US ENVIRONMENTAL PROTECTION AGENCY

SCIENCE ADVISORY BOARD (SAB) STAFF OFFICE

CLEAN AIR SCIENTIFIC ADVISORY COMMITTEE (CASAC)

OXIDES OF NITROGEN PRIMARY NAAQS REVIEW PANEL PUBLIC MEETING

MARRIOTT AT RESEARCH TRIANGLE PARK

4700 Guardian Drive

Durham, North Carolina 27703

OCTOBER 25, 2007

8:36 A.M.

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1	U.S. ENVIRONMENTAL PROTECTION AGENCY

2	CLEAN AIR SCIENTIFIC ADVISORY COMMITTEE

3	PUBLIC MEETING

4	OCTOBER 25, 2007

5	DR. HENDERSON: I want to thank everyone

6  for being so timely in submitted your paragraphs to

7  Angela, and I thank Angela for bringing it all

8  together.  Now that what's being distributed - -

9	SPEAKER: Hello?

10	DR. HENDERSON: Hello.

11	SPEAKER: Rogene, can you, you need to

12  speak into the microphone.

13	DR. HENDERSON: Okay.

14	SPEAKER: Thank you.

15	DR. HENDERSON: What's being passed out

16  is a compilation of what was submitted, and these are

17  all, everything, it's truly a compilation, but I've

18  read it through it, and I compared it with the list,

19  this small list is, these are the points we listed

20  yesterday afternoon that we thought should be included.

21  So, you might, quickly, compare this list with what's

22  in, what you'd submitted to see if we left anything

23  out.

24	But the consideration that we're going to be

25  making is, is this the substance, does this include

Page 4

1	DR. NUGENT: Good morning.

2	DR. LARSON: Tim Larson.

3	DR. NUGENT: Good morning.

4	DR. ULTMAN: Jim Ultman is.

5	DR. NUGENT: Jim?

6	DR. HENDERSON: Jim Ultman.

7	DR. NUGENT: Ultman.  And, Lee Anne, are

8  you on the phone?  Okay, all right, and just a note

9  about public comments.  I'd mentioned yesterday that we

10  were inviting public comments on yesterday's discussion

11  relating to the ISA.  No member of the public has asked

12  me to speak this morning about the ISA.  I'll ask one

13  more time, because we want to be a little structured

14  about how the discussion proceeds.  Are there members

15  of the public who'd like to present some comments?

16	MR. HICE: Angela?

17	DR. NUGENT: Yes?

18	MR. HICE: This is John Hice on the

19  phone.

20	DR. NUGENT: Yes?

21	MR. HICE: I'd like to make a very, very

22  short comment, if I could.

23	DR. NUGENT: Thank you, okay.  I'll write

24  that down, and we'll turn to you in a moment.

25	MR. HICE: Thank you.

Page 3

1  everything you want to say to the Administrator in our

2  letter.  And, it's not the exact words, because Angela

3  and I will have to go through and make it sound like it

4  was written by one person instead of a committee.

5	But, that is, it's not, it's going to be

6  smoothed out, but does it contain the substance of what

7  we want to say?  Can we agree?  Do you feel comfortable

8  with what is written here as a compilation of

9  everything that we want to say to the Administrator in

10  terms of our peer review of the first draft of the ISA?

11  And, while you're reading that, I think with, I'm going

12  to, I have neglected to let Angela do a roll call of

13  who's on the phone.  So, I will turn it back to her

14  while you're reading it.

15	DR. NUGENT: Thank you, Rogene.  As we

16  start this second day, and we complete the discussion

17  of the ISA, and then move ahead to the discussion of

18  the methods document, I wanted to welcome the people on

19  the phone, and make sure everyone in the room knows

20  who's on the phone, and then talk a little bit about

21  the public comment period, here.  So, may I ask,

22  please, what CASAC panel members are on the phone

23  today?  Are the CASAC panel members on the phone right

24  now?

Page 5

1	DR. NUGENT: Let me also mention that we

2  didn't explicitly list on the agenda public comments

3  for the methods document.  And, I would like to know

4  whether, once we complete this ISA discussion, there

5  are members of the public who'd like to present some

6  brief comments on the methods document.  Okay, hearing

7  none, I think we should proceed.  Rogene, John Hice has

8  some remarks, and I propose that we take them now.

9	DR. HENDERSON: Now would be a great

10  time.

11	DR. NUGENT: Thanks.  I think your

12  audio's working well for us here, so please, speak into

13  your phone set, and we'd love, we'd like to hear your

14  comments now, please.

15	MR. HICE: Thank you very much.  I just

16  wanted to reiterate that we'll be providing written

17  comments for the record to EPA by that deadline, it was

18  October 31st.  And I'm sure several other groups will

19  also.  And I would just ask that the CASAC folks take a

20  look through those comments, at their convenience, and

21  add those thoughts to their own as they think about the

22  review of the next draft.  That's all.

23	DR. NUGENT: Thank you.

24	DR. HENDERSON: And I thank you, too.  I,

25  now, can people hear me if I hold the mike up like

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1  this?

2	SPEAKER ON PHONE: It's fine, Rogene, for

3  me.

4	DR. HENDERSON: Okay, that's good.  This

5  is probably easier than dragging that hand mike.  Okay,

6  have, Angela sent the list of substantive material that

7  we want to have in the letter to the Administrator.

8  Have people had a chance to look at it?

9	SPEAKER: Rogene, you talking about the

10  short list or you talking about the big one?

11	SPEAKER: Big one.

12	DR. HENDERSON: I kind of meant the big

13  one.  This list, this small list, that doesn't have a

14  time on it, is just the notes I jotted down when we

15  were talking at the end of the day yesterday, when I

16  said, you know, what are the substantive issues we want

17  to convey to the Administrator.  And these are simply

18  my notes.  We were in agreement yesterday that this

19  list included everything we wanted to say.

20	Now, would, what I'm asking you, now, do you

21  think these were captured in the more formal listing

22  that Angela pulled together from the people who

23  summarized each charge question?   Well, that's a good

24  idea.  Though some of these overlap quite a bit.  We

25  have charge question one that, have you had a chance to

Page 8

1  rates.  I don't know if that information is available.

2  It's not my area quantitatively, but I was looking for

3  it, and I didn't see it in there.

4	DR. HENDERSON: Okay.

5	DR. CRAPO: Also, with respect to

6  question one, I think that this is an appropriate place

7  where we need to ask if there could be a better

8  assessment of issues related to background, and peaks,

9  and variations in exposure, more data about the

10  variations in exposure across groups, so that we know

11  what the, what percent of, or some idea about what

12  fraction of the country are people, or indoors, or

13  outdoors, is exceeding, or not exceeding the current

14  standard, but substantially higher than the current

15  annual average.  So, that the, the focus on an average

16  annual number makes it really hard for me to analyze

17  what the exposures really are.  So, I think we need

18  more data on that side of the table.

19	DR. HENDERSON: Okay.

20	SPEAKER: Well, I think that actually

21  falls directly under question two.

22	DR. CRAPO: Two, that be great.

23	SPEAKER: That's where ambient mon-,

24  concentrations are.  Some of it's there, but maybe just

25  what more might need to be there.

Page 7

1  look at it?  Would you like to have ten minutes just to

2  look at this one, okay.  Gary's nodding his head.

3  Okay, let's, we will just, we're not breaking.  We're

4  just giving you time to read it, because this is

5  important enough.  I'd like for you to have had a

6  chance to look at it carefully.

7  (WHEREUPON, the members read the document.)

8	DR. HENDERSON: I gather from the

9  conversation that is starting that people are

10  approaching the end of their reading.  Are you about

11  ready to move on?  Okay, what I'd like to hear from you

12  first is, is there anything left out of this that

13  should be added?

14	SPEAKER: Are you asking just about

15  question one, or about all of the questions?

16	SPEAKER: Let's go question by question.

17	DR. HENDERSON: You want to go question

18  by question?  Okay.  We'll take charge question one.

19  Is the response written her, does it include everything

20  that you think should be included?  Ron?

21	DR. WYZGA: One of the things that I

22  think could be useful could be, if they could have more

23  quantitative discussion about the rates of

24  transformation of, I guess, emissions into different

25  species of NOx and what are the influences on these

Page 9

1	DR. HENDERSON: Okay, we're looking at it

2  again.  We come to two, does anybody else have things

3  on one, yes, Terry?

4	DR. GORDON: Just the general, when I

5  read over this, I got the feeling that we were, I mean,

6  it's, the ISA is supposed to help us assess things, and

7  seems like some of the things asked to be added were

8  just making it more criteria document like, just making

9  it longer, and not, not helping us decide things.

10	DR. HENDERSON: Well, that's the strug- -

11	DR. GORDON:  Just a caution.

12	DR. HENDERSON: That's the struggle

13  that's going on, and some of this might go in the

14  annex.  I mean, but, we ask that it be condensed, and

15  that the only policy relevant information given.  And

16  what you're saying is, now, we're asking to expand it

17  in - -

18	DR. GORDON: In some areas.

19	DR. HENDERSON: In some areas.  Mary?

20	DR. ROSS: Well, that was a point of

21  clarification I was going to ask for in general.  It

22  says in the ISA's to include material.  Maps, in

23  particular, will make it longer.  So, one of the

24  questions is, can we balance between annexes and have,

25  expand the ISA a little bit more, but add more of the

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1  annexes, too, and just a clarification if that's what

2  CASAC means when they say in the ISA, or it really mean

3  in the ISA.

4	DR. HENDERSON: Okay.  That's a very good

5  point, and if we say ISA, do we really mean the annex,

6  so.

7	DR. WYZGA: And Mary, if these could be

8  cross references to the annex, I think that would be

9  helpful, too.

10	DR. HENDERSON: We'll go on to question

11  two, because that is what James asked for, you think,

12  is that included in this answer to question two?

13	DR. POSTLETHWAIT: Actually, as a present

14  follow up to James' point, I'm wondering about this

15  issue about getting a little better handle on, first of

16  all, exposures.  I don't know what data is available,

17  but even if some relative analyses of speciation of NOx

18  could be included, just to give us a feel.  I mean if

19  NO2 is 95 percent of it, then the rest of it's fairly

20  trivial.  If it's 25 percent of it, then, you know,

21  there's certainly other issues to consider.  And, I

22  think those two things ought to be in the ISA, and not

23  in the annex, so the reader has that, sort of that,

24  visceral feel as he, as they continue on to the health

25  effects portions, et cetera.

Page 12

1  view.

2	So, my recommendation would be much the

3  opposite as, maybe, minimize this, say that monitoring

4  height could be important, but if they're going to

5  address it in the ISA, they should do it in a more

6  conclusive fashion, and look at more monitors where

7  this, where they could pick up this impact.

8	DR. HENDERSON: Okay, I know, Dale, you -

9  -

10	DR. HATTIS: Yeah, I want to slightly

11  disagree with the fact that that's over-emphasized.  I

12  think that's a critical component of the analysis that,

13  if anything, should be extended to an analysis of,

14  actually, what the biases are in, as-, you know, would

15  be, in assuming that the distribution of levels of the

16  existing monitoring sites are representative of outside

17  outdoor levels, because it does mean that you can't

18  really directly com-, without an analysis of that

19  problem, you cannot directly compare the levels

20  inferred from monitors with the, it helps you

21  reconcile,  to a degree that it's possible, the, any

22  concentration response relationships you infer from it,

23  the epidemiological data, with concentration in your

24  response you infer from things like the Australian

25  study and the indoor, other indoor studies, which are

Page 11

1	DR. HENDERSON: Present those, the two

2  points again, so I'll be sure and get them right.

3	DR. POSTLETHWAIT: Well, again, to

4  speciate NOx, whatever's available, and then the issue

5  of what we know about personal exposure, temporal

6  paradigms.

7	DR. HENDERSON: Okay, some of that may

8  not be available in any of the exploits, but we, and I

9  agree with you, then, by healing what you want.  Yes,

10  Ted.

11	DR. RUSSELL: If I might, and this, also,

12  is captured in response to question three.  There's the

13  discussion about the importance of the height of the

14  monitors that shows up both in the last, sort of,

15  section on the response here, as well as in, there's a

16  fairly large bullet in the next one.

17	There's, currently, a pretty large section in

18  the ISA on the impact of monitoring height, and I,

19  actually, found that was much larger than it should be,

20  and maybe even a red herring as such, in terms of how

21  it might be addressed in the ISA.  For one, there's a

22  lot of information out there where you could compare

23  the values between different height monitors, as

24  opposed to just looking at one special study where they

25  did it.  Which, I think, would, gives you a biased

Page 13

1  based on - -

2	DR. RUSSELL: But you now,  tremendously

3  larger impacts horizontally and spatially than

4  vertically, so I think that that's being blown out of

5  proportion, versus where you're placing a monitor close

6  to a road, or you know, four or five hundred meters

7  away from a road in a park, because that's where you're

8  going to have the bigger differences.

9	DR. HATTIS: Well, I think that's, also,

10  an important area, but this is a systematic error, you

11  know, and the other may well be much more - -

12	DR. RUSSELL: No, it's, they're both

13  systematic.

14	DR. HATTIS: The health studies are based

15  upon aggregate exposure, agg-, exposures within big

16  cities, okay.  And those includes both stuff near

17  roadways and not near roadways.  So, essentially, that

18  tends to be biased by the verticality, although, there

19  are, in fact, some sub-populations within cities that

20  are even more exposed, okay, because of their, you

21  know, proximity to roads.  So, I think that the

22  influences are different, even though there may be a

23  bigger overall number, ratio in the near roadway, far

24  roadway.  This other effect, really, is a substantial,

25  why, I say, now, I don't think that it's overemphasized

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1  in the existing document.  I would like to see a fuller

2  analysis of both kinds of effects.

3	DR. HENDERSON: I want to be sure I

4  understand what you're saying here.  What is the

5  difference, say, between, you know, vertically.  Does

6  Albuquerque have a different from San Diego, I mean,

7  they, is that what you're talking about, I mean?

8	DR. HATTIS: No, no, no.  This is a

9  matter of the fact that, the monitors for all the

10  cities are high.

11	DR. HENDERSON: Yeah, and people are

12  breathing down low.

13	DR. HATTIS: And people are breathing

14  down low, so that means that, systematically, the epi

15  studies are based upon concentrations that are

16  measured, that are underestimated.

17	DR. HENDERSON: And what is, what is the

18  difference, the degree of difference, I mean, that

19  you're taking?

20	DR. HATTIS: Well, I think that, that

21  from the, you know, the brief discussion that I

22  remember from the ISA, that that difference is two-,

23  three-fold.  But that's different heights of monitors.

24  If you go down to the ground level, it looks like, you

25  know, that could even be a larger factor.  The fact

Page 16

1  level, it's fairly sparse.

2	DR. HATTIS: Well, whatever the best

3  sources of information are to estimate the effect, you

4  know, they need to be used.  The fact of the matter is

5  that, the existing epidemiological studies are based

6  upon, what appear to be, biased measurements of the

7  concentrations people actually receive.  And,

8  therefore, they are not directly comparable with the

9  indoor measured concentrations that led to the

10  observations in the Australian study and in the, well,

11  Australian study.  So, that's a big problem that needs

12  to be addressed.

13	DR. LARSON: I'm unaware of any, or many

14  NO2 EPA monitors that are actually sited on top of it,

15  is that what we're talking about?  I don't think that's

16  true.

17	DR. GORDON: Well, it just seems that,

18  from this discussion, I'm agreeing with Ted, now,

19  'cause I thought there was a big verticality problem.

20  And if there is more data out there, this chapter

21  doesn't get that across to me.  It says there's a big

22  vertical problem, but they might be variable by site,

23  and that's not brought out.  So, maybe Ted's right.  It

24  should be condensed but expanded in other areas.  I

25  mean they both should be discussed.

Page 15

1  that it's a systematic, you know, biases of several

2  fold can have a big impact on what you might infer is a

3  level that was, you know, protective of public health.

4	DR. LARSON: This is Tim Larson.  I think

5  the EPA monitors are sited, in most cases, in such a

6  way that the inlet height biases are not capturing what

7  you're thinking about, which is the vertical

8  distribution in urban areas, primarily, in confined

9  urban areas.  And that, I agree, is a significant

10  gradient that can be threefold.  But, you're not going

11  to see that at most NO2 monitoring sites, because

12  their, the way their sited, they're, they tend to be in

13  open areas.  And the differences in heights of the

14  inlets in those are-, in those open areas just don't

15  capture the kinds of gradients of exposure that are

16  important.

17	So, doing an analysis of all the inlet

18  heights for all the NO2 monitors that EPA has isn't

19  going to really capture that.  And, unfortunately,

20  there's just not a lot of data on the vertical

21  distribution of the heights in the urban areas that are

22  systematically done.  We're doing a big study in New

23  York City right now, trying to capture some of that,

24  and there is some European data on this subject, but

25  compared to the data that's measured at or near street

Page 17

1	DR. HENDERSON: Well, I hear-, what I

2  hear people saying is that in urban areas, there may be

3  a difference in, there may be a problem with the siting

4  of the monitors, as far as the vertical differences in

5  concentrations with NO2, but we don't have much

6  information.  I hear people saying, we don't need them,

7  we don't know if that's true, so would you like, Dale,

8  in the letter to say that this is a potential problem?

9  That should be addressed.

10	DR. LARSON: There is some literature on

11  this.  I mean, if you could cite that, I, there, it's

12  just not a lot of it.

13	DR. HATTIS: Well, whatever the

14  literature is that's relevant to estimating the

15  population exposures, that are true versus the

16  population exposures that are estimated in the

17  epidemiological studies, that's relevant to judging the

18  levels at which you expect how many of X.

19	DR. HENDERSON: Sure.

20	DR. LARSON: But I think I'm on balance

21  on Ted's, come down on, with Ted on this.  I think

22  relative, the NO2 EPA monitors in urban areas, the

23  biggest gradients are horizontal.  And they're not

24  proximity to roadway per se.  They're, actually,

25  proximity to confined roadways, where you can get up

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1  factors of three to five times differences relative to

2  the same traffic, of the same distance from a road in

3  an unconfined location.  So, you're not talking about

4  twenty percent here.  You're talking about three to

5  five hundred percent differences.  And similarly,

6  factors two to three in the verticality at those

7  confined locations with height of, those are big

8  effects, none of which are being captured by any of

9  this.

10	DR. HENDERSON: For any epi studies,

11  there's always the problem of exposure.  I mean, we're

12  never happy with the exposure.  Now, and, I think this

13  is an example of some of the issues that come up.  I

14  think it should be mentioned in the letter.  As I

15  recall in reading through the document, it was

16  discussed quite a bit, but - -

17	DR. LARSON: Well, the inlet height

18  effect of the monitors is discussed, which I'm not sure

19  is the important parameter.

20	DR. HENDERSON: I think in the letter, we

21  do, we confirmed the fact that we are aware that the

22  exposures, there's always a problem with measuring

23  personal exposures in an epi study.

24	DR. HATTIS: Yeah, but this is not just

25  the usual problem.  This is not, the usual problem is a

Page 20

1  types of measurements that are used in some of the, you

2  know, the better direct studies establishing the

3  effects of the NO2.

4	DR. HENDERSON: To point out the

5  uncertainties associated with the other, go ahead,

6  George.

7	DR. THURSTON: Yeah, right, well, yeah, I

8  agree with that last part that the problem is when you

9  go to compare it to, like, indoor measurements and

10  those measurements.  But, it's not a problem with

11  regard to interpreting and the epidemiology, I think we

12  have to keep that clear, and applying it to for

13  standard setting.  Because, ultimately, you know,

14  you're applying the standards at the central site

15  monitors.

16	So, that's what you want to use in the

17  epidemiology, and the fact that, let's say, those

18  levels, let's say, they were fifty percent of what

19  people were actually exposed to, it, then you would

20  take all the numbers, double them, and then when you go

21  to set the standards, divide them by two.  I mean, it

22  would be a waste of time.

23	So, I think that it's a fact, but it's not a

24  problem that there are differences in the absolute

25  levels between what's at the central site monitor, and

Page 19

1  random error.  And we know how to deal with that.

2	DR. HENDERSON: I understand.  You're

3  saying that this is - -

4	DR. HATTIS: This is a systematic error.

5	DR. HENDERSON: - - systematic because

6  the, you think the inlets are consistently higher than

7  the level of - -

8	DR. HATTIS: Look it, all I know is what

9  I read in the ISA, and this seems to be, you know, what

10  the ISA seems to say.  And then I, sort of, believe

11  that they will have located the monitors at elevated

12  levels.  You know, maybe, and if it's not true, then

13  fine, you know, but.

14	DR. HENDERSON: Well, I, our charge is to

15  advise them on how to improve the ISA, and are you

16  saying you'd like the - -

17	DR. HATTIS: I'd like that, and I think

18  that if it's, you know, if the analysis, if the

19  statements in the ISA are correct, then, you know,

20  maybe they need to be modified with, including the

21  information from a larger literature base.  But, you

22  know, if they are, then it's worth an a-, worth some

23  much more quantitative analysis, because it creates a

24  serious difference between the types of measurements

25  that are used as the basis of the epi studies, and the

Page 21

1  what people experience on, at street level.  But, only,

2  the only place where I, you know, I think it is a

3  problem that I can think of, you know, I agree.

4	When you go, if we're going to put some

5  importance on these indoor studies, we ought to

6  remember that those concentrations are not directly

7  comparable to the central site concentrations.  And

8  that's, I think, the key that Dale brought out.

9	DR. WYZGA: And the clinical studies as

10  well.

11	DR. THURSTON: Yeah, and the clinical

12  studies as well, yeah, that's true.  Because the actual

13  concentrations associated with the NO2 exposures that

14  we measure at the central site monitors are, actually,

15  higher.  And so, that might explain some of the

16  differences that we see between the exposure studies,

17  the indoor studies, and the ambient results.  So, it,

18  yeah, so that's going to have some importance later on

19  in interpreting the results, so that is an important

20  point to bring up in that respect.

21	DR. HENDERSON: Yeah, I can see that- -

22	DR. HATTIS: A condition of the central,

23  there is always random error, addition, to effect, you

24  know, and that's also a problem to be analyzed, but.

25	DR. HENDERSON: Well, okay, I see the

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1  point that, George, that, you know, you just made, and

2  Dale, too, that there is, the, how something comparing

3  the clinical and the indoor dose response first to what

4  you may see in epidemiology.  That can be, I think,

5  clearly stated.  Yes, George, do you have - -

6	DR. THURSTON: I just have one separate

7  comment.  I guess it, I'm not sure if it goes on two or

8  three, but I think two, that I brought up something

9  that I, in my quick review, I don't see reflected with,

10  yesterday, which was that we need to, more clearly,

11  delineate the difference between personal exposures to

12  all NOx versus personal exposures to ambient NOx, and

13  their respective relationships to outdoor central site

14  monitors.  I didn't see that written in here anywhere,

15  and I did bring that up.  And I hope that that's

16  included.

17	DR. LARSON: Well, we had a bullet in

18  section three on trying to look at the alpha, I guess

19  I, the ratio of the outdoor to personal ambient.

20	DR. THURSTON: Is that what that bullet

21  means?

22	DR. LARSON: Yeah, alpha.

23	DR. THURSTON: I didn't get it.

24	DR. LARSON: Okay, we'll fix it.

25	DR. CRAPO: Could I ask a question for

Page 24

1  want to talk about that in the context of the ISA,

2  fine, or context of the other is fine, too.

3	DR. HENDERSON: Were you proposing that,

4  well, this would be quite a few individual comments,

5  but can you explain it to us what it's saying?

6	DR. HATTIS: Yeah.  What this, I need to

7  get it in front of me.  What this is, is, essentially,

8  plotting the, it is, basically, a lo-, what these are

9  called is log normal probability plots.  And,

10  essentially, what's being plotted is the Z score, which

11  is, essentially, the number of standard deviations that

12  each value represents in the distribution.

13	So, that, for example, the first data point

14  here is, generally, the first per-, is the one

15  percentile level.  The next is the, I think the five

16  percentile level, et cetera.

17	But, plotted on a probability scale, so that,

18  if, in fact, the date corresponded to a log normal

19  distribution, which is the usual expectation, then the

20  points would fall on the straight line.  The regression

21  equation in each case is an estimate of the, the

22  intercept is the log of the geometr-, it's an estimate

23  of the log of the geometric mean, and the slope is the,

24  an estimate of the log of the geometric standard

25  deviation, okay.

Page 23

1  clarification as I listened to the conversation.  When

2  we get an average annual level expressed for us, is

3  that what, is that the average over the whole 24-hour

4  day, then averaged annually.  Or is that the high for

5  the day averaged annually.  Are we talking about - -

6	SPEAKER: Everything.

7	DR. CRAPO: - - everything averaged

8  together, so when NO2's have the peaks during the

9  traffic periods of the day, and it goes down very low

10  at night, you're taking these high levels that occur

11  during the day and averaging it out with twelve to

12  twenty hours with, of low levels and getting a fairly

13  low level out of it.  That's, so, we need a lot more

14  information about the peak, 'cause, probably, the

15  average annual is about the last thing we want to look

16  at to assess this st-, this substance.

17	DR. HENDERSON: You know, I think, that's

18  what I have written down for your, what I wrote down

19  for this.  And we need to remember about the pattern.

20	DR. HATTIS: I've made a series of plots,

21  actually, of the distributions of, for different

22  average-, of NO2 levels for different averaging times

23  from the existing data in one of the annex tables.

24  And, so, we can talk about that later.  Yeah, that's

25  the, yeah, that's the graph, so, essentially, so if you

Page 25

1	So, essentially, these, so these, if these

2  log transformed values were normally distributed, they

3  should fall more or less on the line, and they more or

4  less do.  They are not perfect log normal

5  distributions.  In fact, the actual data have, don't

6  have as fat a, in the tails as they should for a

7  perfect log normal.  But, essentially, what this does

8  is to show the change in the slope is, means,

9  essentially, the longer averaging time or, you know,

10  more tightly distributive than the shorter averaging

11  time.  So, the shorter the averaging time that you

12  take, the data are further spread out, just because of

13  regression of the mean effects.  And this says how,

14  how, what?

15	DR. HENDERSON: I mean that's what you

16  need said, isn't it?

17	DR. HATTIS: Yes, and this, basically,

18  quantifies how much less the dispersed the lo-, the

19  yearly and three averages are relative to the one-hour

20  averages.

21	DR. HENDERSON: And that's what James is

22  saying, that they didn't give us much information, I

23  mean, yes.

24	DR. CRAPO: So, let me just ask a real

25  practical question from a real simple mind.  How many,

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Page 26

1  if I, and instead of doing the average annual and

2  saying that was fifteen parts per billion, what would

3  be, if I took the highest one hour from each day, would

4  that be two hundred parts per billion?

5	DR. HATTIS: Those data are in the table,

6  and I didn't plot them.

7	SPEAKER: Actually, they're in the ISA,

8  too.

9	SPEAKER: They're in the hot spot.

10	DR. CRAPO: Right, so what's the answer?

11	SPEAKER: 201.

12  (WHEREUPON, there was a discussion off the record.)

13	DR. CRAPO: Did I guess, I guessed it

14  right on the money?

15	SPEAKER: Yes.

16	DR. HENDERSON: You get a gold star this

17  morning.

18	DR. CRAPO: And the excursion, the high

19  end excursion is from that?  Do we have a significant

20  if the population is exposed 500 ppd?

21	SPEAKER: No, that was an excursion.

22	DR. CRAPO: That is an excursion, I was,

23  that is the excursion, okay.

24	DR. HENDERSON: Well, okay, Ed, go ahead.

25	DR. POSTLETHWAIT: Well, if there are

Page 28

1  proportionally more while I'm breathing more.

2	DR. CRAPO: Ted has just pointed to me

3  that the 200 ppb that we were talking about is probably

4  at fifteen feet up and not at ground level, so that the

5  ground level might twice that level.  What?

6	DR. LARSON: Ron, wait, no way, no way.

7	DR. RUSSELL: More likely at four meters,

8  aren't more of your monitors at four meters than - -

9  (WHEREUPON, there was a discussion off the record.)

10	DR. LARSON: Those kinds of gradients

11  don't exist.

12	SPEAKER: What?

13	DR. CRAPO: You say gradients of that

14  nature don't exist?

15	DR. LARSON: Not that, I mean, not that

16  strong a gradient over three meters.

17	DR. PINTO: Yeah, no, I think you're

18  right, I mean.  I think what I was trying to say was,

19  no, this particular data point, okay, where it was a

20  change in Lakewood, California, downtown Los Angeles,

21  in other words, and is one of the roadside monitors, so

22  you would expect it a, first of all to be very hot; b,

23  you would also expect the inlet to be at, you know, the

24  standard there, at the standard height, which of the

25  order of three meters or so.

Page 27

1  estimates made of personal exposures, won't that

2  capture that issue, as opposed to, when we compare data

3  back just to annual averages, which gets back to the

4  central issue of how much stuff are people really

5  inhaling, versus, you know, what's the average floating

6  around.

7	DR. HATTIS: Not exactly, because it

8  depends upon, on the averaging time for the personal

9  exposures, where you also will have a similar - -

10	DR. POSTLETHWAIT: Well, that's where,

11  that's where temporal plot, if it was possible, would

12  be really useful, even from a qualitative standpoint.

13	DR. HATTIS: Yeah.  But essentially,

14  you'd have to have comparable, you know, different

15  lengths of time averages to be able to compare.  And I,

16  offhand, I don't know whether the internal, the indoor

17  exposures are more variable with time than the outdoor.

18  So, you can have a different, you could have different

19  comparability depending upon the, you know, how, what

20  that looks like.

21	I mean, there's, also, a likely case that the

22  indoor exposures will be correlated with differences in

23  breathing rate.  So, for example, it may well be that

24  while I'm up and about, one of the things I'm doing is

25  cooking on my gas stove, and exposing myself to

Page 29

1	DR. CRAPO: The reason I'm bringing this

2  up is that I think those of us that are really focusing

3  on the health effects are not even in our heads not

4  even correlated to the right thing.  And we're sitting

5  here looking at the ambient levels and thinking 15 ppb

6  average annual, and we're seeing health effects in

7  asthmatics and people living near roadsides.  When, in

8  fact, the people near the roadsides are getting 200

9  ppb.  And our correlation, all these correlation

10  coefficients on the things that we're looking at are,

11  at least, I'm not sure that because we've used a, such

12  a bad metric to correlate what's going on, I don't

13  think that we're thinking correctly on the health

14  effects side.

15	DR. HENDERSON: I think one thing we can

16  emphasize in our letter is the importance of the

17  temporal and spatial variability in the NOx exposures,

18  and how that will vary.

19	DR. CRAPO: Because this makes our

20  biological plausibility, the discussion yesterday,

21  change directions completely.  It puts us, it, we were

22  arguing that we weren't exposing enough to NO2 to get

23  the level.  If these things, if these exposure metrics

24  change, then our whole argument yesterday, the

25  biological plausibility is met, becomes much more

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Page 30

1  likely.

2	DR. RUSSELL: No, maybe Jill wants to go

3  into this further.  I mean, again, the high monitor is

4  Lakewood in downtown Los Angeles.  It's a roadside

5  monitor, so it's going to be high.  You know, actually,

6  some of these monitors are sitting really near

7  freeways.

8	DR. CRAPO: Well, so am I.

9	DR. RUSSELL: Right, but what I'm saying

10  is that, keep in mind, when you're talking about, these

11  monitors, many of these monitors are capturing very

12  much the highest levels that you're going to get,

13  except in a very confined street canyon.

14	DR. CRAPO: Okay, and that's what I'm

15  thinking, is that the high levels that are causing the

16  disease that we're seeing, and we're not understanding

17  who's got that high level, and where it is, and why.

18  As well as, at least, the medical side of us are,

19  because we're not dealing with the numbers in the form.

20  So, I'm just wondering if the, if this is, a large part

21  of our discussion yesterday wasn't confounded by some

22  of us not quite understanding the exposure levels that

23  our sub-populations were being exposed to.  And, you

24  know, the fact that your, having those, no NO2 all

25  night long is irrelevant to the fact that you get up in

Page 32

1  you were, had actually got, a see-, cumulative

2  distribution function, that those are the ones you'd

3  see at the upper tail.  So, I think we are capturing

4  those.  And, actually, in response to your question

5  about the biologic plausibility is, I think it goes

6  both ways, is that in many cases, I think we might be

7  looking at overestimates of what the potential exposure

8  to NO2 is in a general population.  Because a lot of

9  people live out in the suburbs, and you know, again,

10  I'm sort of parochial in knowing at Atlanta, is that,

11  we've got more monitors near busy areas, than we do

12  sort of in the general suburbs.

13	DR. HENDERSON: I, well, again, I think

14  maybe we can cover this by a paragraph discussing the

15  importance of the temporal and spatial variability of

16  the pollutants and this is not special to NOx.  It's

17  always a problem, and that we, that this should be

18  emphasized to discuss in the ISA.  And it is true that

19  we'll extend, but I don't hear anything that's, that

20  couldn't be covered under the importance of temporal

21  and spatial variability, and the, what we listed, as

22  far as monitoring and determining exposures that we, we

23  had discussed this yesterday afternoon, there's the,

24  you know, you have the indoor outdoor exposures, the

25  spatial and temporal variability, the siting of the

Page 31

1  the morning and get a big dose from 8:00 a.m. to 12:00

2  noon or whatever.

3	DR. BALMES: This is John Balmes.  I have

4  to, I need a clarification.  I thought I heard Tim

5  Larson say that most of the site, and I don't have any

6  map in front of me here on the phone.  I heard Tim

7  Larson say that most of the regular monitoring sites

8  are not, they're in open areas and are not necessarily

9  near freeways.  But I just heard that a lot of the

10  monitors are by freeways.  That makes a big difference

11  to me.

12	DR. LARSON: Not a lot of them.  Some of

13  them are, but not a lot of them.

14	DR. BALMES: Right, I think that's

15  important to know.

16	DR. LARSON: Most of them are not.

17	DR. BALMES: Yes.  That was my

18  understanding, too.

19	DR. RUSSELL: Yeah, so I misspoke when I

20  said a lot, but you do have a representative population

21  of ones that are near freeways.

22	DR. BALMES: Right.

23	DR. RUSSELL: And those are the ones, or

24  very heavily traffic roads, and those are the ones that

25  you do see on the one extreme of our population.  If

Page 33

1  monitors, all of that is something that we've already

2  said is very important.  So, I would like to just

3  summarize that in a paragraph in the letter, and

4  emphasize how the differences between the more precise

5  measurement indoor in the clinical studies, and, as

6  opposed to outdoor ambient studies.

7	Does that, would that co-, I mean, we've,

8  you're absolutely ri-, and if you don't have the

9  correct exposure, the response then is, it can't be

10  related to the amount of, precisely  towards lead and,

11  but that stands, that's always a problem with epi

12  studies.  They don't have it for very long exposures.

13	DR. AVOL: Just one small point of

14  information, I think what Joe meant was Lynwood,

15  California not Lakewood.  The Lynwood station is

16  alongside the Long Beach Freeway, and gets several

17  hundred thousand vehicles a day.

18	SPEAKER: Yeah, thanks, Ed.

19	DR. LARSON: Well, as my comments

20  yesterday, and you know, at each of those, you know,

21  two sites, there is a information in the database on

22  distance from major roads.  And you could compile that

23  fairly easily, and probably, compare that with the

24  population, U.S. population at large.

25	DR. HATTIS: I think that'd be a good

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Page 34

1  thing to do to try to see what biases one should expect

2  and what, you know, how do we characterize the

3  variability and the likely exposures in relation to the

4  variability that we see in the monitors.

5	DR. HENDERSON: Is that something, Mary,

6  that could be done?

7	DR. ROSS: We can look into it.

8	DR. PINTO: I mean, perhaps, with help

9  from the program offices, I mean, I tend to think that

10  that sort of effort if, you know, if done well, I mean,

11  could take a bit of time and maybe, even, longer.  I'm

12  thinking in terms of longer than the time scale for

13  setting the next draft to come out.  But we'd have to

14  look into that, Rogene.

15	DR. HENDERSON: Okay, well, let's, I

16  think we've had a good discussion of this issue, which

17  is a, certainly, an important one.  Can we look now

18  beyond the first three charge questions to going to the

19  health, unless there's anybody else has something else

20  on the first three charge questions.  The next four

21  charge questions relate to the health effects.  And,

22  was there, were there things that were left out or

23  that, yes, Ed.

24	DR. POSTLETHWAIT: As part of the charge

25  four things, and this just may be simply an issue of

Page 36

1  Balmes, again.  I think the last sentence in the bullet

2  here, is, contains key information about that the ISA

3  would be improved if a plan or process for integration

4  and study selection is clearly laid out.  So, that it

5  would be clear to some, to a reader, such as Ed, why

6  studies were included.

7	DR. HENDERSON: That's a good point.

8  Yeah.  Are there other things?

9	DR. WYZGA: Rogene, I had a couple of

10  things on five, but.

11	DR. HENDERSON: Okay, Ron, and then

12  Joyce, go ahead.

13	DR. WYZGA: Okay.  I guess, first of all,

14  I'm flattered that my name is mentioned, but I would

15  also mention that John, in number five, John Balmes

16  mentioned some toxicological studies that weren't

17  included.  And I would change the wording to say that,

18  instead of several of the latest NOx human field

19  studies is, basically, several recent epidemiological

20  studies that examine the association between health

21  outcomes and NO2, were, either, not included nor

22  studied correctly, and say, especially, in describing

23  the impacts of other pollutants on the NO2 health

24  associations.

25	DR. HENDERSON: Certainly, and nobody's

Page 35

1  verbiage.  On that third line, where it says only the

2  key studies that support an NAAQS should be included.

3  I wasn't sure what that meant, in terms of, to support

4  what we have now; to support a new one, I mean.  And

5  when you read that, it almost sounds like you, as we

6  discussed yesterday, you could, inadvertently,

7  introduce selection bias on what studies you were

8  reporting, positive versus negative.

9	DR. HENDERSON: Well, this still is from

10  the, has a little history behind it.  And that's what

11  I, how I interpret it.  If you looked at the CD, it

12  includes everything from, you know, a 500 ppm exposure

13  of a toad frog to, you know, something at ambient

14  levels.  And you're right.  How do you choose the key

15  studies.  But I think the meaning of this statement is

16  that, that chapter three could be condensed to even

17  more to make it less like a CD, and more, just includes

18  studies that are relevant for setting a standard.  I

19  think that's the meaning of it, but you're bringing up

20  a problem which we have discussed, CASAC has discussed,

21  and who chooses, you know.  But we came down that it

22  was more beneficial for us doing this review to have

23  the Agency choose what they felt were the key relevant

24  studies.

25	DR. BALMES: But that, this is John

Page 37

1  saying it's going to be mentioned in here, I mean.

2	DR. WYZGA: Okay.

3	DR. HENDERSON: You know, I mean, as I

4  said, I mean, this will not be covered - -

5	DR. WYZGA: But, I guess, part of it is,

6  it's broader than simply the epidemiological is because

7  there's some toxicological studies as well.

8	DR. HENDERSON: Okay, yeah, okay.  And,

9  is that ment-, it's a tox study, yeah, Balmes, oh,

10  yeah.  No, we, it's mentioned there.  Sure, Ron, never

11  in my wildest dreams would I mention names.

12	DR. COTE: This is an opportunity,

13  though, for me to ask people if you, if there are

14  specific papers that you're aware of that we don't

15  have, please give us the references.  Because, you

16  know, we've done this careful lit search, for whatever

17  reason those papers have not popped up.  So, you know,

18  if it's a flaw in the keywords or whatever, so please

19  help us by giving us the specific references rather

20  than.

21	DR. BALMES: So, I will include, this is

22  John Balmes.  I'll include the ones that I referred to

23  yesterday in my written comments.  But the nitrogen

24  dioxide will get the one paper published in 2005.  You

25  don't have to get fancy with the keywords.

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Page 38

1	DR. COTE: Thank you.

2	DR. HENDERSON: Okay, so, Ron and John

3  will provide, you will provide those in your written

4  individual comments.  Then that, then in the letter, we

5  can refer to it.  We can, see individual comments of,

6  with them, okay.  Anything about question six that

7  people have problems with or would like to add.

8	DR. THURSTON: Well, as to the question

9  five.

10	DR. HENDERSON: You back to five, okay.

11	DR. THURSTON: Yeah, well, I mean,

12  actually, the reason I put Ron's name in there was to,

13  so that I knew he would respond to that and clarify

14  that sentence with it.  I figured that, otherwise, he

15  might get ignored and he would make sure it was

16  correct.  So, we could just write members also pointed

17  out, or something, instead of put, naming names here.

18  The other thing is, in the iterations, I don't know,

19  either I didn't have it in the beginning, or it got

20  left out or something, but I would add at the, in the

21  last sentence, just, well, I'm just going to get this,

22  finally, examining the epidemiology results, and I

23  would say, after results, add the words across outcomes

24  as a function of.  Because, the whole idea was to look,

25  not just individually, but look across outcomes and

Page 40

1  you say that yesterday?

2	DR. SHEPPARD: I don't think I was the

3  one that brought that up.

4	DR. WYZGA: Okay.

5	DR. SHEPPARD: Probably is an important

6  point.

7	DR. HENDERSON: Okay, are there more

8  comments on the substance of answers to question five?

9  Go on to six, then.

10	DR. AVOL: I have a question on six.

11  This Ed Avol.  My question is this.  About seven lines

12  in, there's a comment about sensitive populations.

13  There's no comment about genetic susceptibility in

14  that, and I just have a question for whoever wrote

15  this, if that was a conscious exclusion because they

16  don't believe it's sufficient - -

17	DR. CRAPO: It wasn't conscious.  It was

18  late at night in the middle of a bad Rockies game.

19	SPEAKER: That was a good game.

20	DR. CRAPO: So, let's add that, let's

21  just add that.

22	DR. HENDERSON: So, what line, at what

23  line, yeah, where is it, what line is it, that - -

24	DR. AVOL: It's about seven lines down,

25  the last just in, I'm sorry, there's evidence of

Page 39

1  look for coherence.  That's it.

2	DR. HENDERSON: Okay, and I will remind

3  you, as far as wordsmithing, when we finish here this

4  morning, Angela and I will be drafting the actual

5  letter, based on the substance of these comments.  And

6  you will be receiving it for concurrence and review.

7  So, small wordsmithing, you can take care of at that

8  point if you want.  Can we go on to charge question

9  six, then?

10	DR. WYZGA: One, on question five.

11	DR. HENDERSON: Five, I'm still on five.

12	DR. WYZGA: And, is Lianne on the phone?

13	DR. HENDERSON: Lianne wasn't coming on

14  till when, 9:00.  What's Angela's time.

15	DR. NUGENT: Rogene?

16	DR. HENDERSON: Yes.

17	DR. NUGENT: Is Lianne on the phone?  She

18  said she would be on the phone.

19	DR. SHEPPARD: Yeah, I'm here.

20	DR. WYZGA: Okay, Lianne, this is Ron

21  Wyzga.  You said something yesterday, number five,

22  something about, and I wanted to see if I could capture

23  it, about looking more systematically or in a better

24  organized way at the, how one deals with co-pollutants

25  and interpret studies using co-pollutants.   Did I hear

Page 41

1  adverse health effects in sensitive populations such

2  as.

3	DR. CRAPO: And how would you say that,

4  though.  The only ones that have really been studied

5  are the ones that are mentioned here, really.  I mean,

6  genetic is a theoretic thing, but there's no hard study

7  that says this is a gene that creates susceptibility to

8  NO2.

9	DR. HENDERSON: You could add a sentence

10  - -

11	DR. CRAPO: I mean, I believe it's true.

12  I just don't think, I can't think of a study that would

13  prove it.

14	DR. HENDERSON: You could add a sentence

15  saying, genetic polymorphisms may also influence the

16  response.

17	DR. AVOL: I mean, there is some

18  published information from our lab and others on GST,

19  and the sensitive to oxidative stress mechanistic

20  pathways.

21	DR. HENDERSON: We can put into the,

22  genetically perception.

23	DR. POSTLETHWAIT: Will that fall under,

24  stuff under question seven.  I mean, does, six and

25  seven are, essentially, addressing the same chapter in

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Page 42

1  the ISA.  And there is this issue of defining

2  susceptible populations.

3	DR. AVOL: Yeah, that's, I mean, I think

4  that's fine.  I'd be happy to put it into seven.  I

5  just pointed it out there, because it seemed like it

6  was - -

7	DR. POSTLETHWAIT: Right, yeah, I mean,

8  this becomes redundant, just like, you know, I said

9  it's redundant.

10	DR. HENDERSON: Okay, I noted that that

11  should be mentioned.  Are there other things for six or

12  seven?

13	DR. RUSSELL: Rogene, before going on,

14  I'm actually curious.  On the last sentence, that, I

15  mean, to me that's a rather important sentence.

16	DR. HENDERSON: Which question are you -

17  -

18	DR. RUSSELL: Oh, six.  That we concur on

19  the findings and, et cetera, directly result in adverse

20  impacts.  And this comes, you know, I was sitting here

21  a little uncomfortably yesterday about the use of the

22  word likely causal when we, they say the strongest new

23  evidence comes from epidemiologic studies of ED visits

24  and hospitalization.  And I'm an air quality person, so

25  I, the medical end is somewhat beyond me, but,

Page 44

1  whether, in verbiage that, while it may not be the

2  chemical species NO2, per se, certainly, there's a

3  linkage between NO2 in the air and all the other

4  goodies and these adverse health outcomes.

5	DR. CRAPO: I don't remember exactly what

6  I said.  I can tell you that I, last night, I

7  deliberately wrote this sentence very strong, 'cause I

8  wanted to make us talk about it.  I think we have to

9  decide, I mean, this is, I think, the heart of the

10  paper right here in that one sentence.  It tell them

11  whether we really agree or don't agree with the

12  fundamental conclusion of the document.  The, when I

13  get, at the end of the day, I'm impressed that the,

14  it's not, we have to cite the few studies that were

15  negative; but in fact, this is a, it's a ten to one

16  vote in favor of positive, but it's not an equal, half

17  were positive and half were negative.

18	These are, the most of the studies that come

19  out are showing strong effects.  And I do think that

20  it's likely the effects are tracking primarily the

21  products of combustion, which the paragraph says.  The,

22  but the, but there are, overwhelmingly, strong data

23  showing an association that we haven't really dealt

24  with.  And I'm concerned that the biggest problem is in

25  our exposure metric.  I think that our correlation

Page 43

1  recognizing that the epi studies that we've talked

2  about the problems with the monitoring and the spatial

3  variability.  There are some that find associations.

4  There's others that don't.  And, it almost struck me

5  that, I was sitting here going, the strongest new

6  evidence, and you have some studies that go the other

7  direction, and I recognize EPA was, sort of, sitting on

8  the fence on this one, too.  Directly result may just

9  overstate how I think I feel on this.  And I'm

10  wondering how others feel, too.

11	DR. HENDERSON: I think that's a strong

12  statement considering our discussion.  I agree with

13  you.  I don't find, I think we're all trying to figure

14  out is there something here or not, and - -

15	DR. SHEPPARD: Yeah, I agree as well.  I

16  think that's pretty strong.

17	DR. AVOL: I think, in fact, that

18  yesterday in the discussion, John Samet challenged the

19  consistent coherent issue.

20	DR. POSTLETHWAIT: James, yesterday, you

21  and I were talking, and you came up with a really great

22  multi-word descriptor, you know, that might soften this

23  a bit.  And I'm trying to remember what you said.  It

24  was something about, you know, NO2 appears to be a key

25  player, I mean, you said it better than that.  And

Page 45

1  needs with, needs to be with the highest one-hour

2  average.

3	Not, like ozone was before it changed to an

4  eight hour averaging time.  And if we converted all of

5  our data to one-hour averaging time, we might have a

6  lot more confidence in this conclusion.  But I don't,

7  but I can't walk away from the strength of the data

8  that's summarized in the ISA.  It's a very strong

9  document with studies from every dimension from every,

10  from lots of different countries, consistently finding

11  associations with products of combustion that metric

12  was within all.

13	DR. BALMES: So, the, this is John

14  Balmes.  I agree with you, Jim, James, that the

15  epidemiologic data taken as a whole from a

16  stratospheric level are pretty impressive.  My problem

17  is that I don't think the coherence is, necessarily,

18  there with the toxicologic data.  We talked about that

19  yesterday.  And I don't, actually, personally, have a

20  problem with the Agency moving ahead with a new

21  standard if that's the ultimate outcome, based on

22  epidemiologic data.  I do epidemiology.

23	I appreciate its value.  But I think it's, I

24  don't think the toxicology is really there to support

25  the epidemiologic findings.  And it's often that

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Page 46

1  toxicology is behind epi.

2	So, I think we should recognize that, I mean,

3  if we have to say that.  Because, otherwise, people

4  will criticize the document for not, sort of, fairly

5  representing the literature.  And I think, with regard

6  to respiratory infection risk, I think the toxicology

7  is there.

8	But I don't think that we understand why NO2

9  causes, or is associated with a kind of lung function

10  decrements that the children's health study found.  I

11  think that's a very important finding that should be

12  very strongly emphasized in the document.  But I don't,

13  I, certainly, don't understand how that occurs.

14	DR. CRAPO: Would you say the toxicology

15  does support it if we're speaking about 200 ppb instead

16  of 15 ppb?

17	DR. BALMES: Uh - -

18	DR. CRAPO: 'Cause I've changed my mind

19  on that one.

20	DR. BALMES: Well, I think that's a

21  greyer area, but I'm not sure that 200 ppb, the

22  toxicology supports 200 ppb.

23	DR. LARSON: James, Tim Larson, again.

24  15 ppb is your annual average.  The 200 ppb is your

25  one-hour max.  So - -

Page 48

1	DR. LARSON: I'm not disagreeing with

2  your general conclusion, but I'm just saying, to be

3  more precise, those epidemiology studies are probably

4  looking at 24 hour time series.  And those 24 hour

5  averages are certainly at a max greater than 15 ppb.

6	DR. CRAPO: Yeah, and I'm, but I'm also

7  saying that is a, I think that NO is not driven, NO's

8  health effects are not driven by the daily average.

9  That's probably driven by the peak, and - -

10	DR. LARSON: Right, but - -

11	DR. CRAPO: - - and the, and we never

12  looked at the peak in terms of comparison of.

13	DR. LARSON: Right, because a relevant

14  comparison would be the 24 hour versus daily max hourly

15  average.  Because the type, and the epi are based,

16  primarily, I believe, on the 24 hour, but I'm just

17  saying, those are the two numbers to compare.

18	DR. CRAPO: Well, it is except that we're

19  looking at fairly profound health effects, and, I mean,

20  in many of these studies, and - -

21	DR. LARSON: Well, and I'm agreeing with

22  you.  I'm just saying that the change from one day to

23  the next is greater that 15 ppb.  And, you know, in

24  some cases, the one-hour max could be several hundred,

25  and the change from one hour to the next could be

Page 47

1	DR. CRAPO: Well, that's one-hour max in

2  monitors on certain places.  It's not the one-hour

3  personal max.

4	DR. LARSON: Right, but what's the, what

5  is the annual average at that monitor.  I mean, that,

6  in terms of, if there isn't, I mean, there's two things

7  going on here.  One of them is spatial, you know,

8  proximity to roads, et cetera.  The other one is the

9  annual average versus the one-hour average.  Both cause

10  differences in these numbers.  But, when you say 200

11  versus 15, one's a chronic exposure and one of them's

12  acute exposure.

13	DR. CRAPO: Well, I know that, but the

14  toxicology's almost all acute.  And the peaks are

15  acute.  And I, see, yesterday, I was sitting here

16  thinking about the 15 ppb and saying, I've got an order

17  of magnitude or two orders of magnitude difference in

18  my toxicology and my epidemiology.  But, in fact, I

19  don't.  It's, they're coming together.  The lowest

20  threshold effects for NO are, you know, are in some, a

21  few hundred ppb.  We saw that yesterday, where they

22  looked at the lower limits of toxicology having

23  effects.  And now, we've got peak levels at fifteen

24  feet up in the atmosphere, in certain locations,

25  pushing the same levels.

Page 49

1  fairly large, too.  So, I mean, the 15 ppb, it seems

2  like, is, it's not even in the range of what we're

3  talking about.  I mean, that's an annual average, and

4  it just gets washed out, as you say, by all the

5  seasonally flow seasons and all the midnights and

6  everything else, so.

7	DR. AVOL: This is Ed Avol.  Not to go

8  back to discussion of the health effects, but since the

9  lung function changes in the children health study we

10  brought up, let me just point out one perspective.  And

11  that is that in, of course, in looking at lung function

12  growths or decrements in lung function growth among

13  children, we're looking at long-term changes of

14  children that are moving around their communities, and

15  we're looking at those annual averages from those

16  central site monitors in those areas.  And so, while it

17  may be true that close to roadways or at traffic peaks,

18  there are several hundred parts per billion

19  concentrations, in fact, our relationships with those

20  changes in lung function are with the annual average.

21	DR. CRAPO: Well, I understand that

22  factor.  I'm just hypothesizing, I mean, I'm saying

23  that the health effects appear to be real.  And I,

24  biologically, couldn't explain them with the annual

25  average, but then it occurs to me that what's likely

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Page 50

1  happening, maybe I only need to hit my kid with 200 ppb

2  once a week in order to cause adverse changes in his

3  growth of his lung.  And I take him on my freeway for

4  three or four hours a week while I'm driving various

5  places.  So, it could be that that's the problem, and

6  we have-, but my point is, we haven't even analyzed it

7  that way.

8	DR. LARSON: Right.

9	DR. HENDERSON: Well, there is no - -

10	DR. CRAPO: But the health effects are

11  real.  That's what this sentence says.  The health

12  effects are real.  I don't know why yet, but I, there,

13  and it might not, and it might be a surrogate, but

14  they're, but they are so uniform across so many

15  studies, that we have to take them serious.

16	DR. HENDERSON: Now, as far as - -

17	DR. BALMES: This is John Balmes.  I

18  agree with that.  It's, but I, so the, the coherence in

19  the epi, I have, I'm comfortable with.  It's, if people

20  are assuming from that statement that we mean coherence

21  with the toxicology, I don't think we're really there

22  yet.  That's all I'm trying to say.

23	DR. THURSTON: Could I say?

24	DR. HENDERSON: George?

25	DR. THURSTON: Yeah, I don't really think

Page 52

1  supports that, too.

2	DR. CRAPO: Well, I'll say it, 'cause,

3  actually, I wrote it with, we said it several times

4  yesterday, but when, every time you do the study, you

5  find that there's an adverse health effect, which you

6  can link it, like, to the roadway, or to the children's

7  study with an open fuel on their furnace in the home,

8  the powerful correlations that go with this, the fact

9  the primary source of NOx is combustion.  So, it seemed

10  like an obvious to me.

11	DR. RUSSELL: Yeah, that one I have no

12  problems with.

13	DR. HENDERSON: I have no problems with

14  that, either.  I think that's a solid statement, but

15  George, would you repeat your modification of the last

16  - -

17	DR. THURSTON: Yes, I may have it here.

18  CASAC concurs that the epidemiologic findings indicate,

19  we'll see, that current ambient, is directly, no, are

20  associated with.  That's what epidemiology tells us,

21  associations.  Are associated with adverse impacts on

22  the public health, comma, but that the document needs

23  to better - -

24	SPEAKER: Articulate?

25	DR. THURSTON: Well, you could say the

Page 51

1  we're at with, we may end up where this last sentence

2  is, but I don't think we're there yet, in my opinion.

3  So, I mean, I would just say, concur that the

4  epidemiologic findings, you know, indicate, let me see.

5  I had it written down here, too.  Yeah, concurs that

6  the epidemiologic findings indicate that current

7  ambient NO2 exposures are associated with adverse

8  effects on the public health.  But the document needs

9  to better document, or better, you know, lay out the

10  plausibility, a consistency in coherence.  I think that

11  work, that needs to tightened up, and that's where we

12  ought to be focusing this next iteration.  I don't

13  think we're done yet, and this gives the impression

14  we're done.

15	DR. HENDERSON: That we're done.  No, I

16  would agree with that, and I'll let Mary talk on it.

17  Would you write down your modified sentence so that.

18	DR. ROSS: While you're on that subject,

19  I just want to draw your attention to a sentence a few

20  sentences earlier.  CASAC recognizes that the primary

21  associations are between products of combustion and

22  adverse health effects.  That's also a strong

23  conclusion that will have policy implications.  And

24  just wanted to make sure if that's something you agreed

25  with.  It's helpful if you provide why, you know, what

Page 53

1  ISA needs to, yeah, the ISA needs to better document

2  that these findings are plausible, consistent and

3  coherent with, now  do we want to say with toxicology

4  or something with other evidence?

5	DR. CRAPO: Well, to me, I would say, in

6  looking at lots of different medical kinds of issues, I

7  see more consistency of this data than anything,

8  virtually, anything that I make medical decisions on.

9  A lot of consistency across broad settings, where the

10  issue has been plausibility or coherence with the

11  toxicology.  And that was a dose issue.  It was not,

12  there's plenty of toxicology at high dose.  There's no

13  question about if you're talking about 10 ppb, I mean,

14  10 ppm, there's no question it correlates.  So, the

15  whole issue is, to me, the only issue is dose.

16	SPEAKER: Well, yeah, I mean, that is a

17  big - -

18	DR. THURSTON: Well, I just think it

19  needs to be better.  I think you're probably right.

20  There is, having read it, you know, there is a lot of

21  that evidence, but it hasn't been laid out in a way

22  that makes it obvious that where the coherencies are.

23	DR. BALMES: Well, one thing that might

24  be useful is to look at the relationship between these

25  one-hour peak exposures and the annual averages.

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Page 54

1	DR. HENDERSON: I thought that was done

2  in there, but I - -

3	DR. HATTIS: We do have direct evidence

4  in a table in the ISA on that point, that essentially,

5  the 99th percentile of the one-hour maximum is like 72

6  ppb.  It's not the highest is like 200, but that's the

7  highest of 288,000 measurements.  So, I mean, you're a

8  little bit far out on the scale there with the 200.

9  But, certainly, the 99th percentile is about, is 72

10  parts per billion whereas the 99th percentile, the one

11  hour of the yearly averages is 33 parts per billion.

12  So, you have a couple fold there, which gets a little

13  closer to the toxicology, but.

14	DR. HENDERSON: Mary?

15	DR. ROSS: You know, when we talk about -

16  -

17	DR. HATTIS: But that's again, for the

18  monitors that, some of them, which may be close to

19  roadways, but they're still a little high up, so it

20  may, may still be some additional distortions.

21	DR. HENDERSON: Mary?

22	DR. ROSS: We tried to evaluate the

23  short-term exposure studies that looked at different

24  indices, and there's a small discussion on page 5-5 of

25  24 hour studies versus one-hour max studies.  And they

Page 56

1  tended to look at NO2.

2	DR. CRAPO: Yeah, so I mean, you could

3  say it either way, but since they interconvert, you're

4  a little bit wondering what it really is you're.  I

5  mean, is the NO2 a surrogate for NO-, for all the other

6  species.  And so that's why I use them interchangeably,

7  without being very discretionary.  I knew, I need, you

8  should use the same term.

9	DR. HENDERSON: So, you're saying, I

10  mean, what you're suggesting, Ron, is that NOx can be a

11  significant factor?

12	DR. WYZGA: Yes.

13	DR. HENDERSON: Does anybody have an

14  objection, I mean, can we agree on can be?

15	DR. CRAWFORD-BROWN: Now, is that can be

16  in the sentence of can be under some circumstances?

17	DR. WYZGA: Well, we've avoided making

18  definitive conclusion in the last sentence, and we're

19  saying, you know, we're waiting for the document to,

20  basically, organize and, you know, give us a redraft.

21  And it seems to me to make that conclusion that it is,

22  it can be, and I think that's one of the things we're

23  waiting on, you know, the next round, to see whether or

24  not the document supports, you know, it is a

25  significant factor.

Page 55

1  don't find, there's not a lot of difference in the

2  epidemiologic.  Now, that is one-hour max on a given

3  day, but, you know, we did try to evaluate that, and

4  we'll look at if there are any further studies.

5	DR. HENDERSON: Okay, Ron?

6	DR. WYZGA: Rogene, I would say, I guess

7  in the spirit of what we said, if you look at the

8  previous sentence, we, basically, say NOx is a

9  significant factor, and I wonder, given what we said

10  later, if we could change the is to can be.

11	DR. HENDERSON: Yeah, I know, I see

12  (WHEREUPON, Dr. Henderson reviewed the document.)

13	DR. ROSS: And can I ask one more, I'm

14  sorry to keep bothering you but, when you say NOx, do

15  you mean NO2 or NOx, and it's one of the things we

16  battle with all the time is selecting the term.

17	DR. CRAPO: I use them  interchangeably,

18  because we did it yesterday.  I don't think we know,

19  exactly, what the species is, but NO2 seems to be a

20  good surrogate for it, so you could use NO2, but, in

21  fact, you're measuring the, you're measuring the, well,

22  you're using it as a surrogate for NOx, so probably, I

23  think NOx is your better term, because you don't really

24  know it's NO2, do you?

25	DR. WYZGA: Except the studies have

Page 57

1	DR. HENDERSON: Yes, that's the sense

2  that I understood.  Okay, did we, for the NOx issue, we

3  decided to keep the same term.  What did you decide on

4  the - -

5	DR. CRAPO: I like NOx better, because it

6  - -

7	DR. KENSKI: I actually would prefer NO2

8  in the, you know, all of the epi stuff is based on NO2

9  measurements, and the tox stuff is NO2 measurements,

10  and you know, yes, they are, they do interconvert, but

11  you know, the peak, peak, I mean, you know, what we

12  measure as NOx is, what we measure as NO2 is, you know,

13  the difference between NOx and NO-, so I, I don't know.

14  I just think it's better to be consistent and keep

15  that, you know, link with NO2.

16	DR. HENDERSON: The toxicity data is

17  based on NO2, I mean.

18	DR. KENSKI: Right.

19	DR. HENDERSON: Yeah, I mean, the

20  clinical and the - -

21	DR. KENSKI: And what's repor-, and

22  what's reported, granted, it's not, you know,

23  absolutely pure, you know, true NO2, but it's as close

24  to it - -

25	DR. CRAPO: Well, I wouldn't be, I'd be

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Page 58

1  happy to accept either one, as long as that, someplace

2  in it, you defined that three was interconversion and

3  that NO2 is as, is a critical species in the sequence.

4  So, you just make, as long as you define what you're

5  using, that's fine to use the other term, as far as I'm

6  concerned.

7	DR. KENSKI: It just might be good to add

8  a sentence, you know, up front saying that, you know,

9  we acknowledge that, you know, the NO2 that we measure

10  is not, you know, true a hundred percent - -

11	DR. WYZGA: But I think the other thing

12  is that, that we use NO2 with the relationship between

13  NO2 and the other components of NOx may change

14  temporally and spatially, and we don't really have

15  enough evidence to say that it's consistent.  And if

16  that relationship were consistent, then, I think, we

17  could jump to NOx, but it's not consistent.

18	DR. KENSKI: Right, and we're asking for

19  a better, you know, definition of some of those.

20	DR. HENDERSON: Can we go on to seven and

21  eight.  I put in on seven about the genetics.  I

22  thought, I don't know who wrote eight, but I thought

23  that was well written.  It was very clearly written.

24  Somebody wrote that.  It's Doug.  Oh, we, we'll get a

25  my kudos to Doug.  I thought that was well written.

Page 60

1  inherently increased exposure represent susceptibility.

2	DR. HENDERSON: Oh, okay, or   whether it

3  goes in the exposure.

4	DR. COTE: Just as a point of

5  clarification on that.  We tend to talk about

6  susceptible and vulnerable populations, and susceptible

7  is a more innate quality.  And vulnerable being people

8  at increased risk, or individuals at increased risk for

9  some not intrinsic attribute.  So, exposure would be

10  increased vulnerability.

11	DR. POSTLETHWAIT: Then the first bullet

12  needs to be changed to incorporate, not only defining

13  susceptible, but defining vulnerable.  And then, depend

14  upon what the panel feels, you can leave the high

15  exposure in there, or not.

16	DR. HENDERSON: Okay, I see, you, there

17  is the, the people near the roadway are vulnerable

18  because of the high exposure.  That makes sense.  I,

19  and that's what the question asks, susceptible or

20  vulnerable.

21	DR. ROSS: And to expand on that, the

22  vulnerable population includes the two sub-categories,

23  other than the biological, the socio-economic and the

24  geographic were, generally, extrinsically sensitive.

25  So, we could split that vulnerability up into two

Page 59

1  The, we've talked about the multi-pollutant aspects,

2  and I'm, hope-, I think Ellis, probably, you

3  contributed that.  And, that will be, can be worked

4  into the letter as a major point that, you know, after

5  all our discussions, we still have this problem of the

6  multi-pollutant aspects for, when we try to assess the

7  risk of air pollutants, particularly the different

8  oxidant pollutants.  But, let's see if there's any big

9  changes in seven and eight that we want to make.

10  Particularly, anything we want to add.

11	DR. BALMES: I thought I heard yesterday

12  that some people were uncomfortable with the idea of

13  defining a susceptible group relative based on their

14  where they live.  That's the first bullet in, uh - -

15	DR. HENDERSON: Page seven.

16	DR. AVOL: I think Tim's right.  There

17  was some discussion about moving the issues of high

18  exposure locations and near roadway into exposure.

19	DR. POSTLETHWAIT: Yes, and when I  put

20  this together during the Rockies game - -

21	DR. CRAWFORD-BROWN: I don't think the

22  Rockies actually had a game.

23	DR. POSTLETHWAIT: That's what I was

24  thinking.  Yeah, I mean, that's, it can go wherever.

25  The question is is whether it does, does increased,

Page 61

1  components, and that would address, I think, Dr. Avol's

2  questions.

3	DR. AVOL: Yeah, but I think there is a

4  interaction here in the sense that vulnerable

5  populations, those are the high exposure alongside

6  roadways, are likely, are disproportionately likely to

7  be lower SES and get into issues of environmental

8  justice.  And then, they may have biological in that

9  sense, be the former susceptible.  They may also fall

10  into the susceptible population as well.  So, they get,

11  sort of, a double whammy.  But I think that it is true

12  that there are susceptible and vulnerable sub-

13  categories here.

14	DR. HENDERSON: Okay.  Any more for

15  charge question seven?

16	DR. COTE: If you have time, I had a

17  quick question.  The two on this, on the page five, the

18  partial bullet at the top, the last sentence, the

19  chapter did not address biologic plausibility with

20  regard to specific populations, thus it's difficult to

21  attribute health outcomes to direct causal.  I think

22  we're all in agreement when you have biologic

23  plausibility, you're much better off.  Or is this

24  intended to mean, though, if you don't have mechanism

25  of action information, then you can't say there's a

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Page 62

1  causal outcome?

2	DR. POSTLETHWAIT: Well, my intent was

3  to, sort of, throw that open for discussion that, would

4  it make the document more robust to have, why would an

5  asthmatic be more susceptible to NO2 than a normal.

6  For example, what is it about the biology of NO2 that

7  induces susceptibility in a specific subset of the

8  population.  Yes?

9	DR. COTE: Yeah, I think we can make that

10  stronger.  I'm not sure we can actually, and in each

11  case, can be successful, do we not.

12	DR. CRAPO: The asthmatic has a more

13  responsive airway, and greater responsive inflammation,

14  and the NO2 is an irritant, so it could easily be an

15  oxidant.  So, it could easily be - -

16	DR. POSTLETHWAIT: That one's easy.  Some

17  of the others may not be so easy.  And we can't - -

18	DR. LARSON: Are we doing, dealing with a

19  likely causal, and that term.  I mean - -

20	DR. POSTLETHWAIT: Yeah - -

21	DR. LARSON: - - causal is a diff-, is a

22  higher standard than likely causal.  My understanding

23  was, you don't need the biological plaus-, I mean, you

24  don't need the detailed mechanism to go to likely

25  causal.

Page 64

1  you've got injury, repair, growth, and development.

2	DR. COTE: Okay.

3	DR. POSTLETHWAIT: And, which is not, two

4  of those factors are, don't occur in the adult.

5	DR. HATTIS: Yeah, if you want to back

6  off from unique, you might say distinctive.

7	DR. POSTLETHWAIT: Sure.

8	DR. COTE: Thank you.

9	DR. HENDERSON: Okay.  Did you get that,

10  Angela, distinctive.  Let's look at charge question

11  eight and, uh - -

12	DR. AVOL: Could we just go back.

13	DR. HENDERSON: Oh, sure.

14	DR. AVOL: I'm actually, I mean, I think

15  that Ed is right.  It is unique because of the growth

16  aspect.  The tissues are in the period of growth and

17  are more sensitive.  And I think that is a unique

18  attribute.  But it's not a unique population, anything

19  in the population that makes them unique, susceptibles

20  population.

21	DR. HENDERSON: I think we can work that

22  in.  Let's see.

23	DR. LARSON: The first part of the

24  sentence refers to the children's health, California

25  health studies.  The second part refers to children in

Page 63

1	DR. POSTLETHWAIT: Well, in a perfect

2  world, the detailed mechanisms would be wonderful, but

3  I'm not sure we're there yet, or even close.

4	DR. HENDERSON: And regulations have to

5  be decided on, you know, even in the absence of

6  mechanisms for sure.

7	DR. COTE: The second question I had is

8  in the next bullet, the word unique.  I wasn't and sure

9  what was intended.  So, it says a unique and probably

10  susceptible - -

11	DR. POSTLETHWAIT: Hey, Jim Ultman,

12  you're up.

13	DR. HENDERSON: Jim, are you there.  You

14  were there.  Not answering.

15	DR. POSTLETHWAIT: He sent me this.  I

16  cut and pasted it in, so it's his fault.

17	DR. HENDERSON: Oh, okay.

18	DR. COTE: That's o-, it's not, it's not

19  a deal breaker either way, so that's okay.

20	DR. HENDERSON: Well, I - -

21	DR. COTE: Thank you anyway.

22	DR. HENDERSON: Okay.  We can find out.

23	DR. POSTLETHWAIT: I mean, there is some

24  uniqueness in children because of the superimposition

25  of exposure on top of growth and development.  So,

Page 65

1  general.

2	DR. HENDERSON: Yes.

3	DR. COTE: I thought the concept of the

4  injury, repair, growth, development was what was useful

5  for me.

6	DR. HENDERSON: Yes, I, and, maybe, we

7  can put that in, that children, I don't know, are

8  unique in that, you know, injury, growth and repair.

9	DR. POSTLETHWAIT: Actually, you could

10  throw in a fifth variable, which would be dose, 'cause

11  their running around breathing harder, we hope.

12	DR. HENDERSON: Okay, now can we go on to

13  eight, and I, Doug wrote this.  It just seemed like it

14  was very clear and captures many of the concerns that

15  the committee had.  The, a multi-pollutant aspect, I

16  think, it will be something we'll bring up at the end

17  of the letter as a, you know, general concern we have

18  for all airborne pollutants, and maybe we'll suggest

19  the need for, in the future, striving to address, you

20  know, multi-pollutants, rather than one pollutant at a

21  time, a one atmosphere approach, which the Agency is

22  trying to take anyway.

23	DR. LARSON: But, I also thought, based

24  on the discussions yesterday, that there was a general

25  scientific consensus that nitric oxide was not a

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Page 66

1  confounder either in the palliative, its palliative

2  effects, or its, you know,  irritant effects.  There

3  was no, really no information at these concentrations.

4  I guess, we don't really have the EPA summary of all

5  the nitric oxide concentrations, but it just seemed

6  like we had, sort of, generally, concluded that if, in

7  fact, it is a mixture, it's, it doesn't seem to be the

8  nitric oxide that's doing much of anything.  And then,

9  when you, when you, if you eliminate that, you're, sort

10  of, the next most abundant thing is NO2, and then you

11  start going way down in abundant for these other

12  species that we don't know much about in terms - -

13	DR. HENDERSON: I agree, or what I was

14  thinking of multi-pollutant was ultra fines and ozone

15  and - -

16	DR. LARSON: I agree with that, but I'm

17  just saying that, even though we can't, necessarily,

18  say much about that, I think we can say something about

19  the biological plausibility or the lack of it for

20  nitric oxide.  Because that seemed to be a point of

21  confusion early on in yesterday's discussion.

22	DR. HENDERSON: Okay, I think it's pretty

23  clear in the document.  That's where I read it, so in -

24  -

25	DR. LARSON: Yeah, I mean, we're just

Page 68

1  to is a major reorganization of the document to move a

2  lot of information from the earlier parts into chapter

3  five.  That's not what we intended, though.

4	DR. CRAWFORD-BROWN: I need to  answer

5  that, though.  I mean, I certainly would agree that the

6  entire document is the resource to which people need to

7  turn, but I just don't know what findings and

8  conclusions mean if it isn't a summary of the most

9  important and relevant points from the previous

10  chapters.  I, you know, I would think that there will

11  be people who are going to say, look, I don't have time

12  to read your whole document.

13	Tell me what I really need to know as a

14  policy maker, as somebody who's going to try to do a

15  risk assessment, and so forth.  Tell me what I really

16  need to know in order to be able to make those

17  determinations.  You're the scientist.  I'm not the

18  scientist.  So, I just, you know, that chapter needs to

19  be a chapter that does summarize everything from the

20  past as far as relevant conclusions are.

21	DR. COTE: You know, I was going to, I

22  meant to ask this yesterday, if there were specific

23  examples where there were more important conclusions in

24  the body than in the chapter five.  If somebody could

25  note those, just when you see them.  Things were

Page 67

1  re-, I mean, I was just reading it.  It seems, it still

2  seemed to be a point of confusion.

3	DR. HENDERSON: Okay, I got it.  We're

4  coming to the end here, and as again, this is the first

5  time we've tried this sort of process.  And I need to

6  know if everyone on the phone and sitting around the

7  table is co-, if we modify as we have discussed here

8  this morning extensively, if we modify the content of

9  these points, are you comfortable with these, this

10  being the substance of the letter that we send to the

11  Administrator.  Now, I'm not talking about

12  wordsmithing, et cetera.  Because, what will happen is

13  that this draft letter will go to all of you, so if,

14  you know, if you have wordsmithing problems, don't

15  worry about it.  It's the substance of what's in the

16  letter that I want to know if you're comfortable with.

17  And Mary, why are you raising - -

18	DR. ROSS: May I ask one final, about

19  question number eight.

20	DR. HENDERSON: Okay.

21	DR. ROSS: We had actually intended that

22  the entire ISA be the document that serves as support

23  for risk and exposure assessment.  If it is intended

24  that only the conclusions chapter be the resource for

25  risk and exposure assessment, what that's going to lead

Page 69

1  actually were written by the same people, and I think

2  chapter five reflected, as we were working, perhaps,

3  more refinement of thinking, and so, it's a little

4  disturbing if it was better the first, rather than the

5  second round of thinking, so if you ju- -

6		DR. CRAWFORD-BROWN: If we combine a list

7  of the things that are back in the earlier chapters

8  that - -

9	DR. COTE: That should be - -

10		DR. CRAWFORD-BROWN: But I think the main

11  issue had to do, also, with the fact that the writing

12  of chapter five does need to be the bridge to the user

13  of this document, and what that user needs, as

14  important information,  for the kinds of decisions he

15  or she is going to make.  And that's where I didn't,

16  you know, I, personally, I know Ellis felt the same,

17  didn't feel that that connection was quite there, where

18  somebody at chapter five began to ask, what are people

19  actually going to use this for in the end.  And that's

20  why I raise this issue of integrated.  I don't think

21  there's such a thing as integrated outside of the

22  context of the question that somebody is trying to

23  address.

24	DR. COTE: Was it that there weren't

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Page 70

1  of information were missing, or both?

2	DR. CRAWFORD-BROWN: I, but I mean, my

3  personal opinion is that what happens with chapter five

4  is that, it is, what often happens with concluding

5  chapters in theses, for example, where it's just a

6  compilation of things from the earlier chapters.

7  Here's a thing from chapter one, and here's a thing

8  from chapter two.  Rather than somebody,

9  systematically, sorting through and saying, what do we

10  think we really learned from the earlier chapters that

11  are relevant to the kinds of applications that we

12  thought we were directing this report towards.

13	DR. CRAPO: I think a good example is the

14  issue I was talking about a lot this morning about the

15  dose metrics being annual average, and not telling you

16  what the people, the populations were exposed to,

17  actually, in terms of the more toxic elements of the

18  high level exposures.  And then, a discussion of that,

19  so that the person who tries to interpret the health

20  effects data, in relationship to the possible

21  exposures, both for what they know and don't know, is

22  not there in chapter five.  A person that would read

23  that and just think you had, it would just jump right

24  from the exposure data, think it had totally supported

25  all the findings.  And so, I think, that disconnect

Page 72

1  of these 47 statements, or however many it becomes, and

2  that those that are directly relevant to the issue of

3  making a judgment about the standard be highlighted or

4  marked in some way, and that the, so that's the first

5  point.  And the second point, in chapter two, you were

6  asking for examples of then something that was

7  mentioned in chapter two, but didn't show up in the

8  summary that was in chapter five.  And all of the nine

9  statements in chapter five are relevant to the issue of

10  monitoring alone.

11	DR. COTE: Right, I heard that, yes.

12	DR. COWLING: So, I was just thinking to

13  mention those examples.

14	DR. COTE: Thank you, and what you

15  provided on criteria for judgment, I thought was very

16  good, too.

17	DR. CRAPO: I'd like to add one more

18  thing.  I think the biggest thing that might come out

19  of this review of NO cycle is a recommendation that we

20  go to a one-hour daily average instead of an annual

21  average.  And, no matter what the level is set at, it

22  would totally change our science.  But, we ought to

23  set, I think that's what's needed more than anything

24  else, because I think that we're measuring the wrong

25  thing.  And, I would argue that our document ought to

Page 71

1  that we struggled with for two days here needs to be

2  obvious in chapter five.

3	DR. HENDERSON: And I lay a few, John

4  Samet had quite a bit to say about chapter five in his

5  comments.  And he had the, since so many people had the

6  same conclusion that it was really just a listing of

7  the, what, of items from the previous chapters,

8  excluding some, because several people said that, and

9  not an integration of, you know, all five.  So, I think

10  that it really does need attention.

11	DR. COTE: Clearly.

12	DR. HENDERSON: You don't have that many

13  people giving almost the same comments without there

14  being something that - -

15	DR. COTE: No, no, I wasn't disagreeing.

16  I was just trying to get more - -

17	DR. HENDERSON: Just get more examples

18  and - -

19	DR. COTE: Yeah.

20	DR. HENDERSON: Yes, Ellis.

21	DR. COWLING: I would offer two comments.

22  One is George's suggestion yesterday that, and it's

23  relevant to what Doug was just saying about, what is

24  relevant to the decisions that were made next.  And it

25  seems to me that he was suggesting that a scan be made

Page 73

1  set the, ought to, appropriately, set the background

2  for that type of a recommendation, 'cause that's where

3  I think we're headed.  And it's not in there now.

4	DR. HENDERSON: Has the shorter averaging

5  time been considered in the, by the Agency, because in

6  our discussion, I had the same thought, James, and I

7  thought, well, gee, maybe we're looking at the wrong

8  averaging time.

9	DR. CRAPO: Well, both daily and, sure, I

10  mean, one-hour and dailies is, those are two changes to

11  it.

12	DR. HENDERSON: I'm just curious if the

13  Agency has, that's ever come up.

14	DR. ROSS: Well, I mean, you can look in

15  the history of the rule making, and in 1993, actually,

16  you'd have to ask Karen Martin the specific history,

17  but we made an effort to try to breakdown into short-

18  term and long-term exposure discussions.  And within a

19  short term, there are a range of different levels.

20  Many of the epi studies use 24 hour, but we did try to

21  discuss the evidence at, related to averaging time.

22  Tox studies use a whole variety of different exposures.

23  And then, we try to make that available, to the extent

24  we can say something about peak exposures, we will.

25  There aren't many epi studies that look at peak

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Page 74

1  exposures.  I'm not even sure there are many tox

2  studies, but we'll try to bring that up as much as we

3  can.  I mean, we're taking that ho-, as a comment that

4  we need to address.

5	DR. CRAPO: Remember if the ozone field

6  goes that direction, for shorter averaging times and

7  it's, because it's been there for decades, it has

8  really influenced the thinking of the evolution in that

9  field.  This data would suggest that NO2 has a toxic

10  profile similar to ozone.  In fact, it interacts with

11  ozone to make it this toxic product.  So, there's no

12  rationale for having a different, an annual averaging

13  time for NO2, and a short averaging time for ozone.  I

14  would just argue that you can use the science of the

15  ozone science to justify a lot more evaluation of why

16  NO2 ought to have the same type of short-term

17  evaluation on it.  And part of our problem is we set it

18  up wrong thirty years ago, and we've got a bad

19  collection of data to compare everything to.

20	DR. BALMES: I guess the other point that

21  we should emphasize, this is John Balmes, is that if

22  asthma exacerbation is one of the major endpoints that

23  we feel the epidemiology supports, and I certainly

24  think it does, then it makes no, you know, an annual

25  average does not protect asthmatics from exacerbation.

Page 76

1  me, the epi drives it.  We'd, logically, might think,

2  oh, it's a short term for that day that really drives

3  it, but we have to come up with a value, and if all the

4  epi is driven by lo-, the annual averages, we got a

5  tough task.

6	DR. HENDERSON: That's a good point.

7	DR. CRAPO: For particulates, we have

8  two, so we could keep both, then.  We could put a

9  short-term and a long-term standard in.  Well, we

10  couldn't, but the Administrator could.

11	DR. COTE: And if you were, if you're

12  thinking about two different kind of health effects,

13  like lung growth and asthma, there's no reason to think

14  it would be the same.  It might be, but I'm not sure, I

15  don't know.

16	DR. BALMES: And, there's also no reason

17  to have the same type of siting criteria for your

18  monitors if you're going to go to a short-term

19  standard.  Because, I can walk down a street canyon for

20  an hour and get a completely different exposure than I

21  will at a EPA monitoring site for an hour.

22	DR. ROSS: Just to remind people, we're a

23  little ahead of the process here, talking about the

24  standards already and the sited criteria.

25	DR. HENDERSON: No, we tend to jump over

Page 75

1	DR. HENDERSON: Okay, thank you.  I was

2  thinking of the ozone and, you know, the eight hour

3  standard make sense because it's much higher during the

4  daylight hours.

5	DR. CRAPO: And so NO2 is the same- -

6	DR. HENDERSON:  Is, is NO2 in the same -

7  -

8  (WHEREUPON, there was a discussion off the record.)

9	DR. CRAPO: NO's shorter than the ozone

10  peak, isn't it?

11	DR. RUSSELL: It's actually a very

12  different shape.

13	DR. HENDERSON: Yeah, I think we'd have

14  to be a little careful, but you know, I - -

15  (WHEREUPON, there was a discussion off the record.)

16	DR. HENDERSON: Terry, Terry has his hand

17  up, or you want to go to Dale?

18	DR. GORDON: I had a feeling that this

19  conversation was going to go this way, and I was

20  wondering if it did, we went to shorter term.  Are we

21  going to lose something.  It sounds like people are

22  leaning toward a short term, not a long term, and how

23  would that effect the true long-term studies, such as

24  the children's lung growth studies, which might be more

25  correlated epi wise with annual averages.  I mean, to

Page 77

1  to the endpoints, so let's, but, I really would like to

2  draw this together so that we complete our peer review

3  of the ISA document, and Ellis, would, I'll give you

4  the last call before I ask.

5	DR. COWLING: Well, I would just like to

6  support what Jim Crapo has suggested here, with the

7  additional suggestion, and this is where they did do

8  what Karen Martin told us yesterday.  What was in the

9  mind of the Administrator, and what are the policy

10  implications of having an annual standard, and what are

11  the policy implications of having a daily standard, or

12  any other standard.  And it seems to me that we ought

13  to know what was the rationale in 1971, when an annual

14  standard was selected.  And now, and then, we have the

15  other iterations in '93 and so on, what was in the mind

16  of those who made the decisions at that time.  And I

17  think if that is clarified, it would provide a more

18  rational basis for a decision about what is the proper

19  averaging time.

20	DR. BALMES: Ellis, I can tell you one

21  thing.  I was, way back in my youth, I was in the

22  public health service at EPA.  And the very first

23  criteria document, as you know, were very thin, and

24  committees were about five or six people, and the

25  process took a day, so.

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Page 78

1	DR. HENDERSON: Oh, you're making us all

2  jealous.  Anyway, I do want, we are skipping way ahead.

3  We're going to the next step.  And we, before we go

4  there, we need to complete our review of the ISA, which

5  is looking at the science.  So, I want to know if

6  everyone in the room and on the phone is comfortable

7  with the substance of what we're going to put in the

8  letter.  And you will see this, the draft come-, the

9  letter come out, and you will get to, we will seek

10  concurrences.

11	We always do, so, is there anyone who is not

12  comfortable with it?  John Samet, are you on the phone?

13  Oh, he's coming this afternoon, okay.  Well, we have a

14  quorum of the chartered members of CASAC here who are

15  all comfortable with this, so I consider that the

16  charter members have approved this, the substance of

17  this letter that's going to go out.

18	What comes out next is going to be the draft

19  letter, and with Angela's able help, I hope we can get

20  it out fairly soon.  And then, you must look at it very

21  carefully, and we will seek concurrence before it

22  actually goes in.  And any questions about that

23  process?  Well, I thank everybody for cooperating so

24  well with this new way of doing things.  We'll see if

25  it works out.  I don't know if it, it hasn't quite

Page 80

1  and I would ask, the first speaker is going to be

2  Lydia?

3	MS. WEGMAN: Yeah.

4	DR. HENDERSON: Okay, and Lydia, maybe,

5  you know, as you go through, you can introduce the

6  others from the Air office who are going to be

7  participating.  So, it's a real privilege to have Lydia

8  with us.  She always clarifies things.

9	MS. WEGMAN: Well, I don't know about

10  that, Rogene, but thank you very much.  My name's Lydia

11  Wegman, and I am the Director of the Health and

12  Environmental Impacts Division in the Office of Air

13  Quality Planning and Standards.  And we are the folks

14  who will be working on the exposure and risk

15  assessment, and ultimately, the advanced notice of

16  proposed rule making and the proposed rule and final

17  rule.  And I do want to introduce the folks who are

18  with me, or the ones who have done the real work on the

19  scope and methods plan for the exposure and risk

20  assessment.  And Dr. Karen Martin, who will speak in a

21  moment after I'm done, Dr. Scott Jenkins, Dr. Stephen

22  Graham, and Dr. Harvey Richmond.

23	MR. RICHMOND: I'm no doctor.

24	MS. WEGMAN: Oh, no doctor, you should be

25  a doctor, though. You do the work of a doctor.  So,

Page 79

1  reached it conclusion, but all of you, by participating

2  so readily, I think have helped it, and we may continue

3  to do this.

4	The next thing on our agenda was to move on

5  to the next document.  I think maybe it's time for a

6  break, and we'll take a fifteen minute break, then

7  we'll come back and we'll hear from the Air office.

8  And they are going to move us in the direction we keep

9  trying to go.

10  (WHEREUPON, a break was taken.)

11	DR. HENDERSON: If everybody could take

12  their seats.  Thank you, Doug.  Okay.  We're going to

13  be moving on, here comes Ron, if others could take

14  their seats.  We're going to be moving on to a

15  consultation now for our next document, which is the

16  exposure risk assessment methods document.  And, as

17  we've been saying, we keep jumping in this direction

18  from going from the science assessment to wanting to

19  participate in this part of the process.  And this is

20  our opportunity.  As a consultation, this is where we

21  can, early on in the development of this process,

22  provide advice to the Agency on the methods for

23  exposure and risk assessment.  So, we had quite a bit

24  of discussion on exposure assessment this morning.  It

25  is, we're going to hear first, then, from the Agency,

Page 81

1  this is our team on the exposure and risk planning for

2  the NOx review, the primary NOx review, and we'll be

3  coming to talk with some of you next week about our NOx

4  and SOx  secondary review.

5	I first want to say thank you all for taking

6  the time to review the work we've done, and to spend

7  the couple of days you're spending here in RTP, either

8  in person or by phone, to offer us your comments.  Your

9  comments are invaluable to us, and without the work of

10  CASAC, we would not be able to perform our work.

And I

11  just want to say how very important your work is to us,

12  to the Agency as a whole, and to public health.  And

13  thank you very much for all the work that you do.

14	I, also, just want to make one point, as you

15  offer us comments on the scope and methods plan.  As

16  you have seen, and I know several of you have commented

17  on, we've got a tiered assessment, both for the

18  exposure and risk assessments.  And, one of the reasons

19  we have the tiering is that, we don't know whether

20  we'll have the scientific evidence to go through all

21  tiers of these assessments, and we are very much

22  looking to you for advice on how to prioritize these

23  assessments, and what we do need to do, based on what

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Page 82

1  are the resource constraints that we face in our

2  office.  We have constraints, not only in terms of

3  people and money, which are constraints that we always

4  face, and it does seem that we face them more every

5  year with declining budgets.  But, we also have a time

6  constraint in this case.  As you know, we have a court

7  order.  It's currently under review by the public, but

8  we very much anticipate having a final court order that

9  gives us firm dates by which we do have to complete the

10  proposed and final rules, as well as the ISA.  And,

11  that does limit what we can do.  And I want to alert

12  you to that, because I know that there is a desire on

13  all of our parts to do the maximum amount of assessment

14  that we possibly can do with the science that we have.

15  But we will, in fact, be facing some constraints, and I

16  want to seek your help in knowing what is the most

17  important thing to do within the time and resource

18  constraints we have.  So, as you think about these

19  issues and give us your advice today, I'd appreciate it

20  if you kept that in mind.

21	And now, I'm going to turn it over to Karen,

22  who is going to offer a few thoughts on multi-pollutant

23  assessments.

24	DR. MARTIN: Just, while this is, you all

25  have been talking some about the issue of multi-

Page 84

1  step, in deciding how to approach our exposure and risk

2  assessments; what is it we're assessing the risk of.

3  We can,  obviously, make some up-front assumptions, and

4  my comments yesterday were intended to help get your,

5  at least, preliminary thinking to help us do that.  But

6  our assumptions can, then, be further refined, as we go

7  through the process of doing a first phase and a second

8  phase of a risk assessment, so that, in the end, we

9  can, are in the best position to characterize what, in

10  fact, we think our quantitative assessments reflect the

11  risk of, in this case, only SO2, SO2 in combination

12  with other pollutants, SO2 as a surrogate for other

13  pollutants.  All those things are things we are, in the

14  end, going to have to speak very clearly to.  So the

15  more you help us, at this early stage in the game, with

16  some of your thinking at this stage, and recognizing we

17  can further refine that as we go about characterizing,

18  in the end, the results that we do produce.

19	Beyond that, the issue of multi-pollutant

20  standards and multi-pollutant strategies, obviously,

21  has much broader implications for all of our NAAQS

22  reviews, and for what the Office does in implementing

23  programs to address the NAAQS.  And I would just make

24  the observation that, some of the comments I heard, I,

25  perhaps, unintentionally, have the, sort of sounded

Page 83

1  pollutant approaches, and multi-pollutant standards,

2  and multi-pollutant interpretations of scientific

3  evidence, and the question is, the  tangentially

4  related to the subject we're here to talk about, our

5  plan for doing exposure and risk assessment, but it's,

6  obviously,  more broadly related to our ultimate review

7  of these primary and of two standards, and our review

8  of standards in general.  And I just wanted to take a

9  moment and make a few observations about the

10  discussion, and sort of, our view of it.

11	In the context of science assessment

12  documents, it's clearly extremely important that those

13  assessment documents do everything they can to tease

14  out, what do we know about any individual pollutants

15  effects, and what do we know about the interactions of

16  that pollutant with other pollutants, and to what

17  extent can we define specific effects related

18  individual pollutants versus to what extent does the

19  evidence limit us to only making more general

20  observations about associations of air pollution more

21  broadly.

22	All those issues are extremely important, and

23  your discussions are helping, I think, to sharpen the

24  science assessment document in that regard.  It becomes

25  important for us, of course, at least as an initial

Page 85

1  like, there is an inherent mismatch between setting

2  standards for individual pollutants, and crafting

3  control strategies that most efficiently and

4  effectively get at the mix of pollutants that are, in

5  fact, of concern.

6	And I would offer the observation that I

7  don't, really, perceive that to be a mismatch.  It's

8  clearly a distinction, but one can, clearly, have

9  standards for individual pollutants in conjunction with

10  air quality management programs that are very multi-

11  pollutant oriented, and seek to find the most efficient

12  strategies for addressing all the pollutants for which

13  we have standards.  And, you all, I mean, different

14  people have different views on that, but I just wanted

15  to make the observation that there isn't, necessarily,

16  an inherent mismatch, or contradiction in doing those

17  things.

18	The one pollutant that we truly have a multi-

19  pollutant standard for is, of course, particulate

20  matter, which is a collection of thousands of

21  pollutants.  And if you think about it, we have

22  established that as a multi-pollutant standard under

23  the guise of PM mass, and a great deal of the research

24  right now is focused on trying to tease out what are

25  the differing relative toxicities of the individual

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Page 86

1  components within that mix.	So, when we

2  do find ourselves faced with what truly is a multiple

3  pollutant standard, what we set about to do is trying

4  to figure out how to separate it out.  And I think

5  that's sort of informative as to what utility there

6  might be in trying to aggregate all the other

7  pollutants into one standard, with interaction terms,

8  wouldn't our next step, logically, be trying to sort

9  out the relative toxicity.

10	So, I just wanted to offer those

11  observations, in terms of, the issue is really an

12  important one, but perhaps, it's not as much of a

13  mismatch or contradiction as one might originally

14  think.

15	Those were the points, observation points I

16  wanted to offer before we get into it, so if there's

17  nothing else we need to deal with, why don't we just

18  jump in to the overview presentation we wanted to make.

19	DR. HENDERSON: I think that's, that

20  would be good.  Donna has a question.

21	DR. KENSKI: Well, just a response, I

22  guess, to the idea that single pollutant standards

23  don't, necessarily, preclude multi-pollutant controls.

24  Well, I, you know, it's clear that, you know, a control

25  on one pollutant will almost always, you know, have an

Page 88

1  states, it's the Saint Louis area.  And so, we, in

2  fact, are very mindful of that issue.  As far as the

3  planning goes, I think Karen is addressing, you know,

4  the way in which we set standards right now, which does

5  not, in fact, preclude multi-pollutant planning.  And

6  we can set-, you know, at this point, we do need to

7  look at the pollutants individually, but that doesn't

8  prevent us from moving forward to multi-pollutant

9  planning.  And that's, definitely, what we are trying

10  to do.

11	DR. HENDERSON: Thank you.  And so,

12  Karen, are you going to, who is our first speaker for

13  the - -

14	DR. MARTIN: Scott's going to take the

15  lead in covering the opening, and Stephen and Harvey

16  will round out the opening presentation.

17	DR. HENDERSON: Okay.

18	DR. JENKINS: Okay, thanks.  My name is

19  Scott Jenkins, and I'm the health lead for the NO2

20  review and OAQPS.  And I'm going to be talking through,

21  probably, three or four slides on giving a little bit

22  of background on the current approach that we have

23  proposed in the scope and methods plan.  And then,

24  Stephen is going to talk through the exposure part of

25  it, and Harvey is going to talk through the risk part

Page 87

1  effect on other pollutants, it still, you know, the

2  burden on the states to comply with the single

3  pollutant standard requires that they produce a, you

4  know, state implementation plan.  And in that plan,

5  they have to provide for how they're going to control

6  that single pollutant, not multi-pollutants.  So, I

7  think the, you know, it would, while we get these, sort

8  of, indirect, you know, controls on other pollutants,

9  it would be more straightforward, I think, to, you

10  know, have a multi-pollutant approach that really, you

11  know, dictated this, you know, need to control all

12  pollutants, not just single pollutants.  So, while, you

13  know, while, yes, we do get controls, still the burden

14  on states is to demonstrate their control of a single

15  pollutant for a single standard.

16	MS. WEGMAN: Yeah, and I'll just respond

17  briefly.  We are very mindful of the air quality

18  manager port that the NRC issued, and we did, there is,

19  in fact, a subcommittee of the Clean Air Act Advisory

20  Committee that has looked at all the recommendations

21  coming out of the air quality management report,

22  including the one to develop multi-pollutant plans, and

23  we, in fact, have a project going on in our office to

24  pilot multi-pollutant planning with three states, North

25  Carolina, New York, and Illinois, Missouri, four

Page 89

1  of it.

2	Okay, so we're all aware, by now, that our

3  purpose here to solicit feedback on our proposed

4  approach to assessing risks and exposures.  I just went

5  through this, so I'm going to talk through, a little

6  ahead on the schedule a little bit, talk about the

7  previous review, and give a little bit of what, I hope,

8  is historical perspective.  And then, talk about the

9  scope of the plan.

10	Okay, first schedule, and Mary presented the

11  same slide yesterday, so I'm not going to go through

12  anything in detail, other than to point out that the

13  next time we will be soliciting, or will be meeting

14  with CASAC will be Spring of '08, where we'll be asking

15  for feedback on the second draft of the ISA, and the

16  first draft of the risk and exposure assessment, and

17  then, again, September of '08, for the second draft of

18  the risk and exposure assessment.  And then, the final

19  date here, this is our, the date that we anticipate

20  will become our court ordered date.  This is about five

21  months earlier, just to point out, five months earlier

22  than the dates we had originally proposed.

23	Okay, so a little bit of background, and

24  this, and I'm going to expand on this side a little

25  bit, just based on the conversation that we just had

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Page 90

1  prior to the break, and that is, providing a little bit

2  of historical perspective for how the original standard

3  was set.

4	So, the original standard was based on

5  epidemiology studies that were conducted in

6  Chattanooga, Tennessee, basically, where the long-term

7  annual average levels of NO2 were correlated with

8  health effects.  The issue that arose later with those

9  studies was that the issue of confounding with other

10  pollutants, an issue of the measurement approach to,

11  for, from measuring NO2 in the studies.

12	So, what happened was that, the original

13  standard was set based on those long-term epi studies.

14  And then, every review since then has focused,

15  essentially, on the short-term issues.  And the crux of

16  the decisions that the Administrator has made are how

17  well does that existing long-term annual standard

18  protect against short peak exposures.

19	So, I think that'll become clear when I go

20  through the slide a little bit, but that just gives you

21  a little bit of a historical context.

22	So, and their talk-, specifically, about the

23  last review of the NO2 NAAQS, and the Administrator had

24  a, made a couple of conclusions regarding the

25  sufficiency and the necessity of the existing annual

Page 92

1  arrived at was that we conduct-, we and OAQPS

conducted

2  an air quality assessment, essentially, evaluating the

3  relationship between the annual average NO2 levels and

4  short-term one-hour average NO2 levels.  And, as part

5  of that evaluation, we looked at the number of

6  exceedance as a very short-term benchmark values, with

7  the assumption that were just meeting the current

8  standard.

9	So, those benchmark values were derived,

10  again, from these clinical studies that I just

11  mentioned, and, basically, the result was that, if you

12  assume that the existing annual standard is being

13  attained, the short-term levels of NO2 of potential

14  concern would be very unlikely in most parts of the

15  country.  I think Los Angeles had a few exceedances at

16  the .2 ppm level, but that was the only spot where

17  those exceedances were found.

18	So, that was, this was the structure of the

19  la-, the con-, of the decision framework for the last

20  review.  And now, I'm going to move to the current

21  review, and talk just for just a minute about the scope

22  of the planned risk and exposure assessment, and then

23  I'm going to turn it over to Stephen.

24	We hit on this a little bit yesterday, this,

25  using NO2 versus other oxides of nitrogen.  Obviously,

Page 91

1  standard.  The first conclusion was that the existing

2  annual standard will maintain annual NO2 concentrations

3  well below levels, long-term levels that are of

4  potential concern.  And those long-term levels of

5  potential concern were derived from the animal tox

6  literature.  And this is, basically, a fi-, based on

7  findings that if you expose animals for  relatively

8  long periods of time to relatively high levels of NO2,

9  you get emphysema-like lesions in the lung.  And then,

10  we're talking about, at least months of exposure to,

11  say, at least 5 ppm NO2 here.

12	So, it's pretty much, it's pretty easy to see

13  that, yes, the existing annual standard of .053 ppm

14  will protect against those sorts of long-term effects.

15	The other conclusion, and this is, really,

16  more of the focus of the last review, the other

17  conclusion was that the existing annual standard will

18  provide protection against the short-term peak NO2

19  levels that are of concern.  And those short-term

20  levels of concern were derived from the human clinical

21  literature.  This came from a set of studies showing

22  that, in asthmatics, if you expose asthmatics to levels

23  as low as, say, .2 to .3 ppm NO2, you can get increased

24  airway response in this.

25	So, the way that the second conclusion was

Page 93

1  NO2 is but one of the oxides of nitrogen that include

2  both gaseous and particulate species.

3	There are really two issues, I think,

4  embedded in this.  And that is, first, that is using

5  NO2 as a surrogate for the gaseous nitrogen oxide, and

6  the other issue is using, is focusing this review on

7  the gaseous nitrogen oxide.

8	So, regarding the first, the first statement,

9  you know, and I think this was borne out yesterday,

10  we're thinking-, we're planning to use NO2 as a

11  surrogate for the gaseous species, basically, because

12  the lack, relative lack of health effects data, and

13  actually, it came out yesterday, also, the relative

14  lack of monitoring data for gaseous species other than

15  NO2.

16	In the case of the particulate, the second

17  point that I made, the particulate nitrogen oxide, and

18  we made this point in our integrated review plan, and

19  we, this point, also, came up at our last consultation

20  with you last spring, that the particulate species are

21  addressed by the current NAAQS, and the rationale

22  provided right here, basically, the last review for

23  the, of the PM standard concluded that size

24  fractionated particle mass, rather than chemical

25  composition was the most appropriate way to address

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Page 94

1  ambient PM.

2	This conclusion, obviously, is going to be

3  reassessed in the next review, or I should say, the

4  current review, since it's already kicked off. We had

5  the opening workshop.  But at present, it would be

6  redundant to, also, use the NO2 NAAQS to protect

7  against the health effects of particulate nitrogen

8  oxide.

9	Other than that, I just want to point out

10  that the assessment is going to evaluate, this will be

11  a recurring theme throughout Stephen and Harvey's part

12  of the talk, that the current assessment, we're

13  planning to assess both recent ambient levels of NO2,

14  ambient levels that are associated with just meeting

15  the current standard, and ambient levels that are

16  associated with just meeting the potential alternative

17  standards, which will be identified as we move forward.

18  And the assessment's going to focus on both short- and

19  long-term exposures.

20	So, that's all that I had to say in the way

21  of background and introduction.  I'm going to turn it

22  over now to Stephen, who is going to talk us through

23  the proposal, proposed plan for the exposure

24  assessment.

25	DR. GRAHAM: Thank you, Scott.  Could you

Page 96

1  fashion, that is going from, in a sense, a qualitative

2  evaluation and progressing to a quantitative evaluation

3  if, of course, data exists to support that type of an

4  evaluation.

5	So, the tier one, as I mentioned, is a air

6  quality characterization, and the purpose there is to

7  estimate the potential exposures, using the current, as

8  well as historical air quality data that we have

9  available to us, and use that as a surrogate for

10  exposure.  In addition, we are proposing to take a

11  glance at some of these near roadway exposures, using

12  the ambient data, using enhancement factors.  And then,

13  of course, any available concentration data and

14  emissions data that may be available to look at the

15  influence from sources, particular sources that may be

16  outdoors or indoors.

17	The locations that we considered are

18  outlined, based on the, those criteria that is, air

19  quality trans data availability, you know, number of

20  monitors, whether the data are quality assured and

21  comprehensive, and in addition, to some other criteria.

22  And we've selected Los Angeles, Houston, Atlanta,

23  Philadelphia, and Chicago, and possibly, aggregation,

24  based on some of the analyses that are going to be

25  performed here.

Page 95

1  work the clicker?  Sometimes I have a habit of talking

2  with my hands.  Okay, all right, thank you.  So, of

3  course, the general, broad goals of this exposure

4  assessment are to estimate both short-term and long-

5  term exposures, short-term being hourly, and that is

6  associated with these current levels of ambient NO2,

7  and assuming alternative levels of NO2.

8	Also, to develop these quantitative

9  relationships, based on the form of the current

10  standard, which is long-term, annual average and the

11  relationship between that average and the short-term

12  peak concentrations, which was done in the prior review

13  as well.  But in addition, I want to, also, consider

14  local source influences, which we saw was important in

15  the review of the ISA, and the impact on the exposure

16  estimates.

17	As far as the approach, it's already been

18  mentioned that we have three tiers.  The tier one is

19  air quality characterization.  And I'll go through each

20  of these in greater detail, I guess, or of course, it's

21  been in greater detail in the scope of methods

22  document.  Populations considered include the general

23  population, as well as the individuals identified as

24  susceptible or vulnerable.  And the assessment of

25  uncertainty is also going to be approached in a tiered

Page 97

1	The expected output is, of course,

2  descriptive statistics for NO2 in some of these

3  selected locations; relationships between the short-

4  term peak levels and the long-term average levels; and,

5  of course, identification of additional areas to be

6  modeled in the tier two and tier three, dependent on

7  the analysis outcome.

8	Uncertainty will, primarily, be qualitative

9  at this stage, and of course, these tier one exposure

10  assessment, the outcome is going to be used for

11  comparison with some of the health benchmarks, once

12  they are identified.

13	So, in tier two, we've got, the purpose is to

14  improve that relationship.  So, now, we're trying to

15  link the actual concentrations, themselves, to persons,

16  to humans.  And we are going to, of course, consider

17  both the on roadway and, as well as, near roadway,

18  using dispersion modeling and or enhancement factors as

19  well.

20	The model concentrations for other outdoor

21  sources, if there are any identified, as well as the

22  indoor sources, if they are identified as being

23  important in influencing these exposure estimates or,

24  shall I say, the relationship between, I'm sorry, the

25  contribution, the relative contribution between the

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Page 98

1  two, that will be done as well.  And, of course,

2  consider influential factors, that is, time that people

3  do spend in particular microenvironments, as well as

4  the limited decay of NO2 indoors, and populations

5  residing near roadways.

6	The locations, of course, are going to be,

7  it's going to be a more focused analysis, and it's

8  going to be focused on the locations that have been

9  identified in the tier one analysis.

10	And the output is going to be broken up into

11  two different exposure metrics.  We've got short-term

12  exposure outcome, where we have, in addition to the

13  temporal and spatially resolved ambient air quality

14  concentration fields, that account for local sources,

15  like emissions from roadways and other sources that are

16  identified as important.  We've got estimates of the

17  number of individuals who may experience exposures of

18  concern.  Not to suggest that it's an individual

19  analysis.  It's more of a cohort-based analysis.

20	And then, of course, long-term exposure

21  estimates will include annual average exposure levels

22  within a given census tract, and could be considered at

23  a more finer resolution, say a block group or block.

24  And it's not just the annual, but also, I believe,

25  we'll be able to estimate the daily average.

Page 100

1	So, as I said, the locations are the same as

2  those identified previously.  The expected output is

3  going to be the counts of people exposed one or more

4  times to several NO2 levels, based on, of course,

5  health information obtained from the ISA, and because

6  APEX is a time series model, and the averaging time,

7  that is of interest, can be taken out of the, or shall

8  I say developed as an exposure metric.  And we also

9  have counts of personal occurrences of a particular

10  exposure.

11	And the uncertainty can be a little bit more

12  quantitative in a sense.  We can look at, again, model

13  inputs, where data exists for describing both a

14  variability and the  uncertainty in them, and of

15  course, model formulation.  If we have estimates of

16  personal exposure that are available to compare that,

17  as well as microenvironmental concentrations.  That's

18  it.  Thank you.

19	MR. RICHMOND: Thank you, Stephen.  I'm

20  going to walk you through a few slides on the risk

21  assessment.  First of all, overview goals of the risk

22  assessment are to estimate the number of occurrences of

23  short-term air quality events and number of people

24  exposed at, or above, various potential health effect

25  benchmarks associated with alternative NO2 scenarios.

Page 99

1	And, in addition, we've got the ratios of

2  exposure to ambient, which could be useful for

3  extrapolating to other areas that we had not modeled.

4  And uncertainty would be addressed, of course, through

5  various sensitivity analyses, limited sensitivity

6  analyses, based on input distributions and other model

7  inputs, as well as measured comparisons, if there are

8  data that exist for particular microenvironments.  That

9  would be compared to model estimates.

10	In tier three, of course, it's a more refined

11  approach, and here we are focusing on addressing more

12  particulars about human physiology, including time,

13  well, that's not physiology, but time, location,

14  activity patterns, and their physiology.  Using the air

15  concentration fields developed from a tier-two

16  approach, that is where we have the on and near roadway

17  concentrations, and using the EPA's APEX model for

18  estimating exposures.

19	Locations, of course, are built upon what had

20  been identified in the tier one and used in the tier

21  two analysis.  And, oh, I forgot to mention, of course,

22  the APEX model is capable of estimating individual

23  exposure estimates.  It's a time series exposure model.

24  And we also have capabilities to estimate indoor

25  sources using that model.

Page 101

1  If a tier two assessment is conducted, we'd also

2  provide health risk estimates for NO2 health endpoints

3  associated with alternative scenarios.  And for any

4  tier, we'll, of course, identify and characterize key

5  assumptions and the variability and uncertainty

6  associated with the assessments.

7	As Scott and Stephen have said, the scenarios

8  evaluated are for both recent air quality, simulating

9  the current standard, which is a difficult challenge,

10  given the levels are much lower than the current

11  standard; and air quality levels just meeting potential

12  alternative standards, which could be short- or long-

13  term standards.

14	There's a two tiered approach here.  Proposed

15  one is the, in tier one, potential health effect

16  benchmark levels, which will be based on a review of

17  the revised ISA, would be compared to, first, air