U.S. ENVIRONMENTAL PROTECTION AGENCY

SCIENCE ADVISORY BOARD STAFF OFFICE

CLEAN AIR SCIENTIFIC ADVISORY COMMITTEE (CASAC)

SULFUR OXIDES PRIMARY

NATIONAL AMBIENT AIR QUALITY STANDARDS (NAAQS) REVIEW PANEL

PUBLIC MEETING

MARRIOTT AT RESEARCH TRIANGLE PARK

4700 Guardian Drive

Durham, North Carolina 27703

DECEMBER 5, 2007

8:32 A.M.

1	U. S. ENVIRONMENTAL PROTECTION AGENCY

2	CLEAN AIR SCIENTIFIC ADVISORY COMMITTEE (CASAC)

3	PUBLIC MEETING

4	SULFUR OXIDES PRIMARY

5	NATIONAL AMBIENT AIR QUALITY STANDARDS (NAAQS)

6	REVIEW PANEL

7	DECEMBER 5, 2007

8	DR. STALLWORTH:	Can I ask everyone

9	to take a seat, please?	We can't start without our

10	chair, so.	Tim, we're still shuffling and getting

11	settled in.	Tim, can you hear me now?

12	DR. LARSON:	Hello.

13	DR. STALLWORTH:	Hello.	Tim, can

14	you hear us?

15	DR. LARSON:	Yeah.

16	DR. STALLWORTH:	Great.	We're

17	waiting on our chair, actually.	Okay.	Good morning.

18	I want to get started.	I'm Holly Stallworth.	I'm the

19	designated federal officer for the CASAC SOx panel, and

20	I want to open with a short statement.	The CASAC SOx

21	panel is a federal advisory committee, and by EPA

22	policy its meetings and deliberations are held as

23	public meetings that meet the requirements of the

24	Federal Advisory Committee Act.	The Clean Air

25	Scientific Advisory Committee or CASAC is empowered by

1	law to provide advice to the Administrator.	Consistent

2	with requirements of FACA, that's the Federal Advisory

3	Committee Act, the deliberations of the CASAC SOx panel

4	are conducted in public meetings for which advance

5	public notice is given.	The discussions and

6	substantive	deliberations of the panel, its

7	interactions with the public are conducted in sessions

8	where I am present to ensure that requirements of FACA

9	are met.	This includes the requirements for open

10	meetings, for maintaining records, and making available

11	public summaries of meetings and providing

12	opportunities for public comment.	We do expect one

13	public commentor this morning at 9:20 from the American

14	Petroleum Institute.

15	I'll be taking minutes.	We expect to

16	have them approved by the chair and posted in about a

17	month or two, and finally I want to remind folks that

18	everyone on this panel has been approved by the SAB

19	staff office in terms of the absence of any conflict of

20	interest or appearance of a lack of impartiality.	I

21	can't think of any housekeeping issues yet.	So I'll

22	turn it over to Dr. Tony Maciorowski, the Deputy

23	Director of the SAB.

24	DR. MACIOROWSKI:	This will be very

25	brief.	I just want to -- on behalf of the

1	Administrator's Office and the Science Advisory Board,

2	we want to thank you all for being here today.	We

3	particularly want to thank Rogene for chairing this

4	meeting, as once again she's doing Yeoman's work as the

5	chair.	I want to welcome all the CASAC members and all

6	the panelists.	And we want to particularly mention the

7	EPA staff who are prepared to make presentations to

8	you.	Ila Cote is standing here.	I think she'll be the

9	first speaker.	It's my understanding that Lydia Wegman

10	and Karen Martin will not be here this morning, but Dr.

11	Michael Stewart will be sitting in for them this

12	morning.	And welcome all the members of the public,

13	and I turn the meeting over to Rogene.

14	DR. HENDERSON:	Thank you, Tony.

15	I want to emphasize to the group how important this

16	meeting is to review the ISA for the SOx.	This is the

17	second Integrated Science Assessment document we've

18	looked at.	We looked at the NOx document earlier, this

19	same committee, and as I said before, this is a new

20	process, a new way of doing things.	In place of the

21	criteria document we have this Integrated Science

22	Assessment document.	And I know in talking to Ila and

23	Mary, they're working very hard to develop this as a

24	meaningful document, and we have the privilege of being

25	in on advising them on how to make this the most

1	meaningful document for setting standards that we can.

2	So you have an important task before you here, and I

3	look forward to the discussion that's coming.

4	As we did with the NOx document, I have

5	asked specific people to be lead discussants on certain

6	sections of the report.	At the end of the day, those

7	lead discussants, the ones with their names underlined

8	-- I think they're underlined, yes -- will be

9	responsible for pulling together the consensus view of

10	the group, of the whole panel and answering, providing

11	comments on the specific chapters to which you're

12	assigned.	We are doing it a little different with SOx

13	than with NOx.	With NOx it was charge question by

14	charge question.	That resulted in some redundancy in

15	our report because there's so much overlap between the

16	charge questions.	So this time we're going chapter by

17	chapter, which is really what we've done more often in

18	the past, and that's going to avoid some of that

19	redundancy.	Are there any questions from the panel?

20	I'm not letting you introduce yourselves because we

21	just met for NOx, so I'll presume we all know each

22	other.	But if you have any question about how we're

23	doing this and who's responsible for what.	At the end

24	of the day you'll e-mail Holly your draft comments for

25	the chapter and she will collate those, and in the

1	morning we'll have that draft response to the

2	administrator ready for our review for concurrence

3	within the whole panel.

4	So that's how it happens.	It worked

5	well last time, and I expect it to work well this time.

6	Okay.	Now we're going to turn it over to Ila who is

7	going to tell us about this next ISA.

8	DR. COTE:	I actually mostly just

9	want to welcome people.	Thank you for coming to help

10	us again.	Welcome you on behalf of EPA.	If	there's

11	anybody here that doesn't know me, I'm Ila Cote.	I'm

12	the acting Division Director for the ORD effort on the

13	criteria pollutants.

14	Today we're going to talk specifically

15	about the ORD effort on the Integrated Science

16	Assessment, and tomorrow the emphasis will be on the

17	Office of Air and Radiation, OAQPS's effort.

18	So I just wanted to remind everybody a

19	bit of where we were before we went into talking about

20	highlights from the previous review.	I just want to

21	touch briefly on the current process to remind

22	everybody where we are and the schedule, and then

23	Mike's going to pick it up and talk about the history

24	and highlights from the previous review.	As you

25	remember, this is the process that we're working on. We

1	are, we have developed the integrated plan.	You looked

2	at PM, was it last week, two weeks ago?	And we're here

3	at the Integrated Science Assessment.	Tomorrow we'll

4	talk about the Risks of Exposure Assessment, which all

5	lead to the draft announced Notice of Proposed

6	Rulemaking.	So I think everybody remembers where we

7	are in the schedule or in the process.	So this is the

8	schedule.	The integrated plan is, the projected

9	completion date for the draft is April 2007, which is

10	not far away and the final in October 2007.	And the

11	projected CASAC review for the next version is in May,

12	or we've done that and then -- sorry.	My staff is

13	laughing at me.	And then the Integrated Science

14	Assessment, the first draft, is, will be completed in

15	September of '07, which we just had, and then April of

16	'08, and the final in September of '08.	And the CASAC

17	meeting is right here, and then for the final in July

18	of '08.	So that's kind of where we are in the

19	schedule.	I hope you're oriented even if I'm not.	So

20	I'll, unless there are questions, I'll turn it over to

21	Dr. Michael Stewart from the air office.

22	DR. STEWART:	Thank you, Ila.	My

23	name is Dr. Michael Stewart, and I am from OAQPS.	I'm

24	in Karen Martin's group, and she's very sorry she

25	couldn't be here today, but hopefully I'll be able to

1	give sort of a historical context to, from the previous

2	review so that we can keep in mind as we look at the

3	issues during the current review.	And the only thing

4	I'd like to point out with the schedule is that the

5	next time that there's a SOx CASAC meeting will be in

6	July of 2008.	And when we're, after they talk about

7	this second draft in the Integrated Science Assessment,

8	we'll also be looking at the first draft of the Risk

9	Exposure Assessment.	So with that -- next slide,

10	please.

11	So now I'd like to do a brief history of

12	the SO2 NAAQS, and although this slide doesn't look

13	brief, it actually is.	In 1971, EPA --

14	SPEAKER:	Excuse me.	Is it possible

15	to be a little closer to the microphone?

16	DR. STEWART:	Sure.	Is that better?

17	SPEAKER:	Yeah.	We can't hear.

18	DR. STEWART:	Can you hear now?

19	SPEAKER:	Better.

20	DR. STEWART:	Is that better?	In

21	1971, EPA promulgated the first NAAQS for sulfur

22	dioxide.	There was a primary NAAQS.	A 24-hour

23	standard would set at .14 parts per million and an

24	annual standard was set at .03 parts per million.	A

25	secondary NAAQS	is also promulgated with a three-hour

1	standard set at 0.5 parts per million.	In 1988, EPA

2	proposed not to revise the current standards but

3	requested specific comment on adding a one-hour primary

4	standard of 0.4 parts per million.	And this was to

5	protect asthmatics at elevated ventilation rates, for

6	example, while exercising, from short-term 5 to 10-

7	minutes peaks of SO2 exposure.	And this proposal as

8	well as the request for comment was based on a criteria

9	document for PM and sulfur oxides that was published in

10	1982 as well as an addendum to that document published

11	in 1986.	Now during the public comment period for the

12	proposal there were several questions raised as to

13	whether there was an underestimation of both the

14	magnitude of the health affects associated with these 5

15	to 10-minute peaks of sulfur dioxide as well as the

16	size of acceptable population.	In response to this,

17	the EPA published a supplement to the second addendum

18	to the criteria document.	And this documents focused

19	on recently available clinical exposures of asthmatics

20	to SO2, and in that document is also an exposure

21	analysis that provide an estimate of the number of

22	asthmatics at elevated ventilation rates that were

23	likely to be exposed to short-term peaks of SO2.	Based

24	partly on the information in these documents, in 1994,

25	EPA reproposed not to revise the current standards but

1	again requested comment on regulatory alternatives

2	including adding a 5-minute standard of .6 ppm or

3	establishing a new regulatory program under Section 303

4	of the Clean Air Act.	And Section 303 of the Clean Air

5	Act allows for the EPA to have intervention if they

6	find an imminent and substantial endangerment to human

7	health or welfare.	In 1996, EPA published a final

8	decision not to revise the current standards.	EPA did

9	not promulgate a 5-minute standard or any other

10	regulatory program.	This decision was challenged by

11	the American Lung Association and the Environmental

12	Defense Fund.	And a little bit later, in a later slide

13	I'll talk a little bit more about support case.	In

14	1998, the DC Circuit Court of Appeals remanded the

15	decision back to EPA, saying that EPA did not provide

16	adequate rationale for not setting a five-minute NAAQS.

17	In 2006, there was a deadline suit filed for the Center

18	for Biological Diversity stating that EPA had missed

19	its statutory deadlines for reviewing the	NAAQS, and

20	this is actually part of a larger complaint that

21	included statutory deadline misses for the NO2 primary

22	NAAQS as well as for the secondary NO2 and SO2.	And I

23	just want to also mention that currently we have a

24	consent decree in the deadline suit entered, and we

25	have deadlines that are now finalized.	So we have to

1	have a proposal by July 29, 2009 as well as a final

2	rule making by March 2nd, 2010.	And I also want to

3	mention that the current view will also address the

4	issues raised during the 1998 remand.	Next slide,

5	please.

6	So now what I would like to do is just

7	in general touch on the highlights in the previous

8	review and talk about the key health effects identified

9	during the previous review.	Increased respiratory

10	illness and symptoms were associated with long-term

11	exposure to SO2, and aggravation of bronchitis

12	increased mortality and decreased lung function in

13	children were associated with short-term exposure to

14	SO2.	And in this context when I say short-term, I'm

15	talking about more along the lines of 24 hours.	Now

16	it's important to note, and the previous staff papers

17	note that these epidemiologic studies were done at

18	times and in places where there were both high episodes

19	of PM as well as high episodes of SO2, so it was

20	difficult to delineate whether the health effects were

21	from SO2 alone, or PM alone, or some other combination.

22	Also in the previous review, it was found that

23	transient impairment of respiratory function in a

24	significant proportion of exercising asthmatics

25	following 5 to 10 minute exposures of SO2 at levels as

1	low as .6 PPM, and these lung function changes included

2	decreases in FEV1 as well as increases in specific

3	airway resistance.	So the administrators conclusions

4	from the previous review, the existing annual and 24-

5	hour standards are required to protest against health

6	effects associated with long and short-term exposure to

7	SO2, and five-minute peak SO2 levels do not cause a

8	broad public health problem when viewed from a national

9	perspective because they are localized infrequent and

10	site specific and therefore are not the appropriate

11	type of, are not the type of ubiquitous public health

12	problem for which establishing an act would be

13	appropriate.	Thus, a five-minute standard was not

14	adopted.	And also I'll talk about this conclusion

15	based on an exposure analysis conducted by the EPA.

16	Next slide, please.

17	So after the EPA, after the EPA

18	published that it was not going to promulgate a five-

19	minute NAAQS, I eluded to this in the history that the

20	American Lung Association filed a suit, and in 1998,

21	the Court of Appeals for the District of Columbia found

22	EPA failed to adequately explain determination that

23	revisions to the Sox NAAQS were not appropriate.	And,

24	again, the decision was remanded back to the EPA.	The

25	court required EPA to provide an adequate explanation

1	for the conclusions that five-minute exposures to SO2

2	do not amount to a public health problem under the

3	Clean Air Act given an exposure analyses which shows

4	that between 68,000 and 166,000 asthmatics at least

5	once per year are exposed to levels causing adverse

6	effects.	The EPA has not formally answered this

7	remand, but in the time following the remand engaged

8	the American Lung Association in the negotiations.	And

9	out of those negotiations came an increased monitoring

10	effort, and this monitoring effort was trying to get at

11	where these short-term peaks are likely to occur and

12	with what frequency.	And much of that data that has

13	been collected is going to feed into the current

14	review.	So during the current review we're going to

15	conduct a new risk exposure analysis to better estimate

16	the current size of the asthmatic population affected

17	by short-term peaks of SO2.	And we'll also consider

18	whether ruling making under 303 is appropriate.	In

19	addition to the normal, just looking at, the normal 24-

20	hour as well as the existing, the existing standards --

21	I'm sorry -- to see if any changes need to be made to

22	those.	And that's all I have.	Thank you.

23	DR. HENDERSON:	Thank you.	Are there

24	any questions for Michael?

25	DR. BALMES:	Rogene.

1	DR. HENDERSON:	Yes.

2	DR. BALMES:	Whoever is speaking has

3	to be closer to the microphone for us on the phone to

4	hear.

5	DR. HENDERSON:	And that, I'm glad

6	you reminded me.	We forgot, Holly and I forgot to, to

7	introduce people who are on the phone, and I think,

8	Holly, do you need to be the one who, who calls?

9	DR. STALLWORTH:	Could you introduce

10	yourself?

11	DR. HENDERSON:	We've got John

12	Balmes and then others have called in.	Who else is on

13	the phone?

14	DR. LARSON:	Tim Larson is here, but as

15	John said, it's difficult to hear.

16	DR. PINKERTON:	Also Kent Pinkerton

17	from Davis.

18	DR. HENDERSON:	Good.	Okay.	I

19	think people here are speaking very loudly, and so I am

20	wondering if the audio-visual people can help us a

21	little on that because he's got his hand up saying he

22	is.	So we'll, we'll try to improve that because --

23	Ila, did you have something to say?

24	DR. COTE:	Oh, okay.	Frank had --

25	DR. SPEIZER:	You sent me over here so

1	you won't have to hear me.

2	DR. HENDERSON:	No.

3	DR. SPEIZER:	I'd like to ask about

4	this additional monitoring.	Has any of this been

5	reached, reached the peer review literature?	Where are

6	the data and who is looking at them?

7	DR. STEWART:	I think we'll talk more

8	about this tomorrow during the scope and methods plan,

9	but what I can say is that what came out of the result

10	of negotiations with the American Lung Association is

11	that some of the monitors now are actually going to

12	collect 12, five-minute intervals rather than just

13	collecting the five-minute max within an hour.	But,

14	again, we will talk about this some more tomorrow.

15	DR. SPEIZER:	Wait a minute, you just

16	said "are going to."	Hasn't this been done?

17	DR. STEWART:	Well it has, yes.	Yes.

18	DR. HENDERSON:	Are there other

19	questions, and if you're to my right, I really can't --

20	I mean, on the front.	Frank and George are the only

21	ones, you'll have to call out my name.	Okay.	I think

22	you have an additional presentation, I mean, to NCEA?

23	DR. ARNOLD:	Okay.	Thank you very

24	much.	I'm going to address the Integrated Science

25	Assessment that we've been working on to support the

1	Office of Air as they try to build options for the

2	administrator to select.

3	DR. HENDERSON:	Would you give

4	your name?

5	DR. ARNOLD:	Sure, sorry.	I'm Jeff

6	Arnold.	I'm in Mary Ross's branch.	I do atmospheric

7	chemistry.

8	DR. HENDERSON:	Thank you.

9	DR. ARNOLD:	Next slide, please.

10	This is the team.	You've already met Ila Cote, Mary

11	Ross, who is sitting behind us, Dr. Jee Young Kim who

12	is sitting to my left who has been running the SO2

13	team, and the other members of the team from NCEA.

14	Next slide.	This is a list of our expert authors who

15	have contributed to individual sections, chapters of

16	the ISA and sections of the annexes, which support the

17	ISA.	Yes, please.

18	SPEAKER:	I've already recognized

19	those three.

20	DR. ARNOLD:	Great.	Next slide,

21	please.	So what I'd like to do now is just talk

22	generally about the ISA, and what we're going to

23	present today are just really the brightest highlights

24	of the things which have appeared in the ISA because we

25	know that CASAC members have had it now, and have been

1	looking at it, and have provided comments to us that

2	we've gotten and appreciated.	And the things that I

3	want to point up are things out are things that have

4	allowed us to relate the science to the policy making

5	needs of the Office of Air as they go about developing

6	options.	So in the first section we're going to look

7	at source to dose, and this is going to be looking at

8	emissions of SO2, transformations, fate, and ambient

9	concentrations.	Then we're going to try to

10	characterize those as they're important for

11	understanding the health effects, both short-term and

12	long-term exposures.	Next slide, please.

13	The Integrated Science Assessment, as

14	Ila said, and I know this panel is aware, is a new

15	process, and it's an integrated process in multiple

16	ways.	We've been integrating across scientific

17	disciplines.	We've been trying to reduce the size of

18	what was previously the criteria documents for

19	individual NAAQS criteria pollutants, and integrate

20	both across science, as I said; and then integrate more

21	closely with the Office of Air so that we understand

22	how we can best serve them as they go about designing

23	and testing these options; how we can provide the most

24	useful science that will allow them to support the

25	information that they will present to the

1	administrators.	The annexes, as I said, support the

2	ISA, which is the integrated and summary document that

3	the panel has seen and reviewed for us, and this is in

4	response to repeated calls from CASAC, which have been

5	quite useful to us to	produce a sleeker document,

6	something that's more useful, both for the Office of

7	Air and something that's more integrated, something

8	that's easier for CASAC to read and for the public to

9	digest as well.	So there are, as we've designed it

10	now, there are these two forms to the total science

11	review that ISA, which integrates across the

12	information that's been supported in the annexes.	And

13	I'd like to say that this review is for the primary

14	standard for gas phase SO2.	We will be talking a

15	little bit on the chemistry slide later	about the, one

16	of the phase of SO2, which is production of sulfate.

17	However, we're not concerned with particulate sulfate

18	in this review.	Particulate sulfate is being reviewed

19	both under the PM standard, which is now beginning, and

20	we'll be looking at welfare effects there related to

21	visibility, climate.	And we're also looking at

22	secondary effects from particulate sulfate in the

23	combined NO2/SO2 secondary standard for which we've

24	just finished the first draft of the ISA.	Next slide,

25	please.

1	These are the charge questions given to

2	CASAC members to evaluate for the first chapters on

3	exposure to dose.	I won't read them to you since I'm

4	sure you've read them and have designed your comments

5	around them.	I'll just point out that the important

6	part, important parts to us occur in the first, the

7	first bullet, things that are relative to the review of

8	the primary SO2 notes.	And then in the last bullet,

9	things that are important for the evaluation of human

10	health effects, that's sulfur oxides.	And these are

11	the considerations that have conditioned our writing in

12	the ISA, conditioned our selection of science and we've

13	collected it and reasoned through it, summarized it,

14	and then assessed it so that we can provide support to

15	the Office of Air.	Next slide, please.

16	So very generally I just want to say

17	these few summary things about SO2, chiefly produced

18	from fossil fuel combustion, mostly by electric

19	generating units, highly soluble oxidized to sulfate,

20	mostly in cloud droplets.	Dry deposition and

21	conversion to sulfate results in a lifetime SO2 of

22	roughly a few days in the atmosphere.	Sulfate then

23	circulates, depending on precipitation, for about a

24	week.	And what this means -- again, we don't want to

25	focus on sulfate itself, but what this means is

1	lifetimes for SO2 and sulfate means that the sulfur can

2	be dispersed over large areas, largely homogeneous

3	regional ambient exposures, except where you have

4	particular events.	Next slide, please.

5	You see here a depiction for the eastern

6	third of the continental US, the difference in ambient

7	SO2 concentrations from a three-year average, 1989 to

8	'91, before controls, the acid rain program controls

9	went on the large sulfur emitters and the difference in

10	the most recent period for which we have data 2003 to

11	2005.	And you can see now that in 2005 the mean

12	ambient SO2 concentration was roughly PPB.	However,

13	this dramatic improvement in ambient SO2 does still

14	result in local hotspots.	Next slide, please.

15	What we're showing here with a rather

16	busy table that is actually cut down from the table it

17	appears in the ISA is that even with the dramatic

18	reduction of almost 50% in ambient SO2 from the year

19	1990 to 2005, it is still possible to get very large

20	concentrations for one hour exposures.	So you'll see

21	all the way to the right of this slide, the max

22	concentration for one hour can be as high as 700 PPB

23	while the 24-hour and annual average are still quite

24	low, down in the single digit PPBs.	So this is

25	something that we thought would be useful and helpful

1	for the Office of Air.	Next slide, please.

2	Converting from ambient exposures to

3	personal exposures.	We have some summary points here

4	and chief among them is to realize that indoor SO2

5	comes mostly from the infiltration of outdoor air.

6	There are now a few sources of indoor SO2, and because

7	of this and because of the fact that ambient

8	concentrations are now so low, expect for these

9	infrequent peak exposures that I was showing on the

10	previous slide, only five studies have been identified

11	since the last review that characterize personal

12	exposures to present day low concentrations.	Part of

13	the problem with this, with these characterizations is

14	that personal exposures are now at or below the

15	detection limit of most passive samplers, and this

16	introduces uncertainty in the correlations between

17	ambient and personal exposures.	As you see in the

18	bullet down below that, the rations of indoor to

19	outdoor have quite a wide range due to building

20	characteristics.	Indoor heating and ventilation

21	sources varying with season; that is, there are still

22	some people who are exposed to some indoor SO2 from

23	kerosene heaters, and it is also changes with

24	ventilation rates.	People open the windows more or

25	less depending on season and latitude.	These things

1	are changing the ratios.	However, studies with well

2	characterized personal exposures at higher

3	concentrations, that is above the minimum detection

4	limit at these personal exposure batches, have

5	demonstrated positive associations.	And here is an

6	example, one from Brower et al, 1989.	Next slide.

7	DR. HENDERSON:	Before you go on, may

8	I ask a question?

9	DR. ARNOLD:	Sure.

10	DR. HENDERSON:	There's been a lot

11	of press about these sulfur oxides coming from ships,

12	you know traveling along the coast, is that something

13	that you found to be true that's a major contribution

14	or?

15	DR. ARNOLD:	Yeah.	The -- it's a very

16	good question.	The emission of sulfur oxides from,

17	from marine traffic is, is highly uncertain in the

18	current commissions inventory, and there have been

19	efforts over the last few years to look at ship tracks

20	in, ship tracks of SO2 in the transportation corridors.

21	And although this information has been, is recent and

22	we have looked at it, as I say it is very uncertain in

23	the EPA emission inventories.

24	DR. HENDERSON:	Okay.	We have another

25	question, Ed.

1	SPEAKER:	Just as a comment, we'll

2	talk about it more later, but in the context of

3	California, it's not so indecisive, certainly

4	California because we don't have coal fired plants.

5	The sulfur admissions from the harbor, from the ships

6	coming to port to Los Angeles and Long Beach accounts

7	for over half of the sulfur burden SO2 across the

8	basin.

9	DR. ARNOLD:	Yes, I'm sorry.	I

10	didn't mean to suggest that it was unimportant.	I was

11	suggesting that it was uncertain because it hasn't been

12	looked at extensively until very recently, but we have

13	looked at both, both emissions during transit and then

14	during the periods called hoteling when the ships are

15	actually idling at port when things are being moved on

16	and off.	And you're quite right.	And one of the

17	reasons I didn't mention, I alighted over the point

18	that when I was showing the eastern third, when I was

19	showing those spacial temporal plots for the change, we

20	weren't showing the west because, as you know, the SO2

21	problem is much greater in the east.	So you're quite

22	right, and we, we take that comment.	Thank you.

23	DR. HENDERSON:	Okay.	Yeah, go

24	ahead.	Do we -- no.	We've got more XX.

25	SPEAKER:	I just have a question

1	about what you meant by transportation corridor, and I

2	wondered if you had looked at the evidences with regard

3	to the operation of marine engines in the

4	Houston/Galveston/Brazoria non-attainment area?

5	DR. ARNOLD:	That information is, is

6	known to us.	We have not, we have not, we have not

7	specifically addressed that transportation corridor in

8	itself in the ISA.	As you've probably seen, we don't

9	call out a Houston/Galveston shipping channel itself,

10	but that's exactly what I mean.	And the sort of ships

11	you can look at, it's possible to trace SO2

12	concentrations from the ship stacks as they move in the

13	shipping corridors and then as they come into port for

14	these, as we're saying, for these hoteling operations

15	where they're actually idling and still producing SO2.

16	And the port, as it was pointed out in California, is a

17	very large source of that.	So certainly at places

18	where, where there are major ports, you can get a very

19	large local contribution.	Again, since this

20	information is, is new, relatively new in the last few

21	years, the emissions inventories are quite uncertain

22	about, about how to disperse those numbers across the

23	boards.

24	SPEAKER:	So the word transportation

25	corridors could be, could be translated to harbors.

1	DR. ARNOLD:	Both, both harbors and

2	then the ship tracks as they, as the ships are moving

3	into harbor; that's correct.

4	SPEAKER:	Okay.	Thank you.

5	DR. HENDERSON:	Are there any other

6	people who want to ask questions before we move on.

7	Okay.	Go right ahead.

8	DR. JOHNS:	My name is Doug Johns.

9	I'm a health scientist with NCEA, and I'm going to

10	begin the presentation of material related to charge

11	questions four through six dealing with health effects

12	of SO2.	And, again, I'm not going to read through

13	these questions, but you have them.	Next slide.

14	I'd first like to go over the

15	classification system that we use in evaluating the

16	health evidence related to SO2 exposure, and this is

17	described in Chapter 5 of the ISA.	The relationship

18	between SO2 exposure and some adverse health effect was

19	considered causal only when it was supported by strong

20	and consistent evidence from human clinical studies.

21	Where there was strong and consistent epidemiological

22	evidence along with coherent and plausible human

23	clinical or animal toxicological evidence, we

24	considered the relationship to be likely causal.	Where

25	the epidemiological findings are generally strong,

1	consistent but with limited experimental evidence for

2	coherence and plausibility, we concluded the

3	relationship was suggestive, and the relationship

4	between SO2 and health effect was judged to be

5	inconclusive where either the epidemiological evidence

6	of the experimental evidence was strong and consistent.

7	Next slide.

8	Sulfur oxide is highly water soluble and

9	is readily absorbed in the upper airways.	So for

10	individuals breathing through their nose, almost all

11	the inhaled SO2 is absorbed in the nasal passage, and

12	this is depicted in the figure on the left with the

13	yellow and red checkerboard shading representing SO2

14	and the airway.	It shows that very little of the SO2

15	reaches the lower respiratory tract.	However, with

16	exercises there's an increase in ventilation rate along

17	with a shift from nasal to oronasal breathing, which

18	causes, allows a significant fraction of the inhaled

19	SO2 to reach the lower airways, and that's shown here

20	in the figure on the right.	And this is something

21	that's important to remember as we discuss the health

22	effects of SO2. Next slide.	Controlled human studies

23	among exercising asthmatics have consistently

24	demonstrated SO2 induced decrements in FEV1, increases

25	in specific airways resistance, as well as increases in

1	respiratory symptoms following peak exposures to

2	concentrations between 0.5 and 1.0 PPM, and these

3	effects are seen within minutes of the start of

4	exposure.	And the studies conducted over the past 20

5	to 25 years typically looked at effects falling 5 to

6	15-minute exposures.	With increasing concentrations,

7	there is an increase both in severity of response as

8	well as the fraction of subjects that are affected.	It

9	is important to point out here that the effects are

10	generally not enhanced with increasing exposure

11	duration above 10 to 15 minutes, and, in fact, in many

12	studies the effects have been observed to be attenuated

13	when exposures go beyond that period or when there is a

14	repeat exposure separated by 15 to 30 minutes of rest.

15	And finally, just to point out that these respiratory

16	effects have generally not been observed in exercising

17	non-asthmatics at concentrations below 1.0 PPM.	Next

18	slide.	Thank you.

19	So as an example of what I described in

20	the previous slide, this is a study coming from, a

21	study from 1986 looking at SO2 induced changes in

22	specific airways resistance following 10-minute

23	exposures with moderate levels of exercise.	These

24	exposures were done among asthmatics, 27 asthmatics.

25	So this is a cumulative frequency plot with each point

1	along this plot representing the concentration that was

2	estimated to result in a doubling of specific airways

3	resistance for a given individual.	So in the study

4	they found that approximately 25% of the subjects

5	experience this doubling at concentrations below 0.5

6	PPM, and this is relatively, this has been observed in

7	many other studies.	In fact, in some studies up to 50%

8	of the asthmatic subjects experience moderate to severe

9	decrements in lung function at concentrations as low as

10	0.5 to 0.6 PPM, and those effects are usually

11	accompanied by significant increases in respiratory

12	symptoms.	Another thing to point out here is the

13	variability in response with some subjects affected at

14	concentrations below 0.3 PPM while others are not

15	affected at concentrations below 5 PPM.

16	So this is a brief overview of the

17	evidence from human clinical studies.	And if there are

18	any questions.	I think Dr. Jee Young Kim will be

19	discussing the epidemiological evidence.

20	DR. HENDERSON:	Do people have any

21	questions for Doug?	Yes.	Oh, good.	Hi.

22	DR. THURSTON:	Hi.	Yeah.	I really

23	have what I consider a very serious problem with this

24	which is that what you're talking about here primarily

25	is just pure SO2.	Now in the real world people aren't

1	exposed to just pure SO2, and you also, we're going to

2	have a discussion in a minute about the epidemiology,

3	and the epidemiology is showing associations, some very

4	compelling associations at much lower levels.	And one

5	of the questions that I think this document has to

6	address, really confront, is, you know, how can that be

7	with the controlled studies.	What is it that these

8	controlled studies-- and they do tell us things.	But

9	what is it they're not telling us?	And there's

10	evidence out there which is not brought forth in this

11	document about enough-- there is, I think, one study,

12	Jane Koenig's study where she has particles in there

13	and where there are no effects of SO2.	She adds in

14	sodium chloride particles and suddenly there are

15	effects at much lower levels.	This is very information

16	because that's what happens in the real world.	In the

17	real world there are always particles around, and

18	particles are a vector for gases into the lung.

19	There's Mary Anders' work.	So there's, there's

20	controlled studies that have been done.	There's also

21	toxicology in animals.	Mary Ander's work -- I know

22	some people sort of objected to looking back beyond the

23	last 5 years or 20 years, but I think good information

24	is good information whenever it occurs.	And I think

25	the salient point, salient research to be brought

1	forth, irrespective of when it was done.	So I really

2	don't have a problem.	I really don't like that -- I

3	mean, you certainly should emphasize what have we

4	learned since the last document, but you also ought to

5	be looking back and saying, giving a context, which you

6	have done to some extent.	But I really do think the

7	context is important, and studies like Mary Anders'

8	shouldn't be ignored because they're informative about

9	this dichotomy, apparently dichotomy between the

10	clinical studies.	You know, you're saying well there

11	is no effect in normal people above 1, but every one of

12	these documents should say to pure SO2, to pure.	Every

13	time you're just talking about SO2 you should say pure

14	SO2, and then the reader will know, oh, this is not

15	really like what I'm exposed to.	This is not what the

16	populations are exposed to.	And when there's a mixture

17	that's been looked at, I think that's important to note

18	too.

19	So that's, that's my, I guess, major

20	point on this, and I didn't realize we were commenting

21	section by section on a related thing.	You know, in

22	the previous one, in slide number eight, I think, there

23	was no information there about the five-minute data,

24	you know.	I went through this whole ISA, and I had no

25	idea that there were these five-minute data that had

1	been collected for years.	Then I read the other

2	document and I said, my God, look at all this data.	I

3	could really use this to inform my knowledge about what

4	people are exposed to these short -- 'cause let's face

5	it, one of the things we're looking at is should we

6	have this 5-minute or 15-minute standard, and yet those

7	data were not -- at least I didn't see them --

8	presented in the ISA.	And then the other document is

9	saying that all this data are available, so we ought to

10	have key data in there to tell us what's the

11	distribution of those data.	How many are above 50,

12	100, you know, PPD and so forth?	So that is a major

13	need, I think, in the first part, but this issue of the

14	interaction with particles, as I note in my comments, I

15	think is an important issue that needs to be brought

16	forth.	I know you want to take sulfates and put them

17	off to the side so it simplifies your life, but the

18	reality is the SO2 is never present without particles.

19	DR. HENDERSON:	Thank you, George.

20	Are there any other?

21	DR. BROWN:	I just have one quick

22	question.	The slide that gives, you know, causal

23	suggestive, and so forth.	What strikes me about that

24	is I don't even know what it meant.	Not that I don't

25	know what causal means or suggestive means.	That slide

1	in that system looks a lot to me like a sort of hazard

2	identification, which I always have trouble with

3	because everything in some level is going to cause an

4	effect.	So I don't know what causal refers to here.

5	Are we to take it that causal means causal at the

6	levels of exposure that we're going to be considering

7	in this deliberation?	Because if it means causal at

8	some level of exposure, well the answer is always yes,

9	yes, yes, yes, yes.

10	DR. COTE:	I'd like to hear from

11	John 'cause I'm going to sit.

12	DR. SAMET:	If you can go back to

13	that slide.

14	DR. COTE:	And one of the things --

15	DR. SAMET:	Let me comment on those

16	because my comments, I think follow on those.	They

17	actually --

18	SPEAKER:	There they are.

19	DR. SAMET:	So just to comment on

20	these, these bear no resemblance to any of the causal

21	classifications in the SES, and let me, let me tell you

22	what's wrong with it.	First you set up a paradigm in

23	which only experiment leads to a causal determination

24	at the top, which is certainly not consistent with

25	thinking in public health in general.	I mean, if you

1	look at some of the evidence classifications, the

2	agency health care quality and research or whatever it

3	is called these days, they pose the experiment of

4	clinical trial as the highest level of evidence, but

5	that is not required for causal inference.	This, for

6	example, would not lead to cigarette smoking be

7	classified as causally associated with anything if I

8	interrupt these criteria correctly.	Second, you used

9	the word strong.	Strong usually refers to the strength

10	of association, the magnitude of the relative risk.	I

11	would not expect "strong" associations for most of the

12	pollutants that we will be considering, so I'm not sure

13	what you mean by strong.	So, again, in epidemiological

14	discussions we often talk about relative risk of 2, 3,

15	4, 5, and so on where alternative explanations to

16	causation can be set aside, confounding and so on.

17	So I don't see that these work, and if

18	you were to go back and read Surgeon General's report

19	2004 where we looked at this very closely, I think you

20	would see that the thinking here is quite discrepant

21	with those who are thinking about causal inference and

22	public health.	So I, I just can't accept this as a

23	starting point here because this should not take on

24	legs.	This is not correct.

25	DR. COTE:	We, I think, John,

1	largely agree with you.	Unfortunately, we didn't

2	realize we agreed with you until after the NOx meeting,

3	and this document had already gone to you.	And we

4	decided in the presentation to keep it consistent with

5	what was said in the document, but the next time you

6	see this it won't, it will be different and more

7	consistent with, I think, some of the reports that

8	you've pointed out.

9	DR. SAMET:	Yeah.	And I'd be happy

10	to give you some general background.	And, in fact, I

11	recently chaired an IOM committee looking at this issue

12	around decision-making for veterans, and there's three

13	excellent chapters in that book on causal inferences in

14	the report that I'll give you reference to.	But I

15	think you really need to come into line with general

16	thinking here.

17	DR. COTE:	I agree, John.	I think

18	that we just, again, when we didn't quite think this

19	through clearly before the first NOx document and then

20	kind of set it in stone for these two drafts.	So our

21	plan is to revisit those, but I'd appreciate those

22	references also.

23	DR. BROWN:	And what was the answer

24	to mine?	Is it causal at anything remotely approaching

25	the levels we're talking about or just causal at some

1	level of exposure?

2	DR. COTE:	John can help me on this

3	because what I want to say is based on things that he

4	suggested that I read, so just in case I didn't

5	interpret it correctly.	But that question was asked at

6	the last meeting, and I gave you a different answer

7	than I think I would give you now.	At the last meeting

8	I said, yes, what we were interested in was a causal at

9	ambient concentrations, and I think that we're moving

10	more toward what I interpreted at least was laid out in

11	a smoking, Surgeon General's report on smoking.	And

12	that's to be what's the evidence that it's causal, and

13	then the, sort of the dose response assessment part is

14	more of an inference or an implication.	I can't

15	remember the term that was used.	And that's a thing to

16	talk about if that's, is that what people think is

17	appropriate that you do.	It's causal.	We know that it

18	causes these effects, and then the, does it cause it at

19	the dose or the ambient exposures are separate kind of

20	discussion.

21	DR. BROWN:	Okay.	I can go with

22	that.	All I would say is that you needn't have spent

23	any time at all answering the question can it cause

24	adverse health effects at some level of exposure

25	because the answer is always yes.	It doesn't matter

1	what the substance is.	It's always yes so.

2	DR. COTE:	That's part of the problem

3	is I think for many of the very wonderful studies that

4	have been, that have grappled with very difficult

5	issues, it wasn't so clear they were causal.	So much

6	of the emphasis was, you know, developed on having a

7	system that sorts out is it causal.	In this particular

8	case if you apply those schema it looks a little bit,

9	you know, it's kind of like, yeah, it's always causal,

10	and then you get down to discussing is it causal at

11	ambient levels.	So that's kind of a quandary for us

12	that I'd certainly like comment on.

13	DR. HENDERSON:	Well, it sounds like,

14	John, you can be a big help to them, and we will see

15	this document again, right, in --

16	DR. COTE:	Yes.	And I also want to

17	thank Dr. Cowling who had also made some good

18	suggestions on, you know, formal documents that use

19	different approaches to these problems that we've also

20	been utilizing.

21	DR. HENDERSON:	So that's, that's

22	great.	That's exactly what we're here for is to help

23	you get the best ISA possible.	So is there any, any

24	other questions before we go on to Dr. Kim?

25	DR. ARNOLD:	Rogene, if I could just,

1	if I could respond to a point, respond to a point

2	raised by George and then earlier by Frank about the

3	five-minute data and that is that until the, until the

4	new request from the Office of Air had gone out, states

5	were not, and they are still not required to report

6	five-minute data.	And so what this results in is a

7	very poor distribution of monitors that were reporting

8	five-minute data across the country, and it is not

9	actually even across the county as I'm sure you can

10	imagine.	In having looked at the information that went

11	up through the year 2000, there are a very small number

12	of monitors reporting a very small number of

13	observations.	And in those data, the very high

14	concentrations, concentrations greater than 600 PPB

15	were less than .05% even at this, from a very small

16	number of monitors.	What we are working with now in

17	the Office of Air and analysis is going on now and this

18	gets to Frank's question about whether any of this has

19	been published yet.	We're still working on an analysis

20	of the additional information that has been collected

21	since 2000, so that's why that doesn't appear in this

22	version of the ISA.

23	DR. THURSTON:	Can that make it in

24	here?

25	DR. ARNOLD:	To the extent that we

1	can include information that is produced in time for

2	the second draft, sure.

3	DR. HENDERSON:	Okay.	Dr. Kim,

4	you want to -- oh, wait a second.	No.	There's a

5	question.	I'm sorry.

6	DR. SPEIZER:	I just wanted to sort

7	of add a note of completion.	There's another mechanism

8	for exposure of the lung and that is by the absorption

9	of SO2 in the nose, and it actually gets excreted in

10	the lung.	So I think you have to sort of keep in mind

11	that it isn't just a matter of it all being absorbed

12	and goes away.	It's still there and it may very well

13	have its effect through a different kind of mechanism.

14	DR. HENDERSON:	Okay.	Ellis has a

15	point..

16	DR. COWLING:	As a supplement to what

17	George Thurston said a moment ago about the time frame

18	for publication, one of the things that CASAC has been

19	trying to emphasize is it is not just new evidence but

20	new insights about old evidence that we ought to be

21	giving attention to.	The other thing that I'd like to

22	mention has to do with the issue of -- oh, I've

23	forgotten what I wanted to say.	I must apologize to

24	the chair.	I will come back as soon as my memory is --

25	DR. HENDERSON:	Ellis, you just

1	feel free to bring it up whenever it pops up.	I'm very

2	sympathetic to that.

3	SPEAKER:	We all are.

4	DR. HENDERSON:	Okay.	Pending no

5	other questions, we'll move on to Dr. Kim.

6	DR. KIM:	Hi.	I'm Jee Young Kim and

7	I'm an epidemiologist at NCEA.	One thing I do want to

8	clarify before we went into the epi evidence --

9	actually, could you go to the next slide, please.	In

10	epi when we refer to strength, what we were talking

11	about was rather weight of evidence versus the strength

12	of effect.	So when I use the word strong, I'm meaning

13	that there was, you know, there was a lot of evidence

14	that was available that supported the conclusion that

15	we're making.

16	So I'll be presenting an overview of the

17	epidemiological evidence on SO2 health effects,

18	starting with respiratory effects with short-term

19	exposure, which in this case is generally a 24-hour

20	average.	The strongest evidence of SO2 effects in

21	epidemiology comes from the panel studies examining the

22	association between short-term exposure to SO2 and

23	increased respiratory symptoms in children.	As you can

24	see in this floor plot, with exception of that one

25	study at the bottom -- I don't have a laser thing-- at

1	the bottom by Romeo, et al, all the studies are

2	positive, and in several cases statistically

3	significant.	The two recent multi city studies are

4	Mortimer, et al., which is on the top of the figure and

5	Schildcrout, et al. near the bottom of the figure.	And

6	both of these found positive statistically significant

7	associations at the multi day lag.	Oh, thank you.

8	Yeah.	So that's Schildcrout and that's

9	Mortimer right there, and these studies did some

10	analyses or some examination of the co-pollutant

11	issue, and in multi-pollutant models of Mortimer, et al

12	they found that SO2 effect estimate was robust to

13	adjustment for PM-10, NO2 and ozone.	In the case of

14	Schildcrout, they did a combination of pollutants and

15	found that the SO2 effect was indeed most evident when

16	considered in combination with NO2 and carbon monoxide.

17	The Schwartz et al study, which is right here, is an

18	older study, the Harvard Six City study done in 1994,

19	published in 1994, and in this study, once again, there

20	was a positive significant effect that was observed.

21	But in a two pollutant model with PM-10 they found that

22	the effect estimate decreased considerably.	The one

23	thing to note about this was that the PM-10

24	concentrations were very correlated, highly correlated

25	with sulfate particles.	I believe the correlation

1	coefficient was 0.8, and in this case adjusting for PM-

2	10 may have resulted in over-adjustment in the model.

3	So moving onto the next slide, this is a

4	figure depicting studies of all respiratory and asthma

5	hospitalizations and ED visits with co-pollutant

6	adjustment.	Note that these are not all the studies

7	that looked at this association but simply the ones

8	that also presented results on multi-pollutant models.

9	You can see that in some of the studies with these wide

10	confidence intervals, the effect estimate does decrease

11	significantly when adjusting for co-pollutants and in

12	some cases becomes negative, but the other thing to

13	note about these studies is that the Yang, et al.,

14	Llorca, et al and Lin, et al studies for example, they

15	adjusted for four different co-pollutants.	And in the

16	case where these co-pollutants are probably moderately

17	to highly correlated with , this may have not been the

18	best way to examine co-pollutant interactions or

19	compounding by co-pollutants rather.	So, therefore, we

20	focus on the study that had one additional pollutant

21	added into the model and also the ones with tighter

22	confidence intervals, which give us some indication of

23	study power.	For example, in this study by Schwartz

24	here on the top, adjustment for PM-10 did not

25	appreciably affect the effect estimate in New Haven,

1	though it did decrease it in Tacoma where the SO2

2	concentrations are lower.	In Sunyer et al and Anderson

3	et al once again you'll see that the effect estimates

4	did not appreciably change with adjustment for black

5	smoke and NO2.

6	So from this we concluded that the

7	studies with tight confidence intervals, adjusting for

8	one additional pollutant, that generally the effect of

9	SO2 on respiratory health hospitalizations did not, was

10	not, I'm sorry, were generally robust and independent

11	of effects of other co-pollutants.	Next side, please.

12	So many new epidemiological studies

13	supported by evidence from animal tox studies as well

14	as some of the clinical studies provided evidence of a

15	relationship between short-term exposure to SO2 and

16	respiratory health effects ranging from respiratory

17	symptoms and increasing in severity to ED visits and

18	hospitalizations for respiratory causes.	Associations

19	were observed between ambient SO2 concentrations and

20	increased respiratory symptoms in children,

21	particularly among those with asthma or chronic

22	respiratory symptoms.	The recent US multi city studies

23	along with several other single city studies observed

24	these associations at ambient concentrations that are

25	below the current 24-hour average NAAQS, which is 0.14

1	PPM or 140 PPB.

2	One interesting thing to note was that

3	the Harvard Six City study done by Schwartz et al

4	examined the concentration response function of the

5	relationship and observed that no significant increase,

6	and that's a statistically significant increase was

7	observed in the instance of lower respiratory symptoms

8	and	until	you reach 22 PPB, which was around just

9	about the 90th percentile of the distribution of the

10	data that they have for SO2.	And this perhaps suggests

11	that the associations are maybe led by the higher or

12	peak year concentrations in the distribution.	Positive

13	but not always statistically significant associations

14	were observed between ambient SO2 concentrations and ED

15	visits and hospitalizations for all respiratory causes.

16	And these associations were particularly examined and

17	observed in children and older adults.	So from the

18	available evidence that we have, we conclude that there

19	is a likely causal association between short-term

20	exposure to SO2 and respiratory effect.	Yes, Dr.

21	Speizer?

22	DR. SPEIZER:	Yeah.	I'd like to raise

23	an issue, which will come up later again I'm sure, and

24	it has to do with how we look at these data. For the

25	last 50 years there have been studies on SO2, and in

1	probably virtually almost every one of those studies,

2	and this was mentioned earlier, there's a small segment

3	of the population, maybe 10, maybe 20, maybe up to 30

4	or 40% of the population that clearly have significant

5	positive effects.	When you put this in a population-

6	based estimate, often it is null because the dominant

7	population don't have response.	Now it's our ignorance

8	as to what makes these people more vulnerable to , but

9	I think we have to start to think about, but this has

10	sort of been shown over, and over, and over again.	And

11	to ignore it essentially by looking at the mean

12	response of the groups is to really deny the science

13	that we know.	We know that there's an effect there.

14	Now I'm not blaming you guys because that's the way

15	it's always been done, but I think we have to start

16	thinking about different ways of looking at this.	I

17	think we're just sort of sticking our heads in the sand

18	to say that these results are in general null when we

19	know that there are sub-segments of the population

20	which we can't, sometimes we can identify, but most

21	often we can't identify who they are, who are

22	responding and perhaps responding to a very significant

23	adverse effect.	How we're going to deal with this?	I

24	put it on the table because I think we need to discuss

25	it.	I'm not sure I have the answer as to how we're

1	going to deal with it, but I think it is an issue.	I

2	think it really is an issue that we have to deal with.

3	DR. KIM:	Yes.	We certainly agree

4	that there is a wide distribution of individual

5	variability and how we can use that with epi studies

6	I'm not so sure given the current database that we

7	have.	I guess some epi studies do focus on the more

8	susceptible populations such as asthmatic children, but

9	once again it's hard to keep, they don't provide

10	individual results obviously in these papers.	The best

11	data we have is from the human clinical studies

12	examining this, and, of course, those studies don't

13	examine the most susceptible populations anyway.	But

14	we'll consider your comment.

15	DR. BALMES:	This is John Balmes.

16	DR. KIM:	Yes.

17	DR. BALMES:	I would just say that I

18	appreciate the general concern that was brought up

19	about susceptible populations being sort of under, the

20	impact on susceptible populations being under-

21	appreciated, underestimated from the epi studies that

22	focus on the entire population, but I think with	we

23	actually have a better handle than perhaps with ozone

24	or NO2.	Who is most susceptible in that the clinical,

25	the human clinical studies I think clearly identify

1	that asthmatics are much more susceptible than normal

2	individuals.	So I think we're on very strong ground

3	when we say that asthmatics are a susceptible

4	population with regard to SO2 exposure.

5	DR. HENDERSON:	Thank you, John.

6	Are there any others?	I see a hand, George.

7	DR. THURSTON:	I just wanted to pick

8	up on the remark that Dr. Kim made about the multi-

9	pollutant models.	And, you know, I don't know if you

10	want to flip back to that slide, but a lot of them

11	included are what I would call a kitchen sink model.

12	They've thrown in everything but the kitchen sink, and

13	I don't really find those models meaningful because of

14	all the -- and even, you know, in the other document, I

15	quoted him in my comments that they say, "When co-

16	linearity exists," which of course it does, "inclusion

17	of multiple pollutants in models often produces

18	unstable and statistically insignificant effect as to

19	both SO2 and the co-pollutants.	So I don't, I

20	personally feel we shouldn't be showing these.	I think

21	the most you should want to put up there is that there

22	are two pollutants in a model and then look how they

23	co-value, and those should be sensitivity analyses.

24	But, you know, just because somebody publishes these

25	things doesn't mean it's meaningful or that that's what

1	you should present.	And I've run into this in the

2	past.	I wrote sections and I actually remember one

3	time Rick Burnett got on my case because he said, "Well

4	wait a second those aren't, what you have there are not

5	my conclusions from my study, and those are not all of

6	my results."	And I said, "That's right.	Those are my

7	conclusions from your study, not yours because I

8	ignored the kitchen sink models, and so it came up with

9	very different conclusions.	And that's not always

10	going to be the case, but I just think when you put a

11	lot of pollutants in there that are correlated with

12	each other oftentimes what comes out is the one

13	pollutant that is not as correlated with the other

14	pollutants; but that doesn't mean it's causal that's

15	driving the associations.	It really is not very

16	informative, so I'm not sure you should even -- I think

17	you should exclude them.

18	DR. HENDERSON:	Pat Kinney.

19	DR. KINNEY:	I would tend to disagree

20	with that, but I wanted to talk about this table also.

21	I think at least in the way the ISA is currently

22	written, I didn't, I didn't see a very good argument

23	made for this, the conclusion about general robustness

24	that you stated, although I think the way you just

25	explained it gave more detail than I saw in the

1	document.	There is some nuance about studies with

2	tight confidence intervals and studies that, you know,

3	at higher concentrations, you know, that sort of help

4	build that argument.	But, you know, when I just looked

5	at this figure and then I saw the conclusion about

6	general robustness and then, the way that got carried

7	through the entire document and then into the risk

8	assessment document as well, I just thought it really

9	needed to be pinned down much more clearly in the ISA.

10	And, you know, based on this figure, I'm still not

11	convinced that I would say there is general robustness,

12	you know, in spite of what George has said, which is a

13	good point; but I think the central question is really

14	to what extent are these results, these effects we're

15	seeing really due to SO2 as opposed to the mix of

16	pollutants, and can we even say anything about that.

17	I'm not sure that we can, but it's results like this

18	that are the only thing we can look at to help us think

19	about that.

20	DR. HENDERSON:	Yes.	And I agree

21	in this one, I, George would disagree that these

22	shouldn't be presented because I think they are

23	informant about where we are.

24	DR. KIM:	Well, I guess I did want

25	because there's sort of a disagreement here about what

1	is appropriate for multi models in terms of the number

2	of adjustments.	Can we have a little bit more

3	discussion about that to sort of guide us through.

4	Okay.	I was just told that we should probably do this

5	when we discuss Chapter 3 so.

6	DR. HENDERSON:	Well Jon Samet has

7	something to say.

8	DR. SAMET:	Well, I'll comment.	I'll

9	comment here later.	I think this comes out of the crux

10	of interpreting this.	I think the other issue that has

11	to be put on the table is publication bias and how to

12	interpret it because, again, I think statistically

13	significant associations in these sort of multi variant

14	model data are far more	likely to appear than non-

15	significant associations and that issue has to be dealt

16	with.	I think we need a pretty lengthy probably

17	discussion of how to interpret these.	Either, George,

18	either the univariant, bi-variant, or multivariant

19	models in the face of some of the real problems in

20	measurement error and everything else.	And I don't

21	know that this is the time to have that discussion, but

22	I think it should come up when we come on to Chapter 3

23	discussion and in Chapter 5.	The other just passing

24	comment, I won't let you get away with saying weight of

25	evidence and strength are equivalent, and I've never

1	known what weight of evidence means.	EPA people staff

2	love to use that term, and every now and then I do it;

3	and then I saw well like what does that really mean,

4	and if it's a couple of studies out of an infinite

5	universe of epidemiological studies showing

6	statistically significant associations, it's probably

7	not, I guess, a heavy body of evidence; is that the

8	counterpart of weight of evidence?	So be careful.

9	DR. HENDERSON:	Okay.	I thank

10	you, Jon, and I think now we should move on.	Jon has

11	pointed out that we can discuss this at greater lengths

12	later on as the, as we go through the different

13	chapters.	So we'll let you, Dr. Kim, finish your -- or

14	you --

15	DR. KIM:	A couple of findings, one

16	more, please.

17	DR. HENDERSON:	Okay.

18	DR. KIM:	So now the evidence on the

19	effect of short-term exposure of SO2 on cardiovascular

20	morbidity and mortality will be discussed.	Here the

21	effect of SO2 on cardiovascular morbidity is generally

22	inconclusive in both epi studies and human clinical

23	studies.	Some positive associations were indeed

24	observed in the studies of ED visits and

25	hospitalizations. There is a lack of supportive data

1	from panel studies and human clinical studies on

2	preclinical cardiovascular health effects that provide

3	biological plausibility for these absurd associations.

4	For the effect of	short-term exposure

5	to	mortality, we conclude that there is suggestive

6	evidence from epidemiological studies, and this is

7	because several studies observed positive associations

8	in US and Canadian multi city studies.	And probably

9	the one thing to note was that in multi-pollutant

10	models, once again the best evidence we have for, to

11	consider confounding, these effect estimates did tend

12	to decrease.	So the SO2 effect estimates did decrease

13	but in many cases remained positive and in some cases

14	remained statistically significant.	There is also an

15	intervention study from Hong Kong that provides

16	supportive evidence of a reduction in SO2 levels,

17	linking the reduction in	levels with a reduction in

18	deaths.	However, one thing that we should note is that

19	this does not preclude the possibility that it's not

20	per se but something that's emitted along with SO2 such

21	as vanadium or nickel that may be causing these

22	reductions.	Next slide, please.

23	Evidence of health effects from long-

24	term exposure to SO2 are generally inconclusive.	For

25	respiratory morbidity, effects of long-term exposure on

1	respiratory symptoms and lung function were assessed in

2	epidemiologic studies.	While some of these studies did

3	observe positive associations for respiratory symptoms

4	in particular, the general overall evidence-base was

5	inconsistent and the results were mixed.	There was

6	limited animal toxicology studies that cannot fully

7	provide strong biological plausibility.

8	There are two recent epidemiologic

9	studies that observed the association between long-term

10	exposure to SO2 and instance of cancer, and both

11	provided no evidence of an increased risk.	Their

12	animal studies also did not find that SO2 was a

13	carcinogen by itself, but there was some limited

14	evidence of cool carcinogenicity at high

15	concentrations.

16	For adverse birth outcomes, there was

17	some positive associations between SO2 and low birth

18	weight.	However, the results were inconsistent across

19	trimesters of pregnancy, and also most of these studies

20	did not adjust for important potential confounders such

21	as maternal smoking and socioeconomic status.

22	And finally, results from two major US

23	epidemiological studies observed positive and

24	statistically significant associations between long-

25	term exposure to SO2 and mortality, and those were the

1	Harvard Six City study and the American Cancer Society

2	study.	However, several other US and European studies

3	did not observe this association.	So these

4	inconsistent associations and the difficulty and

5	challenge of distinguishing effects by other co-

6	pollutants limit the interpretation of us to state a

7	causal association.	Next slide, please.

8	So these are charge questions 7 and 8,

9	and these deal with the public health impact and

10	adequacy of the ISA to provide support for future risk

11	exposure and policy effectiveness.	Last slide, please.

12	Epidemiological and human clinical studies have

13	evaluated potentially susceptible and vulnerable

14	populations and observed that subjects with respiratory

15	illness, most namely asthma are more susceptible to

16	induced respiratory health effects compared to the

17	general population.	Additional epi evidence also

18	suggests that children and older adults, that's

19	individuals who are 65 years or older, are more

20	susceptible and potentially vulnerable to respiratory

21	health effects from SO2 exposure.	The panel studies

22	found the SO2 concentrations were associated with

23	respiratory symptoms in children but not in adults.	In

24	the ED visits and hospitalizations studies observed

25	slightly larger effect estimates for children and older

1	adults compared to the general adults.	There was one

2	study that specifically examined variability by genetic

3	polymorphisms and found the greater response to SO2 was

4	associated with the homozygous wild type allele for TNF

5	Alpha, and this is in asthmatics.	However, the

6	available evidence is much, much too limited to make

7	any conclusive statements at this time regarding

8	genetic variability of SO2 effects.	And that was the

9	last slide.	If you have any quick questions, we'll

10	take them.

11	DR. HENDERSON:	We'll be

12	discussing this in detail later.	Yeah.	Dale, you

13	wanted to say something?

14	DR. HATTIS:	Yeah.	I am just

15	wondering whether you perhaps would plan in there in

16	the next draft of the ISA to have a more general

17	discussion of the strengths and weaknesses of multi-

18	pollutant epidemiological controls because it seems to

19	me that there might be a variability among the panel in

20	the strength of belief of the efficacy of statistical

21	adjustment for confounders in these multi-pollutant

22	analyses.	It seems to me some serious effort would be

23	warranted to discuss that issue as a general matter.

24	DR. KIM:	Yeah.	What we did for the,

25	both the NOx and the SOx ISA was refer heavily back to

1	the PM and the ozone documents where this was discussed

2	in much greater detail.	What we could do is sort of

3	pull out the salient points and perhaps put it either

4	into the ISA or the annex to those documents.

5	DR. BALMES:	This is a small point from

6	John Balmes, but I can't let it go by.	If you turn to

7	slide two, the list of expert authors, my colleague at

8	UC Berkeley, Kathleen Mortimer is identified as being

9	from Yale.	She got her Ph.D. from Harvard and I think,

10	you know, it would be nice to show where she actually

11	is from.	But she is currently at University of

12	California Berkeley.

13	DR. HENDERSON:	Okay.	So with

14	that I think we will, I offer my thanks to all of you

15	for making this presentation and very clear

16	presentations that's got the discussion going well.

17	We'll be talking with you throughout the day, but I

18	think now we move onto what Holly handles and that is

19	public comment.

20	DR. STALLWORTH:	Hi.	Do we have Howard

21	Feldman on the line?

22	DR. FELDMAN:	Yes.	I'm here.	Thank

23	you.

24	DR. STALLWORTH:	Okay, Howard.	You

25	have five minutes.	Howard is with the American

1	Petroleum Institute and his comments have been passed

2	out.

3	DR. FELDMAN:	Well, thank you very

4	much.	Good morning everyone.	Thank you, Dr.

5	Henderson, for allowing me to call in.	You know, we

6	have a dusting of snow here in Washington, so

7	everything is gridlocked here already.	So I'm Howard

8	Feldman.	I'm with the American Petroleum Institute and

9	API has over 400, nearly 400 member companies involved

10	in the oil and gas industry, and we'd like to thank for

11	the opportunity, for having this opportunity to comment

12	on the SOx ISA.	In conclusion right away, API

13	concludes that the significant revision of the SOx ISA

14	is necessary.	Based on the science we see presented

15	there, we don't find that this version conveys the

16	information that's useful to the Administrator to

17	evaluate the possible need to alter thes form or the

18	level of the SO2 NAAQS.	But we have already put in

19	comments to the docket which go into detail on this.

20	In summary, we find that the SOx ISA inaccurately

21	concludes that SO2 measurements from the ambient

22	monitors of good surrogates were measurement of

23	personal SO2 exposure, so that's going to confound

24	everything.	Since the ISA relies on epidemiological

25	studies to infer health effect, those studies that rely

1	on data from ambient monitors are going to lead to a

2	questionable determination of health effects.	So API

3	finds that the ISA inaccurately characterizes the epi

4	evidence as suggesting that the levels below the

5	current standards cause increased respiratory symptoms,

6	increased ED visits, and hospital admissions, and acute

7	mortality.

8	So in the time I have available today

9	I'm going to focus on two points.	First the

10	overarching finding that API does not believe that ISA

11	accurately reflects the full body of the latest

12	science, and second I'm going to discuss why the

13	available information in the ISA does not indicate that

14	SO2 measurements from ambient monitors are good

15	surrogates for measurement of personal SO2.

16	So first of all we know that under the

17	Clear Air Act the SOx ISA must "accurately reflect the

18	latest scientific knowledge useful in indicating the

19	kind and extent of all identifiable effects on public

20	health, which may be expected from the presence of SOx

21	in the ambient air in varying quantities.	So in other

22	words, the science has to be accurate.	Furthermore,

23	the SOx ISA must include the recent information that

24	will be useful to the administrator.	To do that the

25	SOx ISA must clearly set forth the criteria that led to

1	the selection of particular studies for emphasis, and

2	those criteria must be applied consistently.	And this

3	touches on, a little bit touches on, John just

4	mentioned a little while ago a publication vies.

5	That's one place where you can see some of this playing

6	out as well.	The failure of the present draft of the

7	SOx ISA to this rate is questioned about the document's

8	usefulness.	To be useful, the SOx ISA must present an

9	unbiased evaluation of the evidence.	And we talked

10	about, a little bit, you guys were just mentioning

11	through, what are the criteria?	How do you evaluate

12	things objectively?	CASAC member Douglas Crawford-

13	Brown, made the point recently when we were dealing

14	with the NOx health criteria, he said, and we're going

15	to quote this just for emphasis again, "The chapter

16	follows an EPA tendency to present the evidence as a

17	form of building a legal case in which evidence or a

18	belief is what matters most.	Throughout the chapter

19	and throughout the report there is a focus on the

20	studies that is suggestive of an adverse effect.	With

21	the conflicting studies providing a kind of

22	counterevidence that lowered the judgment from likely

23	causal down to suggestive or down to inconclusive.

24	What is needed instead is a methodology that examines

25	all studies, supportive and counter-supportive, ways of

1	findings systematically by trying to determine why

2	there are conflicting results and then yield a final

3	judgment of causality that reflects this full range."

4	And we think that was very well captured there, and we

5	do appreciate that.	Unfortunately in the SOx ISA, as

6	it's presently drafted, it doesn't meet these

7	standards.	It's scientifically inaccurate and biased

8	in several ways, and, therefore, will not be useable to

9	the administrator without substantial revision.

10	Moving on to foundation of the findings

11	on health impacts from the cited epi studies rests on

12	the assumption that SO2 measurements from ambient

13	monitors are good surrogates for measurements of

14	personal SO2, and API does not find that the ISA

15	provides evidence to support this assumption.	Yet the

16	SOx ISA relies on two long-term cohort studies to state

17	that their reasonably strong associations, okay.	This

18	conclusion is based on a 20-year-old study by Brower,

19	and in a series of more recent studies by Sonnet et al.

20	The studies do not, however, support the SOx ISA

21	conclusion.	The more recent Sonnet et al studies are

22	the most relevant as they involve SO2 ambient exposures

23	more typically found today.	Sonnet et al explains to

24	take care of the no exposure studies showing the

25	ambient SO2 to be a suitable surrogate for personal SO2

1	exposures.	Indeed as EPA recognized in a recently

2	completed NAAQS for PM, okay, the ambient SO2 exposures

3	are poorly, poorly correlated.	Ambient and personal

4	SO2 exposures are poorly correlated. Quoting, "Ambient

5	gases pollutant concentrations including SO2 are not

6	correlated with their corresponding personal exposure

7	concentrations; however, ambient gases concentrations

8	were found to be strongly associated with personal PM

9	2.5 exposures suggesting that ambient gaseous

10	concentrations of ozone, NO2 and SO2 are acting as

11	surrogates as opposed to confounders of PM 2.5 in

12	estimating PM health effects.	This is a very big

13	question this is going to touch on.	We've already

14	touched on multi-pollutant models and how those are

15	going to play through and how those need to be looked

16	at, and how you look at these data and these compounds

17	that are correlated and take them apart and find out

18	what's causing the effect and what's not is critical.

19	While API may question EPA's conclusion in the PM NAAQS

20	review that SO2 was acting as a surrogate with PM 2.5

21	multi-pollutant modeling, it is scientifically

22	incorrect for EPA to reach contrary interpretations of

23	the Sonnet et al study from the PM assessment to the

24	SO2 assessment.	This leads to the misstep of

25	attributing to SO2 exposures effects that the agency

1	has already previously attributed to PM 2.5.	So the

2	SOx ISA should be revised to be consistent with EPA's

3	finding when it reviewed the PM NAAQS that ambient SO2

4	concentrations correlate poorly with personal

5	exposures.	Moreover, the SOx ISA should acknowledge

6	that ambient SO2 measurements are a poor surrogate for

7	personal SO2 exposure in observational epi studies.

8	The time does not allow me to discuss in

9	detail other findings of API's review of the ISA.	Our

10	comments discussed is the SOx ISA inaccurately

11	concludes that there's suggestive evidence of

12	association between ambient SO2 levels and the ED

13	visits and hospitalizations for respiratory causes,

14	inaccurately characterizes the epi evidence as

15	suggestive of association between short-term exposures

16	to SO2 and premature mortality, and inaccurately

17	concludes that new epi studies provide evidence of an

18	association between short-term SO2 and respiratory

19	symptoms.	As a copy of our comments with cited

20	reference are provided with the testimony, I thank you

21	for your consideration.	I'm happy to take any

22	questions that you may have.

23	DR. HENDERSON:	Thank you.	Are

24	there questions?	Okay. Well, thank you very much, and

25	that will end our public comment period unless Holly

1	knows of anybody else.	Nope, nobody else.	I think

2	it's a good time to take a break, a 15-minute break.

3	So if you could come back about five minutes after

4	10:00, I'd appreciate it, and we'll start our

5	discussion of the individual chapters.

6	DR. FELDMAN:	And Regina, may I say

7	that I probably could have gotten a lot more than $53

8	an hour by just going right to API and written my

9	comments directly.

10	DR. HENDERSON:	It's okay.

11	(WHEREUPON, a break was taken.)

12	DR. STALLWORTH: Could everyone take a

13	seat?

14	DR. HENDERSON: We are going to be

15	getting together again, so please take your seats if

16	you will.	Thank you.	We're going to start our

17	discussions by receiving comments from the panel on

18	Chapter 2, which includes responses to charge questions

19	1 through 3, and Christian Seigneur is our first lead

20	discussant.	Christian, are you about -- I want to

21	emphasize, the people who are listed here will make

22	their points, but then it will be open for comments

23	from the whole panel.	So anyone on the panel who wants

24	to make comments on Chapter 2, feel free to do so.

25	DR. SEIGNEUR: Okay.	I'll start with my

1	comments on the ISA.	The first point I want to make is

2	that I got it to be confusing within the ISA.	It

3	starts in Chapter 1 by saying that all oxides are being

4	advised, which would include of course SO2 and sulfate.

5	And then when reading the documents at some point

6	emphasis was on SO2 and after that point then emphasis

7	was on sulfate.	So I felt there was a lack of balance.

8	So I'm not sure whether it should say in Chapter 1 that

9	the emphasis will be on SO2 because sulfate is

10	otherwise somewhere else as PM, or if not, if the

11	emphasis is really on both SO2 and sulfate, then

12	throughout the document, both compounds should be

13	advised.	Examples of sulfate not being advised is

14	point source emissions.	The emissions focus on SO2.

15	The fraction of the emissions which is sulfate is not

16	mentioned in the text, so this could be added.	You

17	know, how much of power plant SOx emissions is sulfate.

18	I think it's a small amount, maybe one person thought

19	so.	For ship emissions, which is becoming a bigger

20	deal, how much is ship emissions for instance.	The

21	preceding relevant background is advised, SO2 I didn't

22	see a value for sulfate for instance.	Another example

23	where the emphasis is on sulfate instead of SO2 is the

24	modeling.	You talk about threshold modeling which

25	would apply to SO2 conversion to sulfate at regional

1	scales, which is sort of applied to regional haze, and

2	PM 2.5.	I didn't see any descriptions of the modeling

3	for SO2 because there we are interested in SO2

4	concentrations near the source, and tomorrow we'll talk

5	about the assessment, which is going to be based on

6	AERMOD.	So I would augment the exclusions	for

7	dispersion models, which has AERMOD in the appendix.

8	So that would bring some better balance.

9	Then getting into more detailed

10	questions about the charge questions 1 through 3, which

11	is for Chapter 2.	One major revision I would like to

12	see is the descriptions of why sulfate is not in the

13	gas phase.	A statement was made that sulfuric acid is

14	water soluble and that's the reason why we find it in

15	droplets and particles.	That is true for droplets.

16	The reason we find it in particles is not because it is

17	water soluble but because it has a low, very low

18	saturation rate for pressure.	Otherwise, we would find

19	nitric acid in particles as well, and we know that we

20	only find nitrates when we have ammonia in nitric acid.

21	So that's a correction which needs to be made.

22	In Chapter 2 there is emphasis of course

23	on the coal-fired power plant source category because

24	it is the largest category right now for SO2 emissions.

25	I think it would be good to mention that this is a

1	source category which is being controlled, not too much

2	for SO2 but for acid depositions, PM 2.5, regional

3	haze, and therefore those emissions are decreasing.	As

4	this is happening other source categories may become

5	more important, and Rogene this morning mentioned ship

6	emissions.	And I think that there should be a better

7	descriptions of ship emissions in the document.

8	Obviously there are uncertainties associated with

9	those, as was mentioned this morning by EPA, but we can

10	less those uncertainties.	I think that should be

11	brought up as a source category of interest.

12	Related to that, I assume that the

13	citing of the SO2 monitors has been based historically

14	on trying to characterize the impact of the major

15	source categories, which probably was power plants.

16	But as now we may refocus on other source categories

17	such as ship emissions.	The question comes up whether

18	the monitoring network needs to be reevaluated in terms

19	of the citing of at least some of those monitors trying

20	to find out what that shows the SO2 concentrations are

21	next to those, either the harbors or the ship channels.

22	There is a need, I think, to increase the descriptions

23	of the SO2 chemistry as it is related to the power

24	plant plumes, seeing as power plants are listed as a

25	major category.	There is a single sentence which gave

1	a range of oxidation rates for SO2 to sulfate, which I

2	think is something like, you know, half to two person,

3	which I think is too simplistic, mainly because the

4	chemistry of SO2 in power plants is evolved throughout

5	the history of the plume.	Near the stack there would

6	be no sulfate formation, mainly because you don't have

7	any oxidant in the plume.	Nitrate oxide has eliminated

8	all the oxidants.	Then as the plume gets dispersed you

9	start to build up the oxidants very slowly, and then

10	you start to have a sort of reaction to sulfate.	And

11	then found downwind in rural area, you have higher NOx

12	in the plume than in the background then your SO2

13	oxidation to sulfate would be faster than it is in the

14	background.	So I think this needs to be pointed out.

15	Most of that description, of course, should go to the

16	annex or to the appendix, but since you are focusing on

17	power plants as one source category needing SO2, I

18	think there is a need for more description there.	I

19	was to be surprised when I got into the annex that the

20	description started with NOx chemistry, and I was

21	wondering actually whether we need to have NOx

22	chemistry in the ISA.	We have another document for

23	that.	Maybe we can just refer to that and then only

24	keep this document focusing on the SOx chemistry,

25	especially since we're trying to keep those documents

1	tight that maybe one good thing to do.

2	And as I mentioned earlier, I think we

3	need to have descriptions of AERMOD in this ISA because

4	it is the model you would be using when you, OAQPS

5	would be using for the methods assessment.	Those are

6	my main points.

7	DR. HENDERSON: Thank you very much,

8	Christian.	Do you have any questions for Christian, or

9	is it clear what he's saying?

10	DR.	LARSON:	I think it's clear, and

11	we appreciate those comments.	And we'll certainly

12	include them in the next draft.	Thanks very much.

13	DR. MACIOROWSKI: Sure.

14	DR. HENDERSON: Okay.	We have Tim Larson

15	next.	Are you on the phone?

16	DR. LARSON: Yes, I am.

17	DR. HENDERSON: Okay.	You have the

18	floor.	DR. LARSON: Thank you.	I will

19	just take the charge, the three charge questions in

20	sequence here.	I think the air quality

21	characterizations are clearly communicated with respect

22	to charge question one.	Again, following up on

23	Christian's comments, the preponderance of below

24	detection limit values and regulatory observations,

25	because of that it is difficult to get an accurate

1	picture of the actual concentrations in most urban

2	areas.	We know that at those monitoring sites it is

3	fairly low.	However, the spatial variability is a bit

4	of a problem because we've only got 12 metropolitan

5	statistical areas with four or more monitors, and some

6	of those are located near industrial sources.	I

7	contrast this with the SAVIAH study by Pikhart where

8	the passive samplers were deployed at over 100 cites to

9	estimate spatial variation at one location.

10	And there's a large discussion about

11	better measurement methods.	I think that's a good

12	thing.	It is not clear, however, that the focus of the

13	analysis should be on a broad regional characterization

14	because I think a lot of the levels will be very low.

15	It might be useful to focus just on areas with

16	relatively high SO2 such as pointed out in the map

17	earlier and perhaps do a more thorough air quality

18	characterization in those areas in a more limited

19	geographical region.	From an epidemiological

20	perspective, the relevant co-pollutants may be

21	different in these higher SO2 regions than in the

22	country at large or in the European and Asian cities

23	where adverse health associations are claimed.

24	I guess the second question on sulfur

25	oxides and human exposure, picking up on previous

1	comments.	I think there's a statement on page 237 that

2	says, "When personal exposure concentrations are above

3	detection limits, a reasonably strong association is

4	observed between personal exposures and ambient

5	concentrations," but this statement is essentially

6	repeated in the conclusion Chapter 5.13, and as best I

7	can tell it is based primarily on the results of Mike

8	Brower's 1989 study.	While this might be a perfectly

9	good study, it was done in one city over two seasons,

10	and it's a very important generalization, but the other

11	studies don't seem to support that, support that same

12	statement as best I can tell.	So if it's true that

13	it's based on that one Brower study, the claim of the

14	linearity, and they're some high associations, I think

15	that ought to be clear because I think right now you're

16	left with the impression that it's based on all those

17	studies.

18	I would say from an epidemiological

19	perspective, the current ambient levels are very low

20	and also poorly mentioned because they're below

21	detection limit in most locations.	I suppose from one

22	sense that's good news, but it makes epidemiology

23	difficult.	There is also insufficient information to

24	predict personal exposure levels from these low ambient

25	levels measured at most community monitors.	I think

1	you're really left perhaps with the pathological

2	perspective based on a limited number of locations and

3	short-term effects at the high end of the concentration

4	distribution, and that's why I say basically that more

5	emphasis perhaps should be focused on the air quality

6	characterization in those regions to compare and

7	contrast the other studies.	Those are my comments.

8	DR. HENDERSON: Thank you very much, Tim.

9	Any questions for Tim from NCEA?

10	DR. ARNOLD: Just a quick point of

11	clarification on Tim's point about the strong

12	association being based on Brower '89.	Tim, if you

13	flip back to the slide we presented this morning, we've

14	actually, in the time since we distributed the draft,

15	ISA, we've taken out the word "strong positive

16	association" there and just left that as an

17	association.

18	DR. LARSON: Okay.

19	DR. ARNOLD: It is in fact, as we cite in

20	that slide, Brower, but there is also the second study,

21	the Sarnet study in 2006, which we refer to in the ISA.

22	DR. HENDERSON: Okay.

23	DR. ARNOLD: We take that point and have

24	de-emphasized our conclusion and we'll reflect that in

25	the second draft.

1	DR. HENDERSON: Thank you.	Donna?

2	DR. KENSKI: Yeah.	Greetings, Rogene.

3	First off I guess I'd just like to --

4	DR. HENDERSON: You need to get close to

5	your mic.

6	DR. KENSKI: Oh, okay.	First off I'd

7	like to congratulate the team because I thought this

8	document was in a lot better shape overall than NOx ISA

9	that we finished a month ago, so I think it's showing

10	some real progress.

11	With respect to the specific charge

12	questions in this category, I thought they did an

13	adequate job with the chemistry, but the description of

14	the air quality data I think could be improved

15	somewhat.	It does a nice job using the CASTNET data to

16	describe regional variability, but the fact is that the

17	CASTNET data are strictly almost exclusively rural

18	monitors.	So while that does show, you know the

19	distribution of background concentrations across the

20	country, it really doesn't address urban

21	concentrations.	And those were to some extent

22	addressed by the 12 cities with the four monitors, but

23	there are other cities with additional monitors.	So I

24	guess what I was hoping for was some distinction

25	between urban concentrations and rural concentrations

1	and also a better assessment of the spatial variability

2	within those urban areas, which can be fairly extreme.

3	There was a lot made about the non-

4	correlation between sulfur dioxide and sulfate, and it

5	seemed to me that the ISA was sort of surprised that

6	those two species were not more highly correlated which

7	actually wasn't so surprising to me.	I guess thinking

8	on their sort of separation in space and time, and the

9	time between the conversion of SO2 to SO4.	But what I

10	was also hoping to see was some additional information

11	about the correlation between sulfur dioxide and its

12	co-pollutants because that's maybe more relevant to

13	helping interpret some of the epi studies.	So I would

14	like to see how those ambient concentrations of SO2

15	correlate with NO2 and CO and PM fine and PM course to

16	the extent that, that data is available.	I think that

17	would be a valuable addition.

18	And with respect to temporal patterns, I

19	think seasonally -- that whole thing with the seasonal

20	data could be summarized a little more efficiently, I

21	think, rather than showing every city and those

22	patterns, you know, annual timelines.	Those parts were

23	nice, but I think you could come up with a more

24	efficient summary of that information and in particular

25	the daily variation, you know, hour by hour, diurnal

1	variation.	That plot was not very effective, and I

2	think everybody's comments noted that particular

3	figure.	I don't know which number it was, but the one

4	that showed daily diurnal variation was not very

5	helpful.

6	I guess I liked that fact that annex two

7	had some NOx chemistry in it, but it was a little

8	disconcerting too, you know.	The only mention that it

9	was going to be there was this little footnote very

10	early on in the document, so I think that could be

11	maybe explained a little better.	But I actually liked

12	that the NOx chemistry was there.	I thought that was

13	helpful.	Oh, and I did point out in my comments with

14	respect to the urban spatial variability and urban

15	gradients, there is a brand new study that's Canadian,

16	but I think really relevant to this effort that could

17	be reviewed.	That's all.

18	DR. HENDERSON: Thank you, Donna.	And

19	Ted Russell?	Where are you Ted?

20	DR. ARNOLD: If we could, I'd just like

21	to maybe make a point of clarification.

22	DR. HENDERSON: Oh, sure.	I'm sorry.	I

23	forgot to ask you if you had questions.

24	DR. ARNOLD: Thanks very much.	Thanks

25	for your comments, Donna.	We really appreciate them,

1	and I think it points out something that we need to

2	perhaps address in terms of the emphasis that we're

3	providing.	We're certainly looking at CASTNET, and

4	we're showing the distributions for looking broadly

5	across the domain.	Table 2.4-2, however, does use the

6	AQS data, and we've split them for inside and outside

7	the CMSAs to try to get to this idea of looking at

8	distributions within cities and then outside of cities

9	as well.	But we certainly take your point, and we'll

10	provide more emphasis on looking potentially at

11	correlations, both across monitors within a CMSA where

12	we have it and then with potential co-pollutants as

13	well.	I'm sure with your experience you realize that

14	part of the problem is that SO2 is not measured

15	everywhere at the same location as the other pollutants

16	that we might be interested in looking at correlations

17	with.	And as to perhaps there was too much emphasis on

18	what you took to be our surprise in looking at the

19	correlation between SO2 and sulfate, there was some

20	perhaps differential in surprise between the

21	atmospheric scientists and the epidemiologists about

22	whether there was going to be correlation between SO2

23	and sulfate, and we were trying to address that

24	question with those plots that were in there.	So we do

25	take that comment.	We tried to make the point about

1	whether there was, we talked about the difference in

2	looking at processing time and why that would be the

3	case and why we got some difference in the correlation

4	across the cities that we did look at.	But we will go

5	back and look at the language on that and try to

6	sharpen that discussion.

7	DR. KENSKI: You know, this Table 2.4-2,

8	it wasn't, I think maybe that was a question I had in

9	here.

10	DR. ARNOLD: I saw that in your written

11	comments.	Yeah.

12	DR. KENSKI: Whether it was including

13	Casnet data or just AQS data.

14	DR. ARNOLD: AQS data from 2003 to 2005.

15	DR. KENSKI: Okay.	So that could be

16	clarified.

17	DR. ARNOLD: Yeah.	We'll certainly put

18	that in the note.	Thanks very much.

19	DR. HENDERSON: Okay.	Now we'll go to comments from Ted

20	Russell.

21	DR. RUSSELL: Okay.	Thanks.	Just a few

22	comments.	First on the measurement techniques.	You

23	talk about the positive and negative possible

24	interferences.	I think in the bottom line what we want

25	to know about are quantitatively what you think the

1	bias and uncertainty are as opposed to just what they

2	may be in that I'd suspect we're actually, this isn't

3	going to play a real role in how we interpret the

4	measurements.	And I think as we indicated on the NOx

5	case, what we really want to know is the information

6	relevant to how we might go forward and interpret the

7	various other studies towards how that would influence

8	setting of the standard, and I think they're, in this

9	case again, it's quantitative information as to the

10	uncertainties, not just what may be positive and

11	negative without really knowing to what degree.

12	We talked somewhat about providing a

13	five-minute data, and I think this should be done

14	wherever it's available, and you say that it's less

15	than 0.05% of the time it's over, whatever, 100 ppb.	I

16	can't recall exactly what it was.	That's still about

17	50 times a year, so it's not -- for a typical monitor

18	-- so it's not a insignificant number of times.	Given

19	that, what I'd do, and I think it does have to be in

20	this chapter, is a nice plot showing the five-minute

21	data, and I'd use something like a PDF so we can get a

22	good idea of the whole distribution would be the

23	approach I'd take.

24	You've got a fairly large section on

25	exposure measurement air, and I was taken actually by

1	one of the first sentences.	The sentence in the second

2	paragraph of that where you say the considerations of

3	exposure air for SO2 are somewhat simplified compared

4	to those for NOx and PM, and, you know, that's only in

5	one dimension.	And that I'd say that actually exposure

6	measurement air for SO2 is probably going to be the

7	biggest of the bunch.	Just if you look at what leads

8	to the higher concentrations, it's typically a fairly

9	localized event that, you know.	It could be a plume

10	that's all of, oh, 3, 4, 5 km if that wide.	So you're

11	actually many a time going to be measuring something

12	that's having an impact on a relatively small amount of

13	a domain, and other times you're going to be missing

14	significant exposures that just aren't being measured.

15	And this really is going to depend upon the geometry,

16	how close your major sources are, etc, and so I would

17	take a little bit more time in discussing the

18	complexities of SO2 exposure measurement air in a

19	typical domain.	One of the ways I'd approach that is

20	for the locations that you have multiple monitors

21	within a single CMSA area.	Look at correlations, the

22	five-minute, one-hour, and 24-hour average

23	concentrations just to -- and you can do one-hour max

24	concentrations -- just to see how well you think you

25	actually, or provide information.	Actually I'd hope

1	the studies themselves did this, to provide information

2	as to how to interpret these, the exposure measurement

3	there.	And you just look through the document right

4	now.	I think it underestimates the complexity there,

5	and then when you start seeing the results from the

6	Sarnet study, etc that there really are questions as to

7	how well ambient monitors really do reflect exposure.

8	And along those lines I'd also for the sites where you

9	do have co-occurring data, show and describe what

10	pollutants SO2 is currently correlating with, including

11	the medals from various PM components, not just

12	sulfate.	You know, see how well it correlates with an

13	array of other pollutants that might also have either

14	effects leading to increasing the impact of SO2 or

15	those that might be impacting the interpretation of

16	your exposure analyses and epi analyses. And I think

17	most of the other things are in my written comments.

18	DR. HENDERSON: Thank you, Ted.	Does

19	NCEA have any, do you have any questions for Ted?

20	DR. ARNOLD: Just a few short points of

21	clarification, I think.	We certainly take the general

22	feeling of the panel that information on finer term

23	ambient monitoring is important, and we will include it

24	to the extend that we can.	We were explaining a little

25	earlier about the problem in using the five-minute data

1	now, and that is that since it's not currently required

2	of the states and they reported voluntarily, they

3	reported for some monitors and not others.	And these

4	monitors come in and out year by year, so it makes it

5	difficult to look across time.	And I just wanted to be

6	a little clearer about it.	We were unclear.	I realize

7	it's hard since we don't actually present the

8	information in the ISA, but the figure of 0.5% does not

9	refer to a single monitor registering 600 ppb but

10	across all the monitors, which were reporting for 10

11	years across the time.	Now we're adding to this.

12	Again, we're extending up with our work with the

13	program office.	We're looking beyond 2000 up to the

14	most recent through 2006.	That doesn't end up

15	producing a large number of additional observations

16	simply because states are taking out monitors in places

17	because we're now so far below the standards.	So to

18	the extent that we can get this information together

19	and get the analysis done, we'll certainly include it

20	in the second draft.

21	DR. RUSSELL: And what you state

22	actually, I think there would be a nice piece you could

23	do with it is showing the correlation between the one-

24	hour average, how well it correlates with your peak

25	five-minute average.

1	DR. ARNOLD: That's right.	And that's

2	one of the things we have been looking at internally,

3	and at the few sites where we have consistent five-

4	minute data, we can certainly do, look at that.

5	DR. RUSSELL: Okay.

6	DR. ARNOLD: Our concern has been to

7	present this in a way that we can emphasize both the

8	uncertainty in the non-random distribution of these

9	observations and not use this or have this be

10	potentially misinterpreted as the basis for

11	generalization across the whole continental US.

12	DR. SPEIZER: But surely wherever you've

13	got a five-minute measurement and you have a one-hour

14	or a 24-hour, that is internally consistent, and you

15	can do an analysis of that irrespective of how

16	representative those five-minute averages are of the

17	country.

18	DR. ARNOLD: That's correct.

19	DR. SPEIZER: And we should see that.

20	DR. ARNOLD: Yes.	And we will provide

21	that.

22	DR. SPEIZER: And if I would, I would

23	suspect that if you plot the five-minute averages,

24	they're fairly logged normally distributed.

25	DR. ARNOLD: I believe that's true, but I

1	don't have that plot with me.

2	DR. SPEIZER: Okay.	In which case you

3	can actually get a lot of extra inference from what

4	distributions you currently have.

5	DR. ARNOLD: Sure.	But my concern is

6	just, I mean, we can say something locally about it,

7	but we can't say anything very regionally about it.

8	DR. HENDERSON: Okay, Ellis?

9	DR. COWLING: I finally remembered what

10	it is that I couldn't remember before, and it's

11	pertinent to these five-minute measurements, which

12	Frank brought up and Ted has emphasized and so on.	And

13	I'd like to make my comments in the context of the

14	early summary that we had about the decisions that were

15	made about the national ambient air quality standards

16	for sulfur oxides.	And on slide 5 we had this very

17	nice history of the SO2 NOx, and I think we should

18	always have a good summary of what the decisions were

19	and why they made those decisions.	Now one of the

20	things that particularly struck my interest in this

21	summary was the fact that EPA made a deal with the

22	American Lung Association.	The American Lung

23	Association have been bringing up this short-term

24	exposure business for a long time, and the EPA, not

25	wishing to change the standards said okay, we'll do

1	some monitoring.	And then we learned that the

2	monitoring was not required to be reported.	I would

3	like to know the rationale for that decision and if

4	possible to know who made that decision.

5	DR. ARNOLD: As you can imagine, Ellis,

6	this is not something that we can respond to.	It might

7	be possible for someone from the Air office to respond

8	to that question, but it's not something that we would

9	consider in the ISA or would try to evaluate.	We will

10	evaluate the data that we have when we have it at the

11	time when we've reached the endpoint for the inclusion

12	of those data for various drafts of the ISA as they

13	come along.

14	DR. COWLING: Well I understand this and

15	I guess this comment should be made when the Air Office

16	people are here, and then I'll make it again, but --

17	and I hope I --

18	DR. ARNOLD: I don't mean to push things

19	off on Lydia, but I'm sure you can -- we appreciate

20	your concern in putting it on the table, but I'm sure

21	you realize it's not something that we can, we can

22	respond to or incorporate in the ISA.

23	DR. HENDERSON: Are Lydia and Karen going

24	to be here later in the day?	Tomorrow, okay.

25	DR. COWLING: Let me, in conclusion,

1	mention that Mississippi does not have an ozone problem

2	because Mississippi has no ozone monitors.

3	And you may know that I've had some

4	experience dealing with comments, and I make comments

5	about that from time to time.	Fort Bend County is the

6	most rapidly growing county within the ozone non-

7	attainment area.	There are no ozone monitors in Fort

8	Bend County.	I don't know exactly why, but it's

9	interesting that Tom Delay has his home base in Fort

10	Bend County, and it's also interesting to be aware that

11	the state of Texas does not install monitors unless the

12	monitors are welcome by the county judge and the

13	members of congress that represent that county.	So if

14	we require measurements of five minute averages or

15	exposures and make a deal with the American Lung

16	Association, and then don't require that they report

17	what they found, I should imagine that the American

18	Lung Association would be pretty T'ed off about -- and

19	I understand.

20	DR. ARNOLD: More importantly, the judge

21	might be pretty ticked off.

22	DR. COWLING: Yeah.	I -- okay.

23	DR. HENDERSON: Well --

24	DR. ARNOLD: I think I, I think I just

25	want to be clear about what's required of the states to

1	report, and that's irrespective of the agreement that

2	may have been struck for the additional findings.	We

3	will certainly use all data which we can collect from

4	the program obviously.

5	DR. COWLING:	And I guess we could

6	try to increase the willingness of the states to

7	provide this if we were to comment in some way.	You're

8	advice about these matters would be very welcome, and

9	Donna is raising her hand I think.	And I look to

10	Donna.	She regulates air quality or helps in that

11	process, and it is very welcome to have someone who

12	actually manages air quality in our CASAC discussions,

13	which are mostly scientists who don't manage anything

14	but their own affairs.

15	DR. HENDERSON: All right.	With that,

16	Donna, do you have any comment on what's required?

17	DR. KENSKI: I do have a comment.	In the

18	quest for five-minute data, one barrier to that data is

19	actually getting into AQS because it's not really set

20	up to deal with five-minute data.	But it's my sense

21	that many of the state organizations who collect, those

22	of them that report the five-minute max data may in

23	fact have the other, you know, other five-minute

24	intervals archived somewhere.	So that might be

25	something you'd want to pursue in, you know, in whether

1	it's, in the next draft of the ISA or with respect to

2	the Health and Exposure Assessment, is trying to track

3	down whether the states, you know, have that data

4	available and could share it with you.

5	DR. ARNOLD:	We'll certainly work

6	with the program offices to establish where those data

7	are and how we can get them.	Thank you.

8	DR. THURSTON: Not to dwell on this too

9	long, but routinely how long do they archive the data

10	for?	I've had a real problem with trying to get

11	filters that they archive 'cause they keep them for

12	like one year and then toss them.	Do they do the same

13	thing with data?	Do they archive them for a few years

14	and then print out a report and they're done?

15	DR. KENSKI: I mean, if there's a

16	requirement to submit, you know, data to assess the

17	NAAQS, but aside from that, then, you know, each state

18	they can throw away whatever they want if it's not

19	required to go into, you know, assessing their

20	compliance with the NAAQS.	But, I mean, states differ

21	widely in their desire to, to figure out the nature of

22	their air quality and problems.

23	DR. THURSTON: Tactfully put.

24	DR. KENSKI: Thank you.	So, you know, so

25	it varies form state to state what's archived and

1	what's available, you know.

2	DR. HENDERSON: Maybe we should go on and

3	let Jim Ultman give his comments.

4	DR. ULTMAN: Thank you.	I just have a

5	couple of things to add.	Relative to figure 2.4-5 on

6	page 213, I found this figure very useful personally.

7	It was labeled as a box plot, and it refers in the text

8	to 95% limits.	So I think there's some discrepancy

9	there.	It's more of a scattergram, but I thought it

10	would be, because it was so useful to me, I thought

11	that in considering different forms of the standard, it

12	would be nice to have consistent plots for all, for

13	three different forms that I think you're reaching for.

14	One is the annual form.	The other would be the daily

15	form, and then the third would be the hourly form. And

16	if there's, I realize that the next figure shows for

17	Steubenville shows kind of a, that kind of a plot for

18	the hourly form, but it could be three consistent

19	plots, you know, that showed scattergrams of some sort.

20	And I know this is very hard for the short standard,

21	but still as close as you could come so you can compare

22	if you use different forms what the distributions would

23	be like.	I think that would be helpful.

24	And then my other comment has to do with

25	dosimetry, dosimetry section, and I think as Frank

1	Speizer already pointed out, there's more to what

2	happens to SO2 than considering the SO2 that reaches

3	the lower airway, lower respiratory tract.	And

4	particularly there's an emphasis in the chapter in the

5	section on dosimetry on the absorption of ozone, I'm

6	sorry, of SO2 by the upper airways as a means of

7	protecting	the lower airways, but two things I wanted

8	to mention that should be stressed at probably in the

9	last part of this section.	First of all, that SO2,

10	which is absorbed by the upper airways is going to

11	circulate and can cause systemic effects.	So to the

12	extent possible, I think systemic effects should be

13	brought in because whether it's absorbed in the upper

14	or lower airways, it's not all going to be reacted

15	within the liquid lining layer.	So you're going to

16	have systemic effects.	So I don't, I'm not sure that

17	there's enough data out there to do much about it

18	quantitatively, but at least to mention, to emphasize

19	that fact.

20	The second point related to that is that

21	only a portion of the absorbed ozone in the upper

22	airways is permanently absorbed, but there's this

23	countercurrent exchange that goes on with heat, with

24	water vapor, and with these xenobiotic gases that are

25	soluble; and that is they're absorbed in the upper

1	airways during inspiration, and then they're desorbed

2	during expiration.	And this is one of the ways the

3	lungs kind of protect the whole organism from

4	xenobiotics and from heat loss.	And this is covered

5	actually.	The studies are quoted in that section on

6	dosimetry, but I think, again, it should be emphasized

7	that this is a protective mechanism and that not all

8	the ozone that's absorbed during inspiration

9	necessarily puts the person at risk because some of it

10	is desorbed.	And if nothing else, this will possibly

11	stimulate other thinking, other studies in this area,

12	even though it may not be directly useful in terms of

13	what we're discussing here.	That's it.

14	DR. HENDERSON: Okay.	Mike, do you have

15	any questions?	Nobody wants to question?	Now I'll

16	open it up to any member of the panel who wants to talk

17	or make comments on chapters, on chapter 2.	Yes, go

18	ahead?

19	DR. POSTLETHWAIT: Hi, Rogene, this is Ed

20	Postlethwait.

21	DR. HENDERSON: Oh, hi, Ed.

22	DR. POSTLETHWAIT: I actually had a

23	question for Jim, what he just brought up, which I

24	think was a great point.	Jim, have you ever looked at

25	the half-life of SO2 once it diffuses in the tissue or

1	the vascular space as to how far downstream it actually

2	might exist, especially the kind of environmental

3	concentrations we're talking about?

4	DR. ULTMAN: No.	I haven't, I haven't

5	that, Ed.	But there's two questions here in terms of

6	half-life; and one would be the decomposition or the

7	reaction of the material in the blood, and the second

8	would be removal by other organs.

9	DR. POSTLETHWAIT: Right.

10	DR. ULTMAN: So it's a pretty complex

11	issue, but I haven't looked at it, no.

12	DR. POSTLETHWAIT: Well because the

13	chapter does mention the business about delivery to the

14	lower respiratory tract via the vascular supply, and,

15	you know, when we're talking fairly low ppb

16	concentrations one wonders what in terms of a mass

17	action how much SO2 you might really be talking about.

18	I would guess the numbers are going to be pretty small.

19	DR. HENDERSON: I don't know, Jim, were

20	you thinking of the oxidation reduction situation that

21	the sulfate would be a reducing agent?

22	DR. ULTMAN: Well I hadn't really been

23	thinking of the specific chemistry involved, no.

24	DR. HENDERSON: I was just trying to --

25	I'm like Ed.	I was thinking when you said that, what

1	would you expect from the blood borne.	It could be

2	sulfite I presume.	At very low levels, what would we

3	expect, but you're right it would be there.	Dale, do

4	you want to go ahead with your comment?

5	DR. HATTIS: Yeah.	I just wanted to

6	point out the issue of the distributions for different

7	time periods was mentioned earlier, and I think that --

8	I like your Table 2.4.2 where you give the percentiles,

9	but I think you could enhance that with some log normal

10	probability plots.	And so I basically made some from

11	those data.	Basically you could see those on page 56

12	of the comments.	It's labeled Figure 1.	And basically

13	what you see there is the orderly progression of

14	increasing variability for decreasing averaging times.

15	And you see particularly that for the one-hour

16	averaging time you have a pretty good correspondence

17	with a log normal distribution as corresponding to the

18	points that fit inline and pretty parallel lines,

19	meaning the same standard deviation, geometric standard

20	deviation essentially for the one-hour maximum versus

21	the one-hour average concentration load slightly

22	translated.	And what that means is that you basically

23	have a geometric standard deviation of a little over

24	three for the one-hour maximum.	So you could do the

25	same thing in parallel with the five minutes, maybe

1	even make some inferences to how much more variable the

2	five minutes average is compared to the one-hour, and

3	that would allow you to make the national projection of

4	how often you get various levels.	So basically what

5	the log normal distribution does for you is it has a

6	convenient way of extending the data essentially to how

7	often you get very high levels versus just more common

8	levels, and that in turn can be used in conjunction

9	with your direct clinical observational data to do some

10	kind of concentration response and expectations for

11	incidents of adverse effects.

12	DR. HENDERSON: Are there -- oh, go

13	ahead, Jon.

14	DR. SAMET: In general comments, I'd like

15	to read this chapter called something like source to

16	dose, and actually see that question answered, which I

17	don't think it does.	So it deals with SO2 but then

18	raises the possibility of surrogates in true causal

19	agents, leaving them general and unspecified.	And

20	isn't this the chapter where if you think that SO2 is

21	undergoing chemical transformation, physical

22	transformation into agents that are actually injurious?

23	There should be some specificity given to that

24	discussion.	So I think this is a critical foundation

25	for determining the epidemiological studies in which

1	this issue will come up, but I don't see this question

2	as answered at all.	I think possibilities are raised

3	and, again, for example on page 241, Relationship of

4	SO2 to the True Causal Factor.	So if you're raising

5	the possibility there is some "true causal factor,"

6	what is it?	What are its physical and chemical

7	properties, and what doses are being delivered to the

8	respiratory tract or?	Also I just don't think these

9	things can be raised and then left dangling because I

10	think this is really fundamental to interpreting our

11	multi-pollutant models.	DR. HENDERSON:

12	Thank you.	Yeah.	Go ahead, Ron.

13	DR. WYZGA: One of the things I think

14	could be helpful in later chapters when we try, and I

15	think we have to do more to try to tie together the

16	information from both the epidemiological studies and

17	the human clinical studies is to have a better

18	understanding, particularly when you look at the time

19	series epidemiological studies.	What's the

20	relationship?	Those tend to use 24-hour SO2

21	measurements.	What's the relationship between those

22	and peak hourly or peak five-minutes?	So I'd like to

23	see some correlations for where we have data between

24	the 24-hour average over time and the peak five-minute

25	for that period, and the peak hourly for that period.

1	It would help me get some understanding to what extent

2	the epidemiological studies are indeed telling us some

3	of the same things as the human clinical studies.

4	DR. HENDERSON: Okay.	Is that something

5	that's possible with the data?	I'm asking NCEA.

6	DR. ARNOLD: Yes.	We think so.	We

7	certainly have epi data and we think we can construct

8	those correlations to the extent that we have.

9	Certainly it's going to, as we've heard this morning

10	already, certainly it's going to be easier with the

11	one-hour data than with the five-minute data, but

12	certainly where we have it we can take a look at that

13	as well.	Thanks very much.

14	DR. HENDERSON: Okay.	Yeah, Lianne.

15	DR. SHEPPARD: Yeah.	I wanted to suggest

16	in this chapter that the presentation needs to be

17	thoroughly revised to really deepen the understanding

18	with respect to the health studies, and so there are a

19	couple of things that I would suggest along that line.

20	One is more thorough analysis -- well also and for the

21	Health Risk Assessment that will follow.	So one is the

22	analysis that was already suggested of relating the

23	five-minute to the one-hour averages.	We also need to

24	have a much better understanding of the spatial

25	distribution of exposure.	SO2 monitors often are cited

1	right next to local sources, and in a time series study

2	that's not really representative of population exposure

3	and could be a very important aspect of measurement

4	error in a time series study.	And there's certainly

5	cities where there are only local source SO2 monitors.

6	I know Seattle is one of them.	And so you would really

7	question the interpretation of a health study that uses

8	population level data in a city like that.	And so I

9	think there needs to be a summary that classifies

10	cities into only local source monitors versus

11	population-oriented monitors versus both, so we can

12	understand how important that is.	There should also be

13	an analysis of land use characteristics so we can get a

14	sense of how important the local sources are in terms

15	of population exposure where there aren't monitors.

16	Let's see.	And then another thing we need to better

17	understand is the analyses of personal or indoor

18	concentrations versus outdoor concentrations in terms

19	of interpretation of exposures that people actually

20	have.	So there is some analysis in the chapter, but I

21	don't think it really gets at that issue clearly

22	enough, and if the apex model is going to be used in

23	the Health Assessment, we need parameters in this

24	chapter that can be brought forward into apex.

25	And then I think that, actually I

1	recommend that a thorough analysis of the AQS data in

2	the context of results that are going to be needed for

3	either the Health Assessment or the interpretation of

4	epi studies and clinical studies be added to the annex,

5	and then the tables and figures be completely revamped

6	to bring forward the key features of that analysis.	A

7	lot of the figures and tables are way too summarized

8	for what we need, and my comments will give specific

9	details on those.

10	DR. ARNOLD: Great.	If we could just add

11	a couple points of clarification to make sure we

12	understand, then we'll go back and look at your

13	comments again and consider those in consideration with

14	the letter, with the letter that comes out of the

15	panel.	If you'd say a little more about what you mean

16	by considering the analysis of land use characteristics

17	when we're looking at questions of local citing.

18	DR.	SHEPPARD: Well, I mean, monitors

19	are not put next to all local sources, and it's going

20	to be really important in terms of characterizing

21	population exposure, particularly susceptible

22	individuals, to have a sense of how much of the area in

23	the United States do you expect to have high exposures.

24	And monitors are only in a few of those places, but

25	with a geographic information system or the point

1	source database, you could, somebody could summarize in

2	a city or over the United States, for instance, which

3	census tracts are expected to have high peak exposures

4	and which aren't.	And that would be very important to

5	bring forward into the Health Assessment.

6	DR. ARNOLD: So if I just, in addition to

7	the plots, the mapped plots that we have now of SO2

8	sources, you would like to see similar plots of where

9	the monitors are and what the relationship between the

10	monitor, the distance let's say as one parameter

11	between the monitor and that source.	And then bend

12	these up.	In some kind of ways you were suggesting

13	whether these are population cited monitors or source

14	receptors.

15	DR. SHEPPARD: Well so I'm making really

16	two different points.	One is just summarizing land use

17	to bring forward into the Health Assessment.	I should

18	go back and look to see what you have in respect to the

19	sources already with respect to that to see how well

20	that's addressed for the Health Assessment.	But the

21	other point that I was making was in terms of, of

22	summarizing the monitoring data with respect to whether

23	it's local source or other important characteristics

24	about sources versus population oriented because that

25	has very important implications for interpretation.

1	For instance, of the time series studies because if you

2	use only a local source monitor in a time series study,

3	it's not representing population exposure, and it's

4	presumably that SO2 estimate is going to be subject to

5	a very high amount of classical measurement error as a

6	result of that.	And so I'd like to see summarized in

7	the document information about citing characteristics

8	with respect to the monitoring data that we have.	And

9	I would recommend that a number of the tables and

10	figures as well be separated by local source versus

11	population-oriented information.

12	DR. ARNOLD: Sure.	And we take that

13	point, and we'll work with the program office which

14	controls the regulations, as I'm sure you're aware,

15	controls the regulations that describe the citing

16	characteristic and perhaps include those in the annex?

17	Is that your idea and be able to bring forward our

18	conclusions about how those could be useful for

19	interpreting the health data.	DR.

20	SHEPPARD: Yes.	So I would suggest adding a pretty

21	extensive analysis of the AQS data in the annex with

22	respect to different questions that would be important

23	for interpreting the epi studies and for use in the

24	Health Assessment and then bringing forward the key

25	features into the ISA from that analysis.	So depending

1	on what exactly it is that you learn, then you decide

2	how to bring that forward.

3	DR. ARNOLD: Thanks very much.

4	DR. ROSS: I'd like to follow up.	And it

5	sounds like since your most interested in health

6	studies, it would be useful to focus on the cities in

7	which health studies were done.	Looking at the

8	epidemiological tables that we have at the end of

9	Chapter 5 and really focus on an in-depth look to the

10	extent data available those cities because that's where

11	you would be interpreting epidemiological --

12	DR. SHEPPARD: Well, you know, that's an

13	important point I think with respect to interpreting

14	the studies that are being recorded, but we also need

15	to keep in perspective that we have the Health

16	Assessment as well where presumably we are, the whole

17	population of the United States is relevant.	And so

18	I'd be careful about restricting that analysis too

19	early, and I would definitely, in terms of the more

20	thorough exploratory analysis that's done in the annex,

21	I would certainly look at that distinction and see if

22	there's something important that needs to be brought

23	forward with that.	But I wouldn't immediately restrict

24	attention to only those cities.

25	DR. ROSS: I was thinking more of the

1	word focus rather than restrict.

2	DR. HENDERSON: Okay.	Does anyone else

3	have comments on Chapter 2, or can we go on to Chapter

4	3?	Oh, we've got lots of comments.	Okay, Terry.

5	DR. GORDON: Something else that might be

6	added to this chapter as brought up by George Thurston

7	earlier, the inclusion -- this chapter's title is

8	Source to Dose, and it's a tremendous bias amount since

9	I was Mary Ander's last student.	But I think that the

10	work by Jacob at Hopkins, and Mary at Harvard, and MIT,

11	and NYU should be included.	I understand for both SO2

12	and NO2 once it becomes part of a particle, it's part

13	of the PM ISA, but in this case because one of the

14	issues we're going to find is the exposure levels at

15	SO2 are so low and we're finding adverse effects, is

16	biological plausibility.	So I think some of the, the

17	Jacob and the Ander data of the acid particle

18	interactions should be included in Chapter 2 and

19	integrated with Chapter 3 where it's missing also just

20	to help us get to the Chapter 4 and 5 in looking at

21	biological plausibility.

22	DR. HENDERSON: Okay.	And who else had

23	their hand up?	Yes, Frank.

24	DR. SPEIZER: I wanted to sort of second

25	what Elizabeth said about getting out the distribution