1
1
ILLINOIS POLLUTION CONTROL BOARD
2 IN THE MATTER OF:
)
3
)
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 )
10
11
12
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.
15
16 BEFORE: MARIA E. TIPSORD, HEARING OFFICER,
17
ILLINOIS POLLUTION CONTROL BOARD
18
100 West Randolph Street
19
Suite 11-500
20
Chicago, Illinois 60601
21
312-814-4925
22
23
24
2
1 APPEARANCES:
2
3
4
MS. MARIE TIPSORD, HEARING OFFICER
5
MS. ALISA LIU, Environmental Scientist
6
MR. ANAND RAO, Senior Environmental Scientist
7
MR. G. TANNER GIRARD, Acting Chairman
8
MR. NICHOLAS J. MELAS,
9
MS. ANDREA S. MOORE,
10
11
12
ILLINOIS ENVIRONMENTAL PROTECTION AGENCY,
13
1021 North Grand Avenue East
14
P.O. Box 19276
15
Springfield, Illinois 62794-9276
16
217-782-5544
17
MS. DEBORAH WILLIAMS,
18
MS. STEPHANIE DIERS,
19
MR. SCOTT TWAIT;
20
21
22
23
24
3
1 APPEARANCES (cont'd):
2
3
4
BARNES & THORNBURG, LLP,
5
One North Wacker Drive
6
Suite 4400
7
Chicago, Illinois 60606
8
312-357-1313
9
MR. FREDRIC P. ANDES,
10
appeared on behalf of the Metropolitan
11
Water Reclamation District;
12
13
NATURAL RESOURCES DEFENSE COUNCIL,
14
101 North Wacker Drive
15
Suite 609
16
Chicago, Illinois 60606
17
312-663-9900
18
MS. ANN ALEXANDER;
19
20
THE CHICAGO LEGAL CLINIC,
21
2938 East 91st Street
22
Chicago, Illinois 60617
23
773-731-1762
24
MR. KEITH HARLEY;
4
1 APPEARANCES (cont'd):
2
3
OPENLANDS,
4
24 East Washington Street
5
Suite 1650
6
Chicago, Illinois 60602
7
312-863-6265
8
MS. STACY MEYERS-GLEN,
9
10
FRIENDS OF THE CHICAGO RIVER,
11
28 East Jackson Boulevard
12
Suite 1800
13
Chicago, Illinois 60604
14
312-939-0490
15
MS. MARGARET FRISBIE,
16
MR. ALBERT ETTINGER.
17
18
19
20
21
22
23 REPORTED BY: SHARON BERKERY, C.S.R.
24
CERTIFICATE NO. 84-4327.
5
1
THE HEARING OFFICER: Back on the
2
record.
3
MS. ALEXANDER: I wanted to start with
4
Gerba prefiled Question No. 3, which is
5
referring to Page 2 of your testimony that
6
pseudomonas was selected for study, in part,
7
because it, quote, "Causes recreational
8
associated, eye, skin and ear infection."
9
And then on Page 3, the adenoviruses are a
10
cause of ear, nose, throat and respiratory
11
infections. Just.
12
To clarify, the risk assessment
13
did not calculate quantitatively risks
14
associated with these types of infections; is
15
that correct?
16
MR. GERBA: For these two organisms,
17
it was done qualitatively.
18
THE HEARING OFFICER: You have to
19
remember to speak up.
20
DR. GERBA: For these two organisms,
21
it was done qualitatively.
22
MS. ALEXANDER: And I also wanted to
23
reference -- now, we were on the attachments
24
to the May 23rd, letter from Geosyntec,
6
1
second attachment Page 3.
2
THE HEARING OFFICER: Excuse me,
3
Ms. Alexander, this will be a new transcript,
4
so that's Exhibit 73.
5
MS. ALEXANDER: Sorry.
6
Exhibit 73, the portion of that
7
which is the letter from Geosyntec dated
8
May 23rd, 2008. Page 3 of the second
9
attachment, there is a statement made in the
10
first paragraph, "Ear and eye infections
11
associated with contact by pseudomonas
12
contaminated water are typically associated
13
with full immersion activities. Since these
14
types of activities are not permitted as
15
designated uses of the CAWS, the incidents of
16
ear and eye exposures are expected to be low
17
and as a result of an accidental or
18
intnetional misuse of the waterway."
19
I direct this question to
20
Dr. Petropoulou. Would I be correct in
21
understanding that if, in fact, you fell into
22
the water, you would be at risk of this from
23
the pseudomonas?
24
MR. ANDES: Can I just -- can you
7
1
repeat the page?
2
MS. ALEXANDER: I'm sorry. Page 3 of
3
the second attachment, which is entitled
4
Review Conducted by USEPA Office of Research
5
and Development, which is, in fact, I believe
6
is the Tim Wade document, I identified
7
earlier in response to that.
8
THE HEARING OFFICER: And that's --
9
what's the date on the cover letter to that?
10
MS. ALEXANDER: The cover letter is
11
dated May 23rd, 2008.
12
DR. TOLSON: It starts with a
13
clarification. It starts on Page 2 and it
14
continues on Page 3.
15
MS. ALEXANDER: Yes. I'm sorry. I
16
was reading from Page 3.
17
But the point be responded to is
18
on Page 2. "Since pseudomonas and adenovirus
19
were found, descriptions of non-GI illness
20
should also be provided, to represent a clear
21
picture of the actual risk associated with
22
recreating in the CAWS." That's the
23
statement being responded to.
24
The response begins on Page 2. I
8
1
read a portion of that response from Page 3
2
concerning non-GI gastrointestinal infection
3
associated with pseudomonas.
4
And my question was, am I correct
5
in understanding that this means you would be
6
at risk of non-GI illness from pseudomonas if
7
you actually fell into the water
8
accidently --
9
DR. GERBA: Are you asking me that
10
question?
11
MS. ALEXANDER: I was actually
12
directing it, initially, to Dr. Petropoulou,
13
because I believe she testified that she had
14
drafted that text.
15
DR. PETROPOULOU: I did. With input
16
from Dr. Tolson.
17
So I would defer that question to
18
Dr. Tolson.
19
MS. ALEXANDER: Okay. Go ahead,
20
either one of you.
21
DR. TOLSON: I won't defer it one more
22
time. I'll go ahead and take it.
23
Pseudomonas can cause
24
folliculitis. It typically requires a
9
1
pre-existing cut. So it's a very difficult
2
thing to sort of estimate what the population
3
pre-existing cuts would be to do that.
4
So there is a potential for
5
folliculitis from pseudomonas. We have not
6
calculated that directly within here,
7
however, the report does go into some
8
information on pseudomonas. Maybe we should
9
refer to that proportion --
10
MS. ALEXANDER: I'm going to get
11
there.
12
DR. TOLSON: Okay.
13
MS. ALEXANDER: I'm sorry, I didn't
14
mean to cut you off. Were you going to
15
continue to that --
16
DR. TOLSON: I was going to discuss
17
pseudomonas and the relationship with
18
pseudomonas between dry and wet and such.
19
But we can -- if we can postpone that, that's
20
fine.
21
MS. ALEXANDER: Yeah, I want to allow
22
you to do that, but I actually had a few
23
questions about it. Perhaps we can address
24
it in that context.
10
1
Because I just wanted to keep the
2
thread here, which is, you mentioned
3
folliculitis. Is that a skin infection?
4
DR. GERBA: Excuse me. I'm more
5
familiar with folliculitis because I've
6
studied it.
7
MS. ALEXANDER: Go ahead.
8
DR. GERBA: Actually, it's usually
9
infections around your hair follicles.
10
That's where it gets the name folliculitis.
11
It's most commonly associated with
12
hot tubs, particularly in the bathing suit
13
area and around the buttocks. And that's
14
where you most commonly see getting
15
folliculitis.
16
Almost all the cases in the
17
United States are associated with hot tubs or
18
other type of artificial waters, generally,
19
in the United States. Although, cases have
20
been associated with swimming in natural
21
waters.
22
And there's one study in Europe
23
that showed a relationship between getting
24
pseudomonas infections and swimming in lake
11
1
water.
2
MS. ALEXANDER: There's also a
3
reference to eye and ear exposures, here and
4
in the language I just quoted and in your
5
testimony.
6
Are those eye and ear infections
7
also folliculitis, or are those a different
8
type of infection?
9
DR. GERBA: Those are different types
10
of infection.
11
MS. ALEXANDER: Okay. Just one
12
second. Bear with me.
13
All right. Now, regarding
14
pseudomonas, I have in front of me the
15
discussion -- at least one of the discussions
16
of it in the risk assessment on Page 129.
17
THE HEARING OFFICER: One twenty-nine
18
of --
19
MS. ALEXANDER: One twenty-nine of the
20
risk assessment document, which I believe is
21
marked as Exhibit 72.
22
THE HEARING OFFICER: Okay. Wait.
23
Seventy-two is what you gave us, the Tim Wade
24
documents.
12
1
MS. ALEXANDER: Oh, I'm sorry.
2
THE HEARING OFFICER: The Geosyntec
3
report is 71.
4
MS. ALEXANDER: This (indicating)
5
is 71. Okay. I apologize.
6
Looking at Page 129, just to read
7
your language, it states, "Perhaps, more
8
importantly, the outfall samples show low
9
levels of pseudomonas -- I'm sorry, lower
10
level pseudomonas in the corresponding wet
11
weather samples. This suggests that the
12
major input for pseudomonas in the waterways
13
are sources other than the WRP effluent.
14
"Therefore, this infection of the
15
WRP effluent would have minor effects on the
16
overall loading of pseudomonas in the
17
waterway and risks associated recreational
18
exposure to the pathogen."
19
Would I be correct in summarizing
20
that the basis for your conclusion that
21
pseudomonas was not a risk is this the
22
statement that wet weather levels are higher
23
than dryer weather levels?
24
DR. TOLSON: I'm sorry the statement
13
1
that pseudomonas is not a risk?
2
MS. ALEXANDER: Basically, you have
3
the statement -- you conclude, "Therefore,
4
disinfection of the effluence would have
5
minor effects on overall loading of
6
pseudomonas." Let me ask the question more
7
broadly.
8
Do you have any other basis for
9
concluding that there was no -- that there is
10
no significant risk from eye, skin and ear
11
infections associated with pseudomonas?
12
MR. ANDES: Other than what?
13
MS. ALEXANDER: Other than the
14
language I just read, stating that lower
15
levels of pseudomonas in the dry weather
16
samples.
17
I mean, is there any other basis
18
for concluding that these types of infections
19
from pseudomonas are not a significant risk?
20
DR. TOLSON: I think -- we did not
21
quantify the exact level of pseudomonas
22
risks -- I'm sorry, the risk, for ear or eye
23
or skin infections. However, if you look at
24
Page -- Table 515 in Exhibit 71, I believe,
14
1
which is the report, it lists the pseudomonas
2
levels in the outfall effluent and also in
3
wet weather samples.
4
So, for example, in the north side
5
channel, the outfall had 1,350 CFUs per ML --
6
is that correct? Thirteen hundred fifty
7
units, where the wet weather -- in other
8
words, in the channel, had 5,427.
9
So it's hard to explain how the
10
effluent disinfection would have affected
11
something the receiving body that was, you
12
know, a four times higher concentration. And
13
that's the basis of my conclusion that
14
disinfection wouldn't change the wet weather
15
concentrations that we see.
16
Is that --
17
MS. ALEXANDER: Did you reach any
18
conclusions as to whether it would change the
19
dry weather concentrations?
20
MR. ANDES: I didn't -- whether what
21
would change?
22
MS. ALEXANDER: Weather disinfection
23
would change the dry weather concentration of
24
pseudomonas?
15
1
DR. TOLSON: Pseudomonas is a little
2
bit different than the other pathogens,
3
because they have such varied sources. The
4
concentrations of pseudomonas out of the
5
effluent we would expect it to decrease
6
probably quite dramatically by most of the
7
disinfection technologies.
8
Our pseudomonas is one of the
9
pathogens that comes from a lot of our
10
sources. We talked within this testimony
11
yesterday about trees and bushes that are
12
nearby the shoreline, those are a significant
13
source of pseudomonas into the waterway.
14
So unlike other pathogens,
15
pseudomonas is more -- is greatly affected by
16
these sort of nonpoint discharges or sources
17
into the waterway.
18
MS. ALEXANDER: Just to be clear,
19
however, these nonpoint discharges are wet
20
weather discharges; is that correct?
21
DR. TOLSON: They can be -- for
22
pseudomonas, they can be both wet and dry.
23
MS. ALEXANDER: Would you say that
24
they are substantially or predominantly wet
16
1
weather?
2
DR. TOLSON: If you want pure
3
speculation, I'd say yes.
4
MS. ALEXANDER: Okay.
5
And I get back to my question, did
6
you specifically do any analysis of the
7
impact of disinfection on dry weather
8
pseudomonas levels in the waterway?
9
DR. TOLSON: Yes, we did. We did
10
evaluate the dry weather days -- we did
11
sample the waterway under dry weather
12
conditions, and we did investigate the
13
effectiveness of disinfection techniques on
14
pseudomonas.
15
And from that conclusion, it would
16
suggest that the effluent could be decreased
17
quite dramatically by disinfection
18
techniques.
19
MS. ALEXANDER: Okay.
20
Now, what -- the reason I
21
highlighted that text on Page 129 is I was,
22
frankly, having a little bit of difficulty
23
finding the discussion that you have
24
characterized elsewhere as a qualitative as
17
1
opposed to quantitative assessment of these
2
impacts of pseudomonas. And by these
3
impacts, I'm referring to the possible ear,
4
eye and skin infections, there are reference
5
to qualitative as opposed to quantitative
6
assessment of that.
7
I was hoping that someone could
8
point me to any text other than what I've
9
highlighted on Page 129 that embodies that
10
qualitative risk assessment of those types of
11
illnesses.
12
DR. TOLSON: Well, the qualitative
13
assessment is the comparison of pathogen
14
concentrations under what way wet weather
15
versus dry weather versus the outflow. So we
16
don't know what that risk is, but we know we
17
can measure the concentrations of wet, dry
18
and outfall and get a sense of whether the
19
contributions to that risk, the magnitude of
20
that risk, who is responsible for it, what
21
the discharges are that are responsible for
22
it.
23
MS. ALEXANDER: Okay. So when you
24
reference --
18
1
DR. TOLSON: Let me follow up --
2
MS. ALEXANDER: I'm sorry, I didn't
3
mean to interrupt.
4
DR. TOLSON: Let me follow up with one
5
more point.
6
The dose response data available
7
to actually do that quantitative assessment
8
is not available. There's also very scant
9
information in the scientific literature
10
about the concentrations in hot tubs that
11
were responsible for outbreaks.
12
And I think Dr. Gerba might be
13
able to speak to that.
14
DR. GERBA: Most all of the outbreaks
15
of folliculitis are due to hot tubs, almost
16
entirely, where there's high concentration.
17
But nobody has ever quantified it, so you
18
couldn't really do a risk assessment on it.
19
Ear infections do take immersion,
20
I think I have to point out to when it's
21
correlated with lake water. And eye
22
infections, the only ones I've seen have
23
usually been immersion, related to
24
recreational activities.
19
1
MS. ALEXANDER: Okay. I just --
2
that's helpful, and I want to summarize to
3
make sure I understand.
4
When you say that you've done a
5
qualitative risk analysis of pseudomonas,
6
what you've done, essentially, is look at the
7
differing levels under different conditions
8
and the impact of disinfection on the levels;
9
is that correct?
10
DR. TOLSON: That is correct. We have
11
been able to assess between wet weather
12
versus dry weather and what are our
13
anticipated effects would be of disinfection,
14
absolutely.
15
MS. ALEXANDER: But no actual analysis
16
of the probabilistic likelihood that anyone
17
is going to get an ear, eye or skin
18
infection?
19
DR. TOLSON: We do not have the data
20
available, nor does anyone else, to sort of
21
do that quantitatively.
22
MS. ALEXANDER: Are any of you
23
familiar with research by lead author
24
Fewtrell, et al., in 1992, finding that at
20
1
one of the contaminated sites studied, the
2
relative risk of respiratory symptoms among
3
exposed individuals was actually higher than
4
the risk of GI symptoms?
5
DR. TOLSON: I'm familiar with a
6
number of his papers, if you let me see that
7
one?
8
MS. ALEXANDER: Okay. I do have
9
something in my hand.
10
And I apologize that I just
11
discovered this morning that this is actually
12
an incomplete copy. I am happy to provide a
13
complete copy as soon as I get my hands on
14
it.
15
This, however, does have a
16
reference to the conclusion that I'm
17
discussing here.
18
MR. ANDES: Is that referenced in the
19
questions?
20
MS. ALEXANDER: No, this is a
21
follow-up to this whole discussion.
22
THE HEARING OFFICER: I've been handed
23
a two-page document entitled Health Effects
24
of White Water Canoeing, by L. Fewtrell,
21
1
F-E-W-T-R-E-L-L, et al. And it's dated June
2
27th, 1992 from the Lancet, L-A-N-C-E-T.
3
I'll mark this as Exhibit 74, if
4
there's no objection?
5
Seeing none, then it's Exhibit 74.
6
(WHEREUPON, a certain document
7
was marked Exhibit No. 74 for
8
identification, as of 9/9/08.)
9
THE HEARING OFFICER: And Ms.
10
Alexander, when you get a complete copy we
11
will mark that.
12
MS. ALEXANDER: Okay.
13
And my initial question, I think,
14
is pending to all three of you, whether any
15
of you have seen this or are familiar with
16
it.
17
DR. TOLSON: I believe I've seen it
18
before, yes.
19
MS. ALEXANDER: Okay. Anybody else?
20
Dr. Gerba?
21
DR. PETROPOULOU: I haven't.
22
MS. ALEXANDER: I'm sorry, I couldn't
23
hear Dr. Gerba.
24
DR. PETROPOULOU: I haven't.
22
1
MS. ALEXANDER: I heard yours, I
2
didn't hear Dr. Gerba.
3
DR. GERBA: Yes, I believe I have.
4
MS. ALEXANDER: You've seen it, okay.
5
MR. ANDES: I can ask -- actually, I
6
think we have another witness who is very
7
familiar with it, who -- in fact, we were
8
going to produce this later anyway. So I
9
don't know if you want to --
10
MS. ALEXANDER: Yes, I understand it
11
was referenced in Dr. Dora Vitch's report. I
12
just wanted to get a brief reaction from
13
these witnesses.
14
Do you have any reason to doubt
15
the accuracy of the report of the data and
16
conclusions, in this document?
17
DR. TOLSON: I'm not really able to
18
comment on that at this point. One, I
19
haven't gone through this in great detail,
20
and so...
21
MS. ALEXANDER: Understood. I just
22
wanted to see if you had any --
23
DR. TOLSON: Sorry.
24
MS. ALEXANDER: -- immediate reaction.
23
1
Anyone else?
2
DR. GERBA: Yes, the thing that struck
3
me was the very concentrations of viruses per
4
ten liters.
5
MS. ALEXANDER: Very high
6
concentrations of --
7
DR. GERBA: About 200 per ten liters.
8
MS. ALEXANDER: Two hundred what
9
per -- I can't quite hear you.
10
DR. TOLSON: One hundred ninety-eight
11
per ten liters.
12
THE HEARING OFFICER: Viruses, I
13
believe he said.
14
DR. GERBA: One hundred ninety-eight
15
viruses per ten liters.
16
MS. ALEXANDER: I also see a reference
17
to 285 fecal colony forming units per
18
deciliter, I believe.
19
Can someone do some quick math on
20
that and translate that into what that would
21
be per -- I think we're usually using colony
22
forming units per 100 millimeters. That's
23
the same thing; correct, per deciliter?
24
Okay. Sorry.
24
1
Okay. So that 285 number for 100
2
milliliters, would it be fair to say that
3
that number is lower than the fecal coliform
4
levels generally measured in dry weather near
5
the outfalls in the CAWS?
6
DR. TOLSON: I have not --
7
unfortunately, I don't have any reading
8
glasses, so I can't read this at all.
9
As it's been characterized, it
10
would seem, that the concentrations in the
11
waterways that are represented by this study
12
are very different than the concentrations
13
that we've seen in the CAWS. That the
14
indicator organisms are very low in this
15
study.
16
The indicator organisms are very
17
low, the pathogen organisms are very high.
18
Compared to the CAWS, where the indicator
19
organisms are very high and the pathogenic
20
organisms are very low. That's probably a
21
significant sort of input to the conclusions
22
that they've drawn here.
23
The other thing that's striking is
24
that, you know, this is a white water
25
1
canoeing. And I believe that they actually
2
took discharge from a water treatment plant
3
to increase the flow of a river where they
4
had this event, if I'm characterizing it --
5
if I recall it correctly.
6
And that's more of a primary
7
contact activity than what we have.
8
MS. ALEXANDER: Do you have any reason
9
to believe that the contribution from the
10
wastewater treatment plants of this situation
11
would have been higher than 70 percent, as it
12
is in the CAWS?
13
DR. TOLSON: Say again?
14
MS. ALEXANDER: Do you have any reason
15
to believe that the percentage contribution
16
of wastewater treatment plant effluent in
17
this waterway was higher than 70 percent,
18
which is the percent in the CAWS?
19
DR. TOLSON: I'm sorry, I'm not
20
familiar with this study well enough from
21
memory.
22
MS. ALEXANDER: I just asked if you
23
had any reason to believe. If the answer is
24
no, that's fine.
26
1
DR. TOLSON: No.
2
MS. ALEXANDER: All right. Moving on
3
from this.
4
Can meningitis be caused by water
5
born pathogens?
6
DR. GERBA: Yes.
7
MS. ALEXANDER: Can meningitis be
8
caused by water born pathogens?
9
DR. TOLSON: Dr. Gerba can --
10
DR. GERBA: Yes.
11
MS. ALEXANDER: Can myocarditis?
12
DR. GERBA: Yes.
13
MS. ALEXANDER: Can encephalitis?
14
DR. GERBA: Yes.
15
MS. ALEXANDER: Okay.
16
And none of those, of course, are
17
GI illnesses; correct?
18
DR. TOLSON: Beg your pardon?
19
MS. ALEXANDER: That none of those are
20
gastrointestinal, they're all different
21
kinds; correct?
22
DR. GERBA: Yes.
23
DR. TOLSON: I'd also like to point
24
out that those are reportable illnesses. So
27
1
we could pole the county health records and
2
see if there were any occurrences of those.
3
MS. ALEXANDER: Right.
4
But you did not study risks of
5
those types of infections in the risk
6
assessment; is that correct?
7
DR. GERBA: Well, we used -- again, we
8
use infection as the limit, which could be
9
taken into that. In other words, that's an
10
endpoint of infection.
11
Your conservative things that
12
estimate you risk by infection is what we
13
did. That's an outcome of infection.
14
MS. ALEXANDER: But, in fact, only
15
studied risk of gastrointestinal illness; is
16
that correct?
17
DR. GERBA: That's right. Because,
18
currently, that's how the U.S. Environmental
19
Protection Agency regulates recreational
20
waters.
21
MS. ALEXANDER: Bear with me one more
22
second while I find a page number.
23
I apologize for the interlude.
24
Not all the pages are -- hard to find things.
28
1
All right. I want to refer to the
2
language on Page 95 of Exhibit 71. I got it
3
right in time, the risk assessment.
4
And that language is, "Since there
5
is a certain degree of correlation between
6
different pathogens, indications of
7
unacceptable levels of gastrointestinal
8
illness may indicate a potential for other
9
effects."
10
My first question is, have you
11
quantified that correlation between GI
12
illness and other unacceptable -- I'm
13
sorry -- in other effects, I should say?
14
MR. ANDES: What page did you say
15
that's on, I'm sorry?
16
MS. ALEXANDER: This is on Page 95.
17
DR. TOLSON: We have not undertaken
18
that as a component of the study.
19
MS. ALEXANDER: Okay. And again, you
20
state that this correlation may exist. I
21
take it you haven't quantified the
22
probability of such a correlation?
23
DR. TOLSON: No, we have not.
24
MS. ALEXANDER: Do you know any other
29
1
researchers that have?
2
DR. TOLSON: I'll refer to Dr. Gerba.
3
I do not personally.
4
DR. GERBA: Say again.
5
MS. ALEXANDER: A quantification of
6
the probability of the correlation between GI
7
illness and other effects, the language used
8
here.
9
DR. GERBA: You mean, in other words,
10
the probability you have a GI was the
11
probability of having another outcome of
12
that?
13
MS. ALEXANDER: Yes. In other words,
14
these other -- I assume it's referring to
15
what's referred to also in the core, which is
16
the ear, skin, eye infections that can
17
result.
18
DR. GERBA: From recreational contact?
19
MS. ALEXANDER: Well, I mean, let me
20
expand the question for any. Because I --
21
what I want to know is whether anybody that
22
you know of has done research to quantify the
23
probability of that correlation?
24
DR. GERBA: Going from GI to like,
30
1
say, meningitis?
2
MS. ALEXANDER: Yeah, any of these
3
other possible effects of water born
4
pathogens.
5
DR. GERBA: Not offhand, no, I
6
can't --
7
MS. ALEXANDER: Okay.
8
DR. TOLSON: If I can add something,
9
though.
10
You know, EPA's bases GI
11
illness -- or uses GI illness for their
12
setting acceptable limits. So I think
13
implicit within that is the understanding
14
that GI is the most sensitive and would be
15
correlated to all illnesses.
16
MS. WILLIAMS: Is there anywhere that
17
you can point us to where they say that?
18
DR. GERBA: I'm not sure what the
19
question revolves about.
20
MS. WILLIAMS: Okay.
21
DR. TOLSON: Off the top of my head I
22
do not know. But that is something that's
23
potentially out there.
24
They had to come up with a
31
1
rationale for using GI illness, which --
2
MS. WILLIAMS: But you don't know what
3
it is?
4
DR. TOLSON: I do not know what it is.
5
MS. ALEXANDER: Okay.
6
DR. TOLSON: And my guess is that they
7
specified it somewhere.
8
MR. ANDES: I'll follow up on that.
9
So your understanding is the way
10
EPA sets these standards, the sense is, if
11
you address GI illness, you're addressing the
12
other issues?
13
DR. TOLSON: That is correct.
14
MR. ANDES: Thank you.
15
MS. ALEXANDER: But you're not
16
offering anything substantive right now to
17
support that assumption?
18
DR. GERBA: I was just -- my thought
19
was that a lot of times gastrointestinal -- I
20
mean, we have respiratory, we have intestinal
21
infections, also. So you can have both by
22
the same agent is the only thought I had on
23
that.
24
So in some ways that might be
32
1
covered, because you can have both diarrhea
2
and respiratory illness from the same agent
3
at the same time.
4
MS. ALEXANDER: I understand that it's
5
possible to get really sick from multiple
6
things at the same time. But I guess what
7
I'm asking is whether you know of any
8
quantification of the likelihood of that
9
correlation.
10
DR. GERBA: I've answered that.
11
MS. ALEXANDER: And it sounds to me
12
like the answer was no.
13
Let me ask another question along
14
those lines. Is it possible in your review
15
that there could be circumstances in which
16
recreators would be at risk of contracting
17
nongastrointestinal illnesses, even if they
18
were not at significant risk of a GI illness?
19
DR. GERBA: There are so many caveats
20
to that.
21
DR. TOLSON: There are a lot of
22
caveats to that. There are potentials,
23
obviously, of getting a respiratory or an ear
24
infection and not getting GI illnesses,
33
1
that's what you're after, sure.
2
MS. ALEXANDER: Okay.
3
MR. ANDES: Can you expand on that?
4
DR. TOLSON: While there is that
5
potential, we believe the predominant illness
6
from recreational exposure to the CAWS is GI
7
illness.
8
MS. ALEXANDER: I understand that's
9
your --
10
DR. TOLSON: Okay.
11
MS. ALEXANDER: -- viewpoint.
12
Let me ask -- this has drawn --
13
sorry, I didn't mark which prefiled question
14
this was. But I'll ask it anyway.
15
Approximately how many types of
16
water born human pathogens are known to be
17
associated with sewage overall? Just an
18
approximation.
19
DR. GERBA: The number of different
20
types?
21
MS. ALEXANDER: Yeah.
22
DR. GERBA: I'd say between 160 and
23
200.
24
MS. ALEXANDER: Okay.
34
1
Did any or all of you review the
2
list of water born pathogens that accompanied
3
Dr. Mary Lynn Yates' testimony submitted in
4
this matter.
5
DR. GERBA: She didn't give a specific
6
list. But she did say there were thousands,
7
I think.
8
MS. ALEXANDER: There was an attached
9
list, which I'm happy -- I mean, we're going
10
to be marking Dr. Mary Lynn Yates' testimony.
11
But for ease of reference, I can just have
12
the list marked separately, if that's all
13
right.
14
I do not recall, unfortunately,
15
which document this was to the testimony, but
16
I will represent that it was an exhibit,
17
which I'm giving you for reference.
18
THE HEARING OFFICER: I've been handed
19
Table 1, Illness Acquired By Ingestion of
20
Water.
21
MS. WILLIAMS: I think it's Exhibit 6
22
to the testimony.
23
MS. ALEXANDER: Thank you.
24
THE HEARING OFFICER: And I believe
35
1
the title of the book is Water Born
2
Transmissions of Infectious Agents, that's at
3
the top.
4
I'm going to mark this as Exhibit
5
75. If there's no objection?
6
Seeing none, it's Exhibit 75.
7
(WHEREUPON, a certain document
8
was marked Exhibit No. 75 for
9
identification, as of 9/9/08.)
10
DR. GERBA: Can I make a comment right
11
away?
12
This has to do with recreational
13
water only. Many of these organisms are
14
not -- do not occur in sewage and are not
15
transmitted by that route.
16
They are -- many of these
17
organisms are what we call water based
18
pathogens, those that grow naturally in
19
water. Did you want me to comment otherwise
20
on this?
21
I -- again I don't see thousands
22
of organisms listed here.
23
MS. ALEXANDER: Yeah. Let me just
24
clarify your comment.
36
1
You say that they are not
2
recreationally associated. Is that what I
3
heard you say?
4
DR. GERBA: No, I said they're not
5
sewage associated.
6
MS. ALEXANDER: They're not sewage
7
associated.
8
But some of them are sewage
9
associated; correct?
10
DR. GERBA: Oh, yes.
11
MS. ALEXANDER: Yes, I understand
12
there are a few of these that are not sewage
13
associated.
14
My only question to you was, with
15
that comment in mind that you made that, you
16
know, we all -- Dr. Yates also recognized in
17
her testimony that not all of these are
18
necessarily sewage related. Do you have any
19
reason to doubt the overall accuracy of this
20
list as your representation of human water
21
born pathogens?
22
DR. GERBA: This is transmitted by
23
recreational waters?
24
MS. ALEXANDER: I'm sorry?
37
1
DR. GERBA: Transmitted by
2
recreational waters? That's what the table
3
says.
4
MS. ALEXANDER: Yes, potentially
5
transmitted by recreation, sorry.
6
DR. GERBA: And that's only the latter
7
part of that. Yes.
8
Again, I don't see thousands of
9
organisms listed here.
10
MS. ALEXANDER: Right. Okay.
11
So that's a subset of them.
12
But the only question would be is
13
it a longer list, is it not, than the list of
14
pathogenic organisms that were included in
15
the risk assessment analysis? Is that
16
correct?
17
MR. ANDES: Well, wait. Do we have to
18
count up whether there's 160 to 200 here? He
19
just testified there's 160 to 200 types.
20
MS. ALEXANDER: I'm sorry, say that
21
again? You have to --
22
MR. ANDES: He just testified there
23
were 160 to 200 types of pathogens.
24
MS. ALEXANDER: Right.
38
1
MR. ANDES: So you're questioning --
2
he has to count these and decide if there are
3
that many?
4
MS. ALEXANDER: No, that wasn't really
5
my question. It was more general than that.
6
MR. ANDES: Okay.
7
MS. ALEXANDER: I mean, I -- in the
8
risk assessment you studied approximately
9
eight, give or take; is that correct?
10
DR. GERBA: That's correct.
11
MS. ALEXANDER: And there are more
12
listed here that are associated with
13
recreational water use; is that correct?
14
DR. GERBA: That's correct.
15
MS. ALEXANDER: Okay. That's all I'm
16
getting at, sorry.
17
DR. GERBA: But I would point out most
18
of these are not transmitted by sewage. Of
19
the recreational ones, that you have in
20
recreational.
21
MR. ANDES: I'd like to follow up on
22
that.
23
Dr. Gerba, is it accurate to say
24
that the eight, according to your testimony,
39
1
that were chosen, were chosen to be
2
representative of what the basic risks are
3
from --
4
DR. GERBA: Sewage contaminated water.
5
We collected the water organisms because they
6
occurred in sewage and had the potential to
7
be transmitted by that route.
8
We also selected to represent what
9
we figured would be the ones most commonly
10
present, ones that could be detected by
11
methods currently available, because methods
12
weren't available for all of these. And the
13
ones would be there in the greatest
14
concentration.
15
So they would present the greatest
16
risk based on knowledge of dose response and
17
the occurrence of waste water.
18
MR. ANDES: Thank you.
19
MS. ALEXANDER: And the longer list
20
concerns illnesses acquired by ingestion of
21
water; correct?
22
DR. GERBA: That's right.
23
MS. ALEXANDER: Okay.
24
And one of the exposure pathways
40
1
that you considered in your risk assessment
2
was ingestion; correct?
3
DR. GERBA: That's correct.
4
MS. ALEXANDER: And a number of those
5
are, in fact, transmitted fecally orally; is
6
that correct?
7
DR. GERBA: That's correct.
8
MS. ALEXANDER: Okay.
9
So in other words, the list of
10
pathogens from which one might be at risk if
11
one fell in the water and gulped a mouthful
12
might, in fact, be longer than, specifically,
13
the list identified as acquired by
14
recreational contact with water; is that
15
correct?
16
DR. GERBA: That's correct.
17
MS. ALEXANDER: Okay.
18
Now, I'll address this initially
19
to Dr. Petropoulou, it's Question No. 2 on
20
the Petropoulou prefiled questions. And the
21
others, if you can chime in afterwards, it's
22
also Tolson No. 6 and Gerba No. 15.
23
But specifically for
24
Dr. Petropoulou, regarding the statement at
41
1
Page 4 of your testimony in which you
2
identify the two bases for selecting a
3
limited subset of pathogens that you studied,
4
these eight give or take that I referred to a
5
moment ago. And those two bases were, one,
6
the existence of past outbreaks caused by
7
these viruses, and, secondly, the existence
8
of USEPA approved SOPs for those pathogens.
9
Is that an accurate
10
characterization?
11
DR. PETROPOULOU: Correct.
12
MS. ALEXANDER: Okay.
13
In your view, are outbreaks an
14
accurate indicator of the actual risk of a
15
particular pathogen?
16
DR. PETROPOULOU: I'll defer the first
17
question to Dr. Gerba.
18
MS. ALEXANDER: Okay.
19
DR. GERBA: Yeah, outbreaks are one
20
indication. But a pathogen can be
21
transmitted by a specific route.
22
MS. ALEXANDER: They're one
23
indication. But is it possible for there to
24
be risk of a type of pathogen and no record
42
1
of outbreaks from that pathogen?
2
DR. GERBA: By a water route, say,
3
or -- yes.
4
MS. ALEXANDER: Sure, by water route.
5
DR. GERBA: Yes.
6
MS. ALEXANDER: One second.
7
Now, I'd like to refer again to
8
the second attachment to that May 23rd, 2008
9
letter, which was a component of Exhibit 73,
10
Page 7 of that.
11
THE HEARING OFFICER: For
12
clarification, you refer to the May 23rd
13
letter, and it may be a copying error again,
14
but we have the May 23rd letter attached to
15
the May 28th letter.
16
MS. ALEXANDER: Yes, I'm sorry. I've
17
been referring to May -- that is the May 23rd
18
letter.
19
THE HEARING OFFICER: Okay.
20
MS. ALEXANDER: And this is Page 7 of
21
the document headed Review Conducted by USEPA
22
Office of Research and Development.
23
THE HEARING OFFICER: Page 7?
24
MS. ALEXANDER: Yes. Are you there?
43
1
Okay.
2
I'm referring to the statement at
3
the bottom, that quoted language from the
4
Office of Research and Development document.
5
It's cited as Page 2.
6
They are quoting language in the
7
document regarding, quote, "No outbreaks
8
tradable to treated waste water." And then,
9
the comment being responded to:
10
"The statement is misleading,
11
because outbreaks are not a reliable health
12
indicator due to problems with consistent and
13
reliable detection. Furthermore, statements
14
such as these require citations and peer
15
reviewed literature, other outside sources to
16
avoid the perception of bias."
17
Now, their response provided is a
18
citation to what purports to be peer reviewed
19
literature. Let me first ask the question,
20
is that document cited peer reviewed, to your
21
knowledge?
22
DR. TOLSON: I think that's beyond
23
our --
24
MR. ANDES: Let me clarify.
44
1
Directly under that citation it
2
points out that the statement the EPA
3
commented on was removed from the final
4
report.
5
MS. ALEXANDER: I understand that.
6
But the subject matter is still relevant,
7
regardless whether the statement is in the
8
report.
9
MR. ANDES: But we don't have the
10
particular statement at issue here in the
11
final report. So you're asking them about
12
the statements in their testimony, not the
13
statement in the draft report.
14
We don't know what that statement
15
was.
16
MS. ALEXANDER: Understood. But the
17
subject matter is exactly the same, which is
18
whether outbreaks are or are not a reliable
19
indicator of risk.
20
And what I am trying to find out
21
is the type of discussion that has taken
22
place with EPA about that. Because EPA here
23
has expressed a concern, and it's not obvious
24
to me how that concern was responded to or if
45
1
it was responded to. And that's what I'm
2
getting at with these questions.
3
MR. ANDES: But I guess the question
4
that they're testifying is not whether
5
outbreaks are a reliable health indicator,
6
it's whether they're relevant to the choice
7
of which particular parameters to look at in
8
doing a study. So if you want to ask him
9
questions about that, that's relevant, but
10
this statement is to a different issue.
11
MS. ALEXANDER: It's the same issue in
12
the sense of what does it matter whether
13
there's been an outbreak or not. And I want
14
to find out what kind of discussion there was
15
with the USEPA on that topic.
16
And I understand that the
17
parameters of the discussion may have changed
18
a little, but the fact of the matter is there
19
is extensive reference, both in the testimony
20
and in the report itself, to the significance
21
of outbreaks. And I want to know what the
22
conversations were with EPA about that, and
23
whether their concerns in any context were
24
responded to.
46
1
DR. TOLSON: I believe the answer to
2
your question is that, you know, we used
3
outbreaks to identify important parameters,
4
important pathogens to carry through the
5
assessment.
6
MS. ALEXANDER: I get that.
7
DR. TOLSON: And that's totally it.
8
MS. ALEXANDER: And EPA made a comment
9
to the effect that outbreaks are effectively
10
of minimal significance. And then a response
11
was provided by Dr. Petropoulou, perhaps in
12
reliance on others, but I'm trying to
13
understand that response.
14
Even though I know that particular
15
statement that prompted the USEPA's concern
16
is not in the record, the issue is still very
17
much a part of this -- a part of the report
18
and a part of discussion.
19
So let me return to my question,
20
which is, there is a citation here to an MWRD
21
paper. And my question -- I'll direct it to
22
Dr. Petropoulou, since she drafted this --
23
is, was that or was that not a peer reviewed
24
document?
47
1
DR. PETROPOULOU: Which document?
2
MS. ALEXANDER: I'm referring to now
3
on Page 8, the -- on Page 8, your response
4
says, "The report includes the following
5
citation for the statements made." And then
6
it cites a document.
7
And my question is, is that
8
document peer reviewed? Because the question
9
asked what about peer review.
10
DR. PETROPOULOU: I do not know.
11
MS. ALEXANDER: Okay.
12
MR. ANDES: I'd like to follow up.
13
The question for any of you is, in
14
terms of the choice of parameters, the
15
parameters that you chose based partly on the
16
existence of outbreaks, did EPA finally go
17
along with the choice of parameters?
18
DR. GERBA: Yes. I've been on EPA
19
advisory committees for years in trying to
20
get them to actually do more than just
21
outbreaks. But EPA's position has always
22
been the drinking water.
23
There hasn't been an outbreak, why
24
are we trying to regulate it. In general,
48
1
it's the opposite thing.
2
What we're really finding most of
3
the time is that they want an outbreak. And
4
the reason you use an outbreak is because we
5
know it can be transmitted by that route.
6
And there's a great deal of
7
uncertainty whether other illnesses can be
8
transmitted by that route if you don't have a
9
documentation of an outbreak. That's the
10
issue.
11
So it's usually the opposite
12
problem we have with the EPA. That's why I
13
don't really see -- usually the EPA is
14
telling us why are you studying it if there
15
hasn't been an outbreak.
16
MR. ANDES: Thank you.
17
MS. ALEXANDER: Beyond what's in this
18
document, did you have any further
19
conversations, any of you, in this meeting or
20
otherwise, with EPA concerning the
21
significance of outbreaks as an indicator of
22
risk?
23
MR. ANDES: Ever?
24
MS. ALEXANDER: In the context of this
49
1
risk assessment, I should say, not ever,
2
ever.
3
DR. PETROPOULOU: I have not.
4
MS. ALEXANDER: Okay.
5
DR. TOLSON: Nor I.
6
MS. ALEXANDER: Okay.
7
DR. TOLSON: I have not had any
8
contacts with anyone.
9
MS. ALEXANDER: All right.
10
Is it possible, in your view, that
11
a substantial number of outbreaks go
12
undetected?
13
DR. GERBA: Yes.
14
MS. ALEXANDER: Okay.
15
Is it possible that pathogens that
16
are more frequently asymptomatic, as in
17
people aren't actually getting sick they're
18
just getting infected, would be less likely
19
to result in outbreaks that are actually
20
traceable to recreation, because the people
21
with the symptoms would not necessarily be
22
the same people who recreated on the water?
23
DR. TOLSON: I don't think we have the
24
data to really speculate on that. So I can't
50
1
address that.
2
MS. ALEXANDER: Dr. Gerba, can you?
3
DR. GERBA: It's too much speculation,
4
I think, to tell you what the impact would
5
be.
6
MS. ALEXANDER: Let me see if I can
7
clarify my question just a little, because I
8
think it may have sounded more speculative
9
than it is.
10
Let's hypothesize a type of
11
illness where only half the people actually
12
exhibit symptoms. If those people don't get
13
sick themselves but pass it onto their
14
friends and their friends all get sick, it's
15
going to be harder to trace those friends'
16
illnesses to recreation on the water body
17
than it is to trace the recreators'
18
illnesses; is that correct?
19
DR. TOLSON: Again, that is still
20
fairly speculative. But let me address the
21
point that I think it -- the underlying point
22
that relates our risk assessment is we do
23
consider that only about half of the
24
people that are ill actually -- or infected,
51
1
actually become ill. And we do consider that
2
those people can transmit illness to their
3
family members.
4
MS. ALEXANDER: I get that about the
5
risk assessment. But my question has to do
6
with outbreaks.
7
And my question is, isn't it
8
likely that outbreaks are even less likely to
9
be detected if the illness in question is not
10
highly symptomatic, such as the people
11
getting sick aren't the ones who are actually
12
on the water?
13
DR. TOLSON: Our testimony here is
14
about this risk assessment, not on public
15
health sort of concerns about outbreaks.
16
Outbreaks really had nothing to do with the
17
assessment.
18
MS. ALEXANDER: Oh, except you did, in
19
fact, rely on the presence or absence of
20
outbreaks as one of the two criteria for your
21
choice of pathogens; is that correct?
22
DR. TOLSON: That is correct.
23
MS. ALEXANDER: Okay.
24
DR. TOLSON: Outbreaks are a good
52
1
indicator of which ones to go after and
2
sample. But they didn't follow through to
3
figure out what the impacts of outbreaks were
4
on illness rates in the Chicago population.
5
That's not part of their assessment.
6
MS. ALEXANDER: You say they are a
7
good indicator, but, in fact, they are far
8
from a perfect indicator; is that correct?
9
DR. TOLSON: That is correct.
10
MS. ALEXANDER: Because, as Dr. Gerba
11
has acknowledged, it's entirely impossible
12
for outbreaks to go undetected.
13
MR. ANDES: Well, I could follow up.
14
Is there a perfect indicator.
15
DR. GERBA: Can I follow up on that?
16
DR. TOLSON: No, there's no --
17
DR. GERBA: When you say follow up,
18
that's largely because limitations in public
19
health, for one thing. Every potential
20
outbreak is not investigated or comes to the
21
public health's attention. Or not everybody
22
calls in every time to the public health
23
department when they have diarrhea or other
24
types of illnesses.
53
1
So it's more of a limitation of
2
public health's ability to respond to that to
3
conduct an investigation. That's probably
4
one of the overlying factors to all of the
5
quantifying certain sources of infection and
6
identifying outbreaks.
7
MS. WILLIAMS: Can I ask a follow-up
8
question?
9
MS. ALEXANDER: Sure.
10
MS. WILLIAMS: I think Ms. Alexander
11
indicates she understood something that I
12
don't think I do. So I want to go back and
13
make sure I do.
14
When we talk about the risk
15
numbers, you know, one in a thousand, two in
16
a thousand, eight in a thousand, I always
17
understood USEPA to use it per 1,000
18
swimmers. Are your numbers based on per
19
1,000 recreators, or do they reflect also
20
people who have not recreated but have
21
contacted illness from someone who did? Can
22
you explain that?
23
DR. TOLSON: Right. We actually ran
24
two sets of numbers.
54
1
One of them for the people that
2
were actually engaged in that. And then,
3
just sort of to be more conservative and take
4
into consideration a potential that that
5
disease could spread to others, we took
6
secondary attack rates, or their family
7
members, and considered them a second pool of
8
people that could be infected, and presented
9
results for those too.
10
MS. WILLIAMS: Are they in separate
11
tables in your report?
12
DR. TOLSON: They are.
13
Do you want me to point to those?
14
MS. WILLIAMS: Yes. Just so I can
15
take a look at them.
16
DR. TOLSON: Sure.
17
We go to Table 513 in Exhibit 71.
18
The bottom two lines there list illnesses
19
primary and secondary, in parentheses.
20
So you can see from at the North
21
Side we have 1.55 per 1,000. And if you
22
include the pool to include secondary --
23
potential secondaries, it's 2.6.
24
MS. WILLIAMS: Okay. Thank you.
55
1
DR. TOLSON: Okay.
2
MS. WILLIAMS: I'll review that. I
3
may have some follow-up later, but thanks.
4
DR. TOLSON: That's fine.
5
MS. ALEXANDER: I'd like to turn now
6
to the second prong of your two-pronged
7
justification for why you picked this limited
8
subset of eight or so pathogens, which was
9
the presence of USEPA approved laboratory
10
standard operating procedures, which we've
11
been referring to as SOP for measurement of
12
the pathogens.
13
And the question is, does the
14
availability of SOPs for a particular
15
pathogen have any relationship to the risk it
16
poses?
17
DR. PETROPOULOU: The availability of
18
EPA approved methods or standard operating
19
procedures relates to the ability to measure
20
the concentration of the organism. And
21
without that concentration, we cannot
22
quantify the risk.
23
So in that sense, it does relate
24
to how we are able to measure the risk but
56
1
not the risk --
2
MS. ALEXANDER: Okay.
3
DR. PETROPOULOU: -- in general of
4
the --
5
MS. ALEXANDER: Not the risk, but your
6
ability to measure it.
7
And now, as we're discussed
8
before, you did, in fact, evaluate two types
9
of pathogens for which there was not an EPA
10
approved SOP; is that correct?
11
DR. PETROPOULOU: Correct.
12
MS. ALEXANDER: So that was not an
13
absolute requirement for inclusion in your
14
subset, it was just one of the factors you
15
considered; is that correct?
16
DR. PETROPOULOU: Actually, we said
17
either EPA approved or standard operating
18
procedures, like the ones that Dr. Gerba's
19
laboratory is using. So we did go beyond the
20
EPA approved methods.
21
We also quantified viruses that
22
the EPA has no approved method but
23
Dr. Gerba's lab has standard operating
24
procedures to use for that.
57
1
MS. ALEXANDER: And, in fact, there
2
are USEPA approved SOPs for shigella; is that
3
correct?
4
DR. GERBA: Shigella, there may be,
5
yes. I'm not familiar --
6
MR. ANDES: I'm sorry, SOPs --
7
DR. GERBA: It is a standard method,
8
yes.
9
MS. ALEXANDER: SOPs.
10
MR. ANDES: Analytical methods, I'm
11
not --
12
MS. ALEXANDER: USEPA approved SOPs.
13
MR. ANDES: It doesn't approve --
14
MS. ALEXANDER: I'm sorry, US --
15
MR. ANDES: It approves only
16
analytical methods.
17
MS. ALEXANDER: I'm sorry, they
18
only --
19
MR. ANDES: Approve analytical
20
methods to put in 40CFR136. I'm sorry, 136.
21
So I'm not sure if you're
22
referring to an approved analytical nitrogen
23
136 or some other EPA generated document, but
24
I don't think it's approved.
58
1
MS. ALEXANDER: Well, I believe -- in
2
terms of just the language of USEPA approved,
3
I believe that is drawn directly from
4
Dr. Petropoulou's testimony.
5
Did you -- I can fish through it,
6
but did you, in fact, refer to USEPA approved
7
SOPs?
8
DR. PETROPOULOU: No. EPA approved
9
methods or standard operating procedures.
10
MS. ALEXANDER: Methods or --
11
DR. PETROPOULOU: Laboratory standard
12
operating procedures. I was not referring to
13
EPA SOPs.
14
MS. ALEXANDER: Okay.
15
DR. GERBA: Let me go back there.
16
I don't know of an EPA approved
17
method for shigella. Usually EPA only
18
approves methods if there is a legal
19
requirement for monitoring in some aspect, or
20
they're conducting a study, which requires an
21
approval, like an information collection
22
rule.
23
However, there is a standard -- it
24
is in standard method, there is a method for
59
1
shigella.
2
MS. ALEXANDER: Okay.
3
DR. GERBA: And we did not decide not
4
to use shigella in this study, because I had
5
questions about how good the method really
6
was. In all of the recreational outbreaks
7
that were associated with, there were usually
8
too many people in the water.
9
In a review for 1971 or 2000, they
10
were all lake waters, where people were
11
believed to be the source through accidental
12
fecal releases -- I hope they were
13
accidental -- into the water.
14
MS. ALEXANDER: I'm not going there.
15
DR. GERBA: And also, shigella is a
16
weak organism, it doesn't survive very well
17
in the environment.
18
MS. ALEXANDER: But, in fact, as you
19
just referenced, there have been recreational
20
outbreaks of shigella?
21
DR. GERBA: Right. Associated with, I
22
belive, fecal releases are too much gluteal
23
fold in the water at one time.
24
MS. ALEXANDER: And my next question,
60
1
which I believe was a prefiled Petropoulou,
2
but I'll just ask it.
3
The question I think has been
4
partly answered, but I want to get at the
5
rest of the answer, which is, did the risk
6
assessment take into account populations that
7
that are potentially more sensitive to
8
pathogens and may more easily become ill or
9
suffer severe effects, such as children,
10
pregnant women and an immunocompromised
11
person?
12
Now, an answer was given earlier,
13
if I recall correctly, that the more
14
sensitive populations were taken into account
15
in the secondary infection rate analysis; is
16
that correct?
17
DR. TOLSON: That is correct.
18
MS. ALEXANDER: Is there any other
19
manner in which sensitive populations were
20
taken into effect?
21
DR. GERBA: You know, again, we
22
determined the risk of infection, so one
23
could always assume that that risk of
24
infection -- and you could apply what the
61
1
outcome would be to those groups, if you
2
wished. You know, because that's the most
3
conservative thing you do.
4
What you're talking about is the
5
result of the infections.
6
MS. ALEXANDER: Okay. So, in fact,
7
your analysis really doesn't address at all
8
whether or not we're dealing with the risk of
9
somebody having a mild case of diarrhea and
10
somebody having a very severe
11
gastrointestinal illness, which might be the
12
result if, say, the person was a young child
13
or was on chemotherapy?
14
DR. TOLSON: That is correct.
15
MS. ALEXANDER: Okay.
16
MR. ANDES: I want to follow up on
17
that.
18
So, as I understand what you're
19
saying, is the risk of illness -- there's no
20
evidence that their risk of illnesses is
21
different for these groups, the severity of
22
the illness?
23
DR. GERBA: Right. That's correct.
24
MR. ANDES: So your risk assessment,
62
1
in terms of how likely that the people will
2
develop infections, does not change?
3
DR. GERBA: It does not change.
4
DR. TOLSON: Just another follow-up on
5
that.
6
On the flip side of that, you
7
know, we do not consider immunity. And I
8
think we touched on this before, that our
9
analysis may be biased, because there may be
10
immunity in the population that we didn't
11
account for.
12
MS. ALEXANDER: Let me --
13
approximately what percent of the population
14
would you say falls into these categories of
15
immunocompromised persons?
16
DR. GERBA: I -- somewhere about 25 to
17
35 percent of the U.S. population. It's
18
largely represented by people -- elderly
19
individuals over 60 years of age.
20
MS. ALEXANDER: And also would you say
21
children?
22
DR. GERBA: And children.
23
MS. ALEXANDER: And --
24
DR. GERBA: Well, when I said
63
1
children, we usually refer to infants, small
2
children.
3
MS. ALEXANDER: Okay.
4
Pregnant women?
5
DR. GERBA: And pregnant women.
6
MS. ALEXANDER: And people on chemo
7
therapy?
8
DR. GERBA: And -- yeah, people out
9
walking around on chemotherapy.
10
MS. ALEXANDER: And people on
11
antirejection drugs for organ transplants?
12
DR. GERBA: Yes.
13
MS. ALEXANDER: And people with HIV?
14
DR. GERBA: Yes.
15
MS. ALEXANDER: This question was
16
Petropoulou No. 3 and also is the subject
17
matter in Gerba No. 19 and Tolson No. 10.
18
And the question is -- specifically, first to
19
Dr. Petropoulou, because the statement's in
20
your testimony.
21
Regarding the statement at Page 5,
22
that although the microbial analytical
23
results were evaluated within the framework
24
of dry and wet weather conditions, "For the
64
1
MRA risk assessments, the dry and wet weather
2
microbial results were integrated into a
3
comprehensive data set representative of all
4
weather conditions on the waterway."
5
And my question is, does this
6
mean -- am I correct in understanding that in
7
assessing post-disinfection risk, you
8
combined data from the wet and dry weather
9
conditions?
10
DR. TOLSON: Yes. In fact, you have
11
to do that in order to assess what the effect
12
of disinfection is.
13
You want to figure out what the
14
overall seasonal population of recreator risk
15
is, you have to consider that it rains, has
16
CSO events and there's dry weather days.
17
We've attenuated one of those sources to the
18
waterway by disinfecting it and then reran
19
the calculations to figure out what the
20
effect would be on the whole population.
21
MS. ALEXANDER: Would it not be
22
possible to run separate analyses for the
23
risk on wet weather days and the risk on dry
24
weather days?
65
1
DR. TOLSON: Sure. In fact, we
2
present data that shows that.
3
MS. ALEXANDER: Well, let's turn to
4
Table 5-14 in Exhibit 71.
5
DR. TOLSON: Table 5-14 was actually
6
my exhibit to my testimony.
7
MS. ALEXANDER: Right, right. It's
8
the same thing.
9
DR. TOLSON: Good.
10
MS. ALEXANDER: So that's your overall
11
summary. But let's turn to page -- I'm sorry
12
Table 59.
13
In fact, there you've broken out
14
wet and dry weather estimates --
15
MR. ANDES: We actually have this
16
one -- that one on the chart.
17
MS. ALEXANDER: Okay. Yeah, for wet
18
and dry weather.
19
But it's not broken out in your
20
overall estimate; is that correct?
21
DR. TOLSON: It is not broken out in
22
the overall estimates. We've presented the
23
data in a number of different ways and tried
24
to stratify it.
66
1
Actually that was one of the
2
comments we got from the EPA and we tried to
3
stratify it in the final report in various
4
fashions. The 5.9 exhibit that you show
5
there addresses the question what happens
6
just under dry, what happens just under wet.
7
MS. ALEXANDER: But only for
8
pre-disinfection; correct? The table is
9
headed Total Expected Illnesses For One
10
Thousand Exposures Using Different Estimates
11
and Pathogen Concentrations With No Effluent
12
Disinfection.
13
So this is the before; right?
14
DR. TOLSON: Correct.
15
MS. ALEXANDER: Why don't you have a
16
comparable after table? In other words,
17
total expected illnesses per 1,000 for wet
18
weather and for dry weather? Or did I miss
19
it?
20
MR. TOLSON: Well, if you put the dry
21
weather in there, you can see from 5.9 that
22
the dry weather lists are very low.
23
MS. ALEXANDER: That wasn't my
24
question, though.
67
1
DR. TOLSON: It would go even lower.
2
MS. ALEXANDER: My question is, did
3
you break it out, or did you not?
4
DR. TOLSON: It is not broken out
5
within the report.
6
MS. ALEXANDER: Okay.
7
MS. WILLIAMS: Was it broken out and
8
not put into the report?
9
DR. TOLSON: Quite possibly. We have
10
that data, but it would be, essentially, zero
11
for every one of those.
12
If you dis --
13
MS. ALEXANDER: Based on what? Do you
14
have any data printed to present to support
15
that?
16
DR. TOLSON: Should I go and talk from
17
it?
18
MS. ALEXANDER: Go ahead.
19
DR. TOLSON: All right. So Table 5.9
20
presents a risk for dry weather, wet weather
21
and dry and wet weather.
22
If you look at just the dry
23
weather results, we have fairly low risk
24
within the waterway. One of the other tables
68
1
that we have in our report shows that the
2
disinfection efficiency is quite high, or
3
some -- against some of the pathogens, maybe
4
99 percent.
5
So you would decrease the
6
pathogens within just the dry weather by
7
99 percent. The risk -- corresponding risk
8
would drop very low.
9
That doesn't happen to the wet
10
weather contributions. Those would not be
11
attenuated by the disinfection.
12
So the overall risks that I
13
presented in the other table, would not
14
change so much.
15
MS. ALEXANDER: Just to clarify, by
16
the way, it's your testimony that
17
disinfection would reduce the pathogens and
18
not just the indicators; correct?
19
DR. TOLSON: That's correct.
20
MS. ALEXANDER: By 99 percent,
21
approximately?
22
DR. TOLSON: Well, there's a table in
23
the report that lists each individual
24
pathogen and the full reduction within that.
69
1
It varies by pathogen and by disinfection
2
technique.
3
MS. ALEXANDER: So what you're saying,
4
essentially, is -- correct me if I'm
5
misinterpreting you -- is that for purposes
6
of dry weather, you would, essentially,
7
eliminate, or largely eliminate, the pathogen
8
risk through disinfection; correct?
9
DR. TOLSON: Correct.
10
MS. ALEXANDER: Okay.
11
DR. TOLSON: We've been a little bit
12
naive about the way we constructed that, in
13
that we consider under dry weather there are
14
no other inputs. So if there are pseudomonas
15
inputs from overhanging vegetation or
16
something like that that's contributing to
17
dry weather, we're not including that.
18
We're assuming that under dry
19
weather the effluent from the waste water
20
treatment plants are the sole contributor to
21
the waterway.
22
MS. ALEXANDER: Okay.
23
DR. TOLSON: So that's the assumption
24
there.
70
1
MS. ALEXANDER: So, essentially, would
2
it be fair to say that the disinfection would
3
not have a substantial impact, in terms of
4
your conclusions on wet weather pathogen
5
levels and -- although, you've just testified
6
that dry weather disinfection would
7
substantially eliminate that risk?
8
DR. TOLSON: You would take a very low
9
risk and you would make it a much lower risk.
10
MS. ALEXANDER: So, essentially, what
11
you've done in Table 14 is combine a
12
situation in which the risk is potentially
13
reduced -- I'm sorry -- will be reduced with
14
one in which you say it won't be reduced;
15
correct? You've essentially combined those
16
two sets of data, the wet and the dry
17
weather?
18
DR. TOLSON: We present the data for
19
the wet weather and the dry weather. In
20
order to figure out the effect of the
21
chlorination or other disinfection
22
techniques, there has to be some assumptions
23
made, because we can't do the experiment out
24
of the waterway.
71
1
The assumptions that I made is the
2
dry weather will, just substantially from the
3
wastewater treatment plant, if you knock that
4
down, what's the overall effect.
5
THE HEARING OFFICER: And,
6
Ms. Alexander, Table 5-14 is the one you were
7
referring to; right? You said Table 14.
8
MS. ALEXANDER: I'm sorry.
9
THE HEARING OFFICER: That's okay.
10
MS. ALEXANDER: I meant 5-14.
11
Let me get to the point, which is,
12
leaving aside the absolute numbers for a
13
moment, I know that you're claiming that
14
they're low and our people say they're
15
higher. Leaving that aside, what you have
16
done here in combining the wet and dry
17
weather post-disinfection risk, would that
18
not mean that the change in the level of
19
risk, since that change is higher for dry
20
weather in the case of disinfection than for
21
wet weather, that you are reducing the level
22
of change in risk by combining these?
23
In other words, the delta is going
24
to be lower if you combine wet and dry
72
1
weather than it would be for dry weather
2
alone?
3
DR. TOLSON: The risk for recreators
4
out on the waterway, though, is affected by
5
wet weather conditions and affected by
6
effluent from the wastewater treatment plant.
7
MS. ALEXANDER: But if you're out on
8
the --
9
DR. TOLSON: It's the only way of
10
speculating the risk without considering what
11
the true pathogen concentrations are in the
12
waterway. We developed data that comes from
13
a fairly extensive data set of pathogen
14
concentrations within the waterway to develop
15
our risk.
16
MS. ALEXANDER: But if I'm out there
17
on my canoe on a dry weather day, as you've
18
defined it, not impacted by the wet weather,
19
I'm not going to be impacted one way or the
20
other by these wet weather risk levels; is
21
that correct?
22
DR. TOLSON: Yeah.
23
MS. ALEXANDER: So if you wanted to --
24
DR. TOLSON: Hold on, let me answer
73
1
your question.
2
MS. ALEXANDER: Sorry. Go ahead.
3
DR. TOLSON: Because I want to refer
4
you to one other exhibit, our Table 5.8
5
within Exhibit 71.
6
You'll see that only 15 percent of
7
the days in Chicago is it truly a dry weather
8
day, as we've defined it within the report.
9
So today is not a dry weather day.
10
MS. ALEXANDER: I understand that, and
11
I'll have a few questions for you about that
12
calculation later.
13
But my point is, is it not true
14
that, given that you have combined a
15
situation in which there is a significant
16
change, leaving aside the absolute levels
17
between pre and post, pre-disinfection and
18
post-disinfection, and you've combined that
19
with a situation in which there is really
20
not, according to you, a significant change
21
between wet weather pre-disinfection and wet
22
weather post-disinfection, does that not mean
23
that the -- this change between the two,
24
between pre and post, is going to be lower
74
1
than if you broke out dry weather, the degree
2
of change would be higher; is that correct?
3
DR. TOLSON: If we had calculated
4
risks where we said, only can go out into the
5
waterway three days after it rained and just
6
looked at that, the risks change or the
7
impact of disinfection would be higher.
8
However, it would be very low chance of risk,
9
whether it's disinfection or nondisinfection.
10
MS. ALEXANDER: Okay. That --
11
DR. TOLSON: We're talking about low
12
numbers versus almost zero numbers. Yes, in
13
fact, the magnitude of the change would be
14
different.
15
But that's a very -- a subset of
16
something that doesn't really -- you can't
17
control exposure of that.
18
MS. ALEXANDER: Okay.
19
And the absolute numbers, of
20
course, are something that will be addressed
21
subsequently in this proceeding. This
22
question only went to the delta --
23
DR. TOLSON: Okay.
24
MS. ALEXANDER: -- as it were.
75
1
MR. ETTINGER: Can I ask one question
2
about this chart?
3
DR. TOLSON: Sure.
4
MR. ETTINGER: You say dry weather,
5
and then you've go North Side, Stickney,
6
Calumet. Where are you assuming this
7
exposure takes place?
8
I assume that the level would be
9
higher if I were to capsize my canoe directly
10
outside the outfall than if I did it two
11
miles downstream.
12
DR. TOLSON: Yeah.
13
MR. ETTINGER: What are you doing --
14
how did you work that out?
15
DR. TOLSON: That's a good question.
16
And, unfortunately, the answer is going to be
17
a little long.
18
But we had to make some
19
assumptions about where the use happened
20
within the waterway and the concentrations
21
happened in the waterway. We don't have data
22
that would specifically tie a person to a
23
specific spot within the UAA.
24
So we collected all the data
76
1
within the segment that we defined as North
2
Side. And we said this is the use within the
3
North Side water -- North Side segment.
4
We tied all of the data that we
5
collected from that North Side and pulled
6
those two together to calculate risk. We
7
don't make an assumption that a person is
8
going to be in any one place any more often
9
than any other place.
10
It may be that they're -- you
11
know, next to the outfalls more often than
12
are not. In which case the risk would be
13
biased low.
14
It may be that they're away from
15
the outfalls or -- in which case the risk
16
would be biased high -- under dry weather.
17
But under wet weather we've got inputs all
18
along the waterway.
19
So the relationship between where
20
you're recreating in the outfalls, probably
21
much less significant.
22
MR. ETTINGER: Okay.
23
MS. ALEXANDER: This question is -- it
24
was a Petropoulou question for a -- similar
77
1
to Gerba 17 and 18 and Tolson 8 and 9. But
2
this is specifically for Petropoulou.
3
Regarding the statement at Page 5
4
of your testimony that the risk assessment
5
found that downstream concentrations -- and
6
that's concentrations of pathogens -- are
7
consistently greater than upstream during dry
8
weather, so within -- the context here is dry
9
weather.
10
For purposes of assessing risk,
11
did you, in fact, combine the average
12
upstream and downstream sampling numbers?
13
DR. PETROPOULOU: First, I think your
14
statement mischaracterizes my testimony.
15
MS. ALEXANDER: Okay.
16
DR. PETROPOULOU: On Page 5, I discuss
17
downstream concentrations are consistently
18
greater than the upstream. I am not
19
referring to pathogens there.
20
The discussions for bacteria
21
results that were analyzed with the ANOVA
22
testing. And that was done only for
23
indicator bacteria.
24
So that statement pertains only to
78
1
indicator bacteria.
2
MS. ALEXANDER: Okay.
3
DR. PETROPOULOU: And with respect to
4
your first question, I will let Dr. Tolson
5
explain the integration procedure for the
6
data.
7
DR. TOLSON: So under dry weather we
8
did include all of the data from each
9
waterway segment collectively at each
10
sampling date to put as one of the inputs
11
into our risk assessment. That included
12
upstream and downstream concentrations.
13
We believe that's probably biased
14
high, though, since under dry weather the
15
data was collected in close proximity to the
16
outfall. It didn't account for the fact that
17
very far downstream of the outfall there is
18
probably considerable additional attenuation
19
that is not captured.
20
MS. ALEXANDER: Let me just make sure
21
I understand though.
22
Your pathogen concentration levels
23
that you assumed were ultimately -- correct
24
me if I am wrong -- an average that included
79
1
both upstream and downstream.
2
DR. TOLSON: That is correct. We did
3
not, as Dr. Lanyon put so elegantly
4
yesterday, people can go upstream or
5
downstream. So we don't know where the
6
exposures happened, but we considered they
7
could go in either direction.
8
The exposure was averaged across
9
the entire place where they could actually be
10
exposed.
11
MS. ALEXANDER: Would it be fair to
12
say that the large majority of the CAWS
13
waterway reaches are downstream of one or
14
more of the treatment plants?
15
DR. TOLSON: Yeah, I do not -- we do
16
not have the data to figure out what the
17
attenuation rate is downstream. I believe
18
that it, obviously, goes to the Mississippi
19
eventually.
20
So there's a lot more downstream
21
than there is upstream.
22
MS. ALEXANDER: Do you have any data
23
showing that most people use both the
24
upstream and downstream portions of the CAWS,
80
1
in roughly equal measure, even though there's
2
a lot more downstream than upstream?
3
DR. TOLSON: We do not have data
4
specifically to that.
5
MS. ALEXANDER: Okay.
6
So, in other words, your
7
assumption, if we're talking about an
8
individual as opposed to the overall
9
analysis, would not hold true for someone
10
that put in their canoe or kayak, say, at a
11
location downstream of the treatment plant
12
outfall and continued to paddle downstream;
13
correct?
14
DR. TOLSON: I believe our
15
concentration estimates in the waterway would
16
be conservative for that scenario.
17
MS. ALEXANDER: What's the basis for
18
that statement?
19
DR. TOLSON: Because we incorporated
20
the downstream concentration immediately
21
below the outfall and we included an upstream
22
concentration, which we'll assume to be on
23
the other end. And we assumed a linear
24
concentration gradient as opposed to normal
81
1
downfall.
2
So, most likely, the average or
3
the mean concentration that that canoe or
4
recreator would be exposed to would be less
5
than the average of the upstream and
6
downstream.
7
MS. ALEXANDER: But, in fact, isn't it
8
possible, based on your results, that the
9
upstream concentrations upstream of the
10
outfall and dry weather were lower than the
11
downstream concentrations?
12
DR. TOLSON: For the indicators, it's
13
really the case. For the pathogens, it's
14
really not that clearcut.
15
Maybe I'll let Dr. Petropoulou --
16
DR. PETROPOULOU: Yeah. As I
17
mentioned in my testimony, for example, if we
18
take cryptosporidium, there was no infectious
19
cryptosporidium upstream or downstream. So
20
you're comparing zero to zero.
21
For viruses, we found that there
22
were many instances were there were
23
detectible viruses upstream but not
24
downstream. Or that the upstream
82
1
concentrations were greater than the
2
downstream. And that was true also for dry
3
weather.
4
So that is true for indicators but
5
not really for pathogens.
6
MR. HARLEY: Can I ask a question?
7
MS. ALEXANDER: Sure. Go ahead.
8
MR. HARLEY: I wanted to see if I
9
could integrate the testimony that you gave
10
about pseudomonas with the question of
11
impacts of disinfection, dry weather and wet
12
weather. Now, for pseudomonas, you indicated
13
that you measured pseudomonas concentrations
14
at outfalls of sewage treatment plants; is
15
that correct?
16
DR. TOLSON: That is correct.
17
MR. HARLEY: And you came up with a
18
level of 1,350 colony forming units per
19
milliliter, I believe you said?
20
DR. TOLSON: That is correct.
21
MR. HARLEY: And during wet weather,
22
when you were not measuring specifically at
23
outfalls, you were measuring 54, 27 colony
24
forming units per milliliter.
83
1
DR. TOLSON: Actually, we have outfall
2
data from the wet weather also. And I think
3
that the 1,350 includes a wet weather event
4
outfall data as well as dry weather.
5
MR. HARLEY: Is the outfall number
6
affected at all by whether or not it's dry
7
weather or wet weather, or is it relatively
8
constant?
9
DR. TOLSON: I'll let Dr. Petropoulou
10
answer that.
11
DR. PETROPOULOU: Is the question
12
specifically to pseudomonas?
13
MR. HARLEY: Why don't we start with
14
pseudomonas, if you please.
15
DR. PETROPOULOU: For example, I think
16
it depends on the size. And by size, I mean
17
the treatment plant.
18
At the North Side during dry
19
weather, the concentration of pseudomonas at
20
the outfall was 1,091 CFU per 100 ML. During
21
wet weather it was 796 CFU per 100 ML.
22
So they are different.
23
MR. ANDES: Tables 3-2(a) and 3-2(b).
24
DR. PETROPOULOU: On the report.
84
1
And I can read the other numbers.
2
MR. HARLEY: You don't need to.
3
DR. PETROPOULOU: Okay.
4
MR. HARLEY: I guess my question is,
5
by disinfection, in light of the fact that
6
we're going to be hearing different testimony
7
from different witnesses based on what's been
8
prefiled about risk, but just talking in
9
terms of affect of disinfection on levels of
10
a pathogen, like pseudomonas, if you
11
disinfect, you're actually getting a benefit
12
in terms of risk reduction, both during dry
13
weather periods and during wet weather
14
periods; is that correct?
15
Because during dry weather -- I'm
16
sorry, I should let you answer that question.
17
DR. TOLSON: The marginal risk
18
reduction under wet weather, though, is not
19
nearly as much as it would be under dry
20
weather. So I think that's what we are
21
getting to.
22
For pseudomonas, it's a little
23
more complicated, because there's probably
24
additional sources that have been described.
85
1
MR. HARLEY: I understand. But you
2
would get a benefit on those dry weather days
3
because you would be removing pseudomonas by
4
controlling what is the clearly primary
5
source of pseudomonas on dry weather days,
6
which is effluent from waste water treatment
7
plants; is that correct?
8
DR. TOLSON: I assume it is. The
9
"clearly" I'm not to sure about.
10
It's not clearly the dominant
11
source, we really don't know that. We made
12
the assumption within our risk assessment
13
that the wastewater treatment plants were the
14
only source.
15
And that's just in ease of
16
calculation of our risk estimates, that was
17
the way that we needed to do it.
18
DR. PETROPOULOU: Actually, I would
19
like to add to that. Because we did look --
20
pseudomonas was not frequently detected
21
during dry weather. I believe it was 80
22
percent of the samples that we collected, or
23
73 percent of the samples that we collected
24
that had detectable pseudomonas.
86
1
So we looked through a statistical
2
evaluation using box plugs to see if the
3
concentration of pseudomonas were
4
statistically different upstream, downstream
5
and at the outfall. And I would point out
6
that figures 321, 322 and 323, they present
7
those results.
8
And, basically, the results showed
9
that, for example, at North Side and at
10
Calumet, the median concentration of
11
pseudomonas were identical virtually, or
12
statistically the same between upstream,
13
downstream, at the outfalls. That was not
14
the case at Stickney, where the concentration
15
at the outfall was greater.
16
The median concentration was
17
greater than upstream and downstream. But
18
the upstream and downstream concentrations
19
are the same.
20
MR. HARLEY: Uh-huh.
21
DR. PETROPOULOU: So you cannot really
22
draw a direct conclusion.
23
MR. HARLEY: In wet weather events, if
24
you removed a contribution for any
87
1
pathogen -- by disinfection, that would
2
reduce the total loading of that pathogen
3
during the wet weather event?
4
DR. TOLSON: That's correct. But, as
5
we've shown, it's just not a great
6
contribution.
7
MR. HARLEY: I understand there's
8
going to be a difference in opinion as to the
9
relative contribution --
10
MR. ANDES: He didn't state there was
11
a difference in opinion, he stated -- let him
12
state his opinion.
13
MR. HARLEY: I did.
14
MR. ANDES: No, I think you
15
interrupted.
16
MR. HARLEY: Oh, did I? I'm sorry. I
17
didn't mean to interrupt you.
18
DR. TOLSON: Yes, but the relative
19
magnitude of that is insignificant compared
20
to the wet weather loads.
21
MR. HARLEY: Thank you.
22
THE HEARING OFFICER: On that note,
23
let's take a ten-minute break.
24
(WHEREUPON, a recess was had.)
88
1
THE HEARING OFFICER: Back on the
2
record.
3
Ms. Alexander, we're still with
4
you.
5
MS. ALEXANDER: I'm just going to jump
6
back in subject matter a little bit to
7
something I missed in my earlier thread.
8
Which is the question, did you
9
consider inhalation as a exposure pathway in
10
the risk assessment? Water inhalation.
11
DR. TOLSON: We considered it in terms
12
of trying to figure out what the proportion
13
or potential ingestion component of
14
inhalation may be to the overall dose.
15
MS. ALEXANDER: Explain that. What do
16
you mean the ingestion component of
17
inhalation?
18
DR. TOLSON: When you breathe in air
19
that might have mists and things that can
20
lodge into your mucous membranes in your
21
mouth, in which case you could swallow it.
22
So it's not going into your lungs, but it
23
could be, in fact, ingested.
24
MS. ALEXANDER: Okay. So you did not,
89
1
in fact, take into account, if I'm
2
understanding you correctly, the impact of
3
inhalation -- or I should say, that exposure
4
pathway of inhalation into the lungs, you
5
took it into account if it goes down the
6
other pipe?
7
DR. TOLSON: Right. For a respiratory
8
illness, we did not -- as we discussed
9
previously, we did not consider it.
10
MS. ALEXANDER: Okay. Now, I am
11
turning to Page 4 of -- make sure I
12
understand what it's Page 4 of. One moment.
13
This is Page 4 of the first
14
attachment to the May 23rd letter, which is
15
attached to the May 28th letter of
16
Exhibit 73, Page 4. You'll see in the middle
17
of the page there's a bullet point GI Illness
18
is the Sole End Point of Risk.
19
And then, in the middle of the
20
paragraph that follows, within the first
21
sentence of the paragraph, "This is a major
22
weakness in the risk assessment," there's the
23
statement, "Pseudomonas and adenovirus were
24
found, so the author should have explored the
90
1
inhalation route to properly examine the risk
2
associated with recreating on this water."
3
MR. ANDES: I'm sorry, what page are
4
you on?
5
MS. ALEXANDER: I'm on Page 4 of the
6
first attachment, which is Review Conducted
7
by USEPA Office of Water, Office of Science
8
and Technology.
9
DR. GERBA: The one -- pseudomonas
10
transmission by recreational water and normal
11
healthy people by inhalation route, I
12
wouldn't even consider that. I don't know
13
why that's even here. I think the person is
14
not familiar with it.
15
It does cause lung infections in
16
certain groups of people, but not
17
recreational exposure. I've never heard of
18
that.
19
The -- one of the problems here
20
you have is what's the dose from, the
21
secondary contact-type of exposure we're
22
looking -- what's the amount we should
23
consider being aerosolized by that route?
24
There is no basis to form that type of
91
1
exposure.
2
MS. ALEXANDER: So --
3
DR. GERBA: And no information on how
4
to do that is provided.
5
DR. TOLSON: And I want to point out
6
that these are the -- this is one of the
7
comments that we had discussions with Tim
8
Wade on --
9
DR. GERBA: Yeah.
10
DR. TOLSON: -- at the meeting.
11
MS. ALEXANDER: Can you please, I'm
12
sorry, define -- describe that discussion
13
concerning specifically respiratory?
14
DR. TOLSON: And at that point,
15
there's a consideration that we would not
16
evaluate that quantitatively within our risk
17
assessment.
18
MS. ALEXANDER: You would not evaluate
19
the inhalation pathway?
20
DR. TOLSON: Correct.
21
MS. ALEXANDER: And what was the basis
22
for that determination that you would not
23
evaluate it? Or your reason for the
24
consensus, I should say.
92
1
DR. TOLSON: It was -- one, it was not
2
the most predominant illness associated with
3
the recreational water, that GI illness was a
4
predominant illness. But the other one,
5
being that there's not a mechanism by which
6
to establish the dose or the dose response
7
for these organisms.
8
MS. ALEXANDER: Okay. So, once again,
9
with respect to the inhalation pathway, we're
10
talking about the mechanism being the main
11
concern --
12
MR. ANDES: That's not what he said.
13
MS. ALEXANDER: -- as opposed to the
14
risk.
15
DR. TOLSON: No. I have -- there were
16
two points there that I made, and I think
17
both are important considerations when
18
looking at respiratory illness and associated
19
with recreational contact, as it were.
20
MS. ALEXANDER: Okay.
21
But the bottom line is, you didn't
22
consider inhalation or associated respiratory
23
illness in this analysis?
24
DR. TOLSON: That is correct.
93
1
DR. GERBA: Let me reiterate. That
2
doing pseudomonas, there would be no -- there
3
is no recreational exposure that would result
4
in a respiratory infection for pseudomonas.
5
I don't know why that's in there.
6
DR. TOLSON: And also to follow up,
7
that we did not evaluate that quantitatively,
8
but qualitatively in terms of the proportion
9
of risks, we would --
10
MS. ALEXANDER: This also
11
references -- I'm sorry.
12
DR. TOLSON: That we perceive from the
13
various illnesses, we did consider it that
14
way.
15
MS. ALEXANDER: Referring to
16
Dr. Gerba's statement just now, I believe the
17
text refers to pseudomonas and adenovirus.
18
DR. GERBA: Right.
19
MS. ALEXANDER: Am I correct in
20
understanding that there are strains of
21
adenovirus that carry with them a risk of
22
respiratory infection?
23
DR. GERBA: That is correct. And the
24
only -- and, in fact, by recreational waters.
94
1
But those are all primary contact
2
swimming-type exposures that resulted in
3
those types of infection, not by the
4
inhalation route.
5
MS. MEYERS-GLEN: If somebody flips
6
over in a canoe and is dumped, or in a kayak,
7
and they get a mouthful of water, then that
8
would be an exposure route for them?
9
DR. GERBA: Yeah.
10
MS. ALEXANDER: Bear with me just a
11
moment.
12
Okay. And this is also following
13
up on an earlier discussion, but this was
14
Tolson Question 11, which is -- I want to
15
clarify, regarding the statement at Page 6 of
16
your testimony. If you'll pull that out.
17
Regarding the statement at Page 6
18
that, "Disinfection at the effluent outfall
19
was predicted to result in a decrease in
20
effluent pathogen loads in the water
21
reclamation plants that have little affect on
22
overall pathogen concentrations in the
23
waterway."
24
The question is, does that
95
1
statement concern wet weather conditions?
2
DR. TOLSON: It concerns neither wet
3
nor dry weather conditions. It concerns the
4
combination of wet and dry, which I think we
5
discussed.
6
MS. ALEXANDER: The combination we
7
discussed earlier.
8
DR. TOLSON: Right.
9
MS. ALEXANDER: Would that statement
10
apply -- well, actually, let me rephrase
11
that.
12
I take it, based on your earlier
13
testimony, that that statement would not
14
apply specifically to dry weather conditions;
15
is that correct?
16
DR. TOLSON: Your question is does
17
disinfection affect pathogen loads in the
18
waterway under dry weather?
19
MS. ALEXANDER: Yeah. Your statement
20
is that -- yes, that disinfection of the
21
effluent outfall --
22
MR. ANDES: I'm sorry, you're not
23
talking from Question 11, though; are you?
24
Because that's not the same as Question 11.
96
1
MS. ALEXANDER: Hold on. Let me find
2
Question 11, just to clarify. It is one of
3
the Tolson questions, I may have mismarked it
4
last night.
5
THE HEARING OFFICER: Yeah, the second
6
part of the question at 11 --
7
MR. ANDES: Okay.
8
THE HEARING OFFICER: -- it says it
9
applies specifically to dry weather
10
conditions. She did rephrase it slightly,
11
but...
12
MS. ALEXANDER: Okay.
13
So my question is, you make the
14
statement, Dr. Tolson, "Disinfection of the
15
effluent outfall, to paraphrase, was
16
predicted to result in a decrease in pathogen
17
loads from the water reclamation plants that
18
have little affect on overall pathogen
19
concentrations in the waterway."
20
And my question is, would that
21
statement be true, specifically for dry
22
weather conditions? And I actually
23
characterized it as, am I correct in
24
understanding it would not be true in view of
97
1
your testimony that disinfection would
2
significantly decrease pathogen loads in dry
3
weather conditions, or overall pathogen
4
concentration, I mean?
5
DR. TOLSON: Disinfection under dry
6
weather only conditions would decrease the
7
pathogens that come out of the waste water
8
treatment plant. However, we can't estimate
9
overall illness rates in the waterway without
10
considering all the sources.
11
MS. ALEXANDER: I'm not talking about
12
illness rates.
13
DR. TOLSON: And if you look at the
14
pathogens, they're low to begin with, so...
15
MS. ALEXANDER: My question, actually,
16
Dr. Tolson, was not about illness rates. I'm
17
talking specifically about your testimony on
18
Page 6 that you say, "Disinfection --
19
ellipsis -- would have little effect on
20
overall pathogen concentrations in the
21
waterway."
22
Do you mean that statement to
23
apply to dry weather conditions specifically?
24
MR. TOLSON: I understand what your
98
1
point is. So you're -- no, under dry weather
2
conditions --
3
MS. ALEXANDER: Okay.
4
DR. TOLSON: -- it may be different.
5
I understand where you're coming
6
from now.
7
MS. ALEXANDER: Okay. I'm sorry,
8
that's all I'm asking.
9
And I take it there are no
10
findings in the risk assessment that would
11
support that statement in dry weather
12
conditions; correct?
13
MR. ANDES: He didn't make the
14
statement. What statement are you asking
15
whether it would be supported?
16
MS. ALEXANDER: Okay. He makes the
17
statement here on Page 6 of his testimony
18
that disinfection of the effluent outfall
19
would have little effect on overall pathogen
20
concentrations in the waterway. Now, correct
21
me if I'm mischaracterizing, but Dr. Tolson
22
just said that statement would not hold true
23
for dry weather, only in the wet and combined
24
wet and dry analysis that was done in the
99
1
risk assessment.
2
And I'm following up to confirm
3
that, in fact, there are no findings that
4
support this conclusion that Dr. Tolson is
5
not purporting to make that this statement
6
would apply during dry weather conditions.
7
That's all.
8
DR. TOLSON: The report --
9
MR. ANDES: I don't know if the answer
10
is yes or no.
11
MS. ALEXANDER: Got lost in that?
12
There's nothing in the risk
13
assessment that supports any conclusion this
14
would apply to dry weather; is that correct?
15
DR. TOLSON: I believe you're pointing
16
out that under our Table 5-14 within the risk
17
assessments, we did not do that for dry
18
weather, we did it for the combined.
19
MS. ALEXANDER: Right.
20
DR. TOLSON: Yeah, we talked about
21
that before. That is correct, we did not
22
present risk under dry weather because we
23
believe that the whole intent of the risk
24
assessment was to look at overall risks,
100
1
including dry and wet weather.
2
And the only way to do that was to
3
consider that it rains in Chicago.
4
MS. ALEXANDER: Okay. All right. I
5
think I've covered this.
6
Petropoulou No. 7, regarding the
7
statement at Page 6 of your testimony that
8
dry weather fecal coliform concentrations
9
upstream of the North Side and Stickney
10
plants were greater than the effluent limit
11
of 400 CFU per 100 milliliters proposed by
12
IEPA.
13
What's your understanding of the
14
significance of that comparison that you
15
make?
16
DR. PETROPOULOU: I actually would
17
like to point out that I also follow with
18
the -- another statement following what you
19
just read in my testimony. And it's the same
20
statement for wet weather.
21
And looking at the result in
22
Tables 32(a) and 32(b) and looking at the
23
fecal coliform concentrations, in the dry
24
weather, as I mentioned, at the North Side
101
1
and at Stickney, the concentrations are
2
greater than the proposed effluent limit.
3
And that is also true more so in the wet
4
weather.
5
And I can read, like in the wet
6
weather, for example, at North Side upstream
7
of the outfall, there is 117,000 fecal
8
coliform CFUs for 100 ML downstream. We
9
measured a hundred thousand CFUs for a
10
hundred ML. The outfall concentration is
11
22,000.
12
Similarly at Stickney, you can see
13
that the upstream concentration is 172,000,
14
the downstream concentration is 230,000. And
15
at the outfall we measure 38,000.
16
The importance -- my view of that
17
is IEPA is proposing this effluent limit to
18
protect the users of the waterway, there are
19
probably other sources to look into in
20
addition to the district's effluence.
21
Because they contribute fairly high
22
concentrations of fecal coliform in the
23
waterway.
24
That's the only significance that
102
1
I see.
2
MS. ALEXANDER: All right. Let me
3
jump back.
4
The data you were just reading
5
from, Table 3(b) is wet weather data; is that
6
correct?
7
DR. PETROPOULOU: That is correct,
8
yes.
9
MS. ALEXANDER: Okay.
10
And just to point out, in the dry
11
weather data, it appears, fairly
12
consistently, that when you're looking at
13
fecal coliform indicators, that upstream the
14
levels are orders of magnitude lower than
15
downstream; is that correct?
16
DR. PETROPOULOU: They are great, yes.
17
MS. ALEXANDER: Yes, okay.
18
I want to get back to my original
19
question, because you may have answered it,
20
but I think I may have lost the thread.
21
Which is, at Page 6 of your testimony, you
22
state that the dry weather, as opposed to wet
23
weather, fecal coliform concentrations
24
upstream of the North Side and Stickney
103
1
plants, and we're looking at these numbers,
2
for instance, 713 at North Side and that
3
Table 3-2(a), 1,061 at Stickney -- actually
4
the number at Calumet 170 would be lower than
5
the 400.
6
But you point out that, I would
7
say, that at least the first two are higher
8
than the 400 fecal colony forming units per
9
100 milliliters that's proposed by the IEPA.
10
And my question is, what is the significance
11
of that comparison?
12
Why is it significant in your view
13
or what -- is there a point that you're
14
making in stating that the concentrations
15
upstream are higher than the required
16
effluent limit being proposed by IEPA?
17
DR. PETROPOULOU: And again, my
18
statement -- I know you selected one of the
19
two statements I made.
20
MS. ALEXANDER: Uh-huh.
21
DR. PETROPOULOU: In order for me to
22
make my point, I would like to include both
23
statements. And that is, look together at
24
both the dry and wet weather conditions for
104
1
the waterway. It's the same significance.
2
There are probably other sources
3
of fecal coliform in the waterway than the
4
district's effluence. That's the
5
significance.
6
MS. ALEXANDER: What levels of fecal
7
coliform indicator bacteria are, generally,
8
found in the effluent from these three
9
facilities? And I mean the range, I
10
understand that it varies.
11
MR. ANDES: I think we already -- that
12
question has already been answered by
13
Mr. Lanyon.
14
MS. ALEXANDER: Well, in fact, it was.
15
I mean, I'll phrase the question differently.
16
In fact, didn't those levels range
17
up to 200,000 fecal colony forming units per
18
hundred milliliters? Is that correct?
19
DR. PETROPOULOU: No, that's not
20
consistent with our findings. When we did
21
the study in dry weather, we found
22
concentrations that range from 42,000 to
23
56,000.
24
And during wet weather, actually,
105
1
the district's outfall contributes one-third,
2
or 50 percent less of that, to the waterway.
3
If you look at the outfall
4
concentrations during wet weather -- for
5
example, at North Side, the dry weather
6
concentration in the outfall was 42,000.
7
During wet weather the district contributes
8
22,000 fecal coliform units. That's like
9
50 percent of what they contribute during dry
10
weather.
11
And similar results are observed
12
for the outfall concentration during wet
13
weather at the district outfall.
14
So the concentration we measured,
15
you can say they were from 22,000 to 38,000
16
in the district's outfall during wet weather
17
and between 42,000 and 56,000 during dry
18
weather.
19
MS. ALEXANDER: I think my point is a
20
little more straightforward than that, or I
21
should say my question is. Let's look
22
specifically at dry weather for a moment.
23
And you cited the outfall numbers
24
during dry weather that we're looking at, 42,
106
1
411, 56, 391, 56, 287, just to quote from
2
Table 3-2(a).
3
Isn't it a fact that those outfall
4
numbers, as in what the plant is discharging
5
now during dry weather, are orders of
6
magnitude higher than what it would be
7
discharging under the proposed IEPA standard?
8
DR. PETROPOULOU: That is correct.
9
MS. ALEXANDER: Okay. So, in other
10
words, a limit of 400 colony forming units
11
per 100 milliliters, as proposed by the IEPA,
12
might be less in some cases than ambient
13
background levels, but it would still result
14
in a significant reduction in the loading of
15
at least indicator bacteria in the water
16
body; is that correct?
17
DR. PETROPOULOU: I can't say that.
18
It depends on the weather conditions.
19
MS. ALEXANDER: I'm talking about dry
20
weather now exclusively, I'm sorry.
21
DR. PETROPOULOU: I can't make that
22
statement. Like -- you're talking about
23
significant and loads, I think that can be
24
calculated, I'm just not prepared to offer an
107
1
opinion on that.
2
MS. ALEXANDER: Well, let me reframe
3
my question, because I think it's a little
4
simpler than, perhaps, how you're
5
interpreting it.
6
If right now, say, as North Side,
7
the fecal coliform level coming out of the
8
outfall are around 42,000, would it be fair
9
to say that they'll be significantly reduced
10
if you put a limitation of 400 on it, and
11
then you're going to go to 42,000 to
12
something other than 400; correct?
13
DR. PETROPOULOU: That is correct.
14
MS. ALEXANDER: Okay. That's all I'm
15
getting at.
16
I want to turn to Table 58 for a
17
moment and just briefly revisit these issues
18
having to do with dry and wet weather days.
19
This is, again, in Exhibit 71.
20
All right. I just wanted to
21
clarify, because this wasn't obvious to me.
22
And that where I'm getting this from is it's
23
Tolson Question 11 and Gerba Question 20.
24
I had framed the question as
108
1
"Describe how you arrived at these numbers."
2
I think there's already been some description
3
of that. So I'm just going to ask a few
4
follow-up questions on that.
5
Was there any overlap between days
6
that were counted as wet weather and days
7
that were counted as post-wet weather? If
8
that question make sense. I can rephrase it
9
if it doesn't.
10
DR. TOLSON: My answer is it's fairly
11
obvious the day after certainly has a
12
relationship to it.
13
MR. ANDES: Are you asking if there's
14
double counting?
15
MS. ALEXANDER: Well, let me ask it --
16
I just want to make sure I understand.
17
Let's say it rained on seven
18
consecutive days. How many of these post-wet
19
weather days would you assume? Would that,
20
then, be seven wet weather days and three
21
post-wet weather days?
22
DR. TOLSON: We didn't fall into that
23
era. We actually took the meteorological
24
data from the year and put it all out and
109
1
figured out how many multi-day bouts of rain
2
we had, and then used the other intervening
3
days where it was dry and calculated those
4
intermediate weather days.
5
MS. WILLIAMS: When you say
6
"meteorological data," can you elaborate a
7
little bit?
8
DR. TOLSON: Yes, we collected -- we
9
asked the district for their rain gauge data,
10
and we used that for the basis of our
11
establishing wet weather days within the 2006
12
recreational season.
13
MS. WILLIAMS: And what if you had
14
rain at one gauge and not at another?
15
DR. TOLSON: The way we did that is we
16
took -- I'm trying to recall exactly how we
17
sorted this out.
18
I believe we had a weather
19
station -- two weather stations, and we
20
actually looked at the analysis for the North
21
Shore and then we looked at the analysis for
22
the Stickney and Calumet together. We tried
23
to account for that within our assessment.
24
But, essentially, it was the same
110
1
way. We looked at all the meteorological
2
data and did not double count days. We took
3
into account if it rained for four days in a
4
row, those each were rain days.
5
And then the days after that were
6
the intervening days. And then days were --
7
had a three-day antecedent period.
8
MS. WILLIAMS: But did it have to rain
9
in the area where the sample was taken to
10
have a rain day? I'm still not sure I'm
11
following.
12
If you only recorded rain at the
13
North Side plant, was it considered a rain
14
day at Stickney for your sampling at
15
Stickney?
16
DR. TOLSON: We had to average out the
17
meteorological data between the different
18
weather stations we had. What we found was
19
that about 40 percent of the days were rain
20
days or CSO days.
21
Thirty percent, stationwide, were
22
the day after it rained, 15 percent were two
23
days after and 15 percent were kind of, at
24
least, two days of dry weather before that
111
1
day. So it's a generalization for the entire
2
Chicago basin, it took into account district
3
weather data.
4
MS. WILLIAMS: I'm not sure I
5
understand, but I think you answered my
6
question.
7
We can go back to Ms. Alexander.
8
DR. TOLSON: Okay.
9
MS. ALEXANDER: Okay. This is Tolson
10
Question No. 13. And there is a question to
11
Dr. Gerba, Question 21, which is,
12
essentially, the same. But regarding
13
Tolson's testimony, the statement at Page 5
14
that "The UAA study was a primary source for
15
exposure use data in the CAWS."
16
The question is, is it possible,
17
in your view, that a water body that was
18
perceived by the public or known to be
19
cleaner than the CAWS, such as, for instance,
20
Lake Michigan, might receive heavier use for
21
activities involving substantial body contact
22
with water? In other words, are people more
23
likely to go kayaking and canoeing in the
24
clean water bodies than one believed to be
112
1
contaminated?
2
MR. ANDES: Are we at -- let me settle
3
that. But I think we could clarify.
4
Are you talking about water bodies
5
that are simply perceived as cleaner or are
6
actually cleaner? What's heavier use? Does
7
that mean more people, does that mean
8
different types of use?
9
I mean, what substantial body
10
contact with water? Those are all -- I'm not
11
sure what any of those phrases mean.
12
MS. ALEXANDER: I'm going to break
13
this down a little bit.
14
First of all, I am talking
15
about -- I mean, I'll say known to be cleaner
16
in the sense that there's publicly available
17
data out there that there is more
18
contamination in one water body than the
19
people who use the water may be aware of it.
20
It's sort of the criterion and the difference
21
I'm talking about.
22
And the question is -- I mean,
23
I'll first ask the basic question. Would you
24
agree that people are probably -- you know,
113
1
maybe more likely, potentially, to engage in
2
incidental contact-type activities, like
3
canoeing and kayaking in the water body known
4
to be cleaner?
5
DR. TOLSON: You're venturing way off
6
into speculation.
7
MS. ALEXANDER: I understand that's
8
not -- let me move on a little bit.
9
DR. TOLSON: Yeah, sorry.
10
MS. ALEXANDER: Did you take in
11
account in any way in this risk assessment
12
the possibility that people might be more
13
willing to conduct themselves in the context
14
of their water activity, such as canoeing and
15
kayaking, in such a way as to increase their
16
bodily contact if they believe the water to
17
be clean, clean? And let me just sort of
18
clarify what I mean by that.
19
Were they -- for instance, did you
20
take into account the possibility that people
21
might be more willing to roll their kiak on
22
Lake Michigan than in the CAWS?
23
DR. TOLSON: No, ma'am, we did not
24
make any assumptions to that rolling.
114
1
MS. ALEXANDER: Or, for instance, the
2
possibility that they might be more likely to
3
jump off their motorboat and go swimming on a
4
hot day in Lake Michigan than in the CAWS;
5
did you consider that?
6
DR. TOLSON: All those questions are
7
really outside of the scope of our study.
8
MS. ALEXANDER: Okay.
9
DR. TOLSON: And I can't really
10
evaluate them.
11
MS. ALEXANDER: I get it. You didn't
12
consider any of that.
13
This is Tolson Question 14 and
14
Gerba Question 22. Is it your understanding
15
that water born pathogen levels can vary with
16
the degree of sunlight on the water, given
17
that sunlight kills pathogens?
18
DR. GERBA: I think that question is
19
misstated. You have pathogen levels, and I
20
think you mean pathogen survival.
21
Because pathogen levels are
22
independent to sunlight.
23
MS. ALEXANDER: So, in other words,
24
you're including activated and deactivated
115
1
pathogens --
2
DR. GERBA: Right. Sunlight is one
3
that does influence particularly the survival
4
of bacteria in water. Not so much viruses.
5
Particularly like adenoviruses,
6
which are more resistant to UV light, which
7
is really the primary component in sunlight,
8
that inactivates microorganisms.
9
Do you want me continue answering
10
the rest of those?
11
MS. ALEXANDER: Yeah. You can go
12
ahead and answer with that clarification.
13
DR. GERBA: Again, the issue is
14
survival with the turbidity of the water.
15
Generally, the more turbid the water, the
16
longer organisms -- water born pathogens, I
17
should say, as stated here, survive in water.
18
And with temperature -- generally, the warmer
19
the temperature and more rapid the organisms
20
get inactivated, in this case, organisms
21
meaning water born pathogens.
22
MS. ALEXANDER: Did your risk
23
assessment account for these variables in any
24
way?
116
1
DR. TOLSON: We actually measure the
2
concentrations in the waterway, and that was
3
the basis for the risk assessment.
4
MS. ALEXANDER: But in determining
5
what -- for instance what days you were going
6
to measure or how you were going to weight
7
the sampling on any given day, you didn't
8
take into account, for instance, whether
9
there was sunlight on the water at the time
10
or whether the water was turbid? You took
11
the samples but you didn't weight those
12
factors, in other words; is that correct?
13
DR. TOLSON: Correct. Let me think
14
about this for a second and see whether that
15
somehow could have biased it high or low.
16
I really -- I can't tell
17
whether -- how not accounting for that would
18
have affected the results. But I don't think
19
it would have affected to a great extent.
20
DR. GERBA: Well, certainly not for
21
adenovirus, because we didn't measure whether
22
they were dead or alive. I would say the
23
turbidity would have a lot to inhibit the
24
effect of sunlight.
117
1
And I don't think the temperatures
2
were really that warm compared to other
3
bodies of water I studied. I don't think
4
either of those, probably in the time span
5
from the outfall that we looked at, would
6
have much of a major influence, certainly for
7
the viruses that are much more resilient and
8
survive better in the water.
9
So I don't think those would be
10
major factors, certainly, for the viruses.
11
MS. ALEXANDER: But temperature,
12
turbidity and sunlight, presumably, vary from
13
day-to-day; is that correct?
14
DR. GERBA: Yeah, that's right. As
15
far as I'm concerned, this place is a cold
16
place compared to Arizona.
17
MS. ALEXANDER: I'm not going to argue
18
with that. Just one second.
19
MS. WILLIAMS: I feel like I want to
20
ask a follow-up, but I'm not sure. I mean,
21
did you look at the temperatures throughout
22
the system?
23
DR. TOLSON: I don't -- actually --
24
MS. WILLIAMS: I mean, you're not -- I
118
1
guess when you make that last statement,
2
you're not taking into account the power
3
generation facility on this waterway; are
4
you?
5
DR. GERBA: Temperatures were measured
6
by the district, but that's all I can say.
7
DR. TOLSON: We measure the pathogen
8
concentrations at the time that we collected
9
those samples. And those represented what we
10
considered to be the concentrations over that
11
day for which that weather type that we
12
measured them on.
13
So if it was a rainy day and we
14
collected rain samples during that day, that
15
concentration we measured was what we
16
assumed.
17
MS. WILLIAMS: I guess I'm just still
18
reacting to the idea that you said that --
19
the rest of us sort of haven't been at the
20
earlier hearings -- that you felt this was a
21
cold system. Compared to what?
22
DR. GERBA: Compared to like Florida.
23
I think Dr. Joan Gross, for example, looked
24
at die-off of clean surface waters, eventual
119
1
viruses.
2
In there we had really clear
3
waters, low turbidity and higher temperatures
4
than you have here. You get more rapid
5
die-off of like enteroviruses in the water.
6
When you get the cooler --
7
MS. WILLIAMS: You're talking about
8
the air temperature --
9
DR. GERBA: Right.
10
MS. WILLIAMS: Not necessarily the
11
water temperature?
12
DR. GERBA: Exactly.
13
No, water. I'm talking water, not
14
air.
15
MS. WILLIAMS: So you're talking about
16
water --
17
DR. GERBA: Usually the water
18
temperatures are related to the ambient air
19
temperatures.
20
MS. WILLIAMS: And did you look at
21
whether that's the case here?
22
DR. GERBA: What the temperatures were
23
you mean?
24
MS. WILLIAMS: Whether there's a
120
1
natural relationship between the air
2
temperature and the water temperature here,
3
in this system?
4
DR. GERBA: It would be an unusual
5
place that didn't, that's all I can say.
6
MS. WILLIAMS: Is it --
7
DR. GERBA: I correlated that.
8
MS. WILLIAMS: Is it an unusual
9
situation to have 70 percent of the flow
10
coming from a water treatment plant?
11
DR. GERBA: I've seen more, but that's
12
a lot of -- I mean, 70 percent, I've seen
13
100 percent before. So it varies.
14
MS. WILLIAMS: Is it usual to have a
15
system with five power generating facilities
16
located in this proximity?
17
DR. GERBA: I can't comment on that.
18
MS. WILLIAMS: I just want to make
19
sure that wasn't part of your -- what went
20
into your statement.
21
DR. GERBA: Oh, no.
22
MS. WILLIAMS: I'm done.
23
DR. GERBA: Those are factors that
24
influence -- I'd have to know the actual
121
1
numbers and degree to tell you how much it
2
might influence it.
3
MS. ALEXANDER: All right. This is
4
Tolson Question 15 and then Gerba
5
Question 23.
6
What was the basis for using dose
7
response data for echovirus as a surrogate
8
for this dose response behavior for
9
adenovirus?
10
DR. GERBA: Excuse me just one second.
11
Let me just say, we use a dose
12
response data for echoviruses, largely
13
because that represents a virus transmitted
14
by the enteric route. Dose response data for
15
that was based on ingestion.
16
And, of course, some of the entero
17
adenoviruses are transmitted by the ingestion
18
route. So we wanted to use a dose response
19
model that included ingestion. There wasn't
20
one available for adenoviruses.
21
The only one for adenovirus
22
available was inhalation. So that was the
23
reason we used it.
24
MS. ALEXANDER: Are you saying there
122
1
is dose response data connected with
2
inhalation of adenovirus?
3
DR. GERBA: Yes.
4
MS. ALEXANDER: Given that fact, why
5
could you not have also done the complete
6
risk analysis of risk of respiratory
7
inhalation-based illness from adenovirus?
8
MR. ANDES: He already explained why
9
he didn't do that analysis.
10
Go ahead and answer.
11
MS. ALEXANDER: Is your answer the
12
reason you gave before -- well, you gave a
13
two-part answer. And one of them was that
14
you believe GI illness is, essentially, the
15
predominant recreation-associated illness.
16
But the other part of the answer that you
17
consistently gave is that there's no dose
18
response data for these types of illnesses.
19
But we have one here for which, in
20
fact, there is dose response data. And my
21
question is, is there a reason you could not
22
have done that analysis, given there is dose
23
response data?
24
DR. GERBA: There was two organisms in
123
1
my last response, there was pseudomonas
2
aeruginosa, there was no --
3
MS. ALEXANDER: Right. I understand
4
that.
5
DR. GERBA: For adenoviruses, there
6
was -- the thing I said was that there was no
7
data to estimate what the aerosol exposure
8
would be from secondary contact recreation.
9
MS. ALEXANDER: Okay. So you did have
10
a dose response, but you didn't have the
11
aerosol inhalation data; is what you're
12
saying?
13
DR. GERBA: That's correct.
14
MS. ALEXANDER: Okay.
15
All right. This is referring to
16
what were Tolson Questions 16 and Gerba 24.
17
I'll represent it was a series of questions
18
concerning the EPA ICR manual and procedures
19
for disinfecting equipment.
20
I'm going to be modifying these
21
questions, based on a document that I was
22
handed yesterday, which I apologize, but I
23
neglected to make copies of in my haste. But
24
it is a letter dated September 5th, 2008 from
124
1
Marsha -- to Marsha Willhite from Coleus,
2
transmitting a letter from Geosyntec
3
Consultants dated August 22nd, 2008 to Thomas
4
Granato of MWRD from Dr. Petropoulou.
5
And then, attached to
6
Dr. Petropoulou's letter is an errata sheet
7
for the risk assessment, which includes some
8
information about Tolson 16 and Gerba 24.
9
So --
10
THE HEARING OFFICER: Ms. Alexander,
11
is that not Exhibit 59?
12
MS. ALEXANDER: Oh, is that -- I'm
13
sorry. That's been introduced?
14
THE HEARING OFFICER: I believe so, if
15
it talks about the same letter, yes.
16
MS. ALEXANDER: Never mind then.
17
We're talking about Exhibit 59. I apologize
18
for the excess words.
19
So I'm going to be asking you some
20
questions about that. And you guys have it
21
over there, I assume.
22
Am I correct in my understanding
23
that the EPA ICR manual for disinfecting
24
equipment to be used for virus sampling
125
1
requires that the concentration of chlorine
2
to be used to disinfect is .1 percent, and
3
that after chlorination the chlorine needs to
4
be neutralized with sodium biosulphate; is
5
that correct?
6
DR. GERBA: That's right.
7
MS. ALEXANDER: Okay.
8
Now, in the draft -- I shouldn't
9
say draft -- in the final of the risk
10
assessment that was appended to various
11
witnesses' testimony from the district and
12
published on the district's website, it was
13
indicated --
14
THE HEARING OFFICER: Excuse me, which
15
is Exhibit 71?
16
MS. ALEXANDER: Exhibit 71. I'm
17
sorry.
18
THE HEARING OFFICER: Okay. For the
19
record, it's better if we --
20
MS. ALEXANDER: I apologize.
21
THE HEARING OFFICER: That's okay.
22
MS. ALEXANDER: It was indicated at
23
Page 16 of Exhibit 71 that, essentially, this
24
procedure was not followed; is that correct?
126
1
DR. PETROPOULOU: No, that is not
2
correct. We had a typographical error with
3
respect to the concentration of the bleach
4
that we used for the disinfection.
5
In our sampling and quality
6
assurance plans, both for the dry and wet
7
weather, we specified the correct cleaning
8
and sterilization method for the equipment,
9
that's what the district followed. We have
10
made the correction in this errata sheet for
11
that.
12
That was the purpose of this
13
errata sheet.
14
THE HEARING OFFICER: The errata sheet
15
attached to Exhibit 59?
16
DR. PETROPOULOU: Correct.
17
MS. ALEXANDER: Okay. So you
18
characterize the change from the .1 percent
19
solution -- I'm sorry, the .5 percent.
20
The .1 percent is a typographical
21
error; is that correct?
22
DR. PETROPOULOU: That's correct.
23
MS. ALEXANDER: Are the other changes
24
also corrections, in your view, of
127
1
typographical errors?
2
DR. PETROPOULOU: No, they are not.
3
We have omitted to include how we
4
dechlorinated the equipment, and we have
5
added that for clarification.
6
I believe it was Dr. Yates. She
7
raised that as an issue in her testimony.
8
So it brought it to our attention
9
that we should include that in the report
10
just to make sure there's no confusion about
11
it.
12
MS. ALEXANDER: Do you have any lab
13
records that are reflecting specifically this
14
information that you, in fact, dechlorinated
15
the equipment?
16
DR. PETROPOULOU: I believe Dr. Ishal
17
from the district that was overseeing the
18
lab, she has instructions to the lab that
19
include an excerpt of our sampling and
20
analysis plan. And there were instructions
21
to the sampling staff on the boat that
22
included information of how to disinfect
23
equipment.
24
And Dr. Gerba and myself, who were
128
1
on the boat, we did the sampling during the
2
first week. So I know that that's -- it was
3
done properly.
4
MS. ALEXANDER: And just to refer to
5
Item 1 on the errata sheet attached to
6
Exhibit 59, you replace the reference to
7
blue-green monkey kidney with buffalo green
8
monkey kidney.
9
Am I correct in understanding that
10
there is, in fact, no such thing as a
11
blue-green monkey or its kidney?
12
DR. GERBA: No.
13
MS. ALEXANDER: Okay. So that's not
14
any kind of cell culture line. The only cell
15
culture line is buffalo green monkey kidneys
16
used in this analysis.
17
Now, I'm turning next to Tolson
18
Question 17 and Gerba Question 25. I just
19
want to state, as an initial matter, that
20
these questions all characterize them as
21
having to do with sample size and proportion
22
of the sample evaluated.
23
There was an indication in
24
prefiled questions given to Dr. Yates that
129
1
this information is available in appendices
2
to the risk assessment. We were not provided
3
with those appendices until I saw those
4
questions and requested the appendices from
5
Mr. Andes. I have just been provided them.
6
I have not had the opportunity
7
either to completely review those or to
8
discuss them were my expert. I do not know
9
whether any of that will be a problem. I
10
simply state that as a caveat on the record,
11
that that's an issue that might come up at
12
some point down the road.
13
It is possible that some of my
14
fact or clarification questions may be
15
answerable by reference to that data. But we
16
can just proceed and see how that works out.
17
MS. WILLIAMS: Can you just clarify
18
for us, so the rest of us don't have them
19
either, that it's not part of Exhibit 71?
20
MS. ALEXANDER: It's not currently
21
part of Exhibit 71. I -- and I was not
22
planning or referring in my question
23
specifically to that data to the extent the
24
witnesses refer to that information in their
130
1
answers, we may need to admit it into the
2
record and mark it as an exhibit.
3
MR. ANDES: Appendices A, B, C and D
4
to the report, I believe A and B I provided
5
last week.
6
MS. ALEXANDER: Correct.
7
MR. ANDES: I've now provided A, B, C
8
and D. If the Agency wants the whole
9
enormous amount of information on a disk, I
10
have another copy and I can provide that, as
11
well. As soon as I find it under this paper.
12
MS. WILLIAMS: Well, first, I just
13
wanted to understand what was in the record
14
and what's not. So we're clear, then, that
15
there's four appendices and two are in the
16
record and two or not; is that correct?
17
THE HEARING OFFICER: No, none of them
18
are.
19
MS. WILLIAMS: None of them are.
20
MS. ALEXANDER: There's an
21
Attachment A that is part of the Exhibit 71
22
that is in the record, but there are no
23
appendices in the record?
24
MR. ANDES: There are Appendices A, B,
131
1
C and D.
2
MS. WILLIAMS: It seem like that's
3
something that after the hearing we can have
4
supplemented by you guys?
5
MR. ANDES: That would be fine.
6
THE HEARING OFFICER: Yes.
7
MR. ANDES: That is beyond the 350
8
pages of the report.
9
MS. WILLIAMS: Which was submitted
10
like four times; right?
11
MR. ANDES: Yes.
12
THE HEARING OFFICER: We only need it
13
onces this time.
14
MS. ALEXANDER: Referring back to
15
those questions, Tolson 17 and Gerba 25, the
16
general question I have is, how large were
17
the samples that you collected for virus
18
analysis?
19
DR. GERBA: Near the -- by the
20
outfall, 100 liters, and away from the
21
outfall 300 liters.
22
MS. ALEXANDER: Okay.
23
THE HEARING OFFICER: I'm sorry?
24
DR. GERBA: One hundred liters by the
132
1
outfall, and then 300 liters away from the
2
outfall.
3
THE HEARING OFFICER: A train went by
4
as you finished your question, so I couldn't
5
hear it.
6
DR. GERBA: To give you a perspective,
7
that's -- 100 liters, basically, is about 25
8
gallons. And about 75 gallons is about 300
9
liters, to give you a rough idea.
10
MS. ALEXANDER: And what volume from
11
these samples are, typically, analyzed for
12
each of the viruses?
13
DR. GERBA: If it was divided up
14
about -- basically -- I don't know. Do you
15
have the actual ratio?
16
It's in the SOP, but I don't
17
remember off the top of my head. I couldn't
18
give you it right off the top of my head.
19
MS. ALEXANDER: Can you give me an
20
approximation?
21
DR. GERBA: Well -- I tried to do at
22
least 100 liters for each virus, when it was
23
feasible to do that. For the Norovirus, it
24
was not feasible, because of the analytical
133
1
method limits, you only need a few hundred
2
microliters of a concentrate.
3
But we tried to do 100 liters for
4
each of the virus groups for -- away from the
5
outfall, and about 30 liters for each virus
6
at the outfall.
7
MS. ALEXANDER: One second here.
8
I have in my notes -- and I
9
haven't quite found the table yet -- that the
10
typical volume of the sample analyzed for
11
calcivirus was around .2 liters; is that
12
correct?
13
DR. GERBA: It varied from sample to
14
sample, something like two liters.
15
MS. ALEXANDER: It was about that
16
would you say?
17
DR. GERBA: Yeah.
18
MS. ALEXANDER: And if no viruses were
19
detected in that .2 liter sample out of the
20
entire sample, would that have been 100 to
21
300 --
22
DR. GERBA: I'm just saying that
23
without having looked at it. So I'm not
24
quite sure.
134
1
MR. ANDES: Let's not make a statement
2
without looking. Let's go back, because I
3
heard two and I heard .2.
4
DR. GERBA: Yeah, I'd have to look at
5
the exact equivalent volume. I'm not sure if
6
you're giving me the volumes on concentrate
7
assay or the equivalent volume of that
8
concentrated to the water sample that was
9
collected.
10
MS. ALEXANDER: All right. I found
11
that reference.
12
If you turn to Table 3-7, which is
13
Table 3-7 in Exhibit 71, Dry Weather
14
norovirus, paren, (calcivirus results).
15
And then you'll see there is a
16
column in that Equivalent Volume Assay in
17
Liters.
18
DR. GERBA: Right. Right. That's
19
right.
20
MS. ALEXANDER: And you see that it
21
varies. But would I be fair in
22
characterizing that as it all falls out to in
23
the vicinity of .2 liters?
24
DR. GERBA: Yeah, about 200
135
1
milliliters, you're correct.
2
MS. ALEXANDER: All right. And that's
3
out of the entire sample that was drawn,
4
which, as I understand it, would have ranged
5
from 100 to 300 liters?
6
DR. GERBA: I'm sorry, this is --
7
yeah, the equivalent volume of the
8
concentrate, that was actually analyzed by
9
the PCR method. The PCR method has very
10
limited volume that can be assayed, where --
11
compared to, you know, the method of the
12
other two viruses, almost the entire sample
13
was assayed in 100 liter volume.
14
It's just the analytical method
15
here for norovirus is limited to apparently a
16
small sample. But still we are able to
17
protect the virus, particularly during
18
rainfall.
19
MS. ALEXANDER: Okay. But you were
20
only -- in fact, if you only tested, assayed,
21
the .2 liters out of your 100 to 300 liter
22
samples, you wouldn't actually know what was
23
in the other 99.8 percent of the sample
24
because you didn't test it; is that correct?
136
1
DR. GERBA: Right. Let me make sure I
2
understand.
3
There's concentrations that would
4
take 300 liters and you reduce it to 20
5
milliliters.
6
MS. ALEXANDER: Right.
7
DR. GERBA: Is what goes on here. And
8
then you're expanding backwards to that.
9
And usually your assay maybe
10
10 MLs for the adenovirus and ten MLs for
11
what we call the total cultural virus. And
12
then usually several microliters for this.
13
It's important here that this is
14
240 milliliters, by the way, which I hope is
15
a volume nobody ever swallows in the water.
16
The reason for the larger volumes for the
17
other viruses is because they're in such low
18
levels.
19
So, in reality, in terms of what
20
somebody might swallow, the smallest volume
21
that was assayed here was about 100
22
milliliters and the largest was about 410
23
milliliters. So those are relatively what
24
somebody might have actually swallow.
137
1
Even in contact recreation, it
2
would be greater, though, with respect to
3
swallowing.
4
MS. ALEXANDER: The question I'm
5
asking is you did not, in fact, test the
6
entire sample you took in the case of
7
calcivirus; is that correct?
8
DR. GERBA: Oh, no, it was impossible
9
to do that.
10
MS. ALEXANDER: Right. And, in fact,
11
you didn't really test anything close to the
12
entire sample?
13
DR. GERBA: No, it was impossible to
14
do that.
15
MS. ALEXANDER: Okay.
16
DR. GERBA: Not with that analytical
17
method.
18
MS. ALEXANDER: Okay.
19
Tolson Question 18 and Gerba
20
Question 26, what primers were used for the
21
calcivirus analysis?
22
DR. GERBA: Those were primers that
23
were developed by Jan Vanay, now with the
24
Centers For Disease Control and Prevention.
138
1
We used these primers to investigate more
2
than 20 outbreaks of noroviruses in the last
3
several years.
4
So we know they were fairly
5
effective in picking up all the norovirus
6
types that were causing outbreaks, certainly
7
on cruise ships and outbreaks in the
8
United States.
9
MS. ALEXANDER: Specifically on which
10
calciviruses are detected --
11
DR. GERBA: With norovirus -- the
12
human norovirus.
13
MS. ALEXANDER: Okay. Just the human
14
norovirus?
15
DR. GERBA: Uh-huh.
16
MS. ALEXANDER: Okay. Tolson 20 and
17
Gerba 28, can you describe the method that
18
was used to analyze the samples of -- I'm
19
sorry -- for adenovirus?
20
DR. GERBA: That's in the SOP, but,
21
basically, what you do is, again, you take
22
part of the concentrate and we put it on a
23
specific cell line to which adenoviruses are
24
known to be sensitive to. The BGM cell line,
139
1
adenoviruses are not sensitive to -- they
2
don't produce cytopathogenic effects.
3
But in the cell line we use, they
4
do produce cytopathogenic effects. We expose
5
those to cells for 14 days and then we take
6
the negative samples and expose those to the
7
cells for another 14 days, for a total of 28
8
days. And those cell lines show a
9
cytopathogenic effects.
10
We use primers against the human
11
adenoviruses to confirm there was human
12
adenoviruses that we detected. Some human
13
enteroviruses grow on the cell lines, too.
14
So there was a need to confirm that they were
15
adenoviruses.
16
The cell lines that we use will
17
grow adenovirus, most of the adenoviruses, 40
18
and 41, which are the ones that cause
19
gastroenteritis 2, 4, and 7 and several
20
others. But we've been using these to grow
21
various adenovirus serotypes in our
22
laboratory for several years.
23
And we've used -- I should say --
24
the same procedure for detecting adenoviruses
140
1
and other studies on water -- waste water
2
discharges, which have been published in peer
3
reviewed scientific literature.
4
MS. ALEXANDER: I'm sorry, I think you
5
just answered this question and I lost the
6
thread. But my sub-A on that was, which
7
specific serotypes of adenovirus are detected
8
using the BGM cell line that you used? Could
9
you list those for me?
10
DR. GERBA: We use the -- actually,
11
PLC5 cell lines for --
12
MS. ALEXANDER: Oh, PLC5, okay.
13
DR. GERBA: -- the adenoviruses.
14
Because they don't produce cytopathogenic
15
effects in the buffalo green monkey cell
16
line.
17
In this cell line we'll grow 40, *
18
41, 2, 7 and 4, to my knowledge, and probably
19
several of the other types of it. The
20
primers would detect, basically, any of the
21
human adenoviruses.
22
MR. ANDES: In follow-up, do you
23
consider these to be a conservative approach?
24
And, if so, how?
141
1
DR. GERBA: Yeah, I consider -- well,
2
the whole idea of putting adenoviruses in
3
here was a conservative approach. Even
4
though there was no approved EPA method for
5
adenoviruses, the literatures indicate
6
adenovirus were the most abundant viruses in
7
sewage discharges. So we felt we would be
8
neglecting the most abundant virus that could
9
be current in sewage, and that's why this
10
part of the study actually was done.
11
And then we wanted to confirm for
12
sure that it was adenovirus that we detected,
13
that's why we used the primers when we did
14
it. Because we were trying to be
15
conservative here and trying to estimate the
16
greatest number of viruses that would be
17
present in the sewage and in the waterway.
18
So that's why we felt it essential
19
to include the adenoviruses in here. And, as
20
you saw from the results of the study,
21
adenoviruses were in far more abundance than
22
the enterovirus.
23
And if we just used the EPA manual
24
for the total culturable virus, we would have
142
1
missed almost the majority of the viruses we
2
actually detected in the waterway. So I
3
think that premise actually paid out in this
4
study.
5
MS. ALEXANDER: I just -- I'm going to
6
need to ask some follow-up on that for
7
clarification.
8
Did you say that all serotypes of
9
adenovirus are detected using the PCR -- the
10
primers used for PCR analysis?
11
DR. GERBA: All the major human
12
enteroviruses, yeah.
13
MS. ALEXANDER: When you say all the
14
major human enteroviruses...
15
DR. GERBA: I said that, because I
16
don't know if every human -- I'm sorry --
17
adenovirus has ever been tested against this
18
set of primers. I don't know that for
19
certain.
20
MS. ALEXANDER: Okay. So the PCR
21
analysis would have detected the ones you've
22
listed, 5 40, 41, 2, 7 and 4?
23
DR. GERBA: Right.
24
Some of those have been associated
143
1
with water born diseases, too. You know,
2
recreational water, that's why we...
3
MS. ALEXANDER: There are, in fact, 51
4
different types of adenoviruses; correct?
5
DR. GERBA: Well, actually, there's
6
a -- there may actually be 52. Some people
7
are pushing another one, so -- I should point
8
out too, not all the adenoviruses have been
9
clearly associated with disease in humans, by
10
the way, too.
11
Although, they've been found in
12
human fluids and stools and infected with
13
some people, we're not -- we're still not
14
certain whether it involved and caused any
15
type of particular disease in humans beings.
16
MS. ALEXANDER: Now, if I'm
17
understanding you correctly, the PCR analysis
18
that you used for the confirmation, detected
19
more stains of adenovirus than the cell
20
culture analysis; is that correct?
21
DR. GERBA: No, the -- in this case,
22
we used PCR to confirm the presence of
23
adenovirus growing in the cell culture. We
24
only detected viable adenoviruses in this
144
1
study.
2
The PCR here was done on the cell
3
culture as an identification step that we
4
were finding adenovirus. For the norovirus,
5
it was -- we need to not determine viability.
6
We just determined the concentration of the
7
adeno -- norovirus genome in that case.
8
MS. ALEXANDER: Can you just clarify
9
what it means when you say that you
10
confirmed, then, using the PCR analysis? You
11
did the cell culture, you identified the
12
sample as testing either positive or negative
13
through the cell culture for those specific
14
serotypes you identified; correct?
15
DR. GERBA: Right. What happened with
16
the cell culture -- enteroviruses also have
17
the capability of growing in the same culture
18
we use to isolate adenoviruses. So we wanted
19
to make sure we had an adequate number on the
20
number of adenovirus growing in the cell
21
culture.
22
If you look at the raw data, not
23
all samples confirmed as adenoviruses, which
24
were probably -- and some of these were
145
1
probably enteroviruses growing in the cell
2
culture.
3
MS. ALEXANDER: Okay. So let's say
4
you tested the sample, were using the cell
5
culture and it was positive, but you did the
6
PCR analysis and it was negative. That would
7
suggest that what was growing there might
8
have -- was probably, or perhaps,
9
enteroviruses rather than adenoviruses;
10
correct?
11
DR. GERBA: It could be. Or some
12
other type of virus it be could. But there
13
were not many of them, because the
14
adenoviruses tend to grow very well in this
15
type of cell culture, more than other virus
16
types, apparently.
17
MS. ALEXANDER: When that happened,
18
did you go back and check what it was that
19
was growing in there that wasn't adenovirus?
20
DR. GERBA: You know, I think at
21
random we did. I don't know if we did it in
22
this study. In other studies we have done --
23
we've been looking at water and waste water.
24
And I have to go and look at the
146
1
notebooks if we looked at a few of those or
2
not. In other studies they've always -- or
3
not always, but some of them turned out to be
4
enteroviruses or viruses we can't identify.
5
MS. ALEXANDER: Am I correct that
6
there were at least some instances where in a
7
sample you identified it as negative for
8
enterovirus, when testing for enterovirus, it
9
was positive in a cell culture for
10
adenovirus, confirmed as negative, and,
11
therefore, counted as negative for
12
adenovirus, but you didn't go back to check
13
whether there were enteroviruses in there?
14
DR. GERBA: We just counted -- it was
15
viral cytopathogenic effects.
16
MS. ALEXANDER: Okay.
17
DR. GERBA: We do that as a minimum.
18
MS. ALEXANDER: So in other words,
19
just to summarize, there were, at least in
20
some cases, where you found something to be
21
growing in the cell culture but you counted
22
it as a negative and didn't follow up to see
23
what exactly it was that was growing in
24
there?
147
1
DR. GERBA: No. Because we already
2
had an assay on BGM cells that worked well
3
for enteroviruses, and we could be double
4
counting the virus.
5
MS. ALEXANDER: But isn't it a fact
6
that there were at least some situations
7
where you got a negatives specifically on the
8
enterovirus assay, but you got a positive on
9
the cell culture for adenovirus that you
10
confirmed it negative for adenovirus, so it
11
could have been enterovirus instead of --
12
DR. GERBA: No. What we did is --
13
MS. ALEXANDER: -- that was going in
14
there?
15
DR. GERBA: -- if there was viral
16
cytopathogenic effects, we took that sample
17
and then we did PCR analysis to determine
18
whether it was an adenovirus or not.
19
MS. ALEXANDER: Right. And if it
20
wasn't but there was still something growing
21
in there, that could have been enterovirus;
22
correct?
23
DR. GERBA: That is a possibility,
24
yes.
148
1
MS. ALEXANDER: Okay.
2
All right. This is Tolson 21 and
3
Gerba 29. And this refers to Tables 3-5(a)
4
through (f) of Exhibit 71, Risk Assessment.
5
These are the enteric virus results.
6
Can you please describe for me the
7
method used to detect enteric viruses? Just
8
summarize as you did with adenoviruses,
9
please.
10
DR. GERBA: Right. Enteric viruses --
11
we're using that term interchangeably with
12
total culturable viruses.
13
Certain enteric viruses used a lot
14
before molecular methods came in to detect
15
viruses in water. So now there's a tendency
16
to total culturable viruses.
17
Because, basically, the EPA method
18
we used for that, before looking for it,
19
that's using the BGM cell line. You put your
20
sample on the BGM cell line and then you look
21
for the production of cytopathogenic effects
22
that are viral, and you confirm those through
23
another passage.
24
And then those are called total
149
1
culturable virus.
2
MS. ALEXANDER: Okay. One second.
3
Okay. Referring to Exhibit 71,
4
Page 48, Section 3.3.1. That contains a
5
description of this method that you're
6
discussing.
7
In the first paragraph there you
8
characterize Tables 3-5(d) through (f) as
9
presenting a summary of the wet weather total
10
enteric virus analytical results. Is the
11
method you describe capable of detecting
12
total enteric viruses, as in all of them?
13
DR. GERBA: Total culturable enteric.
14
That's a term that's used in the literature
15
for EPA. And EPA uses that, too.
16
But largely, you're really just
17
detecting the enteroviruses. Although some
18
real viruses and other virus types my grow in
19
there.
20
But that's a terminology that's
21
come into use.
22
MS. ALEXANDER: Okay. And hepatitis
23
is an enteric virus; correct?
24
DR. GERBA: That's correct.
150
1
MS. ALEXANDER: And you didn't assay
2
for that?
3
DR. GERBA: No, we did not.
4
MS. ALEXANDER: And the same with
5
rotavirus?
6
DR. GERBA: No, we did not assay.
7
Hepatitis A we did not assay for,
8
because the concentration would be expected
9
to be low because the incidence is fairly
10
low. And hepatitis A there's a vaccine now,
11
which is also driving down the incidence of
12
hepatitis A in the United States. The
13
probability of finding that was pretty low.
14
For rotaviruses, the feeling was
15
that the methods were not very good for
16
looking for rotavirus. There's a cell
17
culture method -- and I developed one of the
18
methods -- it's been used before, and it's
19
very difficult to use.
20
And the volumes you could actually
21
assay out of it, I felt, were too small to
22
really give us any meaningful results to
23
actually do rotaviruses. So that's why we
24
kind of decided against that.
151
1
MS. ALEXANDER: Okay. Turning to
2
Tolson 22 and Gerba 30. And this is
3
regarding the statement in Exhibit 71, the
4
risk assessment that reverse
5
transcription-polymerase chain reaction,
6
RT-PCR, results were used to calculate
7
concentrations of noroviruses in the sample.
8
Can you just give a brief summary
9
of how those calculations were performed,
10
please?
11
DR. GERBA: These calculations are
12
done very similar to most probable number
13
calculations for the coliforms, fecal
14
coliforms, the bacteria that are often used.
15
You take a delusion series of your sample and
16
you look for the number of positives and
17
negatives and then you feed that into a -- on
18
a computer program developed by Hurley and
19
Rosco back in 1983.
20
It calculates the most probable
21
number of concentration in the sample that
22
you are assaying. It's, basically, doing the
23
same thing as doing a most probable number
24
for fecal coliforms.
152
1
MS. ALEXANDER: Okay.
2
And just to kind of make sure I
3
understand this properly, this RT-PCR process
4
tells you how many copies of norovirus RNA
5
there are in your sample; is that right?
6
DR. GERBA: You have to do it by a
7
delusion series. It's a positive negative
8
one.
9
You could do that by using
10
quantitative PCR. But I felt it didn't have
11
the sensitivity we needed, so we do the most
12
probable number.
13
In other words, the sample is
14
positive or negative as you dilute it. In
15
other words, you take an unconcentrated
16
sample and you dilute it one to ten, one to
17
100 and one 101,000.
18
And you are basically looking for
19
an extinction point. You no longer find the
20
positive PCR reaction in a sample that is
21
diluted out far enough. And you do that
22
usually at least in triplicate.
23
MS. ALEXANDER: Okay. Did this
24
analysis involve an assumption as to the
153
1
number of copies of norovirus RNA that are
2
associated with the presence of a certain
3
amount of norovirus? Does that question make
4
sense?
5
DR. GERBA: Yeah. Usually one genome
6
equals one virus, it's believed.
7
MS. ALEXANDER: One to one?
8
DR. GERBA: One to one.
9
MS. ALEXANDER: Okay.
10
Help me understand the statement
11
in the Risk Assessment, Exhibit 71, then,
12
that the ratio of he genomes, paren, (the
13
viron self-culture infectivity units) is one
14
to 100 to one to 46,000.
15
DR. GERBA: That varies with the cell
16
culture line you're using.
17
In other words, if I took -- you
18
adapt viruses to cell culture. If I took a
19
virus, like rotavirus in a stool sample and
20
put in a cell culture sample, the ratio may
21
be one to 40,000 -- 40,000 genomes to one
22
virus.
23
If you adapt that to cell culture
24
over time or use vaccine strains maybe you're
154
1
looking for, that may be down to one in a
2
hundred. The cell culture doesn't
3
necessarily detect all the viruses that are
4
in the sample.
5
MS. ALEXANDER: I'm sorry, how does
6
this fit in with your testimony concerning
7
the one-to-one ratio? Am I comparing apples
8
and oranges? Is that a different thing?
9
DR. GERBA: I think you are. The
10
conservative thing would be to consider each
11
genome one norovirus. One, because this
12
picks up inactivated organisms.
13
MS. ALEXANDER: So you're saying the
14
conservative thing would be to consider it
15
one to one. But am I understanding correctly
16
from the risk assessment, Exhibit 71 on
17
Page 48, that, in fact, you used a ratio of
18
one to 100 to one to 46,000?
19
DR. GERBA: The reason for that is
20
because the only dose response data we have
21
is for cell culture, where the ratio is one
22
to a hundred. So, in other words, the
23
echovirus ratio was 100 genomes to one
24
infectivity unit. That's what was done in a
155
1
dose response curve.
2
So that's why it was benchmarked
3
against that. Because we know from the
4
echovirus data that for every hundred
5
genomes, we would have one infected unit.
6
And that was used to develop the dose
7
response curve.
8
MS. ALEXANDER: Wouldn't it make a
9
pretty big difference in your overall
10
results, whether you use one to 100 or one to
11
46,000 -- in other words, in terms of how
12
many virus you're assuming or correlated with
13
the number of genomes you found?
14
DR. GERBA: Of course. I mean, just
15
changing that ratio, you could make that
16
ratio over to a wide number of things. But
17
in this example, we had something to
18
benchmark it again, so we were trying to
19
bring reality into the risk assessment.
20
MS. ALEXANDER: So you were saying you
21
were benchmarking it against the one-to-one
22
ratio from the dose response data?
23
DR. GERBA: No, the 100. Because that
24
was what we had based on the dose response
156
1
data which was developed in cell culture.
2
In other words, when they
3
developed the dose response data, they used
4
the infectivity in cell culture of the
5
echovirus. And they that for every hundred
6
genomes, approximately, they had one
7
infectious virus in cell cultures what they
8
did the dose response against.
9
So what we did is try to benchmark
10
it against a real situation where we actually
11
knew what the ratio was and we had a dose
12
response curve to go with it.
13
MS. ALEXANDER: All right. So you
14
opted against using the one to one because of
15
this dose response data that you had?
16
DR. GERBA: Right. And we could have
17
used the one to 40,000, for example, which
18
could have been used, too. Because that's
19
about what the ratio from the stool sample
20
for, say, rotavirus is to an infectivity in a
21
human being.
22
So this was the range that we
23
picked.
24
MS. ALEXANDER: Okay. Not to beat the
157
1
dead horse, but just so I understand, the
2
most conservative assumption you could of
3
made would be one to one, the least
4
conservative would be one to 46,000, you
5
chose --
6
DR. GERBA: Right.
7
MS. ALEXANDER: -- the one to 100?
8
DR. GERBA: That's right. That's
9
correct.
10
MS. ALEXANDER: Okay. Moving onto
11
Tolson 23 and Gerba 21, they are the same
12
question.
13
Did the secondary infection rates
14
that you used in your analysis change between
15
the interim dry weather risk assessment
16
completed in November 2006 and the final wet
17
and dry weather risk assessment?
18
DR. TOLSON: Yes, it did.
19
MS. ALEXANDER: Okay.
20
I'm going to present a document
21
and have it marked as an exhibit, just so the
22
rest of the room can understand what we're
23
talking about.
24
(WHEREUPON, a certain document was
158
1
marked Exhibit No. 76 for
2
identification, as of 9/9/08.)
3
MS. ALEXANDER: What I have here to
4
present as the exhibit is the cover page from
5
the interim dry weather risk assessment dated
6
November 2006 and then the relevant table
7
that I'll be talking about, which is
8
Table 4-6.
9
THE HEARING OFFICER: I've been handed
10
Prepared For Protecting Our Water Environment
11
Metropolitan Water Reclamation District of
12
Greater Chicago, Interim Dry Weather Risk
13
Assessment and Human Health Impact
14
Disinfection Versus No Disinfection of the
15
Chicago Area Waterway System.
16
If there's no objection, I'll mark
17
this as Exhibit 76.
18
Seeing none, it's Exhibit 76.
19
MS. ALEXANDER: Okay. Specifically I
20
would like to compare this table -- I'm
21
sorry -- this was marked as No. 76 to --
22
which is Table 4-6 in the dry weather risk
23
assessment to table 5-6 in Exhibit 71.
24
DR. TOLSON: Okay. I'm with you.
159
1
MS. ALEXANDER: I'm not with you yet,
2
hold on.
3
And I would point out, correct me
4
if I'm wrong, that several -- a couple of the
5
numbers in the interim assessment are higher
6
than the numbers in Table 5-6. That's
7
comparing Exhibit 76, Table 4-6 to Exhibit
8
71, Table 5-6. And specifically the entries
9
for salmonella and E. Coli.
10
DR. TOLSON: Also total enteric
11
viruses, yes.
12
MS. ALEXANDER: Now, the lower numbers
13
that are contained in the later iteration,
14
the wet and dry weather risk assessment, for
15
infectivity -- or, I'm sorry, secondary
16
attack rates, would, in fact, have the effect
17
of lowering overall risk; is that correct?
18
DR. TOLSON: It is correct that if the
19
lower the secondary attack rates, the higher
20
the risk.
21
MS. ALEXANDER: Okay.
22
DR. TOLSON: If you'd like, I can
23
explain the rationale --
24
MS. ALEXANDER: Yes.
160
1
DR. TOLSON: -- for this if you --
2
MS. ALEXANDER: You anticipated my
3
next question, which is what was the basis
4
for these changes.
5
DR. TOLSON: Sure. The interim
6
report -- and it wasn't interim drafts, sort
7
of a product here -- we assumed a 50 percent
8
attack rate, which is a fairly conservative
9
assumption. As we refined our estimates, we
10
gathered additional data and took a look at
11
what was available in the literature to sort
12
of hone in to get a better estimate of what
13
those would be.
14
For example, for total enteric
15
viruses, we assumed 50 percent. After some
16
additional conversations with Dr. Gerba, we
17
settled on 25 percent as a conservative, sort
18
of, assumption for transmission.
19
For adenoviruses and
20
caliciviruses, it looked like we kept those
21
the same from our initial assessment. The
22
crypto and giardia results that we had in the
23
interim are actually reversed. So they're
24
corrected in the final.
161
1
But I'd like to point out that
2
the -- for the giardia results, the
3
literature reported from eight to ten
4
percent, we actually assumed 25 percent,
5
which is conservative beyond what the
6
literature cites. And then, for salmonella
7
and for E. coli, we changed our default
8
assumption to 25 percent, which we thought
9
was still an overly conservative estimate of
10
the secondary attack rates for those
11
organisms.
12
If you've noticed, we actually did
13
cite some literature below. And I think in
14
every case, the literature cited value is
15
lower or within the range of the values that
16
we use with our -- as our input assumptions.
17
MS. ALEXANDER: Okay.
18
Tolson 24 and Gerba 32. Did you,
19
in fact, use a Monte Carlo simulation in
20
quantifying risk?
21
DR. TOLSON: That is correct, we used
22
the Monte Carlo simulation.
23
MS. ALEXANDER: Can you provide a
24
brief description of what you did in that
162
1
simulation?
2
DR. TOLSON: Monte Carlo simulations
3
are the mathematical tool to solve problems
4
that don't have an easy analytical solution.
5
You can't just add the numbers up and come up
6
with the equal sign and get a final number.
7
It uses simulations to estimate
8
what the final results would be. The process
9
used here, we use Monte Carlo simulation
10
where we selected from our data set -- and
11
this means our data set of dry weather days,
12
wet weather CSO days -- to represent each
13
simulation's waterway pathogen
14
concentrations.
15
And then we did simulations of a
16
million recreational users, drawing
17
individuals from distributions that included
18
canoeists, fishing and boating, in relation
19
to the proportion for which they are
20
represented in the UAA study.
21
DR. GERBA: If I can point out, in
22
microbial risk assessment, that's common
23
practice to use Monte Carlo simulations. You
24
get a better idea what the distribution of
163
1
risk is.
2
MS. WILLIAMS: Can I just ask, have
3
you done this before though? Have you done a
4
Monte Carlo simulation for microbial risk
5
assessment before?
6
DR. TOLSON: I teach a class on
7
probabilistic risk assessment, a graduate
8
level class, at University of Florida. This
9
is a component of one of the things that I
10
teach within that class, a number of
11
probabilistic risk assessments historically.
12
So yes.
13
MS. WILLIAMS: But I'm just
14
specifically distinguishing between microbial
15
risk versus other types of toxic chemical
16
risks. Was that reflected in your answer?
17
DR. TOLSON: The assessment, sort of,
18
parameters are pretty much the same. My
19
microbial risk assessment experience, I have
20
not relied on probabilistic methods for that,
21
but --
22
MS. WILLIAMS: Until now?
23
DR. TOLSON: That is correct.
24
MR. ANDES: Can you explain a little
164
1
bit more about this methodology?
2
DR. TOLSON: The methodology is common
3
methodology that's employed by the agency and
4
others to sort of assess risk. I have been
5
involved in numerous workshops where we've
6
discussed these, sort of, risk assessment
7
techniques in a very fast style in sort of
8
doing them, so...
9
DR. GERBA: I've been involved in a
10
number of teams doing simulations for
11
microbial risk assessment. It's really just
12
a mathematical technique.
13
You put different numbers in is
14
all you're doing.
15
MS. ALEXANDER: So just to summarize,
16
in other words, the point of a Monte Carlo
17
simulation is to account for a distribution
18
spread of input variables; is that basically
19
correct? In other words, you could account
20
for the fact that there's no exact amount of
21
water that every recreator is going to
22
ingest, but it's rather a range of
23
possibilities? Is that basically right?
24
DR. TOLSON: That is correct.
165
1
MS. ALEXANDER: Okay.
2
DR. TOLSON: The alternative is to do
3
point estimates for all the inputs and
4
develop one point estimate, which takes into
5
account the averages of everything. And the
6
way we did it takes into account the ranges
7
and gives us sort of a range of outputs.
8
MS. ALEXANDER: Can we turn to figure
9
5-2 in Exhibit 71, the risk assessment?
10
THE HEARING OFFICER: Excuse me.
11
Let's go off the record for just a second.
12
(WHEREUPON, discussion was had
13
off the record.)
14
THE HEARING OFFICER: Back on the
15
record.
16
MR. ANDES: First the appendices to
17
the risk assessment report I have on a disk,
18
if I could give you that right now.
19
THE HEARING OFFICER: Is that all four
20
appendices?
21
MR. ANDES: Yes, A, B, C and D.
22
THE HEARING OFFICER: We'll mark that
23
as Exhibit 77.
24
MR. ANDES: I also have, both paper
166
1
and on a disk, the attachments to the EPA
2
July 31st, 2008 Melser letter.
3
MS. MEYERS-GLEN: I'm sorry, we didn't
4
catch that. Could you say that again,
5
please? Attachment what?
6
MR. ANDES: The attachments to the EPA
7
letter of July 31st.
8
THE HEARING OFFICER: Exhibit 77 is
9
the risk assessment appendices. If there's
10
no objection?
11
Seeing none, it's Exhibit 77.
12
(WHEREUPON, a certain document was
13
marked Exhibit No. 77 for
14
identification, as of 9/9/08.)
15
THE HEARING OFFICER: Exhibit 78 will
16
be the CD-ROM that is the appendices to the
17
USEPA letter that was previously admitted as
18
CD-ROM 73. Exhibit 73.
19
MR. ANDES: The last document on that
20
CD-ROM, July 31st, 2008.
21
THE HEARING OFFICER: All right. So
22
wait a minute.
23
Instead of -- I'm going to do
24
something I don't normally do. I'm going to
167
1
enter this as Exhibit 73A. So that it will
2
be clear than it goes with Exhibit 73.
3
And this the appendices to the
4
letter, which was one of last documents on
5
the CD-ROM that is Exhibit 73. So this will
6
be Exhibit 73A. If there's no objection?
7
MS. WILLIAMS: I'm just trying to
8
figure out what I have. Is that what I have?
9
Or do I have both?
10
THE HEARING OFFICER: He gave you
11
two --
12
MS. WILLIAMS: We have one disk, I
13
don't know what's on it. What is this?
14
MR. ANDES: Those are the attachments
15
to the EPA July 31st, 2008 letter.
16
MS. WILLIAMS: So that's 73A?
17
THE HEARING OFFICER: 73A.
18
MS. WILLIAMS: Thank you.
19
THE HEARING OFFICER: And 77 is the
20
appendices, which he gave us both the hard
21
copy and on CD. Or which I have both hard
22
copy and CD.
23
So I'm going to mark the hard copy
24
also, again strangely enough, as 77A.
168
1
Because 77 is the disk. There's no
2
objection?
3
MR. ANDES: Let me clarify. The
4
appendices that I gave you -- the disk marked
5
appendices is 71; isn't it? Isn't the risk
6
assessment report 71?
7
THE HEARING OFFICER: Yes, but I'm
8
going to mark them as 77. Because I don't
9
normally give subsets, but I also then have
10
the same thing in hard copy, I'll call it
11
77A.
12
MR. ANDES: All right. Fine.
13
MS. WILLIAMS: Now, with that --
14
THE HEARING OFFICER: Okay. Wait a
15
minute, I'm confused.
16
These are not the appendices to --
17
MR. ANDES: The appendices to the risk
18
assessment report are only on that disk that
19
says Appendices.
20
THE HEARING OFFICER: These
21
(indicating) are what goes with this
22
(indicating), are the attachments?
23
MR. ANDES: Yes.
24
THE HEARING OFFICER: Okay.
169
1
I'm not marking them as an
2
exhibit. We have them on CD, these will be
3
for our use.
4
So Exhibit 77 is the appendices to
5
the risk assessment, and 73A is the
6
appendices to the letter. I am thoroughly
7
confused, but I think I've got it.
8
All right. No objections?
9
Those are entered.
10
(WHEREUPON, a certain document was
11
marked Exhibit No. 73A for
12
identification, as of 9/9/08.)
13
MS. WILLIAMS: So at this point,
14
though, you have copies of -- you have a disk
15
with appendices, Ms. Alexander has a disk
16
with appendices. Can we just request that
17
the Board upload this exhibit in particular,
18
or no?
19
THE HEARING OFFICER: I have to be
20
perfectly honest with you, John is out this
21
week.
22
MS. WILLIAMS: No, I don't mean --
23
THE HEARING OFFICER: I was going to
24
say, so I can't promise you when this would
170
1
get done.
2
Is it possible to get another CD
3
burned?
4
MR. ANDES: Yeah. If I don't already
5
have one, I can certainly burn another.
6
MS. WILLIAMS: Either one.
7
THE HEARING OFFICER: And we might be
8
able to burn a CD faster than we can get it
9
uploaded, given our staffing concerns this
10
week.
11
MS. WILLIAMS: Either way.
12
THE HEARING OFFICER: All right. That
13
being said, we will start again tomorrow
14
morning with Ms. Alexander.
15
Drs. Gerba, Tolson, Petropoulou,
16
thank you very much.
17
We're adjourned.
18
(WHEREUPON, the hearing was
19
adjourned until 9/10/08 at
20
9:00 a.m.)
21
22
23
24
171
1 STATE OF ILLINOIS)
2
) SS:
3 COUNTY OF COOK )
4
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.
12
IN WITNESS WHEREOF, I do hereunto set my
13 hand at Chicago, Illinois, this 18th day of
14 September, 2008.
15
16
17
Certified Shorthand Reporter
18
19 C.S.R. Certificate No. 84-4327.
20
21
22
23
24