United States Science Advisory K*Hd4tkWpAACAC-95-022 I--'
Environmental Board (1400) September 1995
Protection Agency
s>EPA AN SAB REPORT: PHYSICAL
EFFECTS REVIEW
DOCUMENTS FOR THE CAA
RETROSPECTIVE BENEFIT-
COST ANALYSIS
REVIEW OF THE PHYSICAL EFFECTS
DOCUMENTS FOR CRITERIA AIR
POLLUTANTS AND METHODOLOGY
FOR QUANTIFYING HEALTH EFFECTS
FOR THE CLEAN AIR ACT (CAA)
SECTION 812 RETROSPECTIVE
BENEFIT-COST ANALYSIS
U.S. EnvUonn,enta. Ptotection Agency
SSŁ
60604-
-------
f.
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON, D.C. 20460
OFFICE OF THE ADMINISTRATOR
SCIENCE ADVISORY BOARD
EPA-SAB-CAACAC-95-022
Honorable Carol M. Browner
Administrator
U.S. Environmental Protection Agency
401 M Street, SW
Washington, DC 20460
Subject: Clean Air Act Compliance Analysis Council (CAACAC) Physical Effects
Review Subcommittee (CAACACPERS) Initial Review Pertaining to the
Physical Effects Review Documents for Criteria Air Pollutants and
Methodology for Quantifying Health Effects for the Clean Air Act (CAA)
Section 812 Retrospective Benefit-Cost Analysis
Dear Ms. Browner:
In response to the Congressional mandate of Section 812, of the CAA and at the
request of the Agency's Office of Policy Analysis and Review (OPAR) and the Office of
Policy Analysis (OPA), the Clean Air Act Compliance Analysis Council (CAACAC)
Physical Effects Review Subcommittee (CAACACPERS) reviewed the draft physical effects
documents and the methodology pertaining to quantifying health effects for the Clean Air Act
(CAA) Section 812 retrospective benefit-cost analysis.
The CAACACPERS met on November 15 and 16, 1994 to receive briefings from
Agency staff and discuss issues with the Agency staff and the public. In addition, the
CAACACPERS held a public teleconference on April 12, 1995 and a public meeting on May
18, 1995 to review Agency drafts of additional sections of its overall analysis of the Section
812 Retrospective Benefits and Costs, and to finalize the Council's report. Most of the
findings and recommendations contained in this report were conveyed verbally to the Agency
staff during the second day of the November 15-16, 1994 meeting.
We note that the Agency is attempting to respond to a Congressional directive to
conduct a national assessment. However, it has been recognized from the outset by all the
parties involved that the Agency clearly has limited resources provided to it for this daunting
task, and that many of the actions required of the Agency go beyond the capabilities of
current state-of-the art assessments. Further, while significant human health, human welfare,
R»cycl*dm*cycltbl*
Prtrtid on taptr itat corttin
* bait 75* racydtd Oxr
-------
and ecological benefits result from controlling many air pollutants, it is very difficult to
achieve a credible, much less a thorough and unambiguous evaluation, of the human health,
human welfare, and ecological benefits and costs without a sustained program over the long-
term. In our view, it is clear that the major commitment necessary to make any significant
progress in this area has not yet been made.
Congress and the Agency have to ask themselves whether they want to commit the
time and resources needed for more comprehensive evaluations. The Subcommittee believes
that this exercise is worthwhile, and indeed necessary. Without evaluation, how can the
Agency and the Congress tell which programs are working, which need attention, and which
need to be cut or expanded? In doing such an evaluation, it is important to give a complete
list of effects. Where there is any ability to do so, it is important to quantify and monetize
the benefits - at least within an order of magnitude.
We offer the following specific comments in the belief that constructive advice at this
stage can help the Agency make significant improvements in the assessment process needed
for the Section 812 and other future mandates. We also note that neither Congress nor the
EPA implemented the CAA in a way designed to expedite evaluation. It is not surprising,
therefore, that quantifying benefits and costs is so difficult and uncertain at this point.
a) Coordination and Management: The CAA Section 812 retrospective analysis
and the subsequent prospective analysis are very substantial and important
exercises. However, the retrospective study does not presently appear to be
sufficiently coordinated - either across the various physical effects assessments,
or across all major model components. Various EPA offices and researchers
(and their contractors) have used different strategies to address problems,
which limit the linkages in the study and the consistency of presentation.
Although this study should be pushing the frontiers of benefits assessment, it
is, in fact, well behind many similar studies performed for other governmental
entities in terms of coordination, use of available knowledge, and assessment
of uncertainty.
The project needs more emphasis on careful and forceful coordination, plan-
ning, and consistency. The Agency needs a modeling team leader to structure
model frameworks for physical effects quantification and linkages to other
model components. The leader can assure that the team identifies and ad-
dresses specific critical modeling strategies and issues.
-------
b) A Comprehensive Assessment; In Section 812, Congress specified that the
assessment should be "comprehensive" and that it should "consider all of the
economic, public health, and environmental benefits... [emphasis added]." We
interpret this to mean that Congress was directing the Agency not to be
conservative in the sense of minimizing the likelihood that benefits would be
overstated. Rather, Congress appears to have been asking the Agency to
produce an Assessment that was inclusive of not only well documented and
measured effects and values, but also those effects and values for which there
is limited information. In other words, Congress was asking the Agency to
take some risks by listing and quantifying effects that are not well documented
in the literature so as to reduce the likelihood that it would produce an under-
estimate of the true benefits.
With the notable exception of the analysis of the association between ozone
and mortality, the draft document is not responsive to this congressional
directive. Rather, it appears to have been prepared with an emphasis on
statistical and scientific conservatism. Although this is an understandable,
defensible position for the Agency to adopt for many circumstances (for
example in setting regulations that have to be defended in a legal arena), it
may not inform Congress about all of the possible benefits (or lack of benefits)
associated with implementation of the CAA.
c) Uncertainty Analysis: A major deficiency in the draft document is the lack of
any adequate treatment of uncertainty. The manner in which uncertainty is
treated has important implications for the way in which physical-effects dose-
response functions are developed and expressed. And it is important that the
Assessment present a clear picture of the degree of confidence, or lack
thereof, that readers can place on the components of the Assessment.
d) Ecological Effects: The effects of air pollutants on human health have
dominated this analysis thus far, and it does not appear that ecological effects
will catch up within the short time and limited budget that remain for this
project. However, one of EPA's missions is to protect ecosystems from
adverse effects of pollutants. By definition, a benefit-cost analysis is stated in
terms of dollars. However, some quantification involves effects that cannot be
monetized by current methods. Protocols will be needed to express ecological
and other nonmonetary values and to compare them to values expressed in
monetary terms. For many of the human health effects, valuation in monetary
terms may be all that is needed. However, w,hen ecological effects eventually
-------
are addressed, many ecological values (including non-use values) may not
easily be expressed in monetary terms. Although ecological effects are
difficult to comprehensively quantify and value in economic terms, the absence
of at least a qualitative analysis that is on equal footing with a human health
analysis will be conspicuous and will leave EPA open to sharp criticism.
The enclosed report also provides comments on a number of more technical issues
including: the selection of impacts for quantification; omissions, biases, and uncertainty
analyses; sensitivity analysis; and the over-reliance on clinical, as opposed to epidemiologi-
cal, data.
Lastly, the Council strongly recommend that the Administrator and the Congress
allocate adequate resources to the Agency and other entities to build a core of expertise to
continue the difficult, but necessary exercise pertaining to quantifying health, welfare and
ecological effects. It is important that this effort be sustained over the long term. Such
expertise could logically focus on the many challenges identified in this report to you and the
Congress.
We look forward to receiving your reactions to our recommendations as we continue
our reviews of the documents pertaining to the health effects of air toxics, and to ecological
and welfare effects.
Sincerely,
Jr/Ricnard Schmalensee
Chair, Clean Air Act Compliance
Analysis Council
Science Advisory Board
ENCLOSURE
Dr. Morton Lipr/mann
Chair, CAACAC Physical Effects
Review Subcommittee
Science Advisory Board
-------
NOTICE
This report has been written as a part of the activities of the Science Advisory Board, a
public advisory group providing extramural scientific information and advice to the Administra-
tor and other officials of the Environmental Protection Agency. The Board is structured to
-provide a balanced, expert assessment of scientific matters related to problems facing the
Agency. This report has not been reviewed for approval by the Agency; hence, the comments
of this report do not necessarily represent the views and policies of the Environmental Protection
Agency or of other Federal agencies. Any mention of trade names or commercial products does
not constitute endorsement or recommendation for use.
-------
ABSTRACT
The Physical Effects Review Subcommittee (CAACACPERS) of the Clean Air Act
Compliance Analysis Council (CAACAC) of the Science Advisory Board (SAB) has
reviewed the Agency's draft physical effects documents and the methodology pertaining to
quantifying health effects of criteria air pollutants for the Clean Air Act (CAA) Section 812
retrospective benefit-cost analysis. CAACAC responded to five specific questions raised in
the charge to the Subcommittee and also provided more general comments and suggestions
relating to this topic.
CAACACPERS believes that, despite considerable shortcomings in these documents,
the Agency has laid out a useful framework. The Subcommittee identified a number of
technical issues requiring resolution, and made a number of specific recommendations,
including: more systematically identify and document the selection of impacts to be specifi-
cally included and excluded; conduct sensitivity and uncertainty analyses; more carefully
balance and specify the uses of epidemiological and clinical data; identify a method comple-
mentary to the standard valuation endpoints, so endpoints that do not lend themselves to
monetary valuation can also be considered equitably in a cost-benefit analysis; rectify
inconsistencies in the selection of coefficients; and investigate mitigation behavior. The
Subcommittee offers many other comments and emphasizes where fundamental improvements
are needed.
The Subcommittee strongly recommends that the Administrator and the Congress
allocate adequate resources to the Agency to enhance its core of expertise to continue the
difficult, but necessary exercise pertaining to quantifying human health, human welfare, and
ecological effects over the long term. Such expertise could logically focus on the many
challenges inherent in cost-benefit analyses.
Key Words: Clean Air Act, Cost-Benefit Analysis, Physical Effects, Air Pollutants, Ozone,
Particulate Matter, Lead, Carbon Monoxide, Sulfur Dioxide, Nitrogen Dioxide, Economic
Valuation.
n
-------
SCIENCE ADVISORY BOARD
CLEAN AIR ACT COMPLIANCE ANALYSIS COUNCIL
PHYSICAL EFFECTS REVIEW SUBCOMMITTEE
CHAIR
Dr. Morton Lippmann, Nelson Institute of Environmental Medicine, New York University
Medical Center, Tuxedo, NY
VICE-CHAIR
Dr. A. Myrick Freeman, Department of Economics, Bowdoin College, Brunswick, ME
MEMBERS AND CONSULTANTS
Dr. David V. Bates, Department of Health Care and Epidemiology, University of British
Columbia, Vancouver, BC, CANADA
Dr. Gardner M. Brown, Jr., Department of Economics, University of Washington, Seattle,
WA
Dr. Timothy V. Larson, Department of Civil Engineering, University of Washington,
Seattle, WA
Dr. Lester B. Lave, Graduate School of Industrial Administration, Carnegie Mellon
University, Pittsburgh, PA
Dr. Joseph S. Meyer, Department of Zoology and Physiology, University of Wyoming,
Laramie, WY
Dr. Robert D. Rowe, Hagler Bailly, Inc., Boulder, CO
Dr. George E. Taylor, Jr., Department of Environmental and Resources Sciences,
University of Nevada, Reno, NV
Dr. Bernard Weiss, Department of Health Science, University of Rochester Medical Center,
School of Medicine and Dentistry, Rochester, NY
Dr. George T. Wolff, Environmental and Energy Staff, General Motors Corporation,
Detroit, MI
SCIENCE ADVISORY BOARD STAFF
Dr. K. Jack Kooyoomjian, Designated Federal Official, U.S. EPA, Science Advisory Board
(HOOF), 401 M Street, S.W., Washington, D.C. 20460
Mrs. Diana L. Pozun, Staff Secretary, U.S. EPA, Science Advisory Board (1400F), 401 M
Street, S.W.7 Washington, D.C. 20460
111
-------
TABLE OF CONTENTS
1. EXECUTIVE SUMMARY 1
-2. INTRODUCTION AND OVERVIEW 6
3. METHODOLOGY AND OVERVIEW OF APPROACH 7
4. OVERALL CONCLUSIONS AND RECOMMENDATIONS 8
4.1 Coordination and Management 8
4.2 Selection of Effects for Inclusion in the Assessment 8
4.3 Selection of Pollutant Species for Analysis 9
. 4.4 Health-Effects End Points Selected 10
4.5 Omitted Physical Effects 12
4.6 Uncertainty Analysis 12
4.7 Peer-reviewed literature 12
4.8 Additional Issues and Recommendations 13
REFERENCES R-l
APPENDIX A - SPECIFIC TECHNICAL COMMENTS A-l
APPENDIX B GLOSSARY OF TERMS AND ACRONYMS B-l
IV
-------
1. EXECUTIVE SUMMARY
In response to the Congressional mandate of Section 812 (Appendix A, CAA, 1990),
and at the request of the Agency's Office of Policy Analysis and Review (OPAR) and the
Office of Policy Analysis (OPA), the Clean Air Act Compliance Analysis Council
(CAACAC) Physical Effects Review Subcommittee (CAACACPERS) reviewed draft physical
effects documents and the methodology pertaining to quantifying health effects for the Clean
Air Act (CAA) Section 812 retrospective benefit-cost analysis for criteria pollutants.
In addition to answering the questions in the Charge (see section 2), the Subcommittee
also focused on the broader mandate from Congress regarding the Section 812 study. The
following highlights summarize the main points of this review and are offered in the belief
that constructive advice at this stage can help the Agency make significant improvements in
the assessment process needed for the Section 812 and other future mandates. We also note
that neither Congress nor the EPA implemented the CAA in a way designed to expedite
evaluation. It is not surprising, therefore, that quantifying benefits and costs is so difficult
and uncertain at this point. Congress and the Agency have to ask themselves whether they
want to commit the time and resources needed for more comprehensive evaluations. The
Subcommittee believes that this exercise is worthwhile, and indeed necessary. In doing such
an evaluation, it is important to give a complete list of effects, and when possible, to
quantify and monetize the benefits - at least within an order of magnitude.
The Agency's draft documents reviewed are a first step toward confronting the
challenge of the Congressional mandates of Section 812 of the CAA of 1990. The following
points are offered as a summary of the findings and recommendations of the Subcommittee as
it dealt with the charge and identified major issues:
a) A Comprehensive Assessment: In Section 812, Congress specified that the
Assessment should be "comprehensive" and that it should "consider all of the
economic, public health, and environmental benefits... [emphasis added]."
With the notable exception of the analysis of the association between ozone
and mortality, the draft document is not responsive to this congressional
directive. Rather, it appears to have been prepared with an emphasis on
statistical and scientific conservatism. Although this is a defensible position
for the Agency to adopt for many circumstances (for example in setting
regulations that have to be defended in a legal arena), it may not inform
Congress about all of the possible benefits associated with implementation of
the CAA.
1
-------
b) Coordination and Management: The CAA Section 812 retrospective analysis
and the subsequent prospective analysis are very substantial and important
exercises. However, the retrospective study does not. presently appear to be
sufficiently coordinated - either across the various physical effects assessments,
or across all major model components. Various EPA participants have used
different strategies to address problems, which limit the linkages in the study
and the consistency of presentation. This study should be pushing the frontiers
of benefits assessment, bit it is, in fact, well behind many similar studies in
terms of coordination, use of available knowledge, and assessment of uncer-
tainty.
The project needs more emphasis on careful and forceful coordination, plan-
ning, and consistency, particularly in the area of modeling. The Agency needs
to assure that specific modeling strategies and issues are identified and ad-
dressed
c) Selection of Effects for Inclusion in the Assessment: Balancing the objective of
performing a comprehensive analysis against the cost of completing the
assessment requires a systematic approach to the selection of effects- one that
focuses resources on the most substantial effects for which literature exists for
benefits assessment, while not ignoring other effects of potential interest or
concern. We recommend a more comprehensive approach to the screening of
potential effects and the selection of effects for quantification and valuation.
Specifically, we recommend:
1) Providing a more complete listing and identification of known and
suspected physical effects.
2) Screening known and suspected physical effects to formally identify and
focus on the most substantial impacts for which there is literature to
develop a damage assessment.
3) Employing a consistent format for reporting omissions, biases, and
uncertainties in all study components, and especially in all physical-
effects components.
d) Selection of Pollutant Species for Analysis: The analyses received initially
were restricted not only to the criteria pollutants but, within them, to the
specific entities monitored in the ambient air, i.e., SO2, NO2, and the mass
concentrations of PM10 and PM2 5. This is inappropriate for sulfur oxides
(SOJ, nitrogen oxides (NOJ, and paniculate matter (PM). There were
-------
essentially no analyses made for the effects of other SOX, such as sulfuric acid
aerosol and its neutralization products, of other NOX, such as nitric acid vapor
and nitrate salts, or of other PM components, such as trace metals or toxic
organic particles.
e) Selection of Health End Points: Given that the purpose of this Assessment is
to estimate the economic value of air quality changes resulting from the
implementation of the CAA of 1970, the Subcommittee has reservations about
the specific health endpoints selected for detailed quantitative analysis. An
example of an effect given too much attention is reduced lung function follow-
ing short-tenn peaks in exposure to ozone. In some instances, recent epidemi-
ological evidence of more adverse effects that are also more readily monetized
was overlooked.
f) Omitted Physical Effects: The documents presented to the Subcommittee
specifically address only the health effects of the index pollutants within the
criteria pollutant category. In addition to omitting any discussion of other air
pollutants within the criteria pollutant category, the documents reviewed did
not address health effects of air toxics, welfare effects, and ecological effects.
Although recognizing the limited resources available to EPA to complete this
project, we urge EPA to perform some sensitivity analyses to prioritize the
levels of efforts to be invested in air toxics, and welfare and ecological effects
assessments.
g) Uncertainty analysis is not adequately treated: A major deficiency in the draft
document is the lack of any adequate treatment of uncertainty. It is not too
late to make a decision about how uncertainty will be handled in the assess-
ment. The manner in which uncertainty is treated has important implications
for the way in which physical effects dose-response functions are developed
and expressed.
h) Ozone: The Ozone Section of the document is seriously unbalanced. There is
an inappropriate emphasis on the findings from clinical studies, as well as
questionable interpretation of the clinical study implications. The Assessment
needs to link more closely the results of the clinical, field, and epidemiologic
studies to provide a firmer basis for the health costs of ozone exposures based
on the exposure-response relationships from the studies of exposed popula-
tions.
-------
i) Sulfur Oxides: The stated goal of limiting the analysis to the gaseous sulfur
oxides has not been explained or justified. Most importantly, this section does
not come to grips with:
1) The role of SO2 as a precursor of acidic aerosol formation;
2) The ways in which SO2 emission controls have affected exposures to
acidic sulfate aerosols; and
3) The health benefits of the reductions in such exposures.
j) Participate Matter: The mortality effects of particulate matter are likely to be
the dominant ones in terms of economic impact. It is unfortunate that the draft
is incomplete as it stands in several respects. First, it needs to account for
other acute-mortality studies that satisfy the selection criteria. Second, it must
address the nature and significance of acute mortality in terms of the extent of
life-shortening for those who die in excess on polluted days. Third, it should
consider evidence on differences in mortality risk across age groups, e g,
under 65 years vs. 65 and older. Finally, the biggest deficiency is that it
ignores the differences in annual average (cross-sectional) mortality rates
among communities.
k) Carbon Monoxide: The section on CO presents, in a clear manner, the
current information pertaining to the health risks of exposure. As it notes, the
most consistent data relating low-level concentrations to health measures come
from studies based on latency to anginal pain induced by exercise. Linking
these findings to mortality from heart disease or to accelerated myocardial
damage is a difficult speculative exercise, but offers the most reasonable way
to assess the benefits of reduced exposure. If the lower-bound estimate
includes zero, this can be stated. At a minimum, the Agency should conduct a
preliminary assessment using worst-case assumptions to establish an upper
bound.
1) Nitrogen Oxides: It is defensible to exclude aerosol forms of NOX from this
Section, if they are adequately discussed in Section 3 on Particulate Matter.
However, such an exclusion needs to be stated more explicitly. In the case of
NOX, that still leaves all of the vapor-phase nitrogen oxides to be discussed in
this Section. Thus, this Section is obligated to review the health effects
associated with nitric acid, and possibly nitrous acid (as well as those associ-
ated with NO2).
-------
m) Lead: This is one of the better-written products provided by the Agency. The
Subcommittee notes that the Agency's draft document recognizes the broad
spectrum of lead toxicity and attempts to provide quantitative risk assessments
for a variety of endpoints. This aim, however, misses some of the subtleties
of the lead literature. Specifically:
1) No explicit role is accorded to other measures of neurotoxicity;
2) Cross-sectional and other studies fail to exploit the relevant dose-
response behavioral data;
3) Inadequate attention is paid to the interaction of social class and the
expression of lead toxicity;
4) Effects in adults are accorded a narrow point-of-view
5) Observations of other effects of lead are important to understanding
fully the risk factors
6) Remobilization of stored lead has been ignored
7) The document gives inadequate discussion to the doses and responses
chosen, the approximate nature of the functional form, the perils of
extrapolating very far from the median of the data, and the question of
thresholds
8) There is no discussion of how changes in mean blood lead levels in
adults will be predicted as a function of changes in lead emissions
n) Ecological Effects: The effects of air pollutants on human health have domi-
nated this analysis thus far; and it does not appear that ecological effects will
catch up within the short time and limited budget that remain for this project.
However, one of EPA's missions is to protect ecosystems from adverse effects
of pollutants. Protocols will be needed to express ecological and other
non monetary values and to compare them to values expressed in monetary
terms. Currently, the documents only discuss valuation in monetary terms.
For many of the human health effects, this may be all that is needed. How-
ever, when ecological effects eventually are addressed, many ecological values
(including non-use values) may not easily be expressed in monetary terms.
Although ecological effects are difficult to comprehensively quantify and
monetize, the absence of at least a qualitative analysis that is on equal footing
with a human health analysis will be conspicuous and will leave EPA open to
sharp criticism.
-------
2. INTRODUCTION AND OVERVIEW
The CAACACPERS met on November 15 and 16, 1994 to receive briefings, and
have discussions with the Agency staff and the public. The Subcommittee also conducted a
public teleconference on April 12, 1995 and held a public meeting on May 18, 1995 to
review additional draft documents related to this topic.
The basic charge presented to the Subcommittee is as follows.
a) Are each of the elements of the methodology developed by EPA sufficiently
valid and reliable from a scientific standpoint for purposes of the CAA Section
812 assessments?
b) The Congress and the EPA intend that the CAA Section 812 retrospective
analysis should provide the most comprehensive possible statement about
potential benefits of historical reductions in air pollution. This includes
reporting on the potential significance of effects for which there may be no
scientific consensus regarding the magnitude or even the existence of a specific
effect. Given this statutory and administrative goal, is the methodology
developed by EPA sufficiently comprehensive in terms of plausible physical
health, welfare, and ecological consequences of exposure to the relevant air
pollutant?
c) If the answer to question 2 (above) is negative, what are the physical outcomes
of pollutant exposure which the Agency has omitted?
d) For the physical outcomes already included in the methodology paper, as well
as those which should be considered for inclusion pursuant to question 2
(above), are there potentially relevant data pertaining to quantitative or qualita-
tive estimation of the effect which should be considered for inclusion in the
methodology? What specifically are the SQurces of these data and how might
they be best utilized?
e) What is the strength of the scientific evidence underlying each of the physical
effects functions or models already included in the methodology paper? What
is the strength of each element of additional scientific evidence suggested for
inclusion pursuant to questions 3 and 4 above?
-------
3. METHODOLOGY AND OVERVIEW OF APPROACH
One question posed to the SAB was whether EPA's proposed approach is suitable for
quantifying health effects pertinent to Section 812 of the CAA, with the stated goal of
providing the basis for a benefits analysis that is "sufficiently comprehensive in terms of
plausible health, welfare, and ecological consequences of exposure to the relevant air
pollutant." Unfortunately the current draft of the Overview document fell short of these
aims. The Introduction to the document refers to welfare and ecological effects as well as
health effects, and several passages in the document are applicable to these broader aims.
However, most of the document discusses issues pertinent only to the quantification of a
limited number of effects on human health. We recommend that the title of the Overview be
changed to reflect the limited aims of the present Section 812 Assessment, or that the
analyses be broadened to be consistent with the original aims.
The health overview beginning on page 3 did not accurately describe the approaches
used or say anything about the comparative advantage of each. Toxicological and clinical
studies are needed to establish causality. Quantification is generally a combination of
toxicology (causality, functional form, and sensitive populations) and epidemiology (i.e.,
"real world" conditions and quantification of population response rates).
The issue of mitigation behavior was not addressed in the general methods section or
in any of the chapters provided. Individuals in controlled exposure studies cannot mitigate
exposures, whereas individuals in real life situations sometimes can affect their exposures.
Thus, the results of clinical studies may overstate damages. On the other hand, ignoring
mitigation in epidemiologic studies results in understated damage. For example, the number
of observed health effects per capita for any pollutant level is reduced by mitigation, but
mitigation results in some costs to the affected individuals, such as reduced activities and
increased use of medication.
In redrafting the overview chapter, one option that could be considered is to reorga-
nize by effect rather than by pollutant. This would naturally lead to a discussion of real
world exposures of mixed pollutants as well as to 'secondary' pollutants formed in the
atmosphere. It may allow for a better assessment of the dose/response relationships
discussed at the end of each chapter and avoid the issues associated with "double counting"
of effects. This reorganization of the material would not affect the air quality analy-
ses/modeling activities also associated with this exercise. Perhaps, more importantly, it
could place the modeling exercise in context, because the actual model outputs of a pollutant
mixture could be used rather than the pollutant-by-pollutant output.
-------
4. OVERALL CONCLUSIONS AND RECOMMENDATIONS
4.1 Coordination and Management
The CAA Section 812 retrospective analysis and the subsequent prospective analysis
are very substantial and important exercises. However, the retrospective study does not
presently appear to be sufficiently coordinated - either across the various physical effects
assessments, or across all major model components. Various EPA offices and researchers
(and their contractors) have used different strategies to address problems, which limit the
linkages in the study and the consistency of presentation. Although this study should be
pushing the frontiers of benefits assessment, it is, in fact, well behind many similar studies
performed for state and other federal agencies, in terms of coordination, use of available
knowledge, and assessment of uncertainty.
The project needs more emphasis on careful and forceful coordination, planning, and
consistency. With consistency, important linkages will be made between major study
components, appropriate comparisons of costs and benefits can be made, uncertainty can be
treated in a like manner in all study components, and the level of professionalism will be
consistent in all work elements.
The Agency needs a modeling team leader to structure model frameworks for physical
effects quantification and linkages to other model components. The leader can assure that the
team identifies and addresses specific modeling strategies and issues.
4.2 Selection of Effects for Inclusion in the Assessment
Balancing the objective of comprehensiveness against the cost of completing the
assessment requires a systematic approach to the selection of effects that focuses resources on
the most substantial effects for which literature exists for benefits assessment, while not
ignoring other effects of potential interest or concern. The draft overview chapter provides a
good, short summary of the approach that was taken, and provides reasonably good justifica-
tion for the options selected within that narrowly defined approach. However, we recom-
mend a more comprehensive approach to the screening of potential effects and the selection
of effects for quantification and valuation. Specifically, we recommend:
a) Providing a more complete listing and identification of known and suspected
physical effects.
-------
b) Screening known and suspected physical effects to formally identify and focus
on the most substantial impacts for which literature to develop a damage
assessment exists. Ample research to assist with this screening exists. It is
important that a clear statement be provided on what is included in the
quantification and what is not. Substantiation for the selections of the literature
should also be provided. The selection process should focus on key health,
ecological, and welfare impacts that are defended by the screening, with the
other effects left to be addressed later, if arid when additional resources
become available. The Subcommittee would also like to emphasize that both
monetary and non-monetary values should be looked at; that is, dollar benefit
impacts should not be the only basis for selecting and evaluating impacL.
c) Employing a consistent format for reporting omissions, biases, and uncertain-
ties in all study components, and especially in all physical-effects components.
This reporting can be in tabular form, listing the omission, bias, or uncer-
tainty, the direction of bias (if known), and any comments on the potential
significance of the omissions.
4.3 Selection of Pollutant Species for Analysis
Another major problem with the overview chapter and companion documents is the
lack of any apparent strategic planning leading to a comprehensive framework for analysis.
This is evident from the analyses being not only restricted to the criteria pollutants but,
within them, to the specific entities that are monitored in the ambient air. This is a suitable
limitation for carbon monoxide (CO), but not for sulfur oxides (SOx), nitrogen oxides
(NOx), and particulate matter (PM). Within these pollutant classes, analyses were largely
restricted to the effects of SO2, NO2, and the mass concentrations of PM10 and PM2 5. As a
consequence, essentially no analyses were made for the effects of sulfuric acid aerosol and its
neutralization products, of nitric acid vapor and nitrate salts, of trace metals, or of toxic
organics as either vapors or particles.
The reductionist approach taken also complicates and obscures the opportunities to
take some promising approaches to determining the benefits resulting from the 1970 CAA.
The control costs incurred have largely been associated with source-strength reductions
regarding criteria pollutants themselves and precursors of secondary pollutants. Imposed on
motor vehicles, power plants, space heating, and fuel processing, these controls have led to
known or calculable source reductions in emissions of CO, hydrocarbons, SO2, NOX, and
coarse particles. The SO2 and NOX reductions have also led to less well defined, but
calculable reductions in secondary pollutants such as SOX and NOX aerosols and ozone (O3).
-------
Furthermore, the efforts to control ambient concentrations of O3 and PM have led to
reductions in ambient concentrations of CO, as well as much greater reductions in source
emissions of trace metals and hydrocarbons (as both vapors and aerosols) than any efforts to
control them through NESHAPS (National Emission Standards for Hazardous Air Pollutants)
as hazardous or toxic air pollutants. Analyses should be done to show the effects of: a) NOX
source controls on ambient concentrations of O3 and nitric acid; b) the effect of SO2 and NOX
source controls on ambient concentrations of acidic aerosols and on acidic deposition in the
environment; and c) the effects of reductions in O3 on the formation of acidic aerosols. Such
an analysis most likely would show, for example, that the benefits from NOX source control
lie more in their effect on O3 formation, formation of air toxics through photochemical
reactions, and acidic deposition, than on reduction of health effects directly attributable to
NO2. The overview chapter is incomplete without a discussion of such interrelationships
between the various pollutants within and among the categories of the National Ambient Air
Quality Standard (NAAQS) and NESHAPS pollutants.
4.4 Health-Effects End Points Selected
Given that the purpose of this Assessment is to estimate the economic value of air
quality changes resulting from the implementation of the CAA of 1970, we have reservations
about the specific health endpoints selected for detailed quantitative analysis. An example of
an effect given too much attention is the changes in lung function following short-term peaks
in exposure to ozone. No economic data or methods were identified for estimating the
economic values of such effects. Furthermore, to the extent that changes in lung function are
associated with other symptoms and endpoints that are being modeled, there is a potential for
double counting of effects.
On the other hand, several health end points of potential economic significance were
not modeled. Both economic valuation studies and epidemiological studies support the
development of dose-response functions for a) respiratory hospital admissions, minor
restricted activity days, and acute respiratory symptoms due to exposures to ozone and b)
asthma, restricted activity days, and childhood bronchitis due to exposures to particulate
matter.
Also, the discussions of health effects for each pollutant were inconsistent and
incomplete. The material is presented with limited indication of how it will be used and
integrated into the overall assessment. For example:
10
-------
a) The introductory chapter noted the limited usefulness of clinical (controlled
human exposure) studies for this assessment, yet the ozone chapter focused on
clinical studies with little explanation as to why. The fundamental purposes for
including controlled-exposure studies are to establish a basis for the effects
observed in epidemiologic studies and to establish evidence for effect thresh-
olds. The fundamental reasons for not requiring controlled exposure studies
are the costs to conduct valid exposure analyses (which are not required with
the use of epidemiologic studies) and the limited usefulness of the endpoints
that are measured. These reasons, and others, were not sufficiently discussed.
b) The selection of studies, or of dose-response parameters, was inconsistent. In
some cases a best study was selected by judgement, while in other cases meta-
analysis was used. In these cases, the criteria for selection of studies for
inclusion into the meta-analysis were not made clear. A consistent analysis
framework should be adopted.
c) Inconsistent and limited treatment was given to portraying the range of dose-
response results for use in uncertainty analysis. In some health sections, the
highest and lowest coefficient were reported. In others, a meta-function
standard error was reported (or appeared likely to be the strategy that would
be used). These two approaches have a considerably different interpretation.
Without consistency in the treatment of uncertainty, in the physical-effects
study component, and across all other major analysis components, any propa-
gation of uncertainty may be of limited meaning.
d) Evidence for and against thresholds for health effects was often not discussed.
What are the assumptions EPA uses for the base case, and why? What
sensitivity analysis will be done, and why? Base-case threshold assumptions
can be made and defended, and the analyses can be conducted with alternative
assumptions about what are practical thresholds (below which effects may still
occur but where the dose-response curve may become very flat or where there
is little basis to extrapolate existing data to low levels).
e) Some health effects may overlap. The treatment of double counting should be
addressed in each chapter.
11
-------
4.5 Omitted Physical Effects
The documents presented to the Subcommittee specifically address only the health
effects of the index pollutants within the criteria pollutant category. Discussion of other air
pollutants within the criteria pollutant category, health effects of air toxics, welfare effects
such as effects on forests crops, visibility and materials, and ecological effects was omitted.
Although recognizing the limited resources available to EPA to complete this project, we
urge EPA to perform some sensitivity analyses to prioritize the levels of efforts to be
invested in air toxics, and welfare and ecological effects assessments. No plan to handle this
challenge was apparent in the Methodology Overview document. Expert opinion may
provide the only way to approach this challenge.
4.6' Uncertainty Analysis
A major deficiency in the draft document is the lack of any adequate treatment of
uncertainty. It is now past time to make a decision about how uncertainty will be handled in
the assessment. The manner in which uncertainty is treated has important implications for
the way in which physical-effects dose-response functions are developed and expressed.
The options for dealing with uncertainty include the formal specification and propaga-
tion of uncertainty using probability distributions on key variables and applying Monte Carlo
simulations or other related techniques; the specification of high arid low values for key
parameters and the calculation of upper and lower bounds based on them; and sensitivity
analysis. We prefer the formal analysis of uncertainty because it generates much more
information about the overall uncertainty that results from the combinations of uncertainties
about components of the assessment. For example, using high and low values will usually
lead to unrealistically wide bounds around the true value, at least if the individual component
uncertainties are independent of each other, as they often will be. We also recommend that
important omissions, biases, and uncertainties be listed and their potential significance to the
assessment be discussed.
We note that the CAACAC also discussed this set of issues in its letter of March 24,
1993 to the Administrator (SAB, 1993).
4.7 Peer-reviewed literature
The document clearly presents the case that the analysis will include data from some
literature that is not peer-reviewed. While this is necessary in some instances, we would
strongly argue that the window for inclusion of non peer-reviewed literature be restricted to
12
-------
about two years, sufficient for it to be published. For example, we suggest limiting the use
of non-peer-reviewed literature to supportive analyses rather than core components. Clearly,
if a critical component of the analysis methodology is based on non-peer reviewed literature,
the analysis is suspect. Some explicit criteria for inclusion and exclusion of "gray" literature
needs to be formulated.
4.8 Additional Issues and Recommendations
In addition to answering the specific questions in the Charge, the Subcommittee
broadened its scope of coverage to focus on the broader mandate from Congress regarding
the Section 812 study.
Attempts to quantify the costs of air pollution have been undertaken over the past
three decades, beginning with Ridker and Henning (1967), Ridker (1967), and Lave and
Seskin (1970). These efforts led to more active discussion on the reliability of assuming a
causal relationship from statistical associations. In 1989, a Congressional Research Service
Report to Congress (Congressional Research Service Report, 1989) noted, in the summary:
"..we conclude that though there is no doubt that significant health benefits
result from controlling some air pollutants, it is not currently feasible to
produce an unambiguous evaluation of the health benefits."
In Section 812, Congress specified that the Assessment should be "comprehensive"
and that it should "consider all of the economic, public health, and environmental benefits...
[emphasis added]." We interpret this to mean that Congress was directing the Agency not to
be conservative in the sense of minimizing the likelihood that benefits would be overstated.
Rather Congress appears to have been asking the Agency to produce an assessment that was
inclusive of not only well documented and measured effects and values, but also those effects
and values for which limited information exists. In other words, Congress was asking the
Agency to take some risks of overstating benefits so as to reduce the likelihood that it would
produce an underestimate of the true benefits.
With the notable exception of the analysis of the association between ozone and
mortality, the draft document is not responsive to this Congressional directive. Rather, it
appears to have been prepared with an emphasis on statistical and scientific conservatism.
Although this is an understandable, defensible position for the Agency to adopt for many
circumstances (for example in setting regulations that have to be defended in a legal arena),
it may not inform Congress about all of the possible benefits (or lack of benefits) associated
with implementation of the CAA. The Methodology Overview should discuss the issues of
conservatism in the face of limited information about some effects and describe its approach
to meeting the mandate of Congress to avoid undue conservatism.
13
-------
The Council offers the following comments in the belief that constructive advice at
this stage can help the Agency make significant improvements in the assessment process
needed for the Section 812 and other future mandates. We also note that neither Congress
nor the EPA implemented the CAA in a way designed to generate a database that could be
used to expedite evaluation. It is not surprising, therefore, that quantifying benefits and costs
-in the absence of much relevant data is so difficult and uncertain at this point.
Congress and the Agency have to ask themselves whether they want to commit the
time and resources to future evaluations. The Subcommittee believes that this effort is
worthwhile, and indeed necessary. Without evaluation, how can the Agency and the
Congress tell which programs are working, which need attention, and which need to be cut
or expanded? In doing such an evaluation, it is important to give a. complete list of effects.
Where there is any ability to do so, it is important to quantify and monetize the benefits - at
least, by an order of magnitude.
The Agency should focus its resources on estimating the important benefits within
each program. For example, the Agency can neglect effects that are a factor of ten smaller
than the largest effects in a category — They are unlikely to make a significant contribution.
This rule-of-thumb will allow the Agency to focus its resources on the categories of interest
and not waste time or effort on categories that would not affect the policy implications of the
evaluation.
Currently, the documents only discuss valuation in monetary terms. For many of the
human-health effects, this may be all that is needed. However, when ecological effects
eventually are addressed, EPA might be forced to conclude that many ecological values
(including non-use values) cannot easily be monetized. EPA and the Congress will need
protocols for expressing values in non-monetary terms, and for comparing them to those
values that will be expressed in monetized terms. In effect, a methodology is needed to
decide how to maintain two complementary benefits columns — monetary and non-monetary
values.
Another major problem is that the documents failed to confront the challenge of
Section 812 in the CAA of 1990. The overall need is clearly stated in the first two pages of
the overview chapter (October 11 draft). Thereafter, the focus suddenly narrows to "effect
categories that have a direct effect on human health." Furthermore, the balance of the
overview chapter, and the content of the following six Sections on criteria pollutants, makes
it evident that analyses are focussed almost entirely on acute health responses, with consider-
ably less attention to cumulative tissue damage resulting from long-term, low-level exposures
and their benefits in terms of chronic health-care costs, lost time from work or school, and
diminished quality-of-life in people with chronic health damage.
In order for EPA to be responsive to the mandate of Section 812 of the CAA, its final
report will need to take a broader view of not only human-health effects of criteria pollut-
ants, but also other major class of pollutants and their effects. These include the effects of
14
-------
hazardous air pollutants on human health, as well as the effects of air pollution on visibility,
ecosystems, forest and agricultural productivity, and on welfare effects such as soiling and
damage to materials and equipment. It should be noted that the SAB's CAACACPERS
received draft documents in April, 1995 related to the above topics, discussed them in an
open public meeting on May 18, 1995, and will provide a future advisory document to the
Agency on these issues.
15
-------
REFERENCES1
Allred, E.N., Bleecker, E.R., and B.R. Chaitman, B.R. 1989. Short term effects of carbon
monoxide exposure on the exercise performance of subjects with coronary artery
disease. New England Journal of Medicine 321:1426-1432
Aim, S., Jantunen, M.J., Mukala, K., Pasanen, P., and J. Tuomisto. 1994. Personal
weekly nitrogen dioxide exposure levels of preschool children in Helsinki measured
by Palmes tubes. In: Program Abstracts of the Sixth Conference of the International
Society for Environmental Epidemiology: Research Triangle Park, NC September
18-21, 1994. Abstract 135
Arrow, K., B. Bolin, R. Costanza, P. Dasgupta, C. Folke, C.S. Rolling, B.-O. Jansson, S.
Levin, K.-G. Maler, C. Perrings and D. Pimmental. 1995. Economic growth,
carrying capacity, and the environment, Science. 268:520-521.
Avol, E.L., Linn. W.S., Venet, D.A., Shamoo, J.D., and J.D. Hackney. 1984. Compara-
tive respiratory effects of ozone and ambient oxidant pollution exposure during heavy
exercise. J. Air Poll. Com. Assoc. 34:804-809.
Bates, D.V., Baker-Anderson, M., and R. Sizto. 1990. Asthma attack periodicity: a study
of hospital emergency visits in Vancouver. Environ Research 51:51-70.
Bates, D.V. 1992. Health indices of the adverse effects of air pollution: the question of
coherence. Environ. Research. 59:336-349.
Bates, D. V., and Sizto, R. 1987. Hospital admissions and air pollutants in southern
Ontario: the acid summer haze effect. Environ. Research. 43:317-331.
Bellinger, D. Levitor, A. Waternaux, C., Needleman, H.L., and M. Rabinowitz, 1987.
Longitudinal analysis of prenatal and postnatal lead exposure and early cognitive
development. NEJM 316:1037-1043.
Blodgett, J. 1989. (Report for Congress). Health benefits for air pollution control: A
Discussion. 89-161 ENR. Congressional ResearcTi Service, Library of Congress,
Washington DC
Braum-Fahrlander, C, Ackerman-Liebrich, U. Schwartz, J., Gnehm, H.P., Ritishauser, M.,
and H.U. Wanner. 1992. Air pollution and respiratory symptoms in preschool
children. Am. Rev. Respir. J. 145:42-47.
This "Section contains some references not cited in the body of the report, but which are included for the information of the
reader.
R-l
-------
Brunekreef, B. et al. 1994. Respiratory effects of low-level photochemical air pollution in
amateur cyclists. Am. J. Respir. Crit. Care Med. 150:962-966.
Burnett, R.T., Dales, R.E., Raizenne, M.E., Krewski, D. Summers, P.W., Roberts, G.R.,
Raad-Young, M., Dann, T., and J. Brooke. 1994. Effects of low ambient levels of
ozone and sulphates on the frequency of respiratory admissions to Ontario hospitals,
Environ. Research 65:172-194.
Carson, R.T., Mitchell, R.C., and P.A. Ruud. 1989. Valuing air quality improvements:
Simulating a hedonic pricing equation in the context of a contingent valuation
scenario. Paper presented at the Air and Waste Management Association Conference
on Visinbility and Fine Particles, Estes Park, CO, October 15-19, 1989.
Castellsague, J., Sunyer, J., Saez, M., Murillo, C., and J.M. Anto. 1992. Effect of air
pollution in asthma epidemics caused by soybean dust. Eur Respir J. 5, Supplement
15, August. Abstract PI370, page 413S.
Chestnut, L.G. 1994. Human health benefits assessment of the acid rain provisions of the
1990 clean air act amendments. Draft final report prepared for the the U.S. EPA, by
RCG/Hagler Bailly.
Clean Air Act. 1990. Public Law 101-549, Section 812, 104 STAT 2692, November 15,
1990.
Clean Air Act. 1970. Public Law 91-604. December 31, 1990.
Cody, R.P., Weisel, C.P., Birnbaum, G., and PJ. Lioy. 1992. The effect of ozone
associated with summertime photochemical smog on the frequency of asthma visits to
hospital emergency departments. Environ. Research 58:184-194.
Congessional Research Service. 1989. Health benefits of air pollution control: A discus-
sion. U.S. Library of Congress, Congessional Research Service, Washington DC.
Dietrich, K.N., Kraftt, K.M., Bornschein, R/L., Hammond, P.B., Berger, O., Succop,
P.A., and M. Beir. 1987. Low-level lead exposure: effects on neurobehavioral
development in early infancy. Pediatrics 80:721-730.
Dockery, D.W., Pope, C.A., Xu, X., Spengler, J.D., Ware, J.H., Fay, M.E., Ferris, E.G.,
and Frank Speizer. 1993. An association between air pollution and mortality in six
U.S. cities, NEJM. 329:1753-1759.
Dockery, D.W., and C.A. Pope III. 1994. Acute respiratory effects of particulate air
pollution. Annual Rev. Public Health. 15:107-132.
R-2
-------
Edwards, J., Walters, S., and R.K. Griffiths, R.K. 1994. Hospital admissions for asthma
in preschool children: relationship to major roads in Birmingham, United Kingdom
Arch Environ Health 49:223-227.
Frampton, M.W., Voter, K.Z., Fogarty, J.P., Morrow, P.E., Gibb, F.R., Speers, D.M.,
Tsai, Y., and M.J. Utell. 1994. Airway inflammation and functional responsiveness
to ozone in humans. Am. J. Respir. Crit. Care Med. 149:A150.
Gilmour, M.I., Park, P., and M.K. Selgrade. 1993. Ozone-enhanced pulmonary infection
with streptococcus zooepidemicus in mice. Am. Rev. Respir. Dis. 147:753-760.
Hall, J.V., Winer, A.M., Kleinman, M.T., Lurmann, F.W., Brajer, R.V., and S.D.Colome.
1992. Valuing the health benefits of clean air. Science 255:812-817.
Hatch, G.E., Slade, R., Harris, L.P.,McDonnell, W.F., Devlin, R.B., Koren, H.S., Costa,
D.L., and J. McKee. 1994. Ozone Dose and effect in humans and rats. Am. J.
Respir. Crit. Care Med. 150:676-683.
Hazucha, M.J., Folinsbee, L.J., Seal, E., and P.A. Bromberg. 1994. Lung function
response of healthy women after sequential exposures to N02 and 03. Am J Respir
Crit Care Med 150:642- 647.
Ito, K., and P.L. Kinney. 1995. Variations in PM10 concentrations within two metropolitan
areas and the implications for health effects analyses. Inhal. Tox. 7:735.
Kinney, P.L., Ito, K., and G.D. Thurston. 1995. A sensitivity analysis of mortality/PMIO
associations in Los Angeles. Inhal. Toxicol. 7:59-69.
Kinney, P.L.and H. Ozkaynak. 1991. Associations of daily mortality and air pollution in
Los Angeles County. Environ. Research. 54:99-120.
Koren, H.S., Devlin, R.B., Becker, S., Perez, R., and W.F. McDonnell. 1991.
Time-dependent changes of markers associated with inflammation in the lungs of
humans exposed to ambient levels of ozone. Toxicol. PathoL 19:406-411.
Kreit, J.W., Gross, K.B., Moore, T.B., Lorenzen, T.J., D'Arcy, J., and W.L.
Eschenbacher. 1989. Ozone-induced changes in pulmonary function and bronchial
responsiveness in asthmatics. J. Appl. Physiol. 66:217-222.
Krupnick, A.J., Harrington, W., and B. Ostro. 1990. Ambient Ozone and acute health
effects: Evidence from daily data. J. Environ. Econ. and Mgmt. 18(1): 1-18.
R-3
-------
Kuwano, K., Bosken, C.H., Pare, P.D., Bai, T.R., Wiggs, B.R., and J.C. Hogg. 1993.
Small airways dimensions in asthma and in chronic obstructive pulmonary disease,
Am. Rev. Respir. Dis. 148, 1220-1225.
Laitinen, L.A., Laitinen, A., and T. Haahtela. 1993. Airway mucosal inflammation even in
patients with newly diagnosed asthma. Am. Rev. Respir. Dis. 147:697-704.
Lave, L.B., and E.P. Seskin. 1970. Air Pollution and Human Health, Science. 169:723-
733.
Linder, L, Herren, Monn, C., and H-U. Wanner. 1988. Die wirking von Ozon aur die
koerperliche leistungsf^chigkett. Schweiz Z. Sportmed. 36:5-10.
Lipfejt, F.W., and T. Hammerstrom. 1992. Temporal patterns in air pollution and hospital
admissions. Environ. Research. 59:374-399.
Lippmann, M. 1995. Personal Communication.
McBride, D.E., Koenig, J.Q., Luchtel, D.L., Williams, P.V., and W.R. Henderson, Jr.
1994. Inflammatory effects of ozone in the upper airways of subjects with asthma.
Am. J. Respir. Crit. Care Med. 149:1192-1197.
Moseholm, L., Taudorf, E., and A. Frosig. 1993. Pulmonary function change in asthmatics
associated with low-level S02 and N02 air pollution, weather, and medicine intake: an
8 month prospective study analyzed by neural networks. Allergy 48: 334-344, 1993
Moseler, M. Hendel-Kramer, A., Karmaus, W., Forster, J., Weiss, J.K., Urbanek, R., and
J. Kuehr, J. 1994. Effect of moderate NO2 air pollution on the lung function of
children with asthmatic symptoms. Environ. Research. 67:109-124,
Neas, L. M., Dockery, D.W., Ware, J.H., Spengler, J.D., Speizer, F.E., and B.C. Ferris,
Jr. 1991. Association of indoor nitrogen dioxide with respiratory symptoms and
pulmonary function in children. Am. J. Epidemiol. 134:204-219.
Needleman, H.L., Gunnoe, C., Levitor, A., Reed, R., Peresie, H., Maher, C., and P.
Parrett. 1979. Deficits in psychologic and classroom performance of children with
elevated dentine lead levels. NEJM 300:639-695.
Needleman, H.L., and C.A. Gatsonis. 1990a. J^ow-level lead exposure and the IQ of
children: a meta-analysis of modern studies. JAMA 263:673-678.
Needleman, H.L., Schell, A. Bellinger, D., Leviton, A., and E.N. Allied. 1990b. The
long-term effects of exposure to low levels of lead in childhood: An 11-year follow-
up report. NEJM 322:83-88.
R-4
-------
Ostro, B.D. and Rothschild. 1989. Air pollution and repiratory mortality: An observational
study of multiple pollutants. Environ. Res. 50:238-247
Pope, C.A. III. 1991. Respiratory hospital admissions associated with PM10 pollution in
Utah, Salt Lake, and Cache Valleys. Arch. Environ. Health 46:90-97.
Pope, C.A. III. 1995. Particulate air pollution as a predictor of mortality. Am. J. Resp.
Crit. Care. Med. 151:669-674.
Pope, C.A. Ill, Dockery, D. W., and J. Schwartz. 1995. Review of Epidemiological
evidence of health effects of particulate air pollution. Inhalation Toxicology 7:1-18.
Portney, P.R. and J. Mullahy, J. 1990. Urban air quality and chronic respiratory disease.
Regional Sci. 30:407-418
Portney, P.R. and J. Mullahy, J. 1986. Urban air quality and acute respiratory illness. J.
Urban Econ. 20:21-38
Rae, D. 1983. Benefits of improving visual air quality in Cincinnati: Results of a contin-
gent valuation survey. Electric Power Research Institute, Project 1742. Palo Alto,
CA.
Ridker, R.G. 1967. Economic costs of air pollution: Studies and measurement. Pub:
Praeger, New York, NY.
Ridker, R.G., and J.A. Henning. 1967. The determinants of residential property values
with special reference to air pollution. Rev. of Econ. and Stat. 49 (2): 246-257.
Samet, J.M., Lambert, W.E., Skipper, B.J., Gushing, A.H., Hunt, W.C., Young, S.A.,
McLaren, L.C., Schwab, M., and J.D. Spengler. 1993. Nitrogen dioxide and
respiratory illness in infants Am Rev Respir Dis. 148:1258-1265.
Schwartz, J. 1994. Air Pollution and hospital admissions for the elderly in Detroit,
Michigan, Am. J. Respir. Crit. Care Med., 150:648-655.
Schwartz, J. 1994. PM10, ozone, and hospital admissions for the elderly in Minneapolis-St.
Paul, MN. Arch. Environ. Health 49:366-374.
Schwartz, J., Dockery, D.W., Neas, L.M., Wypij, D., Ware, J.H., Spengler, J.D.,
Koutrakis, P., Speizer, F.E., and E.G. Ferris, Jr. 1994. Acute effects of summer
air pollution on respiratory symptom reporting in children. Am. J. Respir. Crit. Care
Med. 150:1234-1242.
R-5
-------
SAB (Science Advisory Board). 1995. Beyond the horizon: protecting the future with
foresight. EPA-SAB-EC-95-007.
SAB (Science Advisory Board). 1995. Futures Methods and Issues, Technical Annex to
"Beyond the Horizon: Protecting the Future with Foresight." EPA-SAB-EC-95-007a.
SAB (Science Advisory Board). 1994. Clean Air Scientific Advisory Committee comments
on air quality modeling for the section 812 retrospective study. EPA-SAB-CASAC-
LTR-94-009.
SAB (Science Advisory Board). 1993. Science Advisory Board's Review of the Office of
Policy, Planning, and Evaluation's (OPPE) and the Office of Air and Radiation's
(OAR) progress on the retrospective study of the impacts of the Clean Air Act. EPA-
SAB-CAACAC-LTR-93-006.
SAB (Science Advisory Board). 1990a. Reducing risk: setting priorities and strategies for
environmental protection. EPA-SAB-EC-90-02.
SAB (Science Advisory Board). 19905. Report of the ecology and welfare subcommittee:
relative risk reduction project. EPA-SAB-EC-90-02 la.
SAB (Science Advisory Board). 1988. Future risk: research strategies for the 1990's.
EPA-SAB-EC-88-040.
Small, K.A., and C. Kazimi. 1995. On the costs of air pollution from motor vehicles. J.
Transport. Economics and Policy 29:7-32.
Strand, V., Svartengren, M., Rak, S., and G. Bylin. 1994. Effects of N02 exposure on
immediate and late response to inhaled allergen in subjects with asthma. Am J Respir
Crit Care Med. 149:A154.
Suter, G.W., II (editor). 1993. Ecological Risk Assessment, Lewis Publishers, Boca Raton,
FL.
Thurston, G.D., Ito, K., Hayes, C.G., Bates, D.V., andM. Lippmann. 1994. Respiratory
hospital admissions and summertime haze air pollution in Toronto, Ontario: consider-
ation of the role of acid aerosols. Environ. Research 65: 271-290.
Thurston, G., Lippmann, M., Bartoszek, M., and J. Fine. 1994. Summer haze associations
with asthma exacerbations, peak flow changes, and respiratory symptoms in children
at a summer asthma camp In: Program Abstracts of the Sixth Conference of the
International Society for Environmental Epidemiology: Research Triangle Park, NC
September 18-21, 1994. Abstract 227.
R-6
-------
Thurston, G., and P. Kinney. 1992. Daily respiratory hospital admissions and summer haze
air pollution in several New York metropolitan areas. Am. Rev. of Respir. Dis.
145(4:2):A429.
U.S. EPA. 1995. Revised air quality criteria document for ozone and related photochemical
oxidants (CASAC Review Draft, February, 1995). Environmental Criteria and
Assessment Office, U.S. EPA Office of Research and Development.
U.S. EPA Memorandum. 1994. CAACAC Review of Section 812 Retrospective Analysis.
from R.D. Brenner, Director, Office of Policy Analysis and Review and R.D.
Morgenstern, Director, Office of Policy Analysis, to D.G. Barnes, Director, Science
Advisory Board, October 5, 1994
U.S..EPA. 1986. Ozone Criteria Document. EPA-600/8-84-020aF-eF. Washington, DC
U.S. EPA. 1995. Revised air quality criteria document for ozone and related photochemical
oxidants: CASAC review draft. Environmental Criteria and Assessment Office, U.S.
EPA, Ofice of Research and Development.
U.S. GAO. 1994. Air Pollution: EPA's Progress in Determining the Costs and Benefits of
Clean Air legislation, U.S. General Accounting Office, Report to Congressional
Committees.
Ware, J.H. Spengler, J.D., Neas, L.M., Samet, J.M., Wagner, G.R., Coultas, D.,
Ozkaynak, H. and M. Schwab. 1993. Respiratory and irritant health effects of
ambient volatile organic compounds: the Kanawha County Health Study. Am. J.
Epidemiol 137: 1287-1301.
White, M.C., Etzel, R.A., Wilcox, W.D., and C. Lloyd. 1994. Exacerbations of childhood
asthma and ozone pollution in Atlanta. Environ. Research 65:56-68.
Winneke, G., Hrgina, K., and A. Brockhaus. 1982. Neuropsychological studies in children
with elevated tooth-lead concentration. Int. Arch. Occup. Environ. Health 51: 169-
183.
Yule, W., Lansdown, R. Millar, I., and M. Urbanowicz. 1981. The relationship between
blood lead concentration, intelligence, and attainment in a school population: a pilot
study. Dev. Med. Child Neurol. 23: 567-576.
R-7
-------
APPENDIX A--SPECIFIC TECHNICAL COMMENTS
OZONE
General Comments
The Ozone Section of the document is seriously unbalanced. The specific reasons for
this conclusion are provided in the detailed critique that follows, but the imbalance is
primarily the consequence of inappropriate emphasis on the findings from clinical studies, as
well as questionable interpretation of the clinical study implications. The clinical studies are
very important, because they confirm that the functional and symptomatic effects reported in
field studies of natural populations engaged in outdoor recreational activities and/or vigorous
work schedules can be seen under rigorously controlled experimental conditions. They are
also important, because they demonstrate that concurrent lung inflammation, not detectable in
field studies, occurs and that it persists during repeated daily exposures despite the attenua-
tion of functional and symptomatic responses. This provides mechanistic support for the
epidemiological associations observed between repeated exposures and the exacerbation of
asthma. By more closely linking the results of the clinical, field, and epidemiologic studies,
a revised document could provide a firmer basis for the health costs of ozone exposures
based on the exposure-response relationships from the studies of exposed populations.
In this revised discussion, the authors need to recognize that the paradigm for the
quantitative assessment of the pulmonary function responses of humans to exposure to ozone
has recently shifted, as agreed by CASAC (Clean Air Scientific Advisory Committee)
consensus during their meeting in July, 1994 and by the WHO-EURO (World Health
Organization, European Region) Working Group on Air Quality Guidelines at their meeting
in Bilthoven, The Netherlands, October, 1994 (Lippmann, 1995, personal communication).
There is now a body of credible data from field studies on human populations in natural
settings to establish the nature and extent of human pulmonary function responses to ambient
ozone exposures, and their uncertainty. In this new paradigm, the findings in controlled
laboratory studies provide support for the observed effects in natural populations, rather than
the other way around, as stated in the draft chapter.
The effect of ozone on mortality remains to be established, but warrants careful
attention. Although the Kinney and Ozkaynak (1991) studies report positive ozone effects,
other mortality studies have not found a statistically significant ozone relationship. EPA does
not address how it would use the Kinney and Ozkaynak results. Will the coefficient from
LA or NY be used? Or would they be averaged? Will these values be the central coefficient
(ignoring or giving little of no weight to other negative studies)? What confidence will be
given to the selected coefficients and why?
The macro-epidemiology studies are noticeably absent, including those for restricted
activity days (e.g., Ostro et al., 1989; Portney et al., 1986), acute respiratory symptom days
(Krupnick et. al., 1990), and respiratory hospital admissions (Burnett et al., 1994; Thurston
A-l
-------
et al., 1992, 1994, Pope, 1991; Schwartz, 1994a,b). This omission is noticeable because
these endpoints and studies are easier to use than the selected controlled exposure studies,
these endpoints and studies are regularly used in other benefit analyses, and because many of
these endpoints and studies are included in the particulate matter chapter. Related to these
points is our concern with the emphasis in this Section of the draft on physical effects of
uncertain significance for human health and for which there is little or no empirical data on
people's willingness to pay to avoid these effects.
As noted in the prior CAACAC Subcommittee review on transport and transformation
modelling, a potentially major issue arises when attempting to reconstruct historical O3
exposure via simple urban plume (box) models. Historical emissions of NOX were higher
than today. Therefore the spatial distribution of NOX emission densities in urban areas would
be different today in the absence of controls, and thus the spatial distribution of maximum
hourly O3 values would also be different. Simple urban plume models may not adequately
capture this shift in O3 and therefore may improperly characterize the control versus no-
control population exposure difference. One possible approach is to use the O3 predictions
from the RADM (Regional Acid Deposition Model) model exercise to predict the control/no-
control ratios of O3 exposure and then use these ratios to adjust current (present day) O3
levels. This would provide a spatially averaged O3 exposure difference for use in retrospec-
tive analyses.
This section also needs other significant revisions. It must address: standard issues of
thresholds; double counting; omissions, biases, and uncertainties; and the selection of central
dose-response function coefficient values.
Specific Comments
Page 1-3: Line 9 from top: "the average changes in lung function are generally small and are
a matter of controversy in regard to their medical significance." As noted below, the issue is
whether an FVC (Forced Vital Capacity) change is indicative of induced inflammation.
Fuller discussion is needed.
Page 1-8: bottom of page: A recently presented study by Thurston et al. (1994). A full text
of this manuscript would be important, as the abstract does not mention all the important
findings. The authors studied asthmatic children at a summer camp for a week in three
consecutive years. The children had to report to an office (where there was doctor and a
nurse) if they felt they needed medication. Air pollutants were measured at the camp. The
usual decrements in lung function with 03 levels were noted, but in addition there was a
monotonic relationship between the requests for medication and the ozone level at concentra-
tions lower than 100 ppb. This study should also be included in Table 1-3.
Page 1-12: Section 1.2.2: This extended discussion of symptoms does not include any
mention of whether the induction of symptoms is important. Does it indicate that inflation
has occurred? Why does the FVC fall early in ozone exposure? As it stands, it is clinically
A-2
-------
incomplete. See below. Also, the review should cite the recent paper on symptoms in
children participating in the Harvard six-cities study (Schwartz et al., 1994).
Page 1-12: A new section is needed to summarize and discuss the evidence of induced
inflammation in the human lung after ozone exposure. On page 1-21 in section 1.2.7, it is
noted, that : "Indications of ongoing tissue inflammation of subject exposed to O3 have been
reported in several studies." This is far too weak a statement for the contemporary evidence.
The time course of the induced inflammation has been well summarized by Koren and Devlin
and their associates ( Koren, et al., 1991). This reference is useful in this regard.
Page 1-22 (first paragraph): The following statement is quoted from the criteria document:
"However, the time course of this inflammatory response and the O3 exposures necessary to
initiate it, have not yet been fully elucidated" . This is entirely unsatisfactory in the light of
present evidence (Koren, et. a/., 1991). Furthermore, the statement at the end of the second
paragraph on page 1-22 referring to Devlin's work states: "However these results have not
yet been fully evaluated." What does this mean? We recommend that the authors revisit
these issues with experts at HERL (Health Effects Research Laboratories) laboratories of
EPA. One would have expected an up-to-date and sophisticated discussion of these issues in
this document.
A more suitable summary would state:
"It has been well established that an early effect of ozone is to cause an inflammatory
response in the human lung. The pattern of increases in the cells in bronchoalveolar
lavage specimens after ozone exposure in normal subjects, followed by the appearance
of inflammatory mediators for as long as 18 hours after the exposure, has been
convincingly shown."
The relationship between the onset of symptoms and the reduction in FVC, with the
onset of inflammation is less clear. It appears that the magnitude of induced function defect
and the severity of the inflammatory response are not closely associated (Frampton et. al.,
1994); if this is the case, then the question arises of whether the use of the function test
response as a guide to safe exposure level is appropriate. What is the clinical significance of
an induced inflammatory response? in normal subjects? in "asthmatics? These question must
be directly addressed.
It should also be noted that the effect of ozone (120 or 240 ppb) in inducing a
inflammatory response in the nose of asthmatic and non-asthmatic subjects has been studied
(McBride et. al., 1994). This showed that an inflammatory response was found in asthmatic
but not in normal subjects.
Page 1-14: Section 1.2.5: Aggravation of existing respiratory disease:
This section s'hould contain a synthesis of information on asthma. The statement quoted here
A-3
-------
from the 1986 Ozone Criteria Document is inappropriate, as it is seriously out of date. The
Draft Ozone Criteria Document (U.S. EPA, 1995) recently submitted by EPA to CASAC
includes a full and up-to-date summary of the known effects of ozone; the clinical and
epidemiological data bases are well covered. Additionally, a synthesis of present data on
asthma would have told the reader:
a) Exacerbations of asthma (including fatal asthma) are now believed to be due to
acute inflammation in the airways (Laitinen et. al., 1993; Kuwano et. al.,
1993).
b) The early and prolonged induction of airway inflammation by ozone is well
documented.
c) Although in quantitative terms the function test response and the bronchial
reactive response in asthmatics to ozone may be similar to that in normals, the
effect in asthmatics is exerted on an already depressed level of function, and
an already aggravated airway responsiveness. Thus the inference invited from
the quotation from the 1986 Ozone Criteria Document, that ozone is not more
of a risk to asthmatics than to normals, is not an accurate representation of the
circumstances. Kreit's 1989 paper (Kreit et al., 1989) is quoted, but misinter-
preted.
d) Based on the nasal lavage studies, asthmatics show an inflammatory response
to ozone that is not shown by non-asthmatics (McBride et. al., 1994).
e) There is now strong epidemiological evidence (see below) that asthma is made
worse by existing ozone levels.
In the light of these observations, the comment on Page 1-28 in the second line:
"However, there is no consensus about the magnitude of the difference in sensitivity between
asthmatics and other individuals" should be deleted.
Page 1-17: Section 1.2.6: This section is seriously out of date. References in Tables 1.5 and
1.6 include several as abstracts which have now been completely published (White, et. al.,
1994; Cody, et. al., 1992; Thurston, et. al., 1994; Burnett et. al., 1994; and Lipfert and
Hammerstrom, 1992), and one that is not mentioned (Schwartz, 1994a). To summarize this
very large bank of epidemiological data:
a) The Ontario data has now been analyzed by four different groups of investiga-
tors (Bates and Sizto, 1987): Lipfert and Hammerstrom, 1992: Thurston et.
al., 1994b: and Burnett et. al., 1994). All find a strong association of respira-
tory hospital admissions with ozone.
A-4
-------
b) Although in the eastern Great Lakes region, ozone is associated with peaks of
acid aerosol, several studies indicate that the primary effects relationship is
with ozone. PM10 effects appear to be additional and separate.
c) In Burnett's analysis of admissions to 168 hospitals in Ontario between 1983
and 1988 (Burnett, et. al., 1994), there is a monotonic relationship between
respiratory admissions and ozone the day before. These data should be used
in economic estimates and assumed to apply in the Northeast of the continent.
d) White's data (White et. al., 1994) show a direct association between hospital
emergency visits and ozone levels in Atlanta. The levels of acidity here are
not much different from those in New Jersey. Together with Cody's data
from eight New Jersey hospitals (Cody et. al., 1992), the conclusion should be
drawn that ozone at levels below 120 ppb is aggravating asthma.
e) Schwartz's recently published data on hospital admissions for pneumonia in the
elderly in Detroit (Schwartz, 1994a) are supportive. He has been able to show
separate effects for PM10 and for ozone.
This document should have analyzed the Lipfert, Burnett, Thurston, Cody, and White
and Schwartz data, and presented a synthesis of ozone impact on emergency visits and on
hospital admissions as a basis for cost estimates.
Page-1-22: Section 1.2-8: The effect of ozone on macrophage is noted here, but this should
be under Section 1.1. The discussion is also incomplete because the reader is not told the
possible significance of this experimental finding. Does it indicate that ozone levels might
affect the incidence or severity of pneumonia? (See comment under Page 1-17 above on
Schwartz's recent study of pneumonia in Detroit).
Page 1-22: Section 1.2.9: It is true that animal-exposure data are important for estimating the
likelihood of chronic effects of ozone. But the point should be mentioned that it is difficult
to extrapolate from rat data to humans, because the rat lung has been shown to be less
sensitive to ozone than the human lung, probably because a lower concentration of ozone is
delivered to the periphery of the rat lung than to the human. See Hatch et. al., (1994) for a
recent discussion of this. This important work was done at the HERL in North Carolina.
Page 1-28: Section 1.4.1. It is surprising to find the development of complex formulae to
calculate pulmonary function test responses to ozone, together with symptomatic responses in
Section 1.4-2, when the strength of the epidemiological data has been denied. An individual
does not go to a hospital emergency department, much less get admitted, complaining of a
2% loss of FEV, (Bates, 1992). This misplaced emphasis represents a serious lack of
balance.
A-5
-------
SULFUR OXIDES
The stated goal of restricting this section to the gaseous sulfur oxides has not been
explained or justified. It could be justified by a disclaimer that the particulate sulfur oxides
would be fully covered in Section 3 - Particulate Matter, if that were indeed the case. This
issue will be addressed further in our comments on Section 3. In any case, the stated goal is
not followed because an extensive, if inconclusive text on the historic PM-SO2 epidemiology
is included in this section.
Most importantly, this section does not come to grips with: (1) the role of SO2 as a
precursor of acidic aerosol formation; (2) the ways in which SO2 emission controls have
affected exposures to acidic sulfate aerosols; and (3) the health benefits of the reductions in
such exposures. Without such considerations, this section is woefully inadequate.
PARTICULATE MATTER
General Comments
There is little doubt that particulate matter (PM) causes health problems. The
questions are: Which particles? Which effects? And what is the dose-response relationship?
Recent reviews which address particulate matter should be cited, and the following points
should be noted:
a) In the past, PM dose-response studies have focused on total PM10 and health
effects (or even TSP), although a few had started to look at constituents of
PM10. EPA takes this approach, as well, in its draft document.
b) In the past year, considerable new evidence allowed investigation into the
relative significance of some constituents (e.g., SOX aerosols), and
c) This issue should be investigated by the Agency. There will still remain issues
of attribution, verification, and double counting; however, considering the
newer literature will provide a much clearer picture of the likely health effects.
The mortality effects are likely to dominate in terms of economic impact. It is
unfortunate that the draft is incomplete as it stands in several respects. First, it needs to
account (as does Table 3-13) for other acute-mortality studies that satisfy the selection
criteria. Second, it must address the nature and significance of acute mortality in terms of
the extent of life-shortening for those who die in excess on polluted days. Third, it should
consider evidence on differences in mortality risk across age groups, e g., under 65 years vs.
65 and older. Finally, the biggest deficiency is that it ignores the differences in annual
average (cross-sectional) mortality rates among communities (Dockery et. at., 1993, Pope et
a/., 1995).
A-6
-------
The secondary aerosols formed in the atmosphere from SO2 and NOX precursors can
often account for 25 to 40% of the ambient PM. While the NOX aerosol health effects
literature is meager and inconclusive, the SOX aerosol literature is not. Extensive evidence of
health effects associated with exposure to strong acid aerosol (H+) exists, and even more
literature relating exposures to health effects associated with exposures to SO4= exists.
Whether SO4= itself produces such effects is an open question, because ambient SO4= may
simply indicate the presence of H+. In any case, SO4= often shows closer associations to the
effects, than do simultaneous measurements of PM10 or PM2.5, and is often a major mass
fraction of PM2 5.
The Sox aerosol health-effects literature cannot be ignored in the benefits analysis.
Either it must be included in a revised Section 3, or alternatively in a revised Section 2.
. Although a consensus regarding the effects of PM on certain health endpoints,
including mortality, is rapidly evolving, a major issue still remains regarding the application
of the results to a retrospective benefits analysis. Specifically, how are we to estimate
historical PM10 concentrations in the U.S. given the fact that we only have TSP (Total
Suspended Particulates) values for most of the past 25 years? One approach is to bound the
PM10 values over time. A reasonable lower bound on historical PM10 is to assume that it has
remained constant at present-day values. An upper bound can be derived assuming that
present-day PM10 to TSP ratios, on a city-by-city basis, have remained constant over time.
This would allow a reconstruction of historical PM10 based on historical TSP. This latter
approach represents an upper limit on historical PM10 because it is certain that emissions of
larger particles (> 10 /xm) have been controlled more than emissions of smaller particles
(< 10 fim) over the past 25 years in the U.S.
An alternative approach would be to use historical measurements of sulfate to assess
fine particle concentration trends over time. Paniculate sulfate measurements do exist over
time, as well as site-specific comparisons with various fine-particle mass measurements.
This analysis presumably would fall within the bounds described above. The danger with
this approach is that it could be misconstrued as supportive of a hypothesis that sulfate
particles are the causative agent.
CARBON MONOXIDE
The CO document presents, in a clear manner, the current information pertaining to
the health risks of exposure. As it notes, the most consistent data relating low-level concen-
trations to health measures come from studies based on latency to anginal pain induced by
exercise. Linking these findings to mortality from heart disease or to accelerated myocardial
damage is a difficult speculative exercise but offers the most reasonable way to assess the
benefits of reduced exposure.
Behavioral effects, which played a large role in the earlier CO literature, have
diminished iri"importance with the inability of investigators to reliably reproduce such effects.
A-7
-------
Exercise performance in healthy subjects suggests diminished capacity at environmentally
relevant CO levels, but the data are rather sparse and the question has been pursued only at
high levels of activity in standardized situations. The document should point out the potential
importance of modifications in voluntary exercise.
Overall, this Section seemed on track and well done until it concluded (p. 4-14, #1
lines, 5, 6) that: "A concentration- response function based on the Allred et al. (1989) data
will not be developed and used in the current assessment." Why not? The results of this
multi-center controlled human exposure study are important, along with the results of other
related and consistent clinical lab studies, because they address cardiac ischemia, a significant
risk to health, and show that subjective responses are correlated with objective measures.
Specifically, the time to onset of angina is linked to changes apparent on electrocardiograms.
Much, weaker and less conclusive results were used for this purpose in other Sections. If the
lower-bound estimate includes zero, this can be stated. At a minimum, the Agency should
conduct a preliminary assessment to either establish order of magnitude values, or a worst
case bounding analysis .
NITROGEN OXIDES
General Comments
As noted in Section 2 on Sulfur Oxides, it is defensible to exclude aerosol forms of
NOX from this Section, if they are adequately discussed in Section 3 on Particulate Matter.
However, such an exclusion needs to be stated more explicitly. In the case of NOX, that still
leaves all of the vapor-phase nitrogen oxides to be discussed in this Section. Thus, this
Section is obligated to review the health effects associated with nitric acid, and possibly
nitrous acid (as well as those associated with NO2). It fails to do so and is, therefore,
deficient. The draft is also deficient in its treatment of NOX chemistry. It should be noted
that the only relevant equilibrium is between NO and NO2, not the other nitrogen oxides.
The conclusion that outdoor NO2 concentrations are "poor predictors of personal
exposures" ignores the recent work done in Los Angeles (Neas, et al., 1991). They co-
located NO2 passive monitors both indoors and outdoors and regressed these weekly values
against personal badge values. The outdoor values accounted for between 40 and 50 percent
of the personal exposure; the remainder was attributed to indoor values. These recent results
temper the conclusions of the chapter. Additionally, recent European work on N02 showing
detrimental effects on asthmatic children, should also be looked at by the Agency (Moseler et
al, 1994).
Detailed Comments
Page 5-2: Section 5.2-1: The recent work from HERL showing that preexposure to
NO2 in healthy women increases the effect of a subsequent exposure to O3, should be cited
A-8
-------
(Hazucha et. al, 1994,). It is important to note that NO2 pre-exposure exerts an effect not
only on the subsequent O3 effect on FEV1; but also in increasing the airway responsiveness.
The recent Swedish work should be noted (Strand et. al., 1994), even though it is still
only in Abstract Form. In studies of 18 asthmatics sensitive to birch or timothy grass,
-exposure to 0.5 ppm NO2 at rest for 30 minutes was shown to increase the late asthmatic
reaction when the subject was subsequently exposed to the allergen. The immediate reaction
was unchanged.
Page 5-9: Section 5.3:
The reasons for thinking that asthmatics may be a sensitive group have been described
above. In an 8-month panel study of asthmatics in Denmark, Moseholm and his colleagues
(Moseholm et. al., 1993) found that both SO2 and NO2 exposures were associated with
worsening of the asthmatic state. This paper might be quoted.
Page 5-11: Last paragraph:
Surely it would be useful to develop a risk estimate regardless of the sources and
nature of the exposure to NO2. It will never be possible to determine exactly, for each
individual in society, what made up the cumulative exposure. The quotation from the NO2
Criteria Document at the head of this page stresses the consistency of the observations, and
recent work provides a basis for estimating the exposures. Outdoor NO2 can only add to
indoor levels.
The Subcommittee agrees that some recent data showing an increased risk of asthma
exacerbation in Birmingham, England, associated with closer residence to a major highway
(Edwards et. al., 1994) do not allow identification of the nature of the hazard (which might
as well be PM10 as NO2), far less an estimate of exposure. Nor does the note that the
asthma associated with exposures to the dust from soybeans in Barcelona only occurred after
several days of NO2 being elevated (Castellsague et. al., 1992) permit a risk estimate. The
significant correlation that was reported between outdoor NO2 levels and hospital emergency
visits for acute respiratory disease in the elderly in Vancouver (Bates et al., 1990) can be
used in cost estimates, however, because the regression can be computed.
If none of these strategies is deemed solid enough to compute a damage associated
with outdoor NO2 levels, the document should end with some such statement as:
The contemporary data indicate that raised NO2 levels (both indoor and outdoor) are
associated with adverse health outcomes. Currently, the data are not solid enough to
permit a damage estimate - but it is clear that any damage estimates which ignore
completely the effects of NO2 are necessarily underestimates.
With the above caveats, this section provides a useful and generally well-balanced
review of a notoriously difficult pollutant.
A-9
-------
LEAD
General Comments
This is one of the better-written products provided by the Agency. The Subcommittee
notes that the Agency's draft document recognizes the broad spectrum of lead toxicity and
attempts to provide quantitative risk assessments for a variety of endpoints. This aim,
however, misses some of the subtleties of the lead literature. Specifically:
a) No explicit role is accorded to other measures of neurotoxicity: The document
focuses on IQ (Intelligence Quotient) as "the predominant measure of neurotoxicity." Other
indications of adverse central nervous system (CNS) actions are recognized indirectly, but no
explicit role is accorded them. For example, Section 6.1 emphasizes effects on hematopoie-
sis, but fails to mention the even more critical effects on neuro-chemistry. We do not expect
a comprehensive review of such data in a document of this kind, but they should be
acknowledged given that the primary developmental effects are expressed in behavioral
toxicity.
b) Cross-sectional and other studies fail to exploit the relevant dose-response behavioral
data: Section 6.2.2-2.2 (Cross- Sectional and Other Studies) mentions conduct disturbances
as one criterion of toxicity, but fails to cite some relevant data. For example, Needleman et.
al., (1979) demonstrated a clear dose-response relationship between tooth lead levels and
items on a teacher rating scale describing such disturbances. Yule et. al. (1981) observed a
similar relationship. Such data provide transparent connections between exposures and
adverse effects that supplements the IQ data. The data of Needleman et. al. (1990a,b; 1979)
which show a correlation between tooth lead values in the early primary grades and subse-
quent success in high school, are also important guides to the evaluation of risks and
benefits.
c) Inadequate attention is paid to the interaction of social class and the expression of lead
toxicity: Although mentioned (page 7), inadequate attention is paid to the interaction of
social class and the expression of lead toxicity. It is not solely the Cincinnati studies (Carson
et al., 1989; Rae, 1983) that demonstrate such a phenomenon. Winneke et al., (1982), in
Dusseldorf, reported similar results. Such interactions should be included in any attempts to
describe benefits.
d) Effects in adults are accorded a narrow point-of-view: Section 6.2.2.1 (Effects in
Adults) focused on evidence for a threshold. In other sections, a Lowest Observed Adverse
Effect Level (LOAEL), which is actually the criterion under discussion, was modified by
uncertainty factors. Why was lead treated differently?
A-10
-------
e) Observations of other effects of lead are important to understanding fully the risk
factors: Section 6.2.3 notes a relationship between higher prenatal blood lead levels and
reductions in gestational age and birth weight. Such observations are important not only for
estimating lead's contribution to infant mortality but for examining the contributions of lead
to reduced IQ scores. Lowered gestational age and birth weight are risk factors for a variety
of developmental disturbances.
f) Remobilization of stored lead has been ignored: The document notes the transfer of
lead from mother to fetus but does not fully describe the hazards of excessive bone stores in
the mother which may be recruited during pregnancy. Similarly, the release of bone stores
of lead during aging may provide another kind of risk.
g) Dose-response relationships: The dose-response relationships are the key to benefits
estimation, because this proyides the basis for quantification. The documents give inadequate
discussion to the doses and responses chosen and the appropriate caveats. The approximate
nature of the functional form, the perils of extrapolating very far from the median of the
data, and of the question of thresholds need to be discussed. Much more attention should be
given to discussing the quantification of the dose-response function and what legitimate uses
of the equations are.
h) Modeling adult lead uptake and changes in blood lead levels: There is no discussion
of how changes in mean blood lead levels in adults will be predicted as a function of changes
in lead emissions.
ECOLOGICAL EFFECTS
The following comments are based on our review of several reports from an outside
contractor (Industrial Economics, Inc.) that reviewed valuation methods and their applicabil-
ity to this Assessment. These reports were provided to the Subcommittee as background.
Their review was not part of the charge to Subcommittee.
General Comments
The objective of the documents delivered prior to the review meeting was to present
the elements of the methodology by which the EPA will provide a comprehensive analysis of
the potential benefits and liabilities from changes in air quality in the United States. The
research is designed to evaluate in an aggregate and comprehensive manner impacts due to
air quality on: (i) human health; (ii) natural and intensively-managed ecosystems (and at-risk
cohorts); (iii) visibility; and (iv) materials. The documents provided by the Agency excluded
items ii - iv. Comments are offered relative to items ii-iv in anticipation of how the Agency
plans to develop the methodology.
As it often appears to happen in other cost-benefit analyses, human health has
dominated this analysis thus far; and it does not appear that ecological effects will catch up
A-ll
-------
within the short time and limited budget that remain for this project. However, one of EPA's
missions is to protect ecosystems from adverse effects of pollutants. No other Federal
agency has this as a primary mandate (U.S. EPA/SAB, 1990b), whereas other agencies share
the mandate to protect human health. It seems likely that this Assessment will once again
highlight our lack of information to quantify ecological effects with adequate certainty.
This Subcommittee is concerned that natural resource valuation is likely to be simply
an addendum to the evaluation provided for human health. If so, it would inaccurately
reflect the mission of the Agency, the overwhelming data demonstrating a linkage between
human health and sustainability of natural resources, and the intrinsic value of natural
ecosystems (U.S. EPA/SAB, 1990b).
Although consideration of ;ssues of economic valuation is beyond the scope of the
Subcommittee charge from the Agency, the Subcommittee offers this additional commentary
for consideration. Ecological effects are difficult to comprehensively quantify and value in
economic terms. However, the absence of at least a qualitative analysis that is on equal
footing with a human health analysis will be conspicuous and will leave EPA open to sharp
criticism. Quantitative valuation clearly has difficulties associated with translating ecological
effects into monetary terms in the valuation process (U.S. EPA/SAB, 1990a). Congress and
the EPA Administrator should be reminded of this continuing deficiency. Although the value
assigned to a single human life and other morbidity effects might at first appear to be so high
as to overshadow any other possible cost-benefit categories, some people believe non-use
ecological values might be significant relative to the monetary value of human lives — if only
enough effort was expended to fully valuate ecosystem functions in monetary and non-
monetary terms. Until such efforts are supported, Congress will not be presented with a
truly comprehensive view of the benefits associated with implementing the CAA. Quantita-
tive ecological risk assessment (Suter, 1993) might provide an approach to deriving a
valuation methodology. We encourage the Agency not to ignore this quantitative methodol-
ogy.
The effort to address physical (including biological and ecological) effects can best
proceed if the exposure modeling is done in a way that complements, the effects research. In
the past, most of the exposure modeling has been done from the perspective of the atmo-
spheric sciences community, whereas most of the effects research is done from the perspec-
tive of the biologists. The isolation of the disciplines has resulted in analyses that often can
not be linked in the respective camps.
Finally, it was clear that the Congress anticipated that the research would be compre-
hensive, exhaustive and integrative. However, the picture that emerged in the documents and
discussions was one of isolated, fragmented activities without a cohesive framework. Given
the scope of the project, it is imperative that the fragmentation be replaced with an approach
that is far more integrated. Otherwise, inadequate results are predictable.
A-12
-------
Specific Comments
Specific comments on quantification and assessment of ecosystem impacts follow:
a) Wildlife: Wildlife were not mentioned in the background documents provided to the
Subcommittee, even though surface-water quality and fisheries were mentioned. If human
health is a concern regarding rural air pollution, it seems reasonable to believe that at least
some mammalian and perhaps non-mammalian wildlife species might also be adversely
affected by rural air pollution. Although little is known about wildlife toxicology, it is likely
that there are adverse effects of air pollution on wildlife. This assessment should acknowl-
edge the probability of some adverse effects; therefore, some positive expected benefits of
reduced air pollution, benefits of reduced air pollution will not be counted).
b) Pollutants: For aquatic ecosystems, acidification (an indirect effect of SOX and NOJ and
air toxics are much more important than CO, O3 and PM. The background document
appeared to implicitly recognize this. The roles of SOX and NOX should be made clear. And
the importance of airborne toxics (e.g., metals in addition to lead) to ecosystems should be
emphasized. Ecological risk assessment techniques that recently have been developed at Oak
Ridge National Laboratory appear to be the most appropriate methods for evaluating the
effects of air toxics that are transferred into aquatic ecosystems. Such techniques were not
mentioned in the documents available to the committee.
c) Ecological services: It is difficult to decipher how this issue is being handled, and we
encourage that the document be specific. Ecological systems provide "services" that need to
be addressed including nutrient cycling, water processing, air cleansing, recreation, wildlife
habitats, pollutant degradation, etc. These are benefits that society derives and values.
d) Food-web transport: Ecological systems process pollutants in the environment. In
many cases, the processing degrades chemicals to innocuous forms. In other cases, transport
and transformation of chemicals through terrestrial and aquatic food webs result in increasing
toxicity and in biomagnification. Notable cases are mercury (via methylation) and polycyclic
aromatic hydrocarbons (via food web contamination).
e) Geographical scale: The scale of the evaluation was not discussed, and the issue is not
trivial. Many of the pollutants have residence times that result in their distribution being
hemispherical and/or global (e.g., ozone, mercury, trace organics). If the scale of the
analysis is simply regional or continental, the assessment process will not capture the
significance of changes outside of the continental United States.
f) At-risk cohorts: It is widely recognized that there is a standard of error or margin of
safety used as a basis for air quality standards, particularly with respect to human health
(i.e., appropriate to protect sensitive members of the population). The same concept is also
A-13
-------
appropriate in some aspects of welfare effects but is handled in separate legislation (e.g.,
PSD legislation, Endangered Species Act). The emphasis was supposed to be on at-risk
cohorts in both human and non-human effects. Although at-risk cohorts were supposed to be
considered in evaluating human and non-human effects, the ecological-effects reports ignored
the concept of at-risk cohorts.
g) Aggregate effects across pollutants: Will the effort appropriately address interactions
among pollutants? The literature strongly suggests that a pollutant-by-pollutant analysis is
inaccurate and too simplistic. This also applies to human-health and welfare effects.
h) Concept of sustainability: Ecological sustainability involves "impacts on the environ-
ment that are irreversible or of long duration compared to human perspectives" (U.S.
EPA/SAB, 1990b, p. 35); furthermore, the sustainability of human activities is determined
by the resilience of the ecological systems on which economies depend (Arrow et al., 1995).
In the ecological literature, this concept has emerged as one means of developing a better
appreciation for the value of ecosystems. We encourage EPA to be cognizant of this
approach.
A-14
-------
APPENDIX B GLOSSARY OF TERMS AND ACRONYMS
ARDS
CAA
CAACAC
CAACACPERS
CASAC
CD
CNS
CO
COHb
COM
COI
COPD
CV
d
dl
EC
EFC
EPA
F
FEF
FEV
FEV,
FVC
g
HERL
H2SO4
IQ
JAMA
K&O
LA
LOAEL
m
m3
Micron (/urn)
MRADS
N/A
NAAQS
NAPAP
NESHAPS
Acute Respiratory Disease Syndrome
Clean Air Act
Clean Air Act Compliance Analysis Council (U.S. EPA/SAB)
Clean Air Act Compliance Analysis Council, Physical Effects Review
Subcommittee (U.S. EPA/SAB)
Clean Air Scientific Advisory Committee (U.S. EPA/SAB)
Criteria Document
Central Nervous System
Carbon Monoxide
Carbon Monoxide Bound to Hemoglobin
Coefficient of Haze
Cost of Illness
Chronic Obstructive Pulmonary Disease
Contingent Valuation
deci- (1/10 of a particular unit of measure)
deci-Uter (1/10 Liter)
Executive Committee (U.S. EPA/SAB)
Environmental Futures Committee (U.S. EPA/SAB/EC)
U.S. Environmental Protection Agency (U.S. EPA, or "The Agency")
Degrees Fahrenheit
Forced Expiratory Flowrate
Forced Expiratory Volume
Forced Expiratory Volume (in one second)
Forced Vital Capacity
gram
Health Effects Research Laboratory (U.S. EPA/ORD)
Sulfuric Acid
Intelligence Quotient
Journal of the American Medical Association
Kinney and Qzkaynak
Los Angeles (California)
Lowest Observed Adverse Effect Level
Moles, also meters
Cubic Meters
A unit of length equal to one thousandth of a millimeter, or about
0.000039 inch
Multiple Restricted Activity Days
Not Applicable
National Ambient Air Quality Standard
National Air Pollution Assessment Program
National Emission Standards for Hazardous Air Pollutants
B-l
-------
NY
NOX
03
OPA
OPAR
OPPE
ORD
ORNL
PERS
Pb
PM
PM10
PM15
ppb
ppm
PSD
RADs
RADM
RHA
SAB
S02
SO4
SOX
TSP
U.S.
M
vs
VSL
WHO-EURO
WTP
New York
Nitrogen Oxides
Ozone
Office of Policy Analysis (U.S. EPA)
Office of Policy Analysis and Review (U.S. EPA)
Office of Policy, Planning and Evaluation (U.S. EPA)
Office of Research and Development (U.S. EPA)
Oak Ridge National Laboratory (A U.S. Department of Energy Facil-
ity)
Physical Effects Review Subcommittee of the CAACAC (U.S.
SAB/CAACAC)
Lead
Paniculate Matter
Particulate Matter (<2.5 /*m in aerodynamic diameter)
Particulate Matter (< 10 /*m in aerodynamic diameter)
Particulate Matter (< 15 jwm in aerodynamic diameter)
Parts rjer Billion
Parts ger Million
Prevention of Significant Deterioration
Regional Acid Depositions
Regional Acid Deposition Model
Respiratory Hospital Admission
Science Advisory Board (U.S. EPA)
Sulfur Dioxide
Sulfate (as in H2S04)
Sulfur Oxides
Total Suspended Particulates
United States
micro (10~6) in combination with specific units
Versus
Value of Statistical Life
World Health Organization, European Region
Willingness to Pay
B-2
-------
DISTRIBUTION LIST
Deputy Administrator
Assistant Administrators
EPA Regional Administrators
EPA Laboratory Directors
Office of the Administrator:
Science Advisor to the Administrator
Office of Cooperative Environmental Management
Deputy Assistant Administrator for Air and Radiation:
Director, Office of Policy Analysis and Review (OPAR)
Director, Office of Air Quality Planning and Standards (OAQPS)
Deputy Assistant Administrator for Policy, Planning and Evaluation:
Director, Office of Policy Analysis (OPA)
Director, Office of Regulatory Management and Evaluation (ORME)
Director, Office of Strategic Planning and Environmental Data (OSPED)
Deputy Assistant Administrator of Research and Development:
EPA Headquarters Libraries
EPA Regional Libraries
EPA Laboratory Libraries
National Technical Information Service
Library of Congress
U.S. Environmental Protection Agency
Region 5, Library (PL- 12J)
77 West Jackson Boulevard, 12th Floor
Chicago, IL 60604-3590
------- |