INFORMAL PUBLIC HEARINGS FOR THE PROPOSED RULE

ON OCCUPATIONAL EXPOSURE TO

RESPIRABLE CRYSTALLINE SILICA

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UNITED STATES DEPARTMENT OF LABOR

OCCUPATIONAL SAFETY & HEALTH ADMINISTRATION

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March 19, 2014

9:30 a.m.

Frances Perkins Building Auditorium

200 Constitution Avenue, N.W.

Washington, D.C. 20210

BEFORE: 	DANIEL F. SOLOMON

	   	Administrative Law Judge

U.S. DEPARTMENT OF LABOR (DOL):

KRISTEN LINDBERG

Attorney, Office of the Solicitor

ANNE RYDER

Attorney, Office of the Solicitor

IAN MOAR

Counsel for Health Standards, Office of the Solicitor

OCCUPATIONAL SAFETY & HEALTH ADMINISTRATION (OSHA):

WILLIAM PERRY

Acting Director, Directorate of Standards and Guidance

STEPHEN SCHAYER

Office of Physical Hazards

TIFFANY DeFOE

Office of Chemical Hazards - Metals

JANET CARTER

Office of Chemical Hazards - Metals

B.J. ALBRECHT

Chemist, Salt Lake Technical Center

JOSEPH COBLE, Sc.D., CIH

Director, Office of Technological Feasibility

DAVID O'CONNOR

Director, Office of Chemical Hazards - Non-Metals

DANIEL JOHANSEN

Chemist, Salt Lake Technical Center

PEER REVIEWERS:

KENNY CRUMP, Ph.D.

GARY GINSBERG, Ph.D.

BRIAN MILLER, Ph.D.

Institute of Occupational Medicine

U.S. CHAMBER OF COMMERCE:

HENRY CHAJET

Attorney, Jackson Lewis

JONATHAN BORAK, M.D.

President, Jonathan Borak and Company

CHRISTOPHER M. LONG, Ph.D.

Principal Scientist, Gradient

PETER A. VALBERG, Ph.D.

Principal Scientist, Gradient

PATRICK HESSEL, Ph.D.

Epidemiologist

THOMAS A. HALL, Ph.D., CIH

Former Professor, University of Oklahoma

ROBERT LIECKFIELD, CIH

Bureau Veritas HSE Laboratory

GERHARD KNUTSON, Ph.D., CIH

President, Knutson Ventilation

WILLIAM B. BUNN, III, M.D., J.D., M.P.H.

Consultant, Navistar

AMERICAN CHEMISTRY COUNCIL (ACC):

NEIL KING

Attorney, American Chemistry Council's Crystalline Silica Panel

LOUIS ANTHONY (TONY) COX, JR., Ph.D.

President, Cox Associates

OTHER PARTICIPANTS:

DAVID F. GOLDSMITH, M.S.P.H., Ph.D.

George Washington University

DR. ROBERT PARK

Risk Evaluation Branch, NIOSH

CHRIS TRAHAN

Building and Construction Trades Department, AFL-CIO

FRANK HEARL

Chief of Staff, NIOSH

ROSA KEY-SCHWARTZ

Division of Applied Research and Technology, NIOSH

DARIUS D. SIVIN, Ph.D.

Health and Safety Department, United Auto Workers

INDEX

										PAGE

INTRODUCTION

Judge Daniel F. Solomon					  	   PAGEREF Intro \h  267

INTRODUCTION OF PEER REVIEWERS

William Perry								   PAGEREF IntroPeerReviewers \h  267

U.S. CHAMBER OF COMMERCE

	Jonathan Borak, M.D.		 			   PAGEREF Chamber1Borak \h  272

	Christopher M. Long, Ph.D.	 			   PAGEREF Chamber2Long \h  297

	Peter A. Valberg, Ph.D.	 				   PAGEREF Chamber3Valberg \h  309

	Patrick Hessel, Ph.D.		 			   PAGEREF Chamber4Hessel \h  323

	Questions								   PAGEREF Chamber5QbyPeers \h  337

AMERICAN CHEMISTRY COUNCIL (ACC)

	Louis Anthony (Tony) Cox, Jr., Ph.D.		   PAGEREF Chem1Cox \h  375

	Questions 							   PAGEREF Chem2QbyPeers \h  400

U.S. CHAMBER OF COMMERCE

	Thomas A. Hall, Ph.D., CIH	 			   PAGEREF ChamberTwo1byHall \h  432

	Robert Lieckfield, CIH		 			   PAGEREF ChamberTwo2byLieckfield \h  441

	Gerhard Knutson, Ph.D., CIH	 			   PAGEREF ChamberTwo3byKnutson \h  447

	William B. Bunn, III, M.D., J.D., M.P.H.	   PAGEREF ChamberTwo4byBunn
\h  461

	Questions 							   PAGEREF ChamberTwo5byPeers \h  471

ADJOURNMENT								   PAGEREF ADJOURN \h  549

EXHIBITS

EXHIBITS		DESCRIPTION				 	PAGE

Exhibit 6		Reserved - Chamber of Commerce 					PowerPoint
PAGEREF e6m \h  336

Exhibit 7		American Chemistry Council

			PowerPoint 			  		   PAGEREF e7mr \h  429

Exhibit 8		Silica vial, 5.6				   PAGEREF e8_10mr \h  470

Exhibit 9		Silica vial, 12.7				   PAGEREF e8_10mr \h  470

Exhibit 10	Silica vial, 25.5		  		   PAGEREF e8_10mr \h  470

Exhibit 11	Reserved - Photo of silica vials	   PAGEREF e11mr \h  470

Exhibit 12	Checkoway study			  	   PAGEREF e12mr \h  496

P R O C E E D I N G S

(9:30 a.m.)

		JUDGE SOLOMON:  Okay, we're on the record.

		I'm Daniel Solomon.  I'm an administrative law judge with the United
States Department of Labor.  My address is 800 K Street, Northwest, 4th
Floor, Washington, D.C.  The zip code is 20001-8002.

		To get started this morning, Mr. William Perry will introduce the
peer reviewers.  Is that right, Mr. Perry?

		MR. PERRY:  Yes, Your Honor.

		JUDGE SOLOMON:  Just state your name again, for the record, because
some of the people weren't here yesterday.

		MR. PERRY:  Thank you, Your Honor.

		I'm Bill Perry.  I'm Acting Director in the Directorate of Standards
and Guidance for OSHA.  Today and tomorrow, we have most of the members
of the expert panel that conducted the peer review on OSHA's preliminary
health effects analysis and quantitative risk assessment.  They are here
in the audience to listen to witnesses today and tomorrow.

		We have Mr. Bruce Allen, Dr. Kenny Crump, Dr. Gary Ginsberg,
Dr. Brian Miller -- all the way from Scotland, and Dr. Andrew Salmon.
 And unfortunately, two of our other peer reviewers, Dr. Murray
Finkelstein and Dr. Noah Sayshus (ph.) did not -- had schedules that
did not permit them to attend, but we do have most of the panel present
here today.  Thank you.

		JUDGE SOLOMON:  Okay.  So the presentation this morning is from the
United States Chamber of Commerce.  Do you want to introduce the members
of the panel?  First of all, would you state your name for the record,
please?

		MR. CHAJET:  Good morning, Your Honor, members of the panel, peer
reviewers, and members of the audience.  Thank you for being here with
us this morning.  I am Henry Chajet.  I am a shareholder at the law firm
of Jackson Lewis.  We are of counsel to the United States Chamber of
Commerce.  We have a series of scientific, engineering, and economic
presentations that are written and in the rulemaking record.

		We will present summaries of those today, this afternoon, and we are
on for another day, I believe, on Friday.  So with that, let me
introduce my witnesses, if I may.

		JUDGE SOLOMON:  Sure.

		MR. CHAJET:  First of all, I just want to say a word about the Chamber
of Commerce.  The Chamber is the largest business organization in the
world.  It represents the interests of more than three million
businesses of all sizes, sectors, and regions, from small to
multinational corporations, and local chambers to leading industry
associations.

		To address the OSHA proposal, the Chamber has engaged a panel of some
of the nation's most distinguished scientists, physicians, engineers,
and experts on occupational health, as well as leading experts on
regulatory economics and on statistical analysis.

		Today we present some of that testimony focused on the science, and
later we'll present on other issues.  So our expert witnesses are led
and chaired by Dr. Jonathan Borak, who is behind me and to my left.
Dr. Borak is a clinical professor of epidemiology and public health, a
clinical professor of medicine, and a member of the Yale University
program in occupational environmental medicine.  He's also President of
Jonathan Borak and Company, a professional services consulting firm with
extensive expertise in occupational and environmental health.

		Also on our panel and sitting to my right is Dr. Peter Valberg.
Dr. Valberg is a principal at Gradient, an environmental consulting
company in Cambridge.  He works in the areas of human health risk
assessment and inhalation toxicology.  He has 30 years of experience on
the faculty of the Harvard School of Public Health, where his research
centered on how inhaled particles and gases affect cell function, and
how particle dose relates to the risk of lung disease.

		At Gradient, Dr. Valberg has provided air quality and public health
expertise to the Department of Justice, the United States Environmental
Protection Agency, the National Academy of Sciences, and a variety of
private and public clients.  He's a fellow of the Academy of
Toxicological Sciences, and he's authored more than 100 peer-reviewed
articles on how environmental exposures might lead to adverse health
affects.

		Dr. Chris Long is another one of our experts on the reviewing panel.
He is a principal scientist at Gradient, and he specializes in air
pollution exposure assessment and inhalation risk assessment.  Prior to
joining Gradient he received his doctorate in environmental health from
the Harvard School of Public Health, where he conducted a research study
to characterize particulate matter mass concentrations, size
distributions, and chemical composition inside and outside residential
homes.

		Dr. Long has prepared approximately 25 peer-reviewed journal articles
or book chapters in the general areas of indoor and outdoor air
pollution exposures and risk assessment and on inhalation toxicology.
He is certified as a diplomate of the American Board of Toxicology.

		Also joining our panel is Dr. Patrick Hessel, sitting behind me and
to my right.  Dr. Hessel is an epidemiologist with a focus on
occupational environmental lung disease.  He holds a master's in
environmental health from the University of Minnesota, and a doctorate
in epidemiology from the University of Pennsylvania.  He has conducted
research on pneumoconiosis, specifically silicosis and asbestosis,
asthma and respiratory cancers.  I will introduce the rest of our panel
in the next part.

		JUDGE SOLOMON:  Okay.  We're sort of pressed for time this morning,
and the Chamber of Commerce has advised me that they're going to take
about an hour and a half.  We will have some questioning from the peer
reviewers, then we will have some questioning from the public, and then
OSHA will comment.

		Now, we'd like to be able to do all of that before lunch.  We have
another panel that's scheduled to come in at 1 o'clock.  So do you want
to begin with your presentation?

		MR. CHAJET:  Yes.  Dr. Borak will chair our session and begin with
his presentation.

		DR. BORAK:  Thank you.  Good morning.  My first question, actually,
before I do anything, is to make sure I've got the right buttons.

		I am summarizing comments that I've submitted, and I've expanded them
a little bit.  And what I would like to do is provide a background which
really addresses a single question, which is the extent to which there
are data that reflect on the adequacy of the permissible exposure limit
of 100.  And my premise, ultimately, said quickly and summarized, is
that there is not such direct empirical data.

		This is a slide which I think by now is more than familiar to
everybody in the room, and which Mr. Perry indicated had, in fact,
continued to decline in -- at least his comments yesterday, and which
shows a 93-plus percent decline in the rate of silicosis deaths.
Yesterday there were certain questions about the meaningfulness of the
slide, and I want to talk about it from a slightly different
perspective.

		One of my concerns has to do with the long latency of silicosis, and I
think it's an issue that pertains largely to interpreting the data that
are on the table.  OSHA in its post-rulemaking, or in this case the
background document, that's shorthand for a very long named document,
which is a summary of medical information and a risk assessment, which
was part of the 2010 docket, says that the latency period for silicosis
is 10 to 30 years after first exposure.

		In fact, review of the literature of some of the more important, kind
of classical silicosis case reports indicates that the latency is
actually significantly longer.  The Hnizdo and Sluis-Cremer report of
South African gold miners with 313 cases indicates a mean latency of 35
years and a range of 18 to 50.

		The Vermont granite workers by Costello and Graham reports a series of
38 deaths and a much larger number of workers, and says that 92 percent
had latency greater than 30 years.

		de Klerk and Musk, in Australian gold miners, presents a large series,
with 630-plus cases of silicosis in which the peak incidence of
silicosis was actually 45 years after first exposure.

		A more interesting study from several standpoints is the very large
Chinese cohort study, which continues to be the subject of ongoing
publications as recently as the last few months subsequent to the OSHA
rulemaking.  That's this cohort often referred to as the Chen cohort.

		But there is this one very interesting study from 2006 that speaks to
the latency.  It's published in a journal that I think few of us
actually subscribe to, but which is available, at least through the Yale
Library and probably others, in which a consideration of latency and
progression was made.

		OSHA cites this paper in its documents as having a latency period of
22.9 years, but there's a different side to that if you look at the
context of the exposures.  This is a table that comes from that paper,
and what you can see is that OSHA has taken the weighted average latency
for a period of close to 40 years.

		The left column describes the year of first diagnosis.  And what is
really striking when you look at this is the fact that the latency
described in this paper, over the course of the 30 or so years of the
captured time, tripled, that the typical latency went from about 11 or
12 years to about 33 to 36 years.

		That's striking.  That doesn't have a very obvious biological basis.
And it's useful to look to see what might have provided such a wide
range of latencies.

		Chen, another paper in that series, this one from '92 in the Journal
of Occupational Medicine, speaks of the facts that operations in this
cohort, this included 20 mines of four types and 9 or 8 pottery
factories, and that operations began before 1949.

		They included workers who had been exposed for at least one year,
working between '72 and '74, but not those who started in '70 to '74.
Many of the workers had preceded for quite a long time.

		And in that paper they provide some insights into the levels of dust
to which people were being exposed, and you can see that the ranges in
that study went up to close to 25 or 30 mg/m3.  We're talking two to
three times the OSHA PEL and the TLV for nonspecific particulate.

		And in 2006, in another reiteration and follow-up of that study, they
described something of the time distribution of those exposures, that
during the 1950s until about 1958, when the first exposure controls were
implemented, that the average exposures were in the range of 10 to 25
mg/m3, and at that time they did not use dust protection on individuals.
 There was no personal protection.

		That those levels, starting around 1958 or 1960 fell dramatically, but
they still remained in the area of 4 to 8 mg/m3 -- once again, we're
talking total dust, not crystalline silica, and then gradually
progressed downward.  So we're looking at a rather dramatic high end and
a rather striking decline.

		And I'm so happy, because when I looked at these slides last night on
an iPad, this didn't project, so I'm just a happy camper now.

		This is a figure that comes from the 2012 Chen study.  This is after
those dust measures have been converted to respirable silica and
crystalline, and the three mines which are the subject, or the three
cohorts which are the subject of the Yang study, which I've just shown
you, are in the purple, the red, and the green.

		And they just serve to emphasize the dramatic step-down and the period
of exposure, that these were not average exposures.  You can average
them, but there was no typical or average.  They were really
time-dependent.

		And what I've done here is to say that if we blocked out the first or
three tranches of the diagnostic group and look at those that were most
recent in the last 15 or 20 years, what you see is that the weighted
latency period for those workers is in the range of 30-plus years, not
the lower period.

		It serves to do two things.  It serves to reemphasize that the average
latency or the mean or the median, however you want to take a central
tendency, is longer than estimated in the OSHA proposed rulemaking
documents, and secondly, I think it provides some interesting insight
into the question of dose rate as opposed to simply cumulative dose.

		I think that it's hard to escape the fact that there was just an
enormous dose rate during those early 8 or 10 years or more, when people
were being exposed to humongously high, extraordinarily high levels.
And that is probably a component of both the development of disease and
the rate or progression of disease.

		We can also look at the latency issue looking at the SENSOR data.
This is a point I'm going to make very quickly because it's kind of
reiterative.  David Weissman yesterday already described this in his
testimony from NIOSH, that the SENSOR data really does not pertain to
those cases that are being found nowadays.

		But what I'm looking at here, or showing you here, is a figure that
comes from the most recent 2012 NIOSH publication of the SENSOR data,
and that shows the decades of first exposure of those cases entered into
the SENSOR registry between 1993 and 2006.  The little blue box on the
far right side simply shows you the period of time during which case
ascertainment was being made.

		This shows you what would have been a 30-year latency if all of those
cases had been detected on the first day of that recognition period.  If
I move that out to the midpoint in that recognition period, you see that
there's a very small proportion that have less than at least a 30-year
latency, and 40 years, clearly more.

		And these are, in fact, the data that come from the most recent three
SENSOR publications regarding effective latency and onset of silicosis.
In the 1997 publication from Michigan, 96.3 percent of the cases
recognized between '87 and '95 had first been exposed before OSHA, in
fact, came about, and clearly before the PEL was enacted.

		In the second series, 90.5 percent, and the most recent -- the one
that I just showed you, distribution, 87 percent of those cases were
exposed before the adoption of the OSHA Act and the promulgation of the
PEL.

		Simply to say that it is difficult to use those SENSOR data for the
purposes of trying to evaluate the current day risk of exposures,
because the exposures that contributed to SENSOR data predated the OSHA
PEL.

		OSHA has relied upon SENSOR data, and also a couple of other related
studies, Goodwin and Rosenman, to estimate the under-reporting of silica
cases.  And Patrick Hessel will discuss some of the methodological
limitations of those two studies, and discuss some of the limits to
their use for the purpose of trying to extrapolate and estimate
under-reporting.

		Then there's another interesting aspect, which is the long duration of
survival after the diagnosis of silicosis.  This is -- well, there were
a series, I think the white progresses down with progressive slides, a
large study of Italian silicotics actually compensated for silicosis,
1258 deaths, and the survival time between first diagnosis and death was
a median of 23 years in that series -- large series.

		In the Yang study, which I mentioned a bit earlier, the survival time,
the mean was 21.5 years from diagnosis of silicosis 1 on x-ray, to the
time of death, and 25 percent were longer than 33 years.

		In the pooled IARC study of silicosis, with 170 silicosis deaths,
while there is not a specific, clear statement of the duration of
survival, what you see is that the median duration of exposure was
28 years, and only 9 percent died within a year thereafter, so it's
clear that there was a combination of exposure and duration that would
have been quite a long period of time.

		The implications of the latency and the survival durations are fairly
straightforward, going back to that familiar CDC chart.  If you consider
that a mean latency of 30 years and a mean survival of 20 years -- and
I understand that that's a simplification, but for the moment, if you
assume it, then the fact is that virtually all the cases reported as a
mortality were first exposed in a period that preceded the adoption of
the PEL and the adoption and enactment of the OSHA Act.

		And it suggests that the data have only limited probative value with
respect to whether this speaks to the permissible exposure limit and its
adequacy in protecting workers.

		There are obviously cases of silicosis that are associated with
shorter latency, and I don't mean in any way to ignore those.  Acute
silicosis, a horrific disease which occurs with very, very high
exposures, and which can have an onset in a matter of even weeks, but
certainly within a matter of only a few years, described by OSHA as
being intense exposures, high crystalline silica content, very high
concentrations.

		And accelerated silicosis is generally regarded as being an onset
within 5 or 10 years, again to very high exposures, intense, often
unprotected, substantial overexposures, says OSHA, and extremely high
exposures in the words of NIOSH researchers, which simply serves to say
that to the extent that there is short latency onset of silicosis --
and there is, it does not provide evidence of the PEL's adequacy or
inadequacy, because those short onset cases are almost all exposed to
these extremely high levels, which do not provide insight into a
proposed or enacted 100 µg/m3 PEL.

		So in summarizing this piece, I think that neither the SENSOR data nor
the remaining silicosis-related deaths in the CDC data demonstrate that
the current PEL is not protective, simply because there is high
exposures that predated OSHA, because the shorter latency cases due to
substantial overexposure and unprotected don't count as evidence against
the current PEL.

		And so I think the SENSOR data and the CDC death data actually are not
a factor in the assessment of the adequacy of the current PEL.

		There is also significant evidence from OSHA and others that there is
and has been extremely widespread overexposure to silica despite a
significant and steeply declining trend in exposure levels.

		This is a composition of data, mostly OSHA data.  The first six lines
are from a study by Yassin and colleagues, OSHA scientists looking at
the Integrated Management Information System, a compilation of OSHA
compliance data, and the latter two are German data.  The first one,
actually, is cited in the OSHA preliminary analysis and the second one
is not cited therein.

		And what they show are the levels of exposure in the duration of '79
to 1987, and then the mean between '88 and '03.  And the third column
shows you the extent of the decline in the silica mean exposure levels
over those time periods.

		And what you can see based upon those data, that the decline that did
take place was between -- in those industries, 50 to 85 or 90 percent,
a rather dramatic decline.  Nevertheless, it did not eradicate a
persistent and important overexposure, which I think is something that
needs to be addressed and hopefully will be.

		In the CDC publication, which included the original of that
now-familiar 93 percent decline, CDC said that despite the reductions in
mortality, silica overexposure remains widespread.  The NIOSH
scientists, commenting upon the persistence, said that despite the
existence of enforceable limits on worker exposure to respirable
crystalline silica, substantial exposure continues to occur in the U.S.
That's in 2008.

		And the OSHA background document cites a range of 0.12 to 0.48 --
that is from above the current PEL to above four times the current PEL,
and says that that falls within the range of exposures of particular
interest.  Exposures in this range or not much lower are common today.

		Simply to say that there is a persistent and important ongoing
overexposure, which is clearly a health concern, and which needs to be
addressed.

		Here are some data that reflect specifically on the extent of those
ongoing and current overexposures.  This is from NIOSH 2007, which says
that from '93 to 2003, about 23 percent of the silica levels in coal
mining, 11 percent in metal/nonmetal mining, and approximately 40
percent in the following industries were over the PEL.

		And they go on to speak about iron and steal foundries, construction
machinery except electrical fabricated structures, with at least
one-third of their exposures exceeding the PEL.  These are recent
data -- or not most current data, but these are fairly recent.  These
are not historic.

		These are data that come straight out of the preliminary economic
analysis.  These are the data that were largely but not entirely put
together by Eastern Research Group, and they give a cross-section of
some of the worst offenders in the industries and sectors.

		Looking at the proportion of data that were over the current PEL,
that's the far right hand, or over 250 µg/m3 -- that's the
intermediate or the middle column -- and what you see going through
this is that a very significant proportion of the data cited by OSHA as
current or recent is largely above the OSHA PEL.  And it's a dramatic
and important degree of exceedances, which needs to be addressed and
should be the focus of attention, I think.

		In a series of ongoing studies and others which contribute additional
insight, Mary Ellen Flanagan and her colleagues at the University of
Washington looked at a large number of construction workers, 13
databases including the OSHA IMIS database, 1375 or so personal samples,
found that 13 percent of all of those samples exceeded 1 mg crystalline
silica, and went on to caution that the range of exposure for any tool
or task is extremely broad, spanning three or four orders of magnitude
for most tasks or tools.

		This wide range means that using any measure of central tendency to
represent an activity can seriously underestimate exposures in some
cases.  My point here is to emphasize the extent of the overexposures
that continues to persist in American industries.

		This is a graph from a paper by Stephen Rappaport.  He looked at four
different categories of construction workers.  The red line is the OSHA
PEL.  The black line is the NIOSH REL.  And we're looking at these four
different groups of workers who represent a very large portion of the
construction work industry.  And what we're looking at is a tremendous
number of exposures which exceed the PEL, and even more exceeding the
REL.

		The bottom line seems really simple to me.  It is that there is a
gigantic amount or risk of a very large pool of people who are being
significantly overexposed, and that that database is so great and so
pervasive that it makes evaluation of the PEL as a -- and its adequacy
to be protective almost moot, because it's very hard to attribute any of
the cases being recognized to people who are being exposed at or even
near the PEL.

		Let me remind you of this slide which I showed earlier.  Right now I'm
showing it to you for one very simple reason.  I want you to look at the
left-hand column and just see how bad exposures were in the period of
'79 to '87.  I don't mean to beat the drum on this, but I am going to.

		The point is that if you allow for a 20- or 30-year latency or even
less, as recently as 20 or 25 years ago there were workers who
apparently were being regularly exposed to levels that are just
egregiously high.  And their impact on the pool of silicosis or
silicotics or potentially such people is obvious.  I mean it's really a
rather remarkable thing.

		The OSHA Preliminary Economic Analysis data reflect recent but not
current exposure levels, and it's unclear to what extent that a
significant decline in exposures has continued.  ERG primarily looked at
data from the late '80s to 2001.  OSHA updated a little bit, they say
through 2007, and it's true.

		But the fact is that there's at least a strong trend of decline, and
it's interesting but not documented in the OSHA materials as to whether
that decline has continued.  And I understand but don't know on first
hand that the data that would provide such insight has not been made
generally available.

		Then let's jump from that to issues of the risk assessment.  OSHA, I
think, correctly says essentially that the CDC and SENSOR data are not
sufficient to be able to draw conclusions with regard to the
occupational exposure limit for crystalline silica, and that it is the
dose-response data that are appropriate for that purpose, the
hypothetical risk assessment applications rather than the empirical data
itself.

		OSHA goes on to say that it believes that uncertainty in the exposure
assessment that underlie each of, for example, the 10 studies in the
IARC pooled meta risk assessment represent one of the most important
sources of uncertainty in the risk assessment, and the authors of that
paper concur.

		Nine of the 10 pooled studies used exposure methods that differ from
those in the proposed Notice of Proposed Rulemaking, and go on to say
that:

		"Measurements in all of these various different units and using all of
these different methods require conversion to a common unit for purposes
of conducting a risk assessment.  And one weakness to our data is our
reliance on conversion factors for which, generally, we have no way to
assess the validity."  It's a concern to the underlying nature of that
risk assessment.

		"In addition, the purpose of the analysis was to determine exposure
response trends, not point estimates of risk levels."  And the
cautionary note was that categorical analyses based on broad exposure
groups could be performed using those data.

		OSHA considered the impacts of some of those exposure
misclassifications, particularly the data as described in the toxic
chemical report, use of job-specific average exposure levels, use of
average conversion factors for dust to respirable crystalline silica,
and use of biased conversion factors in the one South African study.

		And Dr. Chris Long -- who's on my right, one over, will detail
numerous other sources of exposure misclassifications and errors and
likely impact on the respirable crystalline silica risk assessment.

		There are also, in addition, concerns over and beyond those of the
exposure misclassifications that have to do with errors in the exposure
measurements themselves.  There's known variability and quantifiable
errors associated with sampling pumps, samplers, laboratory analyses.
And Dr. Tom Hall will discuss -- and Dr. Robert Lieckfield will
discuss this afternoon the variability and errors that characterize
OSHA's proposed sampling methods.

		They will also talk about the magnitude of those errors and raise
concerns about the feasibility of the OSHA-proposed methods for the
purpose of monitoring at the proposed PEL and action level, and the
capacity to meet OSHA's own proficiency standards for accuracy and
precision.

		Now, sampling and analytical errors have not been incorporated into
the risk assessments to the extent that the actual measurements cited in
the text have all been treated as if they were error-free.  Chris Long
will discuss the effects of sampling, analytical, and other measurement
errors on the risk assessment, including bias of effect estimates,
distortion of exposure response curves, and the obscuring of estimates
of threshold concentrations.

		The issue of thresholds is something which is really understated and
needs to be highlighted and dealt with, I think, with more detail in the
final documentation that comes out of OSHA.

		In addition, I point out that the adoption of the ISO/CEN convention,
which provides the advantage of harmonization, which is, in and of
itself, a desirable thing, results in a greater mass of particles
collected for any given exposure level.

		And OSHA says for most workplace conditions, the proposed change to
criteria would increase the mass of respirable dust collected over that
measure over the current criteria.

		And Soderholm has addressed the extent to which that will have an
upward bias on the loading that results and the implicit exposure
levels.  And the problem will be that the exposure levels that are taken
using the ISO/CEN convention will be inconsistent with the exposure data
that underlie the risk assessments.

		The risk assessments have not incorporated the fact that the ISO/CEN
will change the amount of loading and the implicit levels of exposure
that will result from the use of the new pumps.

		Now, the definition of respirable crystalline silica by OSHA, airborne
particles that contain quartz cristobalite and/or tridymite, whose
measurement is determined by a sampling device designed to meet the
characteristics of the respirable size selective samples, is ambiguous,
unfortunately, although we all understand what is intended.

		Because the performance of individual samples, as Tom Hall will tell
you later, vary, the proposed performance-based definition would yield
variable results depending upon the sampler used for any given
environment.  And that will be something which will be discussed during
the afternoon presentation.

		Recommendations to simplify and avoid the ambiguity of that definition
include, one, defining respirable crystalline silica as the quartz that
is contained in the air and not as the particle containing quartz that
is in the air, and to define respirable crystalline silica by size
rather than performance standards of a sampler, given the fact that the
samplers are all somewhat variable and prone to under- and over-sampling
in various and idiosyncratic ways -- not idiosyncratic, predictable but
distinct to each sampler.

		Exposure response thresholds, there is substantial support in the
literature for the view of exposure response thresholds between inhaled
silica and the development of silicosis, that is a threshold function.
And Chris Long will speak to that particular concern and how exposure
measurement errors can contribute to obscuring the exposure response
thresholds.

		He's going to speak, Chris will, with regard to silicosis.  IARC, in
its two monographs on silica, have made the point that there is no
convincing evidence for a direct physical-chemical mechanism for
crystalline silica-induced genotoxicity.  And the question becomes, is
there a direct mechanism of silica-induced lung cancer?

		IARC summarized seven meta-analyses in their most recent monograph and
concluded that there were increased risks of lung cancers among workers
with silicosis, and no increased risk of lung cancer in those without
silicosis.

		I think there's no question in people's minds that silicosis itself
has a threshold.  So the question of whether silicosis is a necessary
precursor becomes a very important aspect of doing the risk assessment
for lung cancer itself.

		There is a very interesting recent paper, I'm sure you are all aware,
by Liu et al., published last summer or early fall and included -- not
included directly in the Notice of Proposed Rulemaking, but included in
any number of the comments that have been submitted, which claims to
break new ground by documenting a substantially increased risk of lung
cancer in those Chinese cohorts of whom we spoke earlier -- I spoke
earlier, who did not have silicosis.

		But the absence of silicosis in that study was defined as negative
chest x-rays.  And it is important to consider -- and surprisingly,
those authors did not -- that there is a very direct dose-relatedness
between level of exposure and probability of false negative chest x-rays
for silicosis.

		Now, that particular set of data comes about from a series of studies
that Eva Hnizdo and colleagues did in 1993 in South Africa, in which a
series of workers, underground miners who were in a healthcare program,
unselected otherwise, and those who went to autopsy were evaluated.

		Of the 500-plus individuals with silicosis in their autopsies, then
pathology studies, their pathology was compared to their most recent
chest x-rays.  And the data showed that the prevalence of or the
prediction of the chest x-rays for negative values declined sharply.
The probability of a false negative increased dramatically in a
dose-related way.

		This is one of the tables from that study.  What we're looking at
there is, on the vertical, the probability of a false negative chest
x-ray, that is, a chest x-ray without silicosis, in a worker
subsequently found at autopsy to have silicosis.

		And what we're looking at along the x-axis is the duration of
exposure.  And those five lines going across reflect different levels of
dust exposure ranging from 100 to 500 micrograms to milligram per cubic
meter.

		And, in fact, when you look at that report, what you see in the
highest exposure group of the Hnizdo cohort, that false negatives --
that negative x-rays with false negatives in the highest exposure group
up to 92 percent of the time.

		That very strong dose-relatedness of false negative x-rays is not
considered in the context of the Liu study, and I suspect -- but it's
beyond my mathematical skills, so let me make that clear, that if one
were to combine the estimates of false negatives in that study with the
actual data, you would find that there was little or no increase in the
risk of lung cancer in those with negative chest x-rays, because in
those groups with positive associations, there would be very high
numbers of people with normal chest x-rays and positive silicosis.

		So I'm concerned that this study is going to be over-read by others,
and so I raise that as a note of caution.

		These are the data, just to indicate again, the levels of exposure --
this is to respirable crystalline silica, in that underground -- in
that study of the Chinese workers, the pottery workers and the three or
four groups of underground miners.

		Interesting to note that the iron and copper workers in the lowest
tier, who would be the group most relevant to evaluating the 100 µg/m3
PEL, were not independently studied.

		In summary, I think that there is a lack of direct evidence that the
100 µg/m3 standard is not protective.  I think that there are no
empirical data on workers at that level.

		There has been and continues to be widespread exposure and
noncompliance, and as a consequence there are lots of workers who
unfortunately are being overexposed, and they are being overexposed in
many of the industries most likely to be associated with silicosis and
silica-related health effects.

		The exposure assessments have been uncertain for a variety of reasons,
including the technical limitations of the measurement sampling and
analysis methods.  And also because of the ways in which the existing
data have been used, there has been a tendency to discount the exposure
response threshold, which are almost certainly true for silicosis and
most probably true for the lung cancer.  Silicosis is a necessary
precursor, and the definition of respirable crystalline silica is
probably too ambiguous, and it will be problematic.  Thank you.

		JUDGE SOLOMON:  Okay.  We've used up approximately half the time that
was allotted, so you also have some time this afternoon.

		MR. CHAJET:  We do.

		JUDGE SOLOMON:  So how can we use, best use, most efficiently use the
rest of your time this morning?

		MR. CHAJET:  I think we should continue to go through the panel.  We
will have, I believe, enough time left to finish the panel.  And if we
combine the time from this afternoon and this morning, I'm sure we'll be
able to complete it.

		JUDGE SOLOMON:  Okay.  Go ahead.

		DR. LONG:  My name is Chris Long, and as Henry mentioned, I'm a
principal scientist at Gradient, an environmental and health science
consulting company based in Cambridge, Massachusetts.

		In the next 10 or 15 minutes or so, I'll be focusing on exposure
measurement errors as potential sources of biased risk estimates, and of
threshold obscuring or threshold shifting effects in the silica worker
epidemiologic cohort studies that are the basis for OSHA's risk
assessment.

		Exposure measurement error, which can be defined quite simply as the
difference between an estimate of worker exposure that is used in an
epidemiology study and an actual personal exposure level, is recognized
to be a common source of uncertainty in most occupational and
environmental epidemiologic studies.

		This is particularly the case for the silica worker cohort studies,
given the general scarcity of exposure measurements across all affected
individuals and exposure time periods of interest.  Both OSHA and its
peer reviewers have acknowledged exposure measurement error to be an
issue of significant importance to OSHA's risk assessment.

		Some of the issues that I'll be discussing will not be new to the OSHA
peer reviewers, since they've also raised them.

		I've organized my comments on exposure measurement error around three
main points.  First, it is now well recognized that exposure measurement
errors can have significant impacts on occupational and environment
epidemiologic studies, with impacts including effect estimates that are
biased high, distorted exposure response curves, and either complete
masking of threshold concentrations or underestimation of threshold
concentrations.

		Second, the silica worker cohort studies are subject to the potential
impacts of a variety of different sources of exposure measurement error.

		Third, OSHA's assessment of exposure measurement error is very
limited, in terms of the sources of exposure measurement error that it
considered, and in its adequacy for addressing questions related to
potential impacts of these errors and risk estimates and thresholds of
response.

		So I'd now like to make a few general comments about exposure
measurement error and its well-recognized ability to bias regression
coefficients, modify exposure response relationships, and either hide or
cause an underestimation of threshold estimates.

		These general comments are based in part on a review paper that I
co-authored, along with several other Gradient scientists for
publication in the peer-reviewed journal, Critical Reviews in
Toxicology.

		This paper, which is titled, "Measurement Error in Environment
Epidemiology and the Shape of Exposure Response Curves," was published
in 2011.  As indicated in the title of the paper, it focused on the
existence and impacts of non-differential exposure measurement error on
the shape of exposure response curves and the estimation of threshold
parameters.

		As discussed in great detail in the paper, it is now well known among
statisticians and epidemiologists that random errors in the values of
independent variables, such as estimates of exposure, can bias
regression results.  This is true for random errors, including both
Berkson type and classical type random errors, as well as systematic
errors.

		Moreover, there are several examples in the literature of how this
bias can sometimes be sufficient to distort the shape of exposure
response curves, and to either completely obscure true thresholds or
result in threshold underestimation.

		Based on our comprehensive review of the epidemiologic and statistical
literature, we concluded in the paper that error in independent
variables, such as exposure variables, tends to smooth out and flatten
and essentially linearize curves from a variety of different types of
regression models.

		Written comments submitted to OSHA provide several examples from the
occupational and environmental epidemiology literature, but I'd like to
highlight one example that I find to be particularly compelling.

		It's from a 2002 paper from the journal, Risk Analysis, titled
"Exposure Misclassification and Threshold Concentrations in Time Series
Analyses of Air Pollution Health Effects."  That was published by
Michael Brauer and several other researchers at the University of
British Columbia.

		The Brauer et al. paper focused on Berkson type random error arising
from the use of community average PM2.5 data from outdoor central site
monitors to represent personal exposures to ambient PM2.5.

		I think important lessons can be drawn from this scenario, where
community average PM2.5 data are used to represent individual personal
exposures for the common scenario in the OSHA risk assessment where
group level average respirable crystalline silica exposure estimates are
assigned to individuals in silica worker studies.

		Brauer et al. conducted simulations where individual level mortality
risks were estimated for exposure response models incorporating the
source of exposure measurement error in different threshold assumptions.

		As persuasively demonstrated by figures in the paper, there is no
evidence of a threshold at the lowest value of the true threshold
parameter.  While the exposure parameter, while the exposure response
curves for the other, higher assumed threshold levels retained some
evidence of non-linearity, the threshold estimates were biased low.

		As we noted in our paper, these findings strongly suggest that the
inability to detect a threshold in many epidemiology studies does not
mean that no threshold exists.

		Next, I'm going to move on to exposure measurement error specific to
the epidemiologic studies of silica-exposed workers.  You know, we
discuss in great detail in our written comments to OSHA how these
studies are likely subject to a number of additional sources of
potential exposure measurement error beyond the three error sources
considered in the assessment of exposure measurement error in OSHA's
report.

		You know, OSHA's analysis considered three sources of exposure
measurement error, namely two sources of Berkson type random error,
specifically the assignment of job-specific average exposure levels from
a job exposure matrix, and secondly the use of average conversion
factors to convert historical dust measurements to gravimetric
respirable silica equivalents.

		In addition, they considered a single source of systematic error,
namely the use of biased conversion factors for converting historical
dust measurements to gravimetric respirable silica equivalents.

		However, in our written comments, we've identified at least 10
additional sources of potential exposure measurement error in a
comprehensive table.  I'm not going to describe each of these additional
sources of exposure measurement error, but a few prominent examples
include the following:

		First, error associated with the estimation of historical levels,
which necessarily results from a general lack of exposure measurement
data for many worker cohorts for time periods prior to the 1950s.

		Second, error from between measurement variability, such as due to
factors such as instrument error, sampling and pump error, which will be
talked about in more detail this afternoon.

		Third, error from between sample duration variability; this can arise
from the use of short-term samples versus full-shift samples.

		Next, error from between sample location variability; this can arise
due to the use of area samples versus personal exposure samples.

		Also error from between sample type variability, due to the use of
measurements targeted to assess compliance versus measurements from
random exposure surveys.

		Following on this comment, I'd now like to briefly discuss some of the
key shortcomings of OSHA's assessment of exposure measurement error that
limit its utility for making any conclusions regarding the role of
exposure measurement error as a source of bias to silica effect
estimates and threshold estimates.

		These key limitations include the following:  First, as I just
discussed, the estimate only considered a small fraction of probable
error scenarios for these kinds of studies.  Second, there are no formal
analyses conducted to determine the error structures of the three
sources of exposure measurement error included in the sensitivity
analyses;	for example, without any formal analysis, the OSHA assessment
simply assumed a purely Berkson type error structure from the assignment
of job-specific average exposure levels for individual exposures.
However, there are a number of published studies that have shown that
this type of exposure measurement error can often have a more complex
error structure with properties of both Berkson type and classical type
random error.

		JUDGE SOLOMON:  While he's taking a break, I neglected to say at the
beginning -- I did say it yesterday, that anybody who has a cell phone
or any other device should make sure that it's off.  And if there's any
conversation, if you need to talk to each other, we would appreciate it
if you go outside and do it.  Go ahead.

		DR. LONG:  Thank you.  Next, another limitation the OSHA assessment
was its assumption of log linear -- it assumed essentially specific
types of models, including log linear models with log-transformed
exposure variables, and it focused on cumulative measures of silica
exposure that obscure both within-person and between-person variability
in exposure rates.

		Just by limiting itself to these types of models, it's just, it's not
known whether other possible models and exposure metrics, such as
non-transfer in exposure variables, are more or less sensitive to
exposure measurement error.

		Another key limitation involved its narrow focus on impacts to
regression coefficients rather than impacts to the shape of exposure
response curves and threshold estimates.  There's very little discussion
in the OSHA report regarding the potential impacts of exposure
measurement error on identification of thresholds.  And this is true
despite peer reviewer comments noting how little attention is given to
the threshold issue.

		Moreover, ToxiChemica, which is the group that performed the
sensitivity analyses that are the centerpiece of OSHA's assessment of
exposure measurement error, noted that exposure response threshold
estimates are imprecise and appear to be highly sensitive to measurement
errors.

		Next, the sensitivity analyses that were conducted by ToxiChemica for
the OSHA assessment were restricted to studies of lung cancer and
silicosis mortality and did not address studies for other health
endpoints including silicosis morbidity and renal disease mortality.
It's thus unclear whether data for these other silica-related health
endpoints are more or less sensitive to exposure measurement error.

		For lung cancer and silicosis mortality, OSHA includes a rather uneven
discussion of the mixed and inconsistent findings of the ToxiChemica
sensitivity analyses that fails to adequately discuss their
implications.

		For example, OSHA concludes that exposure measurement error is
unlikely to be a major source of uncertainty to the estimates of lung
cancer risk, despite finding that a few cohorts were highly sensitive to
the two simulated sources of Berkson type exposure measurement error.

		In particular, one of the studies of South African gold workers, there
was a 70 percent reduction in the effect estimate once the two sources
of Berkson type random error were accounted for.

		In addition, OSHA noticed that the silicosis dataset was found --
silicosis mortality dataset was found to be more sensitive to the
impacts of the three sources of exposure measurement error than the lung
cancer dataset, but offers no discussion of the reasons for this
difference.  Strangely, for silicosis mortality, there really are no
clear conclusions on the significance of the exposure measurement
errors.

		To conclude, I'd like to emphasize that our written comments delve
into these topics in greater detail.  Rather than repeating each of the
conclusions from our written comments, I'd like to highlight two key
conclusions.

		First, overall, is our conclusion that the silica worker cohort
studies are subject to a variety of potential sources of exposure
measurement error beyond just the three types considered in OSHA's
assessment.  Due to this limitation as well as other limitations that
I've discussed, OSHA's assessment is highly limited and insufficient for
ruling out potential biases from exposure measurement errors that can
affect the interpretation and use of exposure response associations from
the epidemiologic studies of occupational exposures to respirable
crystalline silica.

		Accordingly, OSHA fails to provide adequate scientific justification
for the conclusions of its risk assessment.  There's a need for OSHA to
conduct additional analyses to further assess the potential impacts of
exposure measurement errors on its risk assessment findings.

		In particular, you know, this is true with respect to the
identification of possible thresholds of response.  It may be prudent
for OSHA to reanalyze the epidemiologic data using available techniques
for correcting for potential biases from exposure measurement error,
rather than treating the literature exposure estimates as if they're
accurately known and error-free.

		Thank you for your attention.  I'd like to turn it over to my
colleague, Dr. Peter Valberg.

		MR. CHAJET:  Then I guess we should continue.

		JUDGE SOLOMON:  We are going to take a break, but I'll wait until
you're done with the -- with your presentations, unless anybody has
some urgency.  Okay, go ahead.

		DR. VALBERG:  All right, thank you.  My name is Peter Valberg, and
I've spent a fair amount of time in the area of human health risk
assessment, and I'd like to offer a few comments to OSHA with regard to
the Preliminary Quantitative Risk Assessment.

		A key question in the nature of exposure is response relationships, is
the nature and shape and functional form.  For inhaled crystalline
silica, the existence of a threshold -- and by threshold, we mean a no
adverse effect level -- is suggested by several lines of evidence,
including animal toxicology, mechanistic considerations, and some of the
epidemiology studies.

		And as Chris has already mentioned, the peer review panel of 2010
offered some interesting advice pointing to the need for careful
consideration of thresholds, and yet it seemed like the Preliminary
Quantitative Risk Assessment didn't really follow up on this particular
advice.

		For poorly soluble particles like crystalline silica, biological
mechanism and laboratory animal evidence support the idea that
persistent lung inflammation is a necessary step in the development of
both malignant -- both nonmalignant and malignant lung disease.

		A persistent inflammatory state can develop when inhalation exposure
exceeds the ability of the lung to clear deposited particles and to
neutralize free radicals and cytokines that are released by cells in
response to particles retained on lung surfaces.

		We all inhale particles on a daily basis, and our lung defense
mechanisms are capable to deal with these.  And if those lung defense
mechanisms are not overwhelmed, the lung will be able to deal with
particle burdens without becoming diseased.

		In fact, in a recent 2014 article, Dr. Kyle Steenland made the
comment that while there's also some low-level silica exposure on
beaches and in ambient air in general, there's no evidence such
low-level exposure causes effects.

		Thus, it's important to consider or to test those response models that
include the possibility of exposure concentrations of respirable
crystalline silica below which there are no anticipated health effects,
the so-called no adverse effect level.

		And as Chris has already emphasized, the model choice affects this a
great deal, because even if the biological response does have a well
defined no-effect threshold, failing to explicitly recognize and deal
with errors and uncertainties in the assignment of exposure can easily
cause the linear component of the model to dominate and obscure the
threshold.

		Now, in OSHA's Quantitative Risk Assessment document, it appears that
the linear and loglinear exposure response models were the focus.  And,
in fact, on Page 269 of the QRA document, OSHA identifies exposure
response models that it used, and the studies that it selected in the
Quantitative Risk Assessment.

		None of them seemed to test, as far as I could tell, a threshold
model.  On Page 290, OSHA also combines all of these into a table, which
indicates that the emphasis was on linear fitting.

		In fact, OSHA seems to specifically dismiss the idea of a non-linear
model by saying, on Page 272 -- and here I quote from the document
itself, "OSHA believes that the lack of a consistently monotonic
exposure response curve from the spline model lessens its credibility,
since there's no reason to believe that the biological response to
increasing silica exposure should not be monotonic throughout the range
of exposure."

		So the question is, is that really the case?  And I think if we look
at, a little bit, at some of the evidence that can be applied here,
we'll see that there are definitely very strong suggestions that
thresholds do occur.

		In terms of the animal evidence, I think if we look at the rat lungs
which are often used in these kinds of experiments, we see that their
response to so-called poorly soluble particles, of which silica is a
type, they can reach a lung condition called lung overload that is
characterized by persistent inflammation.

		This lung overload state, as far as I can tell, is not discussed in
the OSHA document, and it's characterized by neutrophil influx,
macrophage influx, oxidant and cytokine release, and increased pulmonary
epithelial cell hyperplasia.

		And these kinds of responses represent a generic, so-called epigenetic
mechanisms, whereby the rat lung responds in an exaggerated fashion to
particle inhalation.  As exemplified by the rat model, the triggering of
persistent inflammation is a key threshold element in respiratory
disease and tumorigenicity.

		For exposure levels below the threshold needed to trigger this
persistent inflammatory state, retained particles do not lead to
irreversible adverse biological effects.  They may trigger lung defense
mechanism enhancement, but not irreversible effects.

		Specifically, in an article that is cited by OSHA, Porter, they noted
that the response of the rat lung to inhaled crystalline silica
particles is biphasic, with a below-threshold phase characterized by
increased but controlled pulmonary inflammation.

		They concluded -- and here I quote, "Pulmonary defense mechanisms
were initially able to compensate and control silica-induced pulmonary
inflammation and damage, but after a certain threshold lung burden was
exceeded, these control mechanisms no longer were adequate to prevent
the progression of silica-induced pulmonary disease."			And so it's
these biological mechanisms that need a little more consideration in the
OSHA document.  In fact, Klein and Christopher of the California
Department of Toxic Substances Control reviewed data on crystalline
silica fibrogenicity and carcinogenicity and determined -- and here I
quote from those authors, "The safe level of silica should be based on a
threshold model in which fibrotic lung disease is a necessary
precondition for the appearance of lung cancer."

		That is, these authors recommended that the linearized model not be
used to describe the lung's response to crystalline silica inhalation
because the fibrogenesis appears to be governed by a threshold response.

		Now, there are other papers and literature such as that of McHoney et
al., who suggested that pneumoconiosis following exposure to
silica-containing coal dust is more likely to be caused by iron content
triggering a persistent inflammatory state rather than the silica
content itself.  And I think that the peer review panel also suggested
that the mode of action needs to be more clearly fleshed out in the OSHA
document.

		The OSHA peer review panel raised that in the following way, and here
I actually -- I'm cribbing from the peer review panel, and the quote I
chose here was, "What non-linearities in the biological response might
exist that would be sensitive to dose rate, threshold phenomena such as
exceedance of defense mechanisms or damage requirement needed for
excitation of immune inflammatory processes?"  So it's these kinds of
mode of action considerations that need to be included.

		In fact, as far as I could tell, in the 480-plus-page document, it
appeared that the only place where threshold in the worker epidemiology
studies was discussed was on Page 275, and no specific threshold
study -- threshold testing of any epidemiology study was presented, and
I couldn't find that in the remainder of the document.

		And in terms of the animal threshold values, the threshold value
derived by the Kempel et al. investigators, through a rat-human
comparison, OSHA looked at that and determined that they wanted to
dismiss the implication, starting on Page 329 -- and here I'm quoting
from the OSHA document, "However, OSHA does not believe that the
analysis of Kempel et al. is definitive with respect to a threshold for
silica-related disease."

		Now, I think that there is this indication that threshold is being
disregarded, and here again I will crib from several comments made by
the peer review committee, because I think they phrased the criticisms
very clearly.

		One comment was, "The appropriate model should be, would need to be
selected, including the likelihood of a threshold, at least for
non-cancer effects."  Another comment said, "The lung burden model has a
potential utility as it defines a threshold for lung cancer; however, it
is not explained well and this concept is not used."

		Another comment is, "The issue of threshold is not given proper
attention."  Yet another comment is, "More consideration needs to be
given in the document to model selection and its effect upon risk
estimates."

		Another comment is, "The estimate of risk has not adequately dealt
with uncertainty regarding the inexistence of thresholds for cancer and
non-cancer endpoints."  And, finally, the last quote, "The issue of
possible thresholds should be systematically evaluated for each study."

		Now, in terms of a few other papers, in terms of the mode of action, I
mean, OSHA does not cite a key paper by Borm and colleagues.  I think
the date of that was 2011.  The title of the paper was "The Carcinogenic
Action of Crystalline Silica: A Review of the Evidence Supporting
Secondary Inflammation-Driven Genotoxicity as a Principal Mechanism."

		And in reviewing the data, these authors concluded that inflammation
is a driving force for genotoxicity, and that the genotoxicity of silica
particles would play only a role when you had very high overloading
concentrations, exposures, and deposited doses.

		They also noted, this is very much in agreement with what Dr. Borak
said in terms of IARC's discussion of crystalline silica where they
considered the established mechanistic events as being impaired particle
clearance and -- leading to macrophage activation and persistent
inflammation.

		And in his same review paper of 2014, Dr. Steenland also appears to
endorse this idea, saying, and here I quote, "Both silicosis and lung
cancer are believed to result from the strong inflammatory response that
silica evokes in the lung."  And so there the idea is that whether or
not the inflammatory response can become persistent is going to be
governed by threshold considerations.

		There are -- the QRA document does not sufficiently discuss and
emphasize that some worker epidemiology studies suggest threshold dose
response.  The implication of such evidence needs to be more carefully
explored and considered by OSHA's analysis.

		There was a study by Bohr and Tran, which reviewed quartz exposure in
coal mine dust, and they concluded -- and here I will quote from their
abstract, "A no observed adverse effect level for quartz between 30 and
130 µg/m3 over a 40-year exposure is derived.  It is concluded that
more refined physiologically based pharmacokinetic modeling is needed
for a better estimate," that is to say, to narrow down that range.

		And the OSHA document does discuss the work of Graham and colleagues,
where they studied 2500 Vermont granite workers and how the exposure
related to silicosis development.  But those authors noted that there
were no silicosis deaths in workers hired after 1940 who worked only in
that Vermont granite industry, illustrating the effect of the lowering
of quartz exposures.

		Those authors concluded that a no effect threshold exposures were
likely and that they were in the vicinity of 100 µg/m3 for respirable
silica, and that rigorously observed workplace conditions would prevent
the development of radiographic abnormalities.

		Now, OSHA, of course, was aware of that, but they chose to rely
primarily on the reanalysis of Attfield and Costello, who looked at that
same data and did observe a statistically significant trend when
cumulative exposure was log transformed, but not for untransformed
exposure.  And those same authors also eliminated some of the highest
exposure groups to enhance the dose-response behavior.

		There are a couple of other studies, Pukkala, which I think is
mentioned in the OSHA document, sought to understand alternative
exposure metrics for crystalline silica by examining 43,000 lung cancer
cases in the Finnish Cancer Registry and relating them to the Finnish
Job-Exposure Matrix database.

		The authors noted that the stability in most occupations in Finland is
so high that cross-sectional information on workers' occupation
corresponds rather well to his or her lifelong occupational history.

		And their analysis of possible relationships between crystalline
silica concentrations and lung cancer risk found evidence for a
threshold, in that lung cancer excesses were limited to exposure
concentrations of at least 200 µg/c3.

		They concluded, and here I quote, "The threshold approach may provide
some additional information on the shape of the crystalline silica
exposure response curve."  Now, OSHA does cite to this document, but
they don't really make any reference to the authors' conclusions
regarding the possibility of a threshold.

		Another more recent paper is that of Garber and colleagues, where they
recently published a reanalysis of respiratory disease mortality in
9,000 miners who were enrolled around 1970 and followed up to about
2007.

		They tested for an exposure response to crystalline silica
concentrations but didn't find any statistically significant
associations.  They did find some statistically significant associations
with total dust, generally, which in that case was coal dust.

		And, finally, I think many people are probably aware of the recent
analysis of Morfeld and colleagues which, you know, was probably was not
in the current document because it was published in 2013, and they
considered approximately 17,000 workers from porcelain manufacturing
plants in Germany.

		These workers were screened for silicosis between 1985 and 1987 and
then were observed for mortality and silicosis morbidity through 2005.
Respirable quartz exposure was estimated by combining detailed
individual employment histories with a job exposure matrix on more than
8,000 in historical industrial hygiene measurements.

		The authors estimated a threshold concentration of 250 µg/m3, on the
basis of their analysis, which was also the best fitting model.  That
is, these findings by Morfeld and colleagues in the German porcelain
industry show a silicosis no-effect threshold, where below silica
exposure concentrations of 250 µg/m3, the lung responses did not
progress to silicosis.

		So, in summary, the bottom line is that the OSHA exposure response
modeling focuses on linear no threshold models, and therefore they
discovered such a linear relationship.  And that, however, would be true
even if the response were a threshold one.

		The exposure misclassification, as Dr. Long has mentioned, will lead
to a non-linear -- non-zero linear coefficient even when any
epidemiology data are run through this data.

		Now, as has been recognized in publications by Dr. Tony Cox, the peer
review panel, and others, exposure misclassification error can obscure
and misidentify thresholds in exposure response.  Care must be taken to
analyze worker data for respirable crystalline silica exposure in a way
that allows for some possible threshold behavior.

		Finally, neglecting to include exposure response models in the
uncertainty analysis allows you to make a statistical significance
determination that may in fact be flawed, because so many different
models were tried in order to find the one that gave you the largest
linear coefficient.

		And, consequently, my net conclusion is that more attention needs to
be paid to the possibility of threshold.  Thank you very much.

		DR. HESSEL:  Good morning, Your Honor, folks.  My name is Pat Hessel.
I'm an epidemiologist.  I was asked to review two papers that OSHA
relied upon in their rulemaking.  The first is a paper by Rosenman et
al.  It was done in -- it was published in 2003.

		What they did was to use the Michigan SENSOR data to estimate the
total number of what they called newly recognized silicosis cases in the
United States.  I think newly recognized is a bit of a misnomer because
what they were really trying to do is estimate the number of
unrecognized silicosis cases.

		The cases were reported to that registry by four sources.  There were
hospitals, physicians, the workers' compensation board, and mortality
data.  When cases were reported to the registry, Dr. Rosenman reviewed
them to determine whether they had an appropriate history of exposure
and whether they either had an x-ray consistent with silicosis or biopsy
evidence of silicosis.

		And then to try to figure out from where he was getting the
information, the three nonfatal sources, so the hospitals, the physician
records, and workers' compensation, from those three sources he used
something called a capture/recapture method to try to figure out, given
the overlaps among those three sources, how many cases were likely to be
in the population unrecognized.

		Capture/recapture is used, has been used to estimate wildlife
populations.  You know, you set a bunch of traps, you catch the rabbits,
you mark the rabbits, and a little while later you set some more traps
and you see how many of the rabbits that you've trapped a second time
were marked.

		And on the basis of that, you try to figure out how many rabbits there
are all together.  And he used this method to try to figure out how many
unrecognized silicotics there were.

		The purpose was to try to relate the number of deaths, which is a
fairly easy number to track, to the number of silicotics.  So he
tried -- he was trying to calculate that ratio.

		He had 547 silicotics that were non-death certificate, reported to the
registry in 10 years, 547.  Most of those were reported by hospitals,
407 of them, 111 from physicians, and 84, only 84 from the workers'
comp.

		There were 130 deaths in Michigan during that time where silicosis
appeared somewhere on the death certificate.  Michigan only knew about
110 of these, so Rosenman and colleagues excluded the other 20, so they
excluded 15 percent of the deaths reported in the national statistics.

		Dr. Rosenman then reviewed those records and -- of the deaths, and
he excluded another 23 percent where he said although the silicosis was
on the death certificate, he didn't believe silicosis was either present
or had anything to do with the death.  That left 85.

		He then compared the number of living silicotics from the registry,
that 547, to the 85 deaths, and calculated that there were 6.44 living
silicotics for each silicosis death, 6.44 to 1.  And then he used this
capture/recapture methodology to estimate that there were between --
well, sorry, and then he expanded it to all of the United States, and he
estimated that there were between 3,600 and 7,300 new cases per year of
silicosis in the United States.

		Several concerns about this study: one, I think, has to do with the
time period of deaths.  We've seen the charts.  During that time period,
'87 to '96, there was actually about a 38 percent decline in the number
of deaths in the United States where silicosis appeared somewhere on the
death certificate.

		That declined another 55 percent from the midpoint of that '87 to '96
period, until 2006, which was the last information that I had.
Apparently the information has been updated, and there is continuous
decline.

		Now, obviously, the numbers of cases, of new cases estimated by
Rosenman during that period bear no relevance to the current situation.
Further, we cannot assume that the quantitative relationship between the
numbers of deaths and the numbers of living silicotics today bears any
resemblance to the estimates that were made in Michigan during that time
period.

		As Dr. Borak pointed out, virtually all of the workers in the
Michigan registry during that time period began their exposures prior to
1970.  Rosenman published something in 1997, a paper where he talked
about the same registry, and he talked about the period '87 through '95.

		Now, the 2003 paper was '87 through '96, so it's only a difference of
one year, but in that -- in the 1997 paper, he showed that more than 95
percent of those workers began their exposure prior to 1970, so prior to
the existing PEL.

		I think we also have to consider the population that makes up the
Michigan registry.  In the Michigan registry -- again, this is from
that 1997 paper, 80 percent of silicotics, or 80 percent of the people
reported to the registry, were from iron and steel foundries.  Of
course, that relates to the car industry in Michigan.

		Now, if we look at the NORMS data for, I believe it's 26 U.S. states
that was published by the CDC in 2005, there were only 6 percent of
deaths where silicosis was somewhere on the death certificate, that came
from workers in iron and steel foundries, so 80 percent in Michigan
versus only 6 percent in the NORMS data.

		Also, if we look at the NORMS data, 22 percent of those deaths, where
silicosis appeared somewhere on the death certificate, were either
miners or quarry workers.  In the Michigan registry, this was only
20 -- sorry, only 2 percent, so 22 percent in the NORMS versus only 2
percent in Michigan.

		Now, in their 1997 paper, Rosenman also presented silica monitoring
data for eight of the Michigan iron and steel foundries that had
produced some of his cases.  They did what they called an initial
inspection and follow-up inspections.

		I believe, on the basis of what was in the paper, the initial
inspections were done in the 1980s -- it sounded like the mid-1980s, so
about 15 years after the implementation of the PEL.

		The average concentration for these eight iron foundries -- this is
unweighted average -- was 1.2 mg/m3 of silica, so we're talking 12
times the PEL, and this was in the 1980s.

		If we look further at this study, there was a single x-ray reader that
was used.  It was only Dr. Rosenman.  He was not blinded to the source
of the x-rays.  He knew that these x-rays were being forwarded to him
because somebody thought that they had silicosis.

		Three-quarters of the people in the registry were smokers.  Now, in my
written comments, I talked about the data relating the reading of
radiographic grounded opacities in relation to smoking history, so I'm
not going to go over that.  But I think there is certainly evidence to
suggest that smoking can enhance the likelihood of a false positive
reading of rounded opacities.

		Rosenman then discussed the assumptions of this capture/recapture
method for his setting, and it didn't appear that any of those
assumptions were met.  One of the assumptions was that there were no
losses or entries during the period of investigation, and he showed that
there was indeed influx into the state of Michigan during that 10-year
time period.

		Another assumption he mentioned was that there would be the same
probability of identification by source, and as I said, the vast
majority of these were identified through hospitals and relatively fewer
from the others.  The other, that ascertainment by sources was
independent, and I think he agreed that that assumption was not met.

		So to conclude the discussion of his paper, virtually all the people
on the Michigan registry were exposed to silica prior to the PEL, the
existing PEL.  The exposures experienced by the people in the Michigan
registry during that 10-year time period were at least an order of
magnitude higher or appeared to be an order of magnitude higher than the
existing PEL.

		The exposure settings of the workers in the Michigan registry were not
typical of workers with silicosis in the United States.  Recall, they
were heavily skewed toward the iron and steel foundry workers.

		The x-ray readings were susceptible to bias from lack of blinding and
reflected the interpretations of only a single reader.  I'm not being
critical of Dr. Rosenman's reading.  I don't know if he's a good reader
or not.  Nonetheless, it was only his readings that are being relied
upon.

		And then the assumptions of the capture/recapture method did not
appear to be met.  I think it's safe to assume that the results of that
study cannot be used to estimate the current burden of undiagnosed
silicosis in the United States.

		But now if we look at the OSHA document in the Federal Register, if
you look at Page 56384, it's actually in the third column, the first
full paragraph.  And I'll quote here.  "Based on Rosenman et al., 2003,
the Agency estimates that between 2,700 and 5,475 new cases of silicosis
at an ILO rating of 1/0 or higher occur annually at the present PELs as
a result of silica exposures at establishments within OSHA's
jurisdiction."

		There are a number of things I want to talk about in that regard.  I
tried to figure out where those numbers came from, and in this document,
the most recent number they had for the number of deaths was 161.  And
so I plugged the 161 into Rosenman's formulas in his 2003 paper, and I
actually came up with the 2,700 with rounding error, the 2,700 and the
5,475.

		So it would appear that what the OSHA folks have done is to take that
161, apply Rosenman's method, and come up with these numbers of 2,700
and 5,475.  Now, actually in 2006, which was the last number that I had
access to, the number was around 120.

		If we use that number of 120, Rosenman would have decreased that by
1,500 -- or sorry, by 15 percent.  You remember, Michigan didn't know
about some of those that were known by the national.  If he had reviewed
those, again looking at what he did in the period '87 to '96, he would
have eliminated another 23 percent.

		And also, the national numbers include mines, and the CDC paper, 2003
publication, indicated that about 22 percent of the deaths were from
people in mines, and I don't believe OSHA is responsible for that.  So
they would be reduced by another 22 percent.

		When I --

		JUDGE SOLOMON:  I'm sorry.  I have to -- but is there a way that you
can summarize this in the next couple of minutes?  Because we're sort of
at the end of the allotted time.

		DR. HESSEL:  Yes, the joy of going last.  Yes, I will try.  The
numbers I came up with were less than half of the numbers that OSHA came
up with, but that almost isn't relevant.  The workers in the Rosenman
study were exposed before the PEL was put in place.

		At least some of the Rosenman foundry workers had very high exposures
even after the PEL was established.  And so when the statement is made
that these estimated cases are the result of exposures at the present
PEL, it's a statement that simply cannot be defended.

		I was also asked to review another paper.  I have filed comments on
that other paper.  It's just not a terribly informative paper.  But if
you would like to proceed, I will just refer you to my written comments
on that.  Thank you very much.

		MR. CHAJET:  Your Honor, could we have two minutes just to ask
Dr. Hessel to summarize that other paper?  We'll do it in two minutes.

		JUDGE SOLOMON:  Okay.  Now, you have time this afternoon, or you --

		MR. CHAJET:  We do, and we're happy to make up that time later.

		JUDGE SOLOMON:  Okay.

		DR. HESSEL:  In two minutes, sure.  The Goodwin paper tried to, again,
look at the burden of undiagnosed silicosis.  They took a bunch of
people who had died in hospital from respiratory diseases.  As best they
could, they read the x-rays.  Many of the x-rays were very poor x-rays.

		They found some that showed signs consistent with silicosis, some that
showed signs consistent with asbestosis.  The numbers that they came up
with and the percents they came up with are fairly comparable to what
you would see in an unexposed group of that same age, further
complicated by what they call the noise of these terminal diseases on
the x-rays.

		It was an ill-conceived study that really doesn't tell us much.  We
know that there is some silicosis that is undiagnosed.  Their attempt to
actually produce a number was unsuccessful and uninformative.

		JUDGE SOLOMON:  Okay, thank you.  We're going to take five minutes for
a break.  Then we're going to come back, and we'll have about 10 minutes
of questioning from the peer review.  We'll have about 10 minutes from
the public.  Then we'll have some questions from OSHA.  Then if we have
any time left before lunch, we'll come back to the peer review and to
the public.

		Now, from what -- the way I understand it, we'll have some additional
time this afternoon if we have to go back to the peers and to the
public; is that right?

		MR. CHAJET:  Correct.

		JUDGE SOLOMON:  Okay, so we're going to take five right now.  We're
off the record.

		(Off the record.)

		(On the record.)

		JUDGE SOLOMON:  All right, we're back on the record.  At this time
Ms. Lindberg is going to make a motion, or several motions.

		MS. LINDBERG:  I would just like to ask the presenters if they have
materials that we can include in the record, your presentation materials
and your testimony?

		MR. CHAJET:  Allow me to respond please, as counsel.

		MS. LINDBERG:  Sure.

		MR. CHAJET:  Our comments are in the record.  We have a full set of
comments by each of the witnesses.  They're all part of the record
already.  They were submitted to you.  These comments that they made are
in the transcript, and we have no additional documents that reflect
their testimony.  We stand on the oral testimony and the written
comments.

		MS. LINDBERG:  How about the PowerPoint?  Can we put that in the
record, since no one can -- could see it in the record?

		MR. CHAJET:  I think we could put the PowerPoint in the record, sure.

		MS. LINDBERG:  Okay.  Do you have a copy that I can mark?

		MR. CHAJET:  I do not.

		MS. LINDBERG:  May I use this copy I have here that I have not written
on?

		MR. CHAJET:  I will provide a copy for the record after the close of
the hearing.

		MS. LINDBERG:  Okay.  Let me just say that I will reserve Exhibit
Number 6 for Dr. Borak's PowerPoint presentation.

		MR. CHAJET:  Sure.  Actually, you can reserve Exhibit Number 6 for the
entire PowerPoint, which has a few more slides on it.

		MS. LINDBERG:  Sure, that's fine.

		And then I heard we have some vials here that you would like us to
also include in the record.

		MR. CHAJET:  We'll address those at the beginning of next panel.

		MS. LINDBERG:  Okay.  Great, thank you.

		JUDGE SOLOMON:  Okay.  Mr. Perry, you were going to make some
introductions, members of the peer reviewers?

		MR. PERRY:  Well, I introduced them this morning.  I would request
that they be invited to ask questions of the panel ahead of other
participants.

		JUDGE SOLOMON:  Okay.  I have already said that we'll take about 10
minutes to do this.  So if any of you have questions, we're using this
microphone.  You can come forward and stand behind the microphone.
Please state your name for the record.  Apparently we have the race to
the microphone.

		UNIDENTIFIED SPEAKER:  You probably are --

		DR. CRUMP:  My name is Kenny Crump.  There's been a lot of discussion
this morning of thresholds.  I'd like to ask some questions about those
comments.

		Dr. Borak, in your written comments, you made the statement, "It is
generally impossible to prove a negative."  So you mean by that -- a
threshold is a negative, right?

		DR. BORAK:  No, sir.  I was meaning that it was generally impossible
to prove that there was not something, as a logical premise.  I was not
speaking of the nothing as the threshold.  I was talking about the
impossibility of proving that it doesn't exist.

		DR. CRUMP:  Okay.  So are you saying that -- agreeing that any data,
no matter how extensive, is consistent with no response?  Would you
agree with that?

		DR. BORAK:  I'm sorry.  Could you ask that again, sir?

		DR. CRUMP:  Any data, no matter how extensive, is consistent with some
level of response, in other words, no threshold.

		DR. BORAK:  I must be feeling very dead in my head.

		DR. CRUMP:  Let's take an example.  You have two groups.  One group is
unexposed and one group is exposed.  The unexposed group, there is 0 out
of 100 responders.  The exposed group, they're also 0 out of 100
responders.

		DR. BORAK:  Yes.

		DR. CRUMP:  Can you use that data to reject the hypothesis that there
is no threshold?

		DR. BORAK:  I think you could use the data to suggest that there's no
effect.

		DR. CRUMP:  Can you reject the hypothesis that there is no threshold?

		DR. BORAK:  I'm not sure if it's meaningful to suggest a threshold for
something for which there is no effect.  It's a logical structure that
I'm having difficulty with.

		DR. CRUMP:  Well the scientific method has been described as posing
falsifiable hypotheses and using data to test those hypotheses.  So
declaring an unfalsifiable statement to be true would not be scientific
under that definition of science.

		DR. BORAK:  I didn't think my intention was nearly as profound as your
questions are, sir.  You know, I'm challenged to try to deal with it.
My intent was to say that -- and perhaps I should look at my comment
and be completely clear.

		JUDGE SOLOMON:  Well, let me just say, we're getting very far afield.
Had this been a court proceeding and had there been an objection on
whether or not, A, the question was argumentative and, B, whether the
question was answered, there probably isn't an answer.  So you can take
that inference if you want to do that, and ask another question.

		DR. CRUMP:  Okay.  I'll ask another question.

		DR. BORAK:  Thank you, Your Honor.

		DR. CRUMP:  Dr. Valberg, you also made a number of comments about
thresholds.  And for example, you say that one time, that Kunkel et al.,
2001, analyzed the responses of rats exposed to high levels of inhaled
crystalline silica, and identified a threshold behavior.  And you said,
i.e., a low L for chronic inflammation.

		I have two questions about that.  Identified a threshold behavior, if
it's impossible to prove a negative, how can you identify something
that's impossible to prove?

		DR. VALBERG:  I guess I take a more practical viewpoint of thresholds.
 And if, in fact, you're exposing animals and you do not get a response,
I mean, I would say that that's a -- certainly is consistent with a
hypothesis that you are exposing them to levels that are below a
threshold, and that you would then have to increase the response to
see -- increase the exposure to see whether a response comes about.

		DR. CRUMP:  So you would consider a low L to be a threshold?

		DR. VALBERG:  I guess, constrained by the biases of how many animals
and what the accuracy of the exposure assessment was, et cetera, that if
you have no response, then that is a no effect level, let alone a no
adverse effect level.

		DR. CRUMP:  Okay.  So you do not distinguish between observed adverse
effect level and an adverse effect level?

		DR. VALBERG:  I guess all of science is based on observation, and so
you are giving me the hypothetical of an experiment that reported no
adverse effects.  And so then, I guess, maybe you would have been --
described that as a no observed adverse effect level, and that's -- I
would agree with that, because anything that we do in science is going
to be ultimately based on observation.

		DR. CRUMP:  Yes.  Would you not agree that the same low L could have
come from a study that did not have a threshold, a dose response that
did not have a threshold?  A small increment of increase that did
not -- but did not have a threshold could have risen to the same low L.

		DR. VALBERG:  It could have given a zero response.  That's correct,
and that's because of the statistics of the situation that, yes, if you
have a low responding -- no response doesn't necessarily mean that it
would always be zero if you had tested an infinite number of animals.

		DR. CRUMP:  Yes.

		JUDGE SOLOMON:  Again, we're pressed time, so maybe --

		DR. CRUMP:  Thank you.

		JUDGE SOLOMON:  -- you have another person in line.  Now, maybe we
can come back to this later.  Is that possible?

		DR. CRUMP:  Yes.

		JUDGE SOLOMON:  Okay.  State your name, please.

		DR. GINSBERG:  Gary Ginsberg.  I'm one of the peer review panelists.
And there's a couple of questions I have that would help me in
formulating my final comments on these proceedings.  So I think I'll try
to limit these to two or three questions, and maybe I'll just put them
out first and then see, you know, how the responses go.

		So, Dr. Valberg, regarding the Kunkel et al. study that was just
brought up by Dr. Crump, you talk about a threshold for the
inflammatory process being identified.  You didn't use this terminology,
but in the paper they used the terminology of the Mcrit, or the critical
loading of the lung with silica.

		The specific number is 0.39 mg per gram lung tissue that they identify
in the paper, and you talk about that as a threshold for inflammation.
But my read of that paper is a little different, specifically in that
where they talk about the no L's and low L's in Table 2, they clearly
show that they did not find a no effect level, that the lowest dose was,
in fact, an effect level for the increase in PMNs.

		And they talk about that specifically in the paper as there was no
threshold for that effect.  And then if you look at their graphs, the
PMN graph as well as their graph on alveolar epithelial hypertrophy and
hyperplasia also shows no evidence of a threshold.

		So I think that it's worth, you know, being careful about what, in
that paper, did show a threshold -- you know, the fibrotic, clearly,
the initial instigating events, clearly no threshold, as well as also
their analysis of the variability that might be inherent in their data,
where they look at the Mcrit, the 95 percent lower confidence limit on
the Mcrit not being 0.39 anymore but being 0.0049, which means a much
lower inhalation dose.

		I think it was instead of 0.036 mg/m3, it's 0.007 mg/m3, that would be
the Mcrit for the most sensitive individual.

		And one thing that has been missing, I feel, both from the OSHA
analysis as well as from the comments I've heard so far, is any
discussion of variability in the population that might, on the one hand,
tend to linearalize or obscure -- I'll call it obscure a threshold, not
just error -- measurement errors, as Dr. Long so rightly talked about,
but there's other factors in terms of population variability, as is
brought out in the Kunkel paper, that that Mcrit value could vary.

		So I'm sorry for the long question, but that's one, if you want to
respond back to that.  The other, I wanted to ask Dr. Long, so how much
measurement error do you need?  If you have a threshold, let's say,
that -- a true threshold, if such a thing is possible, of 0.05 mg/m3,
and you have a bunch of measurement error, how big does that measurement
error need to be for you to, say, increase that to 0.15, a threefold
shift?  How does that work?  I'm not a statistician.

		And then the third piece of my triumvirate questioning is that it
appears to me, that -- self-evident, as Dr. Borak talked about things
that seem to just fall out of the data, that there is a number of
studies where the highest dosed groups have a flattening of the response
either to cancer or to silicosis.

		I'm talking about the granite, the Graham study, the diatomaceous
earth studies, the most recent Liu Chinese studies, and a number of
others.  The high dose groups don't have the same kind of dose response.

		And those high exposed people would have the highest measurement error
because they were the ones that were in the bad old days when there was
no PEL, et cetera, et cetera, and the measurements would be -- so it
seems logical to me to think about dropping off the weight put on those
older, higher exposed groups because you've got the biggest errors.

		As you rightly point out, measurement error is important to consider.
And you've got the best data on those workers that have the more modern
measurements.  So those are my three parts.

		JUDGE SOLOMON:  Okay, let's start with Question Number 2 to Dr. Long,
because that's probably the easiest way to marshal the questions.
Dr. Long?

		DR. LONG:  Yes.  I can try to answer that.  I'm not sure that I have a
definitive answer.  I'm not a statistician either, I'm an exposure
assessor, but I can tell you that that's not an easy question to answer.
 It depends.  I mean, there are a number of factors that influence --

		DR. GINSBERG:  Variability in a population.

		DR. LONG:  Yes.  There are a number of factors that influence what
impact exposure measurement error can have, not only the size of the
exposure measurement error but also the error structure, the type of
model that is being used, you know, other sources of variability.
It -- I guess the answer is, it depends.

		JUDGE SOLOMON:  Okay, so Number 3, Question Number 3 goes to validity;
is that right?  Is that what you were really asking about?

		DR. GINSBERG:  I'm just looking for how much measurement error could
affect the threshold.  And do you have a study I could go home and read
that talks specific -- quantitatively about that?  I mean, there's
a -- I've seen a lot.  I've read the Romberg and I've read the 2011
paper.  There's not a lot that's quantitative about that.

		DR. LONG:  There are some quantitative examples in the Romberg paper.
There's a -- I think it's a study by Carolyn Cuckanoff (ph.) that kind
of looks at different sizes of exposure measurement error and how that
influences the shape of the exposure response curve.  So I think that is
a quantitative example.

		But, you know, again, I mean, the answer is, it really depends on a
number of factors.  So it -- I think that's a difficult question to
kind of pinpoint how much error can cause a threshold to be obscured or
underestimated.

		DR. GINSBERG:  So there'll be --

		JUDGE SOLOMON:  Okay, so in order to marshal all this -- okay, this
is like a compound, loaded series of questions.  Why don't we just give
the panel a chance to answer?  Dr. Long has already spoken.  Does
anybody else want to address any of these issues?

		DR. VALBERG:  I'll just respond.  I mean, I really appreciate your
comments on the Kempel et al. paper.  I think you're correct.  I mean,
there is a lot of nuances that need to be considered, and I agree with
your comments.

		I think the issue, in terms of actual affect, of course, then boils
down to discriminating physiological responses which occur in response
to inhaled particles versus ones that are persistent and are
irreversible and become wholly adverse and lead to disease, but I think
you're correct.  I mean, that -- I didn't mean to simplify it.  I had
very limited time.

		JUDGE SOLOMON:  Anybody else?  Okay.  Thank you very much,
Dr. Ginsberg.  We'll come back to some of this, this afternoon.

		Now, are there any of the members of the public who wish to come
forward?  If you do, we'll take about 10 minutes of questioning, and
then we'll go to the OSHA people.  State your names, please.

		DR. GOLDSMITH:  Yes, thank you, Your Honor.  My name is David
Goldsmith.

		JUDGE SOLOMON:  Can you spell your name where the Court Reporter --

		DR. GOLDSMITH:  G-o-l-d-s-m-i-t-h.  I'm going to speak tomorrow, but
I'm here today, and I'm seriously interested in --

		JUDGE SOLOMON:  And in what capacity are you here for?

		DR. GOLDSMITH:  I'm here as a representative of George Washington
University in Georgetown, but I'm not paid by anyone.

		I have just an observation and a question for the panel.  Back behind
you all is this graph of CDC decline in silicosis mortality, and I would
tend to suggest that there is certainly a reason for something positive
to be said about this.

		And the positive things need to be said about efforts and beneficial
effects put forward by industry to lower the exposure to silica dust,
and that has led in part to this decline in mortality rates, in addition
to which it's also clear that OSHA's raised people's awareness about
this.  And that's another possible explanation why there is this clear
decline in silicosis mortality.

		But my question is, is this the right thing to look at?  Shouldn't we
be looking at all of the silica-related disease, not just silicosis?
Shouldn't we be looking at lung cancer, autoimmune disease, kidney
disease, and tuberculosis, which has fallen dramatically at the
beginning of this time frame, as indications of an effective policy put
in place by industry, and a regulation that's been sort of backed up by
OSHA in terms of telling both workers and the community that action is
needed?

		And I think that this is something that needs to be put into some
context, because as I see it, cases of silicosis that were at the
beginning of this period, these individuals are still there, they're
dying of other diseases.  And as -- other diseases as simple as falls
and automobile crashes, heart disease, what have you.

		And so it's somewhat narrowing, in terms of looking at this whole
question about the role of industry and the role of OSHA, to look solely
at silicosis mortality.  And I just would be pleased to hear what the
panel has to say about that.

		DR. BORAK:  Let me take a first cut.  I agree with Dr. Goldsmith.  I
think that the slide that you are seeing is a tribute to an important
public health success.  Whether it's complete or not is a separate
issue.  It reflects a substantial decrease in deaths related to a
preventable cause.  Whether those exposures occurred before or after
OSHA should not diminish the magnitude of the success.  That's the first
thing.

		I spoke of this curve, essentially to speak to whether this
information informed the evaluation of whether the current PEL was
adequately or was not adequately protective.  That's a different issue
than you bring up, and so let me separate these things, because your
question was multi-part.

		First, this is a sign of a success.  It has been a dramatic decrease
in mortality, and additionally I showed some slides which indicated a
dramatic decline in the exposure levels that occurred in this country,
but also in China.  And I presume we could see the same kind of dramatic
decline elsewhere.

		It's clear that the decline was a consequence of industrial activity,
that is say, activity by corporations and companies and others who were
responsible, and it is also attributable to the implementation and
adoption of various regulations and rules.

		And it's clear that in China, the decline occurred when rules came
into effect, from horrific levels.  And I showed you data that come from
the OSHA IMIS database indicating 50 to 90 or 95 percent declines in
ambient silica levels in workplaces, or silicate workplaces, as
discussed by OSHA scientists, and that's a tribute to both industry and
OSHA working together.  And I think that this has been a wonderful
success.  So that's my contribution to answering your question.

		DR. GOLDSMITH:  And don't you also think that we should be looking at
a broader set of diseases than simply looking at silicosis mortality?

		DR. BORAK:  Ah, yes, I think we are looking at a wide array of
diseases.  This happens to be a clearly documented and dramatic
statement regarding one of those most important diseases, one of which
is a signature disease.

		I think that the question is not that -- I, certainly, as a
physician, do not regard any of these diseases as unimportant, either to
people or to the public health.  My concern had to do with whether 100
ppm PEL was or wasn't protective, and whether there were data, okay.
But I certainly would not tell you that these other diseases are
unimportant.  That would be a terrible thing for me to say.

		JUDGE SOLOMON:  Okay.  We're limited with time.  We have one other
member of the public who wants to ask some questions.

		DR. PARK:  Robert Park, NIOSH, from Cincinnati.  There's been a lot of
interest in what's going on at the low end of the exposure response
curve with a special focus on threshold.  I haven't heard any
speculation about the possibility of an increase in the exposure
response at the low end of the curve.

		Maybe something's being up-regulated and there's a threshold.  Maybe
at the very low level, risk is higher than you would predict from a
linear overall exposure response.  Why are we not hearing of that
speculation?

		Secondly, a lot of talk about measurement error.  If there's no
underlying association, that is not going to generate statistically
significant associations.  It's going to generate random estimates of
exposure response.  Half of them will be negative, half of them will be
positive.  If it's a big study, they'll be really small.  If there's no
association, we don't have to worry about measurement error.

		On the question of latency for silicosis, that's just an artifact of
how much exposure the person has had.  If they're at low exposure, it's
going to take longer.  You're going to have a 35-year latency.  If they
have high exposure, if it's high enough it could be one year.  So
defining a threshold based on when silicosis happens is an artifact of
clinical detectability.

		JUDGE SOLOMON:  Let me put a question mark at the end of that.
And -- is that a question?  Or are you just --

		DR. PARK:  Just one more sentence.

		JUDGE SOLOMON:  Okay.

		MR. CHAJET:  I'm going to object --

		DR. PARK:  Therefore, how can one assign a threshold for lung cancer
to this magical threshold, which depends on sort of the history of
average exposure and clinical detectability?

		JUDGE SOLOMON:  Okay.  What's the nature of the objection?

		MR. CHAJET:  Well, I hadn't had a question for the first three
minutes, so if --

		JUDGE SOLOMON:  Well, this is an example of the loaded question, but I
believe that there -- that as long as somebody can answer --

		DR. PARK:  Why isn't there a positive effect at low doses?  That's a
question.  Why aren't you speculating about that?  Why is measurement
error important --

		JUDGE SOLOMON:  Why don't you give them a chance to answer?  Okay,
does anybody want to take that one?

		DR. VALBERG:  Yes, thank you for that question.  And the speculation
about what is the actual nature at very low doses is a good one.  I
think that it is interesting, you know, how would the organism begin to
respond from very low exposures to minute exposures and so forth?

		And it could very well be that there's all sorts of things that go on.
 You may have heard of the word "hormesis," that in fact maybe zero
exposure is actually not as good as some level of exposure.

		DR. LONG:  I wouldn't go that far, but yes.

		DR. VALBERG:  But yes, I'm just saying.  But yes, the shape there is a
little bit unusual.  And I think that part of the reason that I didn't
include it is because the whole idea is a little bit speculative and I
don't -- I'm not meaning to say that we should dismiss it out of hand.
We should keep it in mind, and if we find evidence that can be helpful
in setting standards, we should use it.

		JUDGE SOLOMON:  Okay.  I think at this point we'd better go to the
OSHA questioning.  Thank you very much, Dr. Park.

		Mr. Perry?

		MR. PERRY:  Thank you, Your Honor.  The first panel member to question
the panel will be Steve Schayer from our Office of Physical Hazards.

		JUDGE SOLOMON:  Technical difficulties beyond our control probably
require another microphone.

		(Off microphone discussion.)

		MR. SCHAYER:  Well good morning, and thank you, Bill.  So I have a
question for the panel.  In your written comments to OSHA, you mention
several examples of potentially large sources of exposure measurement
error not considered by OSHA.

		These included between measurement variability, between sampler
variability, between laboratory variability, between sample duration
variability, between sample location variability, between sample type
variability, and error from particle potency variation.

		So I was wondering if you could kind of clarify on what data would
need to be available to address these sources of error.

		DR. LONG:  Great.  Actually, at this afternoon's session we'll be
talking -- we'll be addressing several of these sources of error, in
particular sampling errors, analytical errors, pump errors, so I think
that session will address, you know, provide information on some of the
data sources needed to address them.

		I think, regarding some of the other sources of error, such as between
sample, I mean, looking at, let's say samples that are collected as part
of compliances purposes versus random exposure survey -- data from
random exposure surveys, I mean, those data are available.  I would
think you can characterize, you know, the size of exposure measurement
error.

		So I think, regarding several of the sources of exposure measurement
error, there are data available.  There are data from area samples
versus personal exposure samples.  You can characterize the difference
between them.

		MR. SCHAYER:  Okay, thank you.  Another question that we have as well
is could you please identify some studies that you believe do acceptably
account for the impact of exposure measurement error on exposure
response associations for respirable crystalline silica?

		DR. LONG:  You know, off the top of my head, I can't think of any
studies that have done that.  I can go back and think about that
question and see if I can identify appropriate studies, though.

		MR. SCHAYER:  Okay, thank you.  What about studies of other
occupational epidemiology cohorts?  Can you give us some examples of
other types of occupational studies that have addressed these sources of
measurement error that you've brought up today?

		DR. LONG:  Again, I can't think of any specific studies.  I can go
back and look into that question.  I believe that exposure measurement
error has been addressed in studies of asbestos-exposed workers.  I
can't think of any specific studies off the top of my head, but I can
get back to you with information.

		MR. SCHAYER:  Okay, thank you.  And one other question that I have,
for the studies that Dr. Valberg cited, that showed evidence of a
threshold, these would be Graham, 2001, 2004; Pukkala et al., 2005;
Rushton, 2007; See (ph.), 2007; and Morfeld et al., 2013, we were
wondering if you believe that these studies actually address the sources
of exposure measurement error that you said the OSHA studies had not
addressed.

		DR. VALBERG:  I appreciate that question.  On those particular
studies, I mean, my -- I did not look at exactly how they treated
exposure measurement error, but I think to the extent that they were
able to discover a threshold, they essentially did not have a surfeit of
noise in their exposure data, and that the threshold could be revealed.

		I think one of the key ingredients in looking for thresholds is that
you have to begin with a model that could allow for that possibility in
order to be able to detect it, and then look for some sort of likelihood
as to which model fitting is going to be the better one.

		MR. SCHAYER:  Okay, thank you.  And one other question that I have,
too.  So you've noted today in your comments and also in your written
comments as well as today's testimony that exposure measurement error
can bias regression coefficients, modify the shape of exposure response
curves, and obscure the presence of a threshold.

		So isn't it also the case that exposure measurement error can bias
results towards the null?

		DR. LONG:  Yes, that is true.  It -- yes, as I discussed in response
to Dr. Ginsberg's question, the impact of exposure measurement error
does depend on a number of different factors, and it is true, it can
bias either high or low.

		It can bias towards the null.  It can be a source of positive bias.
Yes, there are examples of that.

		MR. SCHAYER:  Okay.  Thank you very much.  That concludes my
questions.

		JUDGE SOLOMON:  Mr. Perry?

		MR. PERRY:  Next up will be Tiffany DeFoe.

		MS. DeFOE:  Hi.  I think a number of my questions have been pretty
well addressed by some of the previous questioners and by the panel, but
just a couple additional.

		I wanted to follow up on a question that Dr. Ginsberg, I think,
raised.  Dr. Valberg, would you -- well, first, would you quickly just
step through the beginning of the disease process and how it relates to
the possible existence of a threshold effect in silicosis?

		DR. VALBERG:  Yes.  I'd like -- I'd be glad to do that.  I think, one
of the things that's important is that whenever we're -- whenever the
lungs are presented with a challenge of inhaled gases, vapors,
particles, and so forth, the lung defense systems can kick in, if there
in fact is some sort of adverse reaction with the lung tissues.

		And you can have a enhancement of the lung defense mechanisms that
helps you deal with the challenges of everyday particle inhalation that,
in fact, is a psychological response.  And even though you may be able
to detect a difference between exposed lungs versus unexposed lungs,
that difference may or may not necessarily be adverse.

		And so it's the persistent lung inflammation that seems to cause
problems in the long term.  And if you get that, either by virtue of an
overload of the lung or by virtue of particles that are particularly
toxic in their reaction with cells, then that can go on to be
persistent, irreversible, and lead to disease.

		So what I was picking up, in terms of people who have examined this
reaction between silica and the lung, is that the primary step is
inflammation, and that if that gets out of control due to an overload
condition, then you can have lung disease.

		MS. DeFOE:  So the clearance mechanisms are important to preventing
that sort of overload?  Are there other mechanisms?

		DR. VALBERG:  Yes, absolutely.  No, I think that the whole response of
the lung does involve, you know, dissolution, clearance, the removal of
the material from the lung.  And particularly for particles that are
insoluble, then it is of course macrophage clearance, mucociliary
clearance, perhaps clearance to the lymph nodes as well.

		MS. DeFOE:  And it sounded like you -- is it the case that you would
agree with Dr. Ginsberg's statement that these processes vary quite a
bit from individual to individual?

		DR. VALBERG:  Yes.  And that's one thing I meant to respond to
Dr. Ginsberg's question about individual-to-individual variability.
That does indeed exist, and that's another factor that might tend to
obscure a threshold; something that might be steep for a very homogenous
population, if there's variability in a population, then that threshold
can be blunted, if you will.

		And Dr. Ginsberg served on the panel that developed the National
Academy of Sciences' so-called Silver Book, which had to do with
responses to -- on non-carcinogenic effects, that individual
variability is indeed very important.

		The only factor to keep in mind, however, is what is the degree of
individual variability?  That is to say, you need some information on
how much people would vary.  It's not infinite.  I mean, all of us
manage to live in the face of lots of individual challenges.  People
manage to put out drugs into the drug store that we all take, and
seemingly they are in a range that do not, in fact, kill people and are
effective for most people as well.

		So yes, absolutely, individual variability is an important parameter.

		MS. DeFOE:  Are you aware of good studies on the nature of and extent
of the inter-individual variability on these parameters?

		DR. VALBERG:  There are studies on lung responses to particles and
individual variability.  I don't -- I can't, you know, cite them to you
right now, but in fact that's a fairly well-studied field, yes.

		MS. DeFOE:  Thank you.  And then just a clarifying question to
Dr. Borak, you stated earlier that OSHA relied on a hypothetical risk
assessment rather than the empirical data itself.  That was a phrase
that I picked up from your earlier statement.  And I wanted to clarify,
when you said the empirical itself, which data were you referring to?

		DR. BORAK:  I was talking in particular, in the -- what OSHA refers
to as the surveillance data.  And when I refer to the hypothetical, what
I am talking about is the modeled data largely driven by high exposures
in which the low exposure extrapolations are made.  And I think that
those extrapolations have a certain degree of uncertainty and are
thereby hypothetical.

		MS. DeFOE:  So then if you're suggesting that OSHA should rely on the
empirical data itself and you're talking about surveillance data, are
there empirical data available on the exposures of these workers, or on
their use of respiratory protection?

		DR. BORAK:  No.  I think that I agree with OSHA in its original
statement, which was that the surveillance data are insufficient.

		MS. DeFOE:  Okay, so you didn't actually mean that we should rely on
the surveillance data?

		DR. BORAK:  No, no, no.  To the contrary.

		MS. DeFOE:  Okay, thank you.

		MR. CHAJET:  I have just a couple of questions.  Dr. Borak, I wanted
to ask about your recommendation for changing the definition of
respirable crystalline silica in our proposed rule.  In particular, you
say that the definition should be defined by particle size.

		So are you saying the definition should refer to all particles less
than, say, 10 microns in diameter or less?

		DR. BORAK:  It's -- my objection has several parts.  One of them is,
as you will hear this afternoon, and I don't want to take away that
discussion, each of the individual samplers which has been proposed or
might be proposed has a different profile in terms of the sampling
efficiency at various sizes, aerodynamic sizes of particles.

		And so one of the problems is that some samplers will under-sample
very small particles and over-sample larger particles.  And others work
in the other fashion.  This has several implications, not only in terms
of how much appears to be in the air, but also from a biological
standpoint.

		If you believe, at least as I do, that it's perhaps the surface area
of the particles and not their mass which is a major driver of the
toxicology of silica, then those samplers which under-sample small
particles and over-sample large particles will give very misleading
information as to the toxicity of the dust and at the same time will
lead to incorrect assumptions as to whether people are or are not above
or below allowable levels.

		And I think that is one of the things OSHA needs to consider, which is
that there needs to be a absence of such ambiguity, and that one of the
problems has to do with the variability of different samplers, resulting
in variability in terms of the actual data and their implicit or implied
toxigenicity.

		The second has to do with a problem which includes the fact that there
are sometimes errors in which large particles are inadvertently included
in samples, which give misleading readings of mass and so forth.  And I
think it would be very useful if this was not left to a question of
sampler performance, but rather to a standard which was size based.

		MR. CHAJET:  Okay.  Let's see, I think what I was trying to ask,
maybe, was a little bit different.  First, we all understand that these
respirable dust samplers will collect particles of different sizes with
varying degrees of efficiency.

		The larger particles will be collected less efficiently than the
smaller particles.  Do you agree, as a general matter with that?

		DR. BORAK:  I think so.  I'd have to think twice, but for the moment,
yes.

		MR. CHAJET:  Well, I'm trying to figure out, if we define respirable
crystalline silica as being the particles that are less than 10 microns,
meaning the mass of all of these particles, and we express whatever
exposure limit we end up with as a mass of all of these particles, is
there a sampler available that can measure that, if we define respirable
crystalline silica this way?

		DR. BORAK:  I have to admit that I don't know the answer, but this may
or may not be a subject for this afternoon's discussion.

		MR. CHAJET:  I may hold it till then; thank you.  One other thing.  I
can't remember now who it was, but maybe it was you, Dr. Borak, quoting
IARC 97 with respect to what IARC concluded, that the inflammatory
reaction was a likely mechanism for the induction of lung cancer?

		DR. BORAK:  That's correct.

		MR. CHAJET:  Okay.  Have you seen their updated assessment in 2012?

		DR. BORAK:  Yes.  That was quoted just below, on the same slide.

		MR. CHAJET:  Okay.  Then it should be on your slide that what you say
is true, but then they go on to say, "Although reactive oxygen species
can be directly generated by crystalline silica polymorphs themselves,
and can be taken up by epithelial cells, for this reason, a direct
effect on lung epithelial cells cannot be excluded."

		DR. BORAK:  Yes, correct.  I think I actually quoted that last
statement, and that may have been --

		MR. CHAJET:  I don't remember that.

		DR. BORAK:  I'm sorry.  Was that a question?

		MR. CHAJET:  No, no.  I just couldn't remember you quoting that
particular statement.

		DR. BORAK:  Oh, oh.  It's at least in my written comments and is tied,
in part, to the question that Dr. Crump asked me earlier.

		MR. CHAJET:  Okay.  All right.  Let's see.  The only -- just one
other thing.  In your -- and this is the group now, that you all
mentioned a lot of published studies, and Dr. Long, I think, in
response to a question from Mr. Schayer, you talked about perhaps other
occupational epi studies that would be helpful to us.

		I just wanted to make sure.  Have all of these been submitted to the
record already?  Or will you be able to submit anything that you've
talked about in your oral testimony today to the record?

		(Off the microphone discussion.)

		MR. CHAJET:  Ms. Lindberg has a few questions for the panel.

		MS. LINDBERG:  Dr. Borak, I'm going to quote from your comment that
you submitted to the record, Pages 9 to 10.

		DR. BORAK:  I'm sorry, page?

		MS. LINDBERG:  Pages 9 to 10.  And the quote is, "It should be obvious
that because of the widespread noncompliance in silica overexposures
documented by OSHA, and because of frequent noncompliance with
respiratory protection, there is little or no empirical basis for OSHA
to attribute ongoing reports of new silicosis cases to exposures at or
about the current PEL."

		And perhaps it's because I'm an attorney, but it doesn't seem obvious
to me that this proposition is true.  So I guess I'm wondering, have you
been able to or attempted to demonstrate that these new silicosis cases
were linked to silica exposures above the current PELs rather than below
them?

		DR. BORAK:  I have not been able to relate individual cases, nor has
OSHA been able to relate individual cases to levels at or below the 100
level.  I think the weight of evidence is rather compelling and -- at
least rather compelling to me.

		One of them is demonstrated in the slide which is up here, which shows
a dramatic decline in silicosis, despite the persistence of levels above
100 µg.  And there is a lot of data showing that the exceedances and
noncompliance with the current PEL seem to be most commonly found in
those industries that are associated with the highest rates of
silicosis.

		So I make that inference, and it seems to me clear, but perhaps it is
not clear.  It may not be obvious to all.

		MS. LINDBERG:  Just so long as I'm not missing something.

		DR. BORAK:  No, no, no, no.  I think it's a very sharp question, and I
appreciate your asking.

		MS. LINDBERG:	 And then one for Dr. Hessel.  Again, going back to
your comments that you submitted to the record, on Page 6 you described
a case involving thousands of silicosis lawsuits, a multi-district
litigation.

		And you state that the judge found that the cases of alleged silicosis
were mostly fabricated for purposes of the litigation.  You didn't cite
the case, but I went back and I found it and looked at it.  And as far
as I can tell, those cases involved in that litigation were from
Mississippi, Kentucky, Texas, and Missouri.  But that was cited in a
section of your comments on silicosis in Michigan.  So I'm wondering if
there was a link between that litigation and silicosis cases that were
discussed in the litigation.

		DR. HESSEL:  Yes.  Thanks for your question.  I thought you'd
forgotten I was over here.  The point I was making, I don't know if any
of those screening programs had taken place in Michigan.  I know that
the similar kind of bogus asbestos screening -- or asbestosis screening
programs had taken place in Michigan, but I did not know if the
silicosis screening had done, had happened there as well.

		If they had happened -- see, what I was trying to figure out is, we
had so many of these cases that were reported by hospitals.  Now, a
hospital can generate a silicosis on the record by a diagnosis that
would occur in the hospital, or simply by taking a history, a medical
history on admission, and if somebody on admission says, well, you know,
yes, I've got high blood pressure, oh, and I've got silicosis because,
you know, those lawyers told me so.

		So what I'm -- what I was concerned about is that if those kind of
screenings had happened in that jurisdiction, or in Michigan, then
people would be walking around with a diagnosis of silicosis, and they
might present that when they came to the hospital, and the hospital
might just have a more efficient mechanism for referring to the registry
than some of the other situations.

		MS. LINDBERG:  Yes.  I understand your concern.  I was just wondering
if you had any link or any evidence that you could submit that would
actually document that that kind of screening was happening in Michigan
for silicosis rather than asbestosis.

		DR. KESSEL:  Right.  No, I looked hard.

		MS. LINDBERG:  -- the number of cases.

		DR. KESSEL:  Yes, I looked hard, and I couldn't find any.  But that
doesn't mean it didn't happen.  I just don't know that it happened.

		MS. LINDBERG:  All right, thank you.

		MR. CHAJET:  Let me just interject, for the record, we'll try to find
some of that information.  But clearly we had 30,000 or so cases in
front of Judge Jack, and we quote her in our comments where she said,
"This appears to be a false epidemic, or a phantom epidemic."

		Those cases infest your data as well, because when somebody says they
have silicosis, they go into your database.  And that's 30,000 of them
in one case.  So this is not a phantom problem; it's a phantom epidemic,
as Judge Jack said.

		JUDGE SOLOMON:  That's argument and not testimony, by the way.  But
we're at 12 o'clock, so how much more do we have?

		(Off microphone discussion.)

		MS. LINDBERG:  Just one more for you, Dr. Hessel.  OSHA cites one of
your studies on Page 56299 of the proposal for the proposition that once
someone has been diagnosed with silicosis, there is a chance the disease
will get progressively worse, even in the absence of silica exposure.
It looks like it was a study from 1988.  I'm just wondering, do you
think that's a correct interpretation of that study?

		DR. HESSEL:  I think, in the population we were dealing with -- these
are underground mine workers in South Africa exposed to some fairly high
levels, and the majority of the people who developed silicosis did have
progression.

		We found that when we looked at the difference between progression in
relation to exposure before and after onset, exposure after onset was
actually important.  So yes, I believe the data speak for themselves.  I
think we found that in most cases there was progression.

		MS. LINDBERG:  Thank you.

		JUDGE SOLOMON:  Anything else?

		MR. CHAJET:  Just one more.  I'd like to ask Dr. Borak one question
as a follow-up to a response of one of Ms. Lindberg's questions.

		In talking about this graph that's up here again, of the decline in
silicosis mortality over the years -- and I think you were talking
about thresholds, do you regard this, these data, as evidence of a
threshold for silicosis at or above OSHA's current PEL?

		DR. BORAK:  I think that Dr. Goldsmith linked this and -- a
question.  I thought it was Dr. Goldsmith, but somebody asked regarding
this graph and thresholds.  I see no correlation between this graph and
a threshold.

		What I was trying to talk about was the chronology.  I'm sorry to be
blowing into the speaker.  I was simply speaking of the chronology and
in particular the concerns about latency and survivalship and the
relevance of these data to evaluating the effectiveness of the PEL.  I
think they are a tribute to both industry and government intervention.

		MR. CHAJET:  Okay.  Thank you for clarifying that.  That's all, Your
Honor.

		JUDGE SOLOMON:  Okay.  So we're going to come back at 1 o'clock, when
we'll have the Chemistry Council.  So the hearing is continued to 1
o'clock.

		(Whereupon, at 12:03 p.m., a lunch recess was taken.)

A F T E R N O O N   S E S S I O N

(1:00 p.m.)

		JUDGE SOLOMON:  All right, let's go back on the record.  We have
Dr. Cox.  You want to make the introduction?  State your name.

		MR. KING:  My name's Neil King.  I am counsel for the American
Chemistry Council's Crystalline Silica Panel, and I'm just here as kind
of a prop for Dr. Louis Anthony (Tony) Cox, who will be making a
presentation this afternoon.

		DR. COX:  Great.

		JUDGE SOLOMON:  Go Ahead.

		DR. COX:  Okay, so I am Tony Cox.  I'm the President of Cox
Associates, a risk analysis and quantitative modeling firm based in
Denver.  I'm a member of the National Academy of Engineering; editor in
chief of Risk Analysis, an international journal; author of the book,
Improving Risk Analysis; and a fair amount of my life and passion are
devoted to how we can, indeed, do that.

		The American Chemistry Council asked me to critically review the
assumptions and models used by OSHA, and the sources on which OSHA has
relied in this matter, and I've done that.  And I've submitted a fairly
extensive piece of written testimony, back on February 11.

		What I want to do this afternoon is to summarize what I see as being
some high points of that, and to invite, of course, questions and
exploration.

		So let me begin with a preview of what we're going to cover in the
next half hour, a little bit more.  I want to look at what are the
components of a good quantitative risk assessment, as I understand them,
and then say, well, how good is OSHA's risk assessment compared to those
criteria, or by those criteria?

		And then I want to give you my assessment of the scope of the
preliminary QRA that OSHA has.  So is it answering the right questions?