ILLINOIS POLLUTION CONTROL BOARD

2 IN THE MATTER OF:

)

4 WATER QUALITY STANDARDS AND ) R08-9

5 EFFLUENT LIMITATIONS FOR THE ) (Rulemaking-Water)

6 CHICAGO AREA WATERWAY SYSTEM )

7 AND LOWER DES PLAINES RIVER )

8 PROPOSED AMENDMENTS TO 35 ILL. )

9 ADM. CODE 301, 302, 303 and 304 )

TRANSCRIPT OF PROCEEDINGS had in the

13 above-entitled cause on the 9th day of September,

14 A.D. 2008, scheduled to commence at 1:20 p.m.

16 BEFORE: MARIA E. TIPSORD, HEARING OFFICER,

ILLINOIS POLLUTION CONTROL BOARD

100 West Randolph Street

Suite 11-500

Chicago, Illinois 60601

312-814-4925

1 APPEARANCES:

MS. MARIE TIPSORD, HEARING OFFICER

MS. ALISA LIU, Environmental Scientist

MR. ANAND RAO, Senior Environmental Scientist

MR. G. TANNER GIRARD, Acting Chairman

MR. NICHOLAS J. MELAS,

MS. ANDREA S. MOORE,

ILLINOIS ENVIRONMENTAL PROTECTION AGENCY,

1021 North Grand Avenue East

P.O. Box 19276

Springfield, Illinois 62794-9276

217-782-5544

MS. DEBORAH WILLIAMS,

MS. STEPHANIE DIERS,

MR. SCOTT TWAIT;

1 APPEARANCES (cont'd):

BARNES & THORNBURG, LLP,

One North Wacker Drive

Suite 4400

Chicago, Illinois 60606

312-357-1313

MR. FREDRIC P. ANDES,

appeared on behalf of the Metropolitan

Water Reclamation District;

NATURAL RESOURCES DEFENSE COUNCIL,

101 North Wacker Drive

Suite 609

Chicago, Illinois 60606

312-663-9900

MS. ANN ALEXANDER;

THE CHICAGO LEGAL CLINIC,

2938 East 91st Street

Chicago, Illinois 60617

773-731-1762

MR. KEITH HARLEY;

1 APPEARANCES (cont'd):

OPENLANDS,

24 East Washington Street

Suite 1650

Chicago, Illinois 60602

312-863-6265

MS. STACY MEYERS-GLEN,

FRIENDS OF THE CHICAGO RIVER,

28 East Jackson Boulevard

Suite 1800

Chicago, Illinois 60604

312-939-0490

MS. MARGARET FRISBIE,

MR. ALBERT ETTINGER.

23 REPORTED BY: SHARON BERKERY, C.S.R.

CERTIFICATE NO. 84-4327.

THE HEARING OFFICER: Back on the

record.

MS. ALEXANDER: I wanted to start with

Gerba prefiled Question No. 3, which is

referring to Page 2 of your testimony that

pseudomonas was selected for study, in part,

because it, quote, "Causes recreational

associated, eye, skin and ear infection."

And then on Page 3, the adenoviruses are a

cause of ear, nose, throat and respiratory

infections. Just.

To clarify, the risk assessment

did not calculate quantitatively risks

associated with these types of infections; is

that correct?

MR. GERBA: For these two organisms,

it was done qualitatively.

THE HEARING OFFICER: You have to

remember to speak up.

DR. GERBA: For these two organisms,

it was done qualitatively.

MS. ALEXANDER: And I also wanted to

reference -- now, we were on the attachments

to the May 23rd, letter from Geosyntec,

second attachment Page 3.

THE HEARING OFFICER: Excuse me,

Ms. Alexander, this will be a new transcript,

so that's Exhibit 73.

MS. ALEXANDER: Sorry.

Exhibit 73, the portion of that

which is the letter from Geosyntec dated

May 23rd, 2008. Page 3 of the second

attachment, there is a statement made in the

first paragraph, "Ear and eye infections

associated with contact by pseudomonas

contaminated water are typically associated

with full immersion activities. Since these

types of activities are not permitted as

designated uses of the CAWS, the incidents of

ear and eye exposures are expected to be low

and as a result of an accidental or

intnetional misuse of the waterway."

I direct this question to

Dr. Petropoulou. Would I be correct in

understanding that if, in fact, you fell into

the water, you would be at risk of this from

the pseudomonas?

MR. ANDES: Can I just -- can you

repeat the page?

MS. ALEXANDER: I'm sorry. Page 3 of

the second attachment, which is entitled

Review Conducted by USEPA Office of Research

and Development, which is, in fact, I believe

is the Tim Wade document, I identified

earlier in response to that.

THE HEARING OFFICER: And that's --

what's the date on the cover letter to that?

MS. ALEXANDER: The cover letter is

dated May 23rd, 2008.

DR. TOLSON: It starts with a

clarification. It starts on Page 2 and it

continues on Page 3.

MS. ALEXANDER: Yes. I'm sorry. I

was reading from Page 3.

But the point be responded to is

on Page 2. "Since pseudomonas and adenovirus

were found, descriptions of non-GI illness

should also be provided, to represent a clear

picture of the actual risk associated with

recreating in the CAWS." That's the

statement being responded to.

The response begins on Page 2. I

read a portion of that response from Page 3

concerning non-GI gastrointestinal infection

associated with pseudomonas.

And my question was, am I correct

in understanding that this means you would be

at risk of non-GI illness from pseudomonas if

you actually fell into the water

accidently --

DR. GERBA: Are you asking me that

question?

MS. ALEXANDER: I was actually

directing it, initially, to Dr. Petropoulou,

because I believe she testified that she had

drafted that text.

DR. PETROPOULOU: I did. With input

from Dr. Tolson.

So I would defer that question to

Dr. Tolson.

MS. ALEXANDER: Okay. Go ahead,

either one of you.

DR. TOLSON: I won't defer it one more

time. I'll go ahead and take it.

Pseudomonas can cause

folliculitis. It typically requires a

pre-existing cut. So it's a very difficult

thing to sort of estimate what the population

pre-existing cuts would be to do that.

So there is a potential for

folliculitis from pseudomonas. We have not

calculated that directly within here,

however, the report does go into some

information on pseudomonas. Maybe we should

refer to that proportion --

MS. ALEXANDER: I'm going to get

there.

DR. TOLSON: Okay.

MS. ALEXANDER: I'm sorry, I didn't

mean to cut you off. Were you going to

continue to that --

DR. TOLSON: I was going to discuss

pseudomonas and the relationship with

pseudomonas between dry and wet and such.

But we can -- if we can postpone that, that's

fine.

MS. ALEXANDER: Yeah, I want to allow

you to do that, but I actually had a few

questions about it. Perhaps we can address

it in that context.

Because I just wanted to keep the

thread here, which is, you mentioned

folliculitis. Is that a skin infection?

DR. GERBA: Excuse me. I'm more

familiar with folliculitis because I've

studied it.

MS. ALEXANDER: Go ahead.

DR. GERBA: Actually, it's usually

infections around your hair follicles.

That's where it gets the name folliculitis.

It's most commonly associated with

hot tubs, particularly in the bathing suit

area and around the buttocks. And that's

where you most commonly see getting

folliculitis.

Almost all the cases in the

United States are associated with hot tubs or

other type of artificial waters, generally,

in the United States. Although, cases have

been associated with swimming in natural

waters.

And there's one study in Europe

that showed a relationship between getting

pseudomonas infections and swimming in lake

water.

MS. ALEXANDER: There's also a

reference to eye and ear exposures, here and

in the language I just quoted and in your

testimony.

Are those eye and ear infections

also folliculitis, or are those a different

type of infection?

DR. GERBA: Those are different types

of infection.

MS. ALEXANDER: Okay. Just one

second. Bear with me.

All right. Now, regarding

pseudomonas, I have in front of me the

discussion -- at least one of the discussions

of it in the risk assessment on Page 129.

THE HEARING OFFICER: One twenty-nine

of --

MS. ALEXANDER: One twenty-nine of the

risk assessment document, which I believe is

marked as Exhibit 72.

THE HEARING OFFICER: Okay. Wait.

Seventy-two is what you gave us, the Tim Wade

documents.

MS. ALEXANDER: Oh, I'm sorry.

THE HEARING OFFICER: The Geosyntec

report is 71.

MS. ALEXANDER: This (indicating)

is 71. Okay. I apologize.

Looking at Page 129, just to read

your language, it states, "Perhaps, more

importantly, the outfall samples show low

levels of pseudomonas -- I'm sorry, lower

level pseudomonas in the corresponding wet

weather samples. This suggests that the

major input for pseudomonas in the waterways

are sources other than the WRP effluent.

"Therefore, this infection of the

WRP effluent would have minor effects on the

overall loading of pseudomonas in the

waterway and risks associated recreational

exposure to the pathogen."

Would I be correct in summarizing

that the basis for your conclusion that

pseudomonas was not a risk is this the

statement that wet weather levels are higher

than dryer weather levels?

DR. TOLSON: I'm sorry the statement

that pseudomonas is not a risk?

MS. ALEXANDER: Basically, you have

the statement -- you conclude, "Therefore,

disinfection of the effluence would have

minor effects on overall loading of

pseudomonas." Let me ask the question more

broadly.

Do you have any other basis for

concluding that there was no -- that there is

no significant risk from eye, skin and ear

infections associated with pseudomonas?

MR. ANDES: Other than what?

MS. ALEXANDER: Other than the

language I just read, stating that lower

levels of pseudomonas in the dry weather

samples.

I mean, is there any other basis

for concluding that these types of infections

from pseudomonas are not a significant risk?

DR. TOLSON: I think -- we did not

quantify the exact level of pseudomonas

risks -- I'm sorry, the risk, for ear or eye

or skin infections. However, if you look at

Page -- Table 515 in Exhibit 71, I believe,

which is the report, it lists the pseudomonas

levels in the outfall effluent and also in

wet weather samples.

So, for example, in the north side

channel, the outfall had 1,350 CFUs per ML --

is that correct? Thirteen hundred fifty

units, where the wet weather -- in other

words, in the channel, had 5,427.

So it's hard to explain how the

effluent disinfection would have affected

something the receiving body that was, you

know, a four times higher concentration. And

that's the basis of my conclusion that

disinfection wouldn't change the wet weather

concentrations that we see.

Is that --

MS. ALEXANDER: Did you reach any

conclusions as to whether it would change the

dry weather concentrations?

MR. ANDES: I didn't -- whether what

would change?

MS. ALEXANDER: Weather disinfection

would change the dry weather concentration of

pseudomonas?

DR. TOLSON: Pseudomonas is a little

bit different than the other pathogens,

because they have such varied sources. The

concentrations of pseudomonas out of the

effluent we would expect it to decrease

probably quite dramatically by most of the

disinfection technologies.

Our pseudomonas is one of the

pathogens that comes from a lot of our

sources. We talked within this testimony

yesterday about trees and bushes that are

nearby the shoreline, those are a significant

source of pseudomonas into the waterway.

So unlike other pathogens,

pseudomonas is more -- is greatly affected by

these sort of nonpoint discharges or sources

into the waterway.

MS. ALEXANDER: Just to be clear,

however, these nonpoint discharges are wet

weather discharges; is that correct?

DR. TOLSON: They can be -- for

pseudomonas, they can be both wet and dry.

MS. ALEXANDER: Would you say that

they are substantially or predominantly wet

weather?

DR. TOLSON: If you want pure

speculation, I'd say yes.

MS. ALEXANDER: Okay.

And I get back to my question, did

you specifically do any analysis of the

impact of disinfection on dry weather

pseudomonas levels in the waterway?

DR. TOLSON: Yes, we did. We did

evaluate the dry weather days -- we did

sample the waterway under dry weather

conditions, and we did investigate the

effectiveness of disinfection techniques on

pseudomonas.

And from that conclusion, it would

suggest that the effluent could be decreased

quite dramatically by disinfection

techniques.

MS. ALEXANDER: Okay.

Now, what -- the reason I

highlighted that text on Page 129 is I was,

frankly, having a little bit of difficulty

finding the discussion that you have

characterized elsewhere as a qualitative as

opposed to quantitative assessment of these

impacts of pseudomonas. And by these

impacts, I'm referring to the possible ear,

eye and skin infections, there are reference

to qualitative as opposed to quantitative

assessment of that.

I was hoping that someone could

point me to any text other than what I've

highlighted on Page 129 that embodies that

qualitative risk assessment of those types of

illnesses.

DR. TOLSON: Well, the qualitative

assessment is the comparison of pathogen

concentrations under what way wet weather

versus dry weather versus the outflow. So we

don't know what that risk is, but we know we

can measure the concentrations of wet, dry

and outfall and get a sense of whether the

contributions to that risk, the magnitude of

that risk, who is responsible for it, what

the discharges are that are responsible for

it.

MS. ALEXANDER: Okay. So when you

reference --

DR. TOLSON: Let me follow up --

MS. ALEXANDER: I'm sorry, I didn't

mean to interrupt.

DR. TOLSON: Let me follow up with one

more point.

The dose response data available

to actually do that quantitative assessment

is not available. There's also very scant

information in the scientific literature

about the concentrations in hot tubs that

were responsible for outbreaks.

And I think Dr. Gerba might be

able to speak to that.

DR. GERBA: Most all of the outbreaks

of folliculitis are due to hot tubs, almost

entirely, where there's high concentration.

But nobody has ever quantified it, so you

couldn't really do a risk assessment on it.

Ear infections do take immersion,

I think I have to point out to when it's

correlated with lake water. And eye

infections, the only ones I've seen have

usually been immersion, related to

recreational activities.

MS. ALEXANDER: Okay. I just --

that's helpful, and I want to summarize to

make sure I understand.

When you say that you've done a

qualitative risk analysis of pseudomonas,

what you've done, essentially, is look at the

differing levels under different conditions

and the impact of disinfection on the levels;

is that correct?

DR. TOLSON: That is correct. We have

been able to assess between wet weather

versus dry weather and what are our

anticipated effects would be of disinfection,

absolutely.

MS. ALEXANDER: But no actual analysis

of the probabilistic likelihood that anyone

is going to get an ear, eye or skin

infection?

DR. TOLSON: We do not have the data

available, nor does anyone else, to sort of

do that quantitatively.

MS. ALEXANDER: Are any of you

familiar with research by lead author

Fewtrell, et al., in 1992, finding that at

one of the contaminated sites studied, the

relative risk of respiratory symptoms among

exposed individuals was actually higher than

the risk of GI symptoms?

DR. TOLSON: I'm familiar with a

number of his papers, if you let me see that

one?

MS. ALEXANDER: Okay. I do have

something in my hand.

And I apologize that I just

discovered this morning that this is actually

an incomplete copy. I am happy to provide a

complete copy as soon as I get my hands on

it.

This, however, does have a

reference to the conclusion that I'm

discussing here.

MR. ANDES: Is that referenced in the

questions?

MS. ALEXANDER: No, this is a

follow-up to this whole discussion.

THE HEARING OFFICER: I've been handed

a two-page document entitled Health Effects

of White Water Canoeing, by L. Fewtrell,

F-E-W-T-R-E-L-L, et al. And it's dated June

27th, 1992 from the Lancet, L-A-N-C-E-T.

I'll mark this as Exhibit 74, if

there's no objection?

Seeing none, then it's Exhibit 74.

(WHEREUPON, a certain document

was marked Exhibit No. 74 for

identification, as of 9/9/08.)

THE HEARING OFFICER: And Ms.

Alexander, when you get a complete copy we

will mark that.

MS. ALEXANDER: Okay.

And my initial question, I think,

is pending to all three of you, whether any

of you have seen this or are familiar with

it.

DR. TOLSON: I believe I've seen it

before, yes.

MS. ALEXANDER: Okay. Anybody else?

Dr. Gerba?

DR. PETROPOULOU: I haven't.

MS. ALEXANDER: I'm sorry, I couldn't

hear Dr. Gerba.

DR. PETROPOULOU: I haven't.

MS. ALEXANDER: I heard yours, I

didn't hear Dr. Gerba.

DR. GERBA: Yes, I believe I have.

MS. ALEXANDER: You've seen it, okay.

MR. ANDES: I can ask -- actually, I

think we have another witness who is very

familiar with it, who -- in fact, we were

going to produce this later anyway. So I

don't know if you want to --

MS. ALEXANDER: Yes, I understand it

was referenced in Dr. Dora Vitch's report. I

just wanted to get a brief reaction from

these witnesses.

Do you have any reason to doubt

the accuracy of the report of the data and

conclusions, in this document?

DR. TOLSON: I'm not really able to

comment on that at this point. One, I

haven't gone through this in great detail,

and so...

MS. ALEXANDER: Understood. I just

wanted to see if you had any --

DR. TOLSON: Sorry.

MS. ALEXANDER: -- immediate reaction.

Anyone else?

DR. GERBA: Yes, the thing that struck

me was the very concentrations of viruses per

ten liters.

MS. ALEXANDER: Very high

concentrations of --

DR. GERBA: About 200 per ten liters.

MS. ALEXANDER: Two hundred what

per -- I can't quite hear you.

DR. TOLSON: One hundred ninety-eight

per ten liters.

THE HEARING OFFICER: Viruses, I

believe he said.

DR. GERBA: One hundred ninety-eight

viruses per ten liters.

MS. ALEXANDER: I also see a reference

to 285 fecal colony forming units per

deciliter, I believe.

Can someone do some quick math on

that and translate that into what that would

be per -- I think we're usually using colony

forming units per 100 millimeters. That's

the same thing; correct, per deciliter?

Okay. Sorry.

Okay. So that 285 number for 100

milliliters, would it be fair to say that

that number is lower than the fecal coliform

levels generally measured in dry weather near

the outfalls in the CAWS?

DR. TOLSON: I have not --

unfortunately, I don't have any reading

glasses, so I can't read this at all.

As it's been characterized, it

would seem, that the concentrations in the

waterways that are represented by this study

are very different than the concentrations

that we've seen in the CAWS. That the

indicator organisms are very low in this

study.

The indicator organisms are very

low, the pathogen organisms are very high.

Compared to the CAWS, where the indicator

organisms are very high and the pathogenic

organisms are very low. That's probably a

significant sort of input to the conclusions

that they've drawn here.

The other thing that's striking is

that, you know, this is a white water

canoeing. And I believe that they actually

took discharge from a water treatment plant

to increase the flow of a river where they

had this event, if I'm characterizing it --

if I recall it correctly.

And that's more of a primary

contact activity than what we have.

MS. ALEXANDER: Do you have any reason

to believe that the contribution from the

wastewater treatment plants of this situation

would have been higher than 70 percent, as it

is in the CAWS?

DR. TOLSON: Say again?

MS. ALEXANDER: Do you have any reason

to believe that the percentage contribution

of wastewater treatment plant effluent in

this waterway was higher than 70 percent,

which is the percent in the CAWS?

DR. TOLSON: I'm sorry, I'm not

familiar with this study well enough from

memory.

MS. ALEXANDER: I just asked if you

had any reason to believe. If the answer is

no, that's fine.

DR. TOLSON: No.

MS. ALEXANDER: All right. Moving on

from this.

Can meningitis be caused by water

born pathogens?

DR. GERBA: Yes.

MS. ALEXANDER: Can meningitis be

caused by water born pathogens?

DR. TOLSON: Dr. Gerba can --

DR. GERBA: Yes.

MS. ALEXANDER: Can myocarditis?

DR. GERBA: Yes.

MS. ALEXANDER: Can encephalitis?

DR. GERBA: Yes.

MS. ALEXANDER: Okay.

And none of those, of course, are

GI illnesses; correct?

DR. TOLSON: Beg your pardon?

MS. ALEXANDER: That none of those are

gastrointestinal, they're all different

kinds; correct?

DR. GERBA: Yes.

DR. TOLSON: I'd also like to point

out that those are reportable illnesses. So

we could pole the county health records and

see if there were any occurrences of those.

MS. ALEXANDER: Right.

But you did not study risks of

those types of infections in the risk

assessment; is that correct?

DR. GERBA: Well, we used -- again, we

use infection as the limit, which could be

taken into that. In other words, that's an

endpoint of infection.

Your conservative things that

estimate you risk by infection is what we

did. That's an outcome of infection.

MS. ALEXANDER: But, in fact, only

studied risk of gastrointestinal illness; is

that correct?

DR. GERBA: That's right. Because,

currently, that's how the U.S. Environmental

Protection Agency regulates recreational

waters.

MS. ALEXANDER: Bear with me one more

second while I find a page number.

I apologize for the interlude.

Not all the pages are -- hard to find things.

All right. I want to refer to the

language on Page 95 of Exhibit 71. I got it

right in time, the risk assessment.

And that language is, "Since there

is a certain degree of correlation between

different pathogens, indications of

unacceptable levels of gastrointestinal

illness may indicate a potential for other

effects."

My first question is, have you

quantified that correlation between GI

illness and other unacceptable -- I'm

sorry -- in other effects, I should say?

MR. ANDES: What page did you say

that's on, I'm sorry?

MS. ALEXANDER: This is on Page 95.

DR. TOLSON: We have not undertaken

that as a component of the study.

MS. ALEXANDER: Okay. And again, you

state that this correlation may exist. I

take it you haven't quantified the

probability of such a correlation?

DR. TOLSON: No, we have not.

MS. ALEXANDER: Do you know any other

researchers that have?

DR. TOLSON: I'll refer to Dr. Gerba.

I do not personally.

DR. GERBA: Say again.

MS. ALEXANDER: A quantification of

the probability of the correlation between GI

illness and other effects, the language used

here.

DR. GERBA: You mean, in other words,

the probability you have a GI was the

probability of having another outcome of

that?

MS. ALEXANDER: Yes. In other words,

these other -- I assume it's referring to

what's referred to also in the core, which is

the ear, skin, eye infections that can

result.

DR. GERBA: From recreational contact?

MS. ALEXANDER: Well, I mean, let me

expand the question for any. Because I --

what I want to know is whether anybody that

you know of has done research to quantify the

probability of that correlation?

DR. GERBA: Going from GI to like,

say, meningitis?

MS. ALEXANDER: Yeah, any of these

other possible effects of water born

pathogens.

DR. GERBA: Not offhand, no, I

can't --

MS. ALEXANDER: Okay.

DR. TOLSON: If I can add something,

though.

You know, EPA's bases GI

illness -- or uses GI illness for their

setting acceptable limits. So I think

implicit within that is the understanding

that GI is the most sensitive and would be

correlated to all illnesses.

MS. WILLIAMS: Is there anywhere that

you can point us to where they say that?

DR. GERBA: I'm not sure what the

question revolves about.

MS. WILLIAMS: Okay.

DR. TOLSON: Off the top of my head I

do not know. But that is something that's

potentially out there.

They had to come up with a

rationale for using GI illness, which --

MS. WILLIAMS: But you don't know what

it is?

DR. TOLSON: I do not know what it is.

MS. ALEXANDER: Okay.

DR. TOLSON: And my guess is that they

specified it somewhere.

MR. ANDES: I'll follow up on that.

So your understanding is the way

EPA sets these standards, the sense is, if

you address GI illness, you're addressing the

other issues?

DR. TOLSON: That is correct.

MR. ANDES: Thank you.

MS. ALEXANDER: But you're not

offering anything substantive right now to

support that assumption?

DR. GERBA: I was just -- my thought

was that a lot of times gastrointestinal -- I

mean, we have respiratory, we have intestinal

infections, also. So you can have both by

the same agent is the only thought I had on

that.

So in some ways that might be

covered, because you can have both diarrhea

and respiratory illness from the same agent

at the same time.

MS. ALEXANDER: I understand that it's

possible to get really sick from multiple

things at the same time. But I guess what

I'm asking is whether you know of any

quantification of the likelihood of that

correlation.

DR. GERBA: I've answered that.

MS. ALEXANDER: And it sounds to me

like the answer was no.

Let me ask another question along

those lines. Is it possible in your review

that there could be circumstances in which

recreators would be at risk of contracting

nongastrointestinal illnesses, even if they

were not at significant risk of a GI illness?

DR. GERBA: There are so many caveats

to that.

DR. TOLSON: There are a lot of

caveats to that. There are potentials,

obviously, of getting a respiratory or an ear

infection and not getting GI illnesses,

that's what you're after, sure.

MS. ALEXANDER: Okay.

MR. ANDES: Can you expand on that?

DR. TOLSON: While there is that

potential, we believe the predominant illness

from recreational exposure to the CAWS is GI

illness.

MS. ALEXANDER: I understand that's

your --

DR. TOLSON: Okay.

MS. ALEXANDER: -- viewpoint.

Let me ask -- this has drawn --

sorry, I didn't mark which prefiled question

this was. But I'll ask it anyway.

Approximately how many types of

water born human pathogens are known to be

associated with sewage overall? Just an

approximation.

DR. GERBA: The number of different

types?

MS. ALEXANDER: Yeah.

DR. GERBA: I'd say between 160 and

200.

MS. ALEXANDER: Okay.

Did any or all of you review the

list of water born pathogens that accompanied

Dr. Mary Lynn Yates' testimony submitted in

this matter.

DR. GERBA: She didn't give a specific

list. But she did say there were thousands,

I think.

MS. ALEXANDER: There was an attached

list, which I'm happy -- I mean, we're going

to be marking Dr. Mary Lynn Yates' testimony.

But for ease of reference, I can just have

the list marked separately, if that's all

right.

I do not recall, unfortunately,

which document this was to the testimony, but

I will represent that it was an exhibit,

which I'm giving you for reference.

THE HEARING OFFICER: I've been handed

Table 1, Illness Acquired By Ingestion of

Water.

MS. WILLIAMS: I think it's Exhibit 6

to the testimony.

MS. ALEXANDER: Thank you.

THE HEARING OFFICER: And I believe

the title of the book is Water Born

Transmissions of Infectious Agents, that's at

the top.

I'm going to mark this as Exhibit

75. If there's no objection?

Seeing none, it's Exhibit 75.

(WHEREUPON, a certain document

was marked Exhibit No. 75 for

identification, as of 9/9/08.)

DR. GERBA: Can I make a comment right

away?

This has to do with recreational

water only. Many of these organisms are

not -- do not occur in sewage and are not

transmitted by that route.

They are -- many of these

organisms are what we call water based

pathogens, those that grow naturally in

water. Did you want me to comment otherwise

on this?

I -- again I don't see thousands

of organisms listed here.

MS. ALEXANDER: Yeah. Let me just

clarify your comment.

You say that they are not

recreationally associated. Is that what I

heard you say?

DR. GERBA: No, I said they're not

sewage associated.

MS. ALEXANDER: They're not sewage

associated.

But some of them are sewage

associated; correct?

DR. GERBA: Oh, yes.

MS. ALEXANDER: Yes, I understand

there are a few of these that are not sewage

associated.

My only question to you was, with

that comment in mind that you made that, you

know, we all -- Dr. Yates also recognized in

her testimony that not all of these are

necessarily sewage related. Do you have any

reason to doubt the overall accuracy of this

list as your representation of human water

born pathogens?

DR. GERBA: This is transmitted by

recreational waters?

MS. ALEXANDER: I'm sorry?

DR. GERBA: Transmitted by

recreational waters? That's what the table

says.

MS. ALEXANDER: Yes, potentially

transmitted by recreation, sorry.

DR. GERBA: And that's only the latter

part of that. Yes.

Again, I don't see thousands of

organisms listed here.

MS. ALEXANDER: Right. Okay.

So that's a subset of them.

But the only question would be is

it a longer list, is it not, than the list of

pathogenic organisms that were included in

the risk assessment analysis? Is that

correct?

MR. ANDES: Well, wait. Do we have to

count up whether there's 160 to 200 here? He

just testified there's 160 to 200 types.

MS. ALEXANDER: I'm sorry, say that

again? You have to --

MR. ANDES: He just testified there

were 160 to 200 types of pathogens.

MS. ALEXANDER: Right.

MR. ANDES: So you're questioning --

he has to count these and decide if there are

that many?

MS. ALEXANDER: No, that wasn't really

my question. It was more general than that.

MR. ANDES: Okay.

MS. ALEXANDER: I mean, I -- in the

risk assessment you studied approximately

eight, give or take; is that correct?

DR. GERBA: That's correct.

MS. ALEXANDER: And there are more

listed here that are associated with

recreational water use; is that correct?

DR. GERBA: That's correct.

MS. ALEXANDER: Okay. That's all I'm

getting at, sorry.

DR. GERBA: But I would point out most

of these are not transmitted by sewage. Of

the recreational ones, that you have in

recreational.

MR. ANDES: I'd like to follow up on

that.

Dr. Gerba, is it accurate to say

that the eight, according to your testimony,

that were chosen, were chosen to be

representative of what the basic risks are

from --

DR. GERBA: Sewage contaminated water.

We collected the water organisms because they

occurred in sewage and had the potential to

be transmitted by that route.

We also selected to represent what

we figured would be the ones most commonly

present, ones that could be detected by

methods currently available, because methods

weren't available for all of these. And the

ones would be there in the greatest

concentration.

So they would present the greatest

risk based on knowledge of dose response and

the occurrence of waste water.

MR. ANDES: Thank you.

MS. ALEXANDER: And the longer list

concerns illnesses acquired by ingestion of

water; correct?

DR. GERBA: That's right.

MS. ALEXANDER: Okay.

And one of the exposure pathways

that you considered in your risk assessment

was ingestion; correct?

DR. GERBA: That's correct.

MS. ALEXANDER: And a number of those

are, in fact, transmitted fecally orally; is

that correct?

DR. GERBA: That's correct.

MS. ALEXANDER: Okay.

So in other words, the list of

pathogens from which one might be at risk if

one fell in the water and gulped a mouthful

might, in fact, be longer than, specifically,

the list identified as acquired by

recreational contact with water; is that

correct?

DR. GERBA: That's correct.

MS. ALEXANDER: Okay.

Now, I'll address this initially

to Dr. Petropoulou, it's Question No. 2 on

the Petropoulou prefiled questions. And the

others, if you can chime in afterwards, it's

also Tolson No. 6 and Gerba No. 15.

But specifically for

Dr. Petropoulou, regarding the statement at

Page 4 of your testimony in which you

identify the two bases for selecting a

limited subset of pathogens that you studied,

these eight give or take that I referred to a

moment ago. And those two bases were, one,

the existence of past outbreaks caused by

these viruses, and, secondly, the existence

of USEPA approved SOPs for those pathogens.

Is that an accurate

characterization?

DR. PETROPOULOU: Correct.

MS. ALEXANDER: Okay.

In your view, are outbreaks an

accurate indicator of the actual risk of a

particular pathogen?

DR. PETROPOULOU: I'll defer the first

question to Dr. Gerba.

MS. ALEXANDER: Okay.

DR. GERBA: Yeah, outbreaks are one

indication. But a pathogen can be

transmitted by a specific route.

MS. ALEXANDER: They're one

indication. But is it possible for there to

be risk of a type of pathogen and no record

of outbreaks from that pathogen?

DR. GERBA: By a water route, say,

or -- yes.

MS. ALEXANDER: Sure, by water route.

DR. GERBA: Yes.

MS. ALEXANDER: One second.

Now, I'd like to refer again to

the second attachment to that May 23rd, 2008

letter, which was a component of Exhibit 73,

Page 7 of that.

THE HEARING OFFICER: For

clarification, you refer to the May 23rd

letter, and it may be a copying error again,

but we have the May 23rd letter attached to

the May 28th letter.

MS. ALEXANDER: Yes, I'm sorry. I've

been referring to May -- that is the May 23rd

letter.

THE HEARING OFFICER: Okay.

MS. ALEXANDER: And this is Page 7 of

the document headed Review Conducted by USEPA

Office of Research and Development.

THE HEARING OFFICER: Page 7?

MS. ALEXANDER: Yes. Are you there?

Okay.

I'm referring to the statement at

the bottom, that quoted language from the

Office of Research and Development document.

It's cited as Page 2.

They are quoting language in the

document regarding, quote, "No outbreaks

tradable to treated waste water." And then,

the comment being responded to:

"The statement is misleading,

because outbreaks are not a reliable health

indicator due to problems with consistent and

reliable detection. Furthermore, statements

such as these require citations and peer

reviewed literature, other outside sources to

avoid the perception of bias."

Now, their response provided is a

citation to what purports to be peer reviewed

literature. Let me first ask the question,

is that document cited peer reviewed, to your

knowledge?

DR. TOLSON: I think that's beyond

our --

MR. ANDES: Let me clarify.

Directly under that citation it

points out that the statement the EPA

commented on was removed from the final

report.

MS. ALEXANDER: I understand that.

But the subject matter is still relevant,

regardless whether the statement is in the

report.

MR. ANDES: But we don't have the

particular statement at issue here in the

final report. So you're asking them about

the statements in their testimony, not the

statement in the draft report.

We don't know what that statement

was.

MS. ALEXANDER: Understood. But the

subject matter is exactly the same, which is

whether outbreaks are or are not a reliable

indicator of risk.

And what I am trying to find out

is the type of discussion that has taken

place with EPA about that. Because EPA here

has expressed a concern, and it's not obvious

to me how that concern was responded to or if

it was responded to. And that's what I'm

getting at with these questions.

MR. ANDES: But I guess the question

that they're testifying is not whether

outbreaks are a reliable health indicator,

it's whether they're relevant to the choice

of which particular parameters to look at in

doing a study. So if you want to ask him

questions about that, that's relevant, but

this statement is to a different issue.

MS. ALEXANDER: It's the same issue in

the sense of what does it matter whether

there's been an outbreak or not. And I want

to find out what kind of discussion there was

with the USEPA on that topic.

And I understand that the

parameters of the discussion may have changed

a little, but the fact of the matter is there

is extensive reference, both in the testimony

and in the report itself, to the significance

of outbreaks. And I want to know what the

conversations were with EPA about that, and

whether their concerns in any context were

responded to.

DR. TOLSON: I believe the answer to

your question is that, you know, we used

outbreaks to identify important parameters,

important pathogens to carry through the

assessment.

MS. ALEXANDER: I get that.

DR. TOLSON: And that's totally it.

MS. ALEXANDER: And EPA made a comment

to the effect that outbreaks are effectively

of minimal significance. And then a response

was provided by Dr. Petropoulou, perhaps in

reliance on others, but I'm trying to

understand that response.

Even though I know that particular

statement that prompted the USEPA's concern

is not in the record, the issue is still very

much a part of this -- a part of the report

and a part of discussion.

So let me return to my question,

which is, there is a citation here to an MWRD

paper. And my question -- I'll direct it to

Dr. Petropoulou, since she drafted this --

is, was that or was that not a peer reviewed

document?

DR. PETROPOULOU: Which document?

MS. ALEXANDER: I'm referring to now

on Page 8, the -- on Page 8, your response

says, "The report includes the following

citation for the statements made." And then

it cites a document.

And my question is, is that

document peer reviewed? Because the question

asked what about peer review.

DR. PETROPOULOU: I do not know.

MS. ALEXANDER: Okay.

MR. ANDES: I'd like to follow up.

The question for any of you is, in

terms of the choice of parameters, the

parameters that you chose based partly on the

existence of outbreaks, did EPA finally go

along with the choice of parameters?

DR. GERBA: Yes. I've been on EPA

advisory committees for years in trying to

get them to actually do more than just

outbreaks. But EPA's position has always

been the drinking water.

There hasn't been an outbreak, why

are we trying to regulate it. In general,

it's the opposite thing.

What we're really finding most of

the time is that they want an outbreak. And

the reason you use an outbreak is because we

know it can be transmitted by that route.

And there's a great deal of

uncertainty whether other illnesses can be

transmitted by that route if you don't have a

documentation of an outbreak. That's the

issue.

So it's usually the opposite

problem we have with the EPA. That's why I

don't really see -- usually the EPA is

telling us why are you studying it if there

hasn't been an outbreak.

MR. ANDES: Thank you.

MS. ALEXANDER: Beyond what's in this

document, did you have any further

conversations, any of you, in this meeting or

otherwise, with EPA concerning the

significance of outbreaks as an indicator of

risk?

MR. ANDES: Ever?

MS. ALEXANDER: In the context of this

risk assessment, I should say, not ever,

ever.

DR. PETROPOULOU: I have not.

MS. ALEXANDER: Okay.

DR. TOLSON: Nor I.

MS. ALEXANDER: Okay.

DR. TOLSON: I have not had any

contacts with anyone.

MS. ALEXANDER: All right.

Is it possible, in your view, that

a substantial number of outbreaks go

undetected?

DR. GERBA: Yes.

MS. ALEXANDER: Okay.

Is it possible that pathogens that

are more frequently asymptomatic, as in

people aren't actually getting sick they're

just getting infected, would be less likely

to result in outbreaks that are actually

traceable to recreation, because the people

with the symptoms would not necessarily be

the same people who recreated on the water?

DR. TOLSON: I don't think we have the

data to really speculate on that. So I can't

address that.

MS. ALEXANDER: Dr. Gerba, can you?

DR. GERBA: It's too much speculation,

I think, to tell you what the impact would

be.

MS. ALEXANDER: Let me see if I can

clarify my question just a little, because I

think it may have sounded more speculative

than it is.

Let's hypothesize a type of

illness where only half the people actually

exhibit symptoms. If those people don't get

sick themselves but pass it onto their

friends and their friends all get sick, it's

going to be harder to trace those friends'

illnesses to recreation on the water body

than it is to trace the recreators'

illnesses; is that correct?

DR. TOLSON: Again, that is still

fairly speculative. But let me address the

point that I think it -- the underlying point

that relates our risk assessment is we do

consider that only about half of the

people that are ill actually -- or infected,

actually become ill. And we do consider that

those people can transmit illness to their

family members.

MS. ALEXANDER: I get that about the

risk assessment. But my question has to do

with outbreaks.

And my question is, isn't it

likely that outbreaks are even less likely to

be detected if the illness in question is not

highly symptomatic, such as the people

getting sick aren't the ones who are actually

on the water?

DR. TOLSON: Our testimony here is

about this risk assessment, not on public

health sort of concerns about outbreaks.

Outbreaks really had nothing to do with the

assessment.

MS. ALEXANDER: Oh, except you did, in

fact, rely on the presence or absence of

outbreaks as one of the two criteria for your

choice of pathogens; is that correct?

DR. TOLSON: That is correct.

MS. ALEXANDER: Okay.

DR. TOLSON: Outbreaks are a good

indicator of which ones to go after and

sample. But they didn't follow through to

figure out what the impacts of outbreaks were

on illness rates in the Chicago population.

That's not part of their assessment.

MS. ALEXANDER: You say they are a

good indicator, but, in fact, they are far

from a perfect indicator; is that correct?

DR. TOLSON: That is correct.

MS. ALEXANDER: Because, as Dr. Gerba

has acknowledged, it's entirely impossible

for outbreaks to go undetected.

MR. ANDES: Well, I could follow up.

Is there a perfect indicator.

DR. GERBA: Can I follow up on that?

DR. TOLSON: No, there's no --

DR. GERBA: When you say follow up,

that's largely because limitations in public

health, for one thing. Every potential

outbreak is not investigated or comes to the

public health's attention. Or not everybody

calls in every time to the public health

department when they have diarrhea or other

types of illnesses.

So it's more of a limitation of

public health's ability to respond to that to

conduct an investigation. That's probably

one of the overlying factors to all of the

quantifying certain sources of infection and

identifying outbreaks.

MS. WILLIAMS: Can I ask a follow-up

question?

MS. ALEXANDER: Sure.

MS. WILLIAMS: I think Ms. Alexander

indicates she understood something that I

don't think I do. So I want to go back and

make sure I do.

When we talk about the risk

numbers, you know, one in a thousand, two in

a thousand, eight in a thousand, I always

understood USEPA to use it per 1,000

swimmers. Are your numbers based on per

1,000 recreators, or do they reflect also

people who have not recreated but have

contacted illness from someone who did? Can

you explain that?

DR. TOLSON: Right. We actually ran

two sets of numbers.

One of them for the people that

were actually engaged in that. And then,

just sort of to be more conservative and take

into consideration a potential that that

disease could spread to others, we took

secondary attack rates, or their family

members, and considered them a second pool of

people that could be infected, and presented

results for those too.

MS. WILLIAMS: Are they in separate

tables in your report?

DR. TOLSON: They are.

Do you want me to point to those?

MS. WILLIAMS: Yes. Just so I can

take a look at them.

DR. TOLSON: Sure.

We go to Table 513 in Exhibit 71.

The bottom two lines there list illnesses

primary and secondary, in parentheses.

So you can see from at the North

Side we have 1.55 per 1,000. And if you

include the pool to include secondary --

potential secondaries, it's 2.6.

MS. WILLIAMS: Okay. Thank you.

DR. TOLSON: Okay.

MS. WILLIAMS: I'll review that. I

may have some follow-up later, but thanks.

DR. TOLSON: That's fine.

MS. ALEXANDER: I'd like to turn now

to the second prong of your two-pronged

justification for why you picked this limited

subset of eight or so pathogens, which was

the presence of USEPA approved laboratory

standard operating procedures, which we've

been referring to as SOP for measurement of

the pathogens.

And the question is, does the

availability of SOPs for a particular

pathogen have any relationship to the risk it

poses?

DR. PETROPOULOU: The availability of

EPA approved methods or standard operating

procedures relates to the ability to measure

the concentration of the organism. And

without that concentration, we cannot

quantify the risk.

So in that sense, it does relate

to how we are able to measure the risk but

not the risk --

MS. ALEXANDER: Okay.

DR. PETROPOULOU: -- in general of

the --

MS. ALEXANDER: Not the risk, but your

ability to measure it.

And now, as we're discussed

before, you did, in fact, evaluate two types

of pathogens for which there was not an EPA

approved SOP; is that correct?

DR. PETROPOULOU: Correct.

MS. ALEXANDER: So that was not an

absolute requirement for inclusion in your

subset, it was just one of the factors you

considered; is that correct?

DR. PETROPOULOU: Actually, we said

either EPA approved or standard operating

procedures, like the ones that Dr. Gerba's

laboratory is using. So we did go beyond the

EPA approved methods.

We also quantified viruses that

the EPA has no approved method but

Dr. Gerba's lab has standard operating

procedures to use for that.

MS. ALEXANDER: And, in fact, there

are USEPA approved SOPs for shigella; is that

correct?

DR. GERBA: Shigella, there may be,

yes. I'm not familiar --

MR. ANDES: I'm sorry, SOPs --

DR. GERBA: It is a standard method,

yes.

MS. ALEXANDER: SOPs.

MR. ANDES: Analytical methods, I'm

not --

MS. ALEXANDER: USEPA approved SOPs.

MR. ANDES: It doesn't approve --

MS. ALEXANDER: I'm sorry, US --

MR. ANDES: It approves only

analytical methods.

MS. ALEXANDER: I'm sorry, they

only --

MR. ANDES: Approve analytical

methods to put in 40CFR136. I'm sorry, 136.

So I'm not sure if you're

referring to an approved analytical nitrogen

136 or some other EPA generated document, but

I don't think it's approved.

MS. ALEXANDER: Well, I believe -- in

terms of just the language of USEPA approved,

I believe that is drawn directly from

Dr. Petropoulou's testimony.

Did you -- I can fish through it,

but did you, in fact, refer to USEPA approved

SOPs?

DR. PETROPOULOU: No. EPA approved

methods or standard operating procedures.

MS. ALEXANDER: Methods or --

DR. PETROPOULOU: Laboratory standard

operating procedures. I was not referring to

EPA SOPs.

MS. ALEXANDER: Okay.

DR. GERBA: Let me go back there.

I don't know of an EPA approved

method for shigella. Usually EPA only

approves methods if there is a legal

requirement for monitoring in some aspect, or

they're conducting a study, which requires an

approval, like an information collection

rule.

However, there is a standard -- it

is in standard method, there is a method for

shigella.

MS. ALEXANDER: Okay.

DR. GERBA: And we did not decide not

to use shigella in this study, because I had

questions about how good the method really

was. In all of the recreational outbreaks

that were associated with, there were usually

too many people in the water.

In a review for 1971 or 2000, they

were all lake waters, where people were

believed to be the source through accidental

fecal releases -- I hope they were

accidental -- into the water.

MS. ALEXANDER: I'm not going there.

DR. GERBA: And also, shigella is a

weak organism, it doesn't survive very well

in the environment.

MS. ALEXANDER: But, in fact, as you

just referenced, there have been recreational

outbreaks of shigella?

DR. GERBA: Right. Associated with, I

belive, fecal releases are too much gluteal

fold in the water at one time.

MS. ALEXANDER: And my next question,

which I believe was a prefiled Petropoulou,

but I'll just ask it.

The question I think has been

partly answered, but I want to get at the

rest of the answer, which is, did the risk

assessment take into account populations that

that are potentially more sensitive to

pathogens and may more easily become ill or

suffer severe effects, such as children,

pregnant women and an immunocompromised

person?

Now, an answer was given earlier,

if I recall correctly, that the more

sensitive populations were taken into account

in the secondary infection rate analysis; is

that correct?

DR. TOLSON: That is correct.

MS. ALEXANDER: Is there any other

manner in which sensitive populations were

taken into effect?

DR. GERBA: You know, again, we

determined the risk of infection, so one

could always assume that that risk of

infection -- and you could apply what the

outcome would be to those groups, if you

wished. You know, because that's the most

conservative thing you do.

What you're talking about is the

result of the infections.

MS. ALEXANDER: Okay. So, in fact,

your analysis really doesn't address at all

whether or not we're dealing with the risk of

somebody having a mild case of diarrhea and

somebody having a very severe

gastrointestinal illness, which might be the

result if, say, the person was a young child

or was on chemotherapy?

DR. TOLSON: That is correct.

MS. ALEXANDER: Okay.

MR. ANDES: I want to follow up on

that.

So, as I understand what you're

saying, is the risk of illness -- there's no

evidence that their risk of illnesses is

different for these groups, the severity of

the illness?

DR. GERBA: Right. That's correct.

MR. ANDES: So your risk assessment,

in terms of how likely that the people will

develop infections, does not change?

DR. GERBA: It does not change.

DR. TOLSON: Just another follow-up on

that.

On the flip side of that, you

know, we do not consider immunity. And I

think we touched on this before, that our

analysis may be biased, because there may be

immunity in the population that we didn't

account for.

MS. ALEXANDER: Let me --

approximately what percent of the population

would you say falls into these categories of

immunocompromised persons?

DR. GERBA: I -- somewhere about 25 to

35 percent of the U.S. population. It's

largely represented by people -- elderly

individuals over 60 years of age.

MS. ALEXANDER: And also would you say

children?

DR. GERBA: And children.

MS. ALEXANDER: And --

DR. GERBA: Well, when I said

children, we usually refer to infants, small

children.

MS. ALEXANDER: Okay.

Pregnant women?

DR. GERBA: And pregnant women.

MS. ALEXANDER: And people on chemo

therapy?

DR. GERBA: And -- yeah, people out

walking around on chemotherapy.

MS. ALEXANDER: And people on

antirejection drugs for organ transplants?

DR. GERBA: Yes.

MS. ALEXANDER: And people with HIV?

DR. GERBA: Yes.

MS. ALEXANDER: This question was

Petropoulou No. 3 and also is the subject

matter in Gerba No. 19 and Tolson No. 10.

And the question is -- specifically, first to

Dr. Petropoulou, because the statement's in

your testimony.

Regarding the statement at Page 5,

that although the microbial analytical

results were evaluated within the framework

of dry and wet weather conditions, "For the

MRA risk assessments, the dry and wet weather

microbial results were integrated into a

comprehensive data set representative of all

weather conditions on the waterway."

And my question is, does this

mean -- am I correct in understanding that in

assessing post-disinfection risk, you

combined data from the wet and dry weather

conditions?

DR. TOLSON: Yes. In fact, you have

to do that in order to assess what the effect

of disinfection is.

You want to figure out what the

overall seasonal population of recreator risk

is, you have to consider that it rains, has

CSO events and there's dry weather days.

We've attenuated one of those sources to the

waterway by disinfecting it and then reran

the calculations to figure out what the

effect would be on the whole population.

MS. ALEXANDER: Would it not be

possible to run separate analyses for the

risk on wet weather days and the risk on dry

weather days?

DR. TOLSON: Sure. In fact, we

present data that shows that.

MS. ALEXANDER: Well, let's turn to

Table 5-14 in Exhibit 71.

DR. TOLSON: Table 5-14 was actually

my exhibit to my testimony.

MS. ALEXANDER: Right, right. It's

the same thing.

DR. TOLSON: Good.

MS. ALEXANDER: So that's your overall

summary. But let's turn to page -- I'm sorry

Table 59.

In fact, there you've broken out

wet and dry weather estimates --

MR. ANDES: We actually have this

one -- that one on the chart.

MS. ALEXANDER: Okay. Yeah, for wet

and dry weather.

But it's not broken out in your

overall estimate; is that correct?

DR. TOLSON: It is not broken out in

the overall estimates. We've presented the

data in a number of different ways and tried

to stratify it.

Actually that was one of the

comments we got from the EPA and we tried to

stratify it in the final report in various

fashions. The 5.9 exhibit that you show

there addresses the question what happens

just under dry, what happens just under wet.

MS. ALEXANDER: But only for

pre-disinfection; correct? The table is

headed Total Expected Illnesses For One

Thousand Exposures Using Different Estimates

and Pathogen Concentrations With No Effluent

Disinfection.

So this is the before; right?

DR. TOLSON: Correct.

MS. ALEXANDER: Why don't you have a

comparable after table? In other words,

total expected illnesses per 1,000 for wet

weather and for dry weather? Or did I miss

it?

MR. TOLSON: Well, if you put the dry

weather in there, you can see from 5.9 that

the dry weather lists are very low.

MS. ALEXANDER: That wasn't my

question, though.

DR. TOLSON: It would go even lower.

MS. ALEXANDER: My question is, did

you break it out, or did you not?

DR. TOLSON: It is not broken out

within the report.

MS. ALEXANDER: Okay.

MS. WILLIAMS: Was it broken out and

not put into the report?

DR. TOLSON: Quite possibly. We have

that data, but it would be, essentially, zero

for every one of those.

If you dis --

MS. ALEXANDER: Based on what? Do you

have any data printed to present to support

that?

DR. TOLSON: Should I go and talk from

it?

MS. ALEXANDER: Go ahead.

DR. TOLSON: All right. So Table 5.9

presents a risk for dry weather, wet weather

and dry and wet weather.

If you look at just the dry

weather results, we have fairly low risk

within the waterway. One of the other tables

that we have in our report shows that the

disinfection efficiency is quite high, or

some -- against some of the pathogens, maybe

99 percent.

So you would decrease the

pathogens within just the dry weather by

99 percent. The risk -- corresponding risk

would drop very low.

That doesn't happen to the wet

weather contributions. Those would not be

attenuated by the disinfection.

So the overall risks that I

presented in the other table, would not

change so much.

MS. ALEXANDER: Just to clarify, by

the way, it's your testimony that

disinfection would reduce the pathogens and

not just the indicators; correct?

DR. TOLSON: That's correct.

MS. ALEXANDER: By 99 percent,

approximately?

DR. TOLSON: Well, there's a table in

the report that lists each individual

pathogen and the full reduction within that.

It varies by pathogen and by disinfection

technique.

MS. ALEXANDER: So what you're saying,

essentially, is -- correct me if I'm

misinterpreting you -- is that for purposes

of dry weather, you would, essentially,

eliminate, or largely eliminate, the pathogen

risk through disinfection; correct?

DR. TOLSON: Correct.

MS. ALEXANDER: Okay.

DR. TOLSON: We've been a little bit

naive about the way we constructed that, in

that we consider under dry weather there are

no other inputs. So if there are pseudomonas

inputs from overhanging vegetation or

something like that that's contributing to

dry weather, we're not including that.

We're assuming that under dry

weather the effluent from the waste water

treatment plants are the sole contributor to

the waterway.

MS. ALEXANDER: Okay.

DR. TOLSON: So that's the assumption

there.

MS. ALEXANDER: So, essentially, would

it be fair to say that the disinfection would

not have a substantial impact, in terms of

your conclusions on wet weather pathogen

levels and -- although, you've just testified

that dry weather disinfection would

substantially eliminate that risk?

DR. TOLSON: You would take a very low

risk and you would make it a much lower risk.

MS. ALEXANDER: So, essentially, what

you've done in Table 14 is combine a

situation in which the risk is potentially

reduced -- I'm sorry -- will be reduced with

one in which you say it won't be reduced;

correct? You've essentially combined those

two sets of data, the wet and the dry

weather?

DR. TOLSON: We present the data for

the wet weather and the dry weather. In

order to figure out the effect of the

chlorination or other disinfection

techniques, there has to be some assumptions

made, because we can't do the experiment out

of the waterway.

The assumptions that I made is the

dry weather will, just substantially from the

wastewater treatment plant, if you knock that

down, what's the overall effect.

THE HEARING OFFICER: And,

Ms. Alexander, Table 5-14 is the one you were

referring to; right? You said Table 14.

MS. ALEXANDER: I'm sorry.

THE HEARING OFFICER: That's okay.

MS. ALEXANDER: I meant 5-14.

Let me get to the point, which is,

leaving aside the absolute numbers for a

moment, I know that you're claiming that

they're low and our people say they're

higher. Leaving that aside, what you have

done here in combining the wet and dry

weather post-disinfection risk, would that

not mean that the change in the level of

risk, since that change is higher for dry

weather in the case of disinfection than for

wet weather, that you are reducing the level

of change in risk by combining these?

In other words, the delta is going

to be lower if you combine wet and dry

weather than it would be for dry weather

alone?

DR. TOLSON: The risk for recreators

out on the waterway, though, is affected by

wet weather conditions and affected by

effluent from the wastewater treatment plant.

MS. ALEXANDER: But if you're out on

the --

DR. TOLSON: It's the only way of

speculating the risk without considering what

the true pathogen concentrations are in the

waterway. We developed data that comes from

a fairly extensive data set of pathogen

concentrations within the waterway to develop

our risk.

MS. ALEXANDER: But if I'm out there

on my canoe on a dry weather day, as you've

defined it, not impacted by the wet weather,

I'm not going to be impacted one way or the

other by these wet weather risk levels; is

that correct?

DR. TOLSON: Yeah.

MS. ALEXANDER: So if you wanted to --

DR. TOLSON: Hold on, let me answer

your question.

MS. ALEXANDER: Sorry. Go ahead.

DR. TOLSON: Because I want to refer

you to one other exhibit, our Table 5.8

within Exhibit 71.

You'll see that only 15 percent of

the days in Chicago is it truly a dry weather

day, as we've defined it within the report.

So today is not a dry weather day.

MS. ALEXANDER: I understand that, and

I'll have a few questions for you about that

calculation later.

But my point is, is it not true

that, given that you have combined a

situation in which there is a significant

change, leaving aside the absolute levels

between pre and post, pre-disinfection and

post-disinfection, and you've combined that

with a situation in which there is really

not, according to you, a significant change

between wet weather pre-disinfection and wet

weather post-disinfection, does that not mean

that the -- this change between the two,

between pre and post, is going to be lower

than if you broke out dry weather, the degree

of change would be higher; is that correct?

DR. TOLSON: If we had calculated

risks where we said, only can go out into the

waterway three days after it rained and just

looked at that, the risks change or the

impact of disinfection would be higher.

However, it would be very low chance of risk,

whether it's disinfection or nondisinfection.

MS. ALEXANDER: Okay. That --

DR. TOLSON: We're talking about low

numbers versus almost zero numbers. Yes, in

fact, the magnitude of the change would be

different.

But that's a very -- a subset of

something that doesn't really -- you can't

control exposure of that.

MS. ALEXANDER: Okay.

And the absolute numbers, of

course, are something that will be addressed

subsequently in this proceeding. This

question only went to the delta --

DR. TOLSON: Okay.

MS. ALEXANDER: -- as it were.

MR. ETTINGER: Can I ask one question

about this chart?

DR. TOLSON: Sure.

MR. ETTINGER: You say dry weather,

and then you've go North Side, Stickney,

Calumet. Where are you assuming this

exposure takes place?

I assume that the level would be

higher if I were to capsize my canoe directly

outside the outfall than if I did it two

miles downstream.

DR. TOLSON: Yeah.

MR. ETTINGER: What are you doing --

how did you work that out?

DR. TOLSON: That's a good question.

And, unfortunately, the answer is going to be

a little long.

But we had to make some

assumptions about where the use happened

within the waterway and the concentrations

happened in the waterway. We don't have data

that would specifically tie a person to a

specific spot within the UAA.

So we collected all the data

within the segment that we defined as North

Side. And we said this is the use within the

North Side water -- North Side segment.

We tied all of the data that we

collected from that North Side and pulled

those two together to calculate risk. We

don't make an assumption that a person is

going to be in any one place any more often

than any other place.

It may be that they're -- you

know, next to the outfalls more often than

are not. In which case the risk would be

biased low.

It may be that they're away from

the outfalls or -- in which case the risk

would be biased high -- under dry weather.

But under wet weather we've got inputs all

along the waterway.

So the relationship between where

you're recreating in the outfalls, probably

much less significant.

MR. ETTINGER: Okay.

MS. ALEXANDER: This question is -- it

was a Petropoulou question for a -- similar

to Gerba 17 and 18 and Tolson 8 and 9. But

this is specifically for Petropoulou.

Regarding the statement at Page 5

of your testimony that the risk assessment

found that downstream concentrations -- and

that's concentrations of pathogens -- are

consistently greater than upstream during dry

weather, so within -- the context here is dry

weather.

For purposes of assessing risk,

did you, in fact, combine the average

upstream and downstream sampling numbers?

DR. PETROPOULOU: First, I think your

statement mischaracterizes my testimony.

MS. ALEXANDER: Okay.

DR. PETROPOULOU: On Page 5, I discuss

downstream concentrations are consistently

greater than the upstream. I am not

referring to pathogens there.

The discussions for bacteria

results that were analyzed with the ANOVA

testing. And that was done only for

indicator bacteria.

So that statement pertains only to

indicator bacteria.

MS. ALEXANDER: Okay.

DR. PETROPOULOU: And with respect to

your first question, I will let Dr. Tolson

explain the integration procedure for the

data.

DR. TOLSON: So under dry weather we

did include all of the data from each

waterway segment collectively at each

sampling date to put as one of the inputs

into our risk assessment. That included

upstream and downstream concentrations.

We believe that's probably biased

high, though, since under dry weather the

data was collected in close proximity to the

outfall. It didn't account for the fact that

very far downstream of the outfall there is

probably considerable additional attenuation

that is not captured.

MS. ALEXANDER: Let me just make sure

I understand though.

Your pathogen concentration levels

that you assumed were ultimately -- correct

me if I am wrong -- an average that included

both upstream and downstream.

DR. TOLSON: That is correct. We did

not, as Dr. Lanyon put so elegantly

yesterday, people can go upstream or

downstream. So we don't know where the

exposures happened, but we considered they

could go in either direction.

The exposure was averaged across

the entire place where they could actually be

exposed.

MS. ALEXANDER: Would it be fair to

say that the large majority of the CAWS

waterway reaches are downstream of one or

more of the treatment plants?

DR. TOLSON: Yeah, I do not -- we do

not have the data to figure out what the

attenuation rate is downstream. I believe

that it, obviously, goes to the Mississippi

eventually.

So there's a lot more downstream

than there is upstream.

MS. ALEXANDER: Do you have any data

showing that most people use both the

upstream and downstream portions of the CAWS,

in roughly equal measure, even though there's

a lot more downstream than upstream?

DR. TOLSON: We do not have data

specifically to that.

MS. ALEXANDER: Okay.

So, in other words, your

assumption, if we're talking about an

individual as opposed to the overall

analysis, would not hold true for someone

that put in their canoe or kayak, say, at a

location downstream of the treatment plant

outfall and continued to paddle downstream;

correct?

DR. TOLSON: I believe our

concentration estimates in the waterway would

be conservative for that scenario.

MS. ALEXANDER: What's the basis for

that statement?

DR. TOLSON: Because we incorporated

the downstream concentration immediately

below the outfall and we included an upstream

concentration, which we'll assume to be on

the other end. And we assumed a linear

concentration gradient as opposed to normal

downfall.

So, most likely, the average or

the mean concentration that that canoe or

recreator would be exposed to would be less

than the average of the upstream and

downstream.

MS. ALEXANDER: But, in fact, isn't it

possible, based on your results, that the

upstream concentrations upstream of the

outfall and dry weather were lower than the

downstream concentrations?

DR. TOLSON: For the indicators, it's

really the case. For the pathogens, it's

really not that clearcut.

Maybe I'll let Dr. Petropoulou --

DR. PETROPOULOU: Yeah. As I

mentioned in my testimony, for example, if we

take cryptosporidium, there was no infectious

cryptosporidium upstream or downstream. So

you're comparing zero to zero.

For viruses, we found that there

were many instances were there were

detectible viruses upstream but not

downstream. Or that the upstream

concentrations were greater than the

downstream. And that was true also for dry

weather.

So that is true for indicators but

not really for pathogens.

MR. HARLEY: Can I ask a question?

MS. ALEXANDER: Sure. Go ahead.

MR. HARLEY: I wanted to see if I

could integrate the testimony that you gave

about pseudomonas with the question of

impacts of disinfection, dry weather and wet

weather. Now, for pseudomonas, you indicated

that you measured pseudomonas concentrations

at outfalls of sewage treatment plants; is

that correct?

DR. TOLSON: That is correct.

MR. HARLEY: And you came up with a

level of 1,350 colony forming units per

milliliter, I believe you said?

DR. TOLSON: That is correct.

MR. HARLEY: And during wet weather,

when you were not measuring specifically at

outfalls, you were measuring 54, 27 colony

forming units per milliliter.

DR. TOLSON: Actually, we have outfall

data from the wet weather also. And I think

that the 1,350 includes a wet weather event

outfall data as well as dry weather.

MR. HARLEY: Is the outfall number

affected at all by whether or not it's dry

weather or wet weather, or is it relatively

constant?

DR. TOLSON: I'll let Dr. Petropoulou

answer that.

DR. PETROPOULOU: Is the question

specifically to pseudomonas?

MR. HARLEY: Why don't we start with

pseudomonas, if you please.

DR. PETROPOULOU: For example, I think

it depends on the size. And by size, I mean

the treatment plant.

At the North Side during dry

weather, the concentration of pseudomonas at

the outfall was 1,091 CFU per 100 ML. During

wet weather it was 796 CFU per 100 ML.

So they are different.

MR. ANDES: Tables 3-2(a) and 3-2(b).

DR. PETROPOULOU: On the report.

And I can read the other numbers.

MR. HARLEY: You don't need to.

DR. PETROPOULOU: Okay.

MR. HARLEY: I guess my question is,

by disinfection, in light of the fact that

we're going to be hearing different testimony

from different witnesses based on what's been

prefiled about risk, but just talking in

terms of affect of disinfection on levels of

a pathogen, like pseudomonas, if you

disinfect, you're actually getting a benefit

in terms of risk reduction, both during dry

weather periods and during wet weather

periods; is that correct?

Because during dry weather -- I'm

sorry, I should let you answer that question.

DR. TOLSON: The marginal risk

reduction under wet weather, though, is not

nearly as much as it would be under dry

weather. So I think that's what we are

getting to.

For pseudomonas, it's a little

more complicated, because there's probably

additional sources that have been described.

MR. HARLEY: I understand. But you

would get a benefit on those dry weather days

because you would be removing pseudomonas by

controlling what is the clearly primary

source of pseudomonas on dry weather days,

which is effluent from waste water treatment

plants; is that correct?

DR. TOLSON: I assume it is. The

"clearly" I'm not to sure about.

It's not clearly the dominant

source, we really don't know that. We made

the assumption within our risk assessment

that the wastewater treatment plants were the

only source.

And that's just in ease of

calculation of our risk estimates, that was

the way that we needed to do it.

DR. PETROPOULOU: Actually, I would

like to add to that. Because we did look --

pseudomonas was not frequently detected

during dry weather. I believe it was 80

percent of the samples that we collected, or

73 percent of the samples that we collected

that had detectable pseudomonas.

So we looked through a statistical

evaluation using box plugs to see if the

concentration of pseudomonas were

statistically different upstream, downstream

and at the outfall. And I would point out

that figures 321, 322 and 323, they present

those results.

And, basically, the results showed

that, for example, at North Side and at

Calumet, the median concentration of

pseudomonas were identical virtually, or

statistically the same between upstream,

downstream, at the outfalls. That was not

the case at Stickney, where the concentration

at the outfall was greater.

The median concentration was

greater than upstream and downstream. But

the upstream and downstream concentrations

are the same.

MR. HARLEY: Uh-huh.

DR. PETROPOULOU: So you cannot really

draw a direct conclusion.

MR. HARLEY: In wet weather events, if

you removed a contribution for any

pathogen -- by disinfection, that would

reduce the total loading of that pathogen

during the wet weather event?

DR. TOLSON: That's correct. But, as

we've shown, it's just not a great

contribution.

MR. HARLEY: I understand there's

going to be a difference in opinion as to the

relative contribution --

MR. ANDES: He didn't state there was

a difference in opinion, he stated -- let him

state his opinion.

MR. HARLEY: I did.

MR. ANDES: No, I think you

interrupted.

MR. HARLEY: Oh, did I? I'm sorry. I

didn't mean to interrupt you.

DR. TOLSON: Yes, but the relative

magnitude of that is insignificant compared

to the wet weather loads.

MR. HARLEY: Thank you.

THE HEARING OFFICER: On that note,

let's take a ten-minute break.

(WHEREUPON, a recess was had.)

THE HEARING OFFICER: Back on the

record.

Ms. Alexander, we're still with

you.

MS. ALEXANDER: I'm just going to jump

back in subject matter a little bit to

something I missed in my earlier thread.

Which is the question, did you

consider inhalation as a exposure pathway in

the risk assessment? Water inhalation.

DR. TOLSON: We considered it in terms

of trying to figure out what the proportion

or potential ingestion component of

inhalation may be to the overall dose.

MS. ALEXANDER: Explain that. What do

you mean the ingestion component of

inhalation?

DR. TOLSON: When you breathe in air

that might have mists and things that can

lodge into your mucous membranes in your

mouth, in which case you could swallow it.

So it's not going into your lungs, but it

could be, in fact, ingested.

MS. ALEXANDER: Okay. So you did not,

in fact, take into account, if I'm

understanding you correctly, the impact of

inhalation -- or I should say, that exposure

pathway of inhalation into the lungs, you

took it into account if it goes down the

other pipe?

DR. TOLSON: Right. For a respiratory

illness, we did not -- as we discussed

previously, we did not consider it.

MS. ALEXANDER: Okay. Now, I am

turning to Page 4 of -- make sure I

understand what it's Page 4 of. One moment.

This is Page 4 of the first

attachment to the May 23rd letter, which is

attached to the May 28th letter of

Exhibit 73, Page 4. You'll see in the middle

of the page there's a bullet point GI Illness

is the Sole End Point of Risk.

And then, in the middle of the

paragraph that follows, within the first

sentence of the paragraph, "This is a major

weakness in the risk assessment," there's the

statement, "Pseudomonas and adenovirus were

found, so the author should have explored the

inhalation route to properly examine the risk

associated with recreating on this water."

MR. ANDES: I'm sorry, what page are

you on?

MS. ALEXANDER: I'm on Page 4 of the

first attachment, which is Review Conducted

by USEPA Office of Water, Office of Science

and Technology.

DR. GERBA: The one -- pseudomonas

transmission by recreational water and normal

healthy people by inhalation route, I

wouldn't even consider that. I don't know

why that's even here. I think the person is

not familiar with it.

It does cause lung infections in

certain groups of people, but not

recreational exposure. I've never heard of

that.

The -- one of the problems here

you have is what's the dose from, the

secondary contact-type of exposure we're

looking -- what's the amount we should

consider being aerosolized by that route?

There is no basis to form that type of

exposure.

MS. ALEXANDER: So --

DR. GERBA: And no information on how

to do that is provided.

DR. TOLSON: And I want to point out

that these are the -- this is one of the

comments that we had discussions with Tim

Wade on --

DR. GERBA: Yeah.

DR. TOLSON: -- at the meeting.

MS. ALEXANDER: Can you please, I'm

sorry, define -- describe that discussion

concerning specifically respiratory?

DR. TOLSON: And at that point,

there's a consideration that we would not

evaluate that quantitatively within our risk

assessment.

MS. ALEXANDER: You would not evaluate

the inhalation pathway?

DR. TOLSON: Correct.

MS. ALEXANDER: And what was the basis

for that determination that you would not

evaluate it? Or your reason for the

consensus, I should say.

DR. TOLSON: It was -- one, it was not

the most predominant illness associated with

the recreational water, that GI illness was a

predominant illness. But the other one,

being that there's not a mechanism by which

to establish the dose or the dose response

for these organisms.

MS. ALEXANDER: Okay. So, once again,

with respect to the inhalation pathway, we're

talking about the mechanism being the main

concern --

MR. ANDES: That's not what he said.

MS. ALEXANDER: -- as opposed to the

risk.

DR. TOLSON: No. I have -- there were

two points there that I made, and I think

both are important considerations when

looking at respiratory illness and associated

with recreational contact, as it were.

MS. ALEXANDER: Okay.

But the bottom line is, you didn't

consider inhalation or associated respiratory

illness in this analysis?

DR. TOLSON: That is correct.

DR. GERBA: Let me reiterate. That

doing pseudomonas, there would be no -- there

is no recreational exposure that would result

in a respiratory infection for pseudomonas.

I don't know why that's in there.

DR. TOLSON: And also to follow up,

that we did not evaluate that quantitatively,

but qualitatively in terms of the proportion

of risks, we would --

MS. ALEXANDER: This also

references -- I'm sorry.

DR. TOLSON: That we perceive from the

various illnesses, we did consider it that

way.

MS. ALEXANDER: Referring to

Dr. Gerba's statement just now, I believe the

text refers to pseudomonas and adenovirus.

DR. GERBA: Right.

MS. ALEXANDER: Am I correct in

understanding that there are strains of

adenovirus that carry with them a risk of

respiratory infection?

DR. GERBA: That is correct. And the

only -- and, in fact, by recreational waters.

But those are all primary contact

swimming-type exposures that resulted in

those types of infection, not by the

inhalation route.

MS. MEYERS-GLEN: If somebody flips

over in a canoe and is dumped, or in a kayak,

and they get a mouthful of water, then that

would be an exposure route for them?

DR. GERBA: Yeah.

MS. ALEXANDER: Bear with me just a

moment.

Okay. And this is also following

up on an earlier discussion, but this was

Tolson Question 11, which is -- I want to

clarify, regarding the statement at Page 6 of

your testimony. If you'll pull that out.

Regarding the statement at Page 6

that, "Disinfection at the effluent outfall

was predicted to result in a decrease in

effluent pathogen loads in the water

reclamation plants that have little affect on

overall pathogen concentrations in the

waterway."

The question is, does that

statement concern wet weather conditions?

DR. TOLSON: It concerns neither wet

nor dry weather conditions. It concerns the

combination of wet and dry, which I think we

discussed.

MS. ALEXANDER: The combination we

discussed earlier.

DR. TOLSON: Right.

MS. ALEXANDER: Would that statement

apply -- well, actually, let me rephrase

that.

I take it, based on your earlier

testimony, that that statement would not

apply specifically to dry weather conditions;

is that correct?

DR. TOLSON: Your question is does

disinfection affect pathogen loads in the

waterway under dry weather?

MS. ALEXANDER: Yeah. Your statement

is that -- yes, that disinfection of the

effluent outfall --

MR. ANDES: I'm sorry, you're not

talking from Question 11, though; are you?

Because that's not the same as Question 11.

MS. ALEXANDER: Hold on. Let me find

Question 11, just to clarify. It is one of

the Tolson questions, I may have mismarked it

last night.

THE HEARING OFFICER: Yeah, the second

part of the question at 11 --

MR. ANDES: Okay.

THE HEARING OFFICER: -- it says it

applies specifically to dry weather

conditions. She did rephrase it slightly,

but...

MS. ALEXANDER: Okay.

So my question is, you make the

statement, Dr. Tolson, "Disinfection of the

effluent outfall, to paraphrase, was

predicted to result in a decrease in pathogen

loads from the water reclamation plants that

have little affect on overall pathogen

concentrations in the waterway."

And my question is, would that

statement be true, specifically for dry

weather conditions? And I actually

characterized it as, am I correct in

understanding it would not be true in view of

your testimony that disinfection would

significantly decrease pathogen loads in dry

weather conditions, or overall pathogen

concentration, I mean?

DR. TOLSON: Disinfection under dry

weather only conditions would decrease the

pathogens that come out of the waste water

treatment plant. However, we can't estimate

overall illness rates in the waterway without

considering all the sources.

MS. ALEXANDER: I'm not talking about

illness rates.

DR. TOLSON: And if you look at the

pathogens, they're low to begin with, so...

MS. ALEXANDER: My question, actually,

Dr. Tolson, was not about illness rates. I'm

talking specifically about your testimony on

Page 6 that you say, "Disinfection --

ellipsis -- would have little effect on

overall pathogen concentrations in the

waterway."

Do you mean that statement to

apply to dry weather conditions specifically?

MR. TOLSON: I understand what your

point is. So you're -- no, under dry weather

conditions --

MS. ALEXANDER: Okay.

DR. TOLSON: -- it may be different.

I understand where you're coming

from now.

MS. ALEXANDER: Okay. I'm sorry,

that's all I'm asking.

And I take it there are no

findings in the risk assessment that would

support that statement in dry weather

conditions; correct?

MR. ANDES: He didn't make the

statement. What statement are you asking

whether it would be supported?

MS. ALEXANDER: Okay. He makes the

statement here on Page 6 of his testimony

that disinfection of the effluent outfall

would have little effect on overall pathogen

concentrations in the waterway. Now, correct

me if I'm mischaracterizing, but Dr. Tolson

just said that statement would not hold true

for dry weather, only in the wet and combined

wet and dry analysis that was done in the

risk assessment.

And I'm following up to confirm

that, in fact, there are no findings that

support this conclusion that Dr. Tolson is

not purporting to make that this statement

would apply during dry weather conditions.

That's all.

DR. TOLSON: The report --

MR. ANDES: I don't know if the answer

is yes or no.

MS. ALEXANDER: Got lost in that?

There's nothing in the risk

assessment that supports any conclusion this

would apply to dry weather; is that correct?

DR. TOLSON: I believe you're pointing

out that under our Table 5-14 within the risk

assessments, we did not do that for dry

weather, we did it for the combined.

MS. ALEXANDER: Right.

DR. TOLSON: Yeah, we talked about

that before. That is correct, we did not

present risk under dry weather because we

believe that the whole intent of the risk

assessment was to look at overall risks,

100

including dry and wet weather.

And the only way to do that was to

consider that it rains in Chicago.

MS. ALEXANDER: Okay. All right. I

think I've covered this.

Petropoulou No. 7, regarding the

statement at Page 6 of your testimony that

dry weather fecal coliform concentrations

upstream of the North Side and Stickney

plants were greater than the effluent limit

of 400 CFU per 100 milliliters proposed by

IEPA.

What's your understanding of the

significance of that comparison that you

make?

DR. PETROPOULOU: I actually would

like to point out that I also follow with

the -- another statement following what you

just read in my testimony. And it's the same

statement for wet weather.

And looking at the result in

Tables 32(a) and 32(b) and looking at the

fecal coliform concentrations, in the dry

weather, as I mentioned, at the North Side

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and at Stickney, the concentrations are

greater than the proposed effluent limit.

And that is also true more so in the wet

weather.

And I can read, like in the wet

weather, for example, at North Side upstream

of the outfall, there is 117,000 fecal

coliform CFUs for 100 ML downstream. We

measured a hundred thousand CFUs for a

hundred ML. The outfall concentration is

22,000.

Similarly at Stickney, you can see

that the upstream concentration is 172,000,

the downstream concentration is 230,000. And

at the outfall we measure 38,000.

The importance -- my view of that

is IEPA is proposing this effluent limit to

protect the users of the waterway, there are

probably other sources to look into in

addition to the district's effluence.

Because they contribute fairly high

concentrations of fecal coliform in the

waterway.

That's the only significance that

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I see.

MS. ALEXANDER: All right. Let me

jump back.

The data you were just reading

from, Table 3(b) is wet weather data; is that

correct?

DR. PETROPOULOU: That is correct,

yes.

MS. ALEXANDER: Okay.

And just to point out, in the dry

weather data, it appears, fairly

consistently, that when you're looking at

fecal coliform indicators, that upstream the

levels are orders of magnitude lower than

downstream; is that correct?

DR. PETROPOULOU: They are great, yes.

MS. ALEXANDER: Yes, okay.

I want to get back to my original

question, because you may have answered it,

but I think I may have lost the thread.

Which is, at Page 6 of your testimony, you

state that the dry weather, as opposed to wet

weather, fecal coliform concentrations

upstream of the North Side and Stickney

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plants, and we're looking at these numbers,

for instance, 713 at North Side and that

Table 3-2(a), 1,061 at Stickney -- actually

the number at Calumet 170 would be lower than

the 400.

But you point out that, I would

say, that at least the first two are higher

than the 400 fecal colony forming units per

100 milliliters that's proposed by the IEPA.

And my question is, what is the significance

of that comparison?

Why is it significant in your view

or what -- is there a point that you're

making in stating that the concentrations

upstream are higher than the required

effluent limit being proposed by IEPA?

DR. PETROPOULOU: And again, my

statement -- I know you selected one of the

two statements I made.

MS. ALEXANDER: Uh-huh.

DR. PETROPOULOU: In order for me to

make my point, I would like to include both

statements. And that is, look together at

both the dry and wet weather conditions for

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the waterway. It's the same significance.

There are probably other sources

of fecal coliform in the waterway than the

district's effluence. That's the

significance.

MS. ALEXANDER: What levels of fecal

coliform indicator bacteria are, generally,

found in the effluent from these three

facilities? And I mean the range, I

understand that it varies.

MR. ANDES: I think we already -- that

question has already been answered by

Mr. Lanyon.

MS. ALEXANDER: Well, in fact, it was.

I mean, I'll phrase the question differently.

In fact, didn't those levels range

up to 200,000 fecal colony forming units per

hundred milliliters? Is that correct?

DR. PETROPOULOU: No, that's not

consistent with our findings. When we did

the study in dry weather, we found

concentrations that range from 42,000 to

56,000.

And during wet weather, actually,

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the district's outfall contributes one-third,

or 50 percent less of that, to the waterway.

If you look at the outfall

concentrations during wet weather -- for

example, at North Side, the dry weather

concentration in the outfall was 42,000.

During wet weather the district contributes

22,000 fecal coliform units. That's like

50 percent of what they contribute during dry

weather.

And similar results are observed

for the outfall concentration during wet

weather at the district outfall.

So the concentration we measured,

you can say they were from 22,000 to 38,000

in the district's outfall during wet weather

and between 42,000 and 56,000 during dry

weather.

MS. ALEXANDER: I think my point is a

little more straightforward than that, or I

should say my question is. Let's look

specifically at dry weather for a moment.

And you cited the outfall numbers

during dry weather that we're looking at, 42,

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411, 56, 391, 56, 287, just to quote from

Table 3-2(a).

Isn't it a fact that those outfall

numbers, as in what the plant is discharging

now during dry weather, are orders of

magnitude higher than what it would be

discharging under the proposed IEPA standard?

DR. PETROPOULOU: That is correct.

MS. ALEXANDER: Okay. So, in other

words, a limit of 400 colony forming units

per 100 milliliters, as proposed by the IEPA,

might be less in some cases than ambient

background levels, but it would still result

in a significant reduction in the loading of

at least indicator bacteria in the water

body; is that correct?

DR. PETROPOULOU: I can't say that.

It depends on the weather conditions.

MS. ALEXANDER: I'm talking about dry

weather now exclusively, I'm sorry.

DR. PETROPOULOU: I can't make that

statement. Like -- you're talking about

significant and loads, I think that can be

calculated, I'm just not prepared to offer an

107

opinion on that.

MS. ALEXANDER: Well, let me reframe

my question, because I think it's a little

simpler than, perhaps, how you're

interpreting it.

If right now, say, as North Side,

the fecal coliform level coming out of the

outfall are around 42,000, would it be fair

to say that they'll be significantly reduced

if you put a limitation of 400 on it, and

then you're going to go to 42,000 to

something other than 400; correct?

DR. PETROPOULOU: That is correct.

MS. ALEXANDER: Okay. That's all I'm

getting at.

I want to turn to Table 58 for a

moment and just briefly revisit these issues

having to do with dry and wet weather days.

This is, again, in Exhibit 71.

All right. I just wanted to

clarify, because this wasn't obvious to me.

And that where I'm getting this from is it's

Tolson Question 11 and Gerba Question 20.

I had framed the question as

108

"Describe how you arrived at these numbers."

I think there's already been some description

of that. So I'm just going to ask a few

follow-up questions on that.

Was there any overlap between days

that were counted as wet weather and days

that were counted as post-wet weather? If

that question make sense. I can rephrase it

if it doesn't.

DR. TOLSON: My answer is it's fairly

obvious the day after certainly has a

relationship to it.

MR. ANDES: Are you asking if there's

double counting?

MS. ALEXANDER: Well, let me ask it --

I just want to make sure I understand.

Let's say it rained on seven

consecutive days. How many of these post-wet

weather days would you assume? Would that,

then, be seven wet weather days and three

post-wet weather days?

DR. TOLSON: We didn't fall into that

era. We actually took the meteorological

data from the year and put it all out and

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figured out how many multi-day bouts of rain

we had, and then used the other intervening

days where it was dry and calculated those

intermediate weather days.

MS. WILLIAMS: When you say

"meteorological data," can you elaborate a

little bit?

DR. TOLSON: Yes, we collected -- we

asked the district for their rain gauge data,

and we used that for the basis of our

establishing wet weather days within the 2006

recreational season.

MS. WILLIAMS: And what if you had

rain at one gauge and not at another?

DR. TOLSON: The way we did that is we

took -- I'm trying to recall exactly how we

sorted this out.

I believe we had a weather

station -- two weather stations, and we

actually looked at the analysis for the North

Shore and then we looked at the analysis for

the Stickney and Calumet together. We tried

to account for that within our assessment.

But, essentially, it was the same

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way. We looked at all the meteorological

data and did not double count days. We took

into account if it rained for four days in a

row, those each were rain days.

And then the days after that were

the intervening days. And then days were --

had a three-day antecedent period.

MS. WILLIAMS: But did it have to rain

in the area where the sample was taken to

have a rain day? I'm still not sure I'm

following.

If you only recorded rain at the

North Side plant, was it considered a rain

day at Stickney for your sampling at

Stickney?

DR. TOLSON: We had to average out the

meteorological data between the different

weather stations we had. What we found was

that about 40 percent of the days were rain

days or CSO days.

Thirty percent, stationwide, were

the day after it rained, 15 percent were two

days after and 15 percent were kind of, at

least, two days of dry weather before that

111

day. So it's a generalization for the entire

Chicago basin, it took into account district

weather data.

MS. WILLIAMS: I'm not sure I

understand, but I think you answered my

question.

We can go back to Ms. Alexander.

DR. TOLSON: Okay.

MS. ALEXANDER: Okay. This is Tolson

Question No. 13. And there is a question to

Dr. Gerba, Question 21, which is,

essentially, the same. But regarding

Tolson's testimony, the statement at Page 5

that "The UAA study was a primary source for

exposure use data in the CAWS."

The question is, is it possible,

in your view, that a water body that was

perceived by the public or known to be

cleaner than the CAWS, such as, for instance,

Lake Michigan, might receive heavier use for

activities involving substantial body contact

with water? In other words, are people more

likely to go kayaking and canoeing in the

clean water bodies than one believed to be

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contaminated?

MR. ANDES: Are we at -- let me settle

that. But I think we could clarify.

Are you talking about water bodies

that are simply perceived as cleaner or are

actually cleaner? What's heavier use? Does

that mean more people, does that mean

different types of use?

I mean, what substantial body

contact with water? Those are all -- I'm not

sure what any of those phrases mean.

MS. ALEXANDER: I'm going to break

this down a little bit.

First of all, I am talking

about -- I mean, I'll say known to be cleaner

in the sense that there's publicly available

data out there that there is more

contamination in one water body than the

people who use the water may be aware of it.

It's sort of the criterion and the difference

I'm talking about.

And the question is -- I mean,

I'll first ask the basic question. Would you

agree that people are probably -- you know,

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maybe more likely, potentially, to engage in

incidental contact-type activities, like

canoeing and kayaking in the water body known

to be cleaner?

DR. TOLSON: You're venturing way off

into speculation.

MS. ALEXANDER: I understand that's

not -- let me move on a little bit.

DR. TOLSON: Yeah, sorry.

MS. ALEXANDER: Did you take in

account in any way in this risk assessment

the possibility that people might be more

willing to conduct themselves in the context

of their water activity, such as canoeing and

kayaking, in such a way as to increase their

bodily contact if they believe the water to

be clean, clean? And let me just sort of

clarify what I mean by that.

Were they -- for instance, did you

take into account the possibility that people

might be more willing to roll their kiak on

Lake Michigan than in the CAWS?

DR. TOLSON: No, ma'am, we did not

make any assumptions to that rolling.

114

MS. ALEXANDER: Or, for instance, the

possibility that they might be more likely to

jump off their motorboat and go swimming on a

hot day in Lake Michigan than in the CAWS;

did you consider that?

DR. TOLSON: All those questions are

really outside of the scope of our study.

MS. ALEXANDER: Okay.

DR. TOLSON: And I can't really

evaluate them.

MS. ALEXANDER: I get it. You didn't

consider any of that.

This is Tolson Question 14 and

Gerba Question 22. Is it your understanding

that water born pathogen levels can vary with

the degree of sunlight on the water, given

that sunlight kills pathogens?

DR. GERBA: I think that question is

misstated. You have pathogen levels, and I

think you mean pathogen survival.

Because pathogen levels are

independent to sunlight.

MS. ALEXANDER: So, in other words,

you're including activated and deactivated

115

pathogens --

DR. GERBA: Right. Sunlight is one

that does influence particularly the survival

of bacteria in water. Not so much viruses.

Particularly like adenoviruses,

which are more resistant to UV light, which

is really the primary component in sunlight,

that inactivates microorganisms.

Do you want me continue answering

the rest of those?

MS. ALEXANDER: Yeah. You can go

ahead and answer with that clarification.

DR. GERBA: Again, the issue is

survival with the turbidity of the water.

Generally, the more turbid the water, the

longer organisms -- water born pathogens, I

should say, as stated here, survive in water.

And with temperature -- generally, the warmer

the temperature and more rapid the organisms

get inactivated, in this case, organisms

meaning water born pathogens.

MS. ALEXANDER: Did your risk

assessment account for these variables in any

way?

116

DR. TOLSON: We actually measure the

concentrations in the waterway, and that was

the basis for the risk assessment.

MS. ALEXANDER: But in determining

what -- for instance what days you were going

to measure or how you were going to weight

the sampling on any given day, you didn't

take into account, for instance, whether

there was sunlight on the water at the time

or whether the water was turbid? You took

the samples but you didn't weight those

factors, in other words; is that correct?

DR. TOLSON: Correct. Let me think

about this for a second and see whether that

somehow could have biased it high or low.

I really -- I can't tell

whether -- how not accounting for that would

have affected the results. But I don't think

it would have affected to a great extent.

DR. GERBA: Well, certainly not for

adenovirus, because we didn't measure whether

they were dead or alive. I would say the

turbidity would have a lot to inhibit the

effect of sunlight.

117

And I don't think the temperatures

were really that warm compared to other

bodies of water I studied. I don't think

either of those, probably in the time span

from the outfall that we looked at, would

have much of a major influence, certainly for

the viruses that are much more resilient and

survive better in the water.

So I don't think those would be

major factors, certainly, for the viruses.

MS. ALEXANDER: But temperature,

turbidity and sunlight, presumably, vary from

day-to-day; is that correct?

DR. GERBA: Yeah, that's right. As

far as I'm concerned, this place is a cold

place compared to Arizona.

MS. ALEXANDER: I'm not going to argue

with that. Just one second.

MS. WILLIAMS: I feel like I want to

ask a follow-up, but I'm not sure. I mean,

did you look at the temperatures throughout

the system?

DR. TOLSON: I don't -- actually --

MS. WILLIAMS: I mean, you're not -- I

118

guess when you make that last statement,

you're not taking into account the power

generation facility on this waterway; are

you?

DR. GERBA: Temperatures were measured

by the district, but that's all I can say.

DR. TOLSON: We measure the pathogen

concentrations at the time that we collected

those samples. And those represented what we

considered to be the concentrations over that

day for which that weather type that we

measured them on.

So if it was a rainy day and we

collected rain samples during that day, that

concentration we measured was what we

assumed.

MS. WILLIAMS: I guess I'm just still

reacting to the idea that you said that --

the rest of us sort of haven't been at the

earlier hearings -- that you felt this was a

cold system. Compared to what?

DR. GERBA: Compared to like Florida.

I think Dr. Joan Gross, for example, looked

at die-off of clean surface waters, eventual

119

viruses.

In there we had really clear

waters, low turbidity and higher temperatures

than you have here. You get more rapid

die-off of like enteroviruses in the water.

When you get the cooler --

MS. WILLIAMS: You're talking about

the air temperature --

DR. GERBA: Right.

MS. WILLIAMS: Not necessarily the

water temperature?

DR. GERBA: Exactly.

No, water. I'm talking water, not

air.

MS. WILLIAMS: So you're talking about

water --

DR. GERBA: Usually the water

temperatures are related to the ambient air

temperatures.

MS. WILLIAMS: And did you look at

whether that's the case here?

DR. GERBA: What the temperatures were

you mean?

MS. WILLIAMS: Whether there's a

120

natural relationship between the air

temperature and the water temperature here,

in this system?

DR. GERBA: It would be an unusual

place that didn't, that's all I can say.

MS. WILLIAMS: Is it --

DR. GERBA: I correlated that.

MS. WILLIAMS: Is it an unusual

situation to have 70 percent of the flow

coming from a water treatment plant?

DR. GERBA: I've seen more, but that's

a lot of -- I mean, 70 percent, I've seen

100 percent before. So it varies.

MS. WILLIAMS: Is it usual to have a

system with five power generating facilities

located in this proximity?

DR. GERBA: I can't comment on that.

MS. WILLIAMS: I just want to make

sure that wasn't part of your -- what went

into your statement.

DR. GERBA: Oh, no.

MS. WILLIAMS: I'm done.

DR. GERBA: Those are factors that

influence -- I'd have to know the actual

121

numbers and degree to tell you how much it

might influence it.

MS. ALEXANDER: All right. This is

Tolson Question 15 and then Gerba

Question 23.

What was the basis for using dose

response data for echovirus as a surrogate

for this dose response behavior for

adenovirus?

DR. GERBA: Excuse me just one second.

Let me just say, we use a dose

response data for echoviruses, largely

because that represents a virus transmitted

by the enteric route. Dose response data for

that was based on ingestion.

And, of course, some of the entero

adenoviruses are transmitted by the ingestion

route. So we wanted to use a dose response

model that included ingestion. There wasn't

one available for adenoviruses.

The only one for adenovirus

available was inhalation. So that was the

reason we used it.

MS. ALEXANDER: Are you saying there

122

is dose response data connected with

inhalation of adenovirus?

DR. GERBA: Yes.

MS. ALEXANDER: Given that fact, why

could you not have also done the complete

risk analysis of risk of respiratory

inhalation-based illness from adenovirus?

MR. ANDES: He already explained why

he didn't do that analysis.

Go ahead and answer.

MS. ALEXANDER: Is your answer the

reason you gave before -- well, you gave a

two-part answer. And one of them was that

you believe GI illness is, essentially, the

predominant recreation-associated illness.

But the other part of the answer that you

consistently gave is that there's no dose

response data for these types of illnesses.

But we have one here for which, in

fact, there is dose response data. And my

question is, is there a reason you could not

have done that analysis, given there is dose

response data?

DR. GERBA: There was two organisms in

123

my last response, there was pseudomonas

aeruginosa, there was no --

MS. ALEXANDER: Right. I understand

that.

DR. GERBA: For adenoviruses, there

was -- the thing I said was that there was no

data to estimate what the aerosol exposure

would be from secondary contact recreation.

MS. ALEXANDER: Okay. So you did have

a dose response, but you didn't have the

aerosol inhalation data; is what you're

saying?

DR. GERBA: That's correct.

MS. ALEXANDER: Okay.

All right. This is referring to

what were Tolson Questions 16 and Gerba 24.

I'll represent it was a series of questions

concerning the EPA ICR manual and procedures

for disinfecting equipment.

I'm going to be modifying these

questions, based on a document that I was

handed yesterday, which I apologize, but I

neglected to make copies of in my haste. But

it is a letter dated September 5th, 2008 from

124

Marsha -- to Marsha Willhite from Coleus,

transmitting a letter from Geosyntec

Consultants dated August 22nd, 2008 to Thomas

Granato of MWRD from Dr. Petropoulou.

And then, attached to

Dr. Petropoulou's letter is an errata sheet

for the risk assessment, which includes some

information about Tolson 16 and Gerba 24.

So --

THE HEARING OFFICER: Ms. Alexander,

is that not Exhibit 59?

MS. ALEXANDER: Oh, is that -- I'm

sorry. That's been introduced?

THE HEARING OFFICER: I believe so, if

it talks about the same letter, yes.

MS. ALEXANDER: Never mind then.

We're talking about Exhibit 59. I apologize

for the excess words.

So I'm going to be asking you some

questions about that. And you guys have it

over there, I assume.

Am I correct in my understanding

that the EPA ICR manual for disinfecting

equipment to be used for virus sampling

125

requires that the concentration of chlorine

to be used to disinfect is .1 percent, and

that after chlorination the chlorine needs to

be neutralized with sodium biosulphate; is

that correct?

DR. GERBA: That's right.

MS. ALEXANDER: Okay.

Now, in the draft -- I shouldn't

say draft -- in the final of the risk

assessment that was appended to various

witnesses' testimony from the district and

published on the district's website, it was

indicated --

THE HEARING OFFICER: Excuse me, which

is Exhibit 71?

MS. ALEXANDER: Exhibit 71. I'm

sorry.

THE HEARING OFFICER: Okay. For the

record, it's better if we --

MS. ALEXANDER: I apologize.

THE HEARING OFFICER: That's okay.

MS. ALEXANDER: It was indicated at

Page 16 of Exhibit 71 that, essentially, this

procedure was not followed; is that correct?

126

DR. PETROPOULOU: No, that is not

correct. We had a typographical error with

respect to the concentration of the bleach

that we used for the disinfection.

In our sampling and quality

assurance plans, both for the dry and wet

weather, we specified the correct cleaning

and sterilization method for the equipment,

that's what the district followed. We have

made the correction in this errata sheet for

that.

That was the purpose of this

errata sheet.

THE HEARING OFFICER: The errata sheet

attached to Exhibit 59?

DR. PETROPOULOU: Correct.

MS. ALEXANDER: Okay. So you

characterize the change from the .1 percent

solution -- I'm sorry, the .5 percent.

The .1 percent is a typographical

error; is that correct?

DR. PETROPOULOU: That's correct.

MS. ALEXANDER: Are the other changes

also corrections, in your view, of

127

typographical errors?

DR. PETROPOULOU: No, they are not.

We have omitted to include how we

dechlorinated the equipment, and we have

added that for clarification.

I believe it was Dr. Yates. She

raised that as an issue in her testimony.

So it brought it to our attention

that we should include that in the report

just to make sure there's no confusion about

it.

MS. ALEXANDER: Do you have any lab

records that are reflecting specifically this

information that you, in fact, dechlorinated

the equipment?

DR. PETROPOULOU: I believe Dr. Ishal

from the district that was overseeing the

lab, she has instructions to the lab that

include an excerpt of our sampling and

analysis plan. And there were instructions

to the sampling staff on the boat that

included information of how to disinfect

equipment.

And Dr. Gerba and myself, who were

128

on the boat, we did the sampling during the

first week. So I know that that's -- it was

done properly.

MS. ALEXANDER: And just to refer to

Item 1 on the errata sheet attached to

Exhibit 59, you replace the reference to

blue-green monkey kidney with buffalo green

monkey kidney.

Am I correct in understanding that

there is, in fact, no such thing as a

blue-green monkey or its kidney?

DR. GERBA: No.

MS. ALEXANDER: Okay. So that's not

any kind of cell culture line. The only cell

culture line is buffalo green monkey kidneys

used in this analysis.

Now, I'm turning next to Tolson

Question 17 and Gerba Question 25. I just

want to state, as an initial matter, that

these questions all characterize them as

having to do with sample size and proportion

of the sample evaluated.

There was an indication in

prefiled questions given to Dr. Yates that

129

this information is available in appendices

to the risk assessment. We were not provided

with those appendices until I saw those

questions and requested the appendices from

Mr. Andes. I have just been provided them.

I have not had the opportunity

either to completely review those or to

discuss them were my expert. I do not know

whether any of that will be a problem. I

simply state that as a caveat on the record,

that that's an issue that might come up at

some point down the road.

It is possible that some of my

fact or clarification questions may be

answerable by reference to that data. But we

can just proceed and see how that works out.

MS. WILLIAMS: Can you just clarify

for us, so the rest of us don't have them

either, that it's not part of Exhibit 71?

MS. ALEXANDER: It's not currently

part of Exhibit 71. I -- and I was not

planning or referring in my question

specifically to that data to the extent the

witnesses refer to that information in their

130

answers, we may need to admit it into the

record and mark it as an exhibit.

MR. ANDES: Appendices A, B, C and D

to the report, I believe A and B I provided

last week.

MS. ALEXANDER: Correct.

MR. ANDES: I've now provided A, B, C

and D. If the Agency wants the whole

enormous amount of information on a disk, I

have another copy and I can provide that, as

well. As soon as I find it under this paper.

MS. WILLIAMS: Well, first, I just

wanted to understand what was in the record

and what's not. So we're clear, then, that

there's four appendices and two are in the

record and two or not; is that correct?

THE HEARING OFFICER: No, none of them

are.

MS. WILLIAMS: None of them are.

MS. ALEXANDER: There's an

Attachment A that is part of the Exhibit 71

that is in the record, but there are no

appendices in the record?

MR. ANDES: There are Appendices A, B,

131

C and D.

MS. WILLIAMS: It seem like that's

something that after the hearing we can have

supplemented by you guys?

MR. ANDES: That would be fine.

THE HEARING OFFICER: Yes.

MR. ANDES: That is beyond the 350

pages of the report.

MS. WILLIAMS: Which was submitted

like four times; right?

MR. ANDES: Yes.

THE HEARING OFFICER: We only need it

onces this time.

MS. ALEXANDER: Referring back to

those questions, Tolson 17 and Gerba 25, the

general question I have is, how large were

the samples that you collected for virus

analysis?

DR. GERBA: Near the -- by the

outfall, 100 liters, and away from the

outfall 300 liters.

MS. ALEXANDER: Okay.

THE HEARING OFFICER: I'm sorry?

DR. GERBA: One hundred liters by the

132

outfall, and then 300 liters away from the

outfall.

THE HEARING OFFICER: A train went by

as you finished your question, so I couldn't

hear it.

DR. GERBA: To give you a perspective,

that's -- 100 liters, basically, is about 25

gallons. And about 75 gallons is about 300

liters, to give you a rough idea.

MS. ALEXANDER: And what volume from

these samples are, typically, analyzed for

each of the viruses?

DR. GERBA: If it was divided up

about -- basically -- I don't know. Do you

have the actual ratio?

It's in the SOP, but I don't

remember off the top of my head. I couldn't

give you it right off the top of my head.

MS. ALEXANDER: Can you give me an

approximation?

DR. GERBA: Well -- I tried to do at

least 100 liters for each virus, when it was

feasible to do that. For the Norovirus, it

was not feasible, because of the analytical

133

method limits, you only need a few hundred

microliters of a concentrate.

But we tried to do 100 liters for

each of the virus groups for -- away from the

outfall, and about 30 liters for each virus

at the outfall.

MS. ALEXANDER: One second here.

I have in my notes -- and I

haven't quite found the table yet -- that the

typical volume of the sample analyzed for

calcivirus was around .2 liters; is that

correct?

DR. GERBA: It varied from sample to

sample, something like two liters.

MS. ALEXANDER: It was about that

would you say?

DR. GERBA: Yeah.

MS. ALEXANDER: And if no viruses were

detected in that .2 liter sample out of the

entire sample, would that have been 100 to

300 --

DR. GERBA: I'm just saying that

without having looked at it. So I'm not

quite sure.

134

MR. ANDES: Let's not make a statement

without looking. Let's go back, because I

heard two and I heard .2.

DR. GERBA: Yeah, I'd have to look at

the exact equivalent volume. I'm not sure if

you're giving me the volumes on concentrate

assay or the equivalent volume of that

concentrated to the water sample that was

collected.

MS. ALEXANDER: All right. I found

that reference.

If you turn to Table 3-7, which is

Table 3-7 in Exhibit 71, Dry Weather

norovirus, paren, (calcivirus results).

And then you'll see there is a

column in that Equivalent Volume Assay in

Liters.

DR. GERBA: Right. Right. That's

right.

MS. ALEXANDER: And you see that it

varies. But would I be fair in

characterizing that as it all falls out to in

the vicinity of .2 liters?

DR. GERBA: Yeah, about 200

135

milliliters, you're correct.

MS. ALEXANDER: All right. And that's

out of the entire sample that was drawn,

which, as I understand it, would have ranged

from 100 to 300 liters?

DR. GERBA: I'm sorry, this is --

yeah, the equivalent volume of the

concentrate, that was actually analyzed by

the PCR method. The PCR method has very

limited volume that can be assayed, where --

compared to, you know, the method of the

other two viruses, almost the entire sample

was assayed in 100 liter volume.

It's just the analytical method

here for norovirus is limited to apparently a

small sample. But still we are able to

protect the virus, particularly during

rainfall.

MS. ALEXANDER: Okay. But you were

only -- in fact, if you only tested, assayed,

the .2 liters out of your 100 to 300 liter

samples, you wouldn't actually know what was

in the other 99.8 percent of the sample

because you didn't test it; is that correct?

136

DR. GERBA: Right. Let me make sure I

understand.

There's concentrations that would

take 300 liters and you reduce it to 20

milliliters.

MS. ALEXANDER: Right.

DR. GERBA: Is what goes on here. And

then you're expanding backwards to that.

And usually your assay maybe

10 MLs for the adenovirus and ten MLs for

what we call the total cultural virus. And

then usually several microliters for this.

It's important here that this is

240 milliliters, by the way, which I hope is

a volume nobody ever swallows in the water.

The reason for the larger volumes for the

other viruses is because they're in such low

levels.

So, in reality, in terms of what

somebody might swallow, the smallest volume

that was assayed here was about 100

milliliters and the largest was about 410

milliliters. So those are relatively what

somebody might have actually swallow.

137

Even in contact recreation, it

would be greater, though, with respect to

swallowing.

MS. ALEXANDER: The question I'm

asking is you did not, in fact, test the

entire sample you took in the case of

calcivirus; is that correct?

DR. GERBA: Oh, no, it was impossible

to do that.

MS. ALEXANDER: Right. And, in fact,

you didn't really test anything close to the

entire sample?

DR. GERBA: No, it was impossible to

do that.

MS. ALEXANDER: Okay.

DR. GERBA: Not with that analytical

method.

MS. ALEXANDER: Okay.

Tolson Question 18 and Gerba

Question 26, what primers were used for the

calcivirus analysis?

DR. GERBA: Those were primers that

were developed by Jan Vanay, now with the

Centers For Disease Control and Prevention.

138

We used these primers to investigate more

than 20 outbreaks of noroviruses in the last

several years.

So we know they were fairly

effective in picking up all the norovirus

types that were causing outbreaks, certainly

on cruise ships and outbreaks in the

United States.

MS. ALEXANDER: Specifically on which

calciviruses are detected --

DR. GERBA: With norovirus -- the

human norovirus.

MS. ALEXANDER: Okay. Just the human

norovirus?

DR. GERBA: Uh-huh.

MS. ALEXANDER: Okay. Tolson 20 and

Gerba 28, can you describe the method that

was used to analyze the samples of -- I'm

sorry -- for adenovirus?

DR. GERBA: That's in the SOP, but,

basically, what you do is, again, you take

part of the concentrate and we put it on a

specific cell line to which adenoviruses are

known to be sensitive to. The BGM cell line,

139

adenoviruses are not sensitive to -- they

don't produce cytopathogenic effects.

But in the cell line we use, they

do produce cytopathogenic effects. We expose

those to cells for 14 days and then we take

the negative samples and expose those to the

cells for another 14 days, for a total of 28

days. And those cell lines show a

cytopathogenic effects.

We use primers against the human

adenoviruses to confirm there was human

adenoviruses that we detected. Some human

enteroviruses grow on the cell lines, too.

So there was a need to confirm that they were

adenoviruses.

The cell lines that we use will

grow adenovirus, most of the adenoviruses, 40

and 41, which are the ones that cause

gastroenteritis 2, 4, and 7 and several

others. But we've been using these to grow

various adenovirus serotypes in our

laboratory for several years.

And we've used -- I should say --

the same procedure for detecting adenoviruses

140

and other studies on water -- waste water

discharges, which have been published in peer

reviewed scientific literature.

MS. ALEXANDER: I'm sorry, I think you

just answered this question and I lost the

thread. But my sub-A on that was, which

specific serotypes of adenovirus are detected

using the BGM cell line that you used? Could

you list those for me?

DR. GERBA: We use the -- actually,

PLC5 cell lines for --

MS. ALEXANDER: Oh, PLC5, okay.

DR. GERBA: -- the adenoviruses.

Because they don't produce cytopathogenic

effects in the buffalo green monkey cell

line.

In this cell line we'll grow 40, *

41, 2, 7 and 4, to my knowledge, and probably

several of the other types of it. The

primers would detect, basically, any of the

human adenoviruses.

MR. ANDES: In follow-up, do you

consider these to be a conservative approach?

And, if so, how?

141

DR. GERBA: Yeah, I consider -- well,

the whole idea of putting adenoviruses in

here was a conservative approach. Even

though there was no approved EPA method for

adenoviruses, the literatures indicate

adenovirus were the most abundant viruses in

sewage discharges. So we felt we would be

neglecting the most abundant virus that could

be current in sewage, and that's why this

part of the study actually was done.

And then we wanted to confirm for

sure that it was adenovirus that we detected,

that's why we used the primers when we did

it. Because we were trying to be

conservative here and trying to estimate the

greatest number of viruses that would be

present in the sewage and in the waterway.

So that's why we felt it essential

to include the adenoviruses in here. And, as

you saw from the results of the study,

adenoviruses were in far more abundance than

the enterovirus.

And if we just used the EPA manual

for the total culturable virus, we would have

142

missed almost the majority of the viruses we

actually detected in the waterway. So I

think that premise actually paid out in this

study.

MS. ALEXANDER: I just -- I'm going to

need to ask some follow-up on that for

clarification.

Did you say that all serotypes of

adenovirus are detected using the PCR -- the

primers used for PCR analysis?

DR. GERBA: All the major human

enteroviruses, yeah.

MS. ALEXANDER: When you say all the

major human enteroviruses...

DR. GERBA: I said that, because I

don't know if every human -- I'm sorry --

adenovirus has ever been tested against this

set of primers. I don't know that for

certain.

MS. ALEXANDER: Okay. So the PCR

analysis would have detected the ones you've

listed, 5 40, 41, 2, 7 and 4?

DR. GERBA: Right.

Some of those have been associated

143

with water born diseases, too. You know,

recreational water, that's why we...

MS. ALEXANDER: There are, in fact, 51

different types of adenoviruses; correct?

DR. GERBA: Well, actually, there's

a -- there may actually be 52. Some people

are pushing another one, so -- I should point

out too, not all the adenoviruses have been

clearly associated with disease in humans, by

the way, too.

Although, they've been found in

human fluids and stools and infected with

some people, we're not -- we're still not

certain whether it involved and caused any

type of particular disease in humans beings.

MS. ALEXANDER: Now, if I'm

understanding you correctly, the PCR analysis

that you used for the confirmation, detected

more stains of adenovirus than the cell

culture analysis; is that correct?

DR. GERBA: No, the -- in this case,

we used PCR to confirm the presence of

adenovirus growing in the cell culture. We

only detected viable adenoviruses in this

144

study.

The PCR here was done on the cell

culture as an identification step that we

were finding adenovirus. For the norovirus,

it was -- we need to not determine viability.

We just determined the concentration of the

adeno -- norovirus genome in that case.

MS. ALEXANDER: Can you just clarify

what it means when you say that you

confirmed, then, using the PCR analysis? You

did the cell culture, you identified the

sample as testing either positive or negative

through the cell culture for those specific

serotypes you identified; correct?

DR. GERBA: Right. What happened with

the cell culture -- enteroviruses also have

the capability of growing in the same culture

we use to isolate adenoviruses. So we wanted

to make sure we had an adequate number on the

number of adenovirus growing in the cell

culture.

If you look at the raw data, not

all samples confirmed as adenoviruses, which

were probably -- and some of these were

145

probably enteroviruses growing in the cell

culture.

MS. ALEXANDER: Okay. So let's say

you tested the sample, were using the cell

culture and it was positive, but you did the

PCR analysis and it was negative. That would

suggest that what was growing there might

have -- was probably, or perhaps,

enteroviruses rather than adenoviruses;

correct?

DR. GERBA: It could be. Or some

other type of virus it be could. But there

were not many of them, because the

adenoviruses tend to grow very well in this

type of cell culture, more than other virus

types, apparently.

MS. ALEXANDER: When that happened,

did you go back and check what it was that

was growing in there that wasn't adenovirus?

DR. GERBA: You know, I think at

random we did. I don't know if we did it in

this study. In other studies we have done --

we've been looking at water and waste water.

And I have to go and look at the

146

notebooks if we looked at a few of those or

not. In other studies they've always -- or

not always, but some of them turned out to be

enteroviruses or viruses we can't identify.

MS. ALEXANDER: Am I correct that

there were at least some instances where in a

sample you identified it as negative for

enterovirus, when testing for enterovirus, it

was positive in a cell culture for

adenovirus, confirmed as negative, and,

therefore, counted as negative for

adenovirus, but you didn't go back to check

whether there were enteroviruses in there?

DR. GERBA: We just counted -- it was

viral cytopathogenic effects.

MS. ALEXANDER: Okay.

DR. GERBA: We do that as a minimum.

MS. ALEXANDER: So in other words,

just to summarize, there were, at least in

some cases, where you found something to be

growing in the cell culture but you counted

it as a negative and didn't follow up to see

what exactly it was that was growing in

there?

147

DR. GERBA: No. Because we already

had an assay on BGM cells that worked well

for enteroviruses, and we could be double

counting the virus.

MS. ALEXANDER: But isn't it a fact

that there were at least some situations

where you got a negatives specifically on the

enterovirus assay, but you got a positive on

the cell culture for adenovirus that you

confirmed it negative for adenovirus, so it

could have been enterovirus instead of --

DR. GERBA: No. What we did is --

MS. ALEXANDER: -- that was going in

there?

DR. GERBA: -- if there was viral

cytopathogenic effects, we took that sample

and then we did PCR analysis to determine

whether it was an adenovirus or not.

MS. ALEXANDER: Right. And if it

wasn't but there was still something growing

in there, that could have been enterovirus;

correct?

DR. GERBA: That is a possibility,

yes.

148

MS. ALEXANDER: Okay.

All right. This is Tolson 21 and

Gerba 29. And this refers to Tables 3-5(a)

through (f) of Exhibit 71, Risk Assessment.

These are the enteric virus results.

Can you please describe for me the

method used to detect enteric viruses? Just

summarize as you did with adenoviruses,

please.

DR. GERBA: Right. Enteric viruses --

we're using that term interchangeably with

total culturable viruses.

Certain enteric viruses used a lot

before molecular methods came in to detect

viruses in water. So now there's a tendency

to total culturable viruses.

Because, basically, the EPA method

we used for that, before looking for it,

that's using the BGM cell line. You put your

sample on the BGM cell line and then you look

for the production of cytopathogenic effects

that are viral, and you confirm those through

another passage.

And then those are called total

149

culturable virus.

MS. ALEXANDER: Okay. One second.

Okay. Referring to Exhibit 71,

Page 48, Section 3.3.1. That contains a

description of this method that you're

discussing.

In the first paragraph there you

characterize Tables 3-5(d) through (f) as

presenting a summary of the wet weather total

enteric virus analytical results. Is the

method you describe capable of detecting

total enteric viruses, as in all of them?

DR. GERBA: Total culturable enteric.

That's a term that's used in the literature

for EPA. And EPA uses that, too.

But largely, you're really just

detecting the enteroviruses. Although some

real viruses and other virus types my grow in

there.

But that's a terminology that's

come into use.

MS. ALEXANDER: Okay. And hepatitis

is an enteric virus; correct?

DR. GERBA: That's correct.

150

MS. ALEXANDER: And you didn't assay

for that?

DR. GERBA: No, we did not.

MS. ALEXANDER: And the same with

rotavirus?

DR. GERBA: No, we did not assay.

Hepatitis A we did not assay for,

because the concentration would be expected

to be low because the incidence is fairly

low. And hepatitis A there's a vaccine now,

which is also driving down the incidence of

hepatitis A in the United States. The

probability of finding that was pretty low.

For rotaviruses, the feeling was

that the methods were not very good for

looking for rotavirus. There's a cell

culture method -- and I developed one of the

methods -- it's been used before, and it's

very difficult to use.

And the volumes you could actually

assay out of it, I felt, were too small to

really give us any meaningful results to

actually do rotaviruses. So that's why we

kind of decided against that.

151

MS. ALEXANDER: Okay. Turning to

Tolson 22 and Gerba 30. And this is

regarding the statement in Exhibit 71, the

risk assessment that reverse

transcription-polymerase chain reaction,

RT-PCR, results were used to calculate

concentrations of noroviruses in the sample.

Can you just give a brief summary

of how those calculations were performed,

please?

DR. GERBA: These calculations are

done very similar to most probable number

calculations for the coliforms, fecal

coliforms, the bacteria that are often used.

You take a delusion series of your sample and

you look for the number of positives and

negatives and then you feed that into a -- on

a computer program developed by Hurley and

Rosco back in 1983.

It calculates the most probable

number of concentration in the sample that

you are assaying. It's, basically, doing the

same thing as doing a most probable number

for fecal coliforms.

152

MS. ALEXANDER: Okay.

And just to kind of make sure I

understand this properly, this RT-PCR process

tells you how many copies of norovirus RNA

there are in your sample; is that right?

DR. GERBA: You have to do it by a

delusion series. It's a positive negative

one.

You could do that by using

quantitative PCR. But I felt it didn't have

the sensitivity we needed, so we do the most

probable number.

In other words, the sample is

positive or negative as you dilute it. In

other words, you take an unconcentrated

sample and you dilute it one to ten, one to

100 and one 101,000.

And you are basically looking for

an extinction point. You no longer find the

positive PCR reaction in a sample that is

diluted out far enough. And you do that

usually at least in triplicate.

MS. ALEXANDER: Okay. Did this

analysis involve an assumption as to the

153

number of copies of norovirus RNA that are

associated with the presence of a certain

amount of norovirus? Does that question make

sense?

DR. GERBA: Yeah. Usually one genome

equals one virus, it's believed.

MS. ALEXANDER: One to one?

DR. GERBA: One to one.

MS. ALEXANDER: Okay.

Help me understand the statement

in the Risk Assessment, Exhibit 71, then,

that the ratio of he genomes, paren, (the

viron self-culture infectivity units) is one

to 100 to one to 46,000.

DR. GERBA: That varies with the cell

culture line you're using.

In other words, if I took -- you

adapt viruses to cell culture. If I took a

virus, like rotavirus in a stool sample and

put in a cell culture sample, the ratio may

be one to 40,000 -- 40,000 genomes to one

virus.

If you adapt that to cell culture

over time or use vaccine strains maybe you're

154

looking for, that may be down to one in a

hundred. The cell culture doesn't

necessarily detect all the viruses that are

in the sample.

MS. ALEXANDER: I'm sorry, how does

this fit in with your testimony concerning

the one-to-one ratio? Am I comparing apples

and oranges? Is that a different thing?

DR. GERBA: I think you are. The

conservative thing would be to consider each

genome one norovirus. One, because this

picks up inactivated organisms.

MS. ALEXANDER: So you're saying the

conservative thing would be to consider it

one to one. But am I understanding correctly

from the risk assessment, Exhibit 71 on

Page 48, that, in fact, you used a ratio of

one to 100 to one to 46,000?

DR. GERBA: The reason for that is

because the only dose response data we have

is for cell culture, where the ratio is one

to a hundred. So, in other words, the

echovirus ratio was 100 genomes to one

infectivity unit. That's what was done in a

155

dose response curve.

So that's why it was benchmarked

against that. Because we know from the

echovirus data that for every hundred

genomes, we would have one infected unit.

And that was used to develop the dose

response curve.

MS. ALEXANDER: Wouldn't it make a

pretty big difference in your overall

results, whether you use one to 100 or one to

46,000 -- in other words, in terms of how

many virus you're assuming or correlated with

the number of genomes you found?

DR. GERBA: Of course. I mean, just

changing that ratio, you could make that

ratio over to a wide number of things. But

in this example, we had something to

benchmark it again, so we were trying to

bring reality into the risk assessment.

MS. ALEXANDER: So you were saying you

were benchmarking it against the one-to-one

ratio from the dose response data?

DR. GERBA: No, the 100. Because that

was what we had based on the dose response

156

data which was developed in cell culture.

In other words, when they

developed the dose response data, they used

the infectivity in cell culture of the

echovirus. And they that for every hundred

genomes, approximately, they had one

infectious virus in cell cultures what they

did the dose response against.

So what we did is try to benchmark

it against a real situation where we actually

knew what the ratio was and we had a dose

response curve to go with it.

MS. ALEXANDER: All right. So you

opted against using the one to one because of

this dose response data that you had?

DR. GERBA: Right. And we could have

used the one to 40,000, for example, which

could have been used, too. Because that's

about what the ratio from the stool sample

for, say, rotavirus is to an infectivity in a

human being.

So this was the range that we

picked.

MS. ALEXANDER: Okay. Not to beat the

157

dead horse, but just so I understand, the

most conservative assumption you could of

made would be one to one, the least

conservative would be one to 46,000, you

chose --

DR. GERBA: Right.

MS. ALEXANDER: -- the one to 100?

DR. GERBA: That's right. That's

correct.

MS. ALEXANDER: Okay. Moving onto

Tolson 23 and Gerba 21, they are the same

question.

Did the secondary infection rates

that you used in your analysis change between

the interim dry weather risk assessment

completed in November 2006 and the final wet

and dry weather risk assessment?

DR. TOLSON: Yes, it did.

MS. ALEXANDER: Okay.

I'm going to present a document

and have it marked as an exhibit, just so the

rest of the room can understand what we're

talking about.

(WHEREUPON, a certain document was

158

marked Exhibit No. 76 for

identification, as of 9/9/08.)

MS. ALEXANDER: What I have here to

present as the exhibit is the cover page from

the interim dry weather risk assessment dated

November 2006 and then the relevant table

that I'll be talking about, which is

Table 4-6.

THE HEARING OFFICER: I've been handed

Prepared For Protecting Our Water Environment

Metropolitan Water Reclamation District of

Greater Chicago, Interim Dry Weather Risk

Assessment and Human Health Impact

Disinfection Versus No Disinfection of the

Chicago Area Waterway System.

If there's no objection, I'll mark

this as Exhibit 76.

Seeing none, it's Exhibit 76.

MS. ALEXANDER: Okay. Specifically I

would like to compare this table -- I'm

sorry -- this was marked as No. 76 to --

which is Table 4-6 in the dry weather risk

assessment to table 5-6 in Exhibit 71.

DR. TOLSON: Okay. I'm with you.

159

MS. ALEXANDER: I'm not with you yet,

hold on.

And I would point out, correct me

if I'm wrong, that several -- a couple of the

numbers in the interim assessment are higher

than the numbers in Table 5-6. That's

comparing Exhibit 76, Table 4-6 to Exhibit

71, Table 5-6. And specifically the entries

for salmonella and E. Coli.

DR. TOLSON: Also total enteric

viruses, yes.

MS. ALEXANDER: Now, the lower numbers

that are contained in the later iteration,

the wet and dry weather risk assessment, for

infectivity -- or, I'm sorry, secondary

attack rates, would, in fact, have the effect

of lowering overall risk; is that correct?

DR. TOLSON: It is correct that if the

lower the secondary attack rates, the higher

the risk.

MS. ALEXANDER: Okay.

DR. TOLSON: If you'd like, I can

explain the rationale --

MS. ALEXANDER: Yes.

160

DR. TOLSON: -- for this if you --

MS. ALEXANDER: You anticipated my

next question, which is what was the basis

for these changes.

DR. TOLSON: Sure. The interim

report -- and it wasn't interim drafts, sort

of a product here -- we assumed a 50 percent

attack rate, which is a fairly conservative

assumption. As we refined our estimates, we

gathered additional data and took a look at

what was available in the literature to sort

of hone in to get a better estimate of what

those would be.

For example, for total enteric

viruses, we assumed 50 percent. After some

additional conversations with Dr. Gerba, we

settled on 25 percent as a conservative, sort

of, assumption for transmission.

For adenoviruses and

caliciviruses, it looked like we kept those

the same from our initial assessment. The

crypto and giardia results that we had in the

interim are actually reversed. So they're

corrected in the final.

161

But I'd like to point out that

the -- for the giardia results, the

literature reported from eight to ten

percent, we actually assumed 25 percent,

which is conservative beyond what the

literature cites. And then, for salmonella

and for E. coli, we changed our default

assumption to 25 percent, which we thought

was still an overly conservative estimate of

the secondary attack rates for those

organisms.

If you've noticed, we actually did

cite some literature below. And I think in

every case, the literature cited value is

lower or within the range of the values that

we use with our -- as our input assumptions.

MS. ALEXANDER: Okay.

Tolson 24 and Gerba 32. Did you,

in fact, use a Monte Carlo simulation in

quantifying risk?

DR. TOLSON: That is correct, we used

the Monte Carlo simulation.

MS. ALEXANDER: Can you provide a

brief description of what you did in that

162

simulation?

DR. TOLSON: Monte Carlo simulations

are the mathematical tool to solve problems

that don't have an easy analytical solution.

You can't just add the numbers up and come up

with the equal sign and get a final number.

It uses simulations to estimate

what the final results would be. The process

used here, we use Monte Carlo simulation

where we selected from our data set -- and

this means our data set of dry weather days,

wet weather CSO days -- to represent each

simulation's waterway pathogen

concentrations.

And then we did simulations of a

million recreational users, drawing

individuals from distributions that included

canoeists, fishing and boating, in relation

to the proportion for which they are

represented in the UAA study.

DR. GERBA: If I can point out, in

microbial risk assessment, that's common

practice to use Monte Carlo simulations. You

get a better idea what the distribution of

163

risk is.

MS. WILLIAMS: Can I just ask, have

you done this before though? Have you done a

Monte Carlo simulation for microbial risk

assessment before?

DR. TOLSON: I teach a class on

probabilistic risk assessment, a graduate

level class, at University of Florida. This

is a component of one of the things that I

teach within that class, a number of

probabilistic risk assessments historically.

So yes.

MS. WILLIAMS: But I'm just

specifically distinguishing between microbial

risk versus other types of toxic chemical

risks. Was that reflected in your answer?

DR. TOLSON: The assessment, sort of,

parameters are pretty much the same. My

microbial risk assessment experience, I have

not relied on probabilistic methods for that,

but --

MS. WILLIAMS: Until now?

DR. TOLSON: That is correct.

MR. ANDES: Can you explain a little

164

bit more about this methodology?

DR. TOLSON: The methodology is common

methodology that's employed by the agency and

others to sort of assess risk. I have been

involved in numerous workshops where we've

discussed these, sort of, risk assessment

techniques in a very fast style in sort of

doing them, so...

DR. GERBA: I've been involved in a

number of teams doing simulations for

microbial risk assessment. It's really just

a mathematical technique.

You put different numbers in is

all you're doing.

MS. ALEXANDER: So just to summarize,

in other words, the point of a Monte Carlo

simulation is to account for a distribution

spread of input variables; is that basically

correct? In other words, you could account

for the fact that there's no exact amount of

water that every recreator is going to

ingest, but it's rather a range of

possibilities? Is that basically right?

DR. TOLSON: That is correct.

165

MS. ALEXANDER: Okay.

DR. TOLSON: The alternative is to do

point estimates for all the inputs and

develop one point estimate, which takes into

account the averages of everything. And the

way we did it takes into account the ranges

and gives us sort of a range of outputs.

MS. ALEXANDER: Can we turn to figure

5-2 in Exhibit 71, the risk assessment?

THE HEARING OFFICER: Excuse me.

Let's go off the record for just a second.

(WHEREUPON, discussion was had

off the record.)

THE HEARING OFFICER: Back on the

record.

MR. ANDES: First the appendices to

the risk assessment report I have on a disk,

if I could give you that right now.

THE HEARING OFFICER: Is that all four

appendices?

MR. ANDES: Yes, A, B, C and D.

THE HEARING OFFICER: We'll mark that

as Exhibit 77.

MR. ANDES: I also have, both paper

166

and on a disk, the attachments to the EPA

July 31st, 2008 Melser letter.

MS. MEYERS-GLEN: I'm sorry, we didn't

catch that. Could you say that again,

please? Attachment what?

MR. ANDES: The attachments to the EPA

letter of July 31st.

THE HEARING OFFICER: Exhibit 77 is

the risk assessment appendices. If there's

no objection?

Seeing none, it's Exhibit 77.

(WHEREUPON, a certain document was

marked Exhibit No. 77 for

identification, as of 9/9/08.)

THE HEARING OFFICER: Exhibit 78 will

be the CD-ROM that is the appendices to the

USEPA letter that was previously admitted as

CD-ROM 73. Exhibit 73.

MR. ANDES: The last document on that

CD-ROM, July 31st, 2008.

THE HEARING OFFICER: All right. So

wait a minute.

Instead of -- I'm going to do

something I don't normally do. I'm going to

167

enter this as Exhibit 73A. So that it will

be clear than it goes with Exhibit 73.

And this the appendices to the

letter, which was one of last documents on

the CD-ROM that is Exhibit 73. So this will

be Exhibit 73A. If there's no objection?

MS. WILLIAMS: I'm just trying to

figure out what I have. Is that what I have?

Or do I have both?

THE HEARING OFFICER: He gave you

two --

MS. WILLIAMS: We have one disk, I

don't know what's on it. What is this?

MR. ANDES: Those are the attachments

to the EPA July 31st, 2008 letter.

MS. WILLIAMS: So that's 73A?

THE HEARING OFFICER: 73A.

MS. WILLIAMS: Thank you.

THE HEARING OFFICER: And 77 is the

appendices, which he gave us both the hard

copy and on CD. Or which I have both hard

copy and CD.

So I'm going to mark the hard copy

also, again strangely enough, as 77A.

168

Because 77 is the disk. There's no

objection?

MR. ANDES: Let me clarify. The

appendices that I gave you -- the disk marked

appendices is 71; isn't it? Isn't the risk

assessment report 71?

THE HEARING OFFICER: Yes, but I'm

going to mark them as 77. Because I don't

normally give subsets, but I also then have

the same thing in hard copy, I'll call it

77A.

MR. ANDES: All right. Fine.

MS. WILLIAMS: Now, with that --

THE HEARING OFFICER: Okay. Wait a

minute, I'm confused.

These are not the appendices to --

MR. ANDES: The appendices to the risk

assessment report are only on that disk that

says Appendices.

THE HEARING OFFICER: These

(indicating) are what goes with this

(indicating), are the attachments?

MR. ANDES: Yes.

THE HEARING OFFICER: Okay.

169

I'm not marking them as an

exhibit. We have them on CD, these will be

for our use.

So Exhibit 77 is the appendices to

the risk assessment, and 73A is the

appendices to the letter. I am thoroughly

confused, but I think I've got it.

All right. No objections?

Those are entered.

(WHEREUPON, a certain document was

marked Exhibit No. 73A for

identification, as of 9/9/08.)

MS. WILLIAMS: So at this point,

though, you have copies of -- you have a disk

with appendices, Ms. Alexander has a disk

with appendices. Can we just request that

the Board upload this exhibit in particular,

or no?

THE HEARING OFFICER: I have to be

perfectly honest with you, John is out this

week.

MS. WILLIAMS: No, I don't mean --

THE HEARING OFFICER: I was going to

say, so I can't promise you when this would

170

get done.

Is it possible to get another CD

burned?

MR. ANDES: Yeah. If I don't already

have one, I can certainly burn another.

MS. WILLIAMS: Either one.

THE HEARING OFFICER: And we might be

able to burn a CD faster than we can get it

uploaded, given our staffing concerns this

week.

MS. WILLIAMS: Either way.

THE HEARING OFFICER: All right. That

being said, we will start again tomorrow

morning with Ms. Alexander.

Drs. Gerba, Tolson, Petropoulou,

thank you very much.

We're adjourned.

(WHEREUPON, the hearing was

adjourned until 9/10/08 at

9:00 a.m.)

171

1 STATE OF ILLINOIS)

) SS:

3 COUNTY OF COOK )

I, SHARON BERKERY, a Certified Shorthand

5 Reporter of the State of Illinois, do hereby certify

6 that I reported in shorthand the proceedings had at

7 the hearing aforesaid, and that the foregoing is a

8 true, complete and correct transcript of the

9 proceedings of said hearing as appears from my

10 stenographic notes so taken and transcribed under my

11 personal direction.

IN WITNESS WHEREOF, I do hereunto set my

13 hand at Chicago, Illinois, this 18th day of

14 September, 2008.

Certified Shorthand Reporter

19 C.S.R. Certificate No. 84-4327.