MR. PERRY:  Well, I think I'm asking specifically how could OSHA or
should OSHA use like laboratory testing or that sort of kind of data,
how do we know that -- how do we get from the lab to knowing how well a
controlled approach is going to perform in the field, or should?

		MR. ECHT:  Sure.  I mean the way we've done it typically is to begin
in the lab and end in the field, but there is an alternate approach that
some manufacturers use, particularly German manufacturers, where they do
a worst-case scenario.  They initially start with the test bench method
where they would put a tool, they call a system, the tool, a vacuum
cleaner, in a test bench and, you know, run it over some kind of
substrate, run air by it and sample the air and determine an emission
rate, and then when the emission rate was acceptable, the tool was
acceptable.

		They've since moved to a technique that was validated by the German,
BG Bau was the acronym, I'm not sure what it stands for, where they put
a skilled technician in a closed room with a typical sidewalk or brick
or some kind of substrate, silica containing substrate, and then used a
tool with controls and evaluated its exposure with the control in place,
and when that was within acceptable limits by their standards, that tool
was then considered acceptable for use.

		MR. HEARL:  In a general sense, I think I would turn to your
colleagues at MSHA and look at what they do, because they rather require
a dust control plan to be filed in their coal mines and then require
some sampling to show that that control plan is effective.

		After that, having set parameters of the dust control plan in terms of
water spray pressures and air velocities and so forth, as long as they
keep checking those things which are visually obvious to any inspector
or the operator themselves, they consider things to be in good shape
because they have that background or backup validation sampling data.

		If then an inspector comes in and finds things out of compliance, they
then say the dust control plan is no longer valid, and they have to go
through the whole process of reestablishing it, validating it, and then
they can go forward again.

		So, you know, in terms of what you could do, that's one option.

		MR. PERRY:  Thank you.  It's good ideas.

		Moving to fracking, I have just a couple of questions on the hydraulic
fracturing work that you've done.  In your testimony, you list a number
of engineering control approaches that you've looked at.  Does NIOSH
have any cost information on what it costs to implement those controls?

		MR. KIEFER:  No, we do not.  As I mentioned previously, there are some
that are very straightforward and simple to implement, such as skirting
and so forth which would intuitively be of somewhat low cost.  The
ventilation methods for certain types of applications where it's
necessary, I don't have any information on the costs.

		MR. PERRY:  Okay.  The next best thing would be could you provide some
of the design parameters into the record, things like ventilation
capacities and other kinds of technical information about those controls
that we then could use as a basis for costing perhaps?

		MR. KIEFER:  Sure.  We do have a NIOSH developed control for one of
those --

		MR. PERRY:  Okay.

		MR. KIEFER:  -- release points that we could provide.

		MR. PERRY:  Okay.  Thank you.  One last question on fracking.  It
sounds like from your experience partnering with these hydraulic
fracturing companies, they seem to be very open and receptive to the
idea of wanting to control exposures to silica.  Is that accurate?

		MR. KIEFER:  I would say so.  We have not seen anyone dispute the
science or not fail to recognize that silica is a significant issue in
this industry, and many of these companies have developed very
innovative control methods, some of which they've shared with us, and we
continue to have a good dialogue with a consistent theme of trying to
keep people from being exposed.

		MR. PERRY:  Have any of these companies told you or have they
otherwise represented that the cost of controlling silica are
prohibitive and it's going to be a problem for them?

		MR. KIEFER:  No.

		MR. PERRY:  Okay.  Thank you very much.

		I think at this point, our next questioner is Tiffany DeFoe from our
Office of Chemical Hazards  - Metals who has some questions for the
panel on health effects.

		MS. DeFOE:  In your earlier statement, you said that OSHA's reliance
on cumulative exposure in its risk assessment was a reasonable and
practical choice for silicosis risk assessment.  Would you please
elaborate on why you find it to be reasonable and practical?

		DR. PARK:  Well, there's plenty of precedent in occupational
epidemiology.  This is a exposure that appears to cause an irreversible
effect.  It accumulates over time with increasing cumulative exposure.
There's lots of other exposures and health effects that have been
analyzed with this exposure metric where it proves to be a very useful
predictor, especially, for example, in studies of cancer, cumulative
exposure is just a well-established metric that predicts well outcomes.

		It makes certain assumptions.  For example, cumulative exposure is
simply summing exposure intensity over time.  It doesn't take into
account when the exposure occurred.  So one might think that different
patterns of exposure historically that have the same cumulative exposure
might have different effects, and that's probably true for some health
outcomes, but the fact that it predicts quite well, as cumulative
exposure, implies that that time history is not important for some
outcomes, that the damage progresses and is irreversible and just gets
added up over time, just like the exposure.

		And it's also a relatively easy exposure metric to calculate.  You
don't have to worry about when the exposure occurred.  Just add it up
over time.

		MS. DeFOE:  All right.  You mentioned cancer.  So it sounds like you
think that cumulative exposure is also the most appropriate metric for
cancer as well as --

		DR. PARK:  For lung cancer and many other exposure environments, it's
a good predictor, yep.

		MS. DeFOE:  Is there any evidence of a dose-rate effect for silicosis
at concentrations of interest, around the current PEL or the proposed
PEL?

		DR. PARK:  I don't think that that's been looked at a lot.  That's the
question of whether on a given day the level of exposure contributes to
future risk in a way that's proportional to exposure that day.  If
there's no dose-rate effect, then a little exposure over a long period
could be the same as a lot of exposure over a short period.  That's what
dose rate is all about.

		That's one thing that we looked at in one of our studies.  We looked
at the tin miner cohort in China, and we're examining a number of
questions including whether cumulative exposures is an appropriate
predictor for silicosis, but one of the things we did was calculate
three different metrics, one assuming no dose rate, one assuming that
low exposures are more potent than you would predict on a no dose-rate
effect, and a third one assuming the opposite.

		And so in this study, where there were a 1,000 silicosis cases, a very
big cohort with very good exposure history, this is a mine in China
where they had exposure data going back to the '50s and apparently quite
extensive surveillance, x-rays every two or three years, and this
dataset, comparing those three metrics, cumulative exposure without a
dose-rate effect was by far the best predictor.  So that's not
definitive, but it's some pretty good evidence that there's not a large
dose-rate effect, and if anything, it looks like there's a negative
dose-rate effect; that is, the metric calculated with, in this case, the
square root of exposure summed over time did better than using the
square of exposure.

		So that implies that lower exposures are a little bit more effective
than you would predict just from a standard cumulative exposure
perspective.

		MS. DeFOE:  So if I understand correctly, you mean that there was some
evidence that the lower exposure had a little bit higher exposure
response?

		DR. PARK:  Yes.

		MS. DeFOE:  Thank you.  Now, in your comments, you also noted that
there is evidence of attenuation of exposure response at higher
exposures in some studies, for example, in the NIOSH risk assessment,
for NMRD mortality and silicosis incidence.  Is this type of attenuation
unusual to see in studies of workers?

		DR. PARK:  No, it's pretty common.  There's a publication by Steiner
et al. that talks about this and gives other examples.  There is a lot
of speculation about why that is, what's going on, and one can think of
several possibilities.  One is the so-called healthy worker survivor
effect.  People with long durations and large cumulative exposures tend
to be healthier people than the short-term employee population partly
because people that get sick leave the workforce, and if that were the
case, then you would expect the long-term people to be a healthier
population to begin with and maybe show less of a net effect even though
they might still be responding the same way.

		Another explanation might be that there's some variability in
susceptibility and that some of the higher susceptibility subpopulation
is being depleted.  They're getting sick and they're leaving.  That
would be another explanation.

		A third explanation might be that there's some physiological repair
process in some cases.

		So there's lots of possibilities from a risk assessment perspective.
It doesn't really matter what they are.  What we want to do is really
model what's going on down at the low end of the exposure response,
which is why in the studies you referred to, we as part of the analysis
excluded observation time when cumulative exposure exceeded a certain
level, 10 mg/m3-years, I think, just so that the linear model was better
fitting at the low end.  It gave us a better estimate of risk at low
exposures.

		MS. DeFOE:  Is there any reason to believe that the higher exposure
data that I think you just said you looked at, eliminating from the set,
was there any reason to believe that it might be less reliable than the
remainder of the dataset?

		DR. PARK:  The higher exposure data?  Well, it's got many fewer cases
for one thing.  As one goes to the higher exposure, it's fewer and fewer
cases.  So it was a less certain estimate to begin with.  Other than
that, I don't think there's any difference in reliability.  There might
be different confounding factors, which I alluded to.

		MS. DeFOE:  Let's see here.  Earlier, Dr. Park, when you were in the
process of answering a question I think it was from Mr. King, about the
use of a variety of modeling choices, and whether modeling analyses that
you or others had done had adjusted the significance level to account
for the exploration of multiple modeling choices, you responded that you
don't think that's a legitimate approach, but then time ran out and you
didn't get to finish the thought, I felt like.  Would you be willing to
elaborate now on why you don't think that's a legitimate approach?

		DR. PARK:  Yes.  Because going into the investigation, we have prior
knowledge.  We have a lot of prior experience that would favor some
models over others.

		Now, there is a more formal way that that could be handled.  For
example, there's something called Bayesian model averaging where people
say, well, let the numbers decide, you know, don't pick one model, pick
a mixture, and let the statistical procedure figure out what it ought to
be.  That also basically says we're ignorant.  It's just saying we're
not going to take responsibility for the decision.  We'll let the
numbers do it.

		There's another variation that would make more sense, which is in any
Bayesian process, you can define your prior.  So you can say you think
this model has a high relative value based on other experience and this
model has a very low value, and you can put weights on those in the
Bayesian process.  You could do that.  So you could formalize the
process that we basically do informally, and like I said, we're pretty
partial toward linear effects unless there's some evidence to the
contrary, and also in the absence of sort of biological support for it.

		MS. DeFOE:  In the studies that we're talking about, do you think that
the Bayesian approach you just mentioned would be necessary to get a
sense of what's going on with the model form?

		DR. PARK:  No, and I don't know how to do it.

		MS. DeFOE:  Let me see here.  Several commenters have noted an
association between or a statistical association between silicosis and
lung cancer in the respirable silica literature.  Does this association
indicate a common mechanism or a kind of causal relationship between the
two diseases?

		DR. PARK:  I'll comment on that, and then David and others might want
to as well.

		That's a very difficult question to answer empirically.  The problem
is, as everybody knows, there is exposure misclassification.  Even in a
workplace history where we can identify some groups that we think have
roughly the same exposure, so-called homogeneous exposure zones, there's
still going to be some variability within those.  There's going to be
some workers that have higher exposure than others just because of the
nature of their work, where they're working and so forth.

		So there's that variability that is inherent in any analysis, and what
silicosis is saying is some people have more exposure than others.  So
within one of those homogeneous exposure zones, the people that have
silicosis, you can pretty much say they had higher exposures and the
ones that didn't have silicosis had lower exposures.  So silicosis is a
predictor of lung cancer just because it's improving your exposure
classification.

		It would be very hard to do a study that separates that effect.  It's
possible that lung cancer and silicosis have a similar pathway.  They
might both depend on reactive oxygen species or something but have no
connection to each other.  So they're two independent risks, but they're
going to be highly correlated because they're responding to the same
physiological insult.

		The other reason why this comes up is that silicosis isn't detectable
until there's splotches on the lung that are visible in x-rays.  So
prior to that point, somebody could have developing lung disease and you
just can't see it.

		So, of course, people that have silicosis are going to have higher
lung cancer, and it's going to look like a threshold because you didn't
see the silicosis in other people that have lower lung cancer risk.

		To really separate those two, you'd have to do a really big study.
You'd have to have some measures, independent measures of lung
physiological pathology, and see what's going on with silicosis as a
necessary condition for development of lung cancer.

		David, you want to add anything?

		MR. WEISSMAN:  Yeah.  I don't have much to add to what Bob said except
to say that it would be a hypothesis that you would require silicosis to
get silica-related lung cancer.  And there's quite a bit of reason as
Bob said to think that the two processes don't require each other, and
it would be extraordinarily difficult to sort things out in human data
for the reasons that Bob talked about, and also as laid out, IARC talks
about this in their 100C monograph.

		MS. DeFOE:  Thank you.  And just one last from me.  In your response
to a previous question about the CDC's analysis of decline in silicosis
mortality trends in the U.S., based on data from the NIOSH National
Occupational Respiratory Mortality System database, or the NORMS
database, I believe you stated that these data were not used as a basis
for OSHA's risk assessment, and therefore any challenge to the quality
of the NORMS database wouldn't undermine the results of OSHA's risk
assessment.  Did I understand that correctly?

		MR. WEISSMAN:  Well, absolutely.  I mean the surveillance data might
be an ancillary piece of information that could be motivational if you
know that there are cases, but the surveillance data doesn't contain
information about exposure and health effects, and it's not what would
be used in a quantitative risk assessment.  So it's really not germane
to the risk assessment.

		MS. DeFOE:  You just answered my second question.  So thank you.

		MR. PERRY:  I believe our last panel member to ask questions of the
NIOSH Panel is Stephen Schayer from our Office of Biological Hazards,
I'm sorry, Physical Hazards.

		MR. SCHAYER:  Hi.  Thank you.  So my first question is actually about
thresholds.  So various public commenters have stated that the exposure
response for both silicosis and for lung cancer may have a threshold.
And so we're wondering if NIOSH is aware of any research that would
support the existence of a threshold effect for either silicosis or lung
cancer?

		DR. PARK:  Yes, there's two large studies that are discussed in some
detail in the proposed rule involving a pooling of populations in
Europe.  One was looking at lung cancer and the other at silicosis, and
there's publications from those studies.

		There's two tables that I'd like to draw your attention to, and I have
copies of them here which I can provide.  These are tables that show the
estimated risk at levels of cumulative exposure, and they also give the
average cumulative exposure in each of those levels and the numbers of
cases and so forth.

		So with those tables, you can actually calculate what was the
equivalent exposure level for 45 years that would give you that
cumulative exposure, and then you can see, was there a trend in the risk
that goes down this table and how far down does it go.  And there is a
trend that goes to levels of exposure that are far below 50, let alone
100, down to like 10.  I don't have them with me.  I'm not looking at
them at the moment, but I'd be happy to provide those.  So the
assumption there --

		JUDGE SOLOMON:  Let me ask you.  Where are those located?  If someone
were to find them, were they published?

		DR. PARK:  The tables are published.  What I've done is added two
columns to the tables to show the numbers that I'm talking about.  I
have copies here that I can submit.

		JUDGE SOLOMON:  Where were they published?  If you don't have it, you
can just provide it later on, but it's a lot easier if you put it into
the record.

		MR. SCHAYER:  Yes.  If you could submit that to the record, if you
could, that would be great.

		DR. SCHULTE:  Bob, just to clarify, you were arguing a threshold, but
you started out indicating that there was evidence on the question, and
just to be clear, this is evidence that there is not a threshold.

		DR. PARK:  This is evidence that if there's a threshold, it's very
low.  So one of them was on silicosis, and that was published in
Occupational and Environmental Medicine, 2002, and the other one was in
the Journal of Epidemiology, 2007, looking at lung cancer.

		So this argument that I've made, looking at what the average exposure
was over 45 years that would result in that risk, also depends
critically on this whole question of dose rate, of course, because these
are studies where the people actually worked anywhere from 0 to maybe 20
years, and we're extrapolating out to 45 years, which we can't really do
unless we can be pretty confident that there's no traumatic dose rate.

		MS. KRAMER:  If you don't need those tables to answer your next couple
questions, if you can't, you know, anticipate that, if you could pass
them over, that would be great.

		MR. SCHAYER:  Okay.  So thank you.  So another question that I had was
also I was wondering if you could --

		JUDGE SOLOMON:  If we could wait a second.

		MR. SCHAYER:  Oh, sure.

		JUDGE SOLOMON:  You want to mark those?

		MS. KRAMER:  Your Honor, we'd like to mark these tables as Hearing
Exhibit Number 5 and request that they be entered into the record of
this hearing.

		JUDGE SOLOMON:  Without objection, they are entered into evidence.

(Whereupon, the document referred to as Hearing Exhibit 5 was marked and
received in evidence.)

		MR. SCHAYER:  So my next question, we were wondering if you could kind
of generally discuss the role of epidemiological studies in risk
assessment and if they provide evidence that exposure to a particular
chemical causes a particular disease.

		DR. PARK:  Well, like any scientific endeavor, it's hard to prove a
theory.  You can disprove competing theories.  What that means in
epidemiology is you can prove an association.  Whether it's causal or
not is interpretation.  So one has to ask, are there other plausible
explanations for that association, had they been controlled with the
availability data?  Is there other information, confounding information
that we don't have, that could possibly account for the association, and
so forth?

		So, in general, it's a judgment and based not only on that study but
on prior knowledge.

		MR. WEISSMAN:  And just to expand on that, I mean everybody recognizes
that in epidemiology, when you see an association, it doesn't
necessarily prove causality.  And everyone's familiar with the Hill
criteria that are a set of criteria to try to infer causality.

		But, in reality, what we really need are multidisciplinary approaches.
 So we look at epidemiology, but we also look at basic bench laboratory
science to help us to understand causality, and you have to look at the
totality of the evidence together.

		MR. SCHAYER:  Okay.  And one other question I had, if silica is
thought to be associated with health effects besides those that OSHA
considered in its risk assessment.

		MR. WEISSMAN:  So I'll jump in and, you know, certainly there are a
number of autoimmune diseases that over the years have been recognized
to be associated, you know, with silicosis.  So things like rheumatoid
arthritis and most recently ANCA-positive vasculitis has been recognized
in several studies as associated with silicosis.

		So I think that that group of autoimmune diseases really isn't
included -- prevention of those isn't included as a potential benefit of
improved control.

		MR. SCHAYER:  Okay.  And how about cardiovascular effects?

		MR. WEISSMAN:  There was a recent study, a Chinese study, that showed
an association between exposure and cardiovascular outcomes.  And so
that's another possibility, although you probably don't have the data
that you need to quantitatively look at benefits there.

		DR. PARK:  Historically there were, at much higher silica exposure
levels, a clear kind of heart disease, but we're probably not seeing
that at this range.

		MR. SCHAYER:  The study that you were just talking about,
cardiovascular effects, do we have that?  Okay.

		MR. WEISSMAN:  That was one of the two I believe that we had mentioned
in our comments to you.

		MR. SCHAYER:  Okay.  Okay.  Great.  Okay.  Thank you.  Those are my
questions.

		MR. PERRY:  And I misspoke before.  We actually have a different last
panel member who has a few questions for the NIOSH Panel, Dr. Iannucci.

		MS. IANNUCCI:  Okay.  I just have a few questions on medical
surveillance.  The first one's on spirometry.  Considering that lung
function may be affected by exposures not related to silica exposures
such as smoking, is spirometry testing beneficial as part of silica
medical surveillance?

		MR. WEISSMAN:  The answer to that would be yes.  I mean one of the
silica associated outcomes that we're looking for is chronic obstructive
pulmonary disease, and even though there are other things that can
potentially cause COPD, that can affect the spirometry, if you do see
excessive declines, it gives the opportunity to address those things,
too.

		So we would recommend spirometry, and we believe that the frequency
that you recommended, every three years, is appropriate.

		MS. IANNUCCI:  Okay.  Thank you.  Okay.  We already talked about CT
scans in reference to tumors.  Should OSHA consider CT scans to be
equivalent to x-rays for detecting silicosis?

		MR. WEISSMAN:  So you've laid out in your Federal Register Notice that
early literature with CT showed that it was superior for showing large
opacities and that later literature on CTs has shown that it's more
sensitive than plain chest radiography for detecting silicosis.

		That said, the radiation from CT is much more than the radiation that
somebody gets from plain chest radiography.  So I wouldn't recommend CT
as a routine substitute for chest radiography, but let's say a worker
had a chest CT scan done as part of a clinical workup, and you happened
to have that information.  I would accept a CT scan not showing evidence
of silicosis as appropriate for surveillance and a fine substitute for
plain chest radiography in that particular situation.

		MS. IANNUCCI:  Okay.  And one last question.  If OSHA were to apply
medical removal and protection similar to Part 90 for coal dust miners,
what would be the criteria for removal of workers to jobs with low dust
exposure and why?

		MR. WEISSMAN:  Well, what we use in Part 90 in our Coal Workers'
Health Surveillance Program is evidence of changes of pneumoconiosis on
the chest film of category 1.0 on the ILO classification system.  And I
would think that you would want to use some sort of parallel kind of
approach if you were to have a Part 90, you know, a sort of low dust of
job specification in this rule.

		MS. IANNUCCI:  Okay.  And is there any reason why you're requesting
removal at a low level of severity?

		MR. WEISSMAN:  Because as we touched on before, in our comments, once
somebody develops evidence of interstitial lung disease, really the best
thing that we can do is eliminate further exposure that would exacerbate
the situation for them.

		MS. IANNUCCI:  Okay.  Thank you.

		MR. PERRY:  Your Honor, I think that completes the questioning of our
panel.

		JUDGE SOLOMON:  Okay.  We're sort of at the end here, but I think the
interest of justice require that unfortunately I probably need to ask a
question or two.

		In 2000, the Department of Labor passed regulations that involved
silicosis, and I just wondered, is there a "legal version" of silicosis
as there is a legal version of pneumoconiosis, which is consistent with
silicosis?

		MR. WEISSMAN:  Not to my knowledge.  As you know, for coal mine dust,
legal pneumoconiosis includes not only interstitial lung disease but
also COPD, you know, as evidenced by spirometry, and I'm not aware of a
parallel for silica.

		JUDGE SOLOMON:  Right.  But you were talking about exactly the same
testing.  It's exactly the same testing.  So I assume that the criteria
would be pretty much the same.  So the findings in 2000 primarily went
to smoking, what was the combination of smoking, let's say, and mining
exposure.  Is there something like that in the silicosis area?

		MR. WEISSMAN:  Not to my knowledge.  Not to my knowledge that there's
a way to apportion.

		JUDGE SOLOMON:  I don't think we apportion.  I think that the
regulations actually state that if it in any way affects the breathing,
it could be the spirometry, it could be the blood gas studies, and it's
probably compensable.

		So I'm sorry that I had to be a buttinsky, and I don't have any
further questions.

		So if there's nothing else today, we will convene again tomorrow at
9:30.  Is that correct?

		MS. LINDBERG:  Yes, Your Honor.

		JUDGE SOLOMON:  Okay.  So the time is now 4:17, and this hearing is
continued.

		(Whereupon, at 4:17 p.m., the hearing was continued, to resume the
next day, Wednesday, March 19, 2014, at 9:30 a.m.)

C E R T I F I C A T E

	This is to certify that the attached proceedings in the matter of:

INFORMAL PUBLIC HEARINGS FOR THE PROPOSED RULE

ON OCCUPATIONAL EXPOSURE TO

RESPIRABLE CRYSTALLINE SILICA

March 18, 2014

Washington, D.C.

were held as herein appears, and that this is the original transcription
thereof for the files of the United States Department of Labor,
Occupational Safety & Health Administration.

			      						         					____________________________

			         	ED SCHWEITZER

			         	Official Reporter

_________________________

		Continued

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