence limits correspond to ± 1.8 mg SO-/100 cm/day for  a  given

hydrogen peroxide reading and ± 0.18 mg S02/m3 for a given lead  dioxide

reading.


     In other words, estimates of SOp levels derived from lead dioxide sulfation

rate measurements, especially 24-hr estimates, can only be roughly compared

with SOp estimates obtained by the hydrogen peroxide method at other geographic

sites or at later times at the same location(s).   Also, comparisons between

sulfation rate readings may only be meaningful when such readings differ by
                                o
the equivalent of about 180 ug/m  of SOp.  Some of the types and magnitudes

of errors encountered in the British application of lead dioxide gauges  to

measure SOp levels are summarized in Table 1-1.  As shown in Table 1-1,

several problems (e.g., humidity and temperature effects) result in the  lead

dioxide method being essentially useless for 24-hr, measurements and in their

otherwise having a rather large (±180 ug/m  2a) error band associated  with

them.

     Based on some of the above problems, when the National Survey began in

1961 it was recognized that the lead dioxide method could not provide  the

24-hour SOp measurements necessary for correlation with mortality and morbidity

effects investigated by epidemiology studies.  The hydrogen peroxide method

for S09 was, therefore, adopted as being more  valid than the old  lead dioxide

gauge sulfation method.  Because many of the staff making the measurements

would be the same people who had been servicing particle deposit  gauges and

the lead candles without detailed technical  knowledge  of the analyses,  however,
 E.
an Instruction Manual (IM) issued by WSL in  1966 had to be  quite  detailed  and

clearly readable by people with no training  in analytical techniques.
                                   1-21

-------
                                                    TABLE  1-1.    SUMMARY  OF  EVALUATION  OF  SOURCES .^MAGNITUDES.  AND DIRECTIONAL BIASES OF ERRORS
                                                                                 ASSOCIATED WITH BRITISH  S0; WASUHWIlfS
                             Tl«*
                            •wrloel
                                                 evthod
                                     Reported tevrc*
                                       of error
                                Direction and eagnltcd* ef
                                      reported error
         likely general <*a>act en
            Brltiih SOj date
                           Pro-19C1
                           1W1-1*00
                            (Brlttih Hot1«««1
                            Air P»l. Swvey)
                                              194* •luldt  Mualdlty (RM)
                                                            Te*»>*rature (T)

                                                            Wind speed (W)
                                   (Overall  erron)

                                   Siting ef Step I*  Line
                                    Intake:
                      •ere»ld*
r\>
                                                                Reaction rat* Increaiet with RH.
                                                                ((•action rale Incraatat 2S
                                                                 per S* rite.
                                                                Reaction rat« IncrcaMt
                                                                 • I Hi VS.
                                                             a. toe mar beller chlemeyi  §4) -  100 MO/*  ov*rMtlMt1ofl.
                                                             B. toe n»«r »«ff»Ut)or.       Sffi -  70 p«rc«nt und*r«it1«t1on.

                                                            Saaclt Una Adtorptten:               ,
                                                             a. Good cara & claantng      10 )>e/a>   SO ufl/*
                                                                 annuity Bean.
Tltratlon frror:
 a.  Normal-iharp color
    change of Indicator at
    pH 4 S
 k.  Cradual color ch*ng» of
    Indicator at pH 45
 C.  Rounding off to 0.1 •!
    ef alkali voluea
                                                           (vaewratlan of reagent:
                                                           Teaperature and Pretture:
                                                            a.  Correctloni - norael
                                                            b.  large a/ at filter
                                                                                              thly

                                                                                          n lig/a1  ondereatlMtla*) an 1M ef
                                                                                           •ua»er iee|>l*>  In urftan areas.
                                                                                          unc>r.

                                                                      Varlasle poattlv* »1*». molar hlfh win* ami.


                                                                      CM to  «•>  U t UO iif/e1 (ID).
                                                                                                       Occatienal (pro*, rare) aawtttv* (la*.
                                                                                                       Occatlonal (prob. rare) negative blat.


                                                                                                       »*»>1»1* fcneral 10 MS/"1 «*«atlf« kla
                                                                                                       Occailonal 40-MS negative blai.
                                                                                                       Likely rare SO-MS negative b1e>.
                                                                                                                                 Negligible la
                                                                                                                                  of data.
                                                                                                                                                ct.   Pr*
                                                                                                                                 -SZ negative blai en nigh SO.-tS deys.
                                                                                                                                 »S» potlttve bias en ton SO^'BS dayi.
Negligible le»*ct.   r
 of data.
Likely occn tonal  9-10
                                                                                                d tZX prwltlon

                                                                                                ative klm.
                                                                                                                                 negligible li»>*ct.   ,
                                                                                                                                 Occatlonal 5-10 po/»  negetlv* kin.
                                                                                                                                 Occailonal negatlv* klat ef up te W
                                                                                                        >» uc/a  *«f. klM OB IIS of  timur
                                                                                                        ~ia*pUi  In urb*n are«i.
                                                                                                        Occailonal nea. blei  In eewntrv ar«a«-
                                                                                                        «p t* 80  ug/B1 dally  data &  up U  IMS
                                                                                                        aonthly lean  In  tuner.
                                                                                                                t %
                                                                                                                                 aa «f d»U.
                                                                                                       ActMl i 10 Mt/"3 rreclslm level.'

                                                                                                       Added t S pf/to1 precltlm «rror.c
                                                                     »-10G> pot. kill for SO, **U <1N      .
                                                                     7.S-1SX pot. klat for SO, of 100-700 »>«/•••
                                                                     1.2S-7.SX pot. blat for ». of 700-400 uo/» .
                                                                     <}.2SX pot. blai for SO. dlta >400 po/oi •
                                                                     General 5S neg. blat In SO. iaU.
                                                                     Occailonal - tlOS negative blai In SO.
*Data fro*) 196S-1968 eait clearly lapected.

bO«ta fro* 1966-1967 eait clearly lapacted.

£At MK In errer.

-------
     As mentioned above, the lead peroxide  method was  selected because its


sensitivity, reliability and precision were demonstrated  to  be isuch better


than that obtained in comparison to the lead dioxide method.  More


specifically, the British Standard for sulfur dioxide  determination by the


hydrogen peroxide method states that replicate determinations can be  expected


to be within ±20 ug/m  for concentrations up to 500 mg/m   and within  ±4  percent

                                 o                      /^T^yf7"/" V
for concentrations above 500 ug/m ; and an OECD Working Parting  stated the


accuracy of the method to be ±10% at levels >100 ug/m  .   However, as  summarized


in Table 1-1, numerous sources of errors have been  encountered  in the practical


application of the method in collecting data for the British National Survey


over the past 15-20 years.


     Certain of the sources of error listed in Table 1-1, it can be  seen,


resulted in relatively small errors, whereas others produced errors  ranging up


to 50-100% in magnitude.  Also, some errors appear to  have been restricted to


affecting data from only limited locations (usually unspecified as  to specific


names of localities) or during only limited time periods.  Many of  these types


of errors appear to have been detected fairly quickly and steps taken to


successfully correct or minimize them.  Still other sources of  errors exist


(e.g., those from reagent evaporation), which have  likely affected essentially


all British National Survey SOp data.  Some of these appear to remain uncorrected


to this date, in some cases more than 10 or 15 years after they were first


detected and brought to the attention of Warren Spring Laboratory officials


responsible for overseeing quality control for the  entire National  Air  Pollution


Survey.  See Chapter 3 for a more detailed discussion of each type of error.


     Taking the above information into account for  present purposes, it would


be extremely difficult to determine precisely which errors affected  particular
                                   1-23

-------
 National  Survey data  sets employed in British epidemiology and other studies

 discussed later in  this  document.  That would likely  require a thorough examina-

 tion,  on  a time- and  site-specific basis, of records  detailing Information  on

 how each  pertinent  data  set was  collected and WSL quality control  assessment

 rep"orts for the data  sets.  Alternatively,  in later evaluations  of British

 epidemiology studies  one could accept the following overall evaluation and  set

 of conclusions  by the WSL (1975) regarding  British National Survey air pollution

 data (emphases  added):

     The actual  degree of accuracy attained  in the Survey  is not  known.
     Input data  are  scrutinized by WSL staff, and subjected to computer
     checks, and any reflectances, titres, or air flows  which are abnor-
     mally high  or low or show unusually abrupt  changes  from one  day to
     the next are queried and data known to  be invalid are excluded from
     the annual  summary tables.   Such checks can however eliminate only
     some  of the gross errors.  More information will  become available on
     accuracy when current (1974) plans to institute additional quality
     control, e.g.,  on reagent solutions, are put into operation.
     However, although the accuracy of the Survey data cannot at  present
     be quantified,  many  of the errors discussed in the  previous  para-
     graphs will cancel out when  data are averaged over  periods of a few
     months or a year, or for groups of sites.   The remainder tend to
     show up as  anomalies when data are compared with  past or subsequent
     data  at the same  site or with data from other sites;  anomalies of
     this  kind have  been  commented upon throughout the Reports.   Members
     of Warren Spring  Laboratory  staff have  devoted a  large effort over
     the years to site visiting and checking on  procedures.   It  is their
     experience  that the  vast majority of the  instruments  are maintained
     and operated with reasonable care and accuracy.   The  Laboratory is
     therefore confident  that the accuracy is  sufficient for  the  type of
     data  analyses carried out in the present  series  Of  reports.

Presumably, it is the  opinion of  the WSL  and British  epidemiologists that the

accuracy of the  survey data  is also sufficient to meet the original objectives

of the Survey, ie. to  assess the  benefits  accruing  from  the  Clean Air Act of

1956, which requires use  of  the  survey  air quality  data  along with community

health endpoint  evaluations  in order  to  define quanititative air pollution/health
                                    1-24

-------
effects relationships.   That this presumption is likely correct is  further



attested to by the long history of reliance on these data by British epidemio-



logists, such as in the making of statements regarding such quantitative relation-



ships in innumerable journal articles and reviews appearing during  the past



twenty years, up to and including the very recent review by Holland et al.  (1979).



Daily Smoke Measurements of the United Kingdom National Survey--The



general technique for the British Smoke shade (BS) measurement is described in



detail in Chapter 2, and a detailed critical assessment of the measurement



procedure is provided in Chapter 3 to allow for evaluation of the precision,



accuracy, and reliability of the measurements.  Also, details of the BS



measurements are provided by an Instruction Manual (IM) issued by Warren



Spring Laboratory in 1966.  At the start of the National Survey in  1961 (WSL,



1961) it was recognized:  "The daily instrument, while comparatively simple in



design and operation gives reliable results jm good hands* and seemed the best



choice for the National Survey."  WSL circulated the specifications of the



apparatus and methods to all the cooperating organizations as careful, uniform



work was essential if the results from the different sites throughout the



country were to be comparable.  However, WSL found that detailed instructions



were necessary as most of the Local Authority staff making the measurements



had no training in analytical techniques.  These methods were reviewed by an



O.E.C.D. Working Party and a report "Methods of Measuring Air Pollution"



(OECD, 1964) was prepared, which was accepted into the British Standards



Specification 1747, Parts 2 and 3.  The Manual of Instruction (WSL, 1966)



incorporated the improvements in techniques, "but apparatus and procedures  are
                                    1-25

-------
specified in much greater detail  to assist operation by observers  with no
technical knowledge."*
     Partly due to the lack of analytical  training of survey monitoring site
operators, and other factors as well,  various  errors were encountered in
carrying out BS measurements for the National  Survey.
     Table 1-? summarizes information discussed in Chapter 3 on the sources,
magnitudes and directional biases of errors associated with British smoke
measurements during the past 30 to 40 years.   For example, prior to 1961, the
use of weights for sealing purposes led to highly variable errors  in BS
measurements due to leakage at filter clamps,  and steps were taken to require
screw-down clamps as standard procedure as part of the later British National
Survey work implemented after 1961.  It is not clear to what extent any specific
British BS data sets from the 1950s may have been affected by the clamp leakage
problem, but one must assume that such errors  could not have often been very
large or serious and that the WSL took appropriate steps to eliminate or
invalidate any data in gross error as they were detected via their quality
control efforts in the late 1950s.   Analogously, there is evidence that WSL
did take steps to inform users of pre-1961 BS  data of errors arising from (1)
comparing reflectance on filters to photographs of painted stains and (2) use
of reflectance readings below 25 percent,  where the stain was too dark to use
the Clark-Owens DSIR curve.   However, it also appears that only a few investigators
(e.g., Commins and Waller, 1970) took steps to go back and correct published
reports based on the affected pre-1961 data and to publish revised analyses
taking into account corrections for the pre-1961 data errors.
'Underline added for present emphasis.
                                    1-26

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                                TABLE 1-JF.   SUMMARY OF EVALUATION OF SOURCES. MAGNITUDES, AND DIRECTIONAL BIASES OF ERRORS

                                       t
                                        ASSOCIATED WITH AMERICAN S02 MEASUREMENTS
Time
period
Measurement r
method
Reported source
of error
Direction and Magnitude
of reported error
Likely general Impact on American SO^ data
1944-1968
Lead dioxide.
1969-1975
 (EPA CHESS
 PROGRAM)
West-Gaeke
 Pararosanallne.
Humidity (RH).
Temperature (T).

Wlndspeed (WS).

Saturation of Reagent
 (sulfatlon plate mainly).
                                  (Overall Errors).
Spillage of reagent
 during shipment.

Tine delay for reagent-
 SO- complex.
                                  Concentration dependence
                                   of sampling method.
                                  Low flow correction.
                                  Bubbler train leakage.
                                  (Overall errors).
Reaction rate Increases with RH.
Reaction rate Increases 2X per 5°
 rise.
Reaction rate Increases with WS.

Variable underestimation beyond
 pt. where 15X of PbO. on plate
 reacted.
18% of total volume SOX of time;
 occasional total loss

SO, losses of 1.0, 5, 25. and
 75X at 20. 30, 40, and 50°C,
 respectively.

Underestimation of unspecified
 magnitude at dally SO. >200
 ug/m3.               Z

±10X to SOX variable error.
                                                Small underestimation error of
                                                 unspecified magnitude.
"November, 1970. to April,  1973. CHESS Program data  Impacted before error corrected.
Applies to CHESS  Program SO,  data  from  all years  1970-1975
cAs summarized by  Congressional  Investigative Report (IR,  1976).
                                     Variable positive bias, especially In s
                                     Variable positive bias, especially in s
                                                                                                    Variable positive bias, especially in summer.

                                                                                                    Possible large negative bias, especially for 30-
                                                                                                     day samples for summer monthly readings.
                                                                                     Generally wide ± error band associated with data.
                                                                                      Possible negative bias up to >100X. mainly in
                                                                                      summer, with 30-day reading.
                                     Half of SO
                                      mean of
0, data likely negatively biased by
17X; some up to 100X.
                                     Usually small (<5X) negative bias, but consistent
                                      negativebsummer bias up to 25X at 40°C temp,
                                      extreme.

                                     Probable general negative blas.ln daily,
                                      monthly,  and yearly S02 data.


                                     Usually error of < 110X; occasionally up to
                                      t SOX in daily, but dampened statistically In
                                      annual mean.

                                     Slight negative bias suspected.
                                                                                     From Nov., 1970, to Dec., 1971, data biased
                                                                                      low by 50-100X.  From Nov.. 1971. to
                                                                                      conclusion of CHESS Prograa In 1975, fall-
                                                                                      winter data appear valid but summer data biased
                                                                                      low by maximum of 60-80X.  From 1972 to1975
                                                                                      annual  average data approximately 15-2.0X  low.
                                                                                      Dally data highly random, not useful.

-------
     Probably of much greater concern than the pre-1961 BS measurement errors



are those encountered after the establishment and initial  implementation of



the British National  Survey in 1961.   These include certain errors, e.g., the



"computer error of 1961-1964," (see Figure 1-1),  which were eventually detected



by WSL and resulted in steps being taken to correct affected BS data in



National  Survey data  banks.   It is clear,  however,  that whereas users of the



affected data may have been informed of such errors by WSL, virtually none of



them have taken steps to (1) alert recipients of  publications containing



analyses based on the affected data of the likely inaccuracies or ranges of



error involved; (2) to reanalyze the study results  based on the affected data



sets; or (3) to reissue or publish anew any revised analyses.   In fact, even



some Warren Spring Laboratory quality control literature prepared and published



during the 1960s or 1970s and still in use may contain incorrect information



and recommended standard procedures for BS measurements based on analyses



"contaminated" by computer errors or other problems summarized in Table 1-2



and discussed in more detail in Chapter 3.   One such example of this relates



to ambiguities in the use of certain correction factors in calculating BS



values, which have been questioned by Ellison (1968).



     In regard to determining which British BS data sets and related epide-



miology studies are affected by different post-1961 National Survey errors,



it is again presently very difficult, as was the  case with British SO- measure-



ments, to specify with any confidence the nature  and magnitude of specific



errors impacting particular studies.   This would  probably require thorough



examination of records and WSL quality control reports concerning each of the



pertinent data sets.   On the other hand one can project that certain data



sets and British epidemiology studies were almost certainly affected by some



subset of BS measurement errors and these are taken into account in evaluating
                                   1-28

-------
             500
                      A - BRITISH STANDARD CURVE
                      B - DSIR INTERIM CURVE
                      C — DSIR -CLARK • OWENS CURVE
                      O- 1961 TO 19&4 NATIONAL SURVEY CURVE
                                   DARKNESS INDEX
Figure 1-1.
Comparison of smoke  calibration curves for Eel reflactometer,
Whatman No. 1 paper  and a 1-in diameter filter.  From WSL (1967)
The computer followed  curve D during 1961-64 instead of the
correct curve(s) B and C.
                                    1-29

-------
such studies later this  Chapter.   For example,  published reports of the



"Ministry of Pensions"  (1965)  and  Douglas  and Waller (1966) studies contain



specific reference to usage of National  Survey  data from the 1961-64 period



and, therefore,  the results of those studies  should be reevaluated in light



of measurement errors reported by  the WSL  for that period.



1.3.2.2  American Approaches



American S00 Measurements—Turning to American  measurement approaches,  different



types of measurement methods for a given pollutant were adopted by various



local, state,  and federal  agencies in establishing or expanding air quality



monitoring systems that  proliferated across the United States during the



1950s and 1960s.   Rather than  discuss methods used for S0? measurements by



all of the different American  air  monitoring  systems, main emphasis is  placed



here on the discussion  of only certain key American applications of measurement



methods for SO  that are of crucial  importance  for later discussions of



quantitative relationships between health  effects  and atmospheric levels of



sulfur dioxide.   These  include mainly applications of S0_ measurement methods



as employed in the EPA  "CHESS  Program" as  the single largest attempt to



define quantitative relationships  between  air pollution and health effects.



     In regard to sulfur oxides measurement approaches used in the United States,



lead dioxide or other "sulfation rate" measurement methods were, as in Britain,



widely employed prior to the early 1960s for  assessing S0_ air levels.



However, probably to a  somewhat greater extent  than in Britain, sulfation



rate measurement techniques continued to be  used later into the mid or late



1960s by some monitoring programs  in the United States or in connection with



certain community health epidemiology studies,  as  discussed later in this
                                   1-30

-------
chapter.   As shortcomings of the "sulfation" methods became more widely


recognized, however, their use was generally abandoned and more specific


methods for the measurement of SO- or other sulfur oxide compounds were


adopted, as was done in Britain. The hydrogen peroxide acidimetric method


(see OECD, 1965) selected for use in the British National Air Pollution


Survey, however, was not very widely adopted in the United States for S02


measurements.  Rather, versions of West-Gaeke (1956) colorimetric procedures


were much more widely used in the USA.  Conductivity measurements for SO-


(Adams et al., 1971), based on an acidimetric method adaptation often used in


automatic instruments and most suitable for measuring periods of around 24


hours, later began to be applied in the operation of some American air monitor-


ing networks in the 1970s.


     The West-Gaeke method was the method mainly employed in the EPA "CHESS


Program" for determining SO- air levels for inclusion in analyses of community


health end point data in "CHESS" epidemiology studies.  The application of


that method  in the CHESS Program was accordingly most thoroughly discussed in


Chapter 3.  The types of errors in measurement associated with CHESS SO- data

                          *j
are summarized in Table l-^Sy, along with notation of some factors affecting


earlier sulfation methods.  Much of the information on the former subject is


derived from a 1976 Congressional Investigative Report (IR) which contained a


thorough evaluation of EPA CHESS Program air quality measurements and  other


aspects of the Program.


     Looking at the types of errors associated with earlier American use  of


sulfation rate lead dioxide methods, similar effects of  temperature, humidity,


etc., as affected analogous British S02 methods are seen to apply  here to


American data as well.
                                    1-31

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                     TABLE 1-3.   SUMMARY  OF  EVALUATION OF SOURCES, MAGNITUDES, AND  DIRECTIONAL BIASES OF
                                    ERRORS ASSOCIATED WITH  BRITISH  SMOKE (PARTICULATE)  MEASUREMENTS
                     Tim
                    pa Hod
 Measurement
   method
      Reported  source
         of  error
  Direction and magnitude
     of reported error
     Likely general impact
     on published 6S data
                   1944-1950*
                   Pre-1961
Smoke filter
co
ro
                   1961-1964
                   1964-1980
 Leakage st clasp.
 Weights used to make the
   seal.
Highly variable under-
 estimation of BS  levels.
                                            Depending upon observer
                                               and value of 8.
Comparing reflectance to
   photographs  of  painted
   standard stains.
 Reflectance (R) below 25X,  50-100% underestimation.
   stain too dark  with use
   of Clark-Owens  DSIR curve.

 Computer not following      <80S underestimation  at  low
   proper calibration curve.    R if not corrected by WSL
                               (See Moulds,1961)  and
                               discussion of clamp size
                               correction factor.
               Clamp correction factor
                   for other than 1-inch
                   clasp.


               Flow rate - normal 1 day.
               Flow by 8-port with 1
                  reading per week.

               Variability of reading
                   reflectance.
               Averaging reflectance
                  instead.of averaging
                  mass/cm .
               Use of coarse side of
                  filler facing upstrean.
                            Uncertain; derivation
                               cannot be verified.
                               Possible +20X.

                            »3X variation.
                            -10% underestimation.
                            +10X overestination.
                            +2 units of R

                            Highly variable under-
                              estimation due to non-
                              linearity of R.
                              6-15X underestimation.
Probable widespread highly
 variable  negative bias.
                             Probable widespread relatively
                               smalI  negative bias.

                             Occasional  50-100% negative
                               bias  in some  data sets.


                             Negligible for  BS <~1QO pg/«3.
                             Increasing negative bias up to BOX
                              as BS  values increase over 100
                             Possible underestimate  for 2-inch
                                and 4- inch clamps
                             Possible overestimate for 1/2-Inch
                                and 10 cm clamps.

                             Presumed t 3X precision level.
                             10X negative bias on  high BS days.
                             10X positive bias on  low 85 days.
                                                                                                          Error increases with BS level
                                                                                                          at SO ug/M  up to 120X at 400 ug/m
                                                                                                          Probable snail negative bias at low
                                                                                                          BS levels, could be large at high BS

                                                                                                          Occasional negative bias of 6-1SX.

-------
                                                          TABLE  1-3.  (continued)
          Time
         period
Measurement
  method
Reported source
   of error
Direction and magnitude
   of reported error
Likely general Impact
on published BS data
                                      Reading of wrong side of
                                        stained filter.

                                         Leakage at filter clamp
                                         a. Normal, with good care
                                         b. With inadequate care.
                                         c. Careless  loading where
                                            uneven stains are
                                            produced.

                                         Use  of'wrong clamp size
                                         a. Stain  too light R>90X.

                                         b.  Stain  too dark R<25%.
                                              SO-75X underestimation.
                                              1-2% underestimation.
                                              2-BX underestimation.
                                              10-20% underestimation.
                                               Highly variable over-
                                                estimation.
                                               Highly variable under-
                                                 estimation.
                                                         Occasional negative bias
                                                      of 50-75X.


                                                     General 1-2X negative bias.
                                                     Occasional 2-OX negative bias.
                                                     Occasional 10-20% negative bias.
                                                     Data  usage not  recommended.

                                                     Data  usage not  recommended.
t
oo
CO

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     Turning to American applications  of  SOp  measurements  since  the  wide-
spread abandonment of sulfur dioxide  sulfation  rate  methods  in the mid to
late 1960s, several different types of errors were  identified as being associated
with EPA CHESS Program S02 measurements via a thorough  evaluation of the
CHESS Program, as reported in the IR  (1976).  As  can be seen, the magnitudes
of some errors in CHESS SO^ measurements  spanned  about  the same  range as
those seen for British National  Survey S02 measurements and, at  times, derived
from analogous sources of error,  e.g., evaporation  or other  loss of  reagents.
In the case of the American CHESS Program data, however, the specific overall
impact of the various detected errors  on  particular CHESS data  sets  appears
to have been more definitively defined by the work  of the IR (1976); more
specifically, it appears that the CHESS data  generally  tended to be  somewhat
negatively biased in comparison to other  local  or state SOp data from monitoring
sites proximal to the CHESS sites, with the  local and state data judged by
the IR (1976) to be reasonably accurate and  reliable.  The specific  magnitude
of the negative bias for particular years of  CHESS  data is summarized in
Table 14-3, and appears to have been  around  30-40% in some circumstances and
up to around 100% in other cases.
American High-Volume TSP Sampling Measurements—As discussed earlier, the
hi-volume TSP sampler, since its development in the early 1950s, has been the
instrument most commonly used in United States  for measurement of atmospheric
particulate matter; and high-volume TSP readings have most typically been
used in American epidemiology study evaluations of associated air pollution-health
effects relationships.  In contrast,  other particulate matter measurement
approaches (e.g., the coefficient of haze method) saw only relatively  limited
application during the 1950s and early 1960s in certain American locations
                                   1-34

-------
and were infrequently used in estimating quantitative  relationships between
airborne particulate matter and health or welfare effects.   Accordingly,
major emphasis is placed below on the critical  appraisal  of certain key
appjications of hi-volume TSP measurements in the United  States.   As  before,
in discussing American applications for measurement of oxides of  sulfur,  the
present summarization focuses most heavily on evaluation  of applications  of
TSP measurement methods employed as part of the EPA "CHESS Program,"  as the
single most extensive and comprehensive use of such methods as part of American
community health epidemiology studies.  Much of the information is derived
from the 1976 Congressional Investigative Report (IR), which included a
thorough analysis of EPA CHESS Program TSP measurements and comments  regarding
certain local or state TSP measurements.
     The main sources, directions and magnitudes of errors identified as
possibly affecting American TSP measurements are summarized in Table  1-4.  In
addition to various sources of minor errors inherent to the basic TSP sampling
method, certain other nuances of procedures included in the Federal  Reference
Method (40 CFR 50, Appendix B) may have resulted in the introduction of an
additional slight negative bias in TSP data obtained by American researchers.
This, more specifically, pertains to the manner  in which flow rate calculations
are made upon which final TSP concentration determinations are based.
     The Federal  Reference procedure calls for the averaging of the  initial
and final recorded airflow rates.  However, as described in Appendix  3-A  of
Chapter 3, the uncontrolled flow rate drops more rapidly at the start of  the
run than at the end of the run.  Therefore, a  linear  approximation leads  to  an
 t.
overestimate  of the flow rate, which will  reduce the  measured  value.  Consequently,
                                    1-35

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               TABLE 1-4.  SUMMARY OF EVALUATION OF SOURCES,  MAGNITUDES,  AND DIRECTIONAL BIASES  OF  ERRORS
                              ASSOCIATED WITH AMERICAN TOTAL  SUSPENDED PARTICULATE (TSP) MEASUREMENTS

Tine
period
Measurement
method
Reported source
of error
Direction and magnitude
of reported error
Likely general Impact
on published BS data
1954-1980    High-Volume TSP
Time Off (Due to power
  failure).
Weighing error.
Flow measurement (with
  control).
Flow measurement (without
  control)
a. Constant TSP—Average
    of flows.
   1. Low TSP level.
   2. High TSP level.
b. Rising TSP-Average of
   flows.
c. Falling TSP-Average of
   flows.
Aerosol evaporation on
  standing.
Condensation of water vapor.
Foreign bodies on filter
  (Insects).
Windblown dust into filter
  during off-mode.

Wind speed effect on pene-
  tration of dust Into the
  Hi-Vol shelter.
Wind direction effect due to
 H1-Vol Asymmetry
Artifact formation, NO,
  sor.               3
Variable underestimation.

±2% random variation.
±2% random variation.
                                                                 2% underestimation.
                                                                 5-10% underestimation.
                                                                 10-20% underestimation

                                                                 10-20% overestimatlon.

                                                                 1-2% underestimation.

                                                                 5% overestimatlon.
                                                                 Generally small  over-
                                                                  estimation.

                                                                 Generally small  over-
                                                                  estimation.
                                                                 Less penetration at high
                                                                  windspeed.

                                                                 Higher penetration when
                                                                  normal  to sides.
                                                                 5-10 ug/m  overestimate.
Negligible impact, rare negative bias.

Negligible Impact.
Negligible Impact.
                              Negligible Impact.
                              Possible 510% negative bias.
                              Possible 10-20% negative bias.

                              Possible 10-20% possible bias.

                              Probable negligible Impact.

                              Possible 5% positive bias.
                              Possible 5% positive bias.

                              Occasional (rare) positive bias.


                              Occasional (rare) negative bias.


                              Probable Increase 1n random (±) error.

                              Occasional positive bias.

-------
                                                 TABLE 1-4.(continued).
   Time
  period
  Measurement
    method
  Reported source
     of error
Direction and magnitude
   of reported error
Likely general Impact
on published BS data
1969-1975
 (EPA CHESS
 Program).
Fed. Reference
 Method Standard
 HI-Vol Sampler
Loss of sampling material
 1n field.
                                   Loss of sampling material
                                    In mailing.
                                   Evaporation of organic sub-
                                    stances.


                                   Wlndflow velocity and
                                    asymmetry.
                                   (Overall errors).
   No specific estimate of
    magnitude of error; but
    would be underestimation.

   Reported 4-25X apparent
    loss; max. likely due to
    crustal (sand, etc.)
    fall-off from selected
    Utah sampling sites.

   No specific estimate of error
    magnitude, but not likely to
    exceed 5% underestimation.

   No specific estimate of error
    magnitude; but most likely to
    increase random variation of
    small underestimation.
Probable slight negative bias
 1n Utah winter data.  No known impact
 on other CHESS TSP data.

Probable general small <10X negative bias;
 occasional 25% negative bias.
                                                                                      Probable slight negative bias
                                                                                       of <5X for TSP data from urban/
                                                                                       industrial areas.

                                                                                      Negligible Impact or slight
                                                                                      negative bias.
                                                                                      Generally <10% negative bias;
                                                                                      occasional 10 to 30% negative bias.

-------
all TSP data computed in this manner have a slight negative bias which is

likely usually of the order of 5 percent; on occassion,  however, under

circumstances where the flow rate may have fallen below 40 ft /min, larger

errors (up to approximately 15 percent)  may have been introduced.  Assuming

that monitoring site operators in the United States adhere to the recommended

Federal Reference Method procedures, then this type of bias is likely

inherent in essentially all American TSP data collected without flow rate

control or recording.  Despite such problems, it can be seen that the maximum

range of uncertainty derived from the various errors associated with American

TSP measurements is generally less than  20 percent in either a positive or

negative direction on a random (±) basis.

     Errors in addition to general TSP measurement errors reported by the

1976 Congressional Committee Investigative Report (IR, 1976) to affect CHESS

Program TSP measurements during 1969-1975 are broken out and listed

seperately in Table 1-4.  Some of those  errors (e.g., loss of sample

materials in filter removal from the field monitoring apparatus) were

reported by the IR (1976) as likely affecting only very restricted CHESS data

sets.  Others, e.g., errors due to loss  of sample in mailing, appear to have

been more widespread and presumably impacted on many CHESS data  sets.  It is

interesting to note, however, that the IR (1976) concluded that  the net

effect of all of the errors was to introduce, in general, a slight negative

bias of 10 to 30 percent into CHESS TSP data, which is not much  beyond the

range of different types of errors (e.g., linear flow corrections) more

generally associated with American applications of TSP measurements.  Section

IV C 3 of the IR (1976) further concluded that:

    "...the TSP data were by far the best quality data taken  in  the
    CHESS monitoring program.  Differences measured between High and  Low
    sites are probably  reasonable estimates  of the differences  of TSP
    exposures as received by populations  in  these areas."


                                   1-38

-------
  It appears reasonable to concur with the IR (1976) and,  jccordingly,  to



accept CHESS TSP measurements as reasonable estimates of TSP exposures  of



CHESS Program community health study populations, taking into account that



such data may be biased low by no more than 10 or,^r£ mo^fe-,  30 percent.



1.3.2.3  BS-TSP Comparison Studies—In Chapter 3, information is reviewed on



BS-TSP comparisons derived from a number of studies published over the  past



twenty years and reporting results obtained from the sampling of air in many



disparate geographic areas (Britain, other European countries, and the  United



States) and varying time periods (from the early 1950s to the mid 1970s).  It



was earlier hinted at and is now clear from a present perspective, with the



advantage of viewing the various BS-TSP comparison data sets together in



relation to each other, that a nonlinear relationship exists between BS and



TSP measurements obtained with colocated samplers.  That is, regardless of



where or when such readings were obtained, TSP values were usually found to



be two or more times higher than corresponding BS readings up to BS levels of



about 100 |jg/m .  At higher levels, however, the TSP and BS readings tend to



converge toward each other, such that TSP/BS approaches unity at BS levels of


        3                               3
500 jjg/m  or more.  Thus, above 500 pg/m  or so, BS and TSP readings from



colocated samplers are essentially  identical.



     In carrying out analyses of BS-TSP comparison data sets, various investiga-



tors in the past generally employed linear regression analyses  in an effort



to define straight lines that best  fit data points obtained by  them over a



limited range of BS-TSP values (see Figure 1-2).  They also often extrapolated



the thusly defined straight lines to BS-TSP values beyond the range of  their



emperical observations and found inconsistencies  between the  BS-TSP relationships



implied by their line(s) and those  defined by  linear  analyses of  different
                                   1-39

-------
             500
             400
          s
          uT

          §!
          V) \
          tfi I
           !  300 —
             200
             100
                           BS - TSP COMPARISON STUDIES
                             COMMINS-'WALLER!
                             (LONDON, 1955-63)
                           O LEE, ET AL (LONDON, 1970)_
                           OBALL& HUMEj
                             (LONDON, SUMMER 1975)
                     1001    200    300     400    500

                         AMERICAN HI-VOL  TSP. Jig/m3,
                                          600
700
Figure 1-2.
Representative examples  of BS/TSP relationships defined  by  linear
regression analyses  employed to fit BS/TSP comparison data  points
as described in published  reports                           pum«
                                    1-40

-------
BS-TSP comparison data sets obtained at other times or locations.   Such
apparent inconsistencies between BS-TSP relationships, arising from linear
regression analyses of various data sets obtained over limited and often
different ranges of BS-TSP values, have contributed to and reinforced the
view that no consistent relationships exist between BS and TSP measurements
obtained at different locations or even at different times at the same location.
Paradoxically, this view has gained widespread credence despite the concurrent
realization that corresponding BS-TSP readings are nonlinearly related.
     Recognition of the acknowledged nonlinearity of BS-TSP relationships and
the necessity to meet certain boundary conditions defined by emperical observations
and certain theoretical considerations as sine-qua-non starting points led to
the formation of a "bounded nonlinear model" (BNLM) proposed in Chapter 3 as
a unifying concept or means by which to interconvert monthly or annual average
BS and TSP values obtained under vastly different circumstances.  The BNLM
(see Figure 1-3) essentially employs a power function defining a nonlinear
relationship that meets the boundary conditions of (1) BS -* 0, where TSP •* 0
and (2) BS -> TSP, as BS -»• °°; or, in other words, when there is no particulate
matter in the air, both TSP and BS readings must be zero or tend toward zero
and, also, they must tend to converge toward each other as BS values become
very large as observed in empirical BS-TSP comparison studies.  In addition,
the particular BNLM model chosen defines a curve which  fits other empirically-
derived observations to the effect that TSP/BS = 2 at 100 ug/m3 BS and
TSP/BS = 4/3 at 250 ug/m3 BS.  Plotting of corresponding BS-TSP values from
numerous published BS-TSP comparison studies reveals  that the BNLM model  fits
well virtually all presently available BS-TSP comparison data,  in  the  mean.
                                    1-41

-------
     it
     O
     c
     D
                                    O HOLLAND «t (I (1979) • LONDON
                                    A COMMINS and WALLER (1967) -  LONDON
                                    D LEE n tl (19721  ENGLAND
                                    ^ FERRIS tt «l (19731 - BERLIN. NH
                                    O-DALAGER (1975] • ALBORG. DK
                                    9DALAGER(1975) - K0BENHAVN
                                    •OBALL »nd HUME (1977) • LONDON
                                    VKRETZSCHMAR (1975)  ANTWERP
                                    AMERICAN HHVOLTSP.
Figure  1-3.
Measurements of  British  Smoke vs Hi-vol TSP,  showing  a consistent
relation between these measures over the entire range of reported
observations.  Most points  shown are annual mean values; see text  for
discussion.
                                        1-42

-------
     Only the reported results from one recently obtained data set comparing



BS and TSP values from colocated samplers at 16 locations in the United States



appear, at first sight, to be greatly inconsistent with the BNLM model  (see



AISI line in Figure 1-3).   Closer inspection of the study, however, reveals



that numerous methodological errors were made in conducting the study,  including



the failure to follow published standard procedures employed in the collection



of BS data earlier used in British epidemiology studies on the health effects



of particulate matter and, also, in most other BS-TSP comparison studies.



Nevertheless, when the particular methodological errors and other deficiencies



are evaluated, it becomes apparent that some of the basic observations reported



may not be as inconsistent with other published results and the BNLM model  as



initially seems to be the case.  See Chapter 3 for a more detailed discussion



of this matter.



1.3.3  Sources and Emissions



     Sulfur oxides and particulate matter are emitted into the atmosphere from



a variety of sources, both natural and man-made.  Natural particulate matter



emissions include terrestrial dust (windblown soil and rock particles), radioactive



particles, sea spray, volcanoes, biosphere emanations (products of biological



processes), and biomass burning.  Most natural particle mass is greater than 1 urn



in diameter.  On a global scale, natural emissions of sulfur oxides and particulate



matter into the atmosphere greatly exceed man-made emissions.  The latter,



however, tend to be much more concentrated on a local or  regional  scale.



     In the United States, anthropogenic air pollutants,  that  is,  those pollutants



associated with human activities, are primarily caused by the  combustion of



fossil fuels and the smelting of metals.  The marked increase  in  energy consumption



since the middle of the twentieth century has led to a generally  upward trend



in emissions of particulate matter and sulfur oxides.
                                     1-43

-------
     Projections indicate that secondary PM will  account for an increasingly



greater proportion of the total  emissions over the next decade.   (Secondary



particles are formed by atmospheric conversion of gases.)  Most of this increase



wiJl occur in the fine fraction (less that 2-3 urn), and its impact will be



felt over increasingly greater geographic areas.   For example, the use of



higher smoke stacks will result in a longer range transport of SO^-   This



long-range transport creates more secondary fine particulate matter and greater



geographical distribution of particulate pollutants.



     Man-made emissions of sulfur oxides from stationary sources in the



United States are currently estimated at 29 million metric tons per year.



Transportation sources contribute less than 1 million metric tons of sulfur



oxides, or not quite 3 percent of the total emissions.   Of all stationary



sources, utility plants burning coal and oil are the primary contributor



(about 62 percent), while other industrial processes account for about 32



percent, and residential and commercial use of coal and oil accounts for less



than 3 percent.  Emissions vary considerably from one region to another; over



75 percent of the total national emissions come from the eastern half of the



United States.  Annual emissions of sulfur oxides have increased from about 23



million metric tons in 1940 to as high as 35 million metric tons in 1973.



Although the past few years have seen a slight decline in emissions, an  increase



to nearly 40 million metric tons is projected by 1990 unless  reduced by  implementatio



of air regulations.



     Over 90 percent of the national sulfur oxide emissions occur in the form



of sulfur dioxide; the balance consists of  sulfates  in various  forms.  The



quantity and composition of these emissions vary from source  to  source and



depend on factors such as fuel characteristics, operating conditions,  and



emissions-control equipment.
                                     1-44

-------
     The characteristics of participate matter, like those of sulfur oxides,



vary according to source, emissions-control equipment, and other factors.



Man-made emissions of particulate matter amounted to about 12.5 million metric



tons in 1975 in the United States.  The distribution of sources varies geographi-



cally:   the eastern half of the United States accounts for 66 percent of the



national total.  Forty percent of the emissions come from stationary fuel



combustion sources, principally in electric generation and industry and 25



percent from mineral processing.  Additional emissions come from primary metal



production, land vehicles, food and agricultural processes, solid waste disposal,



and other sources.  In addition, there are considerable emissions of fugitive



particulate matter from both industrial (3.3 million metric tons/yr) and



non-industrial (4.9 million tons/yr) sources.



1.3.4  Environmental Concentrations and Exposure



     To protect the public health from air pollution, it is important to know



how many people are likely at risk from pollutant concentrations capable of



inducing adverse effects.  For  financial and technical reasons it is impractical



to obtain direct measurements of pollutant doses incurred by individuals.  It



is necessary,  therefore, to rely on fixed-point air monitoring to estimate



pollutant exposures in representative environments.   Such monitoring is conducted



predominantly  outdoors—in the  ambient air, within the first 100 feet above



the surface.   A meaningful evaluation of population exposure to sulfur  oxides



and particulate matter must include measurements of specific local  and  area-wide



concentrations, data on  particle  size and  composition, and  knowledge of the



number of people  in specific areas and their activity patterns.



     Fixed-point  ambient air monitoring conducted  at  several thousand  sites  in



the United States  over the last three decades  shows a general  trend of declining



pollutant concentrations.  For  example, in the late 1950s,  monitors in five
                                      1-45

-------
heavily industrialized cities  were  recording  annual  arithmetic  mean  concentrations



of total suspended particles  in  the range  of  130  to  195  ug/m .   By the early



1970s, those sites were recording annual means  in the  range of  70 to 115



ug/m3.  By 1978,  only 17 percent of reporting stations in the nation were


                                                      3
exceeding annual  average particulate levels of  75 ug/m  and six percent were



exceeding the levels of 260 ug/m .



     Studies of urban aerosols indicate that  while the mass balance  of total



TSP is similar from city to city, its chemical  composition varies.  Many of



these differences arise from  the type of fossil  fuel used and the type of



industries dominant.  For example,  soot produced  from  the combustion of fuel



oil can vary from 1 to 13 percent of the TSP  mass in a particular area.  Coal



soot, on the other hand, may  account for up to 30 percent of the TSP mass in



some urban areas.



     Sulfur dioxide concentrations  have also  decreased.   In 1964, a  represent-



ative group of 32 SO- monitors across the  nation  averaged about  50  ug/m ,



with the peak station reporting an  annual  average of some 200 ug/m .  By 1971,



their composite average had decreased to about 25 ug/m , and the peak station

                          3

reported less than 50 ug/m .   In 1978, only  one percent of reporting stations

                                                           o
were exceeding the primary annual  standard for SO- (80 ug/m ); and two percent



were exceeding the primary 24-hour  standard  (365 ug/m ).  Sulfur dioxide



levels in the ambient air generally rise and  fall according to the amount of



coal or other fossil fuels burned other than  natural gas.



     Analyses of some specific constituents  of air pollution,  notably  sulfates,



nitrates, and fine particles  (<2.5  ug/m MMD)  indicate that these  constituents



are not declining at the same rate  as the  gross particulate concentrations.



     Sulfate, ammonium, and nitrate ions dominate the fine particle  fractions



in urban and rural areas.  Generally, toxic elements  such as arsenic  and lead
                                     1-46

-------
are associated with the fine fractions, while less toxic elements such as cal-



cium and iron occur more often in the coarse fraction.



     At least 50 percent of atmospheric particulate sulfur occurs in the fine



fraction as sulfates and often accounts for 40 percent or more of the fine



fraction mass.  Most of the sulfate aerosols occur as ammonium salts rather



than as sulfuric acid.  High sulfate levels occur more often in summer than in



winter.



     There are regional differences in trace metal concentrations.  Vanadium



and nickel, for example, are correlated with the use of fuel oil.  Their con-



centrations are, therefore, highest during the winter months.  But in areas



requiring low sulfur  fuels, vanadium and nickel levels are quite  low, since



these elements are removed during fuel desulfurization processes.  Where coal



is used, titanium tends to exist at somewhat higher concentrations.



1.3.5  Transmission Through the Atmosphere



     Pollutants emitted into the atmosphere are transported vertically and



horizontally, transformed physically and chemically,  and deposited by dry and



wet removal mechanisms.  Since each of these processes is a function of  numerous



physicochemical and meteorological variables, source-receptor  relationships



are necessarily complex.  Despite the difficulty  in analyzing  atmospheric



transmission, certain findings have been substantiated.



     Atmospheric  particulate mass is distributed  bimodally  in relation  to



particle size:  fine  particles are smaller than 2.5 micrometers (|jm)  and



coarse particles are  larger than 2.5 urn.  Comparable  masses  of fine  and  coarse



particles have been measured within urban areas.   Outside of urban areas,  the



fine particulate mass tends to exceed the coarse  particulate mass, especially



in the Eastern United States.
                                      1-47

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     Many fine particles are formed in the atmosphere from precursor gases.



Most coarse particles are emitted directly from combustion or industrial pro-



cesses, or are of natural origin, and become suspended in the atmosphere



through human activity.



     A portion of the fine particulate mass is the result of the atmospheric



conversion of sulfur dioxide, nitrogen oxides, and higher molecular weight



hydrocarbons (Cfi+) to particulate sulfate, nitrate, and organic aerosols,



respectively.  The remainder of the fine particulate mass consists of com-



bustion-derived sulfates and carbonaceous particles, lead, small amounts of



other metal-containing particles from combustion and industrial processes, and



small amounts of finely divided dusts.  The coarse particulate mass consists



of substances emitted directly from industrial sources and from combustion



processes, along with substantial amounts of suspended or resuspended dusts of



various types.



     Because their deposition occurs over several days, fine particles can be



transported for distances up to 1000 kilometers or more from their origins or



the origins of their precursor gases.  Finely divided particles formed con-



tinuously by secondary atmospheric reactions are especially likely to undergo



long-range transport and to exist at appreciable concentration  levels.  Since



urban-area sources and large point sources contribute precursors of secondary



particles, concentrations of such particles may become superimposed upon those



of fine particles during transport.



     Gas-to-particle conversion processes depend on a variety  of environmental



parameters, such as solar radiation, concentrations of oxidizing radicals, and



humidity.  Therefore, precursor gas emission  rates alone  are of very  limited



utility in estimating the mass of secondarily formed fine particles.
                                     1-48

-------
     Although it has been known that many factors contribute to sulfate  levels



in the atmosphere, past results suggest that heterogeneous reactions  may play



an important role in determining those levels.   More detailed studies are



necessary to assess the role of these reactions.   Past work has shown the



importance of temperature, oxygen, water, and other parameters in removal



rates.




1.4  WELFARE EFFECTS ASPECTS




     The third volume of this document discusses welfare effects of sulfur



oxides and particulate matter.  This includes information summarized  below on:



effects on vegetation (Section 1.4.1); acidic precipitation formation and



effects (1.4.2); effects on visibility and climate (1.4.3); and materials



damage effects (1.4.4).  Major emphasis is placed in the discussion of lengthy



materials contained in Chapters 7 and 8 on vegetation effects and acidic



precipitation.



1.4.1  Effects on Vegetation



     Terrestrial vegetation is normally exposed to a variety of substances



from the atmosphere.  Among these substances are sulfur oxides, particulate



matter, and other phytotoxic pollutants.  More is known concerning the effects



of sulfur oxides, mainly sulfur dioxide, than about the effects of particulate




matter.



     The sensitivity to sulfur dioxide of plant species and varieties differs



because of the genetic composition of the plants and the influence of environ-



mental conditions on their response.  Temperature, light, humidity, other air



pollutants, soil conditions, and the stage of plant growth all  interact in



affecting the sensitivity of plants to injury from sulfur dioxide and particulate



matter.  Since the ambient air contains many substances other  than sulfur



dioxide and particulate matter, interaction with these other  substances must



be considered when analyzing the effects of sulfur oxides or  particulate



                                     1-49

-------
matter on vegetation.   Mixtures of the substances in the ambient air, some of


which may be nitrogen oxides or ozone, may have adverse growth or foliar


effects of a greater magnitude than the effects from sulfur dioxide alone.
                   i

  -  The response of a given variety or species of plants to a specific air


pollutant cannot be predetermined on the basis of the known response of related


plants to the same pollutant.   Neither can the response be predetermined by a


given response of a plant to similar doses of different pollutants.  The


interplay of genetic sensitivity and environmental influences must be considered


for each plant and pollutant.


     In general, sulfur dioxide must enter a plant to induce toxic effects,


although some toxic actions on plant surface coatings can be induced by surface


contact,alone.  It is generally accepted that entry of sulfur dioxide into a


plant is through leaf openings termed stomata.  Environmental conditions


(e.g., light, temperature, and humidity) that favor open stomata at the time


of exposure permit the assimilation of S0~.   In the plant, S0? is converted to


sulfite or bisulfite and eventually to sulfate.  Sulfite and bisulfite are


approximately 30 times more toxic than sulfate.


     Air pollutants, as do all plant stress-inducing agents, initiate changes


within plant metabolic systems.  Changes in metabolic pathways may lead to


extensive physiological dysfunctions.  If physiological dysfunctions are


severe, visible symptoms may be manifested.   Two basic forms of injury occur:


(1)  injury not visibly expressed that may or may not result in reduction in


growth or loss in yield; and (2)  injury visibly expressed as clinical symptoms


that may be observed, recorded, and evaluated.


     As long as the rate of absorption in plants does not exceed the rate of


conversion of SO- to sulfate, the only effects of exposure to S0? may be


changes in stomatal opening or closing, or biochemical or physiological changes.


If SQ^ exposure concentrations are reduced, abatement of effects may occur.


                                     1-50

-------
     Reduced growth and yield and/or predisposition to ot.ier biotic or abiotic



stress-inducing agents may occur if alterations in plant metabolism or phy-



siology persist for a period of time.  Significant reductions 1n growth and



yield of major forest tree species and agronomic crops have been reported



without the presence of visible symptoms.



     Visible symptoms result from both acute and chronic injury.   Acute injury



symptoms include necrosis or death of cells, tissues, organs, or the entire



plant.  Chronic injury symptoms include plant responses that usually involve



chlorophyll disruption, followed by induction of chlorosis or yellowing of



tissues.  Pigmentation changes resulting in stippling or general discoloration



characterize this type of injury.  Chronic injury results from either high-dose



or low-dose exposure; high-dose exposure may lead rapidly to acute injury.



These terms refer to plant response rather than to the exposure conditions and



the dose received.  Dose-response relationships relate variations in the



length of exposure and pollutant concentration to variations in plant responses



as mediated by the plant response system and the environment.  Dose is defined



as the concentration of pollutant multiplied by the  length of the period of



exposure.



     Variations in exposure  regimens and response measurements frequently make



it difficult to compare the  results of different studies.  The conclusions



listed below are based on a  synthesis of the data discussed  in Chapter 7  and



summarized  in Tables 1-5, 1-6, 1-7.  These conclusions were  formed by summarizing



the dose-response data without considering the confounding environmental



variables:  (1) Significant  suppression in yield of  economically  important



agricultural species by SO-  concentrations  in  the  range  from 0.05  to  0.06 ppm



can occur  if the period of exposure  is at  least two  weeks  in length.   (2) Both
                                      1-51

-------
                TABLE  1-5.   DOSE-RESPONSE INFORMATION SUMMARIZED FROM LITERATURE PERTAINING TO  CULTIVATED  AGRONOMIC
                              CROPS  AS RELATED  TO FOLIAR,  YIELD,  AND  SPECIFIC EFFECTS  INDUCED BY  INCREASING  S02 DOSE
Ul
ro
Cone,
ppm
0.01
0.01
0.015
0.02
0.035
0.02
0.05
0.10
0.03-
0.10
0.3-
0.06
0.10
0.15
0.20
0.035
1.75
0.05
Exposure
time
10 mln
Growing season
Growing season
10 m1n
3 hr for 8 exp,
growing season
Growing season
(2 year)
72 hr/wk for
growing season
24 hr/day
for 30
days
8 hr
10 mln
Exposure.
condition
EC


EC
F/CC
F-ZAP
F/CC
F/CC
EC/SO
EC
Effects on
P1antc Foliar Yield
Corn
Oats X
Wheat X
Bean
Wheat
Winter wheat
Prairie June grass
Barley X
Durham wheat
Spring wheat
Winter wheat X
ev. Yamhin
ev. Ilyslop X
Broadbean
Broadbean
              Species Effect0
                                    i I

Stomata open wider

Light leaf Injury

15X decrease 1n grain weight yield

Stomata open wider

No effect on apparent photosynthesis, no
  effect on the average head length or
  number of grains  per head

S content Increased with Increase In S0«
  concentration; digestibility  of dry
  matter was reduced by 2 years of treat-
  ment; crude protein content In winter
  wheat decreased significantly

Ho effect on yield
                                                                                            0.03 ppm Increased yield 271
                                                                                            0.06-0.15 ppm. no effect
                                                                                            0.06 ppm decreased yield 221)
                                                                                            0.20 ppm decreased yield 70J
                                                                                            Depressed photosynthesis
                                                                                            Stomata open wider; threshold 0.02 pom for
                                                                                             10, mln
                                                                                                                                      Reference


                                                                                                                                        448

                                                                                                                                        159

                                                                                                                                        159

                                                                                                                                        448

                                                                                                                                        394
                                                                                                                                         473

                                                                                                                                         473
                                             473


                                              40


                                              37

-------
                                                    TABLE  1-5.  (continued)
Cone,
 ppm


0.05
0.05
0.10
0.25
    Exposure
      time
5 hr/day; 5 *ay/wk
     for 4 wk
      4 hr
 Exposure.,
condition0
  EC/SO
  EC/SO
    Plantc


   Alfalfa

   Tobacco

   Oats
   Radish
   Soybean
   Tobacco
                      Effects  on
Foliar
Yield
            X
            X
            X
Species Effect*
             261 decrease In  foliage dry weight
             491 decrease In  root dry weight
             22% decrease 1n  leaf dry weight

             No foliar Injury
Reference


   430



   431
0.05
0.20
0.06
0.065
0.13
0.26
0.10
0.10
0.10
   8 hr/day
   5 days/wk
   for 18 days

   68 days
   1-55 days
  EC/SO
  EC/SO
   GC
    20 m1n
    1 hr
    8 hr
   EC


   EC



   GH
   Soybean
   Alfalfa
   Cabbage
Chinese cabbage
  Cucumber
  Eggplant
   Lettuce
   Spinach
    Bean
    Corn

    Bean
                                                 Tobacco
                       No effect on top fresh or dry weight; root
                         fresh or dry weight; plant height; shoot/
                         root fresh or  dry weight  ratio

                       281 decrease 1n  foliage stubble, 451 decrease
                         root dry weight
                       211 decrease In  total protein content, amlno
                         add content,  total nonstructured carbohy-
                         drates, symblotlcally fixed nitrogen           327

                       Foliage Injury threshold 0.13x27 days            140
                       Foliage Injury threshold 0.26x55 days
                       Foliage Injury threshold 0.13x26 days
                       Foliage Injury threshold 0.13x11 days
                       Foliage Injury threshold 0.13x15 days
                       Foliage Injury threshold 0.13x1 day
                       Other  parameters measured such as plant height,
                         number of leaves, top fresh weight, number of
                         flowers,  fresh weight vs. dry weight of roots
                         were not  found to be significantly different
                         from controls

                       Stomata open wider, effect also shown to occur   448
                         In dark

                       Stomata open wider, water-stressed plant had     448
                        wider opening of stomata compared with
                         controls

                       Foliar  Injury threshold for development  of       283
                         fleck-like lesions

-------
en
          Cone,
           ppm

          0.10
          0.10
          0.10
0.125-
1.0
          0.1S
          0.1S


          0.25
         0.11
               Exposure
                 time

             6 hr/day
            for 133 days
               18 days
 6 hr/day
 43 days
 92 days
133 days

 1-3 hr
               18 days
            72 hr/wk for
           growing  season

               18 days
           103.5  hr/wk
            for 20 wk
                   Exposure.
                  condition

                    F/CC
                                            GC
      Plant0

     Soybean




       Pea
Effects on
        YTeT?
Foliar
                                  F/OT
                                           EC/SO
                     GC
     Soybean
      Oats
     Radish
    Sweet pea
   Swiss chard

      Pea
                   F/CC
                    GC
     Barley
   Durham wheat
   Spring wheat

      Pea
                    GC
   Cocksfoot
  Meadowgrass
Italian ryegrass
    Timothy
               Species  Effect6                Reference

No significant effect on growth  or yield;         169
  92nd-day defoliation  was  \2l greater;
  135th-day seed weight was 1% reduced fnw
  control

31 decrease In fresh weight of shoot       i i     204
51 decrease 1n dry weight of shoot
41 decrease 1n tojal nitrogen
301 decrease In H  (buffer capacity)
101 Increase glutamate  dehydrogenase activity
1101 Increase In Inorganic sulfur content
No significant effect on foliar  Injury,  defolla- 171
  tlon fresh weights, seeds/plant, or weight
  of seeds/plant


No foliar Injury                                  32
                     31 decrease 1n fresh weight of shoot             204
                     81 decrease In dry weight of shoot
                     21 decrease 1n tojal nitrogen
                     35S decrease In H  (buffer capacity)
                     321 Increase 1n glutamate dehydrogenase activity
                     140X Increase In Inorganic sulfur content

                     421 decreased yield In Durham wheat; 441         473
                       decreased yield 1n barley; no effect on
                       spring wheat

                     32X decrease In fresh Height of shoot            204
                     26! decrease In dry weight of shoot
                     241 decrease In to.ta1  nitrogen
                     421 decrease In H  (buffer capacity)
                     BOt Increase In glutamate dehydrogenase activity
                     1501 Increase In Inorganic sulfur content

                     401 decrease In total  dry weight                13,14
                     281 decrease In total  dry weight
                     Nonsignificant
                     511 decrease In total  dry weight
                     (Yield  reductions were related to decrease  in
                     leaf areas)

-------
                                                               TABLE 1-5.  (continued)
en
01
           Cone.
             PP»
           0.15
           0.15-
           0.30

           0.15
           0.17
           0.20
           0.25
           0.25
           0.20
           0.30
           0.40
           0.50
           0.60
           0.70

           0.20
           0.20

           0.218
   Exposure
     tine

   24 hr
   7 days
   14 days
   2 hr



   1 hr


   2 hr



   2 hr
   15 days
To maturation

4.5 hr/day
for 4 days
 Exposure,,
condition0

  CC/SD
  EC/SO
   GH
   EC/SO



  EC/SO


   GC
   GC



  EC/SO

  F-ZAP
   P1antc

    Corn
    Rice

   Barley
    Bean
    Com

   Celery

Big plantain


    Bean
 Big mallow

 Broadbean



  Alfalfa


  Alfalfa
   Barley
   Oats

  Alfalfa
   Barley
  Tomato



 Kidney  bean

   Soybean
                     Effects an
Foliar
YfeTo*
               Species Effect6                Reference

Absorbed SO. remained In water-soluble           490
  form and very difficult to assimilate to
  protein

Severe foliar Injury                             288
Ho Injury                                | (
Severe foliar Injury

Increased peroxldase activity, caused            356
  chlorosis of leaves
Increased peroxldase activity, decreased
  buffering capacity of cells, caused
  necrotlc leaf Injury
Caused necrotlc leaf Injury
Caused necrotlc leaf Injury

Decreased photosynthetlc rate, decreased          39
stomatal resistance If RH > 401.  Increased
stomatal resistance If RH < 401

No effect on photosynthesis                      471


Threshold dose for Inhibition of  photosynthesis    30
                                                        No effects at these doses
                                                                        30
            Threshold dose for Initial symptom of tissue
              death, decrease or change In vitamin B..
              Bg, and nlcotlnlc acid content

            151 decrease In total yield
            No visible damage
            201 decrease 1n yield
                                                                       449



                                                                        33

                                                                       201

-------
                                                              TABLE  1-5.  (continued)
I
on
            Concj
             ppm


            0.23
Exposure
  time
14 days
 Exposure.
condition
               Plant0


GH           Buckwheat
              Lucerne
            Red clover
        Little stinging nettle
              Ryegrass
  Effects on
foliar
0.25
0.25
0.25
0.40
o.eo
1.20
0.25
0.25
0.25
0.25
0.25
0.40
0.80
1.20
0.25
0.25
0.29
1 hr
2 hr
Once every wk
(3 hr) to once
1n ^wk (3 hr)
4 hr
8 hr
24 hr
1 hr
3 hr every
2 wk for
growing season
Unknown
Unknown
15 days


F/CC
EC/SO
EC/SO
GC
EC
F/CC
EC
EC
GC
Broadbean
Broadbean
Alfalfa
Barley
Durham wheat
Spring wheat
Broccoli
Tobacco, Bel B,
Tobacco
Broadbean
Begonia
Alfalfa
Barley
Durham wheat
Spring wheat
Pea
Sunflower
Morning glory
Corn
Sorghum
Lettuce



X
X


X



X
               Species  Effect*"                Reference


Caused necrotlc leaf Injury                      356
Caused necrotlc leaf Injury
Caused necrotlc leaf Injury
Increased peroxldase activity
Increased S content In  leaves         i I

Slight swelling of stroma thylakolds of          464
  chloroplast, effect reversible
Stroma thylakolds spread to  granum
  thylakolds, effect reversible

Ho effect on yield                              473
                                                                        It leaf Injury                                   432
                                                                        6t leaf Injury

                                                                        Chlorophyll a decreased more sharply than
                                                                          chlorophyll b                                   40

                                                                        Stomata opened faster and wider In light         286
                                                                          condition; stomata opened longer In darkness

                                                                        Foliar Injury                                    431

                                                                        No effect on yield                               473
                                                                                                   501 decrease In net photosynthesis               62

                                                                                                   lOt decrease In photosynthetlc rate             450
                                                                                                   20-30X decrease 1n photosynthetlc rate
                                                                                                   No effect
                                                                                                   No effect

                                                                                                   Foliar Injury, 30t decrease In thlamlne content  449

-------
                                                             TABLE  1-5.  (continued)
 I
en
Cone,
 ppm

0.30
          0.35

          0.35
                         Exposure
                           time
                         5 hr/day

                         6 day/wk

                         12 days

                         26 days
1 hr
21 days
                  Exposure.
                 condition13
                    EC/SD
EC/SD
EC/SD
               Plant1"

               Barley

               Bean

               Sunflower


               Barley
                                 Effects on
                Foliar
Yield
Alfalfa
Pea
0.38
1.15
1/90
0.40
0.40
0.50
0.60
0.40
0.40
0.45
0.46
0.50- ,
6.00
14 days
3 hr
4 hr
6 hr
6 hr/2 wk
(1-2 exposures)
3 hr for 7
exposures for
growing season
7 hr
30 min
0

EC/SD
EC/SD
EC/SD
F/CC
EC
F/CC
Radish
Oats
Tomato
Apples
Alfalfa
Cotton
Pecan
Pepper
Wheat
Buckwheat
Soybean
X
X




X
X
               Species Effect0                Reference

11% foliar injury; 38% decrease in               292
  dry weight shoot
1% foliar injury; 38% decrease in
  dry weight shoot
5% foliar injury; 41% decrease in
  dry weight shoot

21% foliar injury; 26% decrease in
  dry weight shoot
2% foliar injury; 15% decrease in dry
  weight shoot
16% foliar injury; 29% decrease in
  dry weight shoot
80% decrease in apparent photosynthesis        472

Increase in glutamine content, decrease        205
  in glutamic acid and protein content
    inorganic S accumulated
Necrosis and growth inhibition at 0.35
  x 14 days
Decrease injury at 0.38 and above, inhibited    111
  seed germination, formation of green leaf-
    lets of sprouts, and root growth
Threshold for leaf injury                      174

Increase accumulation total  and soluble         29
  S content

No effect                                      227

No difference found in total  N, protein/total   424
  N ration, chlorophyll, all  plants,  all
    treatments


No accumulative effect on yield,  no effect on
  average head length or number of grains/head  394
                                                                                                  Injury threshold

                                                                                                  Very significant negative linear relation-
                                                                                                    ship between percent leaf area destroyed
                                                                                                    and percent crop loss; 0.66% yield loss
                                                                                                    for every 1% increase 1n foliar injury;
                                                                                                    asymtomatnc plots Increased yield by
                                                                                                    6.02% over controls
                                                                                                                       498


                                                                                                                       102

-------
                                                             TABLE 1-5.  (continued)
en
CO
ConCi
ppn
0.50
0.50
0.50


Exposure
time
1.5 hr
1.5 hr
2 hr »-


Exposure.
condition0
EC/SO

EC


P1antc
Soybean
Oats
Begonia
Petunia
Coleus
Effects on
Foliar Yield
X X
X

X

                                                           Snapdragon
0.50
0.50
0.50
0.50
0.50





2 hr EC
4 hr EC/SO
4 hr EC/SD
4 hrfday EC/SO
for 14 days
5 hr/day
6 days/wk
for 12 days
26 days


Grape
Alfalfa
Broccol 1
Radish
Tobacco
Tomato
Oats
Radish
Soybean
Tobacco
Oats
Barley
Bean
Sunflower
Barley
Bean
Sunflower
X
X
X
X
X
X







            Species Effect0                Reference

71 decrease In short  fresh weight;            172
  trace foliar Injury

Inltlon of leaf Injury                       174

No effect
30t decrease In flower number;  151             2
  decrease In shoot weight               '
No effect; 12% decrease In shoot weight
lit decrease In number of flowers;  no
  effect
1901 Increase In stomatal resistance        371

191 leaf Injury
41 leaf Injury                              431
11 leaf Injury
11 leaf Injury
11 leaf Injury

Foliar Injury occurred to all crops         441
                                                                                                    321 decrease top dry weight;  131 decrease   175
                                                                                                      1n root dry weight;  number  of heads
                                                                                                      unchanged

                                                                                                    241 foliar Injury;  421 decrease In dry      292
                                                                                                      weight shoot
                                                                                                    71 foliar Injury; 311  decrease 1n dry
                                                                                                      weight shoot
                                                                                                    181 foliar Injury;  441 decrease In dry
                                                                                                      weight shoot

                                                                                                    361 foliar Injury;  451 decrease In dry
                                                                                                      weight shoot
                                                                                                    121 foliar Injury;  341 decrease In dry
                                                                                                      weight shoot
                                                                                                    261 foliar Injury;  351 decrease In dry
                                                                                                      weights shoot

-------
                                                    TABLE  1-5.  (continued)
Cone,
 ppm

0.50
1.00
1.50

0.50
0.50


0.56
0.77
0.92

0.60


0.60
0.70
0.70
    Exposure
      time

    4 hr
    5 hr/day
   6 days/ week
   for 14 days
    6 days

    4 hr
    6 hr


    6 hr/day
    5 days/week
    for 14 days

    8 hr/day for
      3 days
6/12, 24 hr/day
    1-7 days
 Exposure^
condition

 GC/G



 EC



 0


 EC/SD



 EC/SD


 EC/SD



 EC/SD




 EC
Plant1"

Red Clover
Broadbean
Sunflower
Tobacco

Pea
Cucumber
Apples
Soybean
White bean
Broadbean
Bean
  Effects on
Foliar    YTeTd
0.75
0.80
0.80-
2.00
0.80-
2.00
3 hr
2 hr
4 hr, 20 min
4 hr, 20 min
EC/SD
F/ZAP
F/ZAP
Al fal fa
Alfalfa
Soybean
Soybean
X
X

X
                Species Effect0                Reference

Increase in vitamin A, fat, protein content       196
  Significant change in plant nutritional
  components
Under drought conditions exposure caused          379
  wider opening of stomata, no effect on
  diffusive resistance

Increased glutamate dehydrogenase; increased       465
  peroxidase activity
Accumulation of significant total and soluble      29
  sulfur
                      7.3%  increase  in foliage injury; 5% increase      227
                        leaf abscission
                      No effects
                      Bifacial necrotic lesion on mature leaves         183

                      20% decrease in photosynthesis after 2 hr
                        fumigation;  after 3-day fumigation, 1           24
                        hr  to full recovery in light condition;
                        no  foliage injury
                      Increase in total amino acids and ammonium,
                        decrease in  aspartic acid glutamic acid
                        and protein  synthesis, all before visible
                        injury present
                      No injury developed                               192
                      Threshold dose for foliar necrosis; 25-50%         30
                        decrease in  net photosynthesis
                      4.5%  decrease  in yield at 1.4 ppm
                      11% decrease in yield at 1.7 ppm                  310
                      15% decrease in yield at 2.0 ppm

                      Epidermal and mesophyll  cell death, the number
                        of  dead mesophyll  cells highly correlated
                        with increase in S02
                      Highest S02 concentration,  significant decrease
                        in seed yield

-------
                                                    TABLE  1-5.  (continued)
Cone,
 ppm
0.90
1.00


1.00


1.00


1.00
1.00
1.0



1.0


1.00


1.50


1.50
Exposure
  time
2 hr
2 hr


3 hr


3 hr


2 hr
 Exposure.
condition

 EC/SO
 GC


 EC/SO


 EC
4 hr
 EC/SO
1 hr/2 days
 for 4 days


6 hr/day
for 3 days

1.5 hr
3 hr

0.75-3 hr


3 hr
 EC/SO



 EC/SO


 EC/SO


 EC/SD


 EC/SO
P1antc
Broadbean
Barley
Polnsettla
eight cultlvars
Alfalfa
Begonia
Petunia
Coleus
Snapdragon
Broccol 1
Bromegrass
Cabbage
Lima bean
Radish
Spinach
Tomato
Geranium
Strawberry
Soybean
Soybean
Alfalfa
Effects
Foliar
X

X



X
X
X
X
X
X
X

X
X
X
X
on
Yield



X
X
X



X
X
X

 30


177



192
               Species Effect6                Reference

261 decrease In net  photosynthesis under          39
  saturated light  conditions; 52t decrease
  1n net photosynthesis under nonsaturated
  light conditions
Threshold dose for foliar necrosis; 30-60
  decrease In net  photosynthesis         ( |

No effect


Leaf necrosis at 315 ppm CO. was 2.8x that
  Induced under 645 ppm C0_

No effect
30t decrease 1n flower number;  191 decrease  1n
  shoot weight
271 decrease In flower number;  191 decrease  In
  shoot weight
141 decrease In flower number;  161 decrease  1n
  shoot weight

381 leaf Injury
651 leaf Injury
701 leaf Injury
251 leaf Injury
461 leaf Injury
491 leaf Injury
331 leaf Injury

Rapid closing of stomata  In low-RH air  after
  exposure; slow closing  1n hlgh-RH  conditions,
  stomata remained open

No effect on growth and development
  Necrotlc lesions, lower leaf surface

91 decrease 1n shoot fresh weights,  41  leaf
  Injury 211-291 decrease 1n shoot  fresh weight

24-941 decrease In shoot  fresh weight;  63-931
  foliar Injury

Leaf necrosis at 315 ppm  CO. was 2.5x that
  Induced under 645 ppm CO,
                                                                                                                                        431
 47



358


172

172



192

-------
                                                    TABLE 1-5.  (continued)
Cone,
 PPM

1.50
2.00
2.0

2.5



3.0



4.00
Exposure
  time
To maturation
                                 Exposure,.
                                condition0

                                 EC/SO
2 hr
                                 EC
               3 hr


               6 hr
               1 hr
               2 hr
               3 hr

               2 hr
                  GC


                  EC/SO
                  GC
                  GC
                  GC

                  EC
Mante

Kidney bean
                  Effects on
Foliar
Begonia

Petunia

Coleus

Snapdragon


Polnsettla        X
eight cultlvars

Apples            X



Polnsettla        X
eight cultlvars   X
                  X

Begonia

Petunia

Coleus

Snapdragon
Yield

  X
  X
Species Effect0
                                                                    Reference
                      201 decrease In root dry weight;  141
                        decrease 1n legume dry weight;
                        171 decrease 1n  seed  dry weight;               33
                        10-301 decrease  In apparent  photo*
                        synthesis.   Increase  In chlorophyll
                        a and b content
                      141 decrease flower number; 221 decrease      ' '   2
                        1n shoot weight
                      321 decrease In flower  number; 241 decrease
                        1n shoot weight
                      301 decrease in flower  number; 201 decrease
                        In shoot weight
                      151 decrease In flower  number; 151 decrease
                        In shoot weight

                      0-18.31 foliar Injury                            177


                      171 Increase In foliar  Injury; 621 Increase      227
                        in lead abscission; 191 decrease In shoot
                        growth
                      0.13.81 foliar Injury                            177
                      1.8-26.81 foliar Injury
                      18.8-96.51 foliar  Injury

                      271 decrease  in flower  number; 331 decrease
                        In shoot weight                                 2
                      421 decrease  In flower  number; 321 decrease
                        in shoot weight
                      301 decrease  in flower  number, 211 decrease in
                        shoot  weight
                      201 decrease  In flower number; 191 decrease In
                        shoot  weight
                  second-order divisions.  Doses within a single study that
                  concentration that  Induced said effect.
*Table arranged by Increasing SO, concentration as first-order and exposure time as
 did not Induce specifically different effects are listed along with the lowest SO.

 F » field or forest surveys
 F/CC • Field, closed chambers
 0/OT • Field, open-top chambers
 F/ZAP • Field, zonal air pollution system
 6 • Greenhouse
 GC • Growth chambers
 EC • Exposure chambers
 EC/SO • Exposure chamber, special design
 0 • Other
c$ee Appendix A for most scientific latin binomials of plants.

*l Indicates study examinated foliar and/or yield effects.  The X does not necessarily imply that an effect was found.

'most prominent or significant effect reported.

-------
the  quality and quantity of the crop can be negatively affected by the concen-



tration of pollutant multiplied by the length of the exposure period.   Unfortunate



variations in exposure regimens and response measurements make it difficult to



compare the results of different studies.



     The concept of dose-response can be demonstrated by a synthesis of the



data presented in Tables 1-5, 1-6, 1-7.   The following conclusions were formed



by summarizing the dose-response data without designating specific associated



exposure conditions:



     o    Yield of economically important agricultural spe cies can be signifi-



          cantly suppressed by SO- concentrations in the range of 0.05 to 0.06



          ppm if the exposure period is sufficiently long (2 weeks).  Both



          crop quality and quantity can be negatively affected.



     o    Fluctuating, long-term (seasonal, annual) SO- exposures averaging



          0.05 ppm or less can cause economically and ecologically undesirable



          effects on productivity and stability of range and forest ecosystems.



     o    As SO- concentrations increase to 0.25 ppm, a variety of agricultural



          crops (such as alfalfa, timothy, range grasses, soybean, barley,



          wheat, cabbage, lettuce, spinach, tobacco, cucumber, eggplant, pea,



          and kidney bean) respond with necrotic foliar injury or suppressed



          yield.  Approximately 70 percent of the cultivated agronomic crop



          species exposed to 0.25 ppm or less respond to the SO- exposure of 1



          hour or longer with changes in stomatal aperture (leaf openings),



          foliar injury or yield effects.  Foliar injury on vegetables and



          suppression of yield are directly related to economic values.



     o    Forest trees species (such as pine, spruce, fir, beech, alder  and



          poplar, representing coniferous and deciduous forest ecosystems)



          respond to 0.25 ppm or  less of S02.  Approximately 90 percent  of the
                                     1-62

-------
TABLE 1-6.   DOSE-RESPONSE INFORMATION SUMMARIZED FROM LITERATURE PERTAINING TO  FOREST TREE  SPECIES
              AS  RELATED TO FOLIAR, -YI£LB, AND SPECIFIC EFFECTS INDUCED BY  INCREASING S02 DOSE
Cone,
ppm
0.001
0.003-
0.09
0.09-
0.12
0.004
0.35
0.006
i- 0.007-
cn 0.01
co
0.007-
0.01
t
0.008
0.011
0.017
0.015
0.019
0.023
0.025
Exposure
time
10 yr avg.
i"
Annual avg
Annual avg
Annual avg
Annual avg
(exposed 5 mo)
Growing season
Annual avg
Annual avg

10 yr avg
Growing season
10 yr avg
Annual avg
Annual avg
Annual avg
6 hr
Exposure.
condition1'
f
F

F
F
F
F

F
F
F
F
F
F
EC/SO
Hwite
Forest trees
Scotch pine

Eastern white pine
White birch
Fir forests
Fir forests

Forest trees
White birch
Forest trees
Conifers
Conifers
Conifers
Eastern white pine
Effects on
Foliar Y1e1d~
X X
X X



X
X X

X X
X
X X
X
X
X
X
                                                                                         Species Effect'
                                           Reference
                                                                           Mo Injury
                                         i I
                                                                           Decreased photosynthesis leading to the
                                                                             death of tree
                                                                           No significant difference In S content of
                                                                             foliage
                                                                           No effect on foliar S content
                                                                           20 +_ 5X growth Increase
                                                                           20 + 5* growth decrease
                                                                           Premature defoliation
Very little chronic foliar Injury
Increased foliar S content; trace to light
  foliar Injury
Mostly chronic foliar Injury; some acute Injury
301 decrease In growth
52t decrease in growth
54! decrease In growth
Threshold dose for needle damage; most
  sensitive clones only
355


369

273
297

296
                                                                                                                       273
                                                                                                                        .54
                                                                                                                       454
                                                                                                                       454
                                                                                                                       193

-------
TABLE  1-6.  (continued)
Cone,
ppm
0.025-
0.037
0.026
0.026-
0.037
0.035
0.038-
0.057
Exposure
time
Annual avg

Growing season
Annual avg

5 mo
Annual avg

Exposure.
condition"
F

F
F

F
F

P1antc
Fir

White birch
F1r

Eastern white pine
Scotch pine

Effects
Foliar
X

X
X

X


on
Yield
X


X


X

0.045
0.045
0.048
0.05
0.15
0.05
0.05
0.05
0.10
0.20
0.05
0.05-
0.10
0.05
0.10
0.20
Growing season
10 yr avg
Growing season
6 hr
49 days
10 wk
5 mo
9 mo
9 mo
9 mo
F
F
F
EC/SO

F/CC
F/CC
F/CC
F/CC
F/CC
Jack pine
Forest trees
White birch
Eastern white pine
Norway spruce
Spruce
Beech
Spruce
Scotch pine
Fir
X
X
X
X
X

X



                                                                              I I
273
296

369
133
            Species Effect0                Reference
Death of groups of trees                     297

Moderate to severe foliar Injury
Rapid death of groups of trees

Foliar Injury
Species occurrence negatively correlated
  with SO. ambient cone.; foliar S content
  positively correlated with SO- ambient
  cone.; foliar S content positively
  correlated with SO. ambient cone.; by
  distance from source
Reduced chlorophyll content, tissue death    273
Acute and chronic foliar Injury
Severe foliar Injury; foliar S  concentration  273
  3x normal
60! of tolerant clones foliar Injury         193
  developed
Foliar Injury                                491
No effects                                   224
Increase In S concentration  proportional     223
  to Increase 1n SO. exposure cone.;
  terminal bud deatn
Decreased foliar buffering capacity; In-     222
  peroxldase activity
Decreased photosynthesis                     222

Decreased pollen viability                   222

-------
     TABLE 1-6.  (continued)







I—1
1
cr>
tn
Cone,
ppm
0.069
0.07
0.10
0.20
0.10
0.15
0.30
0.18-
0.20
0.20-
1.00
Exposure
time
Annual evg
3 days
10 wk
76 days
9 wk
24 hr
1 hr
Exposure.
condition0
r
EC
'" F/CC




    Mantc
     Conifer
Eastern white pine
     Spruce
Black alder
Poplar

Jack pine
Azalea
Flrethom
White ash
White birch
  Effects on
Foliar
9.20

D.20
0.025


0.2S



0.27

0.35
0.40
0.50
12 hr/day
for 7 wk
110 days
2 hr


2 hr



3 mo

3 hr
74 hr

EC/SO


EC/SO


EC/SO



EC

EC/SO
EC

Hybrid poplar

English birch
Eastern white pine
Jack pine
Red pine
Loblolly pine
Short leaf pine
Slash pine
Virginia pine
Pin oak
White birch
Trembling aspen
Yellow pine
Eastern white pine



X
X
X
X
X
X
X


X


X









X
X



               Species Effect0               Reference
701 decrease In growth                         454
Chlorotlc spotting and death of needle tips       19
Decreased CO- uptake; positive correlation     223
  between COf uptake and cambium growth;     (.
  Increase in cone. Induced annual  ring
  width
Increase phenoloxldase activity               491
Decreased leaf area Index and foliar           209
  growth

Inhibited foliar llpld synthesis. Inhibition    286
  reversible; Increase In dose • Increase  1n
  recovery time
No appreciable effect on foliar sorptlon of SO. 367
                                           Slightly decreased height; decreased relative   208
                                             growth rate, relative leaf growth rate, and
                                             relative leaf area expansion rate

                                           No effect on phenyloxldase activity             491

                                           6.51 foliar Injury                               34
                                           4.51 foliar Injury
                                           0.5* foliar Injury

                                           All equally sensitive; most sensitive period     35
                                             8-10 wk of age or older
                                           45X decrease In height growth                   368
                                           1071 Increase In height growth
                                           21 foliar Injury                                217
                                           Chlorophyll  content varied Inversely with        100
                                             concentration

-------
                                                 TABLE  1-6.  (continued)
Cone,
ppm
0.45
0.45
0.5

Exposure
time
6 hr
9 hr/day
for 8 wk
15 mln
30 m1n
60 m1n
120 m1n
Exposure.
condition
EC/SO
,, EC


Plant0
Eastern white pine
Ponderosa pine
Red pine

Effects on
Foliar Yield
X
X


0.50
2 hr
EC/SD

1—
1
en
en
0.50
0.50
3 hr
5 hr
EC/SD
GC
Eastern white pine
Jack pine
Red pine

Trembling aspen

Austrian, Ponderosa
Scotch pine. Balsam,
Fraser, White fir
Blue, White spruce
Douglas fir
0.50



0.65
1.00




1.00
1.07-
6.41
1.83

30 day



3 hr
4 hr




8 hr
30 m1n
to 6 hr
50 m1n

GC



EC/SD
GC




EC
0

0

Chinese elm
Gingko
Norway maple
Pin oak
Trembling aspen
Austrian, Ponderosa.
Scotch pine. Balsam,
Fraser, White fir.
White spruce, Douglas
fir
American elm
Scotch pine
P. pinea
V. nigra
Pine
Spruce
X
X
X
X
X
X





X

X

              Species Effect0              Reference
All tolerant clones developed foliar           193
  Injury
Severe needle tip chlorosis and necrosis       128

                                         i I
•Decreased primary needle chlorophyll con-       78
  tent.
Decrease dry weight of primary needles and
  cotyledons
Further Increase of all of above effects
121 foliar Injury                              34
lit foliar Injury
ZX foliar Injury

US foliar Injury                             217

No Injury                                     399
                                                                                         Severe chlorosis  and  necrosis                 416
                                                                                         Moderate marginal  chlorosis
                                                                                         Moderate marginal  chlorosis
                                                                                         Slight overall  chlorosis
                                                                                         23X foliar Injury                            217

                                                                                         Less than 4t foliar Injury all species        399
                                                                                         Inhibition  of stomatal closing               335

                                                                                         Visible Injury was  proportional  to  foliage    65
                                                                                           S content

                                                                                         SO. absorbed by  exposed  foliage  In  winter-   298
                                                                                           time; S stored In new  shoots

-------
                                                   TABLE 1-6.  (continued)
Cone,
 ppm

2.00
2.00



2.00



2.00
2.00

2.00


3.00
Exposure
  time

2 hr
6 hr



6 hr



6 hr
6.5 hr

12 hr


6 hr
 Exposure,
condition0

   CG
   GC
   GC
   GC

    0
   GC
      P1antc
                        Effects on
Foliar
Yield
Austrian, Ponderosa     X
Scotch pine, Balsam,
Fraser, White fir. Blue,
white spruce, Douglas fir

American elm            X
American elm
Chinese elm

Glnkgo


American elm
Glnkgo
Norway maple
              Species Effect'                Reference

No foliar injury on Douglas fir, firs,         399
  spruce
Pine foliar injury threshold, necrotic
  tips
Induce severe foliar injury; defoliation in     76
  older leaves; significant reduced expansion
  of new leaves; number of emerging leaves
  and root dry weight reduced
No significant reduction in lipid content;      79
  significant decrease 1n new leaf protein
  content; significant decrease In leaf,
  stem, root carbohydrate content
lOOt leaf necrosis                             416
Water-stressed plant increased uptake          335
  of S02
Induced stonatal closing; S content            416
  Increased In plants fumigated In
  light
SOX leaf necrosis                              416
  Table arranged by Increasing SO, concentration as first-order and exposure time as second-order divisions.  Doses within a  single study
  that did not Induce specifically different effects are listed along with the lowest
                                                                      S0_ concentration that Induced  said effect.
  F • field or forest surveys
  F/CC « field, closed chambers
  D/OT » field, open-top chambers
  G/ZAP « field, zonal air pollution  system
  G • greenhouse
  GC » growth chambers
  EC • exposure chambers
  EC/SO • exposure chamber, special design
  0 « other
cS*e Appendix A for most scientific  latin binomials of plants

-------
          species  tested  in  this  range of  SO.  concentrations  (with  2  hour



          exposures)  responded with physiological modifications,  suppressed



          photosynthesis,  foliar  injury, death of buds,  or  suppressed foliar



          or  woody growth.



     o    Non-woody components of native ecosystems  such as lichens and  grasses



          also  respond  to  S0? concentrations below 0.025 ppm.   Responses



          include  suppressed growth,  death, and reduced  diversity in  lichen



          populations and  suppressed  photosynthesis  and  growth  of leaves,



          tillers, and  stubble of grasses.



     o    At  S0_ concentrations between 0.25 and 0.50  ppm (1-8  hours  exposure),



          less  than 50  percent of the agronomic species  tested  responded



          negatively  to the  sulfur dioxide treatments.   At  S0?  concentrations



          less  than 0.25  ppm but  for  multiple  days,  70 to 90 percent  of  the



          species  responded  negatively.



     A comparison  of  the  species  response  to the latter  treatments  at the



concentrations  ranging  between 0.25 to 0.50 ppm with the response to  concentrations



below 0.25 ppm  might  be interpreted as suggesting that plant response is not



positively correlated with dose.   This is  not  the case.   Exposure durations



used in the studies at  the higher SO- concentrations generally  ranged from 1-8



hours while multiple-day exposures were  frequently  used  at  the  lower  concentrations



of SO--  All  agronomic  species responded  to a  concentration of  0.50 ppm  at



exposure durations ranging from  1.5 to 5  hours. A  variety  of responses  occurred,



including physiological modifications, foliar  injury,  and suppressed  growth.



These trends  suggest  that as the  S0»  concentration  is  increased (a) a shorter



exposure duration  is  sufficient  to elicit a plant   response equal to  or greater



than that which occurred at a  lower  concentration;  (b)  responses become more



severe; (c)  plants tolerant at  lower concentrations become sensitive.
                                     1-68

-------
        TABLE 1-7.   DOSE-RESPONSE INFORMATION  SUMMARIZED FROM LITERATURE PERTAINING  TO NATIVE  PLANTS AS
                      RELATED  TO  FOLIAR, YIELD,  AND SPECIFIC EFFECTS INDUCED  BY  INCREASING  S02 DOSE
Cone,
ppn
0.006
0.018
0.01-
0.02
0.015
0.017
0.02
Exposure Exposure.
time condition0 Plant5
6 mo
Annual avg '"
Annual avg
6 mo
29 days
F
f
F
F
GC
Lichens
Lichens
Bryophytes
Lichens
Bryophytes
Ryegrass
                                                                Effects on
                                                              Foliar
                                                         Yield
0.14
22 days  In
2 consecutive
growing  seasons

29 days              GC
22 days  1n 2
consecutive growling
seasons
Ryegrass
0.02
0.02
0.03
0.04
0.08
0.15
0.03
0.04
0.04
0.15
0.05
85 days
Growing season
10 wk
6 mo
51 days
Growing season
GC
GC
GC
F
GC
GC
Ryegrass
Ryegrass
Ryegrass
Lichens
Ryegrass
Ryegrass
               Species Effect0                Reference

Loss of chlorophyll, decreased growth            255


Elimination of many lichen species               256«
                                       i l
Decreased  lichen diversity                       397


Elimination of species                          147

No effect  on net photosynthesis, dark resplra-     87
  tlon, transpiration coefficients, number of
  tillers  and yield


As above effects except visible foliar Injury
  and reduction of specific leaf area
                                                                                    Increased organic S content                      89

                                                                                    Increased organic and Inorganic S content        86

                                                                                    Alleviated S deficiency                        277
                                                                                    Alleviated S deficiency
                                                                                    Alleviated S deficiency
                                                                                    Reduction In yield without symptoms

                                                                                    Tissue death                                  ?' Sa


                                                                                    Decreased concentration glyclne and serlne;     234
                                                                                      Inhibited photoresplratlon pathway
                                                                                    Alleviated S deficiency symptoms                86

-------
                                                     TABLE  1-7.  (continued)
Cone,
  ppm

0.06



0.067



0.073



0.074


0.08


0.09
(Peak)

0.11




0.11


0.11



0.12
0.13
0.25
0.50
1.00

0.13
Exposure
  time
Growing season
26 wk
26 wk
 Exposure.
Condition"   Plantc
             Ryegrass
                                Effects on
                              Foliar"
4 wk


103 5 hr/wk
for 20 wk


9 wk
6 wk
6 wk
GC
    EC
    EC
         Ryegrass
         Ryegrass
18 hr
13 hr/day for
28 days
115 days
4 Mk
0
EC
F/CC
0
Splderwort
Foxtail grass
Ryegrass
Cocksfoot

X
X

   EC
   EC/SO
         Ryegrass


         Grass


         Ryegrass



         Ryegrass
   EC/SD     Ryegrass
             Species  Effect0                Reference

Increase in photosynthesis, respiration       135
  and chlorophyll  content; light  Increase
  In productivity
Increase In dry weight  of  leaves, number       24
  of tillers, dry  weight of stubble and |
  leaf area; SIS decrease  In yield

501 decrease 1n shoot dry  weight  241           25
  decrease In chlorophyll  a content;
  261 decrease In  chlorophyll  b content

Increase In chromosome  aberration rate of     282
  germinating pollen

Foliar Injury as caused by heavy  metals was   236
  Increased by SO- exposure

Decrease 1n weight; accelerated  leaf           42
  senesence
301 decrease 1n leaf area; 45! decrease         12
  In dry weight; decrease  In  number tillers;
  decrease In number of green leaves;
  decrease root/shoot ratios
20% decrease 1n leaf area; 4OT decrease  1n     14
  dry weight; decreased root/shoot  ratio

Significant decrease In leaf  area and  all  dry  13
  weight fractions; decrease  In  number of  leaves
  and tillers
Decrease 1n dry weight  of  leaves, number       24
  of tillers, dry  weights  of  stubble and
  leaf area; 461 decrease  In  yield

Foliar necrotlc lesions and decrease In       135
  net primary productivity at 0.13  ppm
  and above


Decreased productivity                        135

-------
                                                     TABLE 1-7.  (continued)
Cone,
ppm
0.15
0.15
0.15
0.20
0.20
(peak)
0.25
0.27
0.27
0.38
(peak)
0.50-
11.00
0.71

2.00-
0.00
Exposure
time
6 wk
51 days
Growing season
2 hr
55 days
5 wk
14 days
8 wk
6-43 wk
2 hr
1 hr
2 hr
5 hr
8 hr
Exposure.
condition"


GC
GC
F/CC
EC/SD
EC/SO
EC/SO
EC/SO
F/CC
EC/SO

EC/SO
Plant0
Duckweed
Duckweed
Ryegrass
Kentucky
bJuegrass
Ryegrass
Ryegrass
Ryegrass
Ryegrass
Ryegrass
87 Desert
species
Lily

Diplacus
meteromeles
                                                                   Effects on
                                                                           Yield
                                                  Foliar
3.50
1 hr
Acacia
                 Species Effect0               Reference

Decrease in starch content and size of           131
   fronds

Decrease in starch content and growth;           131
   decrease 1n surface area dry weight    ' I
Alleviated S deficiency symptoms; Increase        85
   in S content of foliage, free amino acid
   content, and N/S ratio

Visible foliar Injury                            3?0


Decrease In weight; accelerated leaf sensence     4?


No effect on number of tillers; 17t decrease     188
   In yield

Increase in free amino acid content               11
381 decrease In green weight; 301 decrease        188
   in total dry weight; no reduction in
   number of tillers; 2* senesence

36X decrease In total dry weight                  93


Most plants required more than 2.00 ppm          182
   S0_ to produce foliar injury

Inhibited pollen tube elongation at all           294
  exposure durations


Increase In SO. dose Induced  a progressive        478
  decrease In  photosynthesis  and transpiration

Foliar Injury                                     397

-------
                                                    TABLE 1-7.  (continued)
1 Table arranged by Increasing  SO. concentration as first-order and exposure  time as second-order divisions.  Doses within a single  study
 that did not Induce specifically different effects are listed along with  the  lowest SO. concentration that Induced said effect.

1 F • field or forest surveys
 F/CC • field, closed chambers
 0/OT • field, open-top chambers
 G/ZAP « field, zonal  air  pollution system
 G • greenhouse
 GC • growth chambers
 EC • exposure chambers
 EC/SO « exposure  chamber, special design
 0 • other

 Se« Appendix A for  most scientific latin binomials of plants.

-------
     The lack of short- or long-term monitoring data make^ it difficult to



assess the results of dose-response studies in the field.   When data are not



available to determine whether short-term spike concentrations occurred, then



only long-term averages have been used to define the dose.  Obvious differences



between forests in areas with high SO- concentrations have been observed.



There is usually no exact dose information for short-term influences; therefore,



in most field studies, only long-term averages are used to define the dose.



     As the dose of S02 increases, plants develop more predictable and more



obvious visible symptoms.   Foliar symptoms advance from chlorosis or other



types of pigmentation changes to actual necrotic areas, and the extent of



necrosis increases with exposure.  Studies of the effects of SO- on growth and



yield have demonstrated a reduction in the dry weight of foliage, shoots,



roots, and seeds, as well as a reduction in the number of seeds.  At still



higher doses, reductions in growth and yield increase.  Extensive mortality



has been noted in forests continuously exposed to S0_ for many years.



     The amount of sulfur accumulated from the atmosphere by leaf tissues is



influenced by the amount of sulfur in soil relative to the sulfur requirement



of the plant.  After  low-dose exposure to S0_, plants grown in  sulfur-deficient



soils have exhibited  increased productivity.



     Sulfur dioxide and particulate sulfate are the main  forms  of sulfur  in



the atmosphere, and a plant may  be exposed to these pollutants  in several



different ways.  Dry  deposition  of particulate matter and wet deposition  of



gases and particles bring sulfur compounds into contact with plant  surfaces



and soil substrates.  The effects of  such exposures are more difficult  to



assess than those associated with the entry of S0_  through plant stomata.



Plant response to dynamic physical factors such as  light,  leaf  surface  moisture,



relative humidity, and  soil moisture  may  influence  stomatal  opening and closing,
                                      1-73

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and hence, play a major role in determining sensitivities  of species and



cultivars or the time of sensitivity of each on a seasonal  basis.   Dose-response



relationships are significantly conditioned by environmental conditions before,




during, and following exposure to S02>



     Sulfur accumulation in plants has  been suggested as  a tool  for determining



the levels of sulfur in the atmosphere  of a given area over time.   Such data,



however, cannot accurately define the dose received by a  plant.



     Very few studies have been conducted to determine the sensitivity of



microorganisms to SO- or to explore the interactions of SO- with plant pathogens



such as fungi, nematodes, or bacteria.   Both inhibition and enhancement of



disease processes have been reported, but more data are needed to provide



reliable information on trends.



     In ambient atmospheres, SO- and other pollutants usually exist as diverse



mixtures in which a multiplicity of chemical combinations  can take place.



Therefore, with the possible exception  of a point source  in which vegetation



is exposed to a high dose of SO-, the direct and indirect influences of other



air pollutants in combination with SO-  must be considered.   Major phytotoxic



air pollutants that have been studied in combination with S0_ include ozone,



oxides of nitrogen, and hydrogen fluoride.  The interactions of SO- and 0_



have been most extensively investigated because of the incursions of ozone and



other oxidant precursors into many rural areas, as well as their presence in



urban areas.  Many studies have demonstrated more than additive effects  in



symptom expressions, but relatively few studies have attempted to evaluate the



impacts on growth and yield.  Additionally, pollutant combinations with  SO-



have caused less than additive and/or additive effects depending upon doses



applied.  The influence of various physical and biological factors of the



environment increase in complexity as the pollutants are combined  together



during exposures.



                                     1-74

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     A few studies have examined effects of combinations rf particulate matter



and SO- or participate matter and other pollutants:   (1) increase foliar



uptake of S02; (2) increase foliar injury of vegetation by heavy metals; and



(3) reduce growth and yield.   Because of the complex nature of particulate



pollutants, conventional methods for assessing pollutant injury to vegetation,



such as dose-response relationships, are poorly developed.  Studies have



generally reported vegetation responses relative to a given source and the



physical size or chemical composition of the particles.  For the most part,



studies have not focused on effects associated with specific ambient concentrations.



Coarse particles such as dust directly deposited on the leaf surfaces result



in reduced gas exchange, increased leaf surface temperature, reduced photo-



synthesis, chlorosis, reduced growth, and leaf necrosis.  Heavy metals deposited



either on leaf surfaces or in the soil (and subsequently taken up by the



plant) can result in the accumulation of toxic concentrations of the metals



within the tissue.



     Particulate matter is heterogeneous in size and composition, ranging in



mean diameter from <0.005 urn (molecular clusters) to >100 urn (visible dust



particles).  Particles occur in both solid and liquid phases and vary in



chemical composition from a single chemical species (e.g., H-SO^) to complex



combinations of chemical species.  They are produced directly from stationary



and mobile sources and are also formed secondarily  in the atmosphere through



chemical reactions.



     While coarse particles (>2.0 pm in mean diameter)  settle rapidly,  fine



particles (<2.0 urn in mean diameter) have prolonged atmospheric residence



times and are not strongly influenced by gravity.   Because  of the  complex



nature of particulate matter, dose-response studies are very difficult  to



conduct and data, therefore, are not available  for  making generalized  statements.
                                     1-75

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     Vegetation within terrestrial  ecosystems is sensitive to direct SO-



toxicity, as evidenced by changes in physiology, growth,  development, sur-



vival, fecundity,  and community composition.   Responses of individual organisms



reflect both direct or indirect effects.   Habitat modification by S02 results



in indirect effects occurring.   Nutrient cycling appears  to be a sensitive



indicator of subtle, yet important, environmental modification.   The removal



of certain lichen species can reduce nitrogen fixation in forest ecosystems.



     At the community level, chronic exposure to S0_ may result in a shift in



the species composition due to the elimination of individuals or populations



sensitive to the pollutant.  The tendency for SO- derivatives to accumulate in



the soil may have consequences for the microbiota inhabiting the upper soil



horizons.  The gradual accumulation of pollutant derivatives may cause a



change in soil chemistry and influence nutrient cycling and ecosystem pro-



ductivity.



      Particulate emissions have their greatest impact on terrestrial ecosystems



near  large emission sources, and participate matter in itself constitutes a



problem only in those areas where deposition rates are high.  Most of the



material deposited by wet and dry deposition on foliar surfaces in vegetated



areas is transferred to the soil.  Foliage may serve as a transitional site of



accumulation if previously deposited dry material becomes highly concentrated



during precipitation.  Ecological modifications may occur if the particles



contain toxic elements, even though deposition rates are moderate.   Solubility



of particle constituents is critical, since water-insoluble elements are not



mobile within an ecosystem.  Soils are long-term sites for the  retention of



many  constituents found in particulate matter.  Accumulation in the  soil-litter



layer influences ecological processes such as decomposition, mineralization,



nutrient cycling, and primary production.
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1.4.2  Acidic Precipitation



     Acidic precipitation is a major environmental  concern in many regions  of



the United States,  Canada,  northern Europe,  and Japan.   It has caused measurable



damage to aquatic ecosystems in Scandinavia, eastern Canada,  and the northeastern



United States.   Acidic precipitation has,  by acidifying lakes, induced the



extinction of fish, caused the breakdown of nutritional food  webs, and reduced



life in lakes to a few acid-tolerant species.   Acidic precipitation, in addition,



has damaged national monuments and buildings made of stone.   It also has the



potential for impoverishing sensitive soils, degrading natural terrestrial



ecosystems and for damaging forest ecosystems over the long-term (several



decades).



     In an atmosphere relatively free of natural or man-made  emissions of



sulfur and nitrogen oxides, precipitation would be expected to have a pH of



5.6 due to the presence of carbonic acid formed when atmospheric carbon dioxide



dissolves in water vapor.  The precipitation has become acidic chiefly due to



the large amounts of sulfur and nitrogen oxides being emitted from the combustion



of fossil fuels (particularly coal and oil).  In addition, substances present



in other gases, aerosols, and particulate matter from natural and man-made



sources also contribute to the acidity of precipitation.



     Precipitation acts as a scavenger, bringing to earth substances present



in the atmosphere.  The chemical composition of rain, therefore,  depends on



the substances present in the atmosphere.   On a global  scale  natural emissions



far exceed man's contributions; however, man-made emissions  are  localized  in



specific geographic areas, where they may be concentrated in the atmosphere  or



transported meteorologically to other areas downwind.



     Sulfur and nitrogen oxides are transformed  in  the  atmosphere to sulfates



and nitrates.  Sulfates and nitrates upon hydrolysis  in the  the atmosphere
                                      1-77

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contribute hydrogen ions (H+).   If hydrogen ions are present in significant



quantities, precipitation becomes acidic.   The acidity of precipitation is a



reflection of the balance between the major cations and anions in precipitation,



however, when determining the pH of precipitation all cations and anions



should be measured.   Currently the acidity of precipitation in the northeastern



United States is between 4.0 and 5.0.



     The ratio of sulfuric to nitric acids in precipitation varies from time



to time and place to place.   In much of the eastern United States, the average



annual ratio of sulfuric to nitric acids is currently 2:1; however, nitric



acid is apparently becoming progressively more important as a contributor of



hydrogen ions.  Preliminary estimates suggest that two-thirds of the sulfur



emitted into the atmosphere of eastern North America is probably deposited



there with the remainder leaving the atmosphere of the region and moving



primarily to the east.



     Tall stacks (some as high as 1200 ft.) from power plants have decreased



local pollution problems but may have increased the widespread wet and dry



deposition of sulfur and nitrogen oxides by permitting them to be carried long



distances by air streams.  Analysis of air-mass movements and chemical trans-



formations in the atmosphere indicates that acidic precipitation in one state



or region of the United States or Canada results in large part from emissions



which enter the atmosphere in other states or regions, often many hundreds of



miles from the original source.



     Acidic precipitation is only one special feature of the general phenome-



non of atmospheric deposition.  In addition to precipitation (wet deposition),



dry deposition also occurs.  The major chemical substances that are transferred



into ecosystems via acidic precipitation (wet deposition) are also transferred



into ecosystems by dry deposition when it is not raining or  snowing.   It  is,
                                     1-78

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therefore, Impossible to chemically distinguish the biolos'cal  effects of



acidic precipitations from those of dry deposition.



     The increased deposition of acidic substances into aquatic ecosystems



has, as of 1979, caused hundreds of lakes in the Adirondack Mountain region of



New York State, certain lakes in northern Minnesota, and many hundreds of



lakes in various parts of southern Ontario and Quebec to show acid stress.



Reduction or extinction of fish and other plant and animal populations has



occurred.  Lakes and streams in other regions of the United States and Canada



are also potentially vulnerable to stress by acidic precipitation.  Damage or



injury to aquatic or terrestrial organisms is most likely to occur when a



particularly sensitive life form or life stage (one with a narrow range of



tolerance), developing in poorly buffered waters or soils, coincides in time



and/or space with major episodic injections of acidic precipitation or other



injurious substance.



     The disappearance of fish from lakes and streams usually follows two



general patterns.  One pattern results when sudden short-term shifts in pH



occur, the other results from the  long-term decrease in the pH of the water.



A major episodic injection of acids and other soluble substances  occurs when



these substances present in polluted snow are released in the meltwater during



warm periods in winter or early spring.  The release of pollutants can cause



major and rapid short-term changes in acidity and chemical properties of



stream and lake waters.  Fish kills are a dramatic consequence of such episodic



injections into aquatic ecosystems.



     Equally dramatic  long-term changes  in aquatic  ecosystems  also  occur  from



the wet and dry deposition of acidic substances  because  the  chemical  compo-



sition of precipitation and dry deposition determine  in  part the  chemical



composition of  lake,  stream, and ground waters.   The  terrestrial  watershed
                                      1-79

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also plays a significant role as the chemical  composition of precipitation is



modified by chemical  and biological  weathering and exchange processes which



take place as precipitation washes over vegetation, percolates through the



soil and interacts with the underlying bedrock of the drainage basin in which



the precipitation occurs.   The situation is analogous to a gigantic, regional



scale titration with the lakes and streams acting as receiving vessels for



acidic additions from the atmosphere.   The titration end point of each lake is



predetermined by its hydrology and the capacity of the soils in the drainage



basin to assimilate the incoming acid.  If the soils and drainage basin can no



longer assimilate the incoming acids,  the lake and stream waters are changed



from conditions that are favorable for fish and other aquatic organisms to



conditions that inhibit reproduction and/or recruitment of populations of fish



and other aquatic organisms, some of which are food for fish.



     Prolonged acidity interferes with reproduction and spawning so that



changes in the structure of a population occur over time.  These changes



include a decrease in population density and a shift in size and age of the



population to one consisting primarily of larger and older fish.  The process



is  insidious, and effects on yield are often delayed and not recognizable



until the population is close to extinction.  This is particularly true for



late maturing species with long lives.  Large increases in the mortality rate



are not necessary to bring about population extinction.  Even relatively small



increases (5 to 50 percent) in mortality of fish eggs and fry can decrease



yield and bring about population extinction.  Many populations of freshwater



fish become extinct at a pH below 5.0 while the reproduction of many species



of  aquatic organisms is inhibited at pH's between  6.0 and 5.0.  Increasing



acidity of freshwater habitats causes shifts  in species, populations and



communities of most aquatic organisms to occur.  Virtually all  trophic  (food)



levels are affected.



                                      1-80

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     Interference with normal  reproductive processes in fish occurs,  not only



because of acidity of the water, but also due to increased concentrations of



certain metallic cations, notably aluminum, which become mobilized in acidified



lakes and streams.  The metallic cations may originate from the lake  or stream



watershed or be introduced in wet and dry deposition.   Among the inorganic



substances are elements such as manganese, zinc, copper, iron, boron, flourine,



bromine, aluminum, lead, iodine, nickel, cadmium, vanadium, mercury,  and



arsenic.  The underlined elements in the list above are essential  micronutrients



that are required by plants in small amounts.  However, at concentrations



above the amount required, these same elements, can be toxic to plants and



animals.  The non-esssential elements can also be toxic to plants  or  animals



when present in large amounts or when their mobility and solubility is increased



due to soil acidity.  Also the deposition of these metallic substances in



precipitation can affect the foliage and roots of plants and injure microorganisms



or animals that may ingest the plants.  In addition, these substances can harm



animals (including man) that may drink water containing these elements as well



as aquatic animals (especially fish) that live in the water.



     An indirect effect of acidification, which is potentially of concern to



human health is the possible contamination of edible fish and of human water



supplies.  Studies in the United States, Canada and Sweden have revealed the



presence of high mercury concentrations in fish from acidified regions.  Lead



and copper have been found in household plumbing systems with acidified water



supplies.  Persons drinking the water could  suffer from lead or copper poisoning.



     The drainage basins, soils, and wet and dry deposition of acidic substances



link aquatic and terrestrial ecosystems.  Effects of acidic precipitation on



soils may indirectly influence plant productivity by altering the supply and



availability of soil nutrients.  Increased additions of hydrogen  ions may
                                     1-81

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result in a gradual  acidification of the soil.   Soil  acidification increases



leaching of plant nutrients (such as calcium,  magnesium,  potassium, iron, and



manganese) and increases the rate of weathering of most minerals.   It also



makes phosphorous less available to plants.   Acidification also decreases the



rate of many soil microbiological processes  such as nitrogen fixation and the



breakdown of organic matter.   Various processes important in nutrient cycling



and critical in most ecosystems are known to be inhibited by increasing the



soil acidity.   Included among these processes are:   nitrogen fixation by



Rhizobium bacteria on legumes and by the free-living Azotobacter;  mineralization



of nitrogen from forest litter; nitrification of ammonium compounds; and



overall decay rates  of forest floor litter.



     Acidic precipitation increases the solubility and mobility of many cations



in the soil, thus increasing the concentration of trace metal  cations such as



aluminum, manganese, and zinc to toxic concentrations in soil  solutions.



Solubility and mobility of other heavy metals is also enhanced.  These toxic



or nutrient ions leached from the soil are transferred into surface and ground



waters from which they may enter lakes or streams and drinking water.  Plant



nutrients leached in the same way are lost to vegetation.



     Large quantities of hydrogen ions are added to soils as acidic precipitation



and, also, as a result of soil amendment and fertilization practices.  Acidifica-



tion by these processes can be readily controlled through normal soil management



practices such as liming.   Large areas of the United States, however, are not



cultivated and have  soils that are poorly buffered.  These soils are sus-



ceptible to further  acidification.  Many of these soils occur in forest and



wilderness areas.  Some of these soils could benefit from significant quantities



of plant nutrients,  including nitrogen and sulfur being added to soil in



precipitation and by dry deposition.  In some ecosystems these additions may
                                     1-82

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be important in the overall nutrient budgets; however, the additions are



subject to the vagaries of wind and weather.  Some substances, such as ammonium



and sulfate ions, are acidifying in their effects when taken up by plants from



the soil.



     Various specific biological effects of simulated acidic rain have been



demonstrated in controlled field and laboratory experiments.  But reliable



evidence of economic damage to agricultural crops, forests, and other natural



vegetation and to biological processes in soil by naturally occurring acidic



precipitation have been very rarely reported.



     Dry deposition of toxic gases, aerosols, and particulate matter causes



substantial damage to crops in certain regions of the United States.  The



possible effects of acid deposition must be considered together with the



serious economic crop damage caused by sulfur dioxide, ozone, oxides of nitrogen,



fluoride, and hydrogen chloride.



     Direct and  indirect injury to crops and forests  has been reported based



on  laboratory, greenhouse, and field experiments  in which  simulated acidic



rains were used, the following biological effects were observed:



     o    Formation of necrotic lesions and spots on  foliage.



     o    Accelerated erosion of waxes on leaf surfaces.



     o    Loss of  nutrients due to leaching from  exposed plant  surfaces.



     o    Inhibition of nodulation of  legumes leading to decreased  nitrogen



          fixation by symbiotic bacteria.



     o    Reduced yield of marketable  crops.



     o    Reduced  rates of leaf litter decomposition  leading to decreased



          mineralization of organically-bound nutrients.
                                      1-83

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     Soils differ by orders of magnitude in their susceptibility to acidifi-



cation.   Acidic additions are unlikely to damage calcareous (calcium carbonate)



soils, but metal deposition may.   Soils with very low cation exchange capacities



are very susceptible to increased acidification.   In addition,  the consequences



of acidic additions to soils vary greatly.   Such variations depend upon the



rates and recent history of the acidic additions, the character of the vegetation,



natural  rates of acid formation in the soil, and the physical-chemical properties



of the parent material of the soil.



     Acidic precipitation plays an important role in the deterioration of



stone buildings, monuments, and a variety of materials.   Stone has traditionally



been considered one of the most durable building materials used by man.  What



is forgotten is that the structures built with stone which were not durable



have long since disappeared.



     High acidity promotes corrosion of metals because hydrogen ions act as a



sink for the electrons liberated during the critical corrosion process.



Acidic precipitation forms a layer of moisture on the surface of material and



by adding hydrogen and sulfate ions increases corrosion.  Atmospheric sulfur



compounds react with the carbonates in limestone and dolomites, calcareous



sandstone, and mortars to form calcium sulfate.   Blistering, scaling, and loss



of surface cohesion occurs, which in turn induces similar effects in neighboring



materials not in themselves subject to direct attack.  Acid rain may also



leach ions from stonework just as acidic runoff and ground water leaches ions



from soil bedrock.



1.4.3  Effects on Visibility and Climate



     Pollutants released into the atmosphere alter the environment  in  several



ways, such as by reducing visibility and affecting climate.  Visibility  refers



to various characteristics  of the optical environment such as clarity  and
                                     1-84

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trueness of color, as well as the distance over which one can see distant



objects.  Climate is defined as the long-term manifestation of weather at a



given location over a specified period, usually several decades.



     Meteorologically, visibility refers to the greatest distance at which a



bTack object can be distinguished against the horizon sky.  Visibility and



visual range are reduced by atmospheric particles which scatter and absorb



light.  Gases play a relatively minor role in visibility reduction.  Data on



scattering and absorption are used to determine the extinction coefficient, a



measure of the visible range.



      Light scattering by particles, especially fine particles, is the most



important cause of lowered visibility.  Particles with diameters similar to



the wave-length of light (0.1 to 1.0 urn) are the most efficient light scatterers



per unit mass.  Sulfates generally fall within this size range.  An aerosol



composed of particles of 0.5 urn diameter scatters about a billion times more



light than does the same mass of air.



      Sulfates reduce visibility on both local and regional scales.  Considerable



evidence from chemical-mass  balance methods indicates that sulfates, which



constitute approximately 50  percent of the fine aerosol mass  in the atmosphere,



cause more visibility degradation than do other chemical  species.  Ambient



sulfate concentrations and sulfur oxides emission trends  from the  early  and



middle  1960s to the early 1970s closely parallel visibility  trends.  A 30-year



record  of spatial and temporal trends  of coal  use suggests that  increases  in



haziness have been associated with increases  in sulfur  oxides emissions  since



the 1950s.



      Visibility or visual air quality  can be  measured  by  determining  total



extinction, which is the  sum of  light  scattering, and  absorption.   In many



cases,  absorption is assumed to  be small  and  total  extinction is estimated by
                                      1-85

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light scattering.   Visibility measurement approaches include:   the observe



method, in which a black object is viewed against the horizon;  the contrast



telephotometric method, in which the brightness of a black object is compared



with the brightness of the horizon; and the long-path extinction method, in



which the decrease in intensity of a beam of light is measured  as a function



of range.   Indirect methods to measure visibility include scattering and



absorption measurements.  The nephelometric method measures the  scattering



component of extinction.   Absorption can be measured in several ways, such as



by determining the difference between extinction and scattering; however, no



single method has been proven totally effective.



     Pollutants released into the atmosphere may lead to slow and subtle



changes in atmospheric composition and, possibly, climate.  For example, a



fraction of the solar radiation may be absorbed by aerosols, further reducing



the amount of radiation reaching the earth's surface and, at the same time,



heating the aerosol layer itself.   On a hazy day, direct solar  radiation is



reduced to about one-half of that on a clear day.  Most of this light is



diffused as skylight, while there is an overall loss of up to about 10 to 20



percent of the radiation reaching the surface.   Changes in certain measures of



daylight in the Eastern U.S.  are consistent with observed patterns of haziness



and can be attributed to man-made fine particles, including sulfates and



nitrates.   A possible link between haziness, decreased solar radiation, and



decreased surface temperature in the East Central U.S. has been pointed out



recently.




     Atmospheric aerosols, primarily those with strong water affinity, influence



cloud formation.  Essentially all water vapor condensation occurs via nucleation,



i.e., by deposition on cloud condensation nuclei or ice nuclei. Both types of



nuclei are aerosol particles emitted from natural or manmade sources.  Their
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quantity and nucleation properties have an effect on cloudiness,  which in turn



influences the amount of solar energy reaching the earth's surface.  In urban



areas, increases in cloudiness and the quantity of precipitation are well



established.  The incorporation of particles into cloud and fog droplets can




change the quality and quantity of precipitation by altering its chemical



composition.  Effects on visibility and climate of the type summarized above



may exert significant impacts on aesthetic and economic values.



1.4.4  Materials Damage and Soiling Effects



     Atmospheric sulfur oxides and particulate matter damage materials through



deterioration and soiling.  Physical and economic damage functions have been



developed to estimate materials damage from sulfur oxides and particulate



matter. Their accuracy is hampered by problems in identifying dose-response



relationships for specific damage from specific pollutants because of many



variables influencing exposure in the environment.  Damage functions indicate



that reductions in SO- and particulate matter will decrease economic damage.



In most cases, the cost of replacing a product that has suffered premature



damage is far greater than the cost of using protective measures or alternative



materials resistant to damage.



     A principal deleterious  effect of sulfur oxides  is to accelerate the



corrosion of metals to form metal sulfates.  Soluble  sulfates  in rust can



stimulate further corrosion because of their hygroscopicity and electrical



conductivity, while insoluble sulfates in  rust provide corrosion protective




properties.



      Laboratory studies show  that corrosion  is most  severe  under conditions  of



high  SO-  concentration and high  humidity.   Field studies  show that  corrosion



rates  are related to the  amount  of  sulfur  compounds  on  exposed surfaces of




susceptible metals.
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     Many  nonmetallic materials are also damaged by  sulfur oxides  and/or



 soiled  by  particles.  These materials  include paints and  other protective



 coatings,  fabrics,  building materials,  electrical  components, paper,  leather,



 plastics,  and works of art.



     The chemical action  of SO- erodes  paint layers;  light and ozone  cause



 degradation  of  the  polymer.   Paint films permeable to water  may  be penetrated



 by  sulfur  dioxide and aerosols containing  sulfuric acid.  SO- can  sensitize



 dried paint  film, permitting  water to  be absorbed  during  the weathering cycle,



 especially at high  humidity.



     Cotton, rayon, and nylon fabrics  are  damaged  by acids derived from SO-



 Polyester, acrylic, and polypropylene  fibers are damaged—by—ammefmnn—s-tri-fa-te-



.-particles  by acid hydrolysis-



     Certain types  of building stone adsorb S0_ and  undergo  chemical  changes



 that weaken  the material  and  lead to erosion.  Concrete reacts with SO- and



 suffers erosion and spelling  if not protected by paint.   Concrete  is  also



 subject to chemical damage  by sodium sulfate.  The action of SO- has  been



 implicated in the deterioration of ancient buildings.  Sulfate damage has been



 found  in medieval stained glass windows, bronze sculptures,  marble and stone



 statues, and fresco paintings on  lime  plaster.



     Sulfur  dioxide and particles have deleterious effects on electrical



 contacts.  To reduce damage,  contacts  are  electroplated with corrosion-resistant



 metals.



     Sulfur  dioxide is  readily absorbed by paper  and oxidized  to sulfuric  acid



 by  metallic  impurities; the paper then hydrolyzes  and loses  strength. Leather



 also has a high capacity  for absorption of SO  •  the  material is  weakened  by



 hydrolysis of the proteins  that make  up the  collagens in  leather.   The weathering



 of  plastics  has been  attributed  in  part to the  joint action  of  SO- and light.
                                      1-88

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     Airborne particles contribute to corrosion by producing acid electrolytes;



by functioning as nuclei to promote the condensation of water containing SO-



or sulfates; and by forming a solid structure to retain active pollutants such



as chlorides, organic matter, and sulfates.   Deposition of dust and soot on



building materials reduces the esthetic appeal of structures and can also



result in erosion and direct chemical attack.  Fabrics soiled by airborne



particles require more frequent cleaning, which leads to increased costs and



reduces their life.



     Exterior paints are soiled by particles of soot, tarry acids, and various



other constituents such as sulfates of iron, copper, calcium, and zinc.  Staining



and pitting of auto finishes have been traced to iron particles from nearby



industrial operations and to alkali mortar dust from buildings being demolished.



It has been suggested that particles promote the chemical deterioration of



paint by acting as wicks to transfer SO- to the underlying surface.  Acid



smut, emitted mainly from large industrial operations such as oil-fired boilers,



has been shown to cause significant damage to auto finishes, paints, and



fabrics in the area near the source.  The effect is  localized because the



emitted particles are very large and tend to be deposited quickly.  Damage may



be severe because the smut, which may contain as much as 30 percent sulfuric




acid, is highly corrosive.



     A number of  investigators have produced estimates  of the economic  costs



of materials damage.  A significant economic cost  has been  attributed to this




damage, although  the estimates produced  vary greatly.
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1.5  HEALTH EFFECTS ASPECTS
     In the first three chapters (Chapters 11, 12, and 13) of the fourth
volume, information is assessed regarding the uptake,  deposition, and
absorption of sulfur oxides and particulate matter and various health effects
demonstrated to be associated with these pollutants by means of animal toxicology
and human clinical studies.  Such studies offer the advantage of being able to
study biological processes specifically associated with particular pollutant
exposures under highly controlled laboratory conditions.
     The animal toxicology studies are particularly valuable in providing both
qualitative characterization of the full ranges of health effects caused in
mammalian species by SOp and particulate matter exposures and information on
the mechanisms of action underlying such effects.   However, considerable
caution must be applied in extrapolating quantitative  dose-effect relationships
defined in animal studies to humans.
     Of course, some such definition of quantitative dose-effect relationships
can be more directly ascertained by means of human clinical studies.   Such
studies, however, are also somewhat limited, in terms  of the kinds of health
effects potentially characterized by them.   More specifically, only the effects
of short-term (a few hours) exposures or perhaps a few repeated short exposures
are typically investigated in such studies.   Also, the nature of the effects
studied are generally limited to detection of onset of relatively transient
changes in pulmonary or cardiac functions and, at times,  related physiological
or biochemical parameters.   In addition, restrictions  arising from human rights
considerations often result in limitations that preclude thorough investigation
of health effects experienced by the most sensitive members of the population.
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     Community health (epidemiology) studies offer several  Advantages that go
beyond what can be determined by animal  toxicology or human clinical  studies,
in that health effects of both short- and long-term pollutant exposures (including
the presence of other pollutants) can be studied and sensitive members of
populations at special risk for particular effects identified.  In addition,
epidemiology evaluations are not limited to the study of more or less transient
physiological or biochemical effects but also include investigation of both
acute and chronic disease effects induced by S0x and particulate matter pollution
and associated human mortality as well.   Information from epidemiology studies,
then, together with the results from animal and human clinical studies, help
to provide more complete understanding of the health effects of environmental
air pollutants such as sulfur oxides and particulate matter.
1.5.1  Respiratory Tract Deposition and Biological Fate
     Airborne particles and sulfur dioxide are deposited in the various regions
of human and animal respiratory tracts.   Particles are deposited by gravitational
settling, impaction, diffusion, interception, and electrostatic attraction.
Gases are deposited due to convective and diffusional processes.  Chemical and
physical properties of particles and SO^, respiratory tract anatomy, and
airflow patterns during respiration also influence deposition.  In addition,
deposition is influenced by individual respiration and anatomical features,
which can vary considerably.  Nevertheless, the state of knowledge concerning
the deposition of inhaled aerosols and gases is sufficient  to predict  regional
deposition.
     The respiratory tract is usually described in terms of three functional
regions:  (1) nasopharyngeal, (2) tracheobronchial,  and (3) pulmonary. The
deposition of inhaled material depends on its aerodynamic properties.  Material
                                     1-91

-------
soluble in body fluids will  readily enter the blood stream.   Hygroscopic and



deliquescent solid particles can grow in the humid respiratory tract,  depositing



in greater proportion and in larger airways than can insoluble or hydrophobic



particles.



     Relatively insoluble material  deposits in various regions according to



particle size.   If it lands  on ciliated epithelium, either in the nasopharyngeal



or tracheobronchial airways, it will be moved by mucous flow to the throat and



be swallowed.   Relatively insoluble material deposited on nonciliated  surfaces



in the pulmonary regions may be phagocytized by alveolar macrophages,  may



enter the interstitium and remain in the lung for an extended period,  or may



be translocated via lymphatic drainage.   Some material from the pulmonary



region may enter the tracheobronchial region and be cleared via the mucociliary



conveyor.  Very insoluble particles deposited in the pulmonary region  may



remain there for months or years, while similar particles deposited in the



tracheobronchial or nasopharyngeal  regions are cleared in a few days.



     Sulfur dioxide may be deposited directly in the airways or enter  into a



variety of gas-particle chemical and physical reactions.   S0? may dissolve in



liquid droplet aerosols or hygroscopic and deliquescent particles and  thereby



lead to increased deposition deep in the respiratory tract.   The aerodynamic



properties of particles and  the route of breathing affect deposition.



     A nose-breathing person taking 15 breaths per minute with a tidal volume



of 1450 ml would have deposited in the deep lung: 35% of the 0.2 pm particles



inhaled; 25% of the 1 pm particles inhaled; 10% of the 5 urn particles  inhaled;



and almost none of the 10 urn particles inhaled.  During mouth breathing these



deposition percentages would be expected to be about 35 percent, 30 percent,
                                     1-92

-------
55 percent and 10 percent,  respectively.   This difference shows that pulmonary
deposition of large particles is greater during mouth breathing than during
nose breathing.   Some particles that normally are collected in the nasopharyngeal
region during nose breathing may pass the glottis and be deposited in the
upper part of, the tracheobronchial tree during mouth breathing.   One study-   .<
        '/TO       lo                                                          *
          that about 56- percent of 15 urn unit density spheres may enter the
tracheobronchial  tree during mouth breathing, while almost none of these
particles enter the tracheobronchial tree during nose breathing.
     Since many biological studies of inhaled aerosols and SOp involve experi-
mental animals, it is important to understand how humans and animals differ
with respect to pulmonary deposition and clearance.  Small rodents tend to
have smaller lung deposition fractions of particles less than 3 urn D   and
                                                                    QI
somewhat higher pulmonary clearance rates than humans.  In dogs, however,
particle deposition and clearance parallel that in humans.  Mouth-breathing
people bypass most of the nasal filtration of S02 and have much higher lung
exposure than nose-breathing experimental animals.  This may be a very important
factor for humans under heavy work or exercise conditions.  The three functional
regions of the respiratory tract can each be characterized by mechanisms of
deposition, clearance, and potential biological responses.  The respiratory
tract is itself a target of inhaled particles and gases, and it is also the
portal of entry to other organs that may be affected.
1.5.2  Animal Toxicology Studies
     Although major gaps exist in the animal toxicological data base on sulfur
oxides (SO ) and particulate matter (PM), such data can be useful in:
          y\

     (1)  delineating the full range of toxicological effects of SQX and
          PM, including the effects of both very  high-level exposures and
          prolonged low-level exposures;
                                     1-93

-------
     (2)  elucidating potential  mechanisms of toxicity and defining
          structure-function relationships between physico-chemical
          properties of these agents and particular health effects;

     (3)  supporting the findings of human clinical and epidemiological
          studies investigating  analogous health endpoints; and

     (4)  investigating of health effects (e.g., potential mutagenesis or
          carcinogenesis effects), which neither can be experimentally
          induced in human clinical studies nor easily or precisely
          assessed with current  epidemiology methods.

     The use of the toxicological data base from animal studies in order to
make comparisons between man and animals involves assumptions that a chemical
has ultimate mechanisms of toxicity involving chemical and biological structures
which are similar in man and animals.   Although the precise mechanisms underlying
most effects are currently unknown, it is typically acknowledged that common
biochemical  events are probably  involved for both man and other mammalian
animal  species.   For example, if a pollutant is observed to cause toxicity by
destroying a chemical structure  essential for normal activity of a cell membrane
in one  mammalian species, then that cell structure is likely at risk in other
mammalian species and humans. The critical issue then becomes delivery of
the pollutant to that structure  in different animal species and human beings.
Thus, qualitative extrapolation  of the type of effect from animal to man has a
theoretical  basis; and that basis becomes even stronger if the same effect is
observed in  a number of animal species, since species differences in susceptibility
can exist.   As will be discussed later, certain experimental evidence indicates
the occurrence of similar effects in man and animals do occur in cases where
the same biological endpoint has been examined.
                                     1-94

-------
     The current animal toxicological data base on the effects of participate


matter and sulfur oxides is relatively limited.  In addition, sulfuric acid

                                               ^K^J-<^
studies which used whole body exposure chambers a&e- confounded by an ammonia-


induced conversion of I^SO^.  Since such an event would not occur to an


equivalent degree in human exposure chambers, direct quantitative comparison


of animal and human HLSO. exposure effects would not be accurate, and failure


to find an effect in animal studies does not rule out  its possible occurence


in humans in the absence of ammonia*or other agents more often fetmd—rn^anrnraHH


Hv-JB9.-ABd--.testing conditions-.  On the other hand, many animal studies which


have been conducted with SO^, (NH.^SO., and sulfuric  acid used very high


concentrations relative to ambient air and with exposures of short duration


(less than 1 day) and the direct relevance of  such exposure conditions to


assessment of quantitative dose-effect/dose-response relationships for humans


can be questioned.  Turning to a summary of animal study results, note that


certain studies have looked at the effects of  relatively high  levels of  SOp,


particles, or aerosols on pulmonary  system morphology  or function in various


animal species.  Some animal  studies  have also examined the effects of such


exposures on immune system functions  and susceptibility to bacterial or  viral


infections.  Certain key findings are summarized below.


1.5.2.1  Effects of Acute and Chronic Exposure to  Particles or S0,,--The  results


of most of the animal studies discussed in Chapter 12  regarding  the,effects  of
                                                           (Jut~CJK£**J*fiUsX^> ^ I.TK^t/s

acute and chronic exposure to various particles or SO^ alone/\jan^summarized  in


Tables 1-8, 1-9, and 1-10.  Key findings and their possible  implications for


human health assessment are discussed in what  follows.
                                      1-95

-------
                           TABLE 1-8.   SUMMARY OF EFFECTS OF ACUTE EXPOSURE  TO  <1  mg/m3  PARTICLES3  IN ANIMALS
Concentration
0.05 mg/m3 CdCl2
0.1 mg/m3 NiCl2
0.1 mg/m3 CdCl2 or
0.2 mg/m3 CdS04
0.1 mg/m3 H2S04


0.19-1.4 mg/m3 H2S04
0.19 mg/m3 CdCl2
0.25 mg/m3 NiCl2
0.25 mg/m3
ZnS04, (NH4)2 S04
0.4-2.1 mg/m3
(NH4)2S04
0.43 mg/m3
CuS04
0.5 mg/m3
(NH4)2S04
0.5 or 1.0 mg/m3
Duration
2 hr
2 hr
2 hr (CdCl2)
3 hr (CdS04)
1 hr


1 hr
2 hr
2 hr
1 hr

1 hr

1 hr

1 hr

1 hr
Species
Hamster
Hamster
Mouse

Guinea pig


Donkey
Mouse
Mouse
Guinea pig

Donkey

Guinea pig

Guinea pig

Dog
Results
Decreased ciliary beat frequency in trachea.
Decreased ciliary beating frequency in trachea.
Increased susceptibility to streptococcal lung infection.

41% increase in flow resistance and 27% decrease in
compliance. (Higher concentrations did not cause these
effects in a similar study, Reference 53).
Bronchial mucociliary clearance was slowed.
Decreased number of antibody-producing spleen cells.
Decreased number of antibody-producing spleen cells
22% increase in flow resistance

No change in pulmonary resistance or dynamic compliance

No significant change in flow resistance. 11%
increase in compliance.
23% increase in flow resistance and 27% decrease in
compliance.
At the lower concentration, tracheal mucociliary transport
Reference
Adalis et al.157
Adalis et al.156
Gardner et al. ,7Q
Ehrlich et al.
179
Amdur «t,al. "~
Amdur1 /J

Schlesinger et al.
Graham et al.160
Graham et al.160
123
Amdur and Corn
Amdur J
999
Schlesinger et al.

Amdur et a I.130

Amdur et al.130

Wolff et al.224
0.5 mg/m3 NiCl2
2 hr
               Mouse
 was accelerated,  but 1 wk later,  it was depressed.   At
 1 mg/m3,  the rate was depressed,  even at 1 wk post-
 exposure.


Increased  susceptibility to streptococcal lung
 infection.
Adkins et al.155

-------
                                                   TABLE 1-8 (continued).





t— *
1
UD
•-J

Concentration
0.6 mg/m3 CuS04
0.8-1.51 mg/m3
H2S04
0.9 mg/m3
H2S04
0.9 mg/m3
H2S04
0.91 mg/m3
ZnS04
0.93 mg/m3
NH4HS04
a

Duration
3 hr
1 hr
2 hr
2 hr
1 hr
1 hr


Species
Mouse
Donkey
Hamster
Mouse
Guinea pig
Guinea pig


Results
Increased susceptibility to streptococcal lung infection
No change in pulmonary resistance or dynamic compliance.
Decreased tracheal ciliary beat frequency.
No effect on susceptibility to infectious bacterial
pulmonary disease.
4158 increase in flow resistance.
15% increase in flow resistance and 15% decrease in
compliance
•

Reference
Ehrlich et al.
Schlesinger et
-ip-
Grose et al.
Schiff et al.
Gardner *t al.
Amdur and Corn'
AmdurI/0
Amdur et al.13(

                                                                                                                             179
                                                                                                                                 222
                                                                                                                             182

                                                                                                                             145
                                                                                                                             123
this issue completely.  Data are presented for lowest effective concentration tested.   See the text and tables
of Chapter 12 for details.  (See Table 12-8 for more complete details on effects of particles on airway resistance
in guinea pigs.)

-------
                          TABLE 1-9.  SUMMARY OF EFFECTS OF CHRONIC EXPOSURE TO <1 mg/m3  PARTICLES3  IN ANNALS

Concentration
0.08, 0.1 mg/m3
H2S04
0.38, 0.48 mg/m3
H2S04





0.89 mg/m3
H2S04


0.1 mg/m3
H2S04

0.01, 0.15 mg/m3
Pb203; 0.01 mg/m3
PbCl2, 0.11 mg/m3
NiCl2, 0.12 mg/m3
NiO
Duration Species
52 wk, Guinea pig
continuous
78 wk, Monkey
continuous





21 hr/day, Dog
225 or 620
days

1 hr/day, Donkey
5 days/wk,
several mo
3 mo con- Rat
tinuous for
Pb203; 12
hr/day, 6
days/wk, 2 mo
Results
No effects on hematology, pulmonary function.

No hematological changes. At 0.38 mg/m3 there were
bronchiolar epithelial hyperplasia and thickening
of the respiratory bronchioles. Particle size
influenced the effects. Exposure to 0.48 mg/m3 altered
distribution of ventilation early in the exposure
period. Respiratory rate increased at 0.38 mg/m3.
Other functional parameters were not affected.
No morphological changes at 620 days. At 225 days,
CO diffusing capacity was decreased. At 620 days,
CO diffusing capacity was decreased and other pulmonary
function measurements were affected.
After 4 wk erratic bronchial mucociliary rates were
observed. During the second 3 mo of exposure, clearance
was slowed in animals never pre-exposed.
Decreased number of alveolar macrophages after Pb203.
NiO increased the number of alveolar macrophages.
The soluble metals did not change the number of
alveolar macrophages.

Reference
Q? 197
Alarie et al. >iy/

1Q7
Alarie et al .






Lewis et al.89'104



223
Schlesinger et al .


Bingham et al.152'153




aThe toxicity of particles is dependent on particle size.   For simplicity, this table does not address this issue
 compiletely.  Data are presented for lowest effective concentration tested.   See the text and tables of Chapter 12
 for details.

-------
                                                                                                            11
                       TABLE  1-10.   SUMMARY OF EFFECTS OF EXPOSURE TO <13.1 mg/m3 (5 ppm) SULFUR DIOXIDE IN ANIMALS
i
10
V£>
Concentration
0.26 or 2.62 mg/m3
(0.1 or 1 ppm)


0.37, 1.7 or
3.35 mg/m3 (0.14,
0.64, or 1.28 ppm)
0.42 or 0.84 mg/m3
(0.16 or 0.32 ppm)
2.62, 5.24, 13.1 mg/m3
(1, 2, or 5 ppm)
2.62 mg/m3
(1 ppm)
2.62 or 13.1 mg/m3
(1 or 5 ppm)
9.43 mg/m3
(3.6 ppm)
13.1 mg/m3 (5 ppm)

Duration
7 hr/day,
5 days/wk,
25 days

78 wk,
continuous

1 hr

1 hr

1.5 hr/day

24 hr

7 days,
continuous
6 hr/day,
20 days
Species
Rat



Monkey


Guinea pig

Dog

Dog

Rat

Mouse

Guinea pig

Results
0.26 mg/m3 (0.1 ppm) accelerated tracheobronchial
clearance at day 10 and 23. The higher concentration
accelerated clearance at day 10, but at day 25,
clearance was decreased.
No effects on pulmonary morphology or morphology.


Increase in flow resistance.
-
Increased bronchial reactivity to aerosols of a
bronchoconstrictor agent (acetylcholine).
Decreased mucous flow.

Phagocytosis of alveolar macrophages increased after
3 or 4 days in culture.
Exposure to S02, whether alone or in combination with
a virus, produced weight loss.
No change in bacterial clearance.

Reference
Ferin and Leach



on QI
Alarie et al. u>*1


Amdur and Underbill
Amdur et al.
Islam et al.102

Hirsch et al.111

iqc
Katz and Laskfn133

Lebowitz and.
Fairchild
Ry lander ,«-
Rylander et al.
   13.1 mg/m3 (5 ppm)
3 hr/day,      Mouse
1-15 days and
24 hr/day,
1-3 mo
No change in mortality due to a laboratory-induced
 streptococcal infection.
                                                                                                                   Ehrlich
                                                                                                                          178

-------
As indicated by the results summarized- in Tables
                                                                          .
                                                            d-jrlfr virtually  *
                                                             i£*£ JZtf&sv&si*-' J&*feaJ
all particles examined to date cause health effects^  TWy   |nd^vei^ty ,of^
the effects are chemical-specific and concentration dependelit/t  For woclasses /
of effects (histamine release and increased susceptibility to infectious
dfsease), the cation of a given particle species was found to have more influence
on the toxicity than the anion.  For example, in regard to increasing susceptibility
to infection, CdSO. was more toxic than ZnSO., while NaSO. and (NH. )„$(). had
no significant effect even at high concentrations.   Guinea pigs experienced
approximately a 40% increase in airway resistance with exposure either to 0.1
mg/m  HpS04 or 0.5 mg/m  -ZnSO. and- (Nlh)2SO^.   The ranking of toxicological
potency varies with site of deposition or physiological process.  For example,
the ranking of sul fates for airway resistance does not precisely agree with
that for effects on susceptibility to pulmonary infection.  These findings
illustrate the complexity of toxicological responses and show the need for a
broad data base.
     The size of the particle plays a role in the health effects observed.
Unfortunately, no known experimental data compare the effects of particles
which would predominately be deposited in the head vs. the respiratory tract.
Studies generally have been conducted with particles that tend to enter the
deep portions of the lung where gas-exchange occurs.  In studies employing
^SO^ or ZnSO. and (NH.KSO. particles of various sizes that would predominantly
deposit in the gaseous exchange region, it was found that pulmonary flow
resistance increased as particle size decreased.
     As for particulate matter dose-effect relationships, in contrast to
results discussed below for SOp alone, acute (1-2 hr) exposure of the several
different animal species listed to much lower levels of different particulate
                                     1-100

-------
 substances  have been shown to lead to various -pafcfcephysiological  changes,

 e.g.,  slowed mucociliary clearance, increased  flow resistance and compliance,

^anjLJncr4taj>jiU-Jll^F-reyrstflftfHt- and comp44tmce,  and increased susceptibility to

 an infectious bacterial  agent.   Such effects occurred with exposures to such

 pa~rticulate substances as H2$04, ZnS04, CuS04,  and Ni and CdCl2 at levels  as
                    3
 low as 100-200 (jg/m .   Also chronic exposures  of various animal species to

 sulfate aerosols,  as shown on Table 1-8, results in such effects as bronchiolar

 epithelial  hyperplasia,  slowed mucociliary clearance rates, and decreased  CO

 diffusing capacity.  Certain of these changes  occur at chronic exposure levels
                   3
 of 100 to 500 |jg/m  of sulfate aerosol.  Other effects, e.g., altered numbers

 of alveolar macrophages, have also been observed with chronic exposures to

 lead and nickel oxide particle concentrations  of around 100 ug/m .

      Some,  but not all,  animal and controlled human studies have shown that
                                          3
 acute exposure to high (>1 ppm; 2860 ug/m ) concentrations of S0? increases

 airway resistance.  At lower concentrations, only in animal studies on the

 guinea pig, has increased airway resistance been observed, i.e., at 420 to 840
     o
 ug/m .  It appears, however, that the mechanism of 50,,-induced flow resistance

 is likely similar in man and animals, since atropine inhibits the response in

 both types of subjects.   This suggests that the effect of SOp is mediated by

 parasympathetic motor pathways which alter airway smooth muscle tone.

      In contrast to the above, human and animal studies of effects of H2S04 on

 pulmonary function, have yielded variable results.  Certain  concentrations of

 H^SO. increased resistance in some guinea pig studies, but not in  human studies.

 In guinea pigs, but not in humans, H2$04 is far more potent  than S02  in increasing

 resistance.  In guinea pigs, salt  (NaCl) potentiates the  response  to  S02.   In

 some human studies, a similar potentiation occurred.   If  the hypothesis of
                                      1-101

-------
H2S04 formation as a possible explanation were true,  then H2$04 can likely
affect human airway resistance.   However, in other human studies,  SO2 plus
NaCl was not found to result in  potentiation.
     Some possible reasons for this difference in H2$04 action between man and
animals can be offered.   Perhaps the mechanism for H^SO^ has a species
specificity.  In animals histamine release is one of  the hypothesized mechanism.
Man also has histamine stores and reacts to histamine release.   Nonetheless,
the detailed metabolism and action of histamine in man and animals is not fully
known.  Another possible difference between human and animal studies is the
extent neutralization of KUSO. by ammonia in exposure chambers, with much
higher ammonia levels present in animal  chambers from the urine of the test
subjects.  Both human and animal S02 studies, however, have shown  approximately
a 10 percent incidence of more responsive individuals.  It could be possible
that the positive animal studies had an  unusually high incidence of these
"sensitives" and the humans an unusually low incidence of "sensitives".
Another possibility is that the  negative guinea pig studies more closely
reflect the human condition, and neither the resistance of man nor animals is
highly affected by H2S04-
     Mucociliary clearance has also been investigated.  In dogs, rats, and
man, short-term exposure to lower concentrations of S0? and H?S04  generally
accelerated bronchial clearance  of particles, while higher concentrations
slowed clearance.   In donkeys, single or repeated exposures to low concen-
trations of H2S04 appeared to slow bronchial clearance.  Such findings would
imply that these chemicals might increase the residence times of substances in
the lungs that are normally removed faster.  This slowed clearance could
influence susceptibility to infectious disease.  Guinea pigs exposed to S02
experienced an increase in laboratory-induced viral pneumonia.  Some animal
                                     1-102

-------
studies indicate that acute exposure to a variety of sulfates increases
susceptibility to infectious (bacterial) pulmonary disease in mice, probably
by affecting alveolar macrophages and additional host defense mechanisms.
Metal sulfates caused these effects, but much higher concentrations of HpSO.,
(NH4)2S04, and S02 did not.
1.5.2.2  Effects of Exposures to Combinations of SO  and Particles—Some
investigations with animals have focused on the effects of S02 in combination
with particles.  The results of such studies are summarized in Table 1-11.
Long-term exposure of mice to carbon plus S02 or carbon alone caused
alterations in the immune system which were more extensive than those caused
by SOp alone.   Combinations of H^SO. and carbon resulted in greater morphological
effects in the lungs of mice than exposure to carbon alone.  Similar combination
exposures caused more effects on tracheal tissue than did carbon or H2SO.
alone.  In mice exposed acutely to 0- and then to H^SO., an additive effect
was observed on susceptibility to infectious respiratory disease.  However,
this same regimen resulted in antagonistic effects on reduction of tracheal
ciliary beating frequency.  For long-term exposure, the effects of 03 plus
H2S04 on lung morphology species were attributed to 0, alone.  The mechanisms
for the toxicological interactions described above are not known; the effects
of ammonia neutralization of H2$0. during long exposure studies, however,
cannot be ruled out.
     A variety of other chronic studies have been conducted with single chemicals
                                                              3
and pollutant combinations.  At concentrations below 13.4 mg/m   (5.12 ppm) S02
for up to 18 months, there were no morphological or pulmonary functional
changes in monkeys.  A similar level of S02 caused increased pulmonary flow
resistance and decreased lung compliance in dogs after 225 days  of exposure.
                                     1-103

-------
                     TABLE 1-11.  SUMMARY OF EFFECTS OF COMBINATIONS OF PARTICLES3 (<1 mg/m3)  AND  SULFUR  DIOXIDE
                                                    413.1 mg/m3,  5 ppm) IN ANIMALS

Concentration
0.79-0.84 mg/m3
(0.3-0.32 ppm) S02
+0.9 mg/m3
(NH4)2S04, NH4HS04,
or Na2S04
0.94 mg/m3
(0.36 ppm) S02
+0.4 mg/m3 CuS04
(— •
^ 2.62 mg/m3 (1 ppm)
§ S02 + 1 mg/m3 Nad
2.62 mg/m3 (1 ppm)
S02 + aerosols of
metal salts
2. 6 mg/m3 (1 ppm)
S02 + 0.9 mg/m3
H2S04
0.08 mg/m3 H2S04 +
0.45 mg/m3 fly ash
0.28, 2.62, or 13.1
mg/m3 (0.11, 1, or
5 ppm) S02 + 0.56
mg/m3 fly ash
5.24 mg/m3 (2 ppm)
S02 +0.56 mg/m3
carbon
Duration
1 hr
1 hr
1 hr
1 hr
18 mo,
continuous
12 mo,
continuous
78 wk,
continuous
52 wk,
continuous
100 hr/wk,
192 days
Species
Guinea pig
Guinea pig
Guinea pig
Guinea pig
Monkey
Guinea pig
Monkey
Guinea pig
Mouse
Results Reference
130
Additive effect on increased flow resistance. Amdur et al.
Potentiation of increased flow resistance Amdur et al.
At 80% relative humidity, NaCl potentiated the response McJilton et al.
to S02 flow (increased flow resistance).
96
Manganous chloride, ferrous sulfate and sodium Amdur and Underhill
orthovanadate potentiated the response to S02
flow (increased flow resistance).
92
No effects on hematology or pulmonary function. Alarie et al.
Morphological changes in bronchial mucosa. Addition of
0.41 mg/m3 fly ash did not alter the results.
92
No changes on hematology, pulmonary function, or Alarie et al.
morphology.
199
No effects on pulmonary function, morphology, or Alarie et al.
hematology.
Alterations in the pulmonary and systemic humoral immune Zarkower
system.
aThe toxicity of particles is dependent on particle
 text and tables of Chapter 12.
size which is not presented on this table.   For details, see the

-------
                                                 TABLE  1-11.   continued).
  Concentration
Duration
Species
              Results
Reference
  Various  combinations,
   including  1.1 mg/m3
    (0.42  ppm)  S02 +
    0.09 mg/m3  H2S04
16 hr/day
 68 mo
Dog
No changes in pulmonary function after 18 or 36 mo of
 exposure.  Some alterations in pulmonary function after
 61 mo.   Thirty-two to 36 mo after exposure ceased,
 morphological effects were observed (i.e., enlarged air
 spaces  and increased number and size of interalveolar
 pores,  loss of cilia, nonciliated bronchiolar cell
 hyperplasia and loss of interalveolar septa in alveolar
 ducts).   These changes appear similar to centrilobular
 emphysema.
Lewis et al.'
 Hyde et al.    1B6
 Vaughan et al.
,_, The toxicity  of  particles  is  dependent on  particle size which is  not  presented  on  this  table.
  For details,  see the  text  and tables  of Chapter 12,
o
01

-------
                                                           3
Long-term exposure of monkeys to H^SO. (as low as 0.38 mg/m ) caused morpholo-


gical and some pulmonary function changes.  A higher concentration (0.89


mg/m ) caused no structural changes in dogs,  but pulmonary function decrements


were observed.  Guinea pigs were not affected after a one year exposure to 0.1

   ~3
mg/m  H2S04-

     Effects were also noted after chronic exposure to pollutant combinations,


but in most cases the contributions of the individual chemical species to the


effects of the mixture are obscure.  Although various mixtures of S0?, hLSO.,


and fly ash caused pulmonary morphologic changes, no effects on pulmonary


function were found in monkeys.   It appeared that fly ash did not contribute


to the effects.   Fly ash, when combined with S02 or H^SO. did not significantly


affect guinea pigs.  When dogs received mixtures of SO^ and HpSO. for 620


days, the effects on pulmonary function were attributed to the HLSO^ (0.89

    3
mg/m ).  Several morphological changes were observed in the lungs of dogs 32


to 36 months after a 68 month exposure to 1.1 mg/m  (0.42 ppm) S02 plus 0.09

    3
mg/m  H^SO. ceased.  It was hypothesized that these changes were analagous to


an incipient stage of human proximal acinar (centrilobular) emphysema.  It is


not known whether the disease state progressed, abated, or remained stable


over this post-exposure period.   A shorter exposure (approximately 18 months)


to a higher concentration of KLSO. (0.9 mg/m ) plus 2.62 mg/m  (1 ppm) S0?


caused less serious morphological effects in monkeys.  Concentration-time


relationships of effects in the above studies are not clear.   But from the


above-mentioned dog and monkey study, it appears that time of exposure is an


important factor in the development of disease.  However, concentration does


play a role, as evidenced from the concentration-dependent effects after


either acute or chronic exposure.
                                     1-106

-------
1.5.3  Studies on the Oncogenic Properties of SO  and PM
                                                /\

     The oncogenic potential of SCL has been studied, but the findings are not

yet conclusive.   In one series of experiments, hamsters and rats were exposed

for 98 weeks or a lifetime to various regimens of SOp and benzo(a)pyrene, a

known carcinogen.  No lung tumors or other pathological effects were observed

for hamsters.   Rats, however, had an increased incidence of tumors after

                     3                                    3
exposure to 26.2 mg/m  (10 ppm) for 6 hr/day and 9.17 mg/m  (3.5 ppm) S02 plus
       3
10 mg/m  benzo(a)pyrene for 1 hr/day.  In a later study, rats exposed for 6

hr/day to 26.2 mg/m3 (10 ppm) S02 and for 1 hr/day to 10.5 mg/m3 (4 ppm) S02
            3
plus 10 mg/m  benzo(a)pyrene had a cancer (squamous cell carcinoma) incidence

of 19.6 percent.  This incidence contrasts with a zero percent incidence in
                                    o
the group receiving air or 26.2 mg/m  (10 ppm) S02 for 6 hr/day and a 9 percent

incidence in the group exposed for 1 hr/day to 10.5 mg/m  (4 ppm) S0« plus 10

mg/m  benzo(a)pyrene.  (See Table 12-3 in Chapter 12 for details.)  The reports

do not specifically state whether the 26.2 mg/m  (10 ppm) SOp was given before,

during, or after the exposure to 10.5 mg/m  (4 ppm) SOp plus benzo(a)pyrene.
Thus, it is difficult to speculate on potential prompter/or initiator effects.

     In another study, mice were exposed to T310 mg^m  (500/ppm) 50^ for a

min/day, 5 days/wk for a lifetime.  This exposure increased the carcinoma

incidence in females from 0 to 18 percent.  No such change occurred in the

males.   Primary pulmonary neoplasias increased in both males and females.  The

investigators conclude that the increased incidence of primary lung tumors is

a result of an S0?-induced inflammatory reaction, "followed by a state of

apparent tolerance, which accelerates the inherent tendency of these mice to

develop lung tumor spontaneously but does not justify the classification of

S02 as a chemical carcinogen as generally understood."  From the single  study
                                     1-107

-------
of S02 alone in mice and the two studies of S02 plus benzo(a)pyrene in rats,
no definitive conclusions can be drawn about the carcinogenic or co-carcinogenic
potential of S02<   However, the data reported thus far do justify some concern,
and these issues need to be more extensively addressed in further experimental
research.
     It is commonly believed that fundamental similarities exist between the
molecular mechanisms of both mutagenesis and carcinogenesis.   This assumption
is based on the theory that a chemical interaction with DMA and/or other
critical cellular macromolecules initiates a genetic change which may lead to
carcinogenic transformation.  Therefore, the demonstration of mutagenic activity
for a substance is generally taken as strong presumptive evidence for the
existence of carcinogenic activity.   It follows that an investigation of the
mutagenicity of a substance may be predictive of carcinogenic potential, and
may serve as an early warning of a possible threat to human health.
1.5.4  Experimental Investigations of Human Subjects
     Studies of human subjects exposed to sulfur oxides and particulate matter
explore physiological and sensory responses to these pollutants under controlled
conditions.   A major limitation of such studies is that they do not reflect
the long exposure durations which typically occur in the ambient environment.
However, they may reflect short-term peak exposures, such as may occur in
certain urban situations.  The results of human clinical studies discussed in
Chapter 13 are summarized in Tables 1-12 to 1-14 below.
     The typical response to S02 exposures is an increase in pulmonary flow
resistance.   Most subjects respond to short exposures of 5 ppm (13,000 ug/tn3),
while other subjects react to lower levels of S02-  Significant decreases in
nasal mucous flow rate have been demonstrated at 1 ppm; 2620 ug/m  .  Pulmonary
                                     1-108

-------
1-u.  rutMDMMrr EFFECTS of AEMSOLS
Duration of
Concentration exposure (.Ins)
SO. (1.6 - 5 pp.) 5
MCI 0.22 u. MB
SO (9-60 pp.) S
MCI (OB - 0.95 UB)

SO (0.5, 1.0 and 5.0 pp.) IS
Saline panicles 7.0 u.

Ibid 30

SO (1.1 - 3.6 pp.) . 30
NK1 2.0-2.7 M«/m
MB • 0.25 M"
SO (1-2. 4-7. 14-17 pp.) 30
Nici 10-30 mg/m
MB 0.15 UB
SO (1 pp.) 60
NiCl 1 «g/«
MB 0.9 M og « 2.0 M"
Ibid 60

AsmnnluB sulfata 150
100 MO/"

6
Aamonlua blsulfate 150
85 MO/" aerosol s1u
distribution
g,4 jaa_tn»»4ll__^
0. 35-5.0 BB/B3 H-SO. 15
MB 1 M"


3-39 Bo/"3 H-SO. 10-60
MB 1-1.5 M"


SO- (1-60 pp.) plus Variable
H;O- to for. H-SO.
atrosol 2 4
OB 1.8 and 4.6 MB
H.SO. .1st 120
f 1000 MO/.
MB 0.5 M" (00 * 2-59)
H SO aerosol . 10
10, 100. 1000 MB/"
MB 0.1 MB
H-SO. (75 MO/"3) i20
HMD 0.48 - 0.81 M"
H-SO. (0. 100, -300, 60
Or 1,000 MO/"
MMO 0.5 MB
(oo • 1-9)



Number of '
subjects
13
10

9

9
(asthmatics)

10

12
9
(asthmatic!)

(normals)

5 (normal)
4 (ozone
sensitive)
(asthmatics)
16

15


Variable



24


10


6 normal
6 asthmatics

6 normal
6 asthmatics
10






Source
Mask
Mask

Orel

(Mask
(Exercise for
10 .1 mites)

Oral

Oral
Oral

Mask

Chamber
(exercise)


Chamber
(exercise)

Naik (rest)


Hask (rest)
Chamber (rest)


(Rest)


Chamber
(exercise)

Oral


Chamber
(exercise)
Nasal






Effect!
Synerolsttc Increases In
airway resistance with aerosol
Airway resistance greater after
exposure to aerosol than to
exposure to SO. alone
NEF-— significantly greater
dKreeses In aerosol (NaCl)
condition
y y
•flv?0?'ano*tT7oecrease
significantly In aerosol
condition
No effect on pulannary functions

Change! In pulannary function
sl.llar to changes due to SO.
alone not Influenced by aerolol
Significant decreases In V .-_
• Ml V mmmUt MB
max 75X
No pulmonary effects demon
strata*
No changes In pulmonary
functions


No changes In pulmonary
functions

Respiratory rates Increased,
•ax. Imp. and explretory
flow rates and tidal
decreased volu.es
Longer particles due to "wet
•1st" resulted In Increased
flow resistance cough, rales
bronchoconstrlctlon
Airway resistance
Increased especially
with larger particles

No pulmonary function
changet but Increased
trecheobronchlel clearance
No pulmonary function
changes, no alterations
In gas transport
No pulmonary effects
In either group
No pulennary function
effects
Rronclal mucoclllary
clearance t following
100 MB/" »^ut * following
1000 MO/" mucoclllary
clearance distal to trachea
Reference
1 1'
Toyama. 1962
Nakamura. 1964

Snail and Luchilnger.
1969

Koentg et al., 1979

Burton et al., 1969

Frank et al . , 1964
Koenlo. 1979

Koanlg, 1979

•ell and Hackney, 1977;


Klalnman and Hackney, 1978;
Aral et al., 1979

Amour etTl . . 1952


SI. and Pattle, 1957



Toyama and Nakamura,
1964

Newhouse et al., 1978


Sachner et al., 1978


Klalnman and Hackney,
1978; Avol et al., 1979
Ltppmann et el., 1979







-------
                                                                                         TMU 1-13.  EFFECTS OF SO,
 I
I—>
t—'
O
Pollutant
Concentration (PPM)
.17
.17
.40
.SO
1.0
1.0. S.O
1.0. 1.0, S.O
1. 5. 13
1. S. 15
1.1-1.6
1.0. 5.0, 25.0
S.O
1-23
1.1-80
2.5-50
4-6
1-8
5.0
Duration of
Exposure
120 Minutes
120 Minutes
120 Minutes
180 Minutes
120 Minutes
60 Minutes
120 Minutes
1 Minutes
10- 10 Minute*
30 Minutes
10 Minute*
HP to 6 hr/day
4.5 hrs.
60 Minutes
10 Minutes
10 Minute*
10 Minutes
10 Minutes
120 Minutes
Effects Reference
No pulMonary effects Bates and Huucha. 1973;
Hazucha and lates, 197S
No pulannary effects tall et al.. 1977
No pulMonary effects Bodl et al. , 1979
Horvath and Follnsgea. 1977
HNFR decreased 2.7X; delayed Jaeger, et al.. 1979
•sthM* *
ffj^af^tf^^^^^taU. .„, lllMCta UTJ-

Ho effects observed HcJIltan, 1976
Increase In nasal flow Andersen, et al.. 1974
resistance, decrees* In na**l
MUCUS flow
Light exercls* potentiates effect KralSMan, et al. , 1976
af S02; NFF 40V decreased
No change* In pulse rate. Frank, et al. , 1962
respiratory rate. pulMonary flow
resistance Increased at S and 13
POM but less during nasal breathing; I ^ff)
&T t fl&rt '/ jyti. 4ief^TJ^U4^J~ " fi J^&t**^*- ^*?
Increase In U at S0| «bov«7 Frank et al.. 1964 &3L0-&.
Deep breathing produced n* effect* Burton et al. , 1969
Significant decree*** In expire- Anderson, et •!., 1974
tor* flow and FEV, n. decreased
MUCUS flow
Nuttier ef colds slMllar In both Andersen, et al.. 1977
group* but severity let* In SO.
axposed group* *
BronchoconttrlctloM SIM and Pattle, 1169
BronchocomtrlctlM Sla and fettle. 1957
Increased Insptretory and Aba. 1967
respiratory resistance
Airway conductan* decreased Nadel, 1965
reflex effect
Pulse rate, respiratory rate Amur, et al.. 1951
Increased; tidal voluM* decreased
NNFR decreased 8.SX; Increased Nevnouse. et al. 1978
                                                                                                 tricheobronchlal  clearance

-------
1-14.   PULMONARY EFFECTS OF SO. AND OTHER AIR POLLUTANTS
Concentration
S02 (0.37 ppM)
and
03 (0.37 ppM)
S02 (0.37 ppM)
and
03 (0.37 ppH)
S02 (0.40 ppm)
and
0, (0.40 ppM
S02 (5 ppM)
and
N02 (5 ppM)
S02 (5 ppn.)
M02 (5 ppm)
and
03 (0.1 ppM)
S02 (0.12 ppM)
N02 (0.06 ppM)
and
03 (0.025 pp.)
Duration of Nuaber of
exposure (mlns) subjects Source
120 8 Chamber
(exercise)

120 4 (normal) Chamber
4 (ozone (exercise)
sensitive)
4 (from Bates)
120 9 Chamber
(exercise)

120 11 Chamber
(exercise)
120 11 Chamber
(exercise)

120 11 Chamber
(exercise)

Effects
Decrease pulmonary functions
(In synerglstlc effect of
S02 on 03) FRC, FEV-j^ Q.
MMFR, MEFR_~~
Unable to confirm
synerglstlc effects
pulmonary decrement due
to 0, alone
Unable to confirm
synerglstlc effects
changes due to ozone
alone
No changes 1n P , P
pHa or TGr -Rt °2 C02
Increased
No changes In P , P ,
pHa or TGr -RtC02 °2
Increased .

No changes 1n pulmonary
functions

	 TT 	
Reference
Hazucha and
Bates, 1973, 1975

Bell et al., 1977

Horvath and Follnsbee
(1977);
Bedl et al. (1979)
von Nledlng et al., 1979
von Nledlng et al., 1979

von Nledlng et al., 1979


-------
responses to SOp exposure apparently persist for some 5 to 10 minutes, while


the change in mucous flow rates persists  for several  hours following exposure.

Approximately 10 to 20 percent of individuals studied under controlled conditions


appear to be sensitive to exposures as low as 1 ppm SO^.   Effects on certain


sensory functions, (e.g., dark adaptation, odor perception) are evident at S02


concentrations below 1 ppm (2600 ug/m ).

     A number of factors influence responses to SO,,.   Sulfur dioxide is removed


more efficiently if individuals breathe by nose than by mouth.   This removal


is related to the high solubility of SOp  in water;  most of the SO,, in inhaled


air is absorbed in the moist linings of the nose (and upper airways).   When

subjects breathe by mouth, more SOp reaches deeper  areas of the lungs.  Subjects


who exercise at a level requiring mouth breathing show significant decreases
                                                                     o
in pulmonary function at an SOp concentration of 0.75 ppm (1,950 ug/m ).


     Asthmatics may be more sensitive to  S02, but the data on such individuals


are not definitive.  Sensory awareness of the presence of SOp may be decreased


in individuals chronically exposed to SOp.


     The presence of particles with S02 may influence physiologic responses.


Particulate matter may function as a carrier, bringing more SOp into the

lungs, or may induce chemical reactions to convert  SOp into sulfates.   The


presence of aerosols such as NaCl does not appear to modify the pulmonary


response to S02 in most normal subjects.   However,  it has been found that


adolescent extrinsic asthmatic subjects exhibit pulmonary function changes in


the small airways when orally breathing 1 ppm S02 and NaCl aerosols.  One


study shows that brief exercise during this exposure induces changes  in both

large and small airways.
                                     1-112

-------
     Results of a chamber study indicated synergistic effects on pulmonary


functions in response to a combination of ozone (0.37 ppm) and sulfur dioxide


(0.37 ppm).  This synergisic effect has not been demonstrated in more recent


studies suggesting that the effect reported in the earlier study may have been


caused by the presence of some other substances in the exposure chamber.


     Few studies have examined the effects of exposure to sulfuric acid and


sulfates.  Sensory responses to sulfuric acid have not been clearly defined.


Pulmonary functions do not appear to be influenced by exposure to hLSO. at

                               2
concentrations up to 1,000 pg/m .   Mucociliary transport in the airways distal


to the trachea is affected more by H^SO. exposure than is transport in the


trachea.   This effect depends upon the concentration levels of HpSO., i.e.,

                    3
exposure to 100 ug/m  increases bronchial clearance, while exposure to 1,000


ug/m  reduces clearance.  No adverse pulmonary effects have been reported in

                                                                 3
normal or asthmatic subjects after 2.5 hour exposures to 100 ug/m  ammonium

                    3
bisulfate or 85 ug/m  ammonium sulfate.


1.5.5  Community Health Observational Studies


     Animal  and clinical studies provide incomplete information about the


health effects of sulfur oxides and particulate matter.   The principal


limitations of animal studies are problems with extrapolating quantitative


dose effect dose-response relationships from animal to man and the difficulties


of mounting studies large enough to detect small health effects, particularly


small mortality effects, that may be of public health significance.  Health


effects of chronic exposure typically cannot be assessed in human clinical


studies,  and ethical constraints limit the range and quality of acute exposures


that can be investigated in such studies.  Both types of investigations are


limited in that the mix of pollutants found in the ambient air is difficult to
                                     1-113

-------
characterize and duplicate in the laboratory.   Thus,  the  evidence  from



observational  studies plays an important and crucial  role in  assessing the



health effects of sulfur oxides and particulate matter.



     Observational  or community health studies  also  have  important limitations.



Since the level of exposure is not under the control  of the investigator,



observational  studies can demonstrate associations but not necessarily cause



and effect relationships.  Also, since sulfur oxides  and  particulate matter



have common sources, they frequently covary in  level  in the observational



setting, making it difficult to distinguish health effects of these pollutants



individually.   In addition, other factors such  as temperature or frequency of



smoking may covary with the level of sulfur oxides and particulate matter, so



that effects of pollutants cannot readily be separated from effects of these



other factors.  A final limitation of observational  studies to be  mentioned



here is the difficulty of relating pollution levels  at one or a few community



air monitoring stations to health effects seen  in persons living in the vicinity



of those stations.   Further discussion of these and  other methodological



issues of importance in evaluating observational studies  can be found in



Chapter 14.



     Despite the above limitations, an enormous number of epidemiology studies



have been conducted over the past 30 years in order  to better define both



qualitative and quantitative relationships between  various health effects and



sulfur oxides and particulate matter in the ambient  air;  and Chapter 14 of



this document provides a rather comprehensive and thorough critical assessment



of such studies.  The information contained in Chapter 14 is summarized below.
                                     1-114

-------
1.5.5.1  Overview Summary of Chapter 14 Contents—In Chapter 14,  an extensive
array of information is discussed concerning:   (1)  methodological  considerations
that must be taken into account in evaluating community health epidemiology
studies (Section 14.1); (2)  critical assessment of practical  applications  of
air quality measurement techniques employed in the collection  of  sulfur oxides
and particulate matter data utilized in related community health  studies
(Section 14.2); (3)  critical review of such studies on mortality effects
associated with acute and chronic exposures to sulfur oxides and  particulates
(Section 14.3); (4)  critical review of studies of morbidity associated with
acute exposures to the same pollutants (Section 14.4); and (5) critical
assessment of morbidity effects associated with chronic exposures to sulfur
oxides and particulate matter.  In addition, in the summary and conclusions
section of the chapter, there are discussed other published reviews and critical
evaluations of the subject material and the interpretations derived from such
reviews are compared.
     Through the discussion in Section 14.1 of Chapter 14, it is  seen that
numerous methodological factors, including covarying or confounding variables,
can potentially affect the results and interpretation of community health
studies.  It is also seen, through material summarized in Section 14.2 of the
chapter, that a number of sources of errors have been identified  as having
affected sulfur oxides and particulate matter air quality measurements obtained
in both the United Kingdom and the United States and used in British and
American epidemiology studies which provide the bulk of the information reviewed
in the chapter.  It was further noted that while such errors in air measurements
can at times be fairly large, they also often act to  introduce both positive
and negative biases into air quality data sets that tend  to cancel each  other
                                     1-115

-------
out, especially when considering data grouped or averaged over long time
periods (monthly; annually) from the same sites or across several  geographic
areas classed as "low" or "high" pollution areas.   At other times, however, it
also became clear that certain measurement errors were such as to  introduce
either consistently negative or positive bias into particular British or
American sulfur oxides or particulate matter data sets used in various community
epidemiology studies providing information on quantitative air pollution/health
effects relationships.  It was further noted that such biases due  to air
quality measurement errors must be taken into account in evaluating such
epidemiology studies -- not for the purpose of discrediting such studies but
rather to understand better the error limits likely associated with the reported
quantitative findings derived from them and to thereby allow for more accurate
interpretation of overall patterns of pertinent results.
     Turning to the critical assessments of pertinent community health mortality
and morbidity studies contained in Sections 4.3, 4.4 and 4.5 of Chapter 14,
results of many of the better known and often cited quantitative and qualitative
studies discussed in the chapter are summarized in a series of tables presented
below along with summary statements regarding the results of community health
studies of mortality and morbidity affects associated with short-  and long-term
exposures to sulfur oxides and particulate matter.
Health Effects of Acute Exposure to SO,, and Particulate Matter—Qualitative
studies demonstrating increased mortality effects to be associated with sulfur
oxides and particulate matter air pollution are summarized in Table 1-14.
Note that these studies demonstrate, for example, associations between such
pollution and significantly increased mortality from bronchitis, pneumonia and
heart disease.   Also note that essentially all population groups are affected,
                                     1-116

-------
    TABLE   l-14a  QUALITATIVE ASSOCIATION  OF  GEOGRAPHIC  DIFFERENCES  IN  MORTALITY
                  WITH RESIDENCE  IN AREAS  OF  HEAVY  AIR POLLUTION
Pemberton?and
 Goldberg
Stocks
     138,164-167
     224-225
Gorham
                Q
Gore and Shaddick
 and Hewitt:
Haastrom et al.
 Zeidberg et al
 Sprague et al.
16
 17
Lepper et al.
            227
Jacobs and
 Landoc1/b
                    1950-1952 bronchitis mortality
                     rates in men 45 years of age
                     and older in county boroughs
                     of England and Wales
                    Bronchitis mortality, 1950-1953,
                     in urban and rural areas of
                     Britian, with adjustments for
                     population density and social
                     i ndex

                    1950-1954 deaths, 53 counties
                     of England, Scotland, and
                     Wales

                    Mortality in London, 1954-1958
                     and in 1950-1952, respectively
                    1949-1960 deaths for each  cause
                     in Nashville, Tenn., categor-
                     ized by census tract into 3
                     degrees of air pollution  and
                     3 econimic classes  (levels
                     not accurately determined)
                    1964/1965 mortality rates in
                     Chicago census tracts strati--
                     fied by socioeconomic class and
                     SO  concentration
                    1968/1970 mortality rates
                     in Charleston, S.C. ,
                     industrial vs. non-indus-
                     trial areas
Sulfur oxide concentrations
 (sulfation rates) were con-
 sistently correlated with
 bronchitis death rates in the
 35 county boroughs analyzed

Significant correlation of mor-
 tality from bronchitis and
 pneumonia among men, and from
 bronchitis among females, with
 smoke density

Bronchitis mortality was strongly
 correlated with acidity of
 winter precipitation

Duration of residence in London
 significantly correlated with
 bronchitis mortality, after
 adjusting for social class

Within the middle social class,
 total respiratory disease
 mortality, but not bronchitis
 and emphysema mortality, were
 significantly assoicated with
 sulfation rates and social index.
 White infant mortality rates
 were significantly related to
 sulfation rates

Increased respiratory disease
 death rates in areas of inter-
 mediate and high SO- concen-
 tration, within a socioeconomic
 status, without a consistent
 mortality gradient between the
 areas of intermediate and high
 S0_ concentration

Higher total and heart disease
 mortality rates in  industrial
 area
                                            1-117

-------
                              TABLE l-l4a.(continued)
Morn's et al.
             24
Collins et al.
              287
Beaker et al.
             323
Toyama
      330
Lindeberg
         321
1960-72 mortality rates
 compared to 1959-60 air
 pollution levels

Death rates in children  0-14
 years of age, 1958-1964,
 in relation to social and air
 pollution indices in 83 county
 boroughs of England and Wales
Thanksgiving 1966 Fog,
 New York
Mortality in districts
 of Tokyo
Deaths in Oslo winters
Mortality higher in smokers
 with lower air pollution
 exposures

Partial correlation analysis
 suggested that indices of
 domestic and industrial
 pollution account for a
 differences in mortality
 from bronchopneumonia and
 all respiratory diseases among
 children 0-1 year of age

Complaints of cough, phlegm,
 wheezing, breath!essness, eye
 irritation increased with in-
 creasing air pollution

Bronchitis mortatliy associated
 with dustfall (but not cardio-
 vascular, pneumonia or cancer
 mortality)

Average deaths per week, 1958-65
 winter, correlated with pollution
                                         1-118

-------
both males and females and both the young and the old; the very young (infants)


and the very old, especially the infirm and those with preexisting respiratory


or cardiovascular diseases, however, appear to be at most risk.   Essentially


the same patterns can be discerned for morbidity effects as demonstrated by


qualitative studies summarized in Table 1-15.


     Studies providing evidence of quantitative associations between acute


health effects and air levels of sulfur oxides and particulate matter are


summarized in Table 1-16.  Overall, various British, Dutch, Japanese and


American episodic mortality studies have yielded results that appear to suggest


that mortality effects might occur at or above 300-500 ug/m  S02>   The three


non-episodic mortality studies listed in the table suggest that mortality

                                                         3
effects can be seen when TSP levels reach 500 to 600 ug/m  and S0? concentrations


reach 300 to 500 ug/m .   These three studies summarize a relatively small body


of data from two winters in London and five winters in New York City.  The


stated effect levels may be conservative (high), however, since examination of


the detailed evidence from these studies presented in Section 14.3 of Chapter


14 suggests the possibility of an exposure-response relationship at lower


levels of these pollutants.  More complex time series studies of daily mortality


have also found associations between mortality and these pollutants at lower


levels.  The size of the estimated effects has proved to be sensitive to model


specification and choice of other adjustment variables.  Although the possibility


of mortality effects of TSP and S02 levels below those  cited  in Table 1-16


cannot be excluded, it is unlikely that this question can  be  resolved in the


near future by observational studies.  Thus, the minimum air  levels  at which

                                                                              3
acute mortality increases might be projected to be  seen would be  300-500 ug/m


for both TSP and S02, based on the results summarized  in Table  1-16.
                                      1-119

-------
                TABLE 1-15.  QUALITATIVE STUDIES OF AIR POLLUTION  AND ACUTE
                                    RESPIRATORY  DISEASE
     Study
         Characteristics
      Findings
Angel  et  ai.69
Attack rates of minor respiratory
 illness among 85 London workers,
 examined every 3 weeks, October
 1962-May 1963.
Attack rates were associated
 with weekly average smoke
 and S02 concentrations.
 Levy  et al.70
Schoettlin and
 Landau288
Ze-fdberg et a I.289
Cowan et al.290
Greenberg et al.291
Weill et al.292
 Carroll293
Hospital admissions for respira-
 tory disease in Hamilton,
 Ontario, correlated with
 sulfur oxide/particulate air
 pollution index.

137 asthmatics reporting attacks
 on daily occurrence of asthma,
 September-December, 1956, in
 Los Angeles Basin.

Study during 1 year of 49 adults
 and 34 children with asthma in
 Nashville, Tenn.
History of asthma, and skin tests
 of University of Minnesota
 students, in relation to dust
 from nearby grain elevator.

New York City hospital emergency
 room visits for asthma in
 month of September.
Retrospective study of emergency
 room visits to New Orleans
 Charity Hospital.
Increased hospital admissions on'
 heavy pollution days, except at
 one hospital far removed from
 major pollution sources.
Significantly more asthma on days
 of heavier oxidant pollution.
 No adjustment was made for
 variations in temperature or season

Doubling of asthma attack rates
 in persons living in more
 polluted neighborhoods.  No
 adjustment for demographic or
 social factors.

Significant association between
 grain-dust exposure and
 asthma attacks.
Emergency room visits strongly
 associated with onset of cold
 weather but not with degrees of
 air pollution during the one
 month of study.

Periodic "epidemics" of asthma
 in New Orleans could not be
 traced to any common pollutant
 exposure.
                                          1-120

-------
                              TABLE  1-15 (continued)
   Study
         Characteristics
      Findings
Phelps294
 Meyer295_
"Tokyo-Yokohama asthma" in
 American servicemen stationed
 in Japan after World War II.
Glassej et al.
Chiaramonte
 et al.297
             296
Derrick57
Rao298
Goldstein and
 Black58
Emergency room visits in seven
 New York city hospitals during
 the November 1966 air pollution
 episode.

Emergency room visits at a
 Brooklyn hospital during a
 November 1966 air pollution
 episode.
Nighttime emergency room visits
 for asthma in Brisbane,
 Australia.

Pediatric emergency room visits
 for asthma at Kings County
 Hospital, Brooklyn, October
 1970-March 1971.
Emergency room visits for
 asthma at a hospital in
 Harlem and in Brooklyn,
 September-December 1970 and
 September-December 1971.
Disease primarily in smokers
 attributed to allergic response
 to atmospheric substances that
 could not be characterized.
 Patients improved after leaving
 the area and were immediately
 affected on return.   Some had
 long-term effects afterwards.

Increased emergency room visits
 for asthma in three of seven
 hospitals studied.
Statistically significant
 increase in emergency room
 visits for asthma and for
 all respiratory diseases, con-
 tinuing to 3 days after the
 peak air pollution concen-
 trations.

Negative correlation between
 asthma visits with degrees
 of smoke shade.

Negative correlation of asthma
 visits with degrees of smoke
 shade.  Lack of temperature
 adjustments.  Considerable
 distance of hospital district
 from air monitoring stations.

Temperature adjusted asthma
 rates positively correlated with
 S02 values in Brooklyn but
 not in Harlem.  In 1971 period,
 50-90% increase in asthma
 visits on 12 days of heaviest
 pollution.
                                        1-121

-------
                               TABLE  1-15  (continued)
    Study
         Characteristics
      Findings
Finklea et al.117
Finklea
et al.122 123
Incidence of acute respiratory
 disease, determined at 2-week
 intervals, in parents of
 nursery schoolchildren residing
 in Chicago, December 1969-
 November 1970.
Daily diaries kept by 50
 asthmatics in each of three
 New York City area communi-
 ties, October 1970-May 1971.
Acute lower respiratory
 illness rates were signifi-
 cantly lower among families
 living in neighborhoods
 where air pollution had been
 substantially decreased.
 Rates were adjusted for social
 class, smoking, residential
 mobility, and season of year.
 Cannot quantitate pollutant
 exposures.

Temperature-adjusted attack
 rates significantly correlated
 with total particulates in two
 of the communities.  Increase
 in relative risk from days of
 light to heavy pollution was
 relatively small.   High turnover
 in reporting panels.
*Reference 251
                                       1-122

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TABLE  1-16   SUMMARY TABLE - ACUTE EXPOSURE EFFECTS
Type of Study
Mortality (episodic)
British
Dutch
Japanese
USA
(Non-episodic)

Reference
Table 14-1
Table 14-2
Table 14-2
Table 14-2
Martin and Bradley11
Martin6
Glasser and
Greenburg222
24-hour average pollutant levels
at which effects appear
Effects observed
Excess deaths
Excess deaths
Excess deaths
Excess deaths
Increases in daily mortality
Increases in daily mortality
above the 15 moving average
Increases in daily mortality
TSP ((jg/mj)
546*
300-500
285
570 (5 CoH)
500*
500*
350-450**
S02 ((jg/mj)
994
500
1800
400-532
(1 hr max: 2288)
300
400
524

Morbidity

Martin16
Lawther et al . 53
Greenberg et al.196
Lawther et al . 52
Stebbings. and
Hayes190'
Increases in hospital admissions 500*
for cardiac or respiratory illness
Worsening of health status among
195 bronchi tics
Increased cardio-respiratory
ER visits
Increased clinical condition
in CB patients
Increased symptoms in chronic
bronchitis (CB) patients
344* (250 BS)
357** (260 BS)
529* (400 BS)
344* (250-350 BS)
200 (60 RSP)
(12SS) 8 SN)
400
300-500
715
450
300
100

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                                                   TABLE 1-16  (continued).
Type of Study

Reference
Cohen et al.55
Effects observed
Increased AS attacks
24-hour average pollutant levels
at which effects appear
TSP (Mg/m') S02 (pg/m3)
150 (20SS) 200
                         McCarroll et al.163    Increased ARI daily                160* (1.2 COH)          372
                                                 inc/prev

                         Cassell et al.208 209  Increased ARI average               205* (2 COH)           452
                                                 daily inc/prev

                         Stebbings and          Decreased FEV0<75 (children)           700                 300
                          Fogleman et al.216
"Converted from BS (British Smoke).

-------
     Numerous studies reporting morbidity effects associated with acute



exposures are also listed in Table 1-16.  Worsening of symptoms in bronchitis



patients and increased hospital admissions in Britain were reported to occur



at_TSP and S02 levels of 300 or 350 to 500 ug/m3 or more.  A United States



study, however, found exacerbation of symptoms among bronchi tics at 200 ug/m3

                3

TSP and 100 ug/m  SO,, and asthmatics were reported to show increased attacks


           3                 3
at 150 ug/m  TSP and 200 ug/m  SO,,.  Also, spirometry tests were reported to



show decreases in lung function at 700 ug/m3 TSP and 300 ug/m3 S02.   However,



in another study not listed, van der Lende saw improvement in lung function

                                                             o
among adults when pollution levels were reduced from 245 ug/m  (TSP) and 300



ug/m  (SO,,).  Acute upper and/or lower respiratory illness also has been



reported to occur at levels as low as at 160 ug/m  TSP (24-hour averages).



Overall, then, the summarized results suggest that (1) very severe morbidity



effects, e.g., worsening of symptoms in bronchitic patients, clearly occur at



TSP and SOp levels of approximately 300 or 350 to 500 ug/m , and (2) less



severe but significant morbidity effects may occur with acute exposure at



levels of approximately 150-300 ug/m .   These studies do not, however, provide



a basis for separately estimating the health effects of S02 and particulates.



Since these two forms of pollution have important common sources, their levels



tend to usually vary together over time.



Health Effects of Chronic Exposure to SO,, and Particulate Matter—The results



of qualitative studies on relationships between sulfur oxides and particulate



matter pollution are summarized in Table 117.  Many of the same types of



observations as stated above for population groups at apparent special risk



also apply here; that is, the elderly, the infirm, and children appear to be



most severely affected health-wise by chronic exposures.
                                     1-125

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     Many well-known and often-cited mortality  and  morbidity  studies  that have



been reported as demonstrating quantitative  associations  between  mortality,



illnesses, or decrements in pulmonary function  with chronic (monthly  or annual



average) levels of particulate matter of S02 are  summarized in Table  1-18.   As



seen in that table, the two mortality studies suggest that mortality  effects



can occur at annual levels of 125 to 140 ug/m3  or less of TSP and S02-   In the



morbidity studies, lower respiratory disease, chronic bronchitis, and reduced



pulmonary function results were reported that are indicative  of morbidity



effects likely clearly occurring at annual average  TSP or SO^ levels  of 150 to

        o

250 ug/m  or more.  Other study results summarized  in the table suggest an



association of various morbidity effects with concentrations  in excess of


                   3                                                      3
about 70 to 80 ug/m  TSP and SOp concentration  in excess  of 96 to 107 ug/m .



As with studies of acute effects, many of these studies could be  further



interpreted not only as demonstrating that health effects are exposure-related



but also that they increase as these pollutants increase  over the entire range



of exposures studied and no clear-cut "no effect" level can be determined on



the basis of presently available information.  Also, in general,  these studies



cannot be used to distinguish between the effects of sulfur oxides and particulate



In several studies, however, TSP effects were reported to occur in the presence



of low or non-significant levels of SOp.  (Reference 188, 212, 213, 215, and



257 of Chapter 14, as shown in Table 1-18.)



Health Effects of Atmospheric Sulfates—Conversion to sulfate compounds,



including sulfuric acid, has been proposed as a major pathway by which sulfur



dioxide and possible other sulfur compounds  may exert toxic  effects.   However,



only a few community health studies have attempted to measure and assess



health effects associated with suspended sulfates (SS).  Stebbings and Hays,190
                                     1-126

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   TABLE 1-17      QUALITATIVE STUDIES OF AIR POLLUTION AND PREVALENCE OF CHRONIC
             '  RESPIRATORY SYMPTOMS AND PULMONARY FUNCTION DECLINES
   Study
         Characteristics
      Findings
Fairbatrn and
 Reid265
Mork
    266
Deane  et al.267
Cederlof,39
 Hrubec  et al.40
Comparison of respiratory illness
 among British postmen living
 in areas of heavy and light
 pollution
Questionnaire and ventilatory
 function tests of male trans-
 port workers 40-59 years of age
 in Bergen, Norway and London,
 England
Questionnaire and ventilatory
 function survey of outdoor
 telephone workers 40-59 years
 of age on the west coast of U.S.
Chronic respiratory  symptom
 prevalence  in  large panels  of
 twins in Sweden and in  the
 U.S. Index  of  air pollution
 based on estimated  residential
 and occupational exposures  to
 S02, particulates,  and  CO
Sick leave, premature
 retirement, and death
 due to bronchitis or
 pneumonia were closely
 related to pollution
 index based on visibility

Greater frequency of
 symptoms and lower
 average peak flow rates
 in London.  Differences
 were not explained by
 smoking habits or socio-
 economic factors

Increased prevalence of
 respiratory symptoms,
 adjusted for smoking and
 age, a larger volume of
 morning sputum and a lower
 average ventilatory function
 in London workers, and in
 the English compared with
 American workers.  No
 differences in symptom
 prevalence between
 San Francisco and
 Los Angeles workers,
 although particulate
 concentrations were
 approximately twice as
 high  in Los Angeles

Increased  prevalence of
 respiratory symptoms in
 twins  related to  smoking,
 alcohol consumption,
 socioeconomic character-
 istics, and urban  residence,
 but  not to indices of  air
 pollution
                                        1-127

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      TABLE  1-17.   QUALITATIVE STUDIES  OF AIR  POLLUTION  AND  PREVALENCE  OF  CHRONIC
                RESPIRATORY SYMPTOMS AND  PULMONARY  FUNCTION  DECLINES
    Study
         Characteristics
      Findings
Bates ef al.268-270
Bates271
Yashizo272
Winkelstein and
 Kantor273
Ishikawa et al.275
Fujita et al.276
Comparison of symptom prevalence,
 work absences,  and ventilatory
 function in Canadian veterans
 residing in 4 Canadian cities
10-year follow-up study of
 Canadian veterans initially
 evaluated in 1960,  and
 followed at yearly intervals
 with pulmonary function tests
 and clinical evaluations

Bronchitis survey of 7 areas of
 Osaka, Japan, 1966, among
 adults 40 years of age and over
Survey of respiratory symptoms
 in a random sample of white
 women in Buffalo,  New York
Comparison of lungs obtained at
 autopsy from residents of
 St.  Louis and Winnipeg
Prevalence survey (Medical
 Research Council questionnaire)
 of post office employees in
 Tokyo and adjacent areas, 1962
 and re-surveyed in 1967
Lower prevalence of symptoms
 and work absences and better
 ventilatory function in
 veterans living in the lest
 polluted city

Least decline in pulmonary
 function with age in veterans
 from least polluted city
Bronchitis rates, standardized
 for sex, age, and smoking
 were greater among men and
 women in the more polluted
 areas.   Bronchitis rates
 followed the air pollution
 gradient.

In nonsmokers 45 years of age
 and over, and among smokers
 who did not change residence,
 respiratory symptoms were
 correlated with particulate
 concentrations obtained in
 the neighborhood of residence.
 No association of symptom pre-
 valence with S02 concentrations

Autopsy sets, matched for age,
 sex and race, showed more
 emphysema in the more polluted
 city.  Autopsied groups may
 not reflect prevalence of
 disease in general population

Two-fold increase over time in
 prevalence of cough and sputum
 production in same persons,
 irrespective of smoking habits.
 Change was attributed to
 increasing degrees of air
 pollution
                                          1-128

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    TABLE 1-17.,   QUALITATIVE  STUDIES  OF  AIR POLLUTION  AND  PREVALENCE  OF  CHRONIC
                RESPIRATORY  SYMPTOMS  AND PULMONARY FUNCTION  DECLINES
    Study
         Characteristics
      Findings
Reichel,277
 Ulmer et al.278
Nobuhiro et al.279
Comstock et al.280
Speizer and
 Ferris281-282
Linn et al.283
Prindle et al.284
Respiratory morbidity prevalence
 surveys of random samples of
 population in 3 areas of West
 Germany with different degrees
 of air pollution
Chronic respiratory symptom
 survey of high and low exposure
 areas of Osaka and Ako City,
 Japan

Repeat survey in 1968/1969 of east
 coast telephone workers and of
 telephone workers in Tokyo
Comparison of respiratory
 symptoms and ventilatory
 function in central city and
 suburban Boston traffic poll ice-
 men
Respiratory symptoms and function
 in office working population
 in Los Angeles and San Francisco,
 1973
Comparison of respiratory
 disease and lung  function
 in residents of Seward  and
 New Florence, PA
No differences in respiratory
 morbidity, standardized for
 age, sex, smoking habits,
 and social conditions,
 between populations living
 in the different areas

Higher prevalence of chronic
 respiratory symptoms in more
 polluted areas
After adjustment for age and
 smoking, no significant
 association of respiratory
 symptom prevalence with
 place of residence

Slight but insignificant
 increase in symptoms pre-
 valence among non-smokers
 and smokers, but not
 exsmokers, from the central
 city group.  No group
 differences in ventilatory
 function

No significant difference in
 chronic respiratory symptom
 prevalence between cities;
 women in the more polluted
 community more often reported
 nonpersistent (<2 years)
 production of cough and  sputum

Increased airway resistance in
 inhabitants of more polluted
 community.  Differences  in
 occupation, smoking, and
 socioeconomic  level could
 account for these  differences
                                           1-129

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     TABL€-1-17     QUALITATIVE  STUDIES OF AIR  POLLUTION AND PREVALENCE OF CHRONIC
                RESPIRATORY  SYMPTOMS AND PULMONARY FUNCTION DECLINES
    Study
         Characteristics
      Findings
Watanabe285
Anderson and
 Larsen286
Collins et al.287
Peak flow rates in Japanese
 school  children residing in
 Osaka
Peak flow rates and school
 absence rates in children  6-7
 years of age from 3 towns  in
 British Columbia
Death rates in children 0-14
 years of age, 1958-1964,
 in relation to social  and air
 pollution indices in 83 county
 boroughs of England and Wales
Lower peak flow rates in
 children from more polluted
 communities.   Improved peak
 flow rates when air pollution
 levels decreased

Significant decrease in peak
 flow rates in 2 towns
 affected by Kraft pulp
 mill emissions.   No effect
 on school absences.
 Ethnic differences were
 not studied

Partial correlation analysis
 suggested that indices of
 domestic and industrial
 pollution account for a
 greater part of the area
 differences in mortality
 from bronchopneumonia and
 all respiratory diseases
 among children 0-1 year
 of age
                                          1-130

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                                    TABLE  1-18  SUMMARY TABLE - CHRONIC EXPOSURE EFFECTS
                                                                                                i !•

Type of Study
Mortality (geog. )


Reference
Winkelstein188
Zeidberg and
colleagues16-18
Annual average pollutant levels
at which effect occurred
Effects observed
Increased mortality
Increased mortality
TSP (ug/m3)
125-140
55-60
S02 (ug/m3)
not significant
30

Morbidity

Longitudinal and
 cross-sectional
Ferris
 et al.41 42 46 47
Higher rate of respiratory
 symptoms; and decreased lung
 function
    180
   55
Cross-sectional
 (2 areas)
Sawicki (1972)31
More chronic bronchitis,
 asthmatic disease in smokers;
 reduced FEV%
    250"
  125
Cross-sectional
 study of school-
 children in 4 areas
Lunn et al.96 97
Increased frequency of res-
 piratory symptoms; decreased
 lung function in 5-year olds
    260*
  190
Follow-up of school-
 children in 4 areas
Douglas and Waller90
Increased lower respiratory
 tract infection
197* (130 BS)
  130
Cross-sectional study
 of children in 4 areas
Hammer et al.214
Increased incidence of lower
 respiratory diseases
  85-110
175-250
Cross-sectional study
 of high school
 children in 2 areas
Mostardi and
 colleagues177 258
Lower FVC, FEV0>75 and maximal
 oxygen consumption
  77-109
 96-100
Cross-sectional
 (multiple areas)
Lambert and Reid28
Increased respiratory symptoms
160* (100 BS)
100-150
Cross-sectional
 (3 areas)
Goldberg et al.109     Increased CRD
                                      78-82
                       69-160

-------
                                                            TABLE  1-18 (continued)
 I
t-«

ro
Type of Study
Cross-sectional
(4 areas)
Cross-sectional
and Long (2 areas)
Cross-sectional
(3 areas)
Cross-sectional and
retro- long in 4 areas
(children)
Cross-sectional
2 areas
Cross-sectional
3 areas (children)
Cross-sectional
2 areas (children)
Reference
House et al.108
Sawicki and
Lawrence (1977)181
Rudnick182
Nelson et al.114
Hammer113 257
Shy et al.215
Shy et al.215
Chapman et al.213
i r •
Annual average pollutant levels
at which effect occurred
Effects observed
Increased CRD
Increased Prev CB and AS
Increased persistence, Males
31-50; Increased incidence,
Females, some ages
Increased respiratory symptoms
in boys. Increased Rh in girls
Increased LRD
Increased LRD
Decreased adjusted FEV>75 in
children > 8 years
Decreased adjusted FEV>75
TSP (|jg/mj)
70 (15SS)
169+
221-316*
(150-227 BS)
70
133
(SS=14)
78-82
96-114 (45 RSP)
S02 (pg/m3)
100-150
114-130
108-148
107
<25
69-160
(= and low)

      *Converted from BS  (British  Smoke).

     **Converted from CoH.

-------
for example, reported increased symptoms in patients with 24-hour averages of


12 ug/m3 SS (200 TSP, 60 RSP, 8 SN, 100 S02).  Also, Chapman et al.212 reported


increased chronic respiratory disease prevalence rates in a high pollution


community with an annual average of 15 ug/m3 SS (70 TSP and 107 SOO.   Hammer257


further reported increased lower respiratory disease prevalence rates  in a


high pollution community with an annual average of 14 ug/m  SS (133 TSP and


S02 >17).  Thus, suspended sulfate levels of 12 ug/m3 (daily) or more  and 15


ug/m  (annually) might be interpreted as being important based on those results;


however, certain methodological considerations discussed in Chapter 14 must be


taken into account in qualifying these results.


Respirable Particulates Effects—As discussed in Chapter 11, particles below

       3
15 ug/m  MMAD are important.     Respirable suspended particulates (RSP) £10 urn,


have been measured in only a few American epidemiology studies, e.g.,  those by

       ~i~n 9^7                     iqn                           ?~R ?TI
Hammer,   '"  Stebbings and Hayes,    and Shy and Chapman et al.   J'      The


later study was reported as demonstrating decreased adjusted FEV 75 in children

                                                    3                3
in an area with higher pollution with RSP of 45 ug/m  (96 to 114 ug/m   TSP and

                                    3
S02 very low).  Thus RSP of 45+ ug/m  may be important but, again, acceptance


of these results must be qualified based on certain methodological considerations


discussed in Chapter 14.


1.5.5.2  Methodological Factors Impacting Interpretation of Results—If it


were assumed that all of the results summarized in Tables 1-16 and 1-18 were


derived from methodologically sound studies and were universally accepted as


valid, then the above summary of their results could be accepted as a reasonable


representation of the likely atmospheric particulate and sulfur oxides levels


found to be associated with mortality and morbidity effects.  However, the


matter of the methodological  soundness and validity of various studies has
                                     1-133

-------
been a matter of considerable controversy and discussion during the past
decade.
     Such controversy has derived,  in large part,  from the fact that certain
additional risk factors can often be as important  as the air pollution variables
studied in affecting human health.   For example, as  was alluded to earlier and
discussed more thoroughly in Chapter 14 (Sections  14.1, 14.3, 14.4), it has
been strongly emphasized that smoking is one such  factor,  as are occupational
exposures.  Furthermore, age and sex co-variables  can also be critical in the
evaluation of health effects.  Race or ethnic group  characteristics likely
fall into this catagory as well.   In addition, numerous social  variables may
be highly critical in terms of their existing direct effects on human health,
as well as how they may modify the health effects  of environmental pollutants.
Such social factors include social  economic status (income, education, and
occupational levels and associated social class status), migration, and household
characteristics.  Also, meterological variables such as sudden temperature
changes or shifts in humidity levels may also be critical  co-variables which,
along with air pollutants, might affect health in  a  deleterious manner.
Parental smoking and other sources of indoor pollutants may also be critical.
Other less-well defined social/ environmental variables, such as a greater
degree of crowding in housing conditions, too, may represent a set of "urban
factors" differentially acting to affect health in comparison to "rural"
conditions.
     Many of the studies have attempted to control for at  least some of the
above and other factors.  Most of the studies analyzed, however, have not
controlled for all possible confounding or covarying factors, an extremely
difficult task in practice. Nor have all been able to exquisitely,  control  for
                                     1-134

-------
what factors were taken into account.   In fact, there is not a single study
that has controlled for everything that might have affected its results.
Thus, the likely validity of each study has to be appraised after evaluating
the_ importance of possible confounding variables and co-variables controlled
for or not taken into account by that study.   In many cases, known highly
correlated variables have been controlled for or taken into account and,  in
other cases, comparison study groups have been chosen so as to be similar in
terms of crucial characteristics, making it relatively easy to ascribe likely
validity to their observed results.
     In regard to evaluating other (less well-designed) studies, it should be
noted that some studies exist which indicate that possible confounding variables
are not always as important as they were originally thought to be.  For example,
follow-up studies on an adult cohort previously studied as children by one
group of investigators did not confirm original social class differences
between the groups to be of much significance in accounting for health findings
for the groups later in life, and other studies have shown that household/familial
factors are not necessarily important in all cases in accounting for observed
results.  Therefore, care must be taken not to over-emphasize the relative
importance of potential confounding or covarying factors not ruled out as
possible alternative explanations for the results of a given study.  In other
words, being overly critical where information is lacking to support the
likelihood of a specific confounding factor or co-variable affecting the
pattern of results obtained in a study at a particular time represents as much
of a disservice in trying to achieve an objective, balanced appraisal of study
results under discussion as would any countervailing  lack of reasonable regard
for the potential importance of  such factors.
                                      1-135

-------
     It must also be recognized that no single study alone, no matter how


well-designed or conducted in and of itself completely establishes what comes


to be accepted as a "scientific fact" defining either a relationship between


two or more variables studied or a lack thereof.   Rather, excellence in the


design and conduction of a given study, internal  consistency and biological


plausibility of its results, and their consistency with other known results or


information all help to heighten confidence in the likely existence of relation-


ships indicated by that study's results.   Even greater certainty is attributed


to the probable existence of such relationships if further independent studies,


regardless of particular individual flaws, yield  results consistent with such


relationships.  Thus, consistency in the overall  pattern of results indicative


of particular relationships or the overall "weight of the evidence" from more


than one study are crucial in establishing given  relationships as "scientific


facts" or in determining the degree of certainty  ascribed to them.


1.5.5.3  Quantitative Dose-Response Relationships Defined by Community Health


         Studies—In order to elucidate dose-response relationships established


by community health epidemiology studies of the type reviewed above, numerous


attempts besides the present one have been made to examine both negative and


positive information concerning such studies.   This has usually been done to


determine which are sufficiently sound methodologically to allow for reasonable


conclusions to be drawn from them in evaluating the overall meaning of their


results individually and collectively.   Such attempts include critical reviews

                                        OAt:                       7Aft
and commentaries written by Rail (1974),    Higgins et al. (1974),    Goldsmith


and Friberg (1977),247 Ferris (1978),314a and Waller (1978).314b  They also


include the following evaluative documents appearing in 1978:  an American


Thoraic Society (ATS) review of Health Effects of Air Pollution (Shy et al.,
                                     1-136

-------
      251
1978);    a National Research Council /National Academy of Science (NRC/NAS)
document on Airborne Particles by Higgins and Ferris (1978)    and an NRC/NAS

                                                      ono
document on Sulfur Oxides by Speizer and Ferris (1978)     More recent such



reviews and commentary appearing in 1979 include:   the 1979 World Health



Organization (WHO) document, Environmental Health (8): Sulfur Oxides and

                             31?                                   ^m
Suspended Particulate Matter;     a report by Holland et al. (1979)    written



for the American Iron and Steel Institute and appearing in the American Journal



of Epidemiology; and a reply to that report in the same journal by Shy (1979).



Some of the more salient points of these reviews and commentaries are concisely



highlighted below.



     As will quickly become apparent through the course of the discussion



below, there are certain studies that many reviews consistently rate as being



methodologically sound and their results valid.  Also, when those study results



are viewed together, collectively, fairly consistent patterns of quantitative



relationships emarge regarding exposures to sulfur oxides and parti cul ate



matter associated with the occurence of various types of health effects,



including (1) mortality and morbidity effects associated with acute exposures



to fairly high ranges of air concentrations of those  substances and (2) mor-



bidity effects associated with chronic exposures to lower atmospheric levels



of the same agents.  Given the general concensus that appears to exist  regarding



the validity of these studies, then, there seems to exist very good support



for placing considerable confidence in the overall patterns of quantitative



relationships defined by their collective evaluations.



     In regard to  other reasonably well-designed studies, but  for which less



of a concensus exists regarding  their  likely  validity,  several interesting



points emerge from the  subsequent discussion.   First, it  becomes  apparent
                                      1-137

-------
that, beyond some small  modicum of agreement among the  reviews  concerning

problems associated with certain studies,  the various reviews often differ

considerably in regard to their assessments  of the methodological  soundness or

validity of any given individual study.   This derives mainly from  different

reviewers emphasizing or citing different possible confounding  or  covarying

factors as potentially being important in affecting the results of a given

study.  However, despite whatever flaws might be evaluated by different reviewers

to be associated with the particular individual  studies,  a surprisingly great

degree of consistency exists both between most of the "flawed"  study results

and, also, in comparison with the findings of the other studies alluded to

above as being widely recognized as being valid.   In some cases, however, the

results of some of the supposedly "flawed" studies point toward still  lower

levels of sulfur oxides and particulate matter being associated with significant

mortality or morbidity effects.  Thus, whereas not as much confidence can yet

be placed in such findings as those from the more universally accepted studies,

it is still not appropriate scientifically to completely disregard or ignore

them.  This is especially true in view of the fact that,  all too often, relationships

indicated to exist by "suggestive" evidence derived from numerous  "flawed"

studies are later confirmed by more carefully designed  and conducted "definitive"

studies.


     Tables 1-19 to 1-21 summarize conclusions regarding particular study

results based on critical assessments contained in Chapter 14 of this document

and assessments from other reviews of observational studies of  the health

effects of sulfur dioxide, expressed in ug/m  of SOp,  and particulate matter,
                          3
expressed in terms of ug/m  of total suspended particulates (TSP).  When

exposures were originally obtained in units of black smoke or coefficient of
                                     1-138

-------
haze, they have been converted to TSP for these tables.   The conversion
relationships are discussed in Chapters 3 and 14.   Because information bearing
on the health effects of atmospheric sulfates and the fine fraction of
pa_rticulate matter is insufficient to separately assess the health effects of
these fractions of atmospheric particulates, these measures of pollution level
are not considered in these tables.  These issues are discussed in more detail
in Chapter 14.
     Each row in Tables 1-19 to 1-21 corresponds to an observational study
that has been cited in at least one review.  These studies are grouped
according to whether acute effects were studied, that is, effects associated
with fluctuations in 24-hour average level, or chronic effects were studied,
that is, differences in effects associated with differences in annual average
level.  Within each exposure category, studies showing mortality effects are
listed separately from those showing morbidity effects.  The geographic
location(s) of the populations studied and approximate dates or time periods
covered by each study are given.
     Each column corresponds to one of the particular reviews referenced and
discussed in Chapter 14; and the entries are the air concentrations of of SC^
and TSP interpreted to be associated with  health effects demonstrated by the
different studies listed.  The absence of  stated quantitative values for
TSP/S02 for a given study does not necessarily mean that it was  judged to be
an inadequate study by the particular reviewer(s); rather,  in some  cases,
either no levels were clearly stated in their review or the particular  study
may not have been considered (some studies,  for example, have appeared  after
the publication of several of the  reviews).
                                      1-139

-------
                                                                  TULE 1-19.   SUMMV Of VARIOUS REVIEWERS'  EVALIMTIWK Of QUNHTITATIVE
                                                                            DOSE-RESPOWSE RELATIONSHIPS DERIVED FRO* STUOIES OF
                                                                           PDRTAUTY EFFECTS ASSOCIATED KITH  ACUTE  EXPOSURES TO
                                                                                       S0? AW PARTICULATE MATTER
' " 	 	 — 	 ,

Study
	 : 	
Scott/Btirj«M/
Gore
Lavther13
Glasser 4...
Greenburo."2
Martin L
Bradley"
Martin6
U. K. Ministry
of Pensions
McCarroll
et al.
Greenburg,
„ itil.1S1
1
g Beuchley
Vatanab* ...
i Kanefco""
Composite
Dutch
Compos 1U
British
Conpoilt*
USA
«ppl1nj it «1.
I Waller
Rlggan
et al.

Date

(1954-56)
(1958-59)
(1960-64)

(1958-59)
(1959-60)

(195Z)

(1962-64)

(1953-64)
(1962-66)
(1965-66)

(1960s)

(1955-62)

(1952-64)

(1975)

(1975)
. ,, Goldsulth &
Population (lSJi) M^?* Fr1lwr9 F«"'« W»S $0 IMS TSP WHO "'I"?
(1,74) ,,„,, ,„„, (W7|>) {M7§J WSJSP (WH09) rt^.,. ^^
London 2000/1144* 2000/1000 «»„«.
»00/1040 1000/750
London 750/700 Txinin
750'710 750/710
New York
291/520 750/710
lon*m 750/710
Iond0n 1000/500 *IT««/,»T
417BS/277 500/500 750/700
U. K.
>1000/>1000
H*» York 720/1500 720/1500
800A450
Nev York
720/500 > 570/850*
N~Y°rk -/*» -/300 -/300 -/500
Osaki

Kotterdn
Large
U.K. cities
Urge
U.S. cities

London
54C/994
Pittsburgh

Ware EM
et al. Ch 14
) (1980) (1980)
2000/1000
580/780 33D/524

530/300 500/300
500/400 500/400



570/1500

570/1000
-/500

300/266

300/500

250/250

570/1000

500/7*0
700/300
 (•») Judg«d  to be •etKodologlc^lly sound/valid ttudy.
 (-) Judged  to be Methodologically flawed/Invalid ttudy.
 (7) Judged  to be Methodologically sound, but reservations enpressed.

* Each entry represents  TSP/SO. levels  1n pg/m3 as reported by given
  reviewer.  Exceptions:   BS=Br1t1sh  smoke shade, CoH=  coefficient of  haze.

-------
                                                               TABLE 1-20.  SUMMARY OF VARIOUS  REVIEWERS' EVALUATIONS OF QUANTITATIVE
                                                                         DOSE-RESPONSE RELATIONSHIPS DERIVED FROM STUDIES OF
                                                                        MORBIDITY EFFECTS ASSOCIATED WITH ACUTE EXPOSURES TO
                                                                                     SO  AND PARTICULATE HATTER

Study
IQfi
Greenberg
Lawther52
Lawther53
Martin16
Waller7
Angel59/ .„
Fletcher*"
McCarrol205
Cassell208'209
.- Lawther as.oer
~ Goldsmith3
Lawther as.Der
Golds«1th
Carnow174
Cohen36
Vander Lende74
Hanwer214
Chapman
HaMter113.257
GervoU61
Stebblngs216
Date
1953
1954
1954-68
1959-60
1961-64
1962-63
1963-65
1964-67
1964-65
1966-68
1968
1968-69
1969

1969-71
1969-71
1970s
1975
Rail
Population (1974)
New York
London
London
London
London
London
New York
New York
London
London
Chicago
West Virginia
Netherlands

New York
Birmingham
(S.E. USA)
France
Pittsburgh
Goldsnith & Holland
H'fgglns Frlberg Ferris NAS SOW NAS TSP WHO et al. Shy
(1974) (1977) (1978) (1978? (1978) (1979) (1979) (1979)
3 CoH/700

250/250-500 350/250 350/250 500/500 250 BS/500 350/500
516/340
250/500 350/500
MO/250 250/250 230/250 200/400 (?)


129/264 (*)
68/204 (t)
-/700
150/200 150/200 150/200 (-)
230/300 245/300 140 85/300 (?) 160 BS/-

145/286 (-)
180/26 
-------
                                                           TAILE 1-21   Sl»«A«Y  OF VARIOUS REVIEWERS'  EVALUATIONS OF QUANTITATIVE
                                                                     DOSE-RESPONSE RELATIONSHIPS DERIVED FROM STUDIES OF
                                                                   NOM10ITT EFFECTS ASSOCIATED WITH CHRONIC EXPOSURES TO
                                                                                 SO, AMD PMT1CUUTE MATTE*

Study
U.K. Ministry
of Pension*
DouglasJL
Waller90
w
Ferris43
Fletcher274
ItasUrdl25*
1
C shy**
Bennett
Tessler322
Col ley t Reid
Suzuki *,,.
Hltosugr"
Irving et al.98
Rudnlck182
French306

Data

1946-65
19*6-68
1963-65
1966-67
1950V65
1966-73
1968
1972
1968
1966-67
1971-74
1966
1970
1971-72
1972-73
1972-74
1969-71
1969-71
Gold»1th i
Rill Hlgglni Frlberg Ferris
Population (1974) (1974) (1977) (1978)
BrIUIn 200/200*
BrIUIn 70/90 140/130 230/120
BrIUIn 100/100 100-200/100-200
BrIUIn 180/120
Berlin, N.H. 180/55*
London 420 > 100/260 250/250
Cracow 240/130
Ohio 93/98
*•" York 85-195/50-450
Cincinnati, OH
Kent, Eng. 708V-
France
BrIUIn -/100
Tokyo
B1r>lngha», AL
(S.E. USA)
BHUln
Poland
Chicago
BlretnflhM. AL
(S.E. USA)
Holland
HAS SO MAS TSP WHO «t il. Shy
(1978) (1978) (1979) (1979) (1979)
>100/>100 (-)
230/120 70/90 140BS/140 (?)
100/100 (-) 1-200BS/-
180/120 100/120 200 BS/200 330/180
180/55 180/73 180/- (?) 180/-
250/250 (-)
250/125 170/125 (7) 170/-
110/110 (-)
100/200 (-)
(-)
(7) <100BS/-
(7) 
-------
     One very notable feature of all three tables is the variety of levels



cited for the same studies by different reviewers.  When one considers the



continuous relationship between exposure level and response seen in many of



these studies (for example, the studies by Martin discussed in detail in



Chapter 14), this variation in cited levels can be attributed largely to the



lack of a clear threshold level for effects being defined by these studies.



The other important feature of the table is the variation among reviewers in



the choice of studies considered to have demonstrated health effects.  The



next sections are devoted to a discussion of these differences in interpretation



among reviewers and to a discussion of the studies which bear critically on



differences in conclusions drawn in these various reviews.



Acute Mortality



     Examination of Table 1-19 reveals that considerable agreement exists to



the effect that episodic mortality has occurred definitely above levels of 750


    "3            13 9A~1 307 31 ?                            ^01
ug/ni  TSP and SQ^  >   >   >  *> jn London.  Holland et al.    concluded,

                                                                   o

mostly from British studies, that the critical values were 500 ug/m  TSP and



700 ug/m  S0?.  Interpretation of daily mortality by Martin et al. '   indicate



the effective levels in London could be as low as 500 ug/m  TSP and  300 to 400



ug/m  S02.304'312  Also, new analyses contained in Chapter 14 suggest that the

                                               3

TSP effect  levels may be as low as 200-400 ug/m   in the absence of significant



temperature or other confounding effects.  Similar studies by Glasser et

   220
al.    in New York City would indicate that the levels where mortality has



been seen there could be 2.5 to 5 CoHs (190 to 580 ug/m3  TSP) and  520 ug/m


    307
S02.     This is not all that different from  results found  for  London, but



different reviewers may interpret these results somewhat  differently.  WHO



concluded that  levels above 500 ug/m3 of each  (SOp and particulate matter
                                      1-143

-------
                                                              312
expressed as BS) could definitely produce increased mortality.      On the

other hand, some studies in the Netherlands and in Japan might indicate that
                                                                     3
such mortality increases could occur at levels of TSP around 300 pg/m  with


SO^ at 500 (jg/m3 or above.100'232'302  All  of these effects are tempered by


the particular meteorological conditions present during the study period and


whether only central pollution monitoring states or multiple numbers of

geographically representative sites were used in determining the stated levels


of S0? and particulate matter.   All studies showed mortality effects to occur


predominantly in the infirm, the elderly, and infants.


There is more certainty of effects occurring when either TSP or S02 are at or

above 500 (jg/m .  Mortality effects may be  less certain at levels of TSP


between 300 and 500 pg/m3 at levels of S02  of 500 (jg/m3.

Acute Morbidity


     There is a broader range of opinion, and estimations of effect levels,


associated with the studies of acute morbidity.  The earlier studies by Lawther,


Waller et al. of pulmonary function and of  exacerbation in bronchitics show


various effects when the S0? and BS levels  were higher in London.  Most reviewers

                                                                      3
agree that these effects occurred when TSP  levels were 250 to 350 pg/m  and

                               3
SOp levels were 250 to 500 |jg/m .   As the levels decreased, the acute effects


decreased.  By the winter of 1964-65, the exacerbations were slightly reduced

                                                  3
and less consistent; daily average BS was 129 pg/m  (196 TSP) and daily average


SOp was 264 pg/m  in that winter.   Even during the winter of 1967-68, although


the effects had decreased further, they were significantly correlated with

                                                      3
pollutant concentrations; daily average BS  was 68 pg/m  (121 TSP) and daily


average SO^ was 204 p.g/m  during that winter.  The Greenberg et al. studies in


New York City in the 1960s had also shown increased morbidity during episodes
                                     1-144

-------
                        3                 3
at levels above 300 ug/m  TSP and 700 ug/m  S02_  WHO    concluded that daily


levels above 250 (jg/m  of S02 and BS (-330 TSP) would produce acute effects.


However, several studies have shown effects at levels around or below those


values.  Studies of daily acute respiratory disease symptoms in New York City



families, which included statistical analyses or controls for possible confounders,


showed increased daily symptoms at levels of 160 to 205 ug/m3 TSP and 370 to

        3     205 208 209
450 ug/m  SO,,.   '    '     However, these were only average values over the


winters of the study.  Studies of prevalence rates of acute respiratory symptoms


children in New York City, controlling for confounders indicated increased
                                        3                 1     9~\9
rates associated with levels of 145 ug/m  TSP and 286 ug/m  S02.   ')<     A



similar study in Birmingham showed increased rates at levels of 180 to 220

    •3                •}
ug/rn  TSP and 26 ug/ni  S02.



     Probably one of the most critical s4udy to be considered is that of Cohen

      oc

et al.    They studied 20 asthmatics around a coal -fired power plant.  They



found temperature was most important, but within temperature ranges, pollution


                                                           3                 3
also caused asthma attacks.  The  levels cited were 150 ug/m  TSP and 200 ug/m



S0?, both daily averages.  Various reviews have considered this study



weak,   '   '    ' while others consider it a significant demonstration of


                                     251
competition of environmental factors.     After temperature and one pollutant



were removed, none of the other pollutants entered into the relationship;



thus, no single pollutant could be considered solely responsible for the



increased attack rates.



     On the basis of the above studies, one could conclude that acute  morbidity



could be seen at levels between 145 to 220 ug/m3 TSP and  approximately 200  to



400 ug/m3 SO
                                      1-145

-------
Chronic Morbidity
     The studies summarized under the section of chronic  morbidity include  a
mixture of investigations carried out in population  samples  composed  of random
samples of adults, and adults selected from working  groups and populations  of
children selected by areas of residence.   In addition,  all but a few  of the
studies use a cross sectional method, that is,  they  examine  the population  in
question at one point in time and determine the prevalence of whatever morbid
condition is being assessed.   Alternatively, a few of the investigations
follow a group of people over a period of time.   Although in these studies  the
opportunity to measure the onset of new morbid events exists, eventually all
of the studies actually measure the prevalence of conditions at different
points in time and cannot be used to determine the incidence of new conditions
related to exposure to air pollutants.  The morbid events in each study generally
relate to the prevalence of chronic respiratory symptoms  or  disease states  as
ascertained by standardized questionnaires and/or levels  or  changes in levels
of pulmonary function measured by generally reliable equipment.
     The variation in reported levels of effective exposures from the reviews
which indicate the same studies as providing reliable information probably
reflect one or more of the various problems of with  aerometry or health measurement
errors encountered in this observational assessments (see above).  The inclusion
(or exclusion) of any given study in any particular  review in part reflects the
interpretation by the reviewers of the validity (reliability?) of the measurement
of exposure or health outcomes in that particular study.
     Except for the Holland report which found only  one group of acceptable
studies which provided information on chronic morbidity,   >97 all of the other
reviews found several studies with which to provide  estimates of lowest  levels
                                     1-146

-------
of health effects.  In general, there is a range of agreement between the
reviewers that health effects are measurable at levels of TSP above 180 ug/m3
generally in conjunction with levels of S02 above 120 ug/m3.   There are notable
exceptions in which lower levels are reported to be associated with health
effects.  For example, Ferris   reports TSP levels of 180 ug/m3 in association
with S02 levels of 55 ug/m , however, the S02 measures were made from 30-day
sulfation rates and may not reflect considerably higher peak exposures which
may have occurred.
     More striking in indicating a divergence of levels is the study of Mostardi
and certain other studies reviewed in Chapter 14.   Mostardi indicates effects
at levels of both TSP and S02 approximately 100 ug/m , however, some of the
reviewers rejected his findings because he did not analyze his data on pulmonary
function in adolescents by race in spite of having mentioned that there were
some blacks who would be expected to have lower levels of pulmonary function
in the high exposure group.
     The remaining studies were generally part of EPA sponsored CHESS Program
investigations which have received independent peer review and have been
published in the open literature over the last several years.  In these studies,
increases in chronic morbidity have consistently been found where levels of
                                     3
TSP and/or S02 have exceeded 100 ug/m .  Discussions of published critiques of
shortcomings of a number of these studies are included in Chapters 3 and 14 of
this document and, also, in some of the other reviews listed  in Tables 1-19 to
1-21.  Due to considerable controversy over the results and  interpretation of
many of the CHESS studies, many such quantitative findings regarding air
pollution/health effects relationships need to be qualified  to  take  into
account, for example, certain air quality measurement errors  that tended  to
                                     1-147

-------
bias detected effect levels in a negative direction (i.e.,  toward somewhat



lower levels than those suggested by proximally located local  air sampling



monitors.)  Still, at least some of the CHESS studies,  e.g.,  that by



Hammer113'2   on children in the Southeastern United States (which was



approved as a Harvard doctoral dissertation), appear to be  methodologically



sound, their results well-analyzed statistically and accurately interpreted,



and likely valid.  However, in the absence of much, if  any, comment on some



such studies in the published reviews listed in Tables  1-19 to 1-24, it is



difficult to assign the same level of certainty to their reported effect



levels as those indicated by results from others more widely  critiqued to date



and agreed upon as being valid.   Nevertheless, it should be noted that many of



the quantitative results derived from such studies, especially when known or



suspected errors in aerometry are taken into account, are not badly divergent



from the results obtained in some number of other studies.



     The quantitative relationships defined by many of  the  studies listed in



Tables 1-19 to 1-21 are depicted in Figure 1-4.  Also provided in that figure



are some indications of notable divergence of opinion between certain reviewers,



especially Holland et al. (1979) versus the WHO (1979)  appraisal, the present



EPA (1980) evaluation and several other published appraisals.   The acute and



chronic exposure levels for SOp and particulate matter  (BS  translated to TSp)



evaluated by the WHO (1979) to be associated with mortality and morbidity



effects are indicated by dashed lines in Figure 1-4. Also, presented below



are tables (Tables 1-22 to 1-24) summarizing the conclusions of the WHO (1979)



regarding levels at which mortality and morbidity effects can be expected to



occur and their recommended guidelines for exposure  limits consistent with the



protection of human health.
                                     1-148

-------
| OSAKA (1962)^ | 1
EPA (1980)^)'^
900 — ^

X
800 — ^',
EPA (1980)0' ^
700 —

600 —
r)
* -ACUTE MORTALITY
UJ
2 ROTTERDAM (1960'i)0 ^'
g-iOO 	 	 _ _ _^-__ EP*J.!98°'O'W
5 *™ LONDON (1950-60f[J J"J
§ ACUTE MORBIDITY *
u.
-J
V)
400 ~ LONDON (1958-60)1 1


300— LONDON 0 NETHERLANDS (1969-72)
NEW YORK CITY> (1964-65) /
(1960-70) LJ ~
CHRONIC MORBIDITY ,ri D "•
WEST ^ SHEFFIt ^nSSiS&HOLLAND. ET AL
200 ~ VS'AE WA0~"VRANCE,1973>
(1979)
UK (1946-66) & WHO (1979)
fWlf Af*n MO79I
^7 f*R Af*mAl 1 Qfift 7TI
TOKYO (1970|V 1 j
BERLIN, NH (1967 73)^ WHO (1979)
IT SOUTHEAST U.S.A. (196971) | j
,CHOLLAND, ET AL (1979) | |
N

^©HOLLAND. ET AL (1979)
F —
s
^OHOLLAND, ET AL (1979) —
s
*$' -
<$&'
/
/
HO (1979) —
ACUTE MORTALITY
O MARTIN, ET AL. (1960-64) - LONDON 	
0 GLASSER & GREENBURG (1971) - NYC
C APLING. ET AL, WALLER (1977-78) LONDON
• OTHER STUDIES
ACUTE MORBIDITY 	
D LAWTHER (1970) - LONDON 1950-1975
(E VAN DER LENDE (1975) - NETHERLANDS
f\ COHEN. ET AL (1972) WEST VIRGINIA
(1979) | OTHER STUDIES
CHRONIC MORBIDITY
A LUNN. ET AL (1967, 1970) • SHEFFIELD. UK
A DOUGLAS & WALLER (1966) - UK
A FERRIS. ET AL (1973. 1976) - BERLIN. NH
V SAWICKI (1972) -CRACOW. POLAND —
Y OTHER STUDIES
I 1 1 1
      100
              200
                          TOTAL SUSPENDED PARTICULATES,
Figure
Comparison of interpretations,of studies evaluated  by  Holland
et al. (1979),    WHO (lij^tnft  or otner reviews such as  those
in the NRC/NAS documents    '    and the present chapter.   Aside
from the British studies noted for London and Sheffield,and the
1960-64 New Youk City mortality study, Holland et al.    either
ignored the other studies shown or evaluated them as being in-
valid based on methodological flaws or reinterpretation of their
findings.  "OTHER STUDIES"  not specifically identified in  the
above key include those reported by:  Gervois et al.,17n_Ecance
(1973); Martin10 D London Q958-60); Mostardi et al.   /f"° V
Chicago (1972); Hammer11"5'"7 V Southeast USA (1969-71);
Suzuki and3|jljtosugi V Tokyo (1970).  The dashed lines  depict
WHO (1979)    conclusions regarding S0? and particulate levels
associated with acute (24-hr) mortality, acute morbidity,  and
chronic (annual) morbidity.

                     1-149

-------
   TABLE 1-22.   EXPECTED  EFFECTS OF AIR POLLUTANTS ON HEALTH IN SELECTED
      SEGMENTS  OF  THE  POPULATION:  EFFECTS OF SHORT-TERM EXPOSURES^*
                                     	    n3
Expected effects                         Sulfur dioxideSmoke
24-h mean concentration (ug/m )
                        in
Excess mortality among the elderly              500              500
 or the chronically sick

Worsening of the condition of patients          250              250
 with existing respiratory disease


"Concentrations of sulfur dioxide and smoke as measured by OECD or British
 daily smoke/sulfur dioxide method (Ministry of Technology, UK, 1966;
 Organization for Economic Cooperation and Development, 1965).   These
 values may have to be adjusted in terms of measurements made by other
 procedures.
*From WHO 1979 Criteria Document for Sulfur Oxides and Particulate Matter.
                                  1-150

-------
    TABLE 1-23.   EXPECTED  EFFECTS OF AIR POLLUTANTS ON HEALTH IN SELECTED
        SEGMENTS  OF  THE  POPULATION:  EFFECTS OF LONG-TERM EXPOSURES3*
                                       Annual mean concentration (ug/m )
Expected effects                         Sulfur dioxideSmoke


Increased respiratory symptoms                  100              100
 among samples of the general
 population (adults and children)
 and increased frequencies of
 respiratory illnesses among
 children


Concentrations of sulfur dioxide and smoke as measured by OECD or British
 daily smoke/sulfur dioxide method (Ministry of Technology, UK, 1966;
 Organization for Economic Cooperation and Development, 1965).   These values
 may have to be adjusted in terms of measurements made by other procedures-,2
*From WHO 1979 Criteria Document for Sulfur Oxides and Particulate Matter.
                                      1-151

-------
          TABLE 1-24.  WORLD HEALTH ORGANIZATION GUIDELINES  FOR  EXPOSURE
             LIMITS  CONSISTENT WITH THE PROTECTION OF PUBLIC HEALTH3'*
                                              Concentration (ug/m )
Expected effects                         Sulfur dioxideSmoke


24-h mean                                    100-150          100-150

Annual..arithmetic mean                        40-60            40-60
      _%


*Values for sulfur dioxide and smoke as measured by OECD or British daily
 smoke/sulfur dioxide method (Ministry of Technology, UK, 1966; Organization
 for Economic Cooperation and Development, 1965).   Adjustments may be necessary
 where measurements are made by other methods.   For example» smoke conccntra-t4onr.
 *f-*eO-15D uy/iii  convert to approximately 200-300 po/nT TSP and smptt levels ~
 of 40-607up*rr-ctmven*Uto approximate4y-S^4£0-ug/m3 TSPr
*From WHO ir
                                        1-152

-------
                                                                      7/9/80





      Chapter 1  Introduction, Summary, and Conclusions SO/PM
                                                          A






                         Corrigenda



     Before listing specific errata (deletions/insertions) for Chapter 1   (Volume



I) of the April, 1980, External Review Draft of the EPA criteria document for



sulfur oxides and particulate matter, certain general  comments should be  noted



reguarding anticipated revisions in Chapter 1.



     First, major revisions planned to be made in later current chapters  (2-14)  of



the document, as indicated in ensuing corrigenda materials, will also be  appropriately



reflected in revisions to be made in Chapter 1. For example, certain major revisions



in the text of Chapter 3 noted in corrigenda comments  for that chapter will  be



appropriately reflected in revision of text in Section 1.3.2 (pg. 1-19 to 1-43).



This especially includes introductory materials (4 main points) to be inserted  on



pg. 3-84 at the start of the discussion of comparison  of particulate matter measurement



techniques, as noted later in corrigenda comments for  Chapter 3.  Similarly, revisions



noted in those corregenda comments to be made in Chapter 3 regarding the  discussions



of specific studies comparing COM versus TSP and BS versus TSP measurement results



will be appropriately reflected in Chapter 1 revisions.



     Other major revisions in Chapter 14, noted in the later corrigenda comments



for that chapter, will also be reflected in revisions  of Section 1.5.5 (Community



Health Observation Studies) of Chapter 1.  Of particular importance are major



changes to be made in Tables 1-19 to 1-21 (on pg. 1-140 to 1-42) and accompanying



text regarding summarization of various expert reviewers' evaluations of key quanti-



tative community health studies.  Specific changes in those tables will  include the



following:


                                                                                   13
     (1) In Table  1-19, deletion of all entries except those  for studies by Lawther  ,

                      pop                     11             c

Glasser and Greenburg    , Martin and Bradley   , and Martin  .
                                   -1-

-------
 (2) In Table 1-20, deletion of entries for all  studies except those by Greenburg
 Lawther52'53, Martin16, Waller7, and Van der Lende74.
 (3) In Table 1-21, deletion of entries for all  studies except those by Douglas and
 Waller90, Lambert and Reid28, Lunn et al96'97,  Ferris43, Sawicki181, Mostardi,117'258
 Shy215, and Rudnick182.
     Discussion of tables 1-19 to 1-21, in the  text on pg.  1-143 to 1-152 is to be
 revised such that comments on quantitive air quality levels associated with observed
 health effects will generally be in terms of the original (COM, BS, TSP) particulate
 matter measurement units employed in specific studies  summarized in the table,
 except for comments on interpretative evaluations by particular expert reviewers
 that involved "translation" of COM or BS units  into TSP units.   Further evaluative
 comments are to be added on whether reasonable  interconversions between COH, BS,
 and TSP measurement units can be made and, if so, in what manner and under what
 circumstances. The impact of such interconversion or lack of sound bases to do so
 on interpretation of the epidemiology data base for SO /PM will then be taken into
                                                      /\
 account in text revisions more specifically delineating key conclusions based on
 the epidemiology literature.
     The implications of those conclusions, and others based on information discussed
 in Chapters 11, 12, and 13, for development of  health  criteria  for sulfur oxide and
 particulate matter are to be delineated in an integrative health summary and conclusions
chapter still in the process of being prepared  for addition to  the document.
Relevant text summarizing the most salient features of that chapter, once completed.
is to be added as  the final  portion of Chapter  1 (Volume 1).
                                        -2-

-------