+----------------------------+-----------------------------------------+
| > **Jim Witkowski          | +----+------------------------------+   |
| > \<Ji                     | | To | > Group A-AND-R-DOCKET@EPA   |   |
| m.Witkowski@ipaper.com\>** | +----+------------------------------+   |
| >                          | | cc |                              |   |
| > 10/09/2007 07:23 PM      | +----+------------------------------+   |
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|                            | | S  | > Ozone NAAQS Comments       |   |
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+----------------------------+-----------------------------------------+

Comments attached.

(See attached file: ETC Comments Ozone NAAQS.doc)(See attached file: ETC

Roster.doc)(See attached file: Ozone NAAQS Coalition

Comments.DOC)![](media/image1.png){width="1.8333333333333333in"
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height="0.4895833333333333in"}

October 9, 2007

Submitted via e-mail to: A-AND-R-DOCKET@epa.gov

U.S. Environmental Protection Agency

Mailcode: 6102T

1200 Pennsylvania Avenue, NW

Washington, DC 20460

[Attention]{.underline}: Docket ID No. EPA-HQ-OAR-2005-0172

[Subject]{.underline}: **National Ambient Air Quality Standards for
Ozone**

Proposed Rule, 72 Federal Register 37818, July 11, 2007

Dear Sir or Madam:

The following comments are provided on behalf of the South Carolina
Chamber of Commerce Environmental/Technical Committee ("Technical
Committee") regarding the proposed changes to the National Ambient Air
Quality Standards (NAAQS) for ozone. The South Carolina Chamber of
Commerce ("Chamber"), with over 2000 members, represents a very diverse
group of businesses with interests in South Carolina. The current roster
of Technical Committee members is attached to illustrate the extent of
businesses represented by this committee.

In summary, the Technical Committee feels that the current NAAQS should
be retained as both the primary and secondary standard. The scientific
evidence does not demonstrate that a reduction is needed to protect the
public health. While the science and benefits of changing the standard
are uncertain, the negative economic impacts of tightening the ozone
standard are certain and dramatic for South Carolina.

The Chamber supports an ozone standard that is protective of human
health and the environment. However, we are concerned that lowering the
existing NAAQS at this time is premature, and would cause many of
counties in South Carolina to become "nonattainment," resulting in
significant negative economic impacts, without a corresponding public
health benefit.

This rule making must acknowledge the tremendous progress that has been
made in reducing ambient ozone levels. According to EPA, between 1980
and 2006, the national average for ozone levels has decreased by over 20
percent. Another important consideration is that additional ozone
precursor emission reductions will be achieved by compliance with
existing regulations. These facts also support a position that EPA
should retain the existing NAAQS.

Detailed comments that were prepared by a coalition of impacted
stakeholder groups are attached. This document provides further
information on each of the points raised in this letter and has been
endorsed by the Technical Committee, and therefore should be considered
part of our comments.

Thank you for this opportunity to provide comments and actively
participate in this very important rule making process. The comments
provided, although supported by the Technical Committee membership, do
not preclude member companies from submitting additional comments
directly or through other associations with which they are affiliated.
If you have any questions, please feel free to call me (803) 425-4625.

Sincerely,

James P. Witkowski

Air Subcommittee Chair

SC Chamber of Commerce Environmental Technical Committee

cc: Jack Preston - SCANA

Ben Twilley - SC Chamber of Commerce

Roxie Williamson - SC Chamber of Commerce

Attachments

**Comments on EPA's Proposed Revisions to National Ambient Air Quality
Standards for Ozone**

**October 9, 2007**

**Submitted on behalf of:**

Alliance of Automobile Manufacturers

American Bakers Association

American Chemistry Council

American Coke & Coal Chemicals Institute

American Forest & Paper Association

American Iron and Steel Institute

American Petroleum Institute

American Trucking Associations

Chevron Corporation

Corn Refiners Association

Council of Industrial Boiler Owners

Edison Electric Institute

Engine Manufacturers Association

Exxon Mobil Oil Corporation

Independent Liquid Terminals Association

Institute of Shortening and Edible Oils

National Association of Manufacturers

National Cotton Council

National Mining Association

National Oilseed Processors Association

National Petrochemical & Refiners Ass'n

National Rural Electric Cooperative Ass'n

Portland Cement Association

U.S. Chamber of Commerce

**TABLE OF CONTENTS**

**Page**

**I. INTRODUCTION AND SUMMARY** 1

A. Introduction 1

B. Executive Summary 1

**II. BACKGROUND** 5

A. Requirements for NAAQS 5

B. Historical Context 6

C. EPA's Proposed Rule 7

D. Implications of EPA's Proposed Rule 8

E. Scope of Comments 9

**III. THE HUMAN CLINICAL AND EPIDEMIOLOGICAL**

**STUDIES DO NOT JUSTIFY LOWERING THE PRIMARY**

**STANDARD LEVEL** 10

A. Clinical Evidence on Healthy Subjects 11

B. Clinical Evidence on Asthmatic Subjects 13

C. Epidemiological Asthma Panel Studies 15

D. Epidemiological Studies on Hospital/Emergency Room

Admissions and Mortality 19

**IV. EPA'S EXPOSURE AND RISK ESTIMATES DO NOT**

**JUSTIFY LOWERING THE PRIMARY STANDARD LEVEL** 24

**V. CHANGING THE CURRENT ROUNDING PROCEDURE FOR**

**THE STANDARD IS NOT WARRANTED AT THIS TIME** 28

**VI. THERE REMAIN TOO MANY UNCERTAINTIES TO**

**JUSTIFY ADOPTING A SECONDARY STANDARD THAT**

**IS DIFFERENT FROM THE PRIMARY STANDARD** 29

**VII. CONCLUSION** 32

**VIII. REFERENCES** 33

**EXHIBIT A** Comments of E.R. McFadden, Jr., M.D., on Health
Significance of Asthmatics' Responses Reported in Clinical Studies of
Short-Term Ozone Exposure (excluding his curriculum vitae)

**EXHIBIT B** Excerpts from Statements of Other Physicians Specializing
in

Asthma on Significance of Reductions in FEV~1~ of up to 20 Percent

**I. INTRODUCTION AND SUMMARY**

A.  **Introduction**

On July 11, 2007, the United States Environmental Protection Agency
(EPA) proposed revisions (the Proposed Rule) to the National Ambient Air
Quality Standards (NAAQS) for ozone (O~3~), and established an October
9, 2007 deadline for submission of comments on the Proposed Rule (72
Fed. Reg. 37818 *et seq*.). These comments on the Proposed Rule are
submitted jointly by the trade associations and companies listed on the
cover (the Commenters), which collectively represent a large portion of
the U.S. economy. Several of these associations and companies have
submitted or are submitting separate comments on the Proposed Rule.
However, they have all come together to voice their strong support for
retaining the current NAAQS for ozone and their opposition to adopting
any of the more stringent alternatives proposed by EPA. These comments
focus principally on the primary (health-based) standard, but also
discuss briefly the secondary (welfare-based) standard.

**B. Executive Summary**

Under the Clean Air Act (CAA or Act), primary NAAQS must be set at a
level requisite to protect the public health with an adequate margin of
safety. In 1997, EPA revised the primary NAAQS for ozone from a one-hour
average standard of 0.12 parts per million (ppm) (with one allowable
exceedance per year) to the current 8-hour standard of 0.08 ppm (based
on the annual 4^th^ highest daily maximum 8-hour average concentration
over a three-year period). In the Proposed Rule, EPA proposes to reduce
the level of the 8-hour standard to a level within the range of 0.070 to
0.075 ppm, and to specify that level to three decimal places. EPA also
solicits comment on alternative levels down to 0.060 ppm and up to and
including the current standard level of 0.08 ppm.

EPA relies on five principal lines of evidence to support its proposal
to reduce the level of the standard. As shown in these comments, on each
of those lines of evidence, EPA has consistently overinterpreted the
data in an effort to show the need for a reduction in the standard, when
in fact none of those lines of evidence supports such a reduction. As a
result, the Commenters believe, EPA's conclusions cannot be considered
scientifically valid. The reasons are summarized as follows:

1.  EPA asserts that the controlled human clinical studies provide
    "strong" evidence of "medically significant" effects in healthy
    people exposed to ozone levels at and above 0.080 ppm, with some
    indication of effects at lower levels. In fact, the human clinical
    studies on healthy subjects have not shown medically significant
    effects at levels at and below the current standard level of 0.08
    ppm. Both the lung function changes and respiratory symptoms
    reported in these studies at such levels, both on an average basis
    and in individual subsets of subjects, consist of transient,
    reversible responses that are not of adverse health consequence.

2.  EPA claims that the clinical evidence indicates that asthmatics are
    likely to experience larger and more serious effects than healthy
    people. However, EPA's claims are based on assumptions about
    asthmatics' response profile that have not been established and, in
    any event, do not address the key question of whether the asserted
    effects would occur at levels at and below the current standard. The
    actual clinical studies on asthmatics exposed to ozone (which are
    limited to exposures of around 0.12 ppm and above and most of which
    were available during EPA's 1997 review) show that, at around 0.12
    ppm, asthmatics' responses to ozone exposure, in terms of both lung
    function decrements and respiratory symptoms, are small, transitory,
    and comparable to the types of responses that asthmatics commonly
    experience. As explained by numerous physicians who specialize in
    treating and studying patients with asthma, these types of responses
    are not deleterious to the asthmatics' health. Responses at lower
    ozone levels would be expected to be even less. Overall, EPA has not
    presented any significant new clinical information on asthmatics
    that would warrant a reduction in the standard level.

3.  EPA asserts that epidemiological asthma panel studies show "robust"
    associations between 8-hour ozone concentrations and lung functions
    effects, respiratory symptoms, and medication usage in asthmatic
    children, even at ozone levels below the current standard. The
    studies themselves, however, do not support EPA's assertion,
    because:

    -   Most were conducted in areas with ozone levels higher than the
        current standard;

    -   These studies involve considerable uncertainties as to whether
        the measured ozone concentrations adequately represent personal
        exposures;

    -   At least some of these studies used pulmonary function
        measurements considered to be unreliable;

    -   These studies do not show consistent associations between ozone
        and effects and cannot attribute the effects observed to ozone
        (as opposed to other pollutants or factors); and

    -   These studies are inconsistent with other recent studies which
        have found no associations between ozone concentrations and
        asthma symptoms.

4.  EPA argues that other time-series epidemiological studies show
    associations between short-term ozone concentrations and other
    health effects, including respiratory emergency room visits and
    hospital admissions and (in multi-city studies) premature
    non-accidental mortality, even at ozone levels below the current
    standard. These studies do not support EPA's claims for many of the
    same reasons noted above -- i.e.:

    -   Most were conducted in areas or included a large number of
        cities that would not have met the current standard;

    -   It cannot be assumed that the ambient ozone concentrations
        measured in these studies adequately reflect people's exposures;

    -   EPA has failed to adequately consider model selection;

    -   The studies have inconsistent results and cannot implicate ozone
        (as opposed to other pollutants or factors) as the cause of the
        reported effects; and

    -   The studies on associations between mortality and short-term
        ozone exposure contain implausible findings and are inconsistent
        with the studies of long-term ozone exposure, which EPA concedes
        have shown no consistent relationship between such exposure and
        mortality.

5.  EPA relies on its exposure and risk assessments as indicating
    significant risks if the current standard were just met and thus
    supporting the need to lower the standard. However, EPA has failed
    to take into account the significant uncertainties in these
    assessments. These include:

    -   Uncertainties in the exposure estimates;

    -   Reliance on health effects endpoints which have not been shown
        to be adverse to health or to be causally associated with ozone
        exposures;

    -   Uncertainties regarding the concentration-response relationship
        and regarding a causal link between ozone exposures and effects,
        particularly at levels below 0.08 ppm;

    -   Underestimates of "policy-relevant background"; and

    -   Uncertainties about whether standards below the current level
        would be attainable, such that the asserted health benefits
        could be realized.

> Given these factors, EPA's exposure and risk estimates are too
> speculative to support lowering the primary standard level.

In addition to the lack of adequate support for lowering the level of
the primary standard, EPA has not presented a sufficient justification
for changing the specification of the standard from two to three decimal
places at this time, given that: (a) EPA's air monitoring reference
methods specify a precision of two decimal places for ozone; (b) there
is still uncertainty about the precision of the third decimal place,
particularly in field measurements; and (c) specifying the standard to
the third decimal place implies a degree of precision in the underlying
health effects data that does not exist, due to the uncertainties in
those data.

Secondary NAAQS must specify a level of air quality requisite to protect
the public welfare from any known or anticipated adverse effects. The
current secondary standard was set to be identical to the primary
standard. In the Proposed Rule, EPA concludes that that standard is
inadequate to protect the public welfare from known and anticipated
adverse effects on vegetation; and it proposes to replace that standard
with one of two options: either (a) a cumulative seasonal standard (with
a complex form); or (b) a standard identical to the proposed revised
primary standard. As summarized in these comments, EPA's proposal has
failed to take account of the numerous uncertainties that remain about
the degree to which and levels at which ozone produces adverse effects
on the public welfare and about the extent to which the proposed revised
secondary standard (under either option) would protect the public
welfare from such effects. These uncertainties need to be addressed
before adopting a new and more stringent standard that would produce
substantial and widespread adverse impacts on businesses and
communities, which are also part of the public welfare.

For these reasons, the scientific evidence does not demonstrate that a
reduction in the standard is needed to protect the public health and
welfare. Rather, the Commenters believe that the current standard meets
the statutory requirements and should be retained as both the primary
and the secondary standard.

**II. BACKGROUND**

A.  **Requirements for NAAQS**

Under the CAA, EPA must review NAAQS at least every five years and
revise them "as may be appropriate" in accordance with Sections 108 and
109(b) of the Act (CAA § 109(d)(1)). Primary NAAQS must be set at a
level "requisite to protect the public health" with "an adequate margin
of safety" (CAA § 109(b)(1)). Secondary NAAQS must specify a level of
air quality "requisite to protect the public welfare from any known or
anticipated adverse effects" (CAA § 109(b)(2)). As stated by the Supreme
Court in *Whitman v. American Trucking Ass'ns*, 531 U.S. 457, 476
(2001), "requisite to protect" means "not lower or higher than is
necessary." The comments below demonstrate that the existing standards
are "requisite to protect" the public health and welfare, and that EPA's
proposed revisions are not necessary to meet that objective and
therefore are not justified.

B.  **Historical Context**

In 1997, EPA revised the primary NAAQS for ozone from a one-hour average
standard of 0.12 ppm (with one allowable exceedance per year) to the
current 8-hour standard of 0.08 ppm, based on the annual 4^th^ highest
daily maximum 8-hour average concentration over a three-year period (62
Fed. Reg. 38856, July 18, 1997). In doing so, the Administrator
concluded that "\[t\]he 8-hour averaging time is more directly
associated with health effects of concern at lower O~3~ concentrations
than is the 1-hour averaging time," and that "an 8-hour standard would
limit both 1- and 8-hour exposures" (*id*. at 38861). With regard to the
level of the standard, the Administrator first acknowledged that, as
increasingly stringent standards were evaluated, including an 8-hour
standard of 0.07 ppm, the estimated risks decreased for respiratory
functional and symptomatic effects and for hospital admissions for
respiratory causes (*id*. at 38864). Additionally, the Administrator
acknowledged that there might be no ozone level "below which absolutely
no effects are likely to occur" (*id*. at 38863). Notwithstanding these
observations, the Administrator determined that a standard more
stringent than 0.08 ppm was "not requisite to protect the public health
with an adequate margin of safety" (*id*. at 38868). The Administrator
therefore promulgated a primary 8-hour standard of 0.08 ppm.

With respect to the secondary standard, EPA recognized in 1997 that it
had considerable evidence on the effects of ozone on vegetation. It also
acknowledged that "the available scientific information supports the
conclusion that a cumulative seasonal exposure index . . . is more
biologically relevant than a single event or mean index" (*id*. at
38875). Nevertheless, the Administrator chose to set the secondary
standard equal to the new 8-hour primary standard (*id*. at 38877).
Specifically, the Administrator decided not to set a seasonal secondary
standard due to the "substantial uncertainties" in the estimates of the
increased welfare protection that a seasonal standard would provide
(*id*. at 38877-78). The Administrator concluded that adoption of the
8-hour primary standard as the secondary standard would result in
"significant improvements in public welfare" (id. at 38877).

The primary and secondary standards promulgated in 1997, which were
identical, were not challenged in court as less stringent than
necessary. Rather, they were challenged as overly stringent, but were
ultimately upheld against those challenges. See *American Trucking
Ass'ns v. EPA*, 283 F.3d 355, 378-80 (D.C. Cir. 2002), *upon remand
from* 531 U.S. 457, 476 (2001).

C.  **EPA's Proposed Rule**

In the Proposed Rule, EPA proposes a number of revisions to both the
primary and secondary standards for ozone. For the primary standard, EPA
proposes to retain: (a) use of O~3~ as the most appropriate surrogate
for ambient photochemical oxidants; (b) the 8-hour averaging time to
provide protection against both short-term and prolonged exposures; and
(c) the current form of the standard, which is the 4^th^ highest daily
maximum 8-hour average. However, EPA proposes to reduce the level of the
8-hour standard to a level within the range of 0.070 to 0.075 ppm, and
to specify that level to the nearest thousandth of a ppm. At the same
time, EPA solicits comment on alternative levels down to 0.060 ppm and
up to and including the current level of 0.08 ppm (which is effectively
0.084 ppm due to rounding) (72 Fed. Reg. at 37818).

EPA summarizes in several places the basis for its proposal to lower the
primary standard level (e.g., 72 Fed Reg. at 37870, 37878-79, 37880). As
summarized by EPA, that proposal is based on the following principal
lines of evidence:

1.  Clinical evidence in healthy people exposed to ozone levels at and
    above 0.080 ppm of lung function decrements, respiratory symptoms,
    pulmonary inflammation, and other airway responses (deemed
    "medically significant" by EPA), with some indication of lung
    function decrements and respiratory symptoms at lower levels;

2.  Clinical evidence that EPA believes shows that asthmatics are likely
    to experience larger and more serious effects than healthy people;

3.  Epidemiological evidence of lung function decrements, respiratory
    symptoms, and increased medication usage in asthmatics associated
    with ozone exposures;

4.  Epidemiological evidence of ozone associations for a variety of
    serious health effects, including respiratory emergency room and
    hospital admissions and premature mortality; and

5.  EPA's estimates of exposures and risks associated with just meeting
    the current standard.

With respect to the secondary standard, EPA concludes that the current
standard (which is identical to the primary standard) is "inadequate to
protect the public welfare from known and anticipated adverse
O~3~-related effects on vegetation and the ecosystem," notably, visible
foliar injury, seedling and mature tree biomass loss, and crop
reductions (72 Fed. Reg. at 37899). Further, EPA concludes that a
complex cumulative seasonal form of the standard is more "biologically
relevant" than the current 8-hour standard, although the current 8-hour
form "can also provide substantially improved protection to vegetation
when set at an appropriate level" (*id*. at 37899; see also *id*. at
37905). EPA thus proposes to replace the current standard with one of
two options: either (a) a cumulative seasonal standard; or (b) a
standard identical to the proposed revised primary standard (*id*. at
37818, 37899, 37905).

D.  **Implications of EPA's Proposed Rule**

Under Section 109 of the CAA, EPA does not have authority to base NAAQS
on the economic costs of compliance. However, as recognized by Justice
Breyer in *Whitman v. American Trucking Ass'ns*, 531 U.S. at 494-95,
Section 109 "does not require the EPA to eliminate every health risk,
however slight, at any economic cost, however great"; and it gives the
Administrator the flexibility to consider various contextual factors,
including the severity of a pollutant's effects, the number of those
affected, the distribution of the effects, the uncertainties in the
estimates, and comparative health and welfare consequences, in
establishing the "requisite" primary and secondary standards. These
comments demonstrate that, based on the current scientific evidence, the
proposed changes to the primary and secondary NAAQS for ozone are not
necessary or justified to meet the statutory standard of being requisite
to protect the public health and welfare.

Before doing so, however, we note briefly, for context, that a reduction
in the level of the primary and secondary NAAQS would have substantial
adverse impacts on the regulated community and on States and local
communities. Currently, States are still in the process of executing
implementation plans to meet the current standard (established in 1997,
but delayed due to litigation). These implementation plans include new
restrictions and controls that are expected to significantly reduce
ground-level ozone emissions, as EPA recognizes (EPA, 2007b). Adopting a
more stringent standard before the current standard has been fully
implemented would put a substantial new burden on the States to adopt
new implementation plans before the health and environmental benefits of
the current standard can be evaluated.

Moreover, the reduction of the primary standard to the level proposed by
EPA, 0.070 to 0.075 ppm, would put a large number of additional areas in
the United States into non-attainment, while the adoption of a standard
at the lower alternative level identified by EPA, 0.060 ppm, would
likely result in the majority of the country being so designated when
background ozone levels are taken into consideration (see discussion at
end of Section IV below). Non-attainment designations have significant
adverse consequences for areas so designated. For example, businesses
may be unable to locate new operations or expand existing operations in
non-attainment areas due to the increased costs, delays, and
uncertainties associated with the restrictive permitting regimes
required in such areas. Similarly, businesses and consumers within
non-attainment areas may be subjected to increased costs as a result of
special requirements for vehicles and fuels sold in those areas.

These substantial and widespread adverse impacts can and should be
avoided because the scientific evidence does not demonstrate the need
for the proposed revisions of the standard as being "requisite to
protect" the public health and welfare, as discussed in these comments.

E.  **Scope of Comments**

The Commenters support EPA's proposal to retain the current indicator
(O~3~) and averaging time (8 hours) of the primary standard. These items
are not discussed further in these comments.

The Commenters strongly oppose any reduction in the level of the primary
standard and support the alternative of retaining the current standard
level. In support of this position, Section III demonstrates that the
clinical and epidemiological evidence upon which EPA relies does not
justify its proposed reduction of the standard level. Section IV shows
that EPA's exposure and risk assessments likewise do not justify such a
reduction. Section V presents the Commenters' position that changing the
current expression of the standard to add a third decimal place is not
warranted at this time.

With respect to the secondary standard, Section VI briefly describes the
Commenters' position that, due to the substantial remaining
uncertainties regarding the occurrence of adverse effects on public
welfare at levels below the current standard, as well as the extent to
which a revised standard would provide protection from such adverse
effects, the current scientific information is insufficient to justify a
change in the secondary standard.

> **III. THE HUMAN CLINICAL AND EPIDEMIOLOGICAL STUDIES DO NOT JUSTIFY
> LOWERING THE PRIMARY STANDARD LEVEL.**

As noted above, EPA asserts that the body of human clinical and
epidemiological studies demonstrates that the existing primary standard
of 0.08 ppm is not adequate to protect the public health. Specifically,
EPA asserts that: (1) there is "strong" clinical evidence of "medically
significant" effects in healthy people at exposure levels of 0.080 ppm
and above, with "some indication" of effects at lower levels; (2) there
is "substantial" clinical evidence that asthmatics "are likely to
experience larger and more serious effects than healthy people"; (3)
there is likewise "substantial" epidemiological evidence of such effects
in asthmatics due to ozone (including at levels below the current
standard); and (4) epidemiological studies also show significant
associations of ozone exposure with "a wide range of serious health
effects, including respiratory emergency room visits and hospital
admissions, and premature mortality, at and below 0.080 ppm" (72 Fed.
Reg. at 37879). In reaching these conclusions, as shown below, EPA has
substantially overinterpreted the findings and implications of the
existing human clinical and epidemiological studies. While in some
places EPA recognizes certain uncertainties and limitations associated
with the data, in the end it plays down those uncertainties and
limitations, ignores others, and consistently interprets or
characterizes the data beyond what the data can actually support, in an
effort to show that the current standard is not protective. As a result,
the Commenters believe, EPA's conclusions are not scientifically valid
(see *Daubert v. Merrell Dow Pharmaceuticals, Inc.*, 509 U.S. 579
(1993)).

We recognize that the Clean Air Scientific Advisory Committee (CASAC)
likewise concluded that the existing primary standard is not protective,
and recommended an even more drastic reduction in the standard level (to
a range of 0.060 to 0.070 ppm), relying on the same basic lines of
evidence on which EPA relies (CASAC, 2006b, 2007). However, as also
discussed below, a careful review of the evidence indicates that CASAC
similarly overinterpreted the data and reached conclusions that cannot
be supported by an appropriate evaluation of the evidence.

A.  **Clinical Evidence on Healthy Subjects**

EPA states that several studies (e.g., Folinsbee et al., 1988, 1994;
Horstman et al., 1990; Adams, 2002, 2003, 2006) have reported
statistically significant lung function responses and increased
respiratory symptoms in healthy subjects from prolonged exposures (4-8
hours) to ozone levels in the range of 0.08 to 0.16 ppm (72 Fed. Reg. at
37828-29). With the exception of the Adams studies, these studies were
available at the time of the last standard review in 1997 and thus
provide no new information. EPA relies in particular on the recent
studies by Adams (2002, 2006), since they are the only available human
clinical studies that investigated such effects at levels below the
current standard. These studies investigated effects of ozone on healthy
subjects at levels of 0.08, 0.06, and 0.04 ppm, using both square-wave
(steady-state) and triangular (increasing to a peak and then decreasing)
exposures during a period of 6.6 hours involving considerable exercise.
EPA observes that, in these studies, the author reported no
statistically significant group effects on forced expiratory volume in
one second (FEV~1~) or total symptom score from exposure to any levels
lower than the current standard. However, it notes that a reanalysis by
EPA of the Adams (2006) data did show statistically significant group
FEV~1~ responses at the 0.06 ppm ozone exposure level, that the studies
showed statistically significant lung function decrements in a small
percentage of the individual subjects, and that the author's analysis
also showed some statistically significant respiratory symptom responses
toward the end of the exposure period (72 Fed. Reg. at 37828, 37864,
37875).

Regardless of the statistical significance of the reported responses,
the effects shown in these clinical studies at levels of 0.08 ppm and
below are not medically significant. Both the functional responses and
symptoms reported in these studies were small, transient, and
reversible. For example, the mean functional changes reported by Adams
(2002, 2006) from pre- to post-exposure included FEV~1~ decrements of
around 4-6% at 0.08 ppm and 1-2% at 0.06 ppm (with no reduction at 0.04
ppm). EPA itself recognizes that such functional changes would not
interfere with normal activities and would not constitute adverse health
effects (72 Fed. Reg. at 37850). Similarly, the total mean symptoms
scores reported by Adams (2002, 2006) were 8-10 at 0.08 ppm, and 2-4 at
0.06 and 0.04 ppm out of a possible score of 160. As noted in the
comments of Dr. McFadden (2007) (copy attached as Exhibit A, excluding
his curriculum vitae), these scores indicate that the symptoms were
small and not medically significant.

EPA puts greater reliance on the reported effects in a few individual
subjects. It notes that, based on data from the earlier studies (e.g.,
Folinsbee et al., 1988; Horstman et al., 1990), as interpreted by
McDonnell et al. (1991), about 26%, 18%, and 8% of the subjects had
FEV~1~ decrements \> 10%, 15%, and 20%, respectively, with exposures to
0.08 ppm ozone (72 Fed. Reg. at 37828; EPA, 2007, p. 5-22). EPA observes
further that, in the Adams (2002, 2006) studies, with exposure to 0.08
ppm, 17% of the subjects experienced FEV~1~ decrements \> 10% when the
results were not corrected for the effect of exercise in clean air and
23% experienced such effects after such correction, and that in the
Adams (2006) study, with exposure to 0.06 ppm, 7% of the subjects
experienced such effects after correction for the effect of exercise in
clean air (72 Fed. Reg. at 37828). CASAC likewise relied on such
findings, noting that "26% of the subjects had greater than 10%
decrements \[in FEV~1~\], which can be clinically significant" (CASAC,
2006b, p. 4).

However, these reported responses in a few individual subjects do not
support a reduction in the standard level. To begin with, based on
current data, it is unknown whether these individuals are representative
of any identifiable segment of the population. Indeed, as stated by one
CASAC member (Sverre Vedal), placing great reliance on the occurrence of
effects in such a small number of subjects is "a dangerous precedent --
especially in this case where we are looking at small effects in 3 of 30
vs. 1 of 30, a pitiful number on which to attempt to base policy"
(Vedal, 2007). Moreover, even the individual effects that have been
reported at 0.08 ppm and below are transient responses that have not
been shown to be adverse to health. Contrary to the opinion expressed in
the CASAC (2006b) letter, the occurrence of FEV~1~ decrements in the
range identified by EPA and CASAC (\~ 10-20%) in healthy subjects is not
of medical concern. As discussed in the next section, numerous
physicians have expressed the opinion that reversible FEV~1~ decrements
up to approximately 20% (or more in some cases) are not adverse health
effects even in asthmatics. It follows that such changes in healthy
individuals are of no consequence to their health. Additionally, the
studies do not provide evidence of serious respiratory symptoms in any
specific subset of the subjects.

EPA concludes that evidence of lung function decrements and respiratory
symptoms in some healthy individuals at the 0.06 ppm exposure level is
"too limited to support a primary focus at this level" (72 Fed. Reg. at
37878). In fact, an appropriate interpretation of the data is that the
evidence on such responses in healthy individuals does not support
***any*** reduction in the level of the current standard.

B.  **Clinical Evidence on Asthmatic Subjects**

EPA also claims that the evidence from human clinical studies indicates
that individuals with asthma are likely to experience larger and more
serious effects than healthy people (72 Fed. Reg. at 37826, 37864,
37878). In this regard, EPA presents a fairly lengthy discussion of the
response profile of asthmatics in an effort to demonstrate why this is
so (*id*. at 37846-47). CASAC likewise stated that asthmatics "have been
found to be more sensitive and to experience larger decrements in lung
function in response to ozone exposures than would healthy volunteers"
(citing the Mortimer et al. (2002) epidemiological study discussed in
the next section); and it speculated that if asthmatics had been
included in the clinical studies of Adams, the percentage with lung
function declines \> 10% "would most likely be considerably greater"
(CASAC, 2006b, pp. 4, 10).

These arguments do not take into account the actual clinical studies on
asthmatics exposed to ozone, most of which were included in the 1997
Criteria Document and Staff Paper. Those studies included exposures to
ozone at levels of around 0.12 ppm and higher for various time periods
(ranging from 1-2 hours to over 7 hours), generally combined with
exercise (e.g., Linn et al., 1994; Weymer et al., 1994; Horstman et al.,
1995; Kreit et al., 1989; McBride et al., 1994; Koenig et al., 1985,
1987, 1988). There do not appear to be any clinical studies of
asthmatics exposed to ozone at 0.08 ppm and below. However, even at
exposure levels of around 0.12 ppm, the functional changes and
symptomatic effects observed in these studies are small and not of
health significance, as discussed below.

The functional changes seen in these studies at ozone levels of around
0.12 ppm consisted of mean FEV~1~ decrements well below 10% (and not
statistically significant in most cases). EPA agrees that, even for
asthmatics, such changes are not adverse (72 Fed. Reg. at 37850). As EPA
notes (*id*. at 37846), Horstman et al. (1995) did report that, with
exposure to 0.16 ppm ozone, the asthmatic subjects had a mean reduction
in FEV~1~ of 19%, compared to 10% in the healthy subjects. EPA asserts
that FEV~1~ decrements of 10-20% would constitute adverse health effects
in asthmatics (72 Fed. Reg. at 37850); and CASAC (2006b, p. 12) asserted
that "in asthmatic children, a 10% change \[in FEV~1~\] is indicative of
adverse effects."

The findings of Horstman et al. (1995) at 0.16 ppm were available to EPA
in its last review in 1997 and do not support lowering the current
standard level below 0.08 ppm. Moreover, EPA's (and CASAC's) conclusion
that FEV~1~ reductions of 10-20% in asthmatics are adverse health
effects is not well supported. Numerous physicians who specialize in
studying and treating asthma patients have made clear that reductions in
FEV~1~ of up to 20% are not deleterious to the health of asthmatics. For
example, as explained in the comments of Dr. McFadden (2007) (Exhibit A
hereto), such transient decreases in FEV~1~ of 10-20% commonly occur in
asthmatics (especially overnight), are comparable to the kinds of
bronchoconstrictive responses routinely induced in pulmonary function
tests to diagnose asthma, and are not significant or meaningful to
asthmatics. Many statements by other asthma physicians making similar
points regarding FEV~1~ changes of this magnitude were initially
submitted to EPA in 1995 by the National Mining Association in
connection with comments on the NAAQS for sulfur oxides (NMA, 1995,
Appendix A), and copies were re-submitted as exhibits to the September
18, 2006 comments of a group of trade associations that included most of
the present Commenters on EPA's second draft of the Staff Paper on the
NAAQS for ozone (Alliance of Automobile Manufacturers et al., 2006).
Excerpts from those comments are provided in Exhibit B to the present
comments.

Similarly, the types of symptoms reported in the clinical studies of
asthmatics exposed to ozone levels at around 0.12 ppm, while possibly
greater than those observed in non-asthmatics, were small and do not
indicate a health risk. For example, as discussed by McFadden (2007),
the total symptoms scores reported by Linn et al. (1994) (at 0.12 ppm
ozone) and by Weymer et al. (1994) (at 0.10 and 0.25 ppm ozone) are not
indicative of significant symptoms.

Thus, the clinical studies on asthmatics exposed to ozone levels around
0.12 ppm, most of which were available at the time of the last review,
do not indicate that such exposures produce effects of health concern to
asthmatics. One would expect that the responses of asthmatics at levels
of 0.08 ppm and below would be even less than those reported in these
studies. Such responses are transitory and comparable to the types of
responses that asthmatics commonly experience, and tolerate well, in
response to many non-specific stimuli, such as exercise, cold air,
stress, vigorous laughter, and exposure to common irritants.

EPA's statements in its preamble that are based on mechanistic reasons
relating to asthmatics' response profile are speculative and do not take
into account the actual studies on asthmatics' exposures to ozone. In
his comments, Dr. McFadden (2007) explains that those statements
represent assumptions about the pathogenesis of asthma, but are not
supported by data demonstrating that the types of inflammatory responses
discussed lead to clinical manifestations in terms of exacerbations of
asthma or other adverse health effects. Further, he points out that,
even if they did, the data do not address the question of the level at
which ozone may have such effects and, in particular, whether ozone
would have such effects at levels at and below the current standard. In
fact, the clinical studies discussed above do not indicate that ozone
exposures at such levels would have adverse health effects. Thus, EPA's
statements do not provide a sound quantitative basis for reducing the
standard level.

C.  **Epidemiological Asthma Panel Studies**

EPA asserts that its conclusions about the greater effects of ozone
exposure on asthmatics are further supported by the epidemiological
studies showing that 8-hour average ambient ozone concentrations are
associated, at certain lag times, with measures of lung function, daily
symptoms, and increased medication usage in asthmatic children (72 Fed.
Reg. at 37828-29, 37847, 37865, 37878). These studies consist of asthma
panel studies -- notably, the large U.S. multi-city panel studies by
Mortimer et al. (2002) (the National Cooperative Inner-City Asthma Study
\[NCICAS\]) and by Gent et al. (2003), as well as a number of smaller,
single-city studies. EPA recognizes that these studies do not provide
"direct evidence of a causal link between exposure to ozone and the
occurrence of the effects" (72 Fed. Reg. at 37879). However, it claims
that the studies show "robust" associations between ozone concentrations
and lung function effects, symptoms, and medication usage in asthmatic
children (*id*. at 37829, 37865) and provide "strong evidence" of such
effects (*id*. at 37847), thus supporting its proposal to lower the
standard. (As noted above, CASAC (2006b) also relied on these studies,
notably that of Mortimer et al. (2002).) In fact, a review of these
studies reveals that they do not show such "robust" associations or
"strong" evidence and thus do not support a lowering of the standard.
The reasons are discussed below.

First, as EPA recognizes (72 Fed. Reg.. at 37865), most of these studies
were conducted in areas that would not have met the current ozone
standard. Consequently, the results of such studies cannot be reliably
used to support a reduction in the level of the current standard. EPA
notes that Mortimer et al. (2002) reported statistically significant
associations between 8-hour average ambient ozone concentrations and
lung function decrements even on days when ozone levels above the
current standard were excluded (72 Fed. Reg. at 37865, 37876). That
study, however, is subject to the other serious limitations discussed
below.

Second, there are serious questions about whether the ambient ozone
measurements used in the studies adequately characterize individuals'
ozone exposure. On this subject, EPA provides a discussion that attempts
to discount this problem and, in fact, argues that because ambient
concentrations generally overestimate true personal exposures, the
effects occur at lower levels than indicated by the ambient measurements
(*id*. at 37838-39). EPA fails to recognize, however, that the
assumption that ambient measurements can be used to represent personal
exposures has not been sufficiently validated or demonstrated, and that
the uncertainty regarding this assumption creates uncertainty about
whether the associations reported in the studies in fact show any effect
of ozone at all, particularly since these studies involved other
pollutants as well. EPA does not take into account a number of studies
that have found that ambient concentrations of gaseous pollutants (such
as ozone) do not correlate well with personal exposures to those
pollutants (e.g., Koutrakis et al., 2005; Sarnat et al., 2006; Linaker
et al., 2000; Liu et al., 1997). CASAC recognized these problems in the
context of estimating ozone exposure in time-series studies (CASAC,
2006a, p. 3; 2006b, p. 10), as discussed in Section III.D. The same
problems create uncertainty in the asthma panel studies.

Third, the pulmonary function measure used in many of the panel studies
that EPA relies on, including the study by Mortimer et al. (2002), used
self-reported peak expiratory flow rate (PEFR). Self-reported PEFR
measurements are known to demonstrate high variability and are generally
considered unreliable. The problems include low compliance rates, low
reproducibility of the results, and missing and self-invented data
(Kamps et al., 2001). These concerns were noted by EPA in its draft
Integrated Science Assessment (ISA) for nitrogen oxides. In that
document, EPA stated that "\[r\]eliable data are notoriously difficult
to come by using portable peak flow measuring devices" (EPA, 2007c, p.
3-16) . For this reason, EPA dismissed the results from all nine studies
that failed to demonstrate an association between ambient NO~2~ and
reduced PEFR. Among those nine studies is the study by Mortimer et al.
(2002). In any case, the very small changes in PEFR reported by Mortimer
et al. (2002) (\<2%) are not of clinical significance.

Fourth, the asthma panel studies, which were multi-pollutant studies, do
not show consistent effects of ozone and cannot reliably attribute the
effects observed to ozone, as opposed to other pollutants or other
potential causal factors. For example, Mortimer et al. (2002) attribute
the associations with decreased lung function, increased symptoms, and
increased medication usage to general "summer-time air pollution,"
rather than ozone in particular. Indeed, in that study, when all the
pollutants studied -- including sulfur dioxide (SO~2~), nitrogen dioxide
(NO~2~), and particulates less than 10 micrometers in diameter (PM~10~),
as well as ozone -- were considered, there was no significant
association of effects with ozone (see, e.g., Exponent, 2006; Annapolis
Center for Science-Based Public Policy, 2007). Moreover, this study
found associations only in the morning; no associations were found with
evening pulmonary function or symptoms. As stated by Moolgavkar (2007,
p. 20), if the association with ozone were causal, "one would \[expect\]
to detect this association in the evening in view of the fact that
children are outdoors during the day and exposed to ozone."

The Gent et al. (2003) study has similar limitations, as explained by
Moolgavkar (2007). That study considered only ozone and fine particles;
it did not consider NO~2~, which has been found to be associated with
pulmonary function decrements and respiratory symptoms in other studies,
and it did not control for relative humidity. Further, that study was
conducted using a non-standardized questionnaire to record symptoms.
Also, the study did not show a dose-response relationship between ozone
levels and bronchodilator usage, and the associations reported for
bronchodilator usage are inconsistent with those reported for more
subjective symptoms.

Finally, the asthma panel studies upon which EPA relies are inconsistent
with other recent studies, not mentioned by EPA, which have found no
consistent associations between ozone concentrations and asthma
symptoms. For example, Schildcrout et al. (2006) investigated
associations between exposure to various air pollutants and asthma
exacerbations (daily symptoms and use of inhalers) among asthmatic
children in eight U.S. cities and found no associations of ozone with
these effects. Additionally, while EPA mentions an earlier study by
McConnell et al. (2002) on the onset of asthma (72 Fed. Reg. at 27834),
a later study of associations of air pollution and asthma symptoms by
McConnell et al. (2003) in southern California showed no significant
associations of ozone with such symptoms in multi-pollutant models when
NO~2~ and organic carbon were also considered (see Moolgavkar, 2007).

In short, contrary to EPA's statements in its preamble, the asthma panel
studies show inconsistent and uncertain, not "robust," associations
between ozone concentrations and effects in asthmatics and certainly do
not provide "strong" evidence of such effects due to ozone. In response
to EPA's request for comments on the degree to which these associations
"reflect causal relationships between important health endpoints and
exposure to O~3~ alone at ambient O~3~ levels below the current
standard" (72 Fed. Reg. at 37878), it is apparent that the asthma panel
studies do not present reliable evidence of such causal relationships
and thus do not support a reduction in the standard level.

D.  **Epidemiological Studies on Hospital/Emergency Room Admissions and
    Mortality**

EPA also relies on other time-series epidemiological studies as evidence
of an association between short-term ozone exposure and a wide variety
of serious health effects, including respiratory emergency room visits
and hospital admissions (72 Fed. Reg. at 37832, 37865-66, and 37876) and
premature non-accidental mortality (*id*. at 37835-36, 37844, 37866, and
37876). CASAC (2006b, p. 12) also supported the reliance on these
studies. While EPA claims that some of these studies support causal
associations between health effects and short-term ozone exposure even
at concentrations below the level of the current primary standard, these
studies do not support a lowering of the standard, for the reasons
discussed below.

First, as EPA recognizes, many of the hospitalization studies and nearly
all the emergency room visit studies were conducted in areas that likely
would not have met the current standard (EPA, 2007a, pp. 6-12, 6-13; 72
Fed. Reg. at 37865, 37866). Similarly, the multi-city mortality studies
generally included a large number of cities that were not in attainment
with the current ozone standard and nearly all single-city studies that
showed statistically significant associations with mortality had 98^th^
percentile ozone concentrations indicative of ozone levels that likely
would not have met the current standard (EPA, 2007a, p. 6-16). In these
circumstances, the results of these studies cannot be reliably used to
support a reduction in the level of the current standard. While EPA
notes that an analysis by Bell et al. (2006) of a subset of the data
from the multi-city National Mortality, Morbidity and Air Pollution
Study (NMMAPS) continued to show mortality associations even when only
days with a maximum 8-hour average ozone concentration below 0.061 ppm
were included (72 Fed. Reg. at 37876), that study is flawed in many
significant respects, as described below, and cannot be relied on to
support a reduction in the primary standard level.

Second, the epidemiological studies on hospital/emergency room
admissions and mortality erroneously assume that measurements from one
or more fixed monitors accurately represent individuals' ozone exposure.
As noted above, EPA contends that, in the absence of available data on
personal ozone exposure, ambient measurements represent a good surrogate
for personal exposures and may actually overestimate personal exposures
(72 Fed. Reg. at 37838-39). In fact, however, there is considerable
uncertainty about the validity of using ambient measurements to reflect
personal exposures. For example, Sarnat et al. (2006) found that the
ability of ambient gas monitors to represent personal exposure to such
gases is quite limited, and they concluded that their results "suggest
that time-series health studies based on 24-hour ambient concentrations
may not be able to identify the effects of gases on health, and better
exposure surrogates are needed." Similarly, Koutrakis et al. (2005)
demonstrated, based on studies in Boston and Baltimore, that ambient
concentrations of gaseous pollutants such as ozone do not correlate well
with personal exposure measures of those pollutants. Similar findings
were reported by Liu et al. (1997) (for ozone), Linaker et al. (2000)
(for NO~2~), and Brauer et al. (2002) (for PM~2.5~). In the context of
estimating ozone exposure in time-series studies, CASAC (2006a) stated
(at p. 3):

> "It is known that personal exposure to ozone is not reflected
> adequately, and sometimes not at all, by ozone concentrations measured
> at central outdoor monitoring sites. Typically, personal exposures are
> much lower than the ambient concentrations, and can be dramatically
> lower depending on time-activity patterns, housing characteristics,
> and season. In addition, and of particular importance for the ozone
> time-series studies, there can be no correlation between personal
> concentrations of ozone measured over time and concentrations measured
> at central outdoor sites."

In its later letter, CASAC (2006b) reiterated this problem, noting (at
p. 10) that "Panel members have little insight as to what we would find
if we had actual exposure measurements." Thus, despite the fact that
measured ambient concentrations may generally be higher than personal
exposures, the relationship between the two is so variable and uncertain
that ambient measurements cannot serve as a reliable surrogate for
personal exposures in attempting to attribute any effects seen in the
time-series studies to people's ozone exposure, particularly when other
pollutants are involved.

Third, EPA has failed to adequately consider and critically evaluate
model selection in the epidemiological studies on which it relies. As
Moolgavkar (2007, p. 11) points out: "It has become abundantly clear
that choice of model, particularly adjustment for weather and temporal
trends and choice of lag structure, can significantly influence the
conclusions drawn from time-series studies of air pollution." Moreover,
where the biologically correct models are unknown, as in the case of air
pollution epidemiology, residual bias may occur (Moolgavkar, 2007, pp.
10-11). Similarly, Heuss (2007, pp. 47-49) notes that failure to account
for model uncertainty in the time-series analyses leads to an
overestimation of the certainty of the results of such analyses. In
support of this view, Heuss (2007) cites a study by Koop and Tole
(2004), who used Bayesian model averaging to evaluate model uncertainty
in time-series analyses using an extensive set of pollutants and
meteorological variables from Toronto, Canada, and concluded:

> "Point estimates of the effect of numerous air pollutants all tend to
> be positive, albeit small. However, when model uncertainty is
> accounted for in the analysis, measures of uncertainty associated with
> these point estimates became very large. Indeed they became so large
> that the hypothesis that air pollution has no effect on mortality is
> not implausible. On the basis of these results, we recommend against
> the use of point estimates from time series data to set regulatory
> standards for air pollution exposure."

EPA has not heeded the advice of Koop and Tole, instead relying on
time-series studies without adequately considering the importance of
model selection.

Fourth, the time-series studies reporting associations between ozone
concentrations and hospital admissions or emergency room visits have
inconsistent results and cannot clearly distinguish the effects of ozone
from other potentially causal factors, including both other pollutants
and non-pollutant variables. EPA's Staff Paper recognized that "inherent
limitations in time-series epidemiological studies raise questions about
the utility of such evidence to inform judgments about a NAAQS for an
individual pollutant such as O3 within a mix of highly correlated
pollutants, such as the mix of photochemical oxidants, especially at
ambient O~3~ concentrations below levels at which O~3~-related effects
have been observed in controlled human exposure studies" (EPA, 2007a, p.
6-6). In the Proposed Rule, however, EPA has not taken the cautious
approach indicated by these limitations, but instead has overstated the
likelihood of a causal relationship between exposures to ozone,
especially at lower concentrations, and hospital admissions or emergency
room visits for respiratory disorders. As discussed by the Annapolis
Center for Science-Based Public Policy (2007, p. 4) and Heuss (2007, p.
51), Anderson et al. (1998) evaluated numerous studies of air pollution
and daily asthma emergency room visits or admissions, and concluded that
while there is evidence that the mix of air pollutants, including SO~2~,
NO~2~, fine particles, and ozone, may have an effect on such visits or
admissions, there is no consistency in determining the specific
pollutant responsible. The same remains true today, particularly at
concentrations below the current ozone standard.

Fifth, the multi-city mortality studies -- namely, the NMMAPS study by
Bell et al. (2004, 2006), the European study by Gryparis et al. (2004),
and the meta-analyses by Ito et al. (2005), Levy et al. (2005), and Bell
et al. (2005) -- do not provide reliable or consistent evidence
implicating ozone exposures as a cause of mortality. The reasons for
this include the following:

-   These studies combined the results from many cities to show an
    effect when, in fact, the results from some cities did not show a
    significant positive association between ozone and mortality or
    showed a negative relationship. For example, the NMMAPS study by
    Bell et al. (2004) combined estimates of associations between ozone
    and mortality taken in 95 urban areas to arrive at a national
    average relative risk for mortality, notwithstanding the fact that
    the results from the individual cities ranged from strongly negative
    to strongly positive (see Annapolis Center for Science-Based Public
    Policy, 2007, p. 42). As shown by Moolgavkar (2007, p. 14) and
    McClellan (2007, p. 11), the data from this study show that only 7
    of the 95 cities had statistically significant positive associations
    between ozone and mortality, and about a third of the cities had
    negative coefficients.

-   The multi-city mortality studies and meta-analyses did not
    sufficiently account for other pollutants or other potential causal
    factors. For instance, while Bell et al. (2004) provided an
    adjustment for the potential confounding by PM~10~, they did not
    have the necessary air quality data to provide similar and adequate
    adjustments for the potential confounding effects of fine particles
    (PM~2.5~), which EPA has concluded also cause mortality (see
    Annapolis Center for Science-Based Public Policy, 2007, p. 42).

-   The NMMAPS studies contain several findings that are inconsistent or
    implausible. For example, as explained by Moolgavkar (2007, p. 15),
    the original NMMAPS study showed a negative association between
    ozone and mortality in winter. By contrast, while the extended
    NMMAPS study by Bell et al. (2004) did not report a separate
    analysis for winter, it found a larger effect estimate for the
    full-year analyses than for analyses during the summer months. This
    is at odds with most time-series studies of ozone that looked at
    seasonal effects and implies that there must have been a greater
    effect in winter than in summer, contrary to the original finding.
    Moreover, the Bell et al. (2004) study reported premature mortality
    at such low levels as to imply that ozone-related mortality is
    occurring at levels well below natural background, which is not
    biologically plausible (see Hayes, 2006, p. 5; Annapolis Center for
    Science-Based Public Policy, 2007, p. 42).

-   The meta-analyses of ozone and mortality commissioned by EPA (Ito et
    al., 2005; Levy et al., 2005; Bell et al., 2005) cannot be
    considered to be independent from each other, since there is
    considerable overlap in the cities used in these three
    meta-analyses. In any case, these meta-analyses confirm the
    existence of publication bias in reporting such results and, despite
    the overlap, show a high degree of unexplained heterogeneity in the
    reported results (see Moolgavkar, 2007, p. 15).

-   The findings of acute cardiopulmonary mortality are not coherent
    with the studies of hospital admissions, which report associations
    for respiratory but not cardiac-related admissions.

-   Finally, EPA's conclusion that the mortality studies on which it
    relies suggest that there is an elevated risk of total
    non-accidental mortality associated with acute exposure to ozone is
    inconsistent with studies of long-term ozone exposure, which EPA
    admits have found no consistent association between long-term ozone
    exposure and mortality (72 Fed. Reg. at 37837). The absence of an
    association between long-term exposure to ozone and mortality
    undercuts the conclusion that short-term exposures cause premature
    mortality.

In sum, contrary to EPA's assertions, the time-series epidemiological
studies cited in the Proposed Rule do not provide convincing evidence of
causal associations between exposure to ambient ozone and either
morbidity or mortality. Therefore, these studies do not support a
reduction in the primary standard level.

> **IV. EPA'S EXPOSURE AND RISK ESTIMATES DO NOT JUSTIFY LOWERING THE
> PRIMARY STANDARD LEVEL.**

In addition to the human clinical and epidemiological studies described
in the preceding section, EPA relies on its exposure and risk
assessments as support for its proposal to lower the existing primary
standard of 0.08 ppm (72 Fed. Reg. at 37851-62, 37866-68, 37870-71). EPA
acknowledges, however, that there are significant uncertainties and
limitations associated with these assessments (e.g., *id*. at 37852,
37856, 37858, 37859, 37876, 37880). Given these uncertainties and
limitations, as described in greater detail below, the exposure and risk
estimates do not support lowering the primary standard level.

First, there are substantial uncertainties in the exposure estimates.
EPA simulated ozone population exposure using the Air Pollutants
Exposure Model (APEX), the human inhalation exposure model within the
Total Risk Integrated Methodology framework (*id*. at 37852). While EPA
expresses confidence in the model structure (i.e., the algorithms in
APEX designed to simulate the processes that result in people's
exposures to ozone), EPA acknowledges "important uncertainties" with
respect to the model inputs, including those related to: (a) the
modeling of human activity patterns over an ozone season; (b) the
modeling of variations in ambient concentrations near roadways; (c) the
modeling of air exchange rates that affect the amount of ozone that
penetrates indoors; and (d) the characterization of energy expenditure
for children engaged in various activities (*id*.). Uncertainty with
respect to energy expenditure is particularly important, as it "carries
over to the uncertainty of the modeled breathing rates, which are
important since they are used to classify exposures occurring at
moderate or greater exertion which are the relevant exposures since
O~3~-related effects observed in clinical studies only are observed when
individuals are engaged in some form of exercise" (*id*.).

In addition to the uncertainties associated with the exposure estimate
model inputs, there was substantial variability observed across the 12
urban areas for which exposure estimates were conducted with respect to
the percent of the population subgroups estimated to experience ozone
exposures of concern. As an example, EPA notes that when 2002 ozone
concentrations were simulated to just meet the current primary ozone
standard, the aggregate 12 urban area estimate was that 18% of all
school age children were estimated to experience ozone exposures (at
levels [\>]{.underline} 0.070 ppm), while the exposure estimates in the
12 urban areas considered separately ranged from 1 to 38% (*id*. at
37855). This variability raises significant concerns about the extent to
which the 12 urban areas used in the exposure estimate and,
consequently, the risk assessment, are representative of other cities.

Second, there are substantial uncertainties about the
concentration-response relationship, particularly at levels below 0.08
ppm. Thus, the extrapolations assumed in the risk assessment may not be
valid. EPA acknowledges as much: "key uncertainties include ...
uncertainties associated with the shape of the exposure-response
relationship, especially at levels below 0.08 ppm, 8-hour average, where
only very limited data are available down to 0.04 ppm and there is an
absence of data below 0.04 ppm" (*id*. at 37856). In addition to
uncertainties relating to the shape of the concentration-response
relationship, EPA identified the following uncertainties pertaining to
the concentration-response relationship for that portion of the risk
assessment based on effects reported in epidemiological studies: (a)
those surrounding estimates of the O~3~ coefficients for
concentration-response relationships used in the risk assessment; (b)
those "related to the extent to which concentration-response
relationships derived from studies in a given location and time when
O~3~ levels were higher or behavior and/or housing conditions were
different provide accurate representations of the relationships for the
same locations with lower air quality distributions and/or different
behavior and/or housing conditions"; and (c) those "concerning the
possible role of co-pollutants, which also may have varied between the
time of the studies from which the concentration-response relationships
were derived and the current assessment period" (*id*. at 37856).

Third, the risk estimates based on lung function decrements use a
benchmark of FEV~1~ declines of [\>]{.underline} 15% for healthy
individuals and ≥ 10% for asthmatics. As shown above, these types of
changes are transient, routinely experienced and well-tolerated, and not
of adverse health consequence for either healthy or asthmatic
individuals.

Fourth, the risk estimates based on respiratory symptoms, hospital
admissions, and non-accidental mortality are based on epidemiological
studies which, as shown above, do not reliably implicate ozone, and
certainly not ozone at any specific level, as the causal agent for the
effects reported.

Fifth, EPA itself notes that while the risk assessment assumes a causal
link between ozone exposures and the reported effects, the evidence for
such a causal relationship is uncertain at lower levels:

> "The Administrator particularly notes that as lower standard levels
> are modeled, including a standard set at a level below 0.070 ppm, the
> risk assessment continues to assume a causal link between O~3~
> exposures and the occurrence of the health effects examined, such that
> the assessment continues to indicate reductions in O~3~-related risk
> upon meeting a lower standard level. . . . \[H\]owever, the
> Administrator recognizes that *evidence of a causal relationship
> between adverse health effects and O~3~ exposures becomes increasingly
> uncertain at lower levels of exposure*." (*id*. at 37880, emphasis
> added).

To the extent that this assumption regarding a causal link at lower
ozone levels is invalid, estimated reductions in O~3~-related risk are
artificially inflated.

Sixth, the estimated risks are for ozone levels in excess of
"policy-relevant background" (PRB) (*id*. at 37857). PRB levels were
predicted solely by modeling using the GEOS-CHEM model (*id*.). This
model underestimates PRB. As shown in detail by Lefohn (2006, pp. 2-1 to
2-48), the modeled estimates of PRB are inconsistent with the empirical
ozone monitoring data from Trinidad Head, California, which have been
shown by detailed back-trajectory analyses to be more representative of
PRB in the West. Those empirical data show the occurrence of numerous
hourly average concentrations [\>]{.underline} 0.05 ppm and indicate
that PRB levels are in fact higher than predicted by EPA's model. By
underestimating PRB, EPA's risk assessment *overestimates* sickness and
premature deaths (see, e.g., CRA International, 2006, p. 7-9). EPA's own
sensitivity analysis confirms this overestimation of health effects:
"estimates assuming higher PRB levels results \[*sic*\] in decreased
estimates of non-accidental mortality incidence per 100,000 that are 50%
or greater less than the base case estimates" (EPA, 2007a, p. 5-82).

In addition, EPA's PRB estimates inappropriately excluded certain
emissions contributions that should be included -- notably,
anthropogenic precursor emissions from Canada and Mexico (72 Fed. Reg.
at 37857). This approach artificially inflates the risk estimates and is
unjustified because, notwithstanding treaties that the U.S. may have
with Canada and Mexico, emissions from those countries cannot be
directly controlled by U.S. emissions regulations; and, in any event, it
is unreasonable to assume zero anthropogenic emissions in those
countries. Therefore, anthropogenic precursor emissions from Canada and
Mexico should be considered a part of PRB.

Seventh, in modeling the impact of alternative standards, EPA used a
Quadratic Rollback approach to adjust hourly ozone concentrations (*id*.
at 37853). This approach may overstate the air quality improvements
resulting from emissions reductions and thus overstate the benefits of
stricter standards. EPA has acknowledged that mid-level ozone
concentrations do not necessarily decline at the same rate as peak ozone
concentrations, a factor taken into account by the Quadratic Rollback
method. However, as explained and demonstrated with actual data by
Lefohn (2006, pp. E-9 - E-10 & 4-1 - 4-11), the Quadratic Rollback
approach, which applies uniformly over the ozone season, will not
capture observed month-to-month variations in the rate of ozone
reduction, which are often significant. Therefore, the Quadratic
Rollback approach will overstate improvements in mid-range air quality
in many cases.

Finally, in considering the health benefits of lowering the standard
level, it is important to consider whether such a standard would be
attainable. EPA's focus on the mean background, and failure to consider
the extremes of background, resulted in a failure on the part of the
Agency to adequately evaluate whether the lower primary standard
proposed by EPA is attainable, even with complete elimination of
controllable man-made emissions. Due to the extremes of background, a
standard at the lower level proposed by EPA, 0.070 ppm, would likely be
unattainable in many areas of the country, including areas that are far
removed from any significant man-made sources; and a standard at the
lower alternative level identified by EPA and recommended by CASAC,
0.060 ppm, would likely be unattainable in most areas of the country
because the background levels would leave too little room for any
man-made emissions (see Annapolis Center for Science-Based Public
Policy, 2007 pp. 25-30; Heuss, 2007, pp. 3-6). When EPA established the
current primary standard for ozone, the Administrator specifically
rejected a standard of 0.070 ppm as being too close to background levels
(62 Fed. Reg. at 38868). The same remains true today. Adoption of such a
standard, the attainment of which is dubious for much of the country in
light of extremes of background, would make the development of rational
state implementation plans difficult, if not impossible. And if the
lowered standard is not achievable, that calls into question the
validity of the asserted health benefits of adopting such a standard.

Overall, EPA's exposure and risk estimates are based on a number of
hypothetical assumptions that are highly uncertain. As a result, they
are too speculative to support lowering the primary standard level.

> **V. CHANGING THE CURRENT ROUNDING PROCEDURE FOR THE STANDARD IS NOT
> WARRANTED AT THIS TIME.**

The ozone standard currently specifies the level to the nearest
hundredth of a ppm (two decimal places). EPA is proposing to change the
standard to specify the level to the nearest thousandth of a ppm (three
decimal places) -- i.e., 1 part per billion (ppb). This proposal is
based on EPA's conclusion, in which CASAC (2006b, p. 5) concurred, that
"current monitoring technology allows accurate measurement of O~3~ to
support specifying the 8-hour standard to this degree of precision" (72
Fed. Reg. at 37875). However, the technical capability of current
monitoring technology does not answer the question of the appropriate
rounding procedure to use in evaluating attainment of the standard.

First, while current technology may allow precision in the ppb range,
there remains uncertainty about the third decimal place. For example,
although (as EPA notes) the California Air Resources Board has adopted
an 8-hour ozone standard specified to the nearest thousandth of a ppm
(0.070 ppm), it has recognized that "ozone measurements are uncertain in
the third decimal place, to the degree of plus or minus 0.0003 ppm"
(California Air Resources Board, 2005, p. 6-3). Similarly, Langstaff
(2007) has reported bias estimates for individual monitors in Boston
varying from -7% to +11% in 2003-04. Further, as noted by Langstaff
(2007), interferences from other pollutants and humidity effects can
lead to errors in field measurements. Indeed, EPA's ambient air
monitoring reference methods specify a precision of two decimal places
(0.01 ppm) for ozone concentrations (40 C.F.R. § 53.20, Table B-1).

Moreover, specifying the standard to the third decimal place implies a
degree of precision in the underlying health effects data that does not
exist. EPA recognized this when it adopted the current standard in 1997.
It stated, at that time, that it was specifying the standard to two
decimal places "in part to reflect uncertainties in the health effects
evidence upon which the proposed standard is based," including "the
measurement uncertainty and representativeness inherent in the reported
O~3~ concentrations used in field and epidemiological studies and the
uncertainty in the exposure estimates upon which the quantitative risk
estimates have been based" (62 Fed. Reg. at 38886). As discussed in
prior sections of these comments, those uncertainties remain. EPA has
not explained why those uncertainties should not lead to the same
conclusion reached in 1997.

Given that (a) EPA's current monitoring requirements specify precision
to only two decimal places, (b) there is still uncertainty about the
precision of the third decimal place, particularly in field
measurements, and (c) there are considerable measurement uncertainties
in the underlying health effects studies, as well as uncertainties in
the exposure and risk estimates, the Commenters believe that it would
not be appropriate, at the present time, to make attainment
determinations in the real world based on the implied precision of a
standard expressed to three decimal places. Hence, the Commenters
support the retention of the current expression of the standard as 0.08
ppm.

> **VI. THERE REMAIN TOO MANY UNCERTAINTIES TO JUSTIFY ADOPTING A
> SECONDARY STANDARD THAT IS DIFFERENT FROM THE PRIMARY STANDARD.**

In reviewing the data on the effects of ozone on vegetation, EPA
concludes that the current secondary standard, which is identical to the
primary standard, is inadequate to protect the public welfare from
adverse effects. EPA claims, in particular, that the current standard
would allow ozone levels to remain that "are sufficient to cause visible
foliar injury, seedling and mature tree biomass loss, and crop
reductions to degrees that could be considered adverse" (72 Fed. Reg. at
37899). To justify this change from its 1997 conclusion, EPA relies on
recent field-based evidence on biomass loss in seedlings, saplings, and
mature trees and on foliar injury incidence, as well as exposure and
risk analyses that predict adverse effects on crops and seedlings under
scenarios that would meet the current standard (*id*. at 37893-99). In
addition, EPA concludes that a cumulative seasonal standard is more
appropriate than an 8-hour standard (id. at 37899, 37900, 37905).

As with the health effect evidence, EPA has overstated the conclusions
that can be drawn from the vegetation data. There remain considerable
uncertainties about the degree to which and levels at which ozone
produces adverse effects on the public welfare, as well as the extent to
which the proposed revised secondary standard (under either proposed
option) would protect the public welfare from such effects. In fact,
CASAC (2006b, p. 6) recognized that the evidence "linking specific ozone
concentrations to specific vegetation/ecological effects must continue
to be characterized as having high uncertainties," although it then
failed to take adequate account of those uncertainties in recommending a
more stringent, separate secondary standard. While the present
Commenters will leave a detailed discussion of the uncertainties to
other comments, it is noted that these uncertainties include the
following:

-   There are significant uncertainties about the extent to which the
    new field-based research upon which EPA places heavy reliance is
    reflective of impacts on natural ecosystems. For example, it is
    unknown whether the individual tree growth effects reported in the
    AspenFACE studies in Wisconsin would translate into adverse impacts
    on the multiple tree species that compose an ecosystem, given
    competitive factors and natural ecosystem succession (see Irving
    Consulting, 2006, pp. 7-9). Moreover, the EPA Staff Paper
    acknowledges the "unknown and unquantifiable sources of uncertainty"
    in the TREGRO model used to estimate mature tree risks (EPA,
    2007a, p. 8-2).

-   The Staff Paper likewise recognizes that "\[l\]inking visible foliar
    injury to other plant effects is still problematic" (EPA, 2007a, p.
    8-7).

-   The estimates of crop losses continue to be based on
    concentration-response functions derived from the National Crop Loss
    Assessment Network (NCLAN) studies performed in the 1980s (see EPA,
    2007a, p. 7-52), which were available and considered in the 1997
    decision. The uncertainties relating to those estimates, which were
    recognized by EPA at that time and continue to be recognized (EPA,
    2007a, pp. 7-52 - 7-53), remain.

-   "\[V\]ast rural areas of the U.S., where important crops and natural
    vegetation occur, still do not have O~3~ monitor coverage" (EPA,
    2007a, p. 7-24). As a result, there are insufficient data to
    validate or judge the model predictions. EPA acknowledges the
    "inherent uncertainties in the interpolation that must rely on
    sparse data that, for the most part, are representative of urban and
    near-urban areas" (EPA, 2007a, p. 8-8).

-   The same underestimates of natural background ozone levels and
    failure to adequately consider extremes of background that were
    discussed above with respect to the primary standard lead to
    overestimates of the improvements in vegetative growth that may
    result from reducing the secondary standard (see Irving Consulting,
    2006, p. 6-7). In fact, the proposed secondary standard may be
    within the range of uncontrollable background and thus not produce
    the benefits claimed (see Heuss, 2007, pp.12-14).

-   The extent to which the proposed cumulative seasonal form of the
    standard, known as W126, would provide increased protection of
    vegetation is also uncertain. For example, as shown by Lefohn
    (2006), use of that measure by itself will not reliably predict
    vegetation effects because the same values can lead to very
    different amounts of foliar injury and damage depending on the
    number of peak concentrations [\>]{.underline} 0.10 ppm. Further,
    EPA notes that one of the reasons for selecting the W126 measure is
    that, since the new estimates of PRB are lower than those in the
    last review, this measure would not be significantly influenced by
    concentrations within the range of PRB (72 Fed. Reg. at 37900). This
    rationale, however, is unjustified because EPA's model-predicted PRB
    is underestimated, as shown in Section IV above.

-   In estimating the air quality that would result from just attaining
    the proposed standard, EPA used the Quadradic Rollback approach to
    adjust hourly ozone concentrations. That approach is problematic for
    the same reasons discussed in Section IV.

-   The extent to which the predicted effects on vegetation from ozone
    exposure at levels below the current standard would be adverse to
    the public welfare depends on the intended use of the vegetation and
    its significance to the public. These factors have not been
    adequately explored. Moreover, in terms of evaluating the overall
    impact of the current standard versus the proposed standard on the
    public welfare, the effects on vegetation need to be weighed against
    the adverse effects on local businesses and communities that would
    result from adoption of the revised standard.

-   The current monitoring network is not appropriate for evaluating
    vegetation exposure in terms of spatial coverage and monitor height,
    and it is unclear whether adequate monitoring and modeling tools are
    available to implement a new standard in a different form from the
    primary standard (see Heuss, 2007, pp. 17-18).

In the Proposed Rule, EPA "recognizes that there remain significant
uncertainties in determining or quantifying the degree of risk
attributable to varying levels of O~3~ exposure, the degree of
protection that any specific cumulative, seasonal standard would
produce, and the associated potential for error in determining the
standard that will provide a requisite degree of protection -- *i.e.*,
sufficient but not more than what is necessary" (72 Fed. Reg. at 37905).
As noted above, CASAC likewise recognized the existence of "high
uncertainties" in the evidence on the vegetation/ecological effects of
ozone. However, in its conclusions and proposal, EPA does not take into
account those uncertainties or the others listed above. These
uncertainties need to be addressed before adopting a new and more
stringent standard that would produce substantial and widespread adverse
impacts on businesses and communities with only uncertain benefits to
the public welfare. In this situation, the Commenters believe that the
current information is insufficient to justify adopting either of the
proposed secondary standards, and that the current standard should be
retained while additional research is conducted to address the many
remaining uncertainties.

**VII. CONCLUSION**

For the reasons discussed above, the tremendous costs and other adverse
impacts to businesses and communities that would result from tightening
the standard are not necessary because the scientific evidence does not
demonstrate that a reduction in the standard is needed to protect the
public health and welfare. Accordingly, the Commenters urge EPA to
retain the current standard as both the primary and the secondary
standard.

**VIII. REFERENCES**

Adams, W.C. 2002. Comparison of chamber and face mask 6.6-hour exposures
to ozone on pulmonary function and symptom responses. *Inhalat.
Toxicol.* 14:745-764.

Adams, W.C. 2003. Comparison of chamber and face mask 6.6-hour exposures
to 0.08 ppm ozone via square-wave and triangular profiles on pulmonary
responses. *Inhalat. Toxicol.* 15:265-281.

Adams, W.C. 2006. Comparison of chamber 6.6-h exposures to 0.04 -- 0.08
PPM ozone via square-wave and triangular profiles on pulmonary
responses. *Inhalat. Toxicol.* 18:127-136.

Alliance of Automobile Manufacturers *et al*. 2006. Comments on EPA's
*"Review of the National Ambient Air Quality Standards for Ozone: Policy
Assessment of Scientific and Technical Information (OAQPS Staff Paper --
Second Draft)"*. Submitted to EPA September 18, 2006.

Anderson, H.R., A. Ponce de Leon, J.M. Bland, J.S. Bower, J. Emberlin,
and D.P Strachan. Air pollution, pollens, and daily admissions for
asthma in London, 1987-92. *Thorax* 53:842-848.

Annapolis Center for Science-Based Public Policy. 2007. *The Science and
Health Effects of Ground-Level Ozone*. July 2007.

Bell, M.L., A. McDermott, S.L. Zeger, J.M. Samet, and F. Dominici. 2004.
Ozone and short-term mortality in 95 US urban communities, 1987-2000.
*JAMA* 292:19.

Bell, M.L., F. Dominici, and J.M. Samet. 2005. A meta-analysis of
time-series studies of ozone and mortality with comparison to the
national morbidity, mortality, and air pollution study. *Epidemiology*
16:436-445.

Bell, M.L., R.D. Peng, and F. Dominici. 2006. The exposure-response
curve for ozone and risk of mortality and the adequacy of current ozone
regulations. *Environ. Health Perspect.* 114:532-536.

Brauer, M., J. Brumm, S. Vedal, and A.J. Petkau. 2002. Exposure
misclassification and threshold concentrations in time series analyses
of air pollution health effects. *Risk Analysis* 22: 1183-1193.

California Air Resources Board. 2005. *Review of the California Ambient
Air Quality Standard for Ozone.* Volume II. Staff Report. March 11,
2005.

CASAC. 2006a. Memorandum to Stephen L. Johnson, USEPA Administrator,
from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory
Committee. June 5, 2006.

CASAC. 2006b. Letter to Stephen L. Johnson, USEPA Administrator, from
Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee.
October 24, 2006.

CASAC. 2007. Letter to Stephen L. Johnson, USEPA Administrator, from
Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee.
March 26, 2007.

CRA International. 2006. *Comments on EPA's Draft Ozone Health Risk
Assessment*. September 18, 2006.

EPA. 1997. *National Ambient Air Quality Standards for Ozone; Final
Rule.* 62 Fed. Reg. 38855. July 18, 1997.

EPA. 2007a. *Review of the National Ambient Air Quality Standards for
Ozone: Policy Assessment of Scientific and Technical Information.* OAQPS
Staff Paper (Final). U.S. Environmental Protection Agency, Office of Air
Quality Planning and Standards, Research Triangle Park, N.C.
EPA-452/R-07-003. January 2007.

EPA. 2007b. Clean Air Trends.
<http://www.epa.gov/airtrends/econ-emissions.html>.

EPA. 2007c. *Integrated Science Assessment for Oxides of Nitrogen --
Health Criteria. First Draft*. EPA/600/R-07/093.

Exponent, Inc. 2006. *Comments on EPA's Ozone Staff Paper (Second
Draft).* Submitted to EPA by Alliance of Automobile Manufacturers,
August 18, 2006.

Folinsbee, L.J., W.F. McDonnell, and D.H. Horstman. 1988. Pulmonary
function and symptom responses after 6.6-hour exposure to 0.12 ppm ozone
with moderate exercise. *JAPCA* 38:28-35.

Folinsebee, L.J., D.H. Horstman, H.R. Kehrl, S. Harder, S. Abdul-Salaam,
and P.J. Ives. 1994. Respiratory responses to repeated prolonged
exposure to 0.12 ppm ozone. *Am. J. Respir. Crit. Care Med.* 149:98-105.

Gent, J.F., E.W. Triche, T.R. Holford, K. Belanger, M.B. Bracken, W.S.
Beckett, and B.P. Leaderer. 2003. Association of low-level ozone and
fine particles with respiratory symptoms in children with asthma. *JAMA*
290:1859-1867.

Gryparis, A., B. Forsberg, K. Katsouyanni, A. Analitis, G. Touloumi, J.
Schwartz, E. Samoli, S. Medina, H.R. Anderson, E.M. Niciu, H.E.
Wichmann, B. Kriz, M. Kosnik, J. Skorkovsky, J.M. Vonk, and Z.
Dörtbudak. 2004. Acute effects of ozone on mortality from the "air
pollution and health: a European approach" project. *Am. J. Respir.
Crit. Care Med.* 170:1080-1087.

Hayes, S.R. 2006. Memorandum to Richard Martin, American Petroleum
Institute, Re: Comments on Second Draft of USEPA's Ozone Staff Paper.
Submitted to EPA. Dated August 18, 2006.

Heuss, J.M. 2007. *Comments on Final Ozone Staff Paper and CASAC
Recommendations for Primary and Secondary Ozone Standard.* Prepared for
The Alliance of Automobile Manufacturers. Submitted to EPA. Dated March
1, 2007.

Horstman, D.H., L.J. Folinsbee, P.J. Ives, S. Abdul-Salaam, and W.F.
McDonnell. 1990. Ozone concentrations and pulmonary response
relationships for 6.6-hour exposures with five hours of moderate
exercise to 0.08, 0.10, amd 0.12 ppm. *Am. Rev. Respir. Dis.*
142:1158-1163.

Horstman, D.H., B.A. Ball, J. Brown, T. Gerrity, and L.J. Folinsbee.
1995. Comparison of pulmonary responses of asthmatic and nonasthmatic
subjects performing light exercise while exposed to a low level of
ozone. *Toxicol. Ind. Health* 11:369-385.

Irving Consulting. 2006. *Final Report to UARG on the Vegetation Effects
Sections of the Review of the National Ambient Air Quality Standards for
Ozone, U.S. EPA, July 2006.* September 14, 2006.

Ito, K., S.F. De Leon, and M. Lippmann. 2005. Associations between ozone
and daily mortality. *Epidemiology* 16:446-457.

Kamps, A.W.A., R.J. Roorda, and P.L.P. Brand. 2001. Peak flow diaries in
childhood asthma are unreliable. *Thorax* 56:180-182.

Koenig, J.Q., D.S. Covert, M.S. Morgan, M. Horike, N. Horike, S.G.
Marshall, and W.E. Pierson. 1985. Acute effects of 0.12 ppm ozone or
0.12 ppm nitrogen dioxide on pulmonary function in healthy and asthmatic
adolescents. *Am. Rev. Respir. Dis.* 132:648-651.

Koenig, J.Q., D.S. Covert, S.G. Marshall, G. van Belle, and W.E.
Pierson. 1987. The effects of ozone and nitrogen dioxide on pulmonary
function in healthy and in asthmatic adolescents. *Am. Rev. Respir.
Dis.* 136:1152-1157.

Koenig, J.Q., D.S. Covert, M.S. Smith, G. van Belle, and W.E. Pierson.
1988. The pulmonary effects of ozone and nitrogen dioxide alone and
combined in healthy and asthmatic adolescent subjects. *Toxicol. &
Indus. Health* 4:521-532.

Koop, G., and L. Tole. 2006. Measuring the health effects of air
pollution: To what extent can we really say that people are dying from
bad air? *J. Environ. Econ. Management* 47:30-54.

Koutrakis, P., H.H. Suh, J.A. Sarnat, K.W. Brown, B.A. Couli, and J.
Schwartz. *Characterization of Particulate and Gas Exposures of
Sensitive Subpopulations Living in Baltimore and Boston*. 2005. Health
Effects Institute Report \# 131.

Kreit, J.W., K.B. Gross, T.B. Moore, T.J. Lorenzen, J. D'Arcy, and W.L.
Eschenbacher. 1989. Ozone-induced changes in pulmonary function and
bronchial responsiveness in asthmatics. *J. Appl. Physiol.* 66:217-222.

Langstaff, J. 2007. *Analysis of Uncertainty in Ozone Population
Exposure Modeling*. Memorandum to the Ozone NAAQS Review Docket,
EPA-HQ-OAR-2005-0172-0174. January 31, 2007.

Lefohn, A.S. 2006. *Comments on Key Issues Relating to the EPA Document:
Review of the National Ambient Air Quality Standards for Ozone: Policy
Assessment of Scientific and Technical Information, OAQPS Staff Paper --
Second Draft.* Submitted to EPA. Dated August 18, 2006.

Levy, J.I., S. Chemernski, and A. Sarnat. 2005. Ozone exposure and
mortality. *Epidemiology* 16:458-468.

Linaker, C.H., A.J. Chauhan, H.M. Inskip, S.T. Holgate, and D. Coggon.
2000. Personal exposure of children to nitrogen dioxide relative to
concentrations in outdoor air. *Occup. Environ. Med*. 57:472-476.

Linn, W.S., D.A. Shamoo, K.R. Anderson, R-C Peng, E.L. Avol, and J.D.
Hackney. 1994. Effects of prolonged, repeated exposure to ozone,
sulfuric acid, and their combination in healthy and asthmatic
volunteers. *Am. J. Respir. Crit. Care Med*. 150:431-440.

Liu, L.J., R. Delfino, and P. Koutrakis. 1997. Ozone exposure assessment
in a southern California community. *Environ. Health Persp.* 107:58-65.

McBride, D.E., J.Q. Koenig, D.L. Luchtel, P.V. Williams, 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.

McClellan, R.O. 2007. Statement of Roger O. McClellan Before the Senate
Subcommittee on Clean Air and Nuclear Safety on the Senate Environment
and Public Works Committee, at Hearing on EPA's Proposed Revision to the
National Ambient Air Quality Standards for Ozone. July 11, 2007.

McConnell, R., K. Berhane, F. Gilliland, J. Molitor, D. Thomas, F.
Lurman, E. Avol, W.J. Gauderman, and J.M. Peters. 2003. Prospective
study of air pollution and bronchitic symptoms in children with asthma.
*Am. J. Respir. Crit. Care Med*. 168:790-797.

McDonnell, W.F., P.W. Stewart, S. Andreoni, E. Seal, Jr., H.R. Kehrl,
D.H. Horstman, L.J. Folinsbee, and M.V. Smith. 1997. Prediction of
ozone-induced FEV1 changes: Effects of concentration, duration, and
ventilation. *Am. J. Respir. Crit. Care Med*. 156:715-722.

McFadden, E.R., Jr. 2007. *Comments of E.R. McFadden, Jr., M.D., on
Health Significance of Asthmatics' Responses Reported in Clinical
Studies of Short-Term Ozone Exposures*. Submitted to EPA on October 1,
2007, with cover letter from James R. Bieke, Goodwin Procter. (Copy of
Dr. McFadden's comments attached as Exhibit A without curriculum vitae.)

Moolgavkar, S. 2007. *A Critical Review of the Staff Paper on Ozone*.
Prepared by Suresh Moolgavkar, M.D., Ph.D., Exponent, Inc. June 25.

Mortimer, K.M., L.M. Neas, D.W. Dockery, S. Redline, and I.B. Tager. The
effect of air pollution on inner-city children with asthma. *Eur Respir
J.* 19:699-705.

National Mining Association. 1995. *Comments of the National Mining
Association on proposed Decision Not to Revise the 24-Hour and Annual
National Ambient Air Quality Standards for Sulfur Oxides and
Solicitation of Comment on Additional Regulation of Short-Term Peak
SO~2~ Exposures.* *Appendix A: Comments of Medical Experts on Health
Significance of Reported Effects of Short-Term Sulfur Dioxide Exposures
on Exercising Asthmatics*. Submitted to EPA on April 14, 1995, in Docket
No. A-84-25.

Sarnet, S.E., B.A. Coull, J. Schwartz, D.R. Gold, and H.H. Suh. 2006.
Factors affecting the association between ambient concentrations and
personal exposures to particles and gases. *Environ. Health Perspect.*
114:640-654.

Schildcrout, S.S., L. Sheppard, T. Lumley, J.C. Slaughter, J.Q. Koenig,
and G.G. Shapiro. 2006. Ambient air pollution and asthma exacerbations
in children: An eight-city analysis. *Am. J. Epidemiol.* 164:505-517.

Vedal, S. 2007. *Critique of the Ozone OAQPS Staff Paper*. Attachment to
Letter to Stephen L. Johnson, USEPA Administrator, from Dr. Rogene
Henderson, Chair, Clean Air Scientific Advisory Committee, dated March
26, 2007.

Weymer, A.R., H. Gong, Jr., A. Lyness, and W.S. Linn. 1994. Pre-exposure
to ozone does not enhance or produce exercise-induced asthma. 1994. *Am.
J. Respir. Crit. Care Med*. 149:1413-1419.

**EXHIBIT A**

**Comments of E. R. McFadden, Jr., M.D.,**

**on Health Significance of Asthmatics' Responses**

**Reported in Clinical Studies of Short-Term Ozone Exposure**

September 14, 2007

My name is Regis McFadden. I am the Argyl J. Beams Professor of Medicine
and the Vice-Chairman for Clinical Research, Department of Medicine,
MetroHealth Medical Center, Case Western Reserve University School of
Medicine. My curriculum vitae is attached. I have had long experience in
treating and studying patients with asthma and have published
extensively on exercise-induced asthma, airway reactivity, and the
effects of various stimuli on airway physiology in asthmatics. I have
been particularly interested in examining the relationship between lung
function abnormalities and the development and resolution of acute
episodes of asthma.

I have been asked by a group of industry trade associations and
companies to provide my views on some of the potential issues raised by
the United States Environmental Protection Agency (EPA) in its current
review and proposal regarding the National Ambient Air Quality Standards
for ozone (EPA, 2007). These issues relate to the health significance
for asthmatics of the types of responses that have been reported in
clinical studies of short-term exposures to ozone at levels close to the
current ozone standard of 0.08 ppm. More specifically, I have been asked
to comment on: (1) the health significance for asthmatics of functional
changes involving FEV~1~ decrements [\>]{.underline} 10% but \< 20%
and/or symptomatic responses (discussed by EPA, 2007, p, 37850); (2)
whether the existing clinical studies on healthy subjects exposed to
ozone levels at, above, and below 0.08 ppm have shown medically
significant effects (see EPA, 2007, pp. 37878-79); and (3) whether the
clinical evidence indicates that people with asthma are likely to
experience larger and more serious effects than healthy people (see EPA,
2007, pp. 37878-79).

[General Discussion of Functional and Symptomatic Changes]{.underline}

For a number of reasons, transient decreases in FEV~1~ of 10-20% are not
by themselves significant or meaningful to asthmatics. Such changes are
an expected part of the asthmatic diathesis and commonly occur,
particularly overnight. In fact, until most recently this type of
variation was sought as one of the diagnostic criteria to establish the
presence of the disease. These responses are spontaneously reversible
and short-lived, with rapid onset and prompt abatement. Further, they
are exactly the kinds of quantitative and qualitative
bronchoconstrictive responses that are deliberately provoked in
laboratories during challenges with various airway antagonists such as
methacholine, histamine, exercise, and numerous other stimuli, in order
to diagnose whether a patient has asthma. These are not major effects in
themselves and cannot be extrapolated to longer-term effects. It has
been my experience from examining and studying thousands of patients for
both clinical and research purposes that asthmatics typically will not
begin to sense bronchoconstriction until their FEV~1~ falls about 50%
from normal. By way of comparison, asthmatic patients presenting to a
physician or emergency room for treatment of acute exacerbations of
their illness often have decreases in FEV~1~ of 65-70% from normal.

Similarly, relatively minor complaints, such as wheezing, shortness of
breath, or chest tightness, which are short-lived and disappear promptly
when the stimulus is removed or are eliminated by use of a
bronchodilator, are similar to the kinds of reactions that asthmatics
experience frequently and tolerate well. It is important to appreciate
that the presence and intensity of symptoms are a function of acute
changes in physiology as filtered by the patient's sensory perception.
Failure of perception is rare, whereas heightened sensitivity is
asthmatics is extremely common. I would regard symptoms such as those
described above as more in the nature of temporary annoyances rather
than adverse health effects.

On the other hand, when the functional changes are not promptly
reversible and/or are accompanied by more severe or long-lasting
symptoms, they may be regarded as adverse.

In the present context, in considering whether to reduce the level of
the current ozone standard, the key question is whether exposure to
ozone at levels at and below the current standard produces the latter
types of effects.

[Review of Clinical Evidence]{.underline}

In evaluating this question, I have first reviewed the recent clinical
studies by Adams (2002, 2003, 2006) on the effects of ozone exposures at
0.12, 0.08, 0.06, and 0.04 ppm on healthy subjects. In these studies,
the functional changes reported at ozone levels ≤ 0.08 ppm were quite
minimal and likely non-detectable by the subjects. I would not regard
such events as medically significant. The symptoms reported were barely
discerned and the maximum effect represented only a 6% increase over
control. For example, the total mean symptom scores on the scale
reported by Adams (2006) were only 8-10 units at 0.08 ppm and 2-4 units
at 0.04 and 0.06 ppm out of a possible total score of 160.

The next question is whether asthmatics would likely have larger and
more serious effects at these ozone levels than those observed in the
healthy subjects. Unfortunately, conjecture will not answer this
question and one must base conclusions on data.

To my knowledge there are no data on the effect of ≤ 0.08 ppm of ozone
on asthmatics. However, to provide some insight into the likely
magnitude of the problem, I reviewed a number of earlier studies that
examined the effects on asthmatics of ozone exposures at levels of \~
0.12 ppm and higher (Linn *et al*., 1994; Weymer *et al*., 1994;
Horstman *et al*., 1995; Kreit *et a*l., 1989; McBride *et al*., 1994;
Koenig *et a*l., 1985, 1987, 1988). These studies do not show any major
effects. Both the functional changes and symptoms (where reported) from
ozone exposure at levels of around 0.12 ppm are small. For example, in
the Linn *et al*. (1994) investigation, the mean total symptom scores
for asthmatics at an ozone concentration of 0.12 ppm were in the range
of 20-40 (compared to around 20-30 in clean air) (Fig. 4), while in the
Weymer *et al*. (1994) investigation, the mean total symptom scores
after exposure to ozone at 0.10 and 0.25 ppm were in the range of 13-17
units (compared to \~ 8 in clean air) (Table 4). Given the large total
possible symptom score ranges, these scores are not indicative of
significant symptoms. The total possible symptom score in the Linn *et
al.* trial (1994, p. 437) appears to have been 480 and that in the
Weymer *et al*. investigation (1994, Table 4 note) 520.

Overall, these studies on asthmatics indicate that ozone exposures at \~
0.12 ppm do not produce medically significant functional changes and are
right around the inflection point where one begins to see an increase in
symptoms; however, that increase is small. Based on this information, it
would be expected that asthmatics' responses to ozone exposure at levels
≤ 0.08 ppm would be even less. It is my view that the available data are
not sufficiently robust to indicate that such exposures would present a
significant health concern even to sensitive people like asthmatics.

I have also reviewed the general statements which EPA relies upon to
support its conclusion that asthmatics would be expected to have larger
and more serious effects than healthy people (EPA, 2007, pp, 37826 and
37846-47). As a group, these statements represent a series of
assumptions about the pathogenesis of asthma detailing the purported
events leading to alterations in physiology and subsequent symptomatic
manifestations. While appealing, it must be remembered that they are
indeed only assumptions. There simply are no data to support the
sequence described or to establish how the type and/or magnitude of
inflammation relates to signs, symptoms, and/or the pathogenesis of
asthma. Further, the translation between these types of responses and
the onset or worsening of asthma or an increase in effects of health
significance to asthmatics has not been established. Thus, the
assumption that these responses would lead to clinical manifestations in
terms of exacerbations of asthma or other adverse health effects remains
unproven theory.

Moreover, even if the hypothesized relationships were true, they would
apply to the effects of various stimuli, including ozone *generally*,
but they do not address the specific question of the level at which
ozone would have such effects. Much of the data discussed represent
compilations derived from a series of studies in a variety of models
with different ozone exposure concentrations. Unfortunately, the
applicability and/or precision of such information is not yet
established. Thus, these statements do not tell us whether ozone would
have such effects at concentrations at and below the current standard
level. As discussed above, the actual clinical studies on asthmatics
exposed to ozone do not indicate that ozone exposure at such low
concentrations produces effects that are harmful to asthmatics' health.
For these reasons, I do not think that EPA's statements provide reliable
support for lowering the ozone standard.

**REFERENCES**

Adams WC. 2002. Comparison of chamber and face mask 6.6-hour exposures
to ozone on pulmonary function and symptom responses. *Inhalat.
Toxicol.* 14:745-764.

Adams WC. 2003. Comparison of chamber and face mask 6.6-hour exposures
to 0.08 ppm ozone via square-wave and triangular profiles on pulmonary
responses. *Inhalat. Toxicol.* 15:265-281.

Adams WC. 2006. Comparison of chamber 6.6-h exposures to 0.04 -- 0.08
PPM ozone via square-wave and triangular profiles on pulmonary
responses. *Inhalat. Toxicol.* 18:127-136.

EPA. 2007. *National Ambient Air Quality Standards for Ozone: Proposed
Rule.* Fed. Reg. 72:37818-37919. July 11, 2007.

Horstman DH, Ball BA, Brown J, Gerrity T, and Folinsbee LJ. 1995.
Comparison of pulmonary responses of asthmatic and nonasthmatic subjects
performing light exercise while exposed to a low level of ozone.
*Toxicol. Ind. Health* 11:369-385.

Koenig JQ, Covert DS, Morgan MS, Horike M, Horike N, Marshall SG, and
Pierson WE. 1985. Acute effects of 0.12 ppm ozone or 0.12 ppm nitrogen
dioxide on pulmonary function in healthy and asthmatic adolescents. *Am.
Rev. Respir. Dis.* 132:648-651.

Koenig JQ, Covert DS, Marshall SG, van Belle G, and Pierson WE. 1987.
The effects of ozone and nitrogen dioxide on pulmonary function in
healthy and in asthmatic adolescents. *Am. Rev. Respir. Dis.*
136:1152-1157.

Koenig JQ, Covert DS, Smith MS, van Belle G, and Pierson WE. 1988. The
pulmonary effects of ozone and nitrogen dioxide alone and combined in
healthy and asthmatic adolescent subjects. *Toxicol. & Indus. Health*
4:521-532.

Kreit JW, Gross KB, Moore TB, Lorenzen TJ, D'Arcy J, and Eschenbacher
WL. 1989. Ozone-induced changes in pulmonary function and bronchial
responsiveness in asthmatics. *J. Appl. Physiol.* 66:217-222.

Linn, WS, Shamoo DA, Anderson KR, Peng R-C, Avol EL, and Hackney JD.
1994. Effects of prolonged, repeated exposure to ozone, sulfuric acid,
and their combination in healthy and asthmatic volunteers. *Am. J.
Respir. Crit. Care Med*. 150:431-440.

McBride, DE, Koenig JQ, Luchtel DL, Williams PV, and Henderson WR Jr.
1994. Inflammatory effects of ozone in the upper airways of subjects
with asthma. *Am. J. Respir. Crit. Care Med*. 149:1192-1197.

Weymer AR, Gong H Jr., Lyness A, and Linn WS. 1994. Pre-exposure to
ozone does not enhance or produce exercise-induced asthma. 1994. *Am. J.
Respir. Crit. Care Med*. 149:1413-1419.

**EXHIBIT B**

**Excerpts from Statements of Other Physicians Specializing in Asthma
on**

**Significance of Reductions in FEV~1~ of up to 20 Percent**

*Note: These Statements were initially submitted to EPA in 1995 by the
National Mining Association in connection with comments on the NAAQS for
sulfur oxides (NMA, 1995, Appendix A). Full copies of these experts'
Statements, including the curricula vitae of the experts, were also
provided as exhibits to the September 18, 2006 comments of a group of
trade associations that include the present Commenters on EPA's second
draft of the Staff Paper on the NAAQS for ozone (Alliance of Automobile
Manufacturers et al., 2006).*

-   Dr. Jeffrey Drazen (1995): "\[T\]here is ample precedent that
    transient changes in the FEV~1~ on the average of 20% are well
    tolerated by patients with asthma and place them at no medical
    risk."

-   Dr. Richard Lemen (1995): "\[C\]hanges of 15-10% in FEV~1.0~
    reported in the EPA-cited studies could be largely within the 'noise
    level' of pulmonary function tests. . . . \[Such responses\] are not
    indicative of medically significant effects. Unlike real asthma
    attacks, the changes in FEV~1.0~ and SRaw observed in the SO~2~
    studies, even in the more responsive subjects, are relatively modest
    in magnitude and are transient and quickly reversible, returning to
    normal after a short period. For comparison, asthma patients who
    seek medical treatment for asthma attacks in emergency rooms or
    hospitals generally have much larger decrements in lung function . .
    . , and these changes are not transient but have often persisted for
    hours or days."

-   Dr. Sheldon Spector (1995): "The changes in pulmonary function
    reported in the studies are relatively small, and do not appear to
    lead to any late phase effect which often indicates that an
    inflammatory process is involved. In my experience, using FEV~1~ as
    a measurement, a fall of 20-50% usually does not produce significant
    symptoms."

-   Dr. Edward Eden (1995): "The asthmatics who engage in such exercise
    tolerate readily a drop in pulmonary function of the type shown in
    the SO~2~ studies (i.e., a mean decrease in FEV~1~ of around 10-30%
    with greater changes in the more sensitive subjects)."

-   Dr. Stuart Brooks (1995): "The clinical significance of a 20% to 40%
    fall in FEV-1 for a mild asthmatic capable of vigorous exercise is
    doubtful. An asthmatic may experience such a decrement not
    infrequently, and suffer no serious consequences or be put at any
    increased risk for future detrimental outcomes."

-   Dr. Nicholas Gross (1995): "\[B\]ronchial challenge (provocation)
    tests with methacholine, for example, that are routinely performed
    on asthmatics take a 20% decline in FEV~1~ as their endpoint, which
    means of course that greater decreases will in fact be produced in
    all hyperresponsive subjects. Such tests are performed in thousands
    of clinics and doctors' offices every day and are regarded as safe."

-   Dr. Adam Wanner (1995): "A \[10-25%\] fall in FEV~1~ during
    bronchoconstriction induced by inhaled antigen, or non-allergenic
    bronchoconstricting stimuli . . . is rarely associated with cough,
    wheezing, shortness of breath or other asthma symptoms . . . . This
    may be one of the reasons why a 20% fall in FEV~1~ has been chosen
    by convention as the target bronchoconstriction in bronchial
    provocation testing."

-   Dr. Peter Hamm (1995): "In my experience, . . . such a drop \[in
    FEV~1~ of 30% or more\] will not yield a clinically relevant outcome
    in an \[asthmatic\] individual with sufficient pulmonary reserve."

-   Dr. Byron Cooper (1995): "The EPA staff regarded changes in FEV~1~
    as severe if they exceeded 20%. In fact the 20% figure is the
    minimum considered significant in a pulmonary function lab and is
    deliberately provoked when doing methacholine challenge. Asthmatics
    with a 20% reduction from normal are considered mild."

ENVIRONMENTAL TECHNICAL COMMITTEE

**October 2007**

**([Please Review and Report Any Changes, etc., to Roxie)]{.underline}**

Weston Adams

McAngus Goudelock & Courie

700 Gervais Street, Suite 300

Columbia, SC 29211

(803)227-2322

(803)748-0526

<wadams@mgclaw.com>

Ruth Albright

SynTerra.

148 River Street, Suite 220

Greenville, SC 29601

(864)421-9999

(864(421-9909

[ralbright@synterracorp.com](mailto:ralbright@fletchergroup.com)

Amy Artmeier

MeadWestvaco Corporation

PO Box 118005

Charleston, SC 29423-8005

(843)745-3250

(843)745-3195

ala5@meadwestvaco.com

John Baker

International Paper

4001 McCords Ferry Road

Eastover, SC 29044

(803)353-7440

(803)353-7026

john.baker1@ipaper.com

Matthew Bares

S&ME, Inc.

134 Suber Road

Columbia, SC 29210

(803)561-9024

(803)561-9177

<mbares@smeinc.com>

Marty Barfield

Domtar

585 Willamette Road

Bennettsville, SC 29501

(843)479-0200

(843)479-6603

marty.barfield@n.domtar.com

Richard K. Blackwell

Upstate Alliance

124 Verdae Blvd., Suite 202

Greenville, SC 29607

(864)283-2305

(864)283-2310

<rblackwell@upstatealliance.com>

Ralph R. Bouton, PE

Earth Tech, Inc.

10 Patewood Drive, Ste 500

Greenville, SC 29615-3517

(864)234-3000

(864)234-3058

<ralph.bouton@earthtech.com>

Christine K. Brenk\
Trigon Engineering Consultants

6200 Haris Technology Blvd.

Charlotte, NC 28269-3732

(704)598-1049

(704)598-1050

cbrenk@trigoneng.com

Blake Burgess

Fuss & O'Neill, Inc.

717 Lady Street, Suite E

Columbia, SC 29201

(803)376-6034

(803)376-6035

<bburgess@fando.com>

Carl Burrell

Davis & Floyd, Inc.

PO Box 428

Greenwood, SC 29648-0428

(864)229-4413

(864)229-7119

cburrell@davisfloyd.com

John Cain

ENSR Corporation

810 Dutch Square Blvd, Ste. 202

Columbia, SC 29210-7318

(803)216-0003 ext. 22

(803)216-0708

jcain@ensr.com

Rory Carlisle

Nelson, Mullins, Riley &

Scarborough, LLP

Post Office Box 11070

Columbia, SC 29211-1070

\(803\) 799-2000

\(803\) 256-7500

[rory.carlisle@nelsonmullins.com](mailto:rtc@nmrs.com)

Myra Carpenter\
Michelin North America

PO Box 2846

Greenville, SC 29602

(864)458-1582

(864)458-0782

<Myra.carpenter@us.michelin.com>

Kay Clamp

S. C. Petroleum Council

807 Gervais St

Columbia, SC 29201-3125

(803)799-9588

(803)765-1512

clampk@api.org

Mike Clark

MACTEC

720 Gracern Road

Columbia, SC 29210

(803)798-1200

(803)750-1303

<jmclark@mactec.com>

Ned Cochrane, III

Mount Mills, Inc.

PO Box 3478

Greenville, SC 29602-3478

(864)233-4151

(864)370-3116

<ned@mvmills.com>

Earl Colwell

FN Manufacturing, LLC

PO Box 24257

Columbia, SC 29224-4257

(803)736-0522

(803)736-4169

EARLC@FNMFG.com

David Comen

Kestrel Horizons, LLC

20-B Creekview Court

Greenville, SC 29615

(864)288-6353

(864)288-6354

dcomen@kestrelhorizons.com

Ward Cooper

Flakeboard

PO Box 1017

Bennettsville, SC 29512-1017

(843)479-0267

(843)479-5555

ward.cooper@flakeboard.com

James Council

Council Energy, Inc.

PO Drawer 347\
Orangeburg, SC 29116

(803)534-4360

(803)534-4361

<councillumberco@bellsouth.net>

Karen Crawford

Nelson Mullins Riley & Scarborough

PO Box 11070

Columbia, SC 29211-1070

(803)255-9442

(803)256-9145

karen.crawford@nelsonmullins.com

Barbara Dankmyer

INVISTA

P O Box 7000

Camden, SC 29020-7000

(803)425-3160

(803)425-2481

Barbara.K. Dankmyer@invista.com

Peggi Davis

Sonoco Products Co.

1 North Second Street

Hartsville, SC 29550

(843)383-7991

(843)383-3394

peggi.davis@sonoco.com

David Dempsey

Delta Environmental Consultants, Inc.

2455 Old Knox Road

Spartanburg, SC 29302

(864)948-9491

(864)948-9491

[dgdempsey@charter.net](mailto:ddempsey@deltaenv.com)

Clay Duffie

Mount Pleasant Waterworks

PO Box 330

Mt Pleasant, SC 29465-0330

(843)884-9626

(843)849-2227

<cduffie@mpwonline.com>\
\
John Durkee

Environmental Engineering Sciences

1226 White Tail Path

Charleston, SC 29414-9104

(843)214-0663

e2sciences@bellsouth.net

Robert H. Emmel, Ph.D.

Reeves Brothers, Inc.

PO Box 892

Spartanburg, SC 29304

(864)316-4111

(864)595-2180

<bemmel@reevesbrothers.com>

Vic Ethridge

Clariant Corporation

788 Chert Quarry Road

Martin, SC 29836-3414

\(803\) 584-4321\
(803) 584-0345

<vic.ethridge@clariant.com>

Kathy Ferry

ENSR

810 Dutch Square Blvd.

Suite 202

Columbia, SC 29210-7318

\(803\) 216-0003

\(803\) 216-0708

<kferry@ensr.com>

Paul Monty Felix

Alaglass Pools

RR 1 Box 393

St. Matthews, SC 29135

(803)874-2731

(803)655-5471

<pfelix2997@aol.com>

Gary Fields

Lafarge North America

463 Judge Street

Harleyville, SC 29448-3124

(843)462- 7651

(843)462-7679

gary.fields@lafarge-na.com

Jack Finney

The Gel Group, Inc.

PO Box 30712

Charleston, SC 29417-0712

(843)556-8171

(843)766-1178

<jack.finney@gel.com>

Greg Force

Professional Geologist and President

Force & Associates, Inc.

147 Vera Road, Suite F

Lexington, SC 29072

(803)359-3200

(803)359-6682

<gregforceassociates@alltel.net>

Robby Gallimore

Federal-Moguel Corporation

9104 Alex Harvin Hwy.

Summerton, SC 29148

(803)478-2382

(803)478-2531

robby_gallimore@fmo.com

Eric Gleason

General Electric-Southeast Region

PO Box 648

Greenville, SC 29602-0648

(864)254-2055

(864)254-2469

eric.gleason@ps.ge.com

Tad A. Goetcheus, P.E.

HRP Associates, Inc.

1327-D Miller Road

Greenville, SC 29607

(864)289-0311

(864)281-9846

Tad.goetcheus@hrpassociates.com

Mick Greeson

Progress Energy

Post Office Box 1551

Raleigh, NC 27602

(919)546-5438

(919)546-6153

<mick.greeson@pgnmail.com>

R. Briggs Hamilton

BMW Manufacturing Company

PO Box 11000

Spartanburg, SC 29304-4100

(864)989-5772

(864)801-5772

<briggs.hamilton@bmwmc.com>

Fred Hanna, P.E.

Jordan, Jones & Goulding, Inc.

1411 Gervais Street, Suite 325

Columbia, SC 29201

(803)312-8964

(803)312-8991

fhanna@jjg.com

Bernie F. Hawkins, Jr.

Nelson, Mullins Riley & Scarborough

PO Box 11070

Columbia, SC 29211-1070

(803)255-9581

(803)255-9687

bernie.hawkins@nelsonmullins.com

Dave Heitz

GeoSyntec Consultants

148 River St., Suite 220

Greenville, SC 29601-2465

(864)527-4671

(864)421-9909

<dheitz@geosyntec.com>

Dale L. Herendeen

Bowater Incorporated

5300 Cureton Ferry Road

PO Box 7

Catawba, SC 29704-0007

(803)981-8009

(803)981-8009

<herendeendl@bowater.com>

Kin Hill

Charleston Commissioners of Public Works

PO Box B

Charleston, SC 29402

(843)727-6862

(843)727-7188

<hillfk@charlestoncpw.com>

Mark E. Hollis

Duke Power

526 South Church Street

Charlotte, NC 28202

(980)373-3726

(704)408-9810

<mehollis@duke-energy.com>

Deborah Hottel

McNair Law Firm, P.A.

PO Box 11390

Columbia, SC 29211-1390

(803)799-9800

(803)376-2219

dhottel@mcnair.net

Jay Hudson

Santee Cooper

1 Riverwood Dr.

PO Box 2946101

Moncks Corner, SC 29461

(843)761-4095

(843)761-4156

<jhudson@santeecooper.com>

Susan Jackson

Santee Cooper

P O Box 2946101

Moncks Corner, SC 29461

(843)761-8000

(843)761-4156

<swjackso@santeecooper.com>

Ronnie Jeffcoat

Blue Cross And Blue Shield of SC AA-G05

I-20 at Alpine Road

Columbia, SC 29219

(803)788-0222 ext. 42770

(803)264-6588

ronnie.jeffcoat@bcbssc.com

Charles Jeter

RMT, Inc.

PO Box 16778

Greenville, SC 29606-7778

(864)281-0030

(864)281-0288

charles.jeter@rmtinc.com

David Jones

Cornell Dubilier

140 Technology Pl

Liberty, SC 29657-3300

(864)843-2277

(864)843-3800

djones@cornell-dubilier.com

Max Justice

Parker, Poe, Adams & Bernstein, L.L.P.

Three Wachovia Center

401 South Tryon Street, St.3000

Charlotte, SC 28202

(704)335-9010

(704)334-4706

maxjustice@parkerpoe.com

Tom Kerr

Albemarle Corporation

PO Box 1028

Orangeburg, SC 29116-1028

(803)539-5404

(803)539-5178

tom_kerr@albemarle.com

Tommy Lavender

Nexsen Pruet LLC

PO Box 2426

Columbia, SC 29202-2426

(803)253-8233

(803)253-8258

tlavender@nexsenpruet.com

Randy Lowell

Willoughby & Hoefer, P.A.

930 Richland Street

Columbia, SC 29202

\(803\) 252-3300

\(803\) 256-8062

rlowell@willoughbyhoefer.com

Christina "Chris" Lyon

So. Region Environ. Coor.

Progress Energy

1755 Mechanicsville Road

Florence, SC 29501-1379

(843)661-2253

(843)661-2233

<christina.lyon@pgn.com>

Donna MacInnis

CH2M Hill

4824 Parkway Plaza Blvd.

Suite 200

Charlotte, NC 28217

(704)329-0073 x 264

(704)329-0141

donna.macinnis@ch2m.com

Alan McConnell

Kilpatrick Stockton LLP

3737 Glenwood Ave

Raleigh, NC 27612-5534

(919)420-1798

(919)420-1800

amcconnell@kilpatrickstockon.com

John Mewborn

EMS -- Chemie (North America)

PO Box 1717

Sumter, SC 29151

(803)469-4127

(803)775-6435

jmewborn@sc.rr.com

Richard Middleton

Circle Environmental Inc.

124 Sparkman Drive

Columbia, SC 29209

(803)792-8989

(803)695-9227

[richard@circle.net](mailto:rm@absorbent.biz)

Richard Moore

Kestrel Horizons

1876 Wallenberg Blvd.

Suite A

Charleston, SC 29407

(843)769-4449 Cell(843)693-7003

rmoore@kestrelhorizons.com

Harry Morris

Kestrel Horizons, LLC

20-B Creekview Court

Greenville, SC 29615

(864)288-6353

(864)288-6354

<hmorris@kestrelhorizons.com>

Deano Orr

International Paper

5 W. Hargett St., Suite 914

Raleigh, NC 27602

(919)831-4764

(919)831-4769

<deano.orr@ipaper.com>

D. Vernon Osteen

Washington Sav. River

Building 735-B

Aiken, SC 29808

(803)952-8318

(803)952-6316

<dvernon.osteen@srs.gov>

Beth Partlow

Ogletree, Deakins, Nash, Smoak, and

PO Box 11206

Columbia, SC 29211-1206

(803)252-1300

(803)254-6517

elizabeth.partlow@odnss.com

Jack Preston

SC Electric & Gas

Mail Code P05

Columbia, SC 29218-0001

(803)217-9849

(803)217-7349

jpreston@scana.com

Randy Pulley

ALCOA - Mt. Holly

PO Box 1000

Goose Creek, SC 29445-1000

(843)572-5294

(843)572-5378

randy.pulley@alcoa.com

C. Victor Pyle, III

Ogletree, Deakins, Nash, Smoak, & Stewart, P.C.

1320 Main Street, Suite 600

Columbia, SC 29201

(803)252-1300

(803)254-6517

<vic.pyle@odnss.com>

Glenn Raynor

HOLCIM, Inc.

PO Box 698

Holly Hill, SC 29059-0698

(803)496-2756

(803)496-2763

glenn.raynor@holcim.com

William Ross

SC Truckers Association

PO Box 50166

Columbia, SC 29250-0166

(803)799-4306

(803)254-7148

Kenneth E. Rosenbaum, Jr.

Environmental Resources Mgmt.

498 Wando Park Drr.

Mt. Pleasant, SC 29414

(843)856-4270

(864)856-4283

<ken.rosenbaum@erm.com>

Catherine Saenz

Shaw Industries Group, Inc.

4401 St. Andrews Road

Columbia, SC 29210-4151

(803)750-4379

(803)750-4428

catherine.saenz@shawinc.com

Art Samberg

Golder Associates NC. Inc.

4819 Emperor Boulevard

4^th^ Floor

Durham, NC 27703

(919)313-4813

(919)313-4816

<asamberg@golder.com>

Gary Sanderson

Specialty Polymers

869 Old Richburg Road

Chester, SC 29706

(803)581-0734

(803)385-6077

<gsanderson@specpoly.com>

Margaret Sembos

Genesis Consulting Group

1330 Lady St, Suite 205

Columbia, SC 29201-3300

(803)744-4500

msembos@genesis-consulting-group.com

James C. Serne

TRC Environmental Corporation

5540 Ceterview Drive

Suite 100

Raleigh, NC 27606-3363

jserne@trcsolutions.com

Glenn Shealy

CMC Steel

PO Box 2005

Cayce-West Cola, SC 29171

(803)936-3792

(803)936-3743

<glenn.shealy@cmcsg.com>

Patrick Shirley

ARCADIS

420 Park Avenue

Greenville, SC 29601

(864)241-5332

(864)241-5246

<pshirley@arcadis-us.com>

Alex Shissias

Haynsworth, Sinkler, Boyd P.A.

P. O. Box 11889

Columbia, SC 29211

(803)540-7962

(803)765-1243

<ashissias@hsblawfirm.com>

Jeffrey Silliman

Milliken & Co.

PO Box 1926, M482

Spartanburg, SC 29304-1926

(864)503-1844

(864)503-1887

jeff.silliman@milliken.com

Jay Smaldone

Roche Carolina Inc.

6173 E Old Marion Hwy

Florence, SC 29506-9330

(843)629-4513

(843)629-4552

james.smaldone@roche.com

Tom Stanfield

PBR

201 Metropolitan Drive

West Columbia, SC 29170

\(803\) 732-4473

(803)822-2010

<Tom_stanfield@pbr.com.au>

Jimmy Summers

Senior Project Manager

URS Corp -- North Carolina

6135 Park South Drive, Suite 300

Charlotte, NC 28219-3272

(704)716-0728

(704)522-0063

<Jimmy_summers@urscorp.com>

Arthur Toompas

Cone Mills Corporation

2420 Fairview Street

Greensboro, NC 27405

(336)230-7216

(336)230-7218

<arthur.toompas@mail.cone.com>

Edward Twilley

MeadWestvaco Corporation

PO Box 118005

Charleston, SC 29423-8005

(843)745-3024

(843)745-3708

wet3@meadwestvaco.com

Et William "Bill" Voshell

Lafarge North America

12735 Morris Road Ext

Alpharetta, GA 30004

(678)746-2024

(678)746-2020

<bill.voshell@lafarge-na.com>\
\
Ethan Ware

McNair Law Firm, P.A.

PO Box 11390

Columbia, SC 29211-1390

(803)799-9800

(803)376-2219

eware@mcnair.net

Gary Weinreich

International Paper

700 S. Kaminski Street

Georgetown, SC 29440

(843)545-2291

(803)545-2480

<gary.weinreich@ipaper.com>

Alicia Wilson

Spartanburg Water\
System/Sanitary Sewer District

PO Box 251

Spartanbanburg, SC 29304

(864)253-9632 ext. 157

(864)253-9382

awilson@sws-sssd.org

Jim Witkowski

International Paper

PO Box B

Eastover, SC 29044-0001

(803)353-7916

(803)353-7026

Jim.Witkowski@ipaper.com

Andrew Wolf

Robert Bosch Corporation

8101 Dorchester Road

Charleston, SC 29418

(843)760-7400

(843)760-7678

<andrew.wolf@us.bosch.com>

Greg Yorston

Oakridge Landfill/WM

1047 Highway Church Rd

Elgin, SC 29045-9119

(803)788-3054

(803)736-0995

Greg_Yorston@wastemanagement.com

Lilly Hong Zhang

Eastman Chemical

PO Box 1782

Columbia, SC 29202

(803)791-5074

(803)926-2043

<lhzhang@eastman.com>

Lee W. Zimmerman

McNair Law Firm

Post Office Box 11390

Columbia, SC 29211

\(803\) 799-9800

\(803\) 376-2219

[lzimmerman@mcnair.net](mailto:lzimmeran@mcnair.net)