Document ID: OSHA-2010-0034-3577
Agency: osha
Document Type: Supporting & Related Material
Title: 
Posted Date: 2014-04-21T04:00Z

INFORMAL PUBLIC HEARINGS FOR THE PROPOSED RULE

ON OCCUPATIONAL EXPOSURE TO

RESPIRABLE CRYSTALLINE SILICA

+ + +

UNITED STATES DEPARTMENT OF LABOR

OCCUPATIONAL SAFETY & HEALTH ADMINISTRATION 

+ + +

March 20, 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):

ALLISON KRAMER

Attorney, Office of the Solicitor 

ANNE RYDER

Attorney, Office of the Solicitor

OCCUPATIONAL SAFETY & HEALTH ADMINISTRATION (OSHA):

WILLIAM PERRY

Acting Director, Directorate of Standards and Guidance

TIFFANY DeFOE

Office of Chemical Hazards - Metals

PATRICIA DOWNS

Office of Technologic Feasibility

ANNETTE IANNUCCI

Health Scientist, Office of Chemical Hazards 

- Non-Metals 

ROBERT STONE

Director, Office of Regulatory Analysis - Health

DAVID O'CONNOR

Director, Office of Chemical Hazards - Non-Metals 

JANET CARTER

Office of Chemical Hazards - Metals 

STEPHEN SCHAYER

Office of Physical Hazards 

ROBERT BURT

Acting Deputy Director, Directorate of Standards and Guidance	

LYN PENNIMAN

Director, Office of Physical Hazards

PEER REVIEWERS:

BRIAN MILLER, Ph.D.

Institute of Occupational Medicine 

GARY GINSBERG, Ph.D.

ANDREW SALMON, Ph.D.

KENNY CRUMP, Ph.D.

NATIONAL INDUSTRIAL SAND ASSOCIATION (NISA): 

MARK ELLIS

President

ANDREW O'BRIEN, CIH

Vice President of Safety and Health

Unimin Corporation

JAMES CONRAD, JR.

Attorney, Conrad Law and Policy Counsel

INTERNATIONAL DIATOMITE PRODUCERS ASSOCIATION (IDPA): 

MARK ELLIS

Executive Director

KENNETH MUNDT, Ph.D.

ENVIRON International Corporation

JAMES CONRAD, JR.

Attorney, Conrad Law and Policy Counsel

BRICK INDUSTRY ASSOCIATION (BIA):

ROBERT E. GLENN, M.P.H., CIH

 

ACME BRICK COMPANY:

DR. GARTH TAYLER 

Technical Director 

THOMAS BROWN

Director of Health and Safety

BILL LATHAM

General Counsel and Risk Manager

AMERICAN COLLEGE OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINE (ACOEM):

MICHAEL FISCHMAN, M.D.

AMERICAN THORACIC SOCIETY (ATS):

ROBERT COHEN, M.D.

ASSOCIATION OF OCCUPATIONAL AND ENVIRONMENTAL CLINICS

(AOEC):

TEE GUIDOTTI, M.D.

AMERICAN PUBLIC HEALTH ASSOCIATION (APHA):

ROSEMARY SOKAS, M.D., M.S., MOH

INDIVIDUALS:

CELESTE MONFORTON, Dr.P.H., M.P.H. 

KENNETH ROSENMAN, M.D.

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

JAMES CONE, M.D., M.P.H.OTHER PARTICIPANTS:

LAURA WELCH, M.D.

Building and Construction Trades Department, AFL-CIO

SCOTT SCHNEIDER, CIH

Director of Occupational Safety and Health

Laborers' Health and Safety Fund of North America

DAE WARD

Alabama Power

JIM WEEKS, Sc.D., CIH

Mine Safety and Health Administration

FRANK HEARL

Chief of Staff, NIOSH

DAVID WEISSMAN

Director, Division of Respiratory Disease Studies NIOSH

FRANKLIN MIRER, Ph.D., CIH

CUNY School of Public Health

AFL-CIO

NEIL KING

Attorney, American Chemistry Council's Crystalline Silica Panel

DARIUS D. SIVIN, Ph.D.

Health and Safety Department, United Auto Workers

ELIZABETH NADEAU

Attorney, International Union of Operating Engineers

RAMI KATRIB

Health, Safety and Environment Department 

United Steelworkers Union

AVI MEYERSTEIN

Attorney, Jackson Lewis

U.S. Chamber of Commerce

BOVNAR ANAND, M.D.

INDEX

										PAGE

		

INTRODUCTION

Judge Daniel F. Solomon					  	   PAGEREF a1Solomon \h  559 

NATIONAL INDUSTRIAL SAND ASSOCIATION (NISA)

	Mark Ellis							   PAGEREF b1EllisNISA \h  559 

	Andrew O'Brien, CIH						   PAGEREF b2Obrien \h  563 

	Questions							 	   PAGEREF b3questionsMonforton \h  586 

INTERNATIONAL DIATOMITE PRODUCERS ASSOCIATION

(IDPA)

	Mark Ellis							   PAGEREF c1Ellis \h  617 

	Kenneth Mundt, Ph.D.				  	   PAGEREF c2Mundt \h  621 

	Questions							 	   PAGEREF c3qOsha \h  636 

BRICK INDUSTRY ASSOCIATION (BIA)

	Robert E. Glenn, M.P.H., CIH			  	   PAGEREF d1Glenn \h  653 

	Questions								   PAGEREF d2qbypublic \h  680 

ACME BRICK COMPANY

	Dr. Garth Tayler						   PAGEREF F1Tayler \h  702 

	Thomas Brown							   PAGEREF F2Brown \h  709 

	Bill Latham							   PAGEREF F3Latham \h  715 

	Questions								   PAGEREF F4questions \h  724 

INDEX

										PAGE

AMERICAN COLLEGE OF OCCUPATIONAL AND 

ENVIRONMENTAL MEDICINE (ACOEM); AMERICAN 

THORACIC SOCIETY (ATS); ASSOCIATION OF 

OCCUPATIONAL AND ENVIRONMENTAL CLINICS (AOEC); 

and AMERICAN PUBLIC HEALTH ASSOCIATION (APHA)

	ACOEM - Michael Fischman, M.D. 			  PAGEREF G1Fischman \h  764 

	ATS - Robert Cohen, M.D.					  PAGEREF H1Coeh \h  770 

	

	AOEC - Tee Guidotti, M.D.				  PAGEREF I1Guidotti \h  780 

	APHA - Rosemary Sokas, M.D., M.S., MOH		  PAGEREF J1Sokas \h  787 

	Questions								  PAGEREF J2questions \h  794 

INDIVIDUALS

	Celeste Monforton, Dr.P.H., M.P.H.		  PAGEREF k1Monforton \h  845 

	Kenneth Rosenman, M.D.					  PAGEREF L1Rosenman \h  853 

	David F. Goldsmith, M.S.P.H., Ph.D.		  PAGEREF M1Goldsmith \h  859 

	James Cone, M.D., M.P.H.					  PAGEREF n1Cone \h  866 

	Questions								  PAGEREF O1questions \h  873 

ADJOURNMENT								  PAGEREF adjourn \h  904 

EXHIBITS

EXHIBITS		DESCRIPTION				 	PAGE

Exhibit 13	Mr. Ellis' testimony, NISA	        PAGEREF Ex13 \h  585 	  

Exhibit 14	Mr. O'Brien's testimony		   	   PAGEREF Ex14 \h  586 	   

Exhibit 15	Mr. Ellis' testimony, IDPA	   	   PAGEREF ex15to17 \h  635 	 
  

Exhibit 16	Dr. Mundt's testimony	   	  	   PAGEREF ex15to17 \h  635 

Exhibit 17	IDPA PowerPoint 		   		   PAGEREF ex15to17 \h  635 	    

Exhibit 18	Mr. Glenn's statement/PowerPoint	   PAGEREF Ex18 \h  680 	   

Exhibit 19	Meyer study in CHEST	  		   PAGEREF Ex19 \h  686 	   

Exhibit 20	Epstein article			  	   PAGEREF Ex20 \h  687 	   

Exhibit 21	Castellan article			  	   PAGEREF Ex21 \h  687 	   

Exhibit 22	Dr. Sokas' testimony		 	   PAGEREF Ex22 \h  844 		

Exhibit 23	Reserved - Dr. Cohen's testimony	   PAGEREF E23Cohenreserve
\h  844 

Exhibit 24	Reserved - Dr. Monforton's 

			testimony	 					   PAGEREF E24Montfortonreserve \h  896 

Exhibit 25	Reserved - Dr. Rosenman's 

			testimony	 					   PAGEREF E25Rosenmanreserve \h  903 

Exhibit 26	Dr. Goldsmith's testimony		   PAGEREF Ex26and27 \h  904 	   

Exhibit 27	Dr. Cone's PowerPoint			   PAGEREF Ex26and27 \h  904 

				  

P R O C E E D I N G S

(9:30 a.m.)

		JUDGE SOLOMON:  Let's go on the record.

		Ms. Kramer, do you want to enter your appearance for the record?

		MS. KRAMER:  Sure.  I'm Alison Kramer.  I am with the Office of the
Solicitor here at DOL.

		JUDGE SOLOMON:  So the first organization that will make a
presentation is the National Industrial Sand Association.  And,
Mr. Conrad, you're waving at somebody.  Who is going to start with the
presentation?

		MR. ELLIS:  I am.

		JUDGE SOLOMON:  Okay.

		MR. ELLIS:  Good morning.  I am Mark Ellis and I am President of NISA,
the National Industrial Sand Association.  I am joined this morning by
Andrew O'Brien, the Vice President of Safety and Health for Unimin
Corporation, a NISA member company, and Jamie Conrad, the principal of
Conrad Law and Policy Counsel, who is NISA's counsel in this rulemaking.

		NISA is a nonprofit, 501(c)(6) trade association representing major
North American producers and processors of industrial sand, sometimes
called silica sand.  NISA currently has 31 members and is the oldest and
largest trade association representing the industrial sand industry in
the United States and Canada.

		Industrial sand companies produce 100 percent pure crystalline silica.
 As a result, NISA members generally have longer history of working with
silica and more direct contact with silica than anyone else in industry.
 It is also why beginning in the 1970s, NISA and its member companies
developed what has now become known as the NISA Silicosis Prevention
Program, or SPP.

		NISA members' workplaces are predominantly mining operations and thus
are typically regulated by MSHA and not OSHA for purposes of
occupational safety and health.  NISA has a substantial stake in the
outcome of the OSHA crystalline silica rulemaking, however, for several
reasons.  The most important of these reasons is simple, however.  NISA
members strongly believe that the exposure monitoring and medical
surveillance that they implement under the Silicosis Prevention Program
are the right things to do to prevent health -- protect the health of
their employees and are good for their business' bottom lines.  They
also believe these two practices must be included in a comprehensive
OSHA standard.

		NISA is pleased to offer a unique perspective on the issue of
workplace exposure to crystalline silica and an optimal solution to
challenge -- to the challenge facing OSHA.  

		As we explained in our comments, NISA strongly supports what has come
to be termed the NISA solution, a comprehensive standard that would
require exposure monitoring and medical surveillance at an action level
of 50 µg/m3, while maintaining the current permissible exposure limit,
or PEL, at 100 µg/m3.  This is similar to OSHA's Alternative 1.  And
NISA commends OSHA for offering that alternative first and for stating
that it will, quote, "Strongly consider alternatives that would reduce
the economic impact of the rule," close quote.

		As our comments demonstrate, the NISA solution would substantially
reduce any risk of material impairment from workplace exposure to
crystalline silica rising from the stubbornly high level of
noncompliance with the current PEL.  

		The NISA solution is also economically and technologically feasible. 
The beauty of the NISA solution lies in two concepts that OSHA itself
has seen the extraordinary value of over the years, a potentially
achievable action level and a substance-specific standard.

		First, a potentially achievable action level drives companies that can
need it to lower their exposures to a level that removes them from the
burden of complying with the regulation altogether.  We believe that
positive enticement is a more powerful motivation than the negative
enticement of avoiding an OSHA citation.  

		If the action level were set at 25 µg/m3, few if any companies would
be able to achieve that mark.  Most would devote expenditures and
resources sufficient just to comply with the PEL, and many would only
spend enough not to violate it by much or very often.  

		A potentially achievable action level, however, will drive companies
that can meet it to pay what they might call a regulatory avoidance
premium to avoid having any further compliance obligations under the
rule.  A potentially achievable action level is paramount in making this
rule successful.

		Further, not enough has been said about the simple power of OSHA's
substance-specific standards, of which there are only about 30.  Once
crystalline silica has a dedicated standard, a great deal more attention
will be given to controlling what potential hazard this substance may
present in the workplace, and this will occur no matter what the
exposure level is established.

		The NISA solution plays on the power of the action level and the
substance-specific standards and presents a pragmatic and cost-effective
alternative that should be embraced by labor, industry, and OSHA.

		NISA's principal witness today, Andrew O'Brien, is chair of NISA'S
Silica Health Effects Committee.  He, thus, is ideally positioned to
describe the NISA Silicosis Prevention Program and the extraordinary
results that it has produced.  That experience is what makes us so
confident in saying that OSHA could retain the current PEL and still
eradicate new cases of silicosis.  The key is to include exposure
monitoring and medical surveillance triggered by an action level in a
comprehensive standard.

		Mr. O'Brien also will discuss the silica epidemiology study that NISA
is sponsoring and that could have a profound effect on this rulemaking. 
So with that introduction, I'd like to turn things over to Mr. O'Brien.

		MR. O'BRIEN:  Thanks, Mark.  Good morning.  My name is Andrew O'Brien,
and I am Vice President of Safety and Health for Unimin Corporation.  I
am pleased to testify before you this morning on behalf of NISA
concerning OSHA's proposed rule regarding crystalline silica.

		As Mark just noted, NISA and its member companies strongly support the
promulgation of a crystalline silica rule that requires exposure
monitoring and medical surveillance at the action level of 50 µg/m3,
while retaining the current permissible exposure limit of 100 µg/m3. 

		The focus of my testimony this morning will be twofold.  First, I will
testify regarding NISA's groundbreaking Silicosis Prevention Program, or
SPP, and the profound effect the SPP has had in eliminating the
occurrence of new cases of silicosis in NISA member company workplaces. 
The SPP includes both exposure monitoring and medical surveillance and
the results of the SPP, as shown by annual company reporting within the
association, provide clear support for including both of these practices
as ancillary provisions in a comprehensive OSHA crystalline silica
standard.  I will also comment briefly on the economic feasibility of
exposure monitoring and medical surveillance.  

		Second, I will testify regarding a major epidemiological study that
NISA has commissioned and that is ongoing as we speak.  We expect that
this study will make a substantial contribution to the existing body of
science that exists to date regarding the shape of the dose-response
curve for silicosis in large part because of the extensive data
available for this study, as I will discuss.  We urge OSHA to
incorporate the results of this study in its decision-making process for
the final rule.  

		But, first, let me provide some background on myself and Unimin.  I am
a certified industrial hygienist and a certified safety professional
with a master of science degree in industrial hygiene and an
undergraduate degree in safety engineering.  I am currently the Vice
President of Safety and Health for Unimin Corporation.  Founded in 1970,
Unimin has grown from a small local sand mining company to become a
leading producer of nonmetallic industrial minerals in the worldwide
Sibelco Group.

		We are the largest producer of industrial sand in each of the United
States, Canada, and Mexico, and along with our affiliates in other
countries, we are the largest producer in the world.  Our products are
the fundamental building blocks of nearly every manufacturing process --
sorry, manufacturing and industrial process.  We are a worldwide
supplier to the glass, ceramic, and lighting industries; to oil and
natural gas service companies; and to paint, plastic, rubber, and
composite manufacturers.  

		Our high purity quartz products are the starting point for the world's
semiconductor and solar photovoltaic cell production.  We are also an
integral supplier to the metallurgical and foundry industries, and we
participate in a wide range of civil, industrial, environmental, and
building related applications.  Our products touch the lives of millions
of people daily.

		In my current capacity at Unimin, I am responsible for the safety and
health of Unimin's employees throughout North America, with a current
census of approximately 2,400.  Within this capacity lies Unimin's
occupational health program, which has a significant emphasis on the
prevention of new cases of silicosis.  Routinely quantifying employee
exposure to respirable crystalline silica and regularly conducting
medical surveillance programs are the backbone of Unimin's efforts to
prevent new cases of silicosis.

		Unimin has been a proud member of NISA since 1970.  Unimin has always
believed strongly in NISA's mission.  And Unimin employees have
historically had leadership positions within NISA.  Three of NISA's past
chairmen have been Unimin executives, and a fourth is currently on
NISA's executive committee.  And, as Mark noted, I am chair of NISA's
Silica Health Effects Committee and chair of the Safety and Health
Committee for NISA's umbrella organization, the Industrial Minerals
Association North America.

		The NISA silica health effects committee is responsible for continuing
to steward the NISA Silicosis Prevention Program and for facilitating
the conduct of our ongoing epidemiology study in collaboration with
NISA's epidemiology research task force.  Coordinating efforts among
government and industry representatives, the NISA silica health effects
committee was also largely responsible in facilitating development and
publication of NIOSH's RI 9689, entitled Dust Control Handbook for
Industrial Minerals, Mining, and Processing.

		I am happy to be able to testify today about both the NISA Silicosis
Prevention Program and our epidemiology study and their potential
implications for this rulemaking.  As Mark Ellis explained, the
industrial sand companies produce essentially 100 percent pure
crystalline silica.  As a result, NISA members have generally had longer
histories of working with silica, more direct contact with silica, and
greater challenges due to the 100 percent silica content of our products
than anyone else in industry.

		It is also why, beginning in the late 1970s, NISA and its member
companies reached out to occupational health experts to establish a
voluntary program of employee exposure assessment and medical
surveillance.  The program referred to as the Occupational Health
Program for Exposure to Crystalline Silica in the Industrial Sand
Industry, or OHP, is the basis for the SPP.

		In 1993, the NISA board of directors adopted the goal of preventing
any new cases of silicosis among their employees, with "new" defined as
cases of silicosis produced by exposures at NISA member company
workplaces commencing in 1994.  This definition of "new" recognized that
some number of NISA member companies -- NISA member company employees
might have had silicosis at that time or might subsequently develop it
based on exposures occurring before that date, whether at NISA member
companies or elsewhere, or after that date but before employment at a
NISA member company.

		As a result of this decision and influence by the widespread
establishment of management system approaches, NISA and its members
subsequently incorporated the OHP into a broader Silicosis Prevention
Program.  I'll discuss these two programs in reverse order.

		The scope and elements of the SPP are set out in this guide right
here, excuse me, which is entitled, National Industrial Sand Association
Silicosis Prevention Program, which NISA included as an appendix to its
comments.  The SPP declares "NISA's expectation that all member
companies will implement and manage a comprehensive silicosis prevention
program at all worksites sufficient to eliminate silicosis among its
employees."  

		The SPP currently comprises seven steps: 

		First, strong management commitment to implement a silicosis
prevention program.  This commitment includes not only a commitment to
performing both dust exposure assessment and medical surveillance, but
to sharing data on both dust measurements and chest x-ray results with
other NISA member companies at annual benchmarking sessions.  I'll turn
to that data-sharing process in a moment.

		Second, implementation of the OHP.  The OHP describes in great detail
how respirable crystalline silica exposure monitoring and medical
surveillance are to be conducted by NISA members.

		Third, periodic assessments to quantify worker exposure to respirable
crystalline silica dust.  As the SPP states, it is crucial that NISA
member companies implement and manage a silica exposure program to
collect personal breathing zone samples from all employees exposed to
industrial sand so that periodic measurements of silica exposure and
cumulative exposure assessments can be made.  After all, if you are not
quantifying employee exposure, how do you know whether or not you are
adequately controlling employee exposure?

		Fourth, routine medical surveillance to assess worker health and to
look for indications of silica-related health effects.  The SPP explains
that medical surveillance serves multiple purposes.  It establishes a
baseline for future measurements so that each employee serves as his or
her own control.  It allows detection of abnormalities that might be
consistent with the health effects of silica exposure at an early age --
sorry, early stage when intervention can lead to the prevention of
disease progression.  

		It prevents the development of silicosis that could produce pulmonary
impairment in the worker.  It prevents the development of other
occupational conditions that might be associated with exposure to
silica.  It enables disclosure to the worker of occupational and
non-occupationally related abnormalities for appropriate medical
follow-up.  And it leads to the development of a database on which
epidemiological studies of crystalline silica exposure can be based.

		The fifth element of the SPP is implementation of dust control
equipment or processes.  The SPP encourages NISA member companies to
undertake a program to anticipate, recognize, evaluate, and control
hazardous dust exposures, and to continually monitor the effectiveness
of control strategies.  It emphasizes that the control of hazards from
exposures to respirable crystalline silica and the elimination of
silicosis is the primary and single most important reason for developing
a comprehensive silicosis prevention program. 

		The sixth element is employee involvement in all stages of SPP
implementation.  The SPP recognizes that, in quotes, "A workforce fully
involved in health and safety management, and a system of workers
operating in partnership with management are essential parts of an
effective health and safety program," close quote.  It describes steps
for promoting employee engagement and provides example actions
management can take. 

		The seventh element is smoking cessation programs.  The principal goal
of such programs is to reduce the added impact of smoking on
silica-related health effects.  A related goal is to diminish the
serious adverse health effects that are directly caused by smoking and
exposure to secondhand smoke.

		Of the seven elements of the SPP, the two that are most relevant to
this rulemaking are also the historic core of the SPP, regular personal
sampling of employees' exposure to respirable crystalline silica and
periodic medical surveillance.  The details of these two elements are
spelled out in the current NISA occupational health program on which the
SPP is based, which we also included as an appendix to our comments.

		The OHP begins with an overview of the state of the science regarding
the range of potential health effects of silica exposure.  It then
provides detailed guidance on both dust sampling and medical
surveillance.

		With respect to dust sampling, the OHP's goal is to provide sufficient
detail in sufficiently clear terms that a, quote, "safety officer,
laboratory technician, quality analyst, or any person within a company
who has responsibility for the industrial hygiene program can collect
sufficient personal breathing zone samples from all employees exposed to
industrial sand so that cumulative individual exposure assessments can
be made," end quote.

		Importantly for this rulemaking, what the OHP and our experience show
is that companies don't need to hire outside contractors to competently
conduct exposure monitoring.  Company staff can be trained to do it and
do it competently.  I'll come back to this point in a moment.

		On the subject of medical surveillance, the OHP provides guidance for
both baseline and periodic medical surveillance of employees.  While it
is principally intended for health professionals, it is also written for
any member company employee with responsibility for a safety and health
program since such individual should have a working knowledge of the
elements of the medical surveillance program.

		Multiple citations to the OHP manual in the preamble confirm the
obvious fact that OSHA's proposed medical surveillance requirements are
substantially derived from NISA's OHP manual.  NISA is proud of these
references and appreciates being able to provide a model for such an
important element of silica workplace health.

		Now that I have described what the SPP is, I'd like to turn to what it
has accomplished.  As I mentioned a moment ago, part of the management
commitment that is Step 1 of the SPP is a commitment to sharing data on
both exposure measurement and chest x-ray results with other NISA member
companies at annual benchmarking sessions.  These annual sessions have
occurred every year since 1994.  Each year, SPP participating members
report employee personal dust sampling and chest x-ray data for the
previous year to NISA's staff.  That information is compiled by NISA
staff under my committee's direction.  I then present the information on
a blinded basis to the membership at a special session at the annual
meeting.  

		In these annual reports, respirable crystalline silica exposure data
are presented for the SPP participants as a whole, as well as for
individual company participants.  Information such as the number of
measurements, average percent quartz, and average percent exposure as a
percentage of the PEL for 10 different processes, for example, mining,
bagging, screening, are included in this reporting.

		JUDGE SOLOMON:  Could I stop you for a second?  You're about 20
minutes into about a 30-minute presentation.  And we have, I'm sure
we're going to have some questions.  So could I get some sense, first of
all from the peers here, are you going to ask questions?  I'm not seeing
any hands.

		And from the public, are there -- okay, so there are several people
who want to ask questions.

		MR. CONRAD:  Judge, I just might note in contrast to the last two
days, there are about 110 minutes allocated for presentations today. 
There is another 40 minutes this morning that is not allocated for any
purpose.

		JUDGE SOLOMON:  We were talking -- well, one of the problems is that
we have been running long.  And among ourselves we've been talking about
the fact we probably have to go into the lunchtime.  We probably won't
be finished until about 12:30.

		MR. CONRAD:  Oh, I'm thinking today we may finish early, if anything.

		JUDGE SOLOMON:  Well, what can I say?  That's not the consensus on the
left side of the podium anyway.

		MR. CONRAD:  No.  I mean we're just getting to the good part.  That's
my concern.

		JUDGE SOLOMON:  Okay.  So are we going to be able to get to some
questions?

		MR. CONRAD:  Counselor?

		MS. KRAMER:  Your Honor, we're happy for them to finish their
presentation, assuming they are going to wrap it up in the next 10
minutes that they have been scheduled for.

		MR. CONRAD:  That's fair.

		JUDGE SOLOMON:  Okay.  Are we going to be able to take questions from
the audience?

		MS. KRAMER:  I believe so, yes, sir.

		JUDGE SOLOMON:  All right.

		MR. CONRAD:  Thank you.

		MR. O'BRIEN:  Chest x-ray data are presented within the annual report
as the number of individuals per company with chest x-rays classified as
having a profusion rating of greater than or equal to 1/1 on the ILO
scale.  Those x-rays are generally read by more than one certified B
reader in accordance with the OHP's consensus reading process.  These
presentations allow the membership to evaluate how they are doing
individually and comparatively at controlling exposures and eliminating
new cases of silicosis.  They also allow NISA to assess the
effectiveness of the SPP.  

		A total of 11 companies have reported chest x-ray data since 1994. 
Over this 19-year period, medical surveillance at these companies has
yielded a total of 8 cases with radiographic evidence of silicosis. 
Again, that means greater than or equal to 1/1 on the ILO scale.  Those
eight cases have occurred at a total of three companies.  Those three
companies advise NISA that they do not regard these as new cases,
meaning that in each case the company determined that the silicosis was
attributable to exposures occurring either before 1994, either at the
company or elsewhere, or after that date but before employment at the
company.

		I should note that several NISA members have grown substantially by
acquisition in the past two decades.  The acquired companies typically
had not implemented exposure monitoring, medical surveillance, or other
elements of the SPP, although that certainly changes once they got
folded into the acquiring company.  It is not surprising, therefore,
that along with those new acquisitions, NISA members have inherited
cases of detectable or insipient silicosis.

		Let me pause for a minute to repeat our findings.  A total of 11 NISA
members over a period of 19 years have found 8 cases of silicosis, none
of which were new.  In other words, implementation of the SPP by
participating companies has eliminated the creation of new silicosis
cases amongst those companies' employees, even as those companies were
subject to the current PEL of 100 µg/m3. 

		We recognize that silicosis, while dramatically reduced, is still
being diagnosed elsewhere around the country.  NISA believes that this
disease is caused by the persistently high rates of noncompliance with
current PEL -- with the current PEL that OSHA continues to witness
despite years of focused enforcement.  We further believe that the
absence of an exposure assessment requirement from the current
crystalline silica PEL is the principal reason for this widespread and
often severe noncompliance.

		This conclusion is supported, by the way, by a study of Industrial
Minerals Association-Europe initiative described in our comments, which
found that the exposure monitoring with feedback to the affected
worksites produced a two to threefold reduction in exposure
concentrations.  Quantification of exposure via personal dust sampling
of employees is, thus, key to ensuring compliance with any PEL for
crystalline silica.  

		NISA, therefore, supports OSHA's proposed inclusion of exposure
monitoring, as well as medical surveillance as part of a comprehensive
crystalline silica standard.  We believe that the NISA solution, the
current PEL, supplemented by exposure assessment and medical
surveillance triggered at 50 µg/m3 action level should reduce
significant risk of material health impairment for silicosis sufficient
to meet the requirements of Section 6(b) of the OSHA Act. 

		Unimin has found that the cost of conducting exposure monitoring and
medical surveillance are quite minimal.  These costs, in fact, are
considered insignificant within our company.  We included actual cost
data for five NISA member companies in our comments on Page 24.  The
real cost impact of the proposed rule will be driven by the engineering
controls required to achieve the lower PEL where that can be done.

		But I do want to highlight one way in which OSHA has overstated the
cost of exposure monitoring in our view.  In its cost analysis, OSHA
assumes that employers will use outside contractors to conduct initial
and periodic exposure assessments.  As I mentioned earlier, NISA's
member companies conduct exposure assessments using in-house personnel. 
Obviously, no one can say for certain what the broad variety of
industries covered by OSHA's proposed standard for general industry
would do in response to an exposure-monitoring mandate.

		Clearly, activities involving potential crystalline silica exposures
are absolutely central to what NISA members do, whereas such activities
may be more or less tangential for other regulated industries.  Also,
NISA members have been doing exposure assessment under the SPP since the
1970s, so they have developed substantial expertise in how to do it cost
effectively.  Nonetheless, we believe that some percentage of
OSHA-regulated establishment can and will internalize the function
either at the outset of the rule's effectiveness or as they gather
experience under the rule.

		We do not believe this issue is purely one of business or
establishment size.  Many NISA member companies are small businesses. 
They have nonetheless found that it is more cost effective for them to
train particular staff and acquire the relevant equipment than it is to
hire consultants.  As I explained earlier, our OHP document provides
sufficient detail in sufficiently clear terms that a safety officer,
laboratory technician, quality control analyst, or any person within a
company who has responsibility for the industrial hygiene program can
collect sufficient personal breathing zone samples from all employees
exposed to industrial sand so that cumulative individual exposure
assessments can be made.  We post the OHP on our website and so that
learning is available for companies to view.  

		Given our experience, we urge OSHA to analyze scenarios in which some
percentage of regulated establishments do their own exposure
assessments.  We also urge OSHA to use the data that NISA supplied. 
Three of the five companies included in our sample are among the largest
NISA members on a revenue basis, but another meets the SBA's size
standard for a small business.

		The last topic I'd like to address today is NISA's ongoing silica
silicosis dose-response study.  While the association between silicosis
and exposure to respirable crystalline silica is indisputable, there is
still considerable uncertainty regarding the dose-response relationship
of this association, particularly in the case of chronic simple
silicosis, which is the most common form of silicosis.

		It is unclear, for example, whether there is an effect threshold or
whether, instead, the dose-response curve is linear, even at the lowest
doses.  The slope of that curve is also uncertain.  As a result, there
is uncertainty regarding the degree of risk remaining at various
eight-hour, time-weighted average exposures, including most importantly
the current PEL of 100 µg/m3.  In NISA's view, this degree of
uncertainty is unacceptable for a rulemaking of this magnitude.

		NISA believes that regulatory standard setting ought to be based on
high quality, reliable science.  This is especially true where data of
sufficient quality and quantity exists to produce that science.

		The principal shortcoming affecting the vast majority of published
studies of silicosis risk is the reliance on poor quality or uncertain
exposure measurements.  This undermines the reliability of any
quantitative risk estimates based on those studies, including OSHA's.  

		Many silicosis studies were based on very high exposure to quartz and
lack data on low exposures, so that estimated dose-response conclusions
have to be extrapolated to low doses.  Others lack data for early
exposure years, and so early exposures are based on inferred or
extrapolated concentrations.  Others are based on area sampling, rather
that personal sampling.  Even those that include personal dust sampling
of individuals generally involve measurements taken using the obsolete
particle count approach for all or part of the period evaluated.  

		This latter defect is a serious limitation because it has become
increasingly clear that there is no single defensible conversion factor
from particle count measurements to gravimetric measurements.  No
published study involves so much exposure data, collected rigorously and
consistently via personal samplers, and evaluated gravimetrically with
percentage quartz assessed with x-ray diffraction.

		On the other hand, NISA's two largest member companies, Unimin and
U.S. Silica, possess an extensive database comprising decades of
gravimetric dust sampling and chest x-ray data generated by those
companies' implementation of the SPP.  The exposure data include about
50,000 dust measurements collected systematically since the mid-1970s,
with personal identifiers that will facilitate construction of a job
time exposure matrix.  These exposure samples encompass a large number
of job positions with low to high concentrations, which should ensure a
wide range of exposures for analyses of exposure response.

		Measurements are all reported gravimetrically with a quartz analysis
by x-ray diffraction.  The chest x-ray data similarly encompasses
thousands of chest x-rays generally taken at the beginning of the
individual's employment in the industrial sand industry and every two
years thereafter.

		JUDGE SOLOMON:  Okay, I'm sorry I have to butt in, but you're going to
have to wrap it up.  We're actually over a couple of minutes.

		MR. CONRAD:  Maybe you can answer the -- well, answer it in response
to questions.

		MR. O'BRIEN:  Yeah, let's go to questions.

		MR. ELLIS:  Maybe we can just cover the rest of it in response to
questions.

		JUDGE SOLOMON:  Okay.

		MR. ELLIS:  Your Honor, I think that one thing that we can do is we
can ask that our written testimony be entered into the record.

		JUDGE SOLOMON:  I was going to ask Mr. Conrad if he had any exhibits
he wanted to mark and offer. 

		MR. CONRAD:  I think we have some copies of that.

		MR. ELLIS:  I have it right here.

		MR. CONRAD:  What else is in here?  Have you got it?

		JUDGE SOLOMON:  Okay.  So how are these going to be marked?

		MS. KRAMER:  It looks like this is Mr. Ellis' testimony on top,
followed by Mr. O'Brien's.  Your Honor, we'd like to mark Mr. Ellis'
testimony as Hearing Exhibit 13 and have it be admitted into the record.

		JUDGE SOLOMON:  Okay, without objection, so admitted.

(Whereupon, the document referred to as Hearing Exhibit 13 was marked
and	 received in evidence.)

		MS. KRAMER:  And Mr. O'Brien's written testimony as Hearing Exhibit
14.

		JUDGE SOLOMON:  And that is admitted also.

(Whereupon, the document referred to as Hearing Exhibit 14 was marked
and received in evidence.)

		MS. KRAMER:  Great.

		JUDGE SOLOMON:  Okay.  Ma'am, would you state your name for the
record, please, and spell your last name?

		DR. MONFORTON:  Dr. Celeste Monforton, M-o-n-f-o-r-t-o-n.

		JUDGE SOLOMON:  Okay.  And what do you do for a living?

		DR. MONFORTON:  I am a professorial lecturer at George Washington
University School of Public Health.

		JUDGE SOLOMON:  Are you representing anybody?

		DR. MONFORTON:  No, myself.

		JUDGE SOLOMON:  Okay, go ahead.

		DR. MONFORTON:  Mr. Ellis, the SPP has been recognized as a model and
in place for decades, and I commend the silica sand industry for having
that.  Are you aware of any other industries that have a comparable
program?

		MR. ELLIS:  Not to my knowledge.  I think that NISA and the Silicosis
Prevention Program that we operate under and have for decades really
serves as a model.  NISA, in effect, is the poster child for
implementation of the OSHA compliance standard, you know, the
comprehensive standard.  So I think we are unique in that, and we serve
as a model for others as to what we -- what can be accomplished.

		DR. MONFORTON:  Thank you.  Mr. O'Brien, when did the study you
referred to commence?

		MR. O'BRIEN:  It commenced during 2013, fall of 2013, and we
anticipate it being completed during the second to third quarter of
2015.

		DR. MONFORTON:  Okay.  And would you share with us the names and
affiliations of the individuals who peer-reviewed the protocol?

		MR. O'BRIEN:  I can't give you them specifically.  I know NIOSH was
one of the peer reviewers.  They provided over 100 comments on our
protocol.  I can't recall any other specifics.  That was the important
one.

		MR. ELLIS:  No, I mean I think we provided the protocol to NIOSH just
to verify that we were on the right approach.  As Andy said, we received
over 100 comments, and those were responded to by the investigators.

		MR. O'BRIEN:  It was seven different NIOSH scientists.

		DR. MONFORTON:  Thank you.  At what stage in the NISA protocol are you
at this point?

		MR. O'BRIEN:  I would say we're roughly a quarter of the way through
the protocol cases.  We're in the case identification stage right now,
soon to be moving onto the control identification stage.

		DR. MONFORTON:  Do you recall what the minimal period of follow-up is
for the cohort?

		MR. O'BRIEN:  The inclusion criteria was at least 10 years of
exposure.

		DR. MONFORTON:  And will you be looking at other silica-related
illnesses besides silicosis?

		MR. O'BRIEN:  No.

		DR. MONFORTON:  You answered that one.  With the --

		JUDGE SOLOMON:  Anything else?

		DR. MONFORTON:  One question.  With the SPP, can you describe the
process for notifying workers if they have silicosis or other
silica-related diseases?

		MR. O'BRIEN:  Yeah, I do it personally.

		DR. MONFORTON:  Okay.  

		MR. O'BRIEN:  I conduct a videoconference or a face-to-face meeting
with the individual, cover the ILO form that has been completed by the B
reader, explain the legal obligations we have with respect to reporting
to the regulator and worker compensation systems, and benefits that are
available to them.

		DR. MONFORTON:  Okay, thank you.

		MR. CONRAD:  I note the protocol is an attachment to our comments, so
hopefully it's on the   HYPERLINK "http://www.regulations.gov/" 
regulations.gov  now.

		DR. MONFORTON:  Thank you.

		JUDGE SOLOMON:  Next?  State your name and spell your last name,
please.

		DR. WELCH:  Laura Welch, W-e-l-c-h.  I'm an occupational physician
with the Building and Construction Trades of the AFL-CIO.  I've got a
lot of questions, but just I'll do in order of what I think I want to
hear the answer to the most.

		So I understand with the current case collection that's ongoing now
where you identify them as a 1/1 film and you said there were no new
cases, but the way I figure it, the latency for cases, you are now at 19
years or 20 years, because exposure had to begin in 1994.  Exposure
before that was excluded.  I just wanted to clarify that because that's
a relatively short latency period to be assured that you don't have
cases at your current exposure control.

		MR. O'BRIEN:  Correct.  The cases we're identifying or the cohort is
anyone regardless of when they started or stopped working for Unimin or
U.S. Silica and met the inclusion criteria.  So employees that may have
started in the '60s would be included in the cohort itself, not from
1994 forward.

		DR. WELCH:  But you said that the eight cases that have been
identified were considered to be not new cases.

		MR. O'BRIEN:  Those are eight cases identified by the member companies
and reported to NISA staff, not -- we're talking two different things.

		DR. WELCH:  Right, right.  No, that's what I wanted to know, because
you were saying that you're controlling to 100, a level of 100, and you
think that's sufficient to prevent new cases of silicosis.  But my
understanding is that is based on only 20 years of follow-up because you
identified the exposure for defining a new case of silicosis among the
member companies, not part of your study, as beginning in 1994.  If
someone came in, had exposure prior to that where the exposures may have
been higher, you didn't want to include them in that assessment?

		MR. O'BRIEN:  Well, the NISA board established that cutoff at 1994, so
the declaration of no new cases, correct, is from that date forward.

		DR. WELCH:  Right.  So I just wanted to clarify it's really 20 years
ago.

		MR. ELLIS:  Maybe to just supplement that, it's an ongoing program.  

		MR. O'BRIEN:  Right.

		MR. ELLIS:  We hope to be doing this 20 years from now.

		DR. WELCH:  Right, right.  Okay, great.  The only other thing I
noticed about that, that your case collection and the way you are
reporting it annually is that you used a criteria of 1/1 on the film,
but in your cohort study that you are proposing you are using 1/0.

		MR. O'BRIEN:  Correct.

		DR. WELCH:  Which I think means you would agree with me that 1/0 is a
more sensitive indicator.  Have you had your member companies look to
see if they have identified any 1/0 films, or are you really restricting
it to the 1/1?

		MR. O'BRIEN:  Not as part of the -- not as part of the NISA SPP
reporting process.  You know, and a comment on 1/0 versus 1/1.  My
experience has shown that at the very low profusion levels, x-ray
quality has a huge impact on whether or not disease is detected or is
detectable.  And so I believe that using 1/1 is appropriate given the
fuzziness of the science of B reading at 1/0.

		DR. WELCH:  Okay.  Well, I won't -- I won't ask you more about that. 
I don't agree.  But then, you know, in your current program, and I
should have echoed what Celeste had said, you know, I think your written
comments were great.  You've got some great comments on competent person
and a lot of things that I would say the Building Trades agrees with
some of the points that you made.

		I was curious, in your surveillance program, if you identify -- if a
medical exam identifies an individual with early changes of silicosis,
however you are defining it, what do you do?  Do you change your control
strategy?  Do you change the job for that worker?  What kind of changes
do you make?

		MR. O'BRIEN:  You know, we have an administrative control program that
looks at their current jobs, what the exposures are for those types of
jobs, whether they can be moved into a job with a lower expected
exposure level.  It's just a systematic review of what they are doing
and how we can better protect them moving forward in order to ensure
that there is no progression.

		DR. WELCH:  Okay.  And do you know, I know your program is voluntary
for the medical surveillance.  Do you have an idea of what proportion of
your employees participate?

		MR. O'BRIEN:  Within Unimin, at our silica processing facilities, it's
actually a condition of employment.  If you are going to work at one of
our facilities, you will participate in the program, so it's 100 percent
participation. 

		DR. WELCH:  Okay.  So then it's not fair to call it voluntary.  I mean
voluntary in that they don't have to work there.

		MR. O'BRIEN:  The Unimin program, as far as the medical surveillance
at our industrial sand facilities, is not voluntary.

		DR. WELCH:  Okay, okay.  And then --

		JUDGE SOLOMON:  How much more do you have?

		DR. WELCH:  Well, I had just one question about your study, which has
an enrollment criteria of at least 10 years of exposure, which is then
10 years of latency, essentially.  Do you have any mechanism to provide
x-rays for workers who have left employment, so you could catch
individuals with longer latency down the road?

		MR. O'BRIEN:  We do not, no.

		DR. WELCH:  And do you have any idea what the average latency is of
the group that you have enrolled in the cohort?

		MR. O'BRIEN:  I do not, no, not at this point.

		DR. WELCH:  Okay.  All right, well, thank you.

		MR. O'BRIEN:  Thank you.

		JUDGE SOLOMON:  Okay, state your name and spell your last name.

		MR. SCHNEIDER:  Okay.  It's Scott Schneider, S-c-h-n-e-i-d-e-r.  I'm
with the Laborers' Health and Safety Fund of North America.

		I had a couple of questions.  One of the things is during your
testimony you described the stubbornly high level of noncompliance.  Are
you basing that on the IMIS data, the OSHA, that 30 percent was over --

		MR. ELLIS:  Yeah, correct.

		MR. SCHNEIDER:  So you're assuming that the IMIS data is somehow
representative of the industry, right?

		MR. ELLIS:  You know, I think that we take that data for what it has
said.  We've seen it portrayed graphically showing several decades and
showing essentially 30 percent noncompliance regardless of what decade
is looked at.

		MR. SCHNEIDER:  Right.  So if OSHA, I mean that's -- I mean if OSHA
were randomly inspecting workplaces, I guess you could say that might be
representative.  But if OSHA was targeting high exposure workplaces,
then that 30 percent might be not representative of the entire industry,
correct?

		MR. ELLIS:  Yeah, I mean if --

		MR. SCHNEIDER:  Okay.

		MR. ELLIS:  -- compliance, if it was targeted, would potentially be
different than a general industry survey.

		MR. SCHNEIDER:  Right, right. 

		MR. CONRAD:  But presumably they are looking at the workplaces with
the most exposure to silica.  So they're probably looking at the places
where you would be most concerned about.

		MR. SCHNEIDER:  Right.  Well, they have the site-specific targeting
program where they're trying to go after employers who have the highest
potential for violations, okay.  

		In terms of your exposure measurement, I know you do thousands of
exposure measurements, which is really great and I am very impressed. 
Do you have -- have you entered into the record any information about
what percentage of them were below 100 µg or below 50 µg?

		MR. ELLIS:  No.

		MR. SCHNEIDER:  Okay.  And do you have that information?  Could you
supply that to OSHA?

		MR. ELLIS:  No.  I mean the samples that are collected are the
business of the companies that collect them.  So the association really
doesn't have access to those and can't make them available.

		MR. SCHNEIDER:  But you have summary statistics, though, right?

		MR. ELLIS:  Again, we blind those statistics when the companies report
it.  It's part of what we do to encourage them to participate in the
program.

		MR. SCHNEIDER:  Previously, yesterday, there was some discussion about
how employers claim that in order to assure that they are below a
certain level, like the 100 µg level, they have to control to the
action level, to half of that.  So is that true with NISA companies that
you guys are controlling down to 50 µg to make sure you don't get over
100?

		MR. O'BRIEN:  Well, certainly, within Unimin, we have an internal
target of 50 µg/m3 for a time-weighted average.  And we control to at
least below that in order to ensure the lowest likelihood of exceeding
100.

		MR. ELLIS:  I think that's also part of the rationale for the NISA
solution of maintaining the current PEL and yet instituting exposure
monitoring and medical surveillance at an action level of half that,
knowing that people would have to be below the PEL consistently to make
sure that they don't exceed it on any given occasions. 

		JUDGE SOLOMON:  Do you have any more questions?

		MR. SCHNEIDER:  Yeah, one last question.  So if you are controlling
down to 50 µg regularly, then the study that you're looking at is not
going to really look at the dangers of 100 µg exposures.  It's really
more looking at the dangers at 50 µg.

		MR. O'BRIEN:  No, that's not necessarily correct because the cohort
consists of employees as far back as possible with 10 or more years of
exposure.  And four years ago, exposures were significantly higher than
they are today.  So as contained in our written comments, there is a
wide spread, and that's one of the values of our study, there is a very
wide spread of exposures that can be evaluated.

		MR. SCHNEIDER:  Okay.  Thank you very much.

		JUDGE SOLOMON:  Come forward.  Again, state your name and please spell
your last name.

		MS. WARD:  Dae Ward, W-a-r-d.  I'm with Alabama Power.  I just wanted
to ask you a question.  First of all, do the employees in your
population that you're looking at have predominantly daily exposures to
silica at above what level?

		MR. O'BRIEN:  That's highly variable.  They have daily exposures
absolutely.  And it ranges from sometimes non-detectable, being in a
control room for the majority of the day, to much higher than that.

		MS. WARD:  Do certain provisions of your program require exposures
above a certain level for a number of days, like 30 or 60?

		MR. O'BRIEN:  When we have a single exposure above 50 µg/m3, our
program requires a root cause analysis to be conducted to identify what
may or may not have contributed to that exposure and to determine
whether any corrective actions can be taken to bring exposures back down
below the 50.

		MS. WARD:  Okay.  And what is the employee population that you are
dealing with here in numbers?

		MR. O'BRIEN:  Our industrial sand population is roughly 800 to 900
employees.

		MS. WARD:  And you had how many cases in how long?

		MR. O'BRIEN:  I was speaking to the entire -- the NISA companies, 11
NISA companies that had been participating in the NISA SPP, not
specifically regarding Unimin.

		MS. WARD:  Okay.  And so those, how many cases?

		MR. O'BRIEN:  Eight cases.

		MS. WARD:  Eight cases?

		MR. O'BRIEN:  From 11 companies.

		MS. WARD:  And that would be what employee population?

		MR. ELLIS:  I can't give you an exact number.  I mean I think it
probably would probably reflect maybe 85 percent of the employees in the
industrial sand industry.

		MS. WARD:  Okay, because I'm trying to understand --

		MR. ELLIS:  No raw number.  I can't give you a raw number.

		MS. WARD:  Okay.  Well, it sounds like a very comprehensive program
for an identified health risk for an identified industry.  And I guess
my core question centers around would you recommend the same program,
the same regimented program for industries that don't deal with 100
percent silica, that employees don't even have exposure to silica on a
daily basis, probably less than a dozen, that are currently controlled
by other measures where the exposure may be managed by something else in
the agent, like the arsenic standard.  And would you recommend and do
the same regimented program with medical surveillance and training when
the exposure profile is completely different than 100 percent silica
product?

		MR. ELLIS:  What we have recommended to OSHA as part of our comments
in this testimony is less strict and demanding than what we require of
ourselves under our voluntary program.  We understand that OSHA has
feasibility issues.  And, frankly, that's why we feel that there is a
simplicity and a beauty and a cost-effectiveness in the NISA solution,
because you maintain the current PEL, bring people that are out of
compliance into compliance.  And the way you do that is through the
exposure monitoring and subsequent medical surveillance.  

		MS. WARD:  At given triggers.

		MR. ELLIS:  At given triggers.  And if you are below what we suggest
be the action level, 50 µg, you don't even have to worry about
compliance with the law because you are already in compliance with the
law.

		JUDGE SOLOMON:  We have another witness.

		MS. WARD:  All right, thank you.

		JUDGE SOLOMON:  Okay.  So you are going to be the last witness.  There
is nobody else in line.

		DR. WEEKS:  My name is Jim Weeks.  I'm an industrial hygienist at the
--

		JUDGE SOLOMON:  Spell your last name.

		DR. WEEKS:  W-e-e-k-s.  At MSHA, the Mine Safety and Health
Administration.  I have one question.  You stated that, in the past,
people had significantly higher exposure levels then, which is common
amongst a lot of companies.  The question is did you look at the effect
of that high exposure per se and that high exposure rate per se on any
other health outcomes?  

		For example, was the rate of progression amongst those people exposed
at that level, was it any higher than would be predicted by, say, simply
looking at the cumulative exposure?  Did I make that clear?  Was that a
clear question?

		MR. ELLIS:  I think what you're saying, though, is in our normal
surveillance program that we report on, we basically are identifying
cases that are greater or equal to 1/0.  But we haven't really looked at
whether somebody has progressed from 1/0 to 1/1 or 2/1.

		DR. WEEKS:  So you haven't looked at the rate of progression at all?

		MR. ELLIS:  No, no.

		DR. WEEKS:  All right, thank you.

		JUDGE SOLOMON:  Ms. Kramer, Mr. Perry, do you have questions?

		MR. PERRY:  Yes, thank you, Your Honor, we do.

		JUDGE SOLOMON:  Let me just state this is William Perry.  He has
already identified himself in the record, but I just want to make sure
--

		MR. PERRY:  Thank you, Your Honor.

		JUDGE SOLOMON:  -- everybody in the room knows who you are.

		MR. PERRY:  Yes, same person I was yesterday, I guess.  Yeah, we do
have some questions.  First, I just want to thank the NISA panel for
appearing today and for the information that you submitted to the record
so far, and congratulate you on what seems certainly to be a very
well-run and effective program.

		But just one thing you mentioned, I just wanted to double check.  You
mentioned the Dust Control Handbook.  Did you enter that into the
record?

		MR. ELLIS:  One of the many hats that I wear is also President of the
Industrial Minerals Association North America.  And, in fact, we did
introduce it into the record as part of our comments, and we will be
presenting it next week when we testify.

		MR. PERRY:  Okay, thank you so much.  We'll begin with Tiffany DeFoe.

		MS. DeFOE:  I'm not sure if this microphone is on.

		JUDGE SOLOMON:  Again, technical difficulties beyond our control.  We
have microphones at the table that work.  We know they work.  So do we
want to change?

		MS. DeFOE:  Okay, it's on now.

		JUDGE SOLOMON:  Oh, okay, go ahead.

		MS. DeFOE:  I think it's on now.  Yes, it is.  Thank you.

		JUDGE SOLOMON:  Yeah, that's it.

		MS. DeFOE:  In your description of the exposure-response study that
you are developing -- I'm sorry, let me back up a little bit.  When you
were discussing OSHA's risk assessment, you stated that a problem with
OSHA's risk assessment is that it extrapolates from high to low
concentrations of respirable silica.  And you suggested that the
exposure-response study that you are developing would help address this
issue.  

		Would you please expand on the exposure database for your study and to
what extent it can provide data on health effects among workers exposed
primarily at concentrations below the current PEL?

		MR. ELLIS:  I guess the number, 50,000.

		MR. O'BRIEN:  We have tens of thousands of data points amongst the two
companies, Unimin and U.S. Silica, participating in the study.  Those
exposures range from in the early years above the PEL, sometimes
multiple times above the PEL, to where they are today, which is well
below -- typically well below the PEL.  In fact, well below 50 µg/m3.  

		So we believe that because of that spread of data, based on current
technology and current analytical techniques, gravimetric and x-ray
diffraction, that the data itself is not only significant in quantity
but significant in quality.

		MS. DeFOE:  When you say that exposures are typically below 50 µg,
about how long ago would you say that became typical?

		MR. O'BRIEN:  Within Unimin, I would say that in the past, it became
typical a decade ago, at least a decade ago.

		MS. DeFOE:  Thank you.  In the study protocol, are you planning on
looking at the effects of concentration as well as cumulative exposure?

		MR. ELLIS:  I'm trying to remember.  I can't recall offhand.  We're
not epidemiologists.  But the protocol itself is part of the rulemaking
record.

		MS. DeFOE:  Thanks.  I looked at it, but I didn't see that detail in
it.

		MR. ELLIS:  Okay. 

		MR. O'BRIEN:  I believe the answer is yes.

		MR. CONRAD:  The answer is yes.

		MS. DeFOE:  Thank you.  Now, you mentioned an internal target at
Unimin of 50 µg.  When was this internal target implemented?

		MR. O'BRIEN:  In the early 1990s.

		MS. DeFOE:  Okay, thank you.  And do other member companies have
internal exposure targets as well?

		MR. O'BRIEN:  I believe that they do, but I couldn't speak to the
specifics of those targets or when they were implemented.

		MS. DeFOE:  Okay.  And when the target is exceeded at Unimin, what
measures are taken at that point either with the processes or with extra
protection of the workers?

		MR. O'BRIEN:  There is a root cause analysis conducted immediately,
and that root cause analysis currently often involves a helmet cam
technology where the worker actually wears a helmet cam attached to
their hardhat for the day.  We can record where the worker is, what the
worker is doing over the course of the day, along with real-time aerosol
monitors, and tie the two together with an application developed by
NIOSH called EVADE, Enhanced Video Analysis of Dust Exposure.

		And we use that technology to see where the worker is, what they are
doing, and the real-time data tells us exactly what their exposures are
at that time.  And with that technology, in one shift, we are very
quickly able to see what's happening, why it is happening, and what we
can do to prevent the exposures from occurring in the future.

		MR. ELLIS:  And the worker can see.

		MR. O'BRIEN:  Right.

		MR. ELLIS:  So that they can modify their own behavior. 

		MS. DeFOE:  That's great.  And what about respiratory protection, at
what point is respiratory protection introduced for workers?  Is it just
above the OSHA PEL or is it --

		MR. ELLIS:  At the 50.

		MS. DeFOE:  At 50.

		MR. ELLIS:  Yeah.

		MS. DeFOE:  How long has that practice been in place?

		MR. O'BRIEN:  Since the early '90s, when the internal target was
established.

		MS. DeFOE:  Okay.  Thank you very much.

		JUDGE SOLOMON:  Mr. Perry, we're actually beyond the time that had
been allocated.  How do you want to handle this?

		MS. KRAMER:  If we could just have approximately five more minutes,
Your Honor?

		MR. PERRY:  Next is Patti Downs from our Office of Technologic
Feasibility.

		MS. DOWNS:  And I promise to make this quick.  I just wanted to
confirm, I know you said you have 11 member companies participating in
the silica safety program.  How many companies do you have total?

		MR. ELLIS:  Thirty-one.

		MS. DOWNS:  Thirty-one.  And how many of those companies may have been
eligible for the program at one time but have implemented controls to
stay below the trigger?

		MR. ELLIS:  They're all eligible to participate in the program because
it's a voluntary program.  But we have 11 companies that are actively
participating.

		MS. DOWNS:  And then the rest have either implemented controls or they
don't need to, right?

		MR. ELLIS:  They chose not to participate in the program.

		MS. DOWNS:  Do you know what type of controls they have in place?

		MR. ELLIS:  Not specifically.

		MS. DOWNS:  Okay.  And then I just have some questions about the
in-house sampling that you say you do.  What kind of training did that
require to get people competent to do that sampling?

		MR. O'BRIEN:  We have a three-day program that covers our safety and
health program, everything from our medical surveillance program, our
industrial hygiene program.  It covers not only silica sampling.  It
covers noise sampling, organic solvent sampling, welding fumes sampling,
just the ins and outs of the entire program.

		MS. DOWNS:  Okay, I think that's it.  Thank you.

		MR. PERRY:  And that --

		JUDGE SOLOMON:  Okay.

		MR. PERRY:  Sorry, Your Honor.

		JUDGE SOLOMON:  Are there any other questions that you would have?

		MR. PERRY:  Yes, we have just a few more, a couple more really. 
Annette Iannucci.

		MS. IANNUCCI:  Okay, good morning.  Earlier, in answering a question,
you indicated that if a worker is found to have evidence of silicosis,
you see if he or she can be moved to a lower exposure job.  How often
does this occur?

		MR. O'BRIEN:  Very rarely, as rarely both in an employee being
identified with disease and, therefore, rarely in having to move
someone.

		MS. IANNUCCI:  Okay.  But if someone is identified with disease, you
are usually able to move them to a lower exposure job?

		MR. O'BRIEN:  Typically, yes.

		MS. IANNUCCI:  What happens if you are not able to?

		MR. O'BRIEN:  Often, respiratory protection will be implemented for
that employee, but only with permission from a healthcare professional
indicating that the use of a respiratory will not negatively impact the
health of that worker or the safety of that worker.  And if, for
example, a negative demand type respirator were going to be problematic,
then a powered air-purifying respirator could be offered.

		MS. IANNUCCI:  Okay.  And then just real quick, does your medical
surveillance look for non-silicosis effects and basically what are those
tests to look for those?

		MR. O'BRIEN:  The medical surveillance program is a broad -- it is
essentially a free physical.  It includes blood chemistry, urinalysis,
the whole suite that you would typically get.  We do not -- we, Unimin,
do not specifically look for non-silicosis disease/diseases.  We really
rely on the healthcare professionals evaluating that data to indicate to
us whether or not there is an indication of some other disease process
going on.

		MS. IANNUCCI:  Okay, thank you.

		MR. STONE:  Hi, Robert Stone.  I just had a couple of questions about
your in-house exposure monitoring and the table you have on Page 24. 
First of all, do you know what the size is of the smallest firm that
does in-house monitoring in your association?

		MR. O'BRIEN:  It could be a plant with only six to eight employees.

		MR. STONE:  Really?  Okay.  And you indicate some costs for analytic
-- for analyses, the analytic cost.  Why is there a range?  Doesn't it
typically go out to a lab or do you -- it's just they get discounts for
volume or something?  What would it be?

		MR. ELLIS:  Any of those.

		MR. STONE:  Okay.  And then I just want to note something.  You have
something that's curious.  You show the analytic costs alone range from
$49 to $129, with $129 would be the upper amount.  But for the total
cost, the range is $106 to $127.  And I'm guessing there might be some
odd result as to why the analytic cost alone would be more than the
total cost for a possible maximum.

		MR. O'BRIEN:  I'm looking at that data.  I'd have to go back and take
another look at that.  I understand what you're saying.

		MR. STONE:  Okay, right.  You might just -- it might be something to
clarify later.  And you have these numbers for the five firms, these
estimates for the five firms.  Are there other firms, do you know, in
the 31 -- in your 31 group that also do in-house monitoring?

		MR. ELLIS:  I would wager that most of them do, but we don't have cost
data from them.

		MR. STONE:  Okay.  That's it.

		MR. CONRAD:  Wouldn't you assume maybe that the company that
experienced the $127 maximum cost per sample would manage to have cheap
analytical and it was something else that was more?  I mean that would
be a possible explanation.

		MR. STONE:  I'm sorry, what was that explanation?

		MR. CONRAD:  In other words, the company that had the highest total
cost per sample, which was $127, may have been the company that had the
cheap analytical cost at $49.  So they don't, you know, it wouldn't
necessarily have been the highest analytical, too.

		MR. STONE:  Okay.

		JUDGE SOLOMON:  Ms. Kramer, Mr. Perry, Mr. O'Connor?

		MR. O'CONNOR:  Yes, I just have one quick question here.  In your
written submission, you state with regard to medical surveillance that
it is important for the employer as well as the employee to receive the
results of an employee's medical surveillance examination.  And I just
wanted to ask what impact, if any, you would anticipate if the results
of a medical examination were to go to the employee, but not the
employer?

		MR. O'BRIEN:  Negative.  I think it is important for the operator --
in our environment, we refer to ourselves as operators in the mining
environment.  I believe it is important for operators to also have
access to that information.

		I'm Canadian, and I grew up in the Canadian system whereby Canadian
companies have no access to the medical data.  And the first time that
you are made aware that there is a problem is when a letter shows up
from a compensation system that says you're making people sick.

		Without access to that data, you can't see disease, potentially see
disease beginning and take preventative action to prevent it from
actually having a negative health effect.

		MR. ELLIS:  That's a handicap for several of our Canadian member
companies that participate in the SPP program because they are not in a
position to report what their x-ray surveillance might show.

		MR. CONRAD:  And you also might wonder how epidemiological work could
ever get done if there was no comprehensive databases of exposure
medical surveillance data.

		MR. O'CONNOR:  Thank you.

		JUDGE SOLOMON:  Mr. Perry?

		MR. PERRY:  I just have just one question.  You talked at length about
your action level of 50 µg/m3 and the kind of actions that you take. 
It sounds like then you have a pretty high degree of confidence in your
exposure monitoring results to feel that it gives you information on
which to base reasonable actions.  Is that accurate?

		MR. O'BRIEN:  That's fair.

		MR. PERRY:  Okay, thank you.  Ms. Kramer?

		MS. KRAMER:  Your Honor, I just have a couple of housekeeping matters
and also one question, if that's all right.  I just wanted to follow up
a little bit on Ms. Welch's, I believe, question earlier.  I believe
you said in your written comments that the average NISA member company's
employee's tenure with a NISA member company is 19.7 years.  Is that
right, do you recall?

		MR. ELLIS:  I can't recall.  But if we said it, I'll take your word
for it.

		MS. KRAMER:  Okay.  And they are not followed up with after they leave
--

		MR. ELLIS:  No.

		MS. KRAMER:  -- the employ of the company?

		MR. ELLIS:  No.

		MS. KRAMER:  Okay.

		MR. ELLIS:  They're no longer employees.  That's the distinction.

		MS. KRAMER:  Okay.  And just a couple of, again, housekeeping matters.
 Mr. O'Brien, the plan that you referred to during your testimony, that
was submitted as part of the record, right?  The thing you held up?

		MR. O'BRIEN:  The Silicosis Prevention Program?

		MS. KRAMER:  Yeah.

		MR. O'BRIEN:  Yes, it was.

		MS. KRAMER:  Okay.  And also two other questions about data, would you
be willing to submit the blinded data that's shown at your annual
meetings, since it is blinded and is not really, you know --

		MR. ELLIS:  That's something I'd have to consult with the members
about to see whether they prefer to do that.

		MS. KRAMER:  We'd really like that, if you could get back to us on
that.  And, finally, you mentioned that you have a program, a three-day
program, I believe, whereby you train folks to be able to do the kind of
sampling.  I was wondering if you would be able, willing to submit
either that program or a description of it to the record?

		MR. O'BRIEN:  I suspect we probably could.  I'll check with those up
my chain of command and circle back.

		MS. KRAMER:  Sure.  Thank you so much for coming.

		MR. CONRAD:  I checked our comments.  We said in 2004, a study
calculated the mean tenure for NISA member company employees fitting the
definition of the cohort for the study as being 19.7 years.

		MS. KRAMER:  Okay.

		MR. CONRAD:  That's on Page 19.

		JUDGE SOLOMON:  Okay.  Well, the time allotted for this program was
about six or seven minutes ago.  So what we are going to do is go off
the record for a second so that we can exchange panels.  

		The IDPA panel is supposed to take 30 minutes.  The questions are
supposed to take about 10 minutes from the peers and the public, about
10 minutes from OSHA.  I was to take a break of five minutes.  I don't
know, we'll see when we get close to that. 

		And then the Brick Industry would be starting around 11:25.  And that
means that we go to 12:30 before we would break for lunch.  The way
we're going now, there is no lunch.  So maybe there can be some
accommodation made.  So let's go off the record for a second while we
change the panel.

		(Off the record at 10:37 a.m.)

		(On the record.)

		JUDGE SOLOMON:  The IDPA program.

		MR. ELLIS:  Yes.  Good morning, again.  I am still Mark Ellis.  In
addition to my role as President of NISA, I also serve as the Executive
Director of the International Diatomite Producers Association, or IDPA. 
I am joined now by Dr. Kenneth Mundt of ENVIRON International
Corporation, a consultant to IDPA, as well as Jamie Conrad, who is also
serving as IDPA's counsel for this rulemaking.

		IDPA is a nonprofit 501(c)(6) trade association representing the major
manufacturers of diatomaceous earth products worldwide.  IDPA currently
has five member companies that collectively account for the majority of
the production of diatomaceous earth products worldwide.

		As with NISA, IDPA's members' workplaces are predominantly mining
operations and, thus, are typically regulated by MSHA, not OSHA, for
purposes of occupational safety and health.  IDPA also has a substantial
stake in the outcome of the OSHA crystalline silica rulemaking, however,
for many of the same reasons that NISA does.  The most important of
these reasons is that IDPA members are committed to the safe use of
diatomaceous earth products.  

		IDPA publishes a, quote, Guide to the Safe Handling of Diatomaceous
Earth Products, North America Version, which provides very general
guidance to diatomite distributors and users regarding the benefits of
engineered ventilation controls, safe work practices, and respiratory
protection programs.  

		On its website, IDPA also provides a link to NISA's Occupational
Health Program for Exposure to Crystalline Silica, which you just heard
about from Mr. O'Brien.

		IDPA agrees with NISA that the exposure monitoring and medical
surveillance provisions that OSHA has proposed would provide valuable
additional workplace protections at OSHA-regulated workplaces where
diatomaceous earth products are used.

		Diatomaceous earth, also known as diatomite, is a naturally occurring,
nonmetallic mineral composed of fossilized remains of microscopic,
single-celled, aquatic algae called diatoms.  Diatomaceous earth, as it
naturally occurs, is predominantly composed of amorphous silica, that is
non-crystalline silicon dioxide.  It may also contain small amounts,
typically less than three percent, of naturally occurring crystalline
silica normally in the form of quartz.

		The natural grade of diatomite that results from crushing, drying, and
milling retains its composition.  For most applications, however, this
natural diatomite ore is then either calcined or flux-calcined in a
large rotary kiln.  Calcined grade diatomite may contain from 0 to 40
percent cristobalite, and flux-calcined grades may contain up to 75
cristobalite.

		As a result, IDPA members have longer histories of working with
cristobalite and more direct experience with it than anyone else in the
industry.  It is vitally important to them that OSHA's crystalline
silica rulemaking properly characterize the hazards presented by
cristobalite.

		As IDPA's written comments explain at greater length, IDPA strongly
believes that OSHA has been correctly guided by the evidence in
proposing to abandon the notion, now over a half century old, that
cristobalite is more hazardous than quartz.  We support OSHA's proposal
to set a single PEL, or permissible exposure limit, and a single action
level for both quartz and cristobalite.  Outside of OSHA and MSHA, no
authoritative body besides ACGIH has adopted the notion that
cristobalite is more toxic than quartz, and even ACGIH abandoned that
view 15 years ago.  Setting the same levels for quartz and cristobalite
would bring OSHA into alignment with the rest of the world.

		IDPA's principal witness today, Dr. Kenneth Mundt, has exhaustively
studied the epidemiological literature regarding the toxicity of
cristobalite.  In his testimony today, he will discuss what that review
has led him to conclude regarding the strengths of that literature and
the potential hazards of cristobalite, both absolutely and relatively to
quartz.  I now turn things over to Dr. Mundt.

		DR. MUNDT:  Thank you.  Good morning, Judge Solomon and peer
reviewers, ladies, gentlemen.  My name is Kenneth Mundt.  I am Director
of Applied Epidemiology and Health Sciences, Global Practice Area Leader
at ENVIRON International Corporation.

		I am speaking today as a consultant on behalf of the International
Diatomite Producers Association, or IDPA.  I want to thank my colleagues
Linda Dell and Lee Carlson for their assistance in conducting the review
that I will discuss.

		My purpose today is to summarize the written comments I submitted
during the comment period entitled, "Review of the Epidemiology of
Occupational Exposure to Cristobalite."  Here, I will highlight three
key points based on my review of the epidemiologic literature regarding
lung cancer risks associated with crystalline silica primarily in the
form of cristobalite, as well as silicosis risks.

		First, based on our critical review and synthesis of the published
peer review epidemiological literature on occupational exposure to
respirable crystalline silica primarily in the form of cristobalite and
human health, there is evidence of an increased risk of lung cancer,
silicosis, and nonmalignant respiratory disease among those exposed to
high levels of respirable crystalline silica dust in the form of
cristobalite.

		Second, some of the published epidemiological studies have quantified
exposure, allowing estimation of a dose-response relationship between
exposure to respirable crystalline silica in the form of cristobalite
and risk of disease, including lung cancers and silicosis.  

		The literature offering the potential to quantify the health risks
specifically associated with cristobalite, however, is largely limited
to the study series led by Drs. Checkoway and Hughes from the California
diatomaceous earth cohort and several reports based on that cohort.

		Despite the availability of a number of studies attempting to evaluate
or quantify risks in relation to crystalline silica, few studies are
able to discern risks associated with cristobalite per se, largely
because most occupational settings in which cristobalite is present,
quartz is also present.

		Third, results of the quantified exposure-response analyses between
respirable crystalline silica in the form of cristobalite and lung
cancers and silicosis do not differ from comparable evaluations for
respirable crystalline silica primarily in the form of quartz.  This can
be seen for lung cancer by comparison with a pooled evaluation of lung
cancer risk in 10 cohorts exposed to crystalline silica, published by
Steenland et al. in 2001 and for silicosis by comparison with a
publication by Morfeld and others in 2013, in which the authors
illustrate a method for identifying an exposure threshold for respirable
silica exposure and silicosis morbidity risk based on a large cohort of
German porcelain workers.

		The methods we have used to identify and review the relevant
epidemiological literature are as follows:  Occupational studies
addressing the health risks of cristobalite exposure were identified by
reviewing the OSHA proposed rule for occupational exposure to respirable
crystalline silica, issued September 12, 2013, as well as conducting
searches of PubMed, based on the U.S. National Library of Medicine. 
Titles and abstracts were examined to identify studies that focused on
potential cristobalite exposures.  

		In considering the health risks associated with occupational
cristobalite exposures, the OSHA proposed rule reviewed primary
occupational cohorts exposed to diatomaceous earth or cristobalite
formed during processes in which various forms of silica were subjected
to high heat.  These included studies of, one, diatomaceous earth
workers in California, including Checkoway's reports of 1993, '96, '97,
'99, and Hughes, 1998; two, refractory workers in Italy, specifically,
Merlo, 1991; and, three, pottery workers in the UK, including Cherry,
1998, and McDonald, 1995.  

		Five additional occupational cohort studies addressing potential
cristobalite exposure that were not discussed in the OSHA rule were
identified through PubMed searches.  Diatomaceous earth workers in
Iceland, Rafnsson, 1997; silicon carbide workers in Norway, Bugge, 2011
and 2012; refractory workers in China, Dong, 1995; and a recent update
of the UK pottery workers, Cherry, 2013.

		Information on the key features of each study was abstracted into
Excel spreadsheets, including study type, design, population, location,
comparison group, outcome, method of exposure assessment, exposure
metrics categories, measures of effect and result, 95 percent confidence
intervals, covariates adjusted, likelihood of selection bias, likelihood
of confounding, and overall quality.

		The four primary criteria used to evaluate the quality of the studies
were quantitative exposure measurement used in analysis, preferably at
the individual level; exposure dominated by cristobalite versus mixed
cristobalite and quartz exposure or predominantly quartz exposures;
control for potential confounding by smoking, especially for studies of
lung cancer; and radiographic assessment or confirmation of lung
opacities for studies on silicosis.

		Studies were accordingly classified into three tiers, with Tier 1
being the highest and Tier 3 the lowest, based on whether they met the
quality criteria.  We subsequently summarized the studies including
strengths and weaknesses by type of disease, and then synthesized the
evidence with the greatest emphasis being placed on studies of better
quality, i.e., Tier 1.

		Three studies satisfied the Tier 1 criteria in part because they
included a quantitative exposure assessment for occupational exposure
where the predominant form of respirable crystalline silica was
cristobalite.  These are Checkoway, 1997, 1999, and Hughes, 1998. 
Checkoway, '97 and '98, also -- I'm sorry, '99 -- also considered
potential confounding by smoking for lung cancer.  Hughes, 1998, used
radiographic criteria for obtaining silicosis diagnosis defined as small
opacities with profusion score greater than 1/0 and/or large opacities. 

		The second tier included five studies.  Rafnsson, 1997, studied an
occupational cohort predominantly exposed to cristobalite, but did not
evaluate risk using quantitative exposure estimates.  Bugge, 2011 and
'12, as well as Cherry, 98 and 2013, each used quantitative exposure
estimates and analyses, but studied cohorts either with mixed exposure
to cristobalite and other silica polymorphs or predominantly quartz.  

		The third tier included five studies.  Checkoway, '93 and '96,
reported earlier evaluations of the diatomaceous earth workers cohort
exposed predominantly to cristobalite, but at that time used only
semi-quantitative exposure estimates.  Merlo, '91; Dong, '95; and
McDonald, '95, did not use quantitative exposure in analyses and studied
workers predominantly exposed to quartz but with some potential for
exposure to cristobalite.

		As can be seen in this slide, few occupational studies have been
published that evaluate disease risk in relation to quantified
categories of exposure to respirable crystalline silica primarily in the
form of cristobalite.  This is largely due to the fact that in
occupational settings in which some cristobalite may be present, there
is also considerable quartz present.

		The stronger studies examine disease risk according to categories of
quantitative estimates of cristobalite exposure, specifically among
diatomaceous earth workers.  Note, however, that the reports quantifying
cristobalite exposures were all based on the California diatomaceous
earth workers cohort.  These essentially reflect results on a single
cohort for which mortality and silicosis morbidity were updated over
time, and for which a detailed quantified exposure reconstruction was
performed, that published by Seixas in 1997.

		For lung cancer and nonmalignant respiratory disease mortality,
indirect methods of accounting for smoking were applied, and for smoking
and asbestos exposures -- and smoking and asbestos exposures were
considered as potential confounders in the lung cancer analyses.

		The majority of the studies identified and reviewed were occupational
cohort studies.  However, many reported only SMR analyses relying on an
external referent group.  While these generally are suited for detecting
excesses of lung cancer or other causes of death, they often do not or
cannot quantify exposure-response relationships.  When excess lung
cancers are detected, additional analyses within internal comparison
groups are preferred for evaluating the exposure disease relationships,
especially where confounding such as by smoking and asbestos exposure
for lung cancer is reasonably expected.

		Among the studies of higher relative quality with quantitative
exposure estimation for individual cohort members, excesses of lung
cancer mortality did not occur until cumulative exposures to respirable
crystalline silica in the form of cristobalite equaled or exceeded 5.0
mg per cubic meter years.  This is from Checkoway, 1997.  Similar
findings were presented in a subsequent report for cohort members
separated into groups with and without silicosis.  This is in Checkoway,
1999.

		In a study with quantitative exposure assessment for individual cohort
members that classified as second tier, excess lung cancer mortality was
reported in the second and third cumulative cristobalite exposure
tertiles, namely 0.028 to 0.093 mg per cubic meter years and 0.93 to 2.7
mg per cubic meter years, respectively.  This is from Bugge, 2012.

		The pattern and magnitude of these results could not be distinguished
from those for quartz exposure within this cohort.  As reported, the
Pearson correlation coefficient was .84 between cristobalite and quartz
exposure.  In other words, differences in risk, if any, between
cristobalite and quartz exposure could not be distinguished because of
the high correlation between quartz and cristobalite exposures in this
industry, the production of silicon carbide.  

		In addition, excess lung cancer risk was reported in the study at
lower estimated cumulative cristobalite exposures than in the
diatomaceous earth worker study, although the magnitude of the lung
cancer risk estimates were similar for the highest exposure categories
in both, relative risks around 2.0 at exposure category 0.93 to 2.7 mg
per cubic meter years in Bugge, and around 5 or greater than 5 mg per
cubic meter years in Checkoway.

		Whether this reflects actual differences in exposure levels between
the cohorts or reflects methodological limitations of the exposure
assessment such as exposure misclassification of a shifting of the
estimated exposure distribution cannot be determined.  Ultimately, these
results likely reflect the highly correlated mixture of crystalline
silica types, as well as silicon carbide fiber and dust exposures.

		Although there was low statistical power in many of the reported
studies, disease trends were seen for increasing duration of exposure,
earlier decade or period of exposure, and high levels of cumulative
exposure.  The modest size and overall absence of a quantitative
exposure assessment in most of these studies reviewed, however, limit
the ability of these reports to determine the specific level of exposure
to cristobalite that may be associated with an increased risk of these
diseases.

		Even among the studies of higher relative quality among workers
exposed predominantly to cristobalite, concomitant exposure to quartz,
as well as incomplete control for confounding by smoking and asbestos,
remain likely.  Most Tier 2 and 3 studies included cohort members with
mixed exposures to cristobalite and quartz.

		It is illuminating to place the results reported by Checkoway and
others on the diatomaceous earth workers in the context of comparable
findings of studies of other cohorts predominantly or exclusively
exposed to crystalline silica in the form of quartz.  

		Here we see the only exposure category at which lung cancer risk is
increased among the diatomaceous earth workers, i.e., the highest
exposure category is open-ended.  That one is the relative risk of 2.15
within the dotted box, which defines the size, the shape of the
continents interval around that estimate.

		Therefore, it is not possible to precisely plot the point at which
risk increases.  All previous estimates are at or about the null value. 
However, no increase in lung cancer risk is evident whether considering
quartz or cristobalite below the 5 mg per cubic meter year cut point for
cumulative exposure.

		With respect to nonmalignant respiratory disease, excess mortality was
observed at cumulative exposures of greater than 2.1 and up to less than
5 mg per cubic meter years among the California diatomaceous earth
workers.  

		In the only report evaluating quantitative exposure levels and
silicosis risk, that being Hughes, 1998, radiologic evidence of small
opacities with profusion scores greater than 1.1/0 and/or large
opacities were seen at cumulative exposures in the categories of greater
than 1 to up to 3 mg per cubic meter years and all higher exposure
categories.

		The results for silicosis morbidity among diatomaceous earth workers
can be compared with the results from previously mentioned German
porcelain workers.  That was Morfeld, 2013, based on Mundt, 2011, study
of the German porcelain workers.  

		In proportional hazards analysis, controlling for age, sex, and
smoking, increased hazard ratios for silicosis were reported for
cumulative exposures exceeding 4 mg per cubic meter years and for
average exposures exceeding .15 mg/m3, with higher hazard ratios
reported at higher exposure categories.

		Among diatomaceous earth works with exposure intensities of .5 mg/m3
or more, relative risks were increased among those with more than 3 mg
per cubic meter years cumulative exposure.  Those with the higher
intensity, average intensity, are on the right side of this diagram. 
That group had exposures exceeding .5 mg/m3, compared with those on the
left side who had not exceeded that intensity threshold. 

		Consistent with these findings, toxicologic evidence also suggests
that there is no clear support for the old hypothesis that cristobalite
is more potent than quartz in producing inflammation and fibrosis.  A
recent review not addressed in the OSHA proposed rule was published by
Mossman et al. in 2013.  This review summarizes animal and in vitro
experimental data, allowing comparisons between cristobalite and quartz.
 Animal and in vitro studies have demonstrated that quartz and
cristobalite share common mechanisms of action leading to cell injury,
macrophage activation inflammation, and fibrosis.

		In conclusion, for lung cancers and silicosis, there is limited
epidemiological evidence providing quantitative exposure risk estimates
for cristobalite.  These findings do not suggest any material difference
in risk associated with crystalline silica in the form of cristobalite
versus quartz.  Furthermore, the literature indicates that in
occupational settings where cristobalite might be present, crystalline
silica in the form of quartz is often also present and may be the
dominant form to which workers are exposed.

		Taken as a whole, the toxicological and epidemiological evidence
provide no clear basis for setting a separate occupational exposure
level for crystalline silica in the form of cristobalite versus quartz. 
Therefore, a synthesis of the available epidemiological literature
summarized here lends support to OSHA's proposal for a single
occupational exposure level for crystalline silica.  Thank you.

		JUDGE SOLOMON:  Okay, we are right at about -- we're about two minutes
over what the estimated time would be.  We would have -- give me some
sense of anybody from the peers that want to question?  From the public,
are there people who want to question?  Nobody.  

		So now we are ahead of the time.  Mr. Conrad, do you have any
exhibits that you want to move into evidence?

		MR. CONRAD:  Your Honor, we'll include, as we did the previous panel,
the testimony of Mr. Ellis, Dr. Mundt, and the slides as a set of
three exhibits for inclusion in the record.

		JUDGE SOLOMON:  Okay.  We can make this a composite exhibit or we can
make them into individual exhibits.  What do you want to do?

		MS. KRAMER:  I'd prefer them to be separate exhibits.  If we could
mark Mr. Ellis' testimony as Exhibit 15, Dr. Mundt's as Exhibit 16,
and predictably the PowerPoint as Exhibit 17, Your Honor.

		JUDGE SOLOMON:  So 15 through 17 are admitted into evidence.

(Whereupon, the documents referred to as Hearing Exhibits 15 through 17
were marked and received in evidence.)

		MS. KRAMER:  Thank you.

		JUDGE SOLOMON:  Anything else?  Mr. Conrad?

		MR. CONRAD:  No, thank you.

		JUDGE SOLOMON:  We are going to go to the next panel, which will be --

		MS. KRAMER:  Your Honor, OSHA has some questions.

		JUDGE SOLOMON:  Oh, you do.  I'm sorry.

		MR. PERRY:  Yes, Your Honor, we do.

		JUDGE SOLOMON:  I cut you out.

		MR. PERRY:  Wouldn't want to let Dr. Mundt off scot-free now, would
we.  I believe Janet Carter has a question.

		MS. CARTER:  Thank you so much for the opportunity to ask you
questions today.  I really appreciate it.  I just have a couple of
questions. 

		You cite the use of in vitro data as providing mechanistic support for
your hypothesis.  So do you support the use of in vitro mechanistic data
to supplement an understanding of underlying mechanisms of
silica-related health effects?

		DR. MUNDT:  I have to first disclaim that I am not a toxicologist and
intending to put what I find in the epidemiological literature to be
consistent with what's reported by Mossman et al. in the recent
publication.  So, if you don't mind, I would rather not venture --

		MS. CARTER:  No, no, I appreciate that.  Thank you.

		DR. MUNDT:  Venture that, yes.  Certainly, we appreciate when lines of
evidence converge and support one another, that we have greater
confidence in the interpretation of our own evidence, even the --
especially the epidemiological.

		MS. CARTER:  No, I appreciate that very much.  Thank you very much. 
In your analysis of the available epidemiological data, you did a very
nice job of summarizing your criteria and tiering of the studies.  One
of your criteria was, of course, controlling for confounding of smoking.

		In the Checkoway study, you provided that as a Tier 1 study.  But in
your analysis, the Park et al. study in 2002, you excluded because it
did not -- you felt that it lacked sufficient control for confounding of
smoking.  That was -- I think that was how you phrased or similar how
you phrased it.

		I was wondering if you could expand on how you would ideally handle
smoking data.  I'm asking this because the Park data used very similar
techniques to what's fairly standard in the literature, and I was
wondering what your, as an epidemiologist, what your view of how smoking
data should be handled.

		DR. MUNDT:  Thank you.  I sense and share some frustration with the
ability to account for what is clearly great potential for confounding
from tobacco smoking.  I also, after 30 years of being an
epidemiologist, continue to be amazed at how few places such important
information is actually recorded and retained.  So quick answer in the
ideal is that that information be gathered and made available for
epidemiologic research which requires at the workplace to, in whatever
way possible, create a reasonably detailed smoking history.

		That said, what we have is what we can use.  And often it is an
indication of having ever been a smoker and, at best, the adjustment for
that is crude.  But it does give us an indication of whether confounding
is a large explanation or a relatively minor explanation.  We may not be
able to completely de-confound using that information.

		I think part of the -- there is some development in better methods for
external adjustment, meaning we don't have individual level data, but
gives us at least a sensitivity test for what range of results might
have been due to confounding under certain assumptions. 

		I think at least attempting those is a good idea in most studies,
especially where we're talking about lung cancers or other respiratory
effects that are clearly caused by smoking, as well as its occupational
exposures.

		MS. CARTER:  Thank you very much.  I really appreciate that.

		JUDGE SOLOMON:  Mr. Perry?

		MR. PERRY:  Stephen Schayer, please.

		MR. SCHAYER:  Good morning, Dr. Mundt.  I just have a couple of very
general questions for you.  So, yesterday we heard testimony from
Dr. Cox that association does not inform us about causation.  So I was
wondering if you could tell us how you would go about assessing
causation.

		DR. MUNDT:  How much time do we have, Judge?  I appreciate your
question, and I think I can appreciate what Dr. Cox was referring to
is, obviously, we are bound by the limitations of observational science
in epidemiology.  But that at some point there is accumulated sufficient
evidence that we make the judgment or the inference that, yes, this is
indeed caused by this exposure.  So I think it is enhanced by, from the
previous question, knowledge from say a toxicologic mechanistic.  And
when these start to align, our confidence in that being a casual
association is enhanced.

		I think here, over time, we've had the advantage with the reduction of
exposure to see reduction in disease, which I think just makes it a home
run that the diseases are caused by, therefore can be prevented by
appropriate intervention.

		MR. SCHAYER:  Okay, thank you very much.  And the other question I
had, we also heard testimony yesterday from Dr. Long about exposure
measurement error and bias exposure-response associations.  So this
question is actually about this.  The sources that he mentioned 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 just wondering if you considered these sources of error in
your tiering of the studies for your review or in your own study from
2011 entitled, "Respirable Crystalline Silica Exposure-Response
Evaluation of Silicosis Morbidity and Lung Cancer Mortality in the
German Porcelain Industry Cohort."

		DR. MUNDT:  Yes.  With regard to your first question, I wish I had the
luxury of enough studies to look at the independent contributions of the
various sources of variability that you mentioned.

		As applied to my own study, we engaged some of the best, at least in
Europe, industrial hygienists and chemists that understand the
measurement procedures.  And, in fact, I can't cite it off the top of my
head, but that publication itself cites some of the precursor work that
we did on understanding the variability in the exposures as measured
over time using different instruments.

		Essentially, for those who are unfamiliar with it or uninterested in
looking it up, we went to the museum, brought back the old equipment,
and ran them side-by-side in an exposure chamber to see how do we then
convert the exposure data historically to a single modern standard.  So
it was quite extensive.

		And that I hope partially answers your question or at least points you
toward where you can find a more eloquent answer to your question about
our study and what we did in it.

		MR. SCHAYER:  Okay, thank you very much.

		MR. PERRY:  Tiffany DeFoe?

		MS. DeFOE:  Good morning.  First, I'd like to ask a clarifying
question.  In your slides, when you were discussing I believe was it the
2013 paper by Dr. Morfeld -- I'm not remembering right now.  Is that
his reanalysis of your study on the pottery workers, the German pottery
workers?

		DR. MUNDT:  That's right.  It's essentially a methodologic proposal
for using computer algorithm to identify where the best fit of the data
suggests a range of threshold.  And he uses that and he applies that
method using our data on silicosis and the quantified individual
crystalline silica exposure estimates that we derived in the broader
mortality study that I published prior to that.

		MS. DeFOE:  Okay.  And you said that he concluded that there seemed to
be evidence for a threshold effect around .25 mg/m3?

		DR. MUNDT:  Yes.  I think if you look at his exact language, he cites
a range and that that was -- I think that was the point estimate.  And
he provides a range from .1 to something, .3, thank you.

		MS. DeFOE:  Okay.  Looking at your Table 2 in your 2011 publication,
it looks to me that there are 19 cases of silicosis recorded for workers
with average exposures below .2 mg/m3 and 21 cases for workers above. 
Is this intention with Morfeld's conclusions?

		DR. MUNDT:  I think you have to understand the difference between
those two publications.  The 2011 was not intended to look for a
threshold.  So the categorization of individuals in cumulative exposures
was in groups.  And so part of the results were determined by the
categories we had chosen to put them in ahead of time.  

		It doesn't have the ability to seek the inflection point or the point
in which the statistical analyses suggest the threshold exists and for
which the data fit the model best or the model fit the data best.  So
there is a difference in those intentions.  

		If you just read our study at face value, you don't see a real
increase risk for silicosis until you get up to about 4 mg cubic
crystalline silica exposure.  So that's pretty similar to the .1, if you
just average it out over a 40-year work history.

		MS. DeFOE:  But I thought when they said they were looking for a
threshold effect, they were looking for essentially no effect.  In
silicosis, there is no effective background, correct?

		DR. MUNDT:  Well, the data suggests that there is no effected
background, as well as at low levels of cumulative exposure up to, and
you see the results in the Mundt, 2011, up to 3 or 4 mg per cubic meter
years, after which it is very clear.  Morfeld wanted to refine that from
just the basic categorical description of where risk, increased risk
occurs to a more precise point.  And in the process, he ends up
developing and presenting a methodology.  So I think half the purpose of
that paper is to demonstrate a methodology that could be used on data
like ours for purposes of determining where the point at which disease
risk is now increasing above that of the background.

		MS. DeFOE:  Do you believe there is a background risk of silicosis
among non-occupationally imposed people --

		DR. MUNDT:  Sorry to interrupt you.  I was speaking generically.  I
was speaking about the methodologic purpose of the model as it was
applied just for silicosis, well, yes, you would think that would be
clear that there would be no exposure or no silicosis among levels to
which we are exposed or workers who are mildly exposed up to some point
after which disease risk increases.  It is his methodology that is
intended to determine where that point might lie.

		MS. DeFOE:  Thank you.  And then when you -- I apologize.  I have a
couple of questions written.  Now I need to find the one I need.  On
Page 286 of your 2011 study, you state that formal threshold analyses
may be warranted, however, available numbers of silicosis cases may
limit their precision.  Would you please elaborate on what you mean
here, for example, approximately how many cases of silicosis do you
think would be needed for a threshold analysis to precisely locate a
threshold effect?

		DR. MUNDT:  It largely depends on how you define precisely. 
Obviously, we advanced with the methodologies of seeking a threshold
with the modest numbers of silicosis cases that we have.  For academic
purposes, we would like there to be many more.  Obviously, we would
never want there to be more cases of silicosis.  So we have what we
have, and we made the best effort, I think, collectively and with a
range of experts from various fields, to try to maximize the
informational value of those data without over-interpreting what's
there.

		I'll be the first one to tell you there is a lot of imprecision and,
therefore, say confidence intervals or uncertainty should be respected,
and that the -- I'm hesitant to just focus on a single point number like
the .25, and prefer that you encompass the broader range that was
reported in the Morfeld, on which I was an author and consistently
brought this point to the table.

		MS. DeFOE:  Thank you.  Now, in your -- again, in your 2011 paper, you
discuss your methods and you said that you lagged exposure by 10 years
for the whole cohort and that you did analyses looking at lagged and
unlagged exposures.  And I was -- you presented these analyses for
lagged and unlagged exposures for silicosis, but I wasn't able to find
the results of the lagged analysis for lung cancer.  Was this performed
and, if so, would you describe the results?

		DR. MUNDT:  Yes.  And for the Judge and the audience, I just want to
remind you the study that we are discussing here, the last several
questions is not on cristobalite.  This is a crystalline silica
exposure.

		If you might recall from the first publication on this topic, there
was no increased risk of lung cancer at any category, so lagging becomes
moot.  It was all done, but it would have filled the paper with
predictable findings.  There was no excess and no association, so
nothing to report on lung cancer in our cohort.

		MS. DeFOE:  Thank you.  And my last question on this, would you please
characterize the age of the workers in the overall cohort?  I'm asking
because only nine percent of the studied population was deceased at the
end, and that seems to suggest a fairly young population, but it's not
clear.

		DR. MUNDT:  Again, if you don't have it in the publication in front of
you, it was in the previous one that reported the descriptive qualities
of the cohort and the SMR analyses.

		MS. DeFOE:  Thank you.

		JUDGE SOLOMON:  Mr. Perry?

		MR. PERRY:  I think Patti Downs has a question or two.

		MS. DOWNS:  And, Dr. Mundt, I'll let you off the hook for a minute. 
This question is directed towards Mr. Ellis.  In your written comments,
you said that diatomite is used in thousands of products, right?  And I
was wondering does the IDPA or any of its member companies have product
stewardship programs in place and, if so, what recommendations do you
make?

		MR. ELLIS:  Well, I think that the guidelines that we published on our
website, the safe use guidelines are an example of that product
stewardship.  And then the companies, obviously, can do their own
activities.  But this is a collective activity that they pursued under
the association's umbrella.

		MS. DOWNS:  Okay, thank you.

		MR. ELLIS:  So, yeah, I'd direct you to our website.

		MS. DOWNS:  And do you collect any information from those companies?

		MR. ELLIS:  I collect information from the companies, but relative to
product stewardship, no, I mean.

		MS. DOWNS:  Do those companies, though, do they collect information
from the customers, the end users?

		MR. ELLIS:  I can't speak to that.

		JUDGE SOLOMON:  Mr. Perry?

		MR. PERRY:  Yes.  Ms. Kramer?

		MS. KRAMER:  Dr. Mundt, I'm afraid we're back to you.  I believe you
mentioned earlier that you don't have the luxury of accounting for all
the long list of variables that Stephen listed out that I don't have a
prayer of listing out myself.  Despite that, are you still reasonably
comfortable that the results that you found and analyzed accurately
reflect the actual exposure levels?

		DR. MUNDT:  I do, especially on the time periods where there were
measurements.  Again, and this is in my study with the German porcelain
workers, the oldest measures were probably the least reliable.  And
there is a time period before which there were none.  

		We're often, in epidemiology, faced with the notion of, well, what
were the exposures before there were measurements.  So I would say over
the years, especially the last 20 or 30 years, where measurements were
abundant, you have a high degree of confidence in what the ambient
exposures were in various workplaces.  We, of course, have to assume
that the individuals working in those workplaces similarly were exposed.
 But we know that between worker practices or micro environments, there
would be some variability even within those homogeneous exposure groups
as characterized in the study.

		But what was, I think, encouraging is even at the qualitative level,
we knew that say the dry material handling, the formulation areas had
the highest potential for direct exposure to crystalline silicon form of
quartz, and it was really there that we saw by far the greatest risk of
silicosis.

		MS. KRAMER:  Okay.  Forgive me if this has already been asked.  We're
back to Mr. Ellis.  Do IDPA's members have any difficulty reaching the
current cristobalite PEL?  I would assume, you know, based on your
association with NISA that probably IDPA's members are meeting the
current PEL.

		MR. ELLIS:  I can speak primarily to the ones that do business in the
United States because they are governed by the Mine Safety and Health
Administration.  As you know, unlike OSHA, MSHA has a mandatory
inspection program where they visit mines twice if they are surface
operations or four times if they are underground operations.  And it is
typical that MSHA includes a health component to those inspections. 
And, typically, when they come to a site that has crystalline silica
exposures, they would look for those exposures.  So MSHA actually posts
that data on its website, so I guess I would direct you there rather
than go back to my companies.

		MS. KRAMER:  As you might imagine, we are most interested in the
companies that are governed by OSHA.  Do you have any kind of response
to that?

		MR. ELLIS:  No.  I mean, again, the companies that produce the
material are essentially MSHA regulated.  It's just the fact that we
work with cristobalite that gives us the expertise that we feel can help
inform the OSHA rulemaking.

		MS. KRAMER:  One last housekeeping matter.  The information that's
posted on your website, we could, of course, print that out ourselves,
but we would appreciate it, since you probably have a cleaner copy, if
you could provide us a copy of that and submit it to the record?

		MR. ELLIS:  So the safe use guidelines, for instance?

		MS. KRAMER:  Yeah.

		MR. ELLIS:  Would you like them in Japanese?

		MS. KRAMER:  Could you translate them for us?

		MR. ELLIS:  Okay.  I could do it in English, how about that?  Okay,
thank you.

		MS. KRAMER:  That would be great.

		MR. ELLIS:  Yeah.

		JUDGE SOLOMON:  Anything else?

		MR. PERRY:  No further questions, Your Honor.  And thank you again to
the panel.

		JUDGE SOLOMON:  Okay.  Let me just -- I have to ask a question.  I
think the interest of justice requires it.  There were questions asked
about the relationship to smoking.  And in 2000, regulations were
written for the Department of Labor involving pneumoconiosis.  Silicosis
is a subset of pneumoconiosis.  And the legislative fact finding found
that there was an additive relationship between smoking and mining
generally.  

		So I heard what you said.  Is there -- can you just comment on that?

		DR. MUNDT:  Yes.  I reiterate what you have heard and can be found
elsewhere.  Unfortunately, I can't contribute new insights based on our
cohort which, for various reasons, and possibly because the questioner
correctly pointed out earlier the cohort has only about 10 percent
decedents at this time, and diseases of long latency may yet to express
themselves in that cohort.  So it's a clear --

		JUDGE SOLOMON:  So you need a statistical sampling of what you have.

		DR. MUNDT:  A clear limitation or continue to follow that cohort.

		JUDGE SOLOMON:  Does anybody have any questions based on what I asked?

		DR. MUNDT:  But what I can suggest that we found and it is noted in
the publication that there was a positive correlation with silicosis and
smoking.  And I can't say epidemiologically I can understand it, but I
believe that that goes back to the question of the quality of x-rays. 
Some of the x-rays in our study were from mobile units from many years
ago.  It was essentially a bus that would go from plant to plant.  And
the reading of those is clear that there is something going on in the
film, whether it was really small rounded opacities or whether it was
something else maybe reflecting.  Smoking couldn't be differentiated
there.  So I think that it did come up as a correlate of what we defined
as silicosis in our study.

		JUDGE SOLOMON:  Okay, thank you very much.  We are going to go off the
record and take a break for five minutes.  And then the people from the
Brick Industry will come forward.

		(Off the record at 11:26 a.m.)

		(On the record at 11:35 a.m.)

		JUDGE SOLOMON:  Okay, we are back on the record.  And would you state
your name for the record?

		MR. GLENN:  Yes, it's Bob Glenn, spelled G-l-e-n-n.

		JUDGE SOLOMON:  Okay.  So we have attributed about 50 minutes to the
presentation.  Is it going to take you 50 minutes?

		MR. GLENN:  Yes.

		JUDGE SOLOMON:  Okay, go ahead.

		MR. GLENN:  The primary purpose of my presentation is to discuss the
unique factors related to crystalline silica exposure in the brick
industry that I believe OSHA has not adequately considered and must
reconsider during this silica rulemaking process.

		Based on my review and the scientific evidence, it is my position that
the brick industry should not be regulated based on quantitative risk
assessment derived from exposure-response data from other industries
handling silica-containing materials, but rather derive risk estimates
based on data from the modern clay brick industry.

		To do this, I will cover three points.  First, I will cover the body
of scientific studies demonstrating no significant workplace risk for
brick workers from crystalline silica exposure exists at the current
exposure limit and that any reduction in the crystalline silica PEL is
not scientifically justified.  I strongly believe, therefore, that the
current OSHA PEL for crystalline silica is amply protective of brick
manufacturing workers and should not be reduced for the brick industry.

		Using studies from the Scottish coal workers study by Buchanan et al.,
I will show that using the prediction equations from Buchanan seriously
inflate the cases of radiological silicosis that were actually observed
in a study of brick workers in England and Scotland by the same group,
the Institute for Occupational Medicine.  Dr. Miller, here, of course,
took part in I know one of these studies, perhaps all.

		Thirdly, I'll discuss why lung cancer risks from crystalline silica
exposure is not expected, because epidemiology studies of aluminum-rich
clays are negative for lung cancer risk.  Second, the potency of quartz
containing aluminum-rich clays not only inhibits the development of
fibrosis, but also inhibits mechanisms of carcinogenesis, and that
pulmonary fibrosis is a necessary mechanistic step not only for
silicosis but for other fibrotic lung diseases that increase the risk of
lung cancer.

		I beg your indulgence if I go back.  It is an early study, but when I
started looking at the literature, I did find them quite informative in
a way, and so I'm going to cover some of these early studies.

		The first I found was a study in the United States in 1939,
unpublished, by the West Virginia State Health Department, the
Industrial Hygiene Bureau.  The study was based on inspections and
medical studies of 20 brick plants throughout the state.  According to
census figures at the time, there were just over 1,000 employees in West
Virginia were engaged in production of brick.

		The West Virginia report found the average percent quartz content from
petrographic analyses to be between 10 and 15 percent.  Using that and
putting it into the ACGIH formula of the day, the 15 percent, you would
come up with a TLV of 10 million particles per cubic foot.

		The dust concentrations shown in this table, the average of 43 samples
taken in the grinding area was 201 million particles per cubic foot,
which exceeded the ACGIH TLV for quartz about 20 times.  In the grinding
area, crusher operators exceeded the TLV by 9, pan operators in that
area by 20, screen operators by 24, and general laborers by 11.  These
are multiples of exposures above the PEL, at the time.  They averaged 31
samples from brickmaking or 49 million particles per cubic foot,
exceeded by almost 5 times, and in the brickmaking area, pug mill and
brick machine operators exceeded the TLV by 6, pressers by 8, hackers by
3, and general laborers by 3.

		This is the results of the radiological study.  A medical study was
conducted on 325 workers at 4 of the 20 plants.  The average of the
study was 36 years -- of those studies was 36 years, and the average
length of employment was 10.7 years.  I realize that is a low tenure or
a low latency, but nonetheless NIOSH considered silicosis, chronic
silicosis to occur with 10 or more years of exposure.

		Of the 319 films that were studied, 15 or 4.7 percent were read as
abnormal, being a classification of a G1 or a greater.  Seven were
interpreted with minimal changes, G1.  Two of the seven had brief
employment in the brick industry and histories of long employment in
another dusty industry.  Seven were classified as G2.  Of the seven, one
had long exposure in another dusty industry and brief exposure in brick.
 One was interpreted as N, or nodulation.  There were no cases of
complicated silicosis found.  Notice that the abnormal films were not
observed until exposures were above 10 times the allowable concentration
for the period.

		Following that study, a 1941 study in North Carolina was made and
published by Trice.  There were 28 plants involved.  He used 183
impinger measurements for particle count concentrations.  He found a
range of quartz similar to the West Virginia study and saw a 10 million
particle per cubic foot TLV would be appropriate.  

		Dust concentrations was not as high as the West Virginia study.  The
average of 43 samples taking in the grinding area was 37.9 million
particles per cubic foot -- I'm going to start saying mppcf -- which
exceeded ACGIH TLV for quartz by 4.  The average of 20 samples from
brickmaking was 43.1 mppcf, which exceeded by 4.  Of 51 from the kiln,
the average exposure was only 28.3, or 2 times; however, the kiln area
cleaning of the kiln was exceptionally dusty.  Five measurements were
taken and exceeded the TLV by 14.  

		Health exams including chest x-rays were performed on 1,555 brick
workers.  The chest x-rays were ready independently by two physicians
who were experienced readers from the North Carolina Dusty Trades
Program.  The Dusty Trades Program was an early prevention program that
conducted routine medical examinations of North Carolina workers in
asbestos textile mills, other asbestos exposure situations, quarry sand
plants, and clay operations.

		Both of the physicians reported no evidence of silicosis in any of the
1,555 workers.  And Trice concluded the total absence of silicosis and
other serious pulmonary pathology, which they also looked at, and the
low incidence of other respiratory diseases among the 1,555 indicate
that exposure to dust in North Carolina trades in brick does not
constitute a serious menace to health.

		This next study is a very small study from England.  Keatinge and
Potter reported, published in 1949, there were 144 workers, 100 were
examined medically, 73 underwent chest radiographs, and of those only 1
worker was reported as having changed with silicosis and that was a
Class 5, second stage silicosis.  He had previously been a bricklayer's
laborer.

		The authors referred a paper by Gardner that suggests that while dust
levels are high, the inhalation risk of free silica is not a hazard due
to the alumina in the brick clays inhibiting fibrosis.  I think this has
been the subject of much literature about aluminum being protective for
brick and especially in the clays.

		I next want to look at a comparison of some studies from the same
period in other silica using industries.  This first one is a comparison
at the West Virginia study with a refractory brick study that was made
in Pennsylvania by Fulton et al. and was published in a report as well.

		It is interesting to compare these because, of course, they are from
the same period, time period.  While many of these studies did not
relate silicosis to exposure, no exposure-response relationship, and
those that did were not comparable metrics, for instance they used
average exposure versus cumulative or by tenure only.  It is clear
evidence that the degree of silicosis morbidity in these other worksites
was striking, and it was obvious that a risk of developing silicosis
from quartz exposure and brickmaking was intrinsically different in its
potential to provoke a manifestation of silicosis.  In a comparison of
this study, of the West Virginia brick and tile, they had an overall
prevalence of five percent.  With the Pennsylvania refractory brick
workers from the same period, an overall of 50 percent prevalence of
silicosis was found.

		For the West Virginia clay brick workers exposed to cumulative, this
is cumulative exposure, 9.9 million particles per cubic foot, no cases
developed, whereas a Pennsylvania study exposed to an average, the same
average, 42 percent had silicosis.

		This next is a comparison to two studies, a North Carolina brick study
and a granite study.  This is the Trice study of North Carolina found no
cases of silicosis from 1,555, whereas the studies by Dr. Russell, some
of the early studies of silicosis in Vermont granite workers, found an
overall prevalence at 50 percent.  In the 10 to 14 year group of granite
workers, by that time 96 percent were determined to have silicosis or be
silicotic.  

		The lower part of the slide, you can see a comparison.  The Keatinge
study with a study of pottery workers in West Virginia by Flynn, which
was a public health service study, the Keatinge studies, you'll
remember, had one silicotic of 73.  The prevalence rate in the pottery
was 83.  The fact that the workers had an overall silica prevalence of 8
percent in the pottery as compared to 50 percent in the granite workers
and 50 percent in the refractory brick workers might be related to the
inclusion of quartz and the aluminum-rich clays used in pottery
manufacturing.  The comparison silicosis prevalence is evidence that the
quartz in brick clays behaves differently with regards to the ability of
reduced pulmonary fibrosis and resultant silicosis in these different
industries.

		This is a study by Gillon, Rajan, and Belovsky.  It was made in Canada
in 1972.  This was the Ontario Health Department.  And a total of 77
impinger counts were taken, free silica percentage of the total airborne
dust varied from 13.2 to 24.8.  The 77 impinger samples were taken with
the mean dust counts ranging from 12 million particles per cubic foot to
1,026 million particles per cubic foot.  That is not given for specific
operations; however, plant conditions were extremely dusty across all
plants with mean impinge counts exceeding the TLV by 1.26 to 114 times. 
As you can see in this table, 6 of the 10 plants exceeded the TLV by
more than a factor of 10 and no plants were below the established TLV.

		Regular chest x-rays had been taken on these workers beginning in 1959
and were conducted every 18 months.  The films were recording -- were
read according to the system developed by Drs. Riddle and Brennan, and
it is described in the paper.  Essentially, the system coded the films
from 1 to 9, with codes 5 through 9 designated as pneumoconiosis.  With
the exception of one film that showed diffuse miliary nodulation, Code
5, no chest x-ray patterns consistent with silicosis were found.  

		The one case was a worker who had worked in an iron mine for 13 years
and 2 years in this tile plant.  They attributed these changes to his
former work.  He was removed from the study.

		The authors concluded that even though the workers were exposed to
dust concentrations considerably in excess of the TLV from 8 to 114
times, nevertheless radiological signs of silicosis among workers were
not present.  Moreover, they questioned whether the ACGIH TLVs at the
time of the study was applicable to the brick industry.

		This is a study by NIOSH.  Following the Trice study, 1941, almost 30
years later, North Carolina again became the focus of interest in
silicosis in the brick industry when the North Carolina Department of
Health asked NIOSH to assist in two medical studies of brick workers in
the '70s.  The health department had been conducting annual medical
surveys of brick workers for 10 years, part of this North Carolina Dusty
Trades.  They include chest x-rays and they failed to show an excess of
silicosis or other disease.  That was a note from Dr. Dubner, who at
the time was doing his residency at Duke and working with the health
department.

		Along with mobile health surveys of these workers, the department
conducted an industrial hygiene study by Carstens, who was also a
hygienist with the health department there.  Respiro average dust
concentration ranged from .88 to 2.49 mg/m3.  Despite these high levels,
no cases of silicosis were found around chest examinations for an
estimated 2,000 brick workers statewide.  And this promoted the health
department to request NIOSH to conduct the medical study.

		This is a '78 study.  It was conducted by Stringer and Anderson of
NIOSH and reported on a medical study of 558 brick workers and 592
non-dust exposed controls.  It is one of the few studies that actually
looked at controls from a non-dust population.  Spirometer chest x-rays
and respiratory disease questionnaire data provided no indication of
excess disease associated with the brick workers.  The NIOSH researchers
concluded that there was a lack of statistical evidence to support the
hypothesis of increased respiratory disease among this group of brick
workers compared to the non-dust exposed control group.  

		Results of chest x-rays found few abnormal films, and there was no
significant difference in the number of abnormal between the brick
workers and the current controls.  And this table shows a number in
percentages of abnormal x-rays for males by smoking status for brick
workers in non-dust exposed.  And as you can see, the non-dust exposed
controls have comparable evidence of changes that might be silicosis,
which I think answered partly the background question during the last
session, is there a background of radiographs in a normal population
that appear to be pneumoconiosis, and the answer is yes.

		The 1990 NIOSH -- oops, this is the 1980 NIOSH study of brick workers.
 It was 395 brick workers from 5 plants, and 159 clay pipe workers also
using structural clay to produce the pipe, and 652 non-dust exposed
workers.  Interestingly, the results of the two NIOSH studies are very
similar to the Trice study.  

		Again, pulmonary function data, chest x-rays, respiratory impingers,
and at this time sputum cytology gave no indications of excess
respiratory disease among the brick workers and pipe makers study group
compared to the control population.  This table is from the NIOSH report
and shows a number in percentage of abnormal workers' x-rays for both
brick and pipe workers. 

		It is interesting these two NIOSH studies, the prevalence of abnormal
chest films in the brick workers are comparable to the non-dust exposed
controls, which indicates there is a background of disease in the
general population that needs to be considered when determining whether
the radiologic results of the study population are truly increased.

		This is a study from the Institute for Occupational Medicine.  The
objective of the study by Love was to assess whether exposure to heavy
clay dust containing quartz caused a significant health risk for
silicosis and to develop information regarding the size of the risk. 
Eighteen brick plants in England and Scotland were studied, chosen and
studied between 1990 and 1991.  There were 1,407 respirable dust
measurements which were analyzed for quartz and used for calculating
exposure response.

		The medical study was of 1,925 workers where medical exams included
medical and occupational histories and chest radiographs.  Radiographs
were interpreted according to the ILO guidelines for pneumoconiosis, and
workers were grouped into 12 occupational groups and used in a job
exposure matrix for estimation of cumulative exposure for each worker. 
So this study does look at dust exposure and respiratory disease.

		There were eight workers identified with ILO Category 2/1 or greater. 
The convention in the United Kingdom is to use Category 2/1 as the
threshold for changes consistent with pneumoconiosis because it is
considered to better avoid confusion with subtle changes under the
radiograph of non-occupational diseases that could mimic a
pneumoconiosis condition.

		Seventeen workers had ILO Category 1 small opacities considered by the
researchers as slightly abnormal, but with the possibility that the
pathology observed was not caused by dust exposure.  Thus, there were a
total of 25 workers, or a 1.4 percent prevalence found to have small
radiographic capacities ILO Category 1 or greater. 

		Researchers point out that this prevalence is much less than they
observed in studies of surface coalminers, 4.4 percent; crushed stone
workers, 4.7 percent; and even greater than the non-dust or listing
non-dust exposed postal and telecommunication workers, 2.7 percent.

		Prevalence percentage is greater in what Forbes (ph.) had been found
many other studies of non-dust exposed workers in persons from the
general population.  And there are some papers that OSHA should look at
regarding that; recently Meyer in 1997 did a meta-analysis on the
subject; Dr. Epstein from the University of Pennsylvania in 1984, and
Bob Castellini of NIOSH in 1985, a study of what were termed blue collar
workers.

		Using the data from the Love et al. study, an exposure-response
relationship for a non-smoking worker, age 40, and exposed to respirable
dust concentration of .4 mg/m3, the UK PEL at the time, for 20 years,
would have a 2.1 percent risk of developing ILO category greater and
equal 1/0.  This level is equivalent to a cumulative exposure of 8
mg/m3, which is twice the allowable cumulative concentration at the
current gravimetric equivalent OSHA PEL of .1 mg/m3.

		The last of these studies is a study by Dr. Patrick Hessel, and it
was sponsored by the Brick Industry Association.  It was completed in
May 2006 with a report to the BIA.  The study was published in an
abstract, in the journal of CHEST, and presented the poster at the 2007
meeting of the American College of Chest Physicians, but a full paper
was never published.

		The study included workers at 13 plants producing structural clay
brick from a total of 94 facilities operated by members of the BIA. 
Workers were selected for the study through a process which took account
of the company size, the geographic location, employee age, and
availability of chest radiograph.  Two NIOSH B readers read the
radiographs from 701 workers.  When the two primary readers disagreed on
the interpretation of a film, the chest x-ray was sent to a third reader
for a median, to arrive at a median reading.  None of the chest x-rays
of the 701 workers were consistent with silicosis.  These results are
consistent with the course of other studies in the U.S., United Kingdom,
and Canada.

		This table shows the 11 -- the studies I have discussed with number of
plants, number of workers examined radiographically, and number of
silicosis cases.  In sum, what the data show is that while the studies
found a small prevalence of silicosis in the brick industry, the
incidence of those cases bear no resemblance to what was occurring in
other silica-using industries as a result of workers exposed to
crystalline silica either in terms of number of cases or severity of
findings.  

		Indeed, the silicosis prevalence in the brick industry is well within
the prevalence of changes that has been found in non-dust exposed
populations.  Based on this evidence, it is my opinion that the brick
industry should not be regulated based on a quantitative risk assessment
derived from exposure-response data from other silica-using industries. 
The basis for risk assessment for the brick industry should be limited
to the exposure-response studies conducted in the modern clay brick
operations, i.e., the Love et al. IOM study of heavy clay workers in the
United Kingdom.

		By the way, I looked at the prevalence of these studies.  The total
prevalence in this slide is 0.6 percent, which is lower than any of the
studies that had been done in looking at non-dust exposed workers.  Now,
to be fair, I didn't include the NIOSH, the two NIOSH studies in North
Carolina because they were not different from the controls.  But if I
include those 30 workers, the prevalence becomes 1 percent.  

		The variability in the Meyer study was from 0.21 percent to 11
percent.  And these are people that are non-dust exposed.  The 0.2
percent came from the Bob Castellini study.

		Moving to my second point of a focus of risk estimates and study of
Scottish coal workers seriously inflates cases actually observed in the
UK brick workers and cannot be used for quantitative risk assessment. 
Miller and Soutar here in the front row from IOM use the risk model
developed in the study of Scottish coal workers by Buchanan et al. to
predict cases of silicosis and compare to actual observed cases in the
studies by Love et al. of UK brick workers exposed to quartz contained
in heavy clays that are commonly used in manufacturing of building
brick.

		Employing the Buchanan risk model for coal workers' predicted risk to
brick workers was extremely overstated when compared to actual cases
observed in the Love studies.  This strongly supports the proposition
that exposures to quartz from these two industries have remarkable
differences in fibrogenic potency.

		We've discussed this study before.  This is the Love study.  But just
to recap, the study used by Miller and Soutar in the comparison with the
Buchanan coal workers was this Love study.  Eighteen brick plants, 1,925
workers examined, 25 workers of 1.4 percent found to have small
radiographic opacities greater than ILO 1/0, 8 were identified with ILO
2/1, 17 workers had ILO Category 1 small opacities considered by the
researchers as slightly abnormal but with a possibility that the
pathology observed was not caused by dust exposures.

		I'll try and speed it up here for you.  This is the Buchanan study,
which was used for the prediction equations.  They came from this study.
 And this was a study of a Scottish quarry that had had very high
exposures to sand -- to quartz due to a result of intrusion of sandstone
into the coal seams and sandstone formations in the roof and the floor
which cut out in the gathering of the coal. 

		The Buchanan follow-up study was 547 ex-miners and they had been
examined previously in rounds of examination in the coal, in the IMO
coal study.  Silicosis defined as greater and equal to 1/0, and there
were 203 that progressed at least one category, that's 38 percent, and
of those, 128 of these progressed two or more categories.

		The prediction equations would show that a miner, age 60, at the time
of follow-up, with 15 years exposure to an average concentration of
quartz of .3 mg/m3, the ACGIH quartz limit at the time, would have a 22
percent risk of developing silicosis.

		And this is the curve from the IMO report comparing the Scottish coal
workers with the clay workers.  The results predicted silicosis excess,
greatly in excess of the new few cases observed.  Figures shows that
1,831 men in 8 groups of equal size, an increasing mean cumulative of
respirable dust exposure, quartz exposure, and observed in the group,
frequency observed and predicted for ILO category greater and equal 1/0
and 2/1, and compared that with the brick workers.  So this is the curve
for the predicted at 1/0 for the coal workers, and this is what was
found when actually observed in the brick study.  This is with a 15-year
latency, and this is for the brick study.

		This is a table from the study.  Since the risk are added, the total
of individual risk gives an estimate of total number of cases expected
across a group not stratified by exposure.  Based on the subjects' work
histories and cumulative exposures with a 15-year lag period, the sum of
predicted risk of greater and equal 1/0 is 468, whereas only 26 were
observed in the radiological study of brick workers.

		For Category 2/1, 86 cases were predicted, whereas only 8 were
observed.  As expected, the 15-year lag period reduces the predicted
cases to 331 and 31 for radiographic changes of 1/0 and 2/0,
respectively.  These lag data, too, are still greatly in excess of the
eight observed cases.

		The third point I'll discuss is while cases of lung cancer would not
be expected from exposures to quartz and aluminum-rich clays, there are
no published mortality studies of brick workers that look at cause of
death or lung cancer death.  However, pottery clays are similar to the
structural clays used in brickmaking in that the quartz is occluded in
aluminum-rich layers of bentonite, kaolinite, and illite. 

		The Chinese pottery work of Chen et al., both his 1992 study and his
2005 follow-up, as well as the 1992 study, McLaughlin, of these Chinese
sub-cohort is discussed in the OSHA QRA.

		Chen et al., the 2005 study, this follow-up study was a case control
study of the same cohort study by him, by himself and McLaughlin in
1992.  In the 1992 earlier study by McLaughlin, he did find a weak
association for exposure to crystalline silica and lung cancer. 
However, the Chen 2005 study found no association of the pottery cohort
after adjustment for PAH, polycyclic aromatic hydrocarbons.  

		The Chen nested case control study is considered more robust as it
doubled the cases of lung cancer in the McLaughlin study, 120 versus 62.
 

		The Chen 2005 study used better exposure data as well with estimates
of average values for each facility, job title, and calendar year,
whereas the McLaughlin study only reported estimated percentages of
respirable dust and silica content of total dust.  The Chen study found
that pottery workers had the highest confounding from PAH levels than
any of the other groups studied, and these were groups of metal miners,
tin, tungsten -- I don't recall the exact metals.  

		The relative risk for crystalline silica exposure was found to be 1.1
with a confidence interval of 1.02 to 1.12, without adjusting for the
PAH confounding, the risk of 1.0 with a confidence interval of .96 to
1.09.  A series of studies in this Chinese cohort provides strong
evidence for aluminum-rich clays suppressing any potential
carcinogenesis from quartz.

		Currently, there are some animal studies.  This is a study by Zhang et
al. in 2002.  And I think it, too, shows the role of aluminum-rich clays
in suppressing carcinogenetic.  He examined the effects of coating
silica with aluminum lactate on silica toxicity uptake and
silica-induced DNA damage.  They used appropriately lung epithelial
cells for their test treatment with uncoated quartz and aluminum lactate
coated quartz.  The DNA was assessed using DNA strand breakage.  The
authors concluded that aluminum coating, which could easily occur
naturally, was shown to eliminate the ability of quartz to generate
hydroxyl radicals and exert critical genotoxic effects very likely to
play a role in quartz carcinogenesis.  

		This is a study by Knaapen et al., also an animal experimental study. 
This was an in vivo study of aluminum treatment of DNA damaging
potential of silica in rat lung epithelial cells.  Rats were instilled
with quartz, 2 mgs, either treated with aluminum lactate or native
quartz.  After three days, the animals were sacrificed, and they did
bronchoalveolar lavage.  The lung epithelial cells were isolated, and
DNA strand breakage was determined by single cell gel of
electrophoresis.  The DNA damage was significantly increased in
epithelial cells from the rats instilled with DQ-12 quartz, whereas no
enhanced DNA strand breakage was observed when quartz was treated with
aluminum lactate.

		The authors concluded the study provides evidence that a modification
particle surface with aluminum lactate prevents DNA strand breakage in
epithelial lung cells from quartz-exposed rats.

		I am just going to briefly mention the subject of pulmonary fibrosis
and lung cancer, but I urge OSHA to revisit the role that pulmonary
fibrosis plays in lung cancer.

		There are consistencies in the observational studies of silicotics
that have less potential for a bias for silicosis as a precursor for an
increased relationship with lung cancer, and this can be seen in studies
by Forastiere that were based on death certificates, Amandus and
Castellan, which were part of the dusty trades workers in North
Carolina, and de Klerk and Musk.

		Coupled with the results of recent meta-analyses studies, available
data provides strong support that the development of silicosis is a
mechanistic step that leads to lung cancer.  And these meta-analyses
were by Erren et al., 2009; Kurihara and Wada, 2004; Lacasse et al.,
2009; Pelucchi et al., 2006; and Steenland and Stayner, 1997.

		In addition, there is support from animal studies that aluminum-rich
clays suppress mechanisms of carcinogenesis.  I mentioned Zhang and
Knaapen.  And OSHA should review the evidence for increased lung cancer
risk found in other pulmonary fibrotic diseases.

		Interstitial lung diseases for which the available evidence suggests
an increased risk of lung cancer, and some of these are very strong
increased risk, including idiopathic pulmonary fibrosis, systemic
sclerosis, systemic lupus, rheumatoid arthritis sarcoidosis, and, of
course, certain forms of pneumoconiosis.  And this was reviewed in a
paper by Mossman and Glenn in 2013.

		In conclusion, it's evident from the medical studies of brick workers
that the risk of developing silicosis from exposure to quartz in brick
clays and shale historically is insignificant at exposure levels that
existed in the past, as well as in more contemporary studies of the
industry and that there is no significant workplace risk from
crystalline silica exposure at the current PEL.  

		Using the Scottish coal work equations considered by OSHA to be the
best for risk assessment, the predicted risk of silicosis was seriously
inflated compared to the actual cases observed in the radiological study
of heavy clay workers.

		In my opinion, the only sensible study to be used for setting an
exposure limit for quartz and brick manufacturing would be those of Love
et al.  To use prediction equations from other studies of native quartz,
such as gold miners, coal miners, tin and tungsten miners, as a basis
for occluded quartz and aluminum-rich clays is scientifically
indefensible.

		Regarding lung cancer, there are consistencies in the epidemiological
studies which have less potential for a bias.  These are studies of
silicotics for silicosis as a precursor, for any increased relationship,
lung cancer would support silicosis is a mechanistic precursor, coupled
with the results of meta-analyses studies.  Data provides strong support
that the development of silicosis is a mechanistic step that leads to
lung cancer.  In addition, there is support from animal studies that
aluminum-rich clays suppress mechanisms of carcinogenesis.

		JUDGE SOLOMON:  Right on time.  Are there comments from the peers? 
No?  From the public?  Would those of you with your hands up please form
a line and come forward.

		MS. KRAMER:  Your Honor, if I may while they are queuing?

		JUDGE SOLOMON:  Sure.

		MS. KRAMER:  Mr. Glenn, I believe you have a document that includes
both your PowerPoint and your statement?

		MR. GLENN:  Yes.  Let me --

		MS. KRAMER:  Could you pass that over?

		MR. GLENN:  Let me confer with counsel.  Yes, I will.

		JUDGE SOLOMON:  Let the record reflect that there was a certain amount
of pantomime in the last presentation.

		MS. KRAMER:  Your Honor, I'd like to mark Mr. Glenn's combination
statement and PowerPoint as Exhibit 18 and request that it be entered
into the record.

(Whereupon, the document referred to as Hearing Exhibit 18 was marked
and received in evidence.)

		JUDGE SOLOMON:  State your name.  And I know that we know you, but you
have to spell your last name.

		MR. HEARL:  Sure, my name is Frank Hearl.  It's spelled H-e-a-r-l. 
I'm with NIOSH.  I work here in Washington, D.C.  I have one question
basically, and that is you talked a lot about the brick industry.  What
do you feel or do you have an opinion about the brick as it is used say
like by bricklayers or by stonemasons when it is being cut, is there a
difference between those exposures and the exposures that you described
from the workplace?

		MR. GLENN:  Yeah, thanks very much, Mr. Hearl.  That's why I did
stress that this is related to brick manufacturing.  When you look at
masons or bricklayers, you will find cases of silicosis at a higher
prevalence in those workers.  I'm not sure why.  It could be that the
quartz that's used in the grout or in the masonry has a higher silica
concentration or has a native silica concentration where the particles
are not coated or it could be that cutting brick could change particle
characteristics.

		MR. HEARL:  Okay, thank you.

		JUDGE SOLOMON:  Next?

		MR. WEISSMAN:  David Weissman from NIOSH.  Dr. Glenn --

		JUDGE SOLOMON:  W-e-i-s-s-m-a-n?

		MR. WEISSMAN:  Correct.  Dr. Glenn, you had mentioned a couple of
references about background rates of abnormal ILO readings in the
general population, and I just wanted to ask a question or two related
to that.

		MR. GLENN:  Sure.  And thank you for the honorary doctorate degree.

		MR. WEISSMAN:  My pleasure.  

		MR. GLENN:  I still work for a living.

		MR. WEISSMAN:  So you'd agree that how B readers are used or how
physicians who do ILO classifications are employed is really important. 
It's very important, for example, to use multiple readers and medians of
readings, and it is very important for people to be blinded to how
readings are done and that sort of technical detail, correct?

		MR. GLENN:  I certainly do.  And when I had your job, I also had the
responsibility for B reader program, so I can assure you.  Interesting
thing in the Meyer study is variability in the European studies was much
greater than that in U.S. studies, and I think that can be attributed to
the success of your B reader program, and your certifications and
re-certifications of B readers.

		MR. WEISSMAN:  And I would also comment that for the Epstein study,
that was also an issue because there weren't independent readings done. 
There were two B readers reading together.

		MR. GLENN:  The other problem with the Epstein study, and I think
another reason he found such a high variability was that those were
films for admission in the hospital.  And, of course, these people
obviously were a select population presenting with other conditions.  So
I don't think his study was one of the better studies, certainly.

		The Castellan study which I mentioned, it was interesting because we
used three readers from the American College of Radiology Task Force on
Pneumoconiosis and some of these people were, you know, of course, the
people who started the program, and they were very expert in reading,
classifying films according to the ILO.

		MR. WEISSMAN:  And in their expert hands, only 3 of 1,422 films or 0.2
percent were ILO classified as 1/0 or greater.

		MR. GLENN:  I believe that's right.

		MR. WEISSMAN:  And you also raised the point of the appropriateness of
the comparison population.  So to have a background that would be
relevant to an evaluation of workers, your general population would need
to be same gender or same age, not dust exposed, correct?

		MR. GLENN:  Yes.

		MR. WEISSMAN:  And that was a problem with many of the studies that
were included in the Meyer analysis, correct?

		MR. GLENN:  I'm not sure about that.  I think -- I'm not sure just how
those group, those studies or people studied were selected.

		MR. WEISSMAN:  Well, it included one study that we have already talked
about that was hospitalized proposals.

		MR. GLENN:  Yes.

		MR. WEISSMAN:  Another study that included people who are office
workers in an asbestos plant, and some other studies as well that may
not have been comparable to workers.

		MR. GLENN:  Yeah, the North American studies, Epstein had an 11
percent variability or 11 percent prevalence, which was the highest. 
Castellan had .21.  Kay Kilburn (ph.) in a study had .25.  And then
there were studies in North America by Kennedy and they -- he found 4.5,
4.8, and 2.1 in another study.

		MR. WEISSMAN:  In any event, I guess the point is, is that for many of
these studies, they didn't follow the recommended procedures that you
would use if you were setting up a study and they weren't exactly
comparable to a working population.

		MR. GLENN:  I would have to review, but you are probably correct,
Dr. Weissman.

		MR. WEISSMAN:  Okay, well, thank you.

		JUDGE SOLOMON:  There was no objection, but I have to ask, the
document that you were reading from, is that part of your presentation?

		MR. GLENN:  Yes.

		JUDGE SOLOMON:  The computer?

		MR. GLENN:  Oh, this is a Meyer study.  It's published I think in --

		MS. KRAMER:  Is that in there?

		UNIDENTIFIED SPEAKER:  Yeah, all three of them are in here.

		MS. KRAMER:  Your Honor, we actually have a copy of three of the
studies that Mr. Glenn referred to.  And if this would be a good time,
we'd like to go ahead and mark those and have them entered into the
record.

		JUDGE SOLOMON:  Well, the reason I brought it up was it hadn't been
identified where it came from.  So typically there are two concepts: it
is present recollection refreshed or past recollection recorded.  If
it's recorded, it should be in evidence typically.

		MS. KRAMER:  Sure.

		JUDGE SOLOMON:  So that's why I asked.

		MR. GLENN:  The Meyer study was published in CHEST in 1997, Volume
111, pages 404 to 410.  And the authors were Meyer, Islam, Ducatman, and
Robert McCunney, Dr. McCunney from MIT.

		JUDGE SOLOMON:  Do you want to pass those to me, please?

		MS. KRAMER:  And, Your Honor --

		MR. GLENN:  Well, I don't have them.

		MS. KRAMER:  I have a copy of it right here.  And if it's all right,
I'd like to mark the CHEST publication as Exhibit 19 and have it
admitted into the record.

		JUDGE SOLOMON:  Okay, there is no objection, and it is admitted into
evidence.

(Whereupon, the document referred to as Hearing Exhibit 19 was marked
and received in evidence.)

		MS. KRAMER:  And two other articles, and I'll be quick in deference to
the questioner.  The first one is entitled "Application of ILO
Classification to a Population without Industrial Exposure," and it is
the article by Epstein that Mr. Glenn was referring to earlier.  I'd
like to have that marked as Exhibit 20 and admitted into the record.

		JUDGE SOLOMON:  So admitted.

(Whereupon, the document referred to as Hearing Exhibit 20 was marked
and received in evidence.)

		MS. KRAMER:  And, finally, an article entitled, "Prevalence of
Radiographic Appearance of Pneumoconiosis in an Unexposed Blue Collar
Population."  And that is by Castellan.  That would be marked as Exhibit
21 and is all right with you?

		JUDGE SOLOMON:  Okay.  That is admitted into evidence.

(Whereupon, the document referred to as Hearing Exhibit 21 was marked
and received in evidence.)

		MS. KRAMER:  Great.  Thank you.

		JUDGE SOLOMON:  The reason that I was asking about the document that
he has, is that your statement, Dr. Glenn?

		MR. GLENN:  No, those were papers.  Those are actually scientific
papers that I used in preparing my remarks.

		JUDGE SOLOMON:  Okay.  State your name and spell your last name.

		DR. ROSENMAN:  Yes.  Dr. Ken Rosenman, R-o-s-e-n-m-a-n.  Hi, Bob.  I
haven't seen you in a number of years.

		MR. GLENN:  Yes, how are you doing, Dr. Rosenman?

		DR. ROSENMAN:  So my question is, so you presented this data on the
brick manufacturing workers and there was no latency or duration that I
saw in any of your slides or what you heard.  And since we know that
silicosis occurs 20, 30 years after duration or first exposure, I was
wondering if you had any data that would actually allow us to look at
the prevalence of disease in people who were truly at risk?  So I could
do x-rays on people first day and they could be very high exposure, but
without latency incorporated, I have no idea if, you know, there were
any people at risk in those studies.

		MR. GLENN:  Yeah, I would be happy to review those studies,
Dr. Rosenman.  I'm not sure which ones might have had latency or not. 
I just had to abstract what I could to get through in the time period. 
However, I would tell you, of course, that the ILM study was an
exposure-response study, and you can easily compare it to the OSHA PEL
for silica.

		DR. ROSENMAN:  Well, you can.  But if people have high exposure but
short duration, short latency, you are not going to see positive x-rays
and so it's not going to be useful, and so what percentage of the
population was truly at risk of silicosis in any of those studies.  And
there was nothing presented.

		MR. GLENN:  That could be in my report, in my comments.  I would have
to look.

		JUDGE SOLOMON:  Next?

		DR. GUIDOTTI:  Hello, my name is Tee Guidotti.  The last name is
G-u-i-d-o-t-t-i.  A great deal of your testimony was predicated on the
inhibitory effect of aluminum and alumina on various manifestations
related to cancer risk and inflammation.  And, of course, we know that
for a brief period until it was abandoned for reasons of concern over
fibrosis risk, that powdered aluminum was actually used in practice as a
prophylactic agent and then abruptly stopped because of concern over
respiratory fibrosis of a different type.

		MR. GLENN:  Yes.

		DR. GUIDOTTI:  Are you aware of any studies either based on
epidemiology or otherwise that suggests that either aluminum or alumina
have a protective effect against immunologically mediated effects in the
lung or bronchial inflammation, or infectious disease risk from
opportunistic infections like mycobacteria?

		MR. GLENN:  Such as immune mediated diseases I discussed and related
to increase for lung cancer?

		DR. GUIDOTTI:  But as a protective effect.

		MR. GLENN:  Yeah, I don't.  I do not.

		JUDGE SOLOMON:  Thank you. 

		MR. GLENN:  I should say not in studies of humans.  Only those two
studies that I mentioned in lung cells, lung epithelial cells.

		DR. GOLDSMITH:  My name is David Goldsmith, G-o-l-d-s-m-i-t-h. 
Mr. Glenn, you paid a lot of attention to the very low or apparently
low levels of x-ray prevalence of pneumoconiosis or silicosis in the
brick workers that you studied.  We have heard yesterday and there has
been some discussion about there being other silica-related diseases,
and you mentioned lung cancer related to silicosis.

		But were you -- the cohorts that you studied, did they look at lung
cancer, did they look at autoimmune disease, did they look at kidney
disease?  Were any of these diseases elevated in those studies of brick
workers, or did you solely look at silicosis?

		MR. GLENN:  Thank you, Dr. Goldsmith.  I didn't -- you said I studied
these workers.  I didn't study these workers.  These are published
reports and published papers in the scientific literature.  The best I
could do was take what they gave me of those.  So I don't recall any of
them looking at chronic obstructive pulmonary diseases or such as that,
kidney disease, any of the other end points that there is discussion of
silica being related to.

		DR. GOLDSMITH:  All right, I appreciate that.

		JUDGE SOLOMON:  Okay, thank you.  Mr. Perry?

		MR. PERRY:  Thank you, Your Honor.  I do have a few questions for
Mr. Glenn.  This is Bill Perry from OSHA.  Okay, I'm going to focus on
the Love report a little bit which, well, I mean you have recommended
that that's what we rely on.

		MR. GLENN:  Um-hum.

		MR. PERRY:  So I'll do that.  So on Page 19 of your testimony,
actually 19 and 20, you present a table that compares a number of
different studies.  It includes the Love et al. study on clay workers,
as well as a number of others.  So the Love et al. study is a
cross-sectional study, okay.

		MR. GLENN:  Yes.

		MR. PERRY:  It was a single session of taking x-rays?

		MR. GLENN:  That's correct.  It was an examination of the workers at
one point in time.

		MR. PERRY:  Okay.  I assume you aren't aware of any prospective or
retrospective studies that have been done in the industry?  I didn't see
any in your testimony.  I assume you would have presented it, if there
were.

		MR. GLENN:  That's correct.

		MR. PERRY:  On either.

		MR. GLENN:  Yeah.  That's the only one, only of the studies that has
exposure response information.

		MR. PERRY:  All right.  So on your table, you don't have a value for
cumulative exposure for 4 mg/m3 years.  But for 2 mg/m3 years, you have
a .9 percent risk of silicosis, radiologic silicosis that you get from
the Love study, which is lower than most of the other studies you have
on the table.  A number of them are retrospective studies, a couple are
cross-sectional.  

		But again I think the issue with cross-sectional studies is, as you
know, and we point it out in our health effects chapters, you get
survivor effects.  You don't, you know, you're not following people
through a period of time.  So we actually, I think, classified this
study as one that did not look at retirees, that did not really reflect
anything like a lifetime risk.  So would you agree with that assessment?

		MR. GLENN:  I would have to look at that study again, but I don't --
I'm not sure I wouldn't agree with that, Bill.

		MR. PERRY:  Okay.  So you think the Love study --

		MR. GLENN:  I think based on the whole body of evidence, that it's
clear to me at least that there is something different about aluminum in
brick clays and their fibrogenicity, and I think that is demonstrated in
the Love study as well.  And in the Love report, also, which is much
more comprehensive.

		MR. PERRY:  Right.  And our analysis doesn't fundamentally disagree
with the qualitative statement that, yeah, when you look at the evidence
for clay industries, the risks appear to be lower.  But you recommended
that we evaluate the risk, the quantitative risk using the Love study. 
So I'm just trying to establish, you know, we're interested in figuring
out what the lifetime risk is.

		MR. GLENN:  The other thing you could do, of course, is leave the PEL
where it is for clay brick workers.

		MR. PERRY:  Yes, but I need a reason.  That's what I'm trying to get
at.

		MR. GLENN:  The reason is that the body of epidemiology literature
indicates --

		MR. PERRY:  Okay.  

		MR. GLENN:  -- there is a negligible risk.  It's within the background
of what you would find if we extract these 100 or so people here.

		MR. PERRY:  Okay.  Just as an example on that same table, on Page 19,
you cite the Rosenman et al. study of iron foundry workers, former iron
foundry workers, which has a risk of 2 percent at 2 mg/m3, which is
only about twice the risk of what the Love study is showing at that same
cumulative exposure.

		MR. GLENN:  I don't have that in --

		MR. PERRY:  Well, it's in Page 19 of your written testimony.

		MR. GLENN:  Okay.  

		MR. PERRY:  So, you know, I just wanted to kind of get your take on
how this reflects lifetime risk, which being a cross-sectional study it
really probably cannot.  I mean you do refer to it as an eloquent
report, perhaps don't disagree fundamentally given its design.

		One thing I wanted to point out going to this issue of background risk
that Dr. Weissman questioned you, the Castellan study, that recommended
that as a result of its findings, it recommended that investigators use
three B readers, correct?

		MR. GLENN:  Yes.

		MR. PERRY:  And is that the number of B readers that was used in the
Love study, also?

		MR. GLENN:  Yes, I believe it was.

		MR. PERRY:  Okay, thank you.  

		DR. MILLER:  Actually, I don't know if --

		MR. PERRY:  I'm sorry?  Well, or equivalent, I guess I would say.

		JUDGE SOLOMON:  Let me just state that that was Dr. Miller.  And do
you want to say what Dr. Miller said?

		MR. PERRY:  Yes.  Dr. Miller was questioning my saying that the Love
study used B readers.  It did not, because it is not a U.S. study.  But
they used readers that have equivalent training and competency, as I
understand it.  And he is, for the record, he is nodding yes.  So I
appreciate that.

		The conditions of the facilities that were studied by Love et al., are
they -- would you say that they are pretty similar to U.S. facilities in
the time period that they were studying?  This is a 1999 report, so it's
fairly recent.

		MR. GLENN:  Yeah, that's a recent study.  You know, perhaps that
question could be asked of the next panel, which will have
representatives from the brick industry.  I would expect that our brick
manufacturing is very similar to the United Kingdom, since we copy a lot
of things from them.

		MR. PERRY:  Okay.  Okay.  I think just really one more question about
the Love study, because in their conclusion, although they do
acknowledge that given the high concentrations that were experienced by
a large proportion of the workforce and the relatively low prevalence
they acknowledge might be surprising, but they go on to state,
nevertheless, the estimated exposure-response relation for quartz
suggests considerable risks of radiological abnormality even at
concentrations of 0.1 mg/m3 of quartz.

		So how do you reconcile what you are saying?  This is, if you have the
paper there, it's on page --

		MR. GLENN:  I don't.

		MR. PERRY:  I have, well, I mean you're welcome to look at this.  It's
on Page 132 of --

		MR. GLENN:  What I was looking for and I thought I had it was a
statement that I had made about that the Buchanan study, and it should
-- the predictions from the Buchanan study are not appropriate clay
brick workers, and there possibly should be another consideration for
clay brick workers.  

		MR. PERRY:  I'm sorry.  This is the conclusion that's in the Love et
al. paper.  Based on the study that they did, they are saying that, to
their mind, there are considerable risks of radiological abnormality
even at concentrations of .1 per cubic meter.

		MR. GLENN:  Let me get back to you with some other quotes from that
study as well.

		MR. PERRY:  Okay.  All right, I would invite that.

		MR. GLENN:  That actually questioned whether the Buchanan study should
be used to -- the results of the Buchanan study should be used for
exposure setting in brick.

		MR. PERRY:  Okay.

		JUDGE SOLOMON:  Any other questions?

		MR. PERRY:  No.  I think, Janet?

		MS. CARTER:  Oh, yes.

		MR. PERRY:  Janet Carter has a question or two.

		MS. CARTER:  Dr. Glenn, thank you so much for the opportunity.

		MR. GLENN:  Mr. Glenn, I work for a living.

		MS. CARTER:  Oh, I'm sorry.  As part of your testimony, you provided
supplemental information of an unpublished analysis that you had
provided on the association between rheumatoid arthritis and lung
cancer, acelli (ph.) and lung cancer, systemic sclerosis and lung
cancer, idiopathic pulmonary fibrosis and lung cancer, and sarcosis --
sarcoidosis and lung cancer.

		Are you aware of any experimental animal studies that look at these
associations that can provide a basis for a mechanistic evaluation?

		MR. GLENN:  I am not.  I drew on that because of discussions that I've
had with the late Dr. Hans Weill, where he was of the opinion that
pulmonary fibrosis from whatever cause was the -- should be a
consideration for an increase of lung cancer.  And so I started looking
at the literature, and I was quite surprised to find the enormity of the
studies that show quite a high relationship and risk between some of
these diseases, pulmonary fibrotic diseases and lung cancer.

		MS. CARTER:  Has there been or are you aware if there has been a
systematic evaluation of the types of tumors found in these
immunological-based diseases that could be used to support this type of
association?

		MR. GLENN:  Well, they're really speaking of fibrosis, so I am not
aware of that.

		MS. CARTER:  Well, they are saying -- I mean you are indicating that
the fibrosis caused by these --

		MR. GLENN:  The fibrosis is precursor for --

		MS. CARTER:  Yeah, is causing the lung cancer.  So I was --

		MR. GLENN:  Well, it's an inflammatory response, of course, and we
know inflammatory response is --

		MS. CARTER:  But these are immunologically based diseases.

		MR. GLENN:  I realize that.

		MS. CARTER:  So it could be that the mechanism may be completely
different.

		MR. GLENN:  That could be.

		MS. CARTER:  Okay.  That was all I had.  Thank you.

		MR. PERRY:  No further questions.  Thank you, Mr. Glenn.

		MS. KRAMER:  Actually, I have one question for you and then a very
small housekeeping matter.  I just wanted to check, you didn't note any
in your comments, but are there any standard-setting organizations or
governments that currently treat brick in the silica industry
differently than silica overall?

		MR. GLENN:  I don't think there are, but I'm not positive.

		MS. KRAMER:  Okay.  And the housekeeping matter, this is in no way
related to you, Mr. Glenn, because you had no notice of this.  But for
those of you who are in the audience who may testify later, if you could
bring a copy of your written comments that you have submitted, in case
OSHA or another questioner wants to refer to it, that would be really
helpful.  And, again, Mr. Glenn, thanks for bearing with us since we
didn't give you any notice.

		MR. GLENN:  That's all right.

		JUDGE SOLOMON:  Okay, we are well over time.  So what we'll plan to do
is start at 1:30, so the brick presentation, the Acme Brick Company,
would start at 1:30.  So the hearing is continued until then.

		(Whereupon, at 12:41 p.m., a lunch recess was taken.)

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

		(1:34 p.m.)

		JUDGE SOLOMON:  From Acme Brick Company, Mr. Latham, are you first?

		MR. LATHAM:  Mr. Tayler will be first.

		MR. TAYLER:  Thank you, Your Honor.  My name is Dr. Garth Taylor.  As
the Technical Director of Acme Brick Company, I am responsible for the
direction, development, and coordination of our company's environmental
health and safety, engineering, and research functions.

		I have been involved with the industry, the brickmaking industry in
South Africa, the U.K., and here for over 48 years.  With me today, I
have Mr. Bill Latham on my left and Mr. Tom Brown on my right. 
Mr. Tom Brown is our Director of Health and Safety, and he will be
addressing the impact of the proposed silica rule which will have -- it
will have on our associates and some of the safety issues involved with
this.  Mr. Latham, on my left, is Acme Brick's Risk Manager and General
Counsel.  He will be addressing OSHA's failure to establish its
statutory mandates in regulating silica.  Mr. Latham will summarize our
comments and provide final recommendations from Acme Brick.

		By way of background, Acme has been manufacturing brick for over 122
years, a well-established company in Fort Worth, Texas.  Before the
recession, our full capacity, we employed 3,000 associates.  Our core
business is the manufacture and distribution of clay face brick.  We
also produce concrete block, cut stone, manufactured stone, and
distribute ceramic tile and various other building materials through our
network of sales outlets and distributor network across the country. 
But our core business, over 80 percent of it is clay brick.

		Acme Brick owns 25 brick manufacturing operations situated in the
southwestern part of the country.  And as a result of the great
recession and the downturn in the construction industry, only 16 of
these plants are currently operating, operated by 1,000 or so production
associates. 

		Acme certain appreciates the opportunity today to address the panel
and comment on our experience and concerns with OSHA's decision to
reduce the permissible exposure level, and to impose the significant
additional ancillary regulations pertaining to the respirable silica.

		My comments, I will start with -- the comments that I would like to
talk about will deal with three areas, raw materials that we work with,
the feasibility of achieving compliance, and some of the economic
impacts.  The rule as proposed has the potential to have significant
detrimental impacts on Acme Brick Company and its associates, as well as
the entire brick industry, while providing very little or no
commensurate improvement to the health or well-being of the workers
employed by Acme Brick.

		The raw materials.  Bricks are made from clays, not silica.  The clays
used by Acme Brick are minerals referred to as hydrated alumina
silicates, and they are being formed by the alteration and breakdown of
parent igneous rocks, mostly feldspathic in nature, over the millions of
years.  These minerals are transported by various actions, water
transportation, and are known as sedimentary deposits.  It is important
to realize that most of the silica in these brickmaking clays is
embodied in the alumina silicate crystalline structure and matrix of the
clay mineral.  

		The free quartz which exists in the clay body is an impurity, and its
content is typically minimal, ranging from 10 through to 30-odd percent.
 Quartz levels higher than this in the brick industry produce poor
quality products.  Furthermore, samples of respirable dust analyzed by
x-ray diffraction indicate lower levels, meaning that not all of the
quartz in the material finds its way into the air.  This goes a long way
to explain why the incidence of silicosis and related illnesses are
virtually nonexistent in the clay brick industry, as Mr. Bob Glenn,
I'm sure, has explained this morning in excellent detail.

		The detailed comment report submitted by Bob Glenn on behalf of the
BIA clearly demonstrates the scientific facts of knowledge by OSHA that
the quartz occluded in an alumina silicate clay matrix does not have the
biologic potency or ability to produce pulmonary fibrosis as does
unoccluded quartz.  Furthermore, OSHA acknowledges in their proposal,
proposed rule discussion, that the physical characteristics that are
inherent in brickmaking clays are undoubtedly responsible for the lack
of silicosis cases in the clay brickmaking industry.

		OSHA should, therefore, take note that the materials used by Acme
Brick and, indeed, by the brick industry at large are inherently
composed of alumina-rich clays that directly modify the toxicity of the
quartz particle.  This means that by occluding the quartz particle in a
clay coating, the bioavailability of the particle is decreased.  The
report compiled by Bob Glenn emphasizes that aluminum has been shown to
decline the toxicity of silica in several studies.  I think he went
through that well this morning.

		It is, therefore, imperative that OSHA recognizes these facts
presented in these scientific studies and that it undertakes a balanced
assessment of this vital scientific information.  Should they do this,
they will most certainly conclude that the proposed reduction of the PEL
to 50 µg/m3 cannot be justified.

		The feasibility of achieving compliance over a decade or more.  Acme
Brick has worked diligently to comply with the existing rule.  We have
developed a program designed to address ways and means to meet the
current PEL of 100 µg/m3, and Mr. Brown will cover more detail on
this.  In spite of the application of the best management practices,
engineering solutions, extensive training, work practices, we have found
it difficult in some of the locations to meet the current PEL.  This is
due to the high dust levels generated as a result of the fine platy
nature of clays.  

		The known limitations of engineering solutions and the best work
practices, even those proposed by OSHA, is going to place our company in
a state of ongoing noncompliance coupled with an ongoing program of
extensive testing in an attempt to meet the concentrations which are
barely achievable.  Our likely ability to meet the proposed reduction in
the PEL to 50 µg/m3 would inevitably result in the requirement for
extensive respiratory protection measures placed on our associates,
placing them in unbearable work conditions.  Mr. Brown will address
this further.

		Furthermore, the introduction of an action limit of 25 µg/m3 will
trigger confusion and lead to an ongoing, disruptive, expensive
training, series of training, expensive testing.  The level of 25 µg/m3
is barely detectable, in fact, our current sampling results indicate
many times are non-detect values at this level.  Maintaining this level
of detection is unrealistic and will place most of our plants in a
permanent state of action or, indeed, noncompliance.

		OSHA should remove this action level requirement and maintain the PEL
at 100 µg for the industry to be able to protect its associates.  This
will enable Acme to continue to provide protection of the health and
well-being of its associates in a safe and effective manner over the
longer term.

		The economic impact.  Our practical experience in the application of
engineering solutions, best practices, and management of a
well-structured program has brought us to an industry leading position. 
With some exception previously referred to, our level of compliance and
the protection of our associates are excellent.  We intend to pursue
these standards with ongoing improvements.  

		We have conducted extensive studies of our facilities to determine the
investment requirements that would be needed to come close to meeting
the proposed PEL and ancillary requirements.  Investment in additional
dust collection equipment, ventilation, vacuum systems, decontamination
facilities, change rooms, protective equipment, to name just a few, will
be required.  Operational costs alone are more than three times the OSHA
estimates.  

		The total capital investment required for Acme's 16 operating plants
to attempt to meet these proposed exposure levels would amount to some
$5.565 million, on average $347,812 per plant.  The annualized
additional operating cost to meet the ancillary requirements of the rule
equates to some $2.025 million a year, with an average of $126,593 per
year per plant. 

		We request, respectfully, that OSHA acknowledge this and acknowledge
that the compliance with the proposed revisions of the silica exposure
level be seen as not economically feasible for the clay brick industry. 
Mr. Latham will address this as well.

		So, in conclusion, Acme Brick strongly believes that the current OSHA
PEL for crystalline silica at 100 µg/m3 is amply protective of its
manufacturing workers and should not be reduced.  Acme Brick is very
likely to have to face the prospect of its associates having to be
subjected to unsafe, life-threatening work conditions in order to meet
the ancillary requirements of the rule.  

		So with these comments, Your Honor, I'll pass it over to Mr. Tom
Brown, Director of Safety for Acme.

		MR. BROWN:  Thank you, Garth.  I'd like to make a few points on our
program and how successful it is under the current standard and
protecting our associates.  

		Our brick and block facilities are extremely labor intensive.  And we
have developed a world-class safety program to address the silica
issues.  They take -- all of our associates and all of our teams take
pride in providing input to help reduce all exposures.  We basically
have a team effort at all levels.

		We, at Acme Brick, developed an effective silica action plan to ensure
our associates' exposure to respirable silica is minimum.  Our program
focuses on identifying potential silica exposures through sampling of
all of our positions, whether they are -- we did that, developed it, and
there was numerous positions that we went through.  And in our program,
we have to pass three tests, separate tests, at least seven days apart,
as the standard states, to reach a level that we can go ahead and
determine is a safe level.

		By doing this, we are on an annual basis, we continue a round-robin
again on all those positions.  So we have a very proactive approach to
safety and health with our associates, because they are our greatest
asset, and that is our cultural beliefs is building our safety program.

		In as far as addressing issues, if we were to determine we have a
potential exposure or an exposure, we activate basically our EH&S
specialists, our engineering team, our regional production management,
and our associates, and we develop as a team solutions to these issues
to bring that level back down to an acceptable exposure.  We immediately
implement our respiratory protection plan to protect our associates,
which includes medical monitoring through PFTs, fit testing, education,
and training.

		The majority of our cases require a series of complex solutions,
because no one solution is a fix.  And how we do that?  Basically, we
develop solutions through engineering, containment, suppression,
collection, ventilation, best management practices, education, and
training.  This was what separates us from everyone else as far as our
program because we are that committed to having a safe and healthy work
environment.  

		Now, looking at this current standard, we are able to meet this
standard with the 100 µg/m3, but we still struggle in some of our
positions to obtain that.  We are still working on it.  We have been in
this struggle for over 18 years and developing all kinds of special
solutions for each one of our processes.  So we feel we are the leader
in the brick industry in those solutions.  We work diligently together,
again, to improve the health and safety of our associates and do the
right thing.  That's what it's all about is doing the right thing.

		We have had experience with OSHA in some of our inspections, and they
have been very complimentary of our program and asked us that we should
definitely be a part of the BPP program.  We feel with all of these
commitments that we have from our CEO all the way through our ranks,
everyone is important, and we definitely feel we can achieve the current
standard.  

		But with the new standard, how it is going to impact us, we are
looking at a 50 µg/m3, and with an action level of 25, which is similar
to our program but we use 50 for an action level.  The reason why we do
that is because we want to achieve the 100 µg/m3.  And that is just
part of industrial hygiene best management practices.  

		So in looking at that, currently looking at all of our data, looking
at what we have done over 18 years, it is going to put our industry and
our plants all in, as far as in a permanent noncompliant status because
we feel we cannot achieve the proposed standard in an economic, feasible
way and be able to operate with our current program.

		Taking a look at our current sample data, our technology and the
thousands and thousands of dollars that we have put into our program, we
have been able to achieve the 100.  But we also have other issues that
we would like to address and make you aware of.

		We are in a region in the southwest where temperatures are excess of
100 degrees.  And being a very intensive -- labor intensive business,
for us to meet the proposed standard by putting Tyvek suits or
protective clothing onto our employees in 110, 115 degrees would be in
direct conflict with our heat stress program, because we have to
implement cool-down periods, and we have to implement different things
to address heat stress.  

		With the proposed standard, we have to look at what are we going to do
when we have to put these people on -- when they want to go on break. 
Are we going to have to completely take all the clothes, bag them, have
them shower, and re-enter the workforce with brand new clothing?  They
get three breaks during those times plus a lunch period.  If they leave
the plant, how are we addressing all these things?  Those rules that are
being proposed is going to put really -- as far as the stress on both
our associates and us as far as trying to efficiently operate and
protect our people.

		The other thing is how does OSHA feel we could go ahead and address
these crossover standards like heat stress and other things that we
implement that is in direct conflict with this standard as far as the
proposed ancillary regulations.  So I don't know if you all have ever
worn a respirator in 115 degrees, but it's pretty tough.  And we
wouldn't want to do that because that's a life-threatening situation,
and we deal with it six months out of the year.

		The other thing we deal with is we have dust storm in West Texas.  We
had one in Lubbock the other day, zero visibility.  How do we address
preventing an overexposure of 50 µg/m3 when the background is over the
current PEL just from Mother Nature?  This is going to be a real tough
situation to deal with in real life.  These are real life situations. 
That's why I am trying to make it clear to you all that it's very
important that we study this and make sure that we can abide by the
current standard, because all of our data shows that we are protecting
our employees.

		In conclusion, I'll reiterate that the new proposed standard is
definitely going to put us in a continuous noncompliant state, and
that's where we are going to have to implement the PPE standard on a
continuous basis in all of our positions with protective clothing.  That
is just unacceptable, and we just can't operate.  When it comes to
eliminating hazards, PPE, as you all know, is the last resort, not the
first.  And current technology just does not allow us to feasibly
operate and fix these issues.

		With that, I would like to turn this over to Bill Latham.

		MR. LATHAM:  Your Honor, thank you for this opportunity to present
this evidence to the panel and to the peers.  As you know, I am General
Counsel and Risk Manager.  As part of that, I deal with insurance
purchasing and obtaining that insurance, as well as all the risk
management programs which dovetail into the safety, which is obviously
directed by Mr. Brown.

		But my particular comments are going to deal with the particulars of
the statute which authorize OSHA to regulate or really, in this
situation, add to or change the regulations.  And I know I'm preaching
to the choir and you know what these are, but just for purposes of
addressing them with the facts that Acme currently faces, I wanted to
readdress them.

		First, obviously, your initial mandate is to exercise your regulatory
powers only when there is a reasonable necessity and appropriate to
provide safe and healthful places of employment.  With regard to
specifically dealing with silica or what you consider to be hazardous
agents or hazardous physical agents, there is an additional limitation
which requires you to only deal with circumstances that show the
standards would prevent employees from suffering a material impairment
of health or functional capacity that is technologically and
economically feasible.  

		When you put these two together, the courts have said that you can
only deal with situations which cause a serious problem and that which,
excuse me, are not safe, which is the meaning of that has been given
that it's a significant risk present that can be eliminated or lessened
by changing a practice.  Okay.  So what I'd like to present to you today
and show you some facts from Acme, and our testimony today is only about
Acme and our different industries that we are involved in, one being
particularly the brick industry, but also the concrete block business
and some other ancillary, the natural stone, we cut and fabricate
natural stone, as well as some of the tile.  We don't manufacture it,
but we sell it and deal with it.

		But the four points I'd like to make in this is Acme's workers do not
face a significant risk of harm.  Two, any risk that Acme's associates
may face will not be eliminated or lessened by any additional
regulations.  Three, the elimination of the risk of respirable silica is
neither economically or feasibly -- or technologically feasible.  And,
finally, OSHA's estimates of implementation costs are underestimated.  

		So, first, turning to the first situation of OSHA is authorized to
further require respirable silica, there must be a showing of
significant risk.  As you heard Mr. Glenn and also Dr. Tayler, there
is no question that there is silica in the manufacturing of brick and in
the manufacturing of concrete block.

		Those exposures are at every one of those facilities.  But despite
those exposure levels, Acme has not experienced a single case of
silicosis or even a significant silica-related injury or illnesses. 
That is very significant.  Acme has been around for 122 years.  And
truthfully, anecdotally, the history prior to about 25 years ago is just
from communications with people who have been in our industry a long
time.  

		I have personally reviewed claims records for the past 25 years. 
Based on that review, there has only been three claims that even had a
statement of silica or lung exposures or anything related to that
category.  We use broad kinds of search protocol in order to find
something that might be related to silica.  

		Of those three claims, none indicated a diagnosis of silicosis.  They
didn't even -- they may have used the word "silica" in their statement,
but there was no issue of any illness that was seen to arise out of that
silica.  In fact, there is no deaths, no evidence of cancer, no evidence
of even a prolonged treatment.  In fact, if you look at those three
claims, the maximum medical spent on those claims was $500.  That is
insignificant when you look at examples of silicosis.

		And we are looking at, at our peak, 3,000 employees, and that would be
back in the '05, '06 time frame.  That is over 3 million worker days of
exposures of the silica we've talked about without any of these
significant illnesses.  Even today, with just the 2,200 employees we
have, we are only talking about a little over 2 million worker days
without any silicas.  That is just not a significant risk that Acme has
faced over these years.

		Turning to the second point of OSHA's mandate, there is no reason to
believe any risk of respirable silica exposure can be eliminated or
lessened by a change in the PEL or additional regulations.  That, simply
said, if you don't have any silica exposure today, what else can you do
to decrease that?  And it is pretty simple, we have significant
exposures for some silica, but the technological aspects that were
discussed by Mr. Glenn, as well as Dr. Tayler -- for whatever reason,
and I am no scientist, I'm not here to be a scientist -- but those
indicate no issues of silica or silicosis and silica-related injuries.

		This leads to the third part of the mandate, which is eliminating the
risk of respirable silica must be economically and technologically
feasible.  This is a question that I do have some testimony that I think
I can provide that will be really important for you to consider.

		OSHA's averaged cost of the big brick plant in your preambles
indicates $38,422 of an annual expenditure for the brick plant.  You
also have some analysis of initial cost of about $750 million per brick
plant -- excuse me, I apologize, $750,000 per brick plant for the
improvement to meet these qualifications.

		You have already heard from Dr. Tayler that our estimated cost was
$126,000 per year, per the 16 brick plants that we have.  An additional
$350,000 for the brick plants, the 16 that are still in operation for
capital costs.  In those particular plants, we have already expended
substantial amounts in excess of what we are already talking about just
to meet the additional rules.  As Mr. Brown talked about, we have been
able to meet the 100 PEL that we are required to by law now.  We are
meeting that, but we expended a lot of money to do that.

		Dr. Tayler, in his written remarks, indicates basically a plant that
needs to be basically start from finish to meet these PEL would cost
almost $900,000 in capital expenses, plus an additional $412,000 in
annual operating expenses.

		JUDGE SOLOMON:  You are right at the 30 minutes.

		MR. LATHAM:  All right.  I am very close to being completed.  If you
--

		JUDGE SOLOMON:  Sure.

		MR. LATHAM:  Would it be all right if I continue?

		JUDGE SOLOMON:  Sure.

		MR. LATHAM:  Thank you.  That leaves in the first year, we're talking
at an expenditure of well over $7 million in both capital and operating
costs.  Those amounts are significant for any business and especially
Acme in this situation.  The smaller businesses, which we don't propose
that we are, face those same kinds of numbers, but maybe not as many
plants.

		I'd like to really address really quickly the use of the 2000 and 2006
numbers.  It is very significant to understand that the brick industry,
during 2006, was the highest profitability of any brick industry in
decades.  In fact, for Acme, 2006 was the highest earnings ever made by
the company.  Obviously, since then, the market and the construction
industry have crashed.  And the economic impact of the recession has
been significant.  In fact, we have seen a 40 percent decrease in our
revenues as a result of that.  

		And, more significantly, we have seen a 100 percent decrease in
profits.  And you'd ask how that is possible, but it is possible because
those other nine plants that are sitting there idle still have costs
which have to be covered while they are not operating.  So I know during
the question and answer periods on the webinar by OSHA indicated that,
well, you just raise your prices.  Well, since the 2006 time period,
Acme's prices have decreased 13 percent.  That's our price.  And the
demand for product at this point is still at a lower level despite the
improvements in the economy.

		The construction business is still suffering and is still not going
into full blow.  And so because of that, it's not just a matter of,
okay, we'll go raise our prices.  That's not possible.  So to reach
those levels are really not able to do that.

		Could I just conclude with the recommendations that we'd like to make?

		JUDGE SOLOMON:  Okay.

		MR. LATHAM:  You've heard all of our testimonies and the points that
we've made.  It is Acme's position that it has been a leader in the
industry, in our opinion.  We have done the right thing for OSHA.  And
with that, we have met the current 100 PEL following those requirements.
 To do that, we have had to use lots of different things.  We've tried
and failed, tried and failed, but some things have been successful.  So
we believe that the current PEL and the current regulations are
sufficient for us to meet the safety of our employees, which have been
no issues of silica.  

		In the alternative -- and so, therefore, we would ask that OSHA
reconsider its new proposals and keep the current regulations as they
are.  In the alternative, as I think you've heard from Mr. Glenn, from
Dr. Tayler, and from the testimony from the brick industry, at least
the brick industry ought to be excluded.  The concrete business ought to
be excluded because we do not have any evidence of a significant risk. 
Thank you.

		JUDGE SOLOMON:  Okay.  Just to get some idea, are there any of the
peers, the peer reviewers that have questions?  There are hands already
going up from the public.  Would the public questioners come to the
microphone?  Okay, apparently, we have one questioner, and it is going
to take a while for him to get there.  

		While he is doing that, we have had a controversy over whether we
should consolidate the rest of the witnesses and have one question
period for all of the rest of the witnesses.  One of the witnesses,
Dr. Sokas, is teaching a class and I don't think she -- I don't want to
make an exception for her, but she would have a tough time, I guess,
getting here.  But it could very well be that we could have all of the
remaining speakers come forward so we don't have to waste any time
between speakers, and then have one question and answer period.

		MS. KRAMER:  I think we would probably want to divide the -- I think
it's eight remaining witnesses into possibly two groups.  Is that right,
David?

		MR. O'CONNOR:  Yes, I think at least two groups would be appropriate.

		JUDGE SOLOMON:  Okay.  Well, after this questioning, you're going to
explain that to me.

		MS. KRAMER:  Sure.

		JUDGE SOLOMON:  And we'll straighten that out.  Okay, would you state
your name and please spell your last name?

		DR. MIRER:  My name is Franklin Mirer, M-i-r-e-r, from CUNY School of
Public Health.  And I am scheduled to be a witness later.

		JUDGE SOLOMON:  Right.

		DR. MIRER:  So, first of all, thank you very much for coming and
presenting the information you did.  From your testimony, it is clear
that you collect a lot of air samples in your facility.  Can you say
what arrangements you make to do, to collect those air samples?  Are
they done by plant personnel or external consultants or what?

		MR. LATHAM:  Dr. Tayler, why don't you address that?

		MR. TAYLER:  The silica action program that we conduct, we have a
schedule of sampling programs at each facility.  And we have -- our
organization structure consists of Mr. Tom Brown as the director, and
we have what we call regional coordinators in all of the areas that we
have.  We have four regions.  Each one of these regional coordinators is
certified and trained in the use of these pumps following the OSHA
protocol, and they conduct the testing in the plants on a scheduled
basis.

		Based on the results we get, we have categorized into three
categories, a maintenance category, an action limit category, and an
exceedance category.  And from that we generate the corrective action
plans.

		DR. MIRER:  Okay.  And could you tell me what are the lowest exposure
levels that are reported back to you in this scheme?

		MR. TAYLER:  Some of the very low ones are in areas where the exposure
levels are fairly low, and they can be as low as a point --

		MR. LATHAM:  Non-detectable. 

		MR. TAYLER:  Non-detectable, yeah.

		DR. MIRER:  Well, what is the lowest that is detectable that's
reported in micrograms?

		MR. BROWN:  Around, let's see, consistently a .28.

		DR. MIRER:  .28 µg?

		MR. BROWN:  Um-hum.

		DR. MIRER:  Okay.  Could you describe your medical surveillance
program?

		MR. LATHAM:  Tom?

		MR. BROWN:  Okay.  Our medical surveillance program consists of we do
chest x-rays on pre-employment, and then we, once we implement our
action plan, we have a voluntary program for respirators, and that's
part of subpart D.  And what that does is it allows our associates to
wear respirators without being under any standard.  

		Then once we receive an action level or above limit, they immediately
are put into respirators.  And all of the people in those positions are
PFT'd, which is a pulmonary function test.  We fit test them.  And that
basically is fit testing them with a respirator to make sure that they
know how to don the respirator and get the best protection.  Our medical
monitoring as far as the -- that's about where we stop with our medical
monitoring.

		DR. MIRER:  So no regular chest x-ray?

		MR. BROWN:  No, we do not do --

		DR. MIRER:  No periodic chest x-ray?

		MR. BROWN:  No.

		DR. MIRER:  No periodic PFT, pulmonary function test?

		MR. BROWN:  Annually we do PFTs.

		DR. MIRER:  Okay.  Could you describe your training program for silica
hazards for your employees?

		MR. BROWN:  Okay.  We have a pretty extensive program.  We have every
month the silica day.  Basically, it's a silica emphasis day.  It's not
just silica.  And that came from the OSHA program.  And we implement
that and we go through our plants, we identify any possible hazards that
we might see such as leakage or things of that from conveyors to we have
a continuous auditing program in that respect.  

		We also have basically classroom training and we have training
pertaining to silicosis, and we explain to them what the hazards of
silica overexposure is.  When we go through our sampling, if there is an
exposure in the action limit or above, we explain to them why they have
to go onto respirators, why they have to basically go to this standard
to protect themselves.

		DR. MIRER:  So would you recommend to OSHA that those elements of the
training program go into the standard?

		MR. BROWN:  I think definitely they should --

		DR. MIRER:  I mean informing people of what their exposure level is --

		MR. BROWN:  I think they --

		DR. MIRER:  -- specific things they have to do to protect themselves?

		MR. BROWN:  Well, I think OSHA has addressed that in the protocols. 
In their silica emphasis program, under industrial hygiene sampling best
practices, you have to -- you've got 15 days to explain to those people
what their exposure is.  So we go to the extra limit through the
training and education of silica.

		DR. MIRER:  Okay.  The last question I think is, well, two last
questions.  One is have you looked at the exposure data in the OSHA PEA,
and do you think that that reflects what exposures are in your facility?

		MR. BROWN:  No.

		DR. MIRER:  You haven't looked at it --

		MR. BROWN:  I have not looked at it.

		DR. MIRER:  Okay.  And are you aware of any summary of distribution of
exposures industrywide in the brick industry, other than the OSHA PEA?

		MR. BROWN:  In the BIA, we have done certain studies in conjunction
with NIOSH in the past.

		DR. MIRER:  Are those in the record here, or could you provide them to
the record?

		MR. BROWN:  Yes.

		MR. LATHAM:  We provided those to BIA.  They would have that and
they'll -- I think they're going to testify in a couple of weeks.

		DR. MIRER:  Okay.  Thank you for your time.  Thanks very much for
putting up with my extra questions.

		JUDGE SOLOMON:  Thank you.  Ms. Ryder?

		MS. RYDER:  Sure.  OSHA has some questions.

		MR. O'CONNOR:  Thank you, Your Honor.  And thank you, Mr. Brown,
Mr. Latham, and Dr. Tayler.  I'll turn it over to Bob Burt.

		MR. BURT:  Hi, several questions.  I want to start just to be sure I
understand the size of the company.  You mentioned at the present time
you have a total of employees of 2,222; 1,306 are production associates.
 A production associate is what someone else might call a production
employee, roughly?

		MR. LATHAM:  Yes.

		MR. BURT:  Okay.  And you have 16 operating facilities now?

		MR. LATHAM:  Sixteen operating brick plants.

		MR. BURT:  Brick.

		MR. LATHAM:  We also have six operating --

		MR. TAYLER:  Concrete block.

		MR. LATHAM:  Concrete block plants.  And we have one limestone
facility that fabricates limestone.

		MR. BURT:  But the cost estimates you provide are devoted to the brick
plants; is that correct?

		MR. TAYLER:  Yes.

		MR. LATHAM:  Yes, which are much larger than our concrete block
plants.

		MR. BURT:  Oh, thank you.  Now, you provided in your testimony of
January -- in your letter of January 24th, a very helpful cost table and
some cost estimates.  I'd like to ask some questions to assure that we
can make best use of the data you provided.

		Now, this first table, is that for a specific plant?  In other words,
you have a table and then you have some aggregate estimates.  Is the
table for one specific plant?

		MR. LATHAM:  Are you looking on Page 4?

		MR. BURT:  Yes.

		MR. LATHAM:  Dr. Tayler's --

		MR. BURT:  Yeah.

		MR. TAYLER:  Yes.  You can notice that what I have said here is a
typical shale brick plant, and those numbers relate to that, to a
typical plant.

		MR. BURT:  Okay.  Now, for this typical plant, roughly how many
employees would you say that this plant had or production associates,
whatever you --

		MR. TAYLER:  In total, yeah, total production associates in the plant
of this nature would be approximately 60.

		MR. BURT:  I'm sorry?

		MR. TAYLER:  Sixty.

		MR. BURT:  Sixty?

		MR. TAYLER:  Um-hum.

		MR. BURT:  Okay.  And most of these people are currently controlled --
these people are largely controlled to 100 now, that's our starting
point, of your analysis --

		MR. TAYLER:  Yeah.

		MR. BURT:  -- is that correct?  Now, just to see where we are getting
to, what percentage of these people would you say were currently over
50, the OSHA PEL?  Any idea?  You said you also use it as your action
level.

		MR. TAYLER:  Yeah, you mean the percentage of people that would be
exposed?

		MR. BURT:  Are currently exposed above 50, if you have any idea?  It
would help to interpret how this fits with other things.

		MR. TAYLER:  Of the 60 associates.

		MR. BURT:  If you can add that in a post-hearing comment, it would be
very helpful.

		MR. LATHAM:  Well, it depends -- we can answer that question.  It
depends on the particulars of that day that the testing was, you know. 
We have the backgrounds of higher levels in a West Texas, you know,
which includes Fort Worth, which is where the plant is that's being
referenced in that.

		MR. BURT:  Any detail you can provide on monitoring data, including
the variance, would be very helpful.  I doubt that there are many people
who have as much monitoring data as you seem to have, and it would be
very useful for us to look at that.

		Now, I notice that when you say this is a typical plant, at the same
time when you get the aggregate cost, you don't simply multiply these
costs by say 16 or do you -- no, you don't.  So, in other words, there
is some adjustment for different sizes of different plants in making the
aggregate estimate?

		MR. TAYLER:  Um-hum.

		MR. BURT:  Okay.  Anything that could show us just how we could
reproduce that calculation would be helpful.  Now, the specific costs,
control room improved air filtration, what does that refer to exactly?

		MR. TAYLER:  Control room improved air filtration would involve, well,
let me explain, in a typical brick plant, you would have a grinding
facility.  And in that grinding facility, you would have a control room
that would house the main control, electrical control circuits, and also
the various switch gear for operating the plant.  The operator would be
in and out of that control room.

		MR. BURT:  Okay.  And that's an operating cost per year at that plant?

		MR. TAYLER:  Yes.  Yes.

		MR. BURT:  And fuel and electrical energy, that is for the ventilation
systems, make up air and anything else?

		MR. TAYLER:  Yeah.  It'll be electrical energy for the equipment
operating, and the fuel would be for motorized devices for sweeping and
--

		MR. LATHAM:  Scrubbing.

		MR. BURT:  And what is the labor cost for it?

		MR. TAYLER:  The labor would be involved in the maintenance of the
equipment.  

		MR. BURT:  So that's in addition to the cost listed above for
maintenance?

		MR. TAYLER:  Yes.

		MR. BURT:  And do you have an estimate of how many people will be
needing, as a basis for the medical surveillance and respiratory
protection equipment estimates, do you have any estimates of how many
people will be needing, newly needing respirators or medical
surveillance as part of how you developed this cost?

		MR. TAYLER:  The numbers that we have in the existing arrangement is
what we have used.

		MR. BURT:  Okay.  So this is your existing program?

		MR. TAYLER:  Yeah.

		MR. BURT:  Testing -- go ahead, sorry.

		MR. LATHAM:  Uses the existing program, but it would anticipate an
increase in the number of people.  If you lower that to a 50 µg, then
it would obviously increase the number based on historical data.

		MR. BURT:  Right.  And that was what I was asking was how much, how
many people would need the -- testing equipment refers to?

		MR. BROWN:  It's dealing with the industrial hygiene sample.

		MR. BURT:  So it's, yeah, the sampling equipment.  And testing
personnel is?

		MR. BROWN:  That is the daily sample.

		MR. BURT:  The person who is taking -- this cost is the person who is
taking the sample?

		MR. BROWN:  Sampling, right.

		MR. BURT:  Okay.  And that analysis is reporting his lab and --

		MR. BROWN:  Um-hum.

		MR. BURT:  Okay.  Sorry, we just use slightly different nomenclatures,
and I want to be sure I can map everything together.  Now, you mentioned
you have 16 plants.  Just out of curiosity, why would you not have just
one or two very large plants, given the nature of the industry?  I just
want to understand how it works?

		MR. TAYLER:  The nature of the brick industry is that you would always
want to have your facility within striking distance of the market.  So
over the years, Acme Brick has positioned the plants closer to the
market areas.  And these plants range from '60s vintage plants to more
recently built plants.  It's an inherent structure which Acme Brick has
had in place for many, many years.

		MR. BURT:  Is there any significant foreign competition in the brick
business?

		MR. TAYLER:  No.

		MR. LATHAM:  Hard to get that across the ocean economically.

		MR. BURT:  I was hoping that was the case, but I didn't want to -- I
have been occasionally surprised about that issue.

		MR. LATHAM:  Production costs really are about a third of the cost of
the brick when we have them close.  But when you're, you know, farther
away, it is -- there are some distinctions in the quality or the makeup
of a brick.  Some clays are different.  And I'm talking -- I'm giving
his testimony because I don't really know all that as much as --

		MR. BURT:  Now, you talk about the limited number of worker -- well,
let me ask, before I ask that, what kind of tenure do you have for your
employees?  Do you have people who have been there 5, 10, or 20 years,
or hard to say, or what would --

		MR. TAYLER:  We don't have the number handy, I mean, but --

		MR. BURT:  Sure.

		MR. TAYLER:  -- we have a great deal of employees that have been there
for 10, 20 years, you know.

		MR. LATHAM:  I've been employed at Acme for about almost 10 years, and
I'm a rookie.

		MR. BURT:  Okay. 

		MR. LATHAM:  I have been to more 50-year employee things than I can
count on both hands.  The normal tenure is, and I can't give you
specific, this is anecdotal only, but really 20- and 30-year employees. 
And in that vein, that's why the significance of the workers' comp
claims is important because these workers had been employed prior to the
2000 -- '80s that this thing started, 20, 30 years, so it is
significant.  And part of the reason for that is just the location of
our plants.  They're out in the sticks a lot of times.  And so those
employees work in that plant their entire life.  And so it is
significant that the employees are long-time employees.

		MR. BURT:  Okay.  Well, that covers my questions.  But I did want to
thank you for coming here today and also the effort you put into the
cost estimates that you gave us.  As I said, any additional
documentation that could help us be sure we understand would be very
helpful.  Thank you.

		JUDGE SOLOMON:  Any additional questions?

		MR. O'CONNOR:  Yes, Patti Downs has some questions.

		MS. DOWNS:  Thank you.  I just wanted to go back to the first topic
you discussed, the raw materials you use in your bricks.  What all do
you use in addition to the clay?  You said you make a whole slew of
items from concrete block to --

		MR. TAYLER:  You mean in addition to clay brick in the company?

		MS. DOWNS:  Yeah.

		MR. TAYLER:  Concrete block, which is an aggregate and cement mixture
made into a block.  We have a quarrying operation where we do engineered
limestone, where we cut limestone for commercial work.  And we have a
company that does glass finishes on aluminum frame, glass finishes and
the grid systems.  And then as we mentioned, we have a network of sales
outlets where we retail tile and pavers and various ceramic products.

		MS. DOWNS:  Okay.  But with the concrete -- I'm sorry, clay brick, the
silica is always naturally occurring?  You don't ever add silica to
that, correct?

		MR. TAYLER:  Most of the time, the clay has a certain amount of silica
in it, which we then monitor and control in the way we mine the clays,
because the silica is a valuable aspect to the ceramics of the body to
reduce shrinkage.  So we control that in the way we recover the clay.

		MR. LATHAM:  In other words, if it's got too much clay in it, we don't
use it.  It doesn't make a good brick.

		MR. TAYLER:  Too much silica.

		MR. LATHAM:  I mean silica, not too much clay.

		MS. DOWNS:  Okay, I'm going to come back to that, but I have another
question for you then.  So when you are making the bricks or the blocks,
do you ever produce anything that has a textured surface, or are they
all smooth sided?

		MR. TAYLER:  Well, when you make a clay brick, texture is a very
important part of the aesthetics of the product.  And we do that on the
brick machine.  What happens is there is an extrusion process, and we
have various techniques to produce texture on the surface while it is in
the plastic state.  And from there it gets cut and dried and fired, so
the finish product is already -- is fired rigid with the texture in it.

		MS. DOWNS:  Okay.  So you don't ever have to use any sort of abrasive
blasting or grinding to get that finished?

		MR. TAYLER:  No.

		MS. DOWNS:  Okay.  So back to the percentage of quartz you said is
typical in the block.  I think in your written testimony, I read that it
was 10 to 30 percent.  You said that's pretty average?

		MR. TAYLER:  That's pretty much, yeah.

		MS. DOWNS:  Some of the information I have read in other comments
indicates that there may be a higher percentage.  I'm wondering what is
the highest percentage you would ever produce on request?

		MR. TAYLER:  It's possible to be as high as 40 percent, could be as
high as 40 percent in that.  But you start moving into an area where the
material becomes very brittle and porous.  To meet the ASTM standard for
clay brick, you have to meet certain porosity levels and strength
levels.  So as the silica increases in the body in the form of free
quartz, the strength of that clay body starts declining, porosity goes
up, and it becomes less durable and less desirable.  So that's why I
mentioned the maximum of about 30 is what you normally would find for a
good quality product.

		MS. DOWNS:  Is the same true for a concrete block?

		MR. TAYLER:  Well, that's a totally different situation, because
you're talking about a composite aggregate with a cement addition, so
that's a different situation.

		MS. DOWNS:  You had mentioned that you guys have a very extensive
program to keep your exposures down and that you have implemented a lot
of controls, and you have work practices in place, but that you guys
have found it difficult, if not impossible, in some locations to meet
the current PEL.  I'm wondering what some of the areas or tasks
associated with those higher exposures are, what you have done to reduce
those exposures, and maybe what some of the big obstacles or
difficulties have been in implementing those and getting those numbers
down.

		MR. TAYLER:  Yeah, the difficulties we see are more prevalent with the
shale plants.  Because of the nature of the shale, it's a very platy
material, and through the pulverizing process and the screening and in
the dry grinding process, they become -- the dust alone is quite high in
spite of having a lot of very extensive dust collection.  It's the
material sticks to the conveyor belts, and it is a difficult material to
work with.

		So our protocols when we are dealing with this type of material is to
work hard with the control room situation, to make sure that it is
properly detailed and to minimize exposure, and our associate that works
in that area is controlling that plant from within that control room, so
he is not exposed as much as he should be.

		Most of the time when we have to deal with working in the plant, we
try to deal and do the work in the plant when the plant is shut down. 
We know that silica takes a long time to settle, so we normally don't do
any cleanup or anything until way after the shift is completed.  This
has become part of our best practices.

		MS. DOWNS:  So how often would you estimate that your operators spend
in the control booth versus out in the plant?

		MR. TAYLER:  I would say about half of his time.

		MS. DOWNS:  And then so you're also saying the higher exposures are
basically due to the inherent nature of the material and not because of
the effectiveness of the controls or whether or not they're working
properly?

		MR. TAYLER:  It's a very difficult thing.  With this particular plant,
we have extensive dust collection equipment.  We have state of the art
scraper technologies on all of the belts.  The belt speeds have been
modified to reduce the -- we know that belt speeds have a big impact on
dust.  And so it's a bit of each, you know.  It's the nature of the
material and also the limitations that we see using these various
technologies.

		MR. LATHAM:  A lot of it, too, is the environmental impact, I mean the
environment that we're in.

		MS. DOWNS:  Right.

		MR. LATHAM:  Especially, the West Texas models and --

		MR. TAYLER:  The dryness, yeah.

		MR. LATHAM:  The dryness.  Part of that deals with the clays,
themselves.

		MS. DOWNS:  Okay.  I want to change topics a little here.  You had
mentioned that you guys, you sample of all the positions three times, at
least seven days apart, every year to determine exposures.  Correct?

		MR. BROWN:  Correct.

		MS. DOWNS:  And then if you have anyone who is not in compliance with
the current PEL, you kind of convene a team to figure out what you can
do to reverse -- or to reduce those exposures.  How often do you have to
get that team together?  And I don't need an exact number; if you could
give me a guess, a percentage?

		MR. BROWN:  Well, in the infancy of the program, it was a continuous
situation.  Now that we have basically got things under control and the
majority of our positions to the current PEL, we, I would say probably
20 percent of the time that we have to implement that.

		MS. DOWNS:  And what are your usual conclusions.  Have you guys been
able to identify a trend between what's causing the overexposures?

		MR. BROWN:  Well, I can refer to Dr. Tayler on the percentages and
the variables as far as the material, because that has a great deal of
impact on that.  But as far as what we're seeing is --

		MS. DOWNS:  I'm just wondering like work processes or maybe
inefficient controls, or something that you have tweaked or changed. 
I'm assuming you can't really change the material too much.  There are
some guidelines --

		MR. BROWN:  No.  We've introduced fogging systems.  We've introduced
suppression surfactant.  We've looked at ventilation, which we have had
baghouses and Dust-Hogs, which are a smaller Torit unit, for each
position, and pulling different pickup points off of conveyors,
enclosures over the conveyors.  

		We've looked at settlement, actually weighed the material once it
settles out of the air to see how much we are -- basically how much is
in the air just from a weight standpoint.  That's all part of our note
taking when we do our samples.  We put belt scrapers on all of belts,
make sure those adjustments.  That's all part of our audit program of
our silica action plan.  And we also --

		MR. LATHAM:  The answer to your question is there are just so many
different things you have to do, depending on the circumstance --

		MR. BROWN:  Yeah.

		MR. LATHAM:  -- and everything that there isn't one thing.  You just
kind of have to play it by ear in business to try to --

		MR. BROWN:  Yeah.  And that's what I was going to make the point is
that when you have an issue, depending on what it is, you might end up
having to put an enclosure over this portion, a fogging system here,
ventilation at this end, because you can't just do one thing because
it's not going to fix the problem.  And that's why our engineering team
is a part of that.

		MS. DOWNS:  So this is my last question, I think.  I reserve the right
to change my mind.  So you had some concerns with putting your workers
in Tyvek clothing, you said, because of the contaminated clothing
provision.  What are some of the activities or job tasks that your
workers are doing that their clothing would get that dusty that would
require them to need to change clothes?

		MR. TAYLER:  The most exposure area is in the grinding plant, the
preparation of the raw material.  We also have exposures at the other
end of the process, which we refer to as the monorail, where the brick
move through a packaging station and there is a manual process where the
brick are handled.  That's the area that we really are concerned about
because of visibility.  

		The individual has to be able to see the brick, handle it, and make a
judgment call on the quality, and place the brick either in the rejected
conveyor or into the jig that will feed through to the packaging line. 
So there is a lot of physical.  These gentlemen handle six tons of
material, brick a day, so they are athletes in their own right, and they
have to have good visibility and good mobility. 

		And at those temperatures, even though we do ventilate the work areas,
it's very, very -- we're very fearful of putting them into that sort of
condition where they would have to work with a non-permeable type of
membrane around them, with a lot of sighting problems with doing the
job.  So there just doesn't seem to be a practical solution to the
problem.

		MS. DOWNS:  And just to clarify, so those are really job tasks and
positions where somebody has to be there during the entire operation,
correct?

		MR. TAYLER:  Yes.

		MR. BROWN:  The other thing I wanted to ask a question on was in the
sweeping process, under the current standard, that's what we do, we use
different types of material to like dust sweep and things of that
nature, like a red sawdust that we throw on the floor to make sure we
don't -- that's part of our best management practices.  Under the
proposed standards, sweeping is not allowed.  That's a real problem for
us, because does that mean we have to put in ventilation or central
vacuum systems?  There is a lot of things that we would have to take a
look at.

		Plus, we have huge concreted areas that we use mobilized sweepers. 
And they are not vacuum systems; they are sweepers.  So are those going
to be obsolete and we'll have to go to a different type of equipment? 
And that's a big expense.

		MS. DOWNS:  Do you have any sampling data that would show how much
respirable silica is being kicked up by sweeping or by using those
sweepers?  Have you guys ever looked into that?

		MR. BROWN:  Well, yes, we have.  They are part of the sampling.  But
during -- they're just like our mining equipment; they are all enclosed
cabs and air-conditioned.  So we make sure we have HEPA filters on all
of our filtering systems inside the cab to protect those associates.

		MS. DOWNS:  You don't have any area samples though of how much dust is
being suspended while you are sweeping or using those sweepers?

		MR. BROWN:  No.

		MR. LATHAM:  We just do it on the employees.

		MR. BROWN:  Yes.  That's first.

		MS. DOWNS:  And I think I'm done.  Thank you, gentlemen.

		MR. O'CONNOR:  I believe Mr. Burt has an additional question.

		MR. BURT:  Yeah, just one more question.  You mentioned concern about
the cost of clothing and changing clothing.  Did you include that in
your cost estimate?

		MR. TAYLER:  Yes.

		MR. BURT:  Where is that?

		MR. TAYLER:  That would be under the respiratory protection equipment.

		MR. BURT:  Sorry?

		MR. TAYLER:  The respiratory protection equipment, it would probably
be in there.

		MR. BURT:  Okay, thank you.

		JUDGE SOLOMON:  Anything else?

		MR. O'CONNOR:  Yes.  Dr. Tayler, in your written comments, you
indicated that respiratory protection, when introduced, has resulted in
unsafe working conditions for your associates.  Could you elaborate on
that?  I think you had mentioned heat stress.  Are there other factors
involved there as well?

		MR. TAYLER:  Yeah, as Mr. Brown said, there is a great deal of
labor-intensive activity handling the product at the end of the process.
 And the amount of heat stress that would develop from placing a person
in that type of protective suit would result in some serious health
problems for that person.

		MR. LATHAM:  I think it's health and safety, too.  The monorail system
is such that when you are in that type of a suit, you have the
respirator, you lose vision.  And it's a very quick process, and there
are brick coming from down that line.

		And you've got a line of about, you know, 4 to 10 people that are
involved in it.  There is more than one person, which you would likely
have, if you've got one of those people with exposures above the limits,
then all of those could have that, and their interacting could cause
safety issues with regard to that, too.

		MR. BROWN:  And also we have mandatory eye protection and hardhats
that they are wearing.  So under these Tyvek suits, they would be
wearing a hood, basically a full suit and booties, because they could
not get their shoes contaminated.  So you're putting them in, you know,
like a -- well, what do you call it --

		MR. TAYLER:  Clean room condition.

		MR. BROWN:  Clean room conditions, and we don't have air-conditioned
plants where they're going to be exposed to the elements, and we have --
we deal with heat stress, like I said, we have a very intensive program
to make sure that we've got liquids and Gatorade and cool-down periods
and constant monitoring through buddy systems to make sure these people
are, you know, not falling out, because when you get into those kind of
temperatures, your core temperature can go up fairly quick.  So we have
to ensure that they take in plenty of -- so they don't dehydrate.

		MR. O'CONNOR:  With regard to the use of respirators specifically and
the concerns about unsafe working conditions associated with them, have
you ever used powered air-purifying respirators?  And if so, have they
addressed your concerns with health and safety issues?

		MR. BROWN:  No, we have not used those.  And the reason why, it would
be almost virtually impossible to wear those type of respirators and
perform the tasks that they are doing.  Because you're looking at a
person, if they've got an air-purifying respirator, they're bending over
and pulling brick off of a keel car, and then stacking it.  So they're
constantly moving.  And you've got an air-purifying respirator on, and
you're looking at 12 people lined up about 2 feet apart all the way
down, so it's very difficult for them to wear something like that.

		MR. O'CONNOR:  Okay, thank you.  In Acme Brick's written comments, on
Page 3, there is a statement that in some cases the ambient air may
already contain levels of respirable crystalline silica higher than
allowed by existing OSHA regulations.  And I was wondering what the
basis for that statement was, whether you had any sampling data,
anything that you might be able to provide into the record?

		MR. LATHAM:  I don't think we have a -- we have not done a study. 
Actually, Mr. Brown has done personal observations and taken
measurements, but it was not part of a regular study at some of our West
Texas operations.

		MR. O'CONNOR:  All right, thank you.  I'll turn it over to Annette
Iannucci.

		MS. IANNUCCI:  Hi, good afternoon.  I just wanted to follow up on your
concerns about protective clothing and potential heat stress.  Now,
considering that for grossly contaminated clothing, the proposed
standard offers an option of any means to remove excessive silica dust
from contaminated clothing that minimizes employees' exposure, now would
this be an option for you, a means to clean off the dust from the
clothing?  And would that alleviate your concerns?

		MR. BROWN:  No, because it really depends on which part of the plant
they are coming from as far as what their tasks are and where they are
working.  For instance, we don't use compressed air or anything like
that to blow clothing off.  That's prohibited.  And a vacuum system, we
have tried that, and that's not effective.  It's just too difficult to
decon people with cotton clothing, for instance.  It just makes more
sense to go to disposable type material.

		MS. IANNUCCI:  Okay.  And then just one other quick question.  Do you
have any idea of the percentage of your workers who are using
respirators now?

		MR. TAYLER:  Not many.

		MR. LATHAM:  Very little.

		MR. BROWN:  I would say probably two percent.

		MS. IANNUCCI:  Two percent.

		MR. LATHAM:  We're able to meet the current PEL.

		MR. TAYLER:  Yeah, most of the times.

		MR. LATHAM:  Most of the time.  So they're usually not on a permanent
basis.  They're on --

		MR. BROWN:  No.  It's usually a hiccup in one of those three samples. 
And that's why we sample three times.  We want to make sure we get it
right and continuously provide a healthy work environment.  If we only
did one sample, you could go forever.  This way, that's our quality
control.

		MS. IANNUCCI:  Okay, great.  Thank you.

		JUDGE SOLOMON:  Anything further?

		MR. O'CONNOR:  Yes.  Anne Ryder has a few questions.

		MS. RYDER:  I just have a few questions.  I was wondering, you said
you have an action level of 50 right now.  How often are you able to
stay at that action level?

		MR. BROWN:  Most of our samples are between 50 and 1.

		MS. RYDER:  And 100 mgs?

		MR. BROWN:  And 100, yeah.

		MS. RYDER:  Okay.  And so I just wanted to clarify something you said
earlier.  Do you take remedial action when you are above the action
level or when you're getting results above the PEL?

		MR. TAYLER:  Once we hit the action level, our program dictates that
the manager and his team develop what they call a decap.  It's a plan to
address the problem.  And they would then consult with Mr. Brown and
the engineering team, and they get -- they would develop the best
possible solution, whether it be containment, ventilation, whatever. 
And that would be activated, enacted, and there would be an ongoing
program of testing until we move out of the action limit.

		MS. RYDER:  Until you're at the action level.

		MR. LATHAM:  And it's below 50 is the action provided, yeah.

		MR. BROWN:  No, but it's 50 is --

		MR. LATHAM:  You're at 50, it is?  Okay. 

		MR. BROWN:  Yeah, 50, and immediate respiratory protection.  And
that's why we do the annual PFTs with these potential areas that we
found those inconsistencies, like grinding area, that's typically the
area that we have issues, so because of the variables in the clay.

		MS. RYDER:  Okay.  So when you get results and you're a little above
50, and you have to bring in your team of experts to try to remedy the
situation, is that when you first try to implement some engineering
controls and then you -- are people going into respirators at that
point, too?

		MR. BROWN:  Yes, sir -- yes, ma'am.

		MS. RYDER:  No problem.  So there would be workers who are in
respirators who have exposure below 100?

		MR. BROWN:  That's correct.

		MS. RYDER:  Okay.  All right, and I guess how are you dealing with the
heat stress issues in that situation when your workers are in
respirators?

		MR. BROWN:  To be honest with you, it's a struggle.  What we have
issues with, like on the monorail, like I was telling you, when we have
to put those people on respirators, we have to come up with a solution
real quick because they cannot deal with that.  So --

		MR. TAYLER:  You need to clarify.  We have the N95 respirator, which
is small.

		MR. BROWN:  And I think the biggest thing we have is our
proactiveness, and the quick and the good engineering team that we have,
and our experience.  So we can look at that situation and where we have
improved things in the past, we can implement those things quickly and
then retest.  And where the time comes in is that we have to have three
tests to get to an okay level, basically, to clear them from
respirators.  And that takes three okays, not two okays and an action
level, for instance.  It has to be all consistent.  

		MR. LATHAM:  One thing, too, that's critical.  I mean we're testifying
here on behalf of Acme, but we are one of the largest brick companies. 
The other smaller brick companies don't have the engineering resources. 
They don't have the EH&S resources that we have.  It would be impossible
for them to move as quickly as we can.  And that's something to really
be considered by OSHA.

		MR. BROWN:  And our sampling drives our program.  So we make sure
that, you know, it implements an entire program of all kinds of things
that interact.  And we call it a close-the-loop program when we finish
correcting the problem.

		MS. RYDER:  Okay.  Did you say you do your sampling in-house?

		MR. BROWN:  Yes.

		MS. RYDER:  What type of cyclone are you using?

		MR. BROWN:  Ten mm with I think it's a -- what is it, 37 mm cassette.

		MS. RYDER:  Okay.  And when you get your -- you send out the result,
you send out the sample to a lab and you get the results, how confident
do you feel in the accuracy of those results?

		MR. BROWN:  We do periodic -- well, I do the periodic reviews of that
lab.  It's WOHL out of Wisconsin.  And the reason why we picked that lab
is because OSHA sends their overflow there.

		MS. RYDER:  Oh.

		MR. BROWN:  And so we want to be as accurate as we can.

		MS. RYDER:  Okay.

		MR. BROWN:  Unless you'll let us send it to Salt Lake City.

		MS. RYDER:  Salt Lake, I don't know.

		MR. LATHAM:  You know, one thing to do with that, even that lab at .25
is coming up with some non-detectable areas.  We get some at that level
that says non-detectable.

		MS. RYDER:  Okay.  Now, I think you referred to your silica action
program many times.  Is this a written program?  Is that what you
pointed to?

		MR. BROWN:  Well, that's part of it.

		MS. RYDER:  Is that part of it?

		MR. BROWN:  Yes, it is.

		MS. RYDER:  Is that program something that you could submit to the
record, if you haven't done so already?

		MR. LATHAM:  We'll have to consider that and talk to the guys that are
above all of us here.

		MS. RYDER:  Okay.  I think that's everything.

		MR. O'CONNOR:  Bill Perry has some additional questions.

		MR. PERRY:  Yes.  This is Bill Perry, thank you.  Just a couple of
clarifying questions.  I want to make sure we really understand.  So
when you say sometimes you get non-detects, do you mean at .025 mg or --

		MR. TAYLER:  Yes, sir.

		MR. PERRY:  Because earlier I heard a .25 µg.  Okay, so it's .25 mg.

		MR. TAYLER:  Milligrams, yeah.

		MR. LATHAM:  And blame me for those misstatements.

		MR. PERRY:  That's quite all right.  It's easy.  Okay.  Let's see, you
indicated earlier that about two percent of your associates wear
respiratory protection, but that most of your air samples that you have
taken, most of the time they are between 50 and 100 µg/m3, right?

		MR. TAYLER:  Yes.

		MR. PERRY:  But you have an action level of 50, which then triggers
respiratory protection, so that seems to be a contradiction.  Could you
clarify that for me?

		MR. BROWN:  You have a good point.

		MR. TAYLER:  It's a discipline, really, isn't it?

		MR. BROWN:  Yeah.  It's the majority is below 50.  I'll just state
that.  That was my mistake.

		MR. PERRY:  That's quite all right.  Thank you.  I think, oh, the
sampler, okay.  You said that you use a 10 mm cyclone.  Is it nylon,
aluminum, either?  Is it Dorr-Oliver, SKC?

		MR. BROWN:  We use MSA.

		MR. PERRY:  MSA samplers, okay.

		MR. BROWN:  And they are now -- I think it, what is it, it starts with
a Z.  It's a new company that took it over.  But we use -- they're
really durable.

		MR. PERRY:  Okay.

		MR. BROWN:  And they are calibrated with a primary calibrator
annually.  And we use field calibration.  So the field calibrators are
calibrated every six months.

		MR. PERRY:  Very good.  Okay, thank you very much.  Appreciate it.

		MR. O'CONNOR:  And I think that concludes our questioning.

		JUDGE SOLOMON:  Okay.  Do you have any exhibits, Mr. Latham, that you
were going to --

		MR. LATHAM:  We've submitted our written statements already, and we
didn't have any slides or anything.  But we'll look at what you've asked
and try to find answers to that.

		MS. KRAMER:  Okay.

		MR. LATHAM:  I hopefully made a list and we'll get back, well, we'll
find that.

		MS. KRAMER:  What you can do is you could send that back during the
post-hearing comment period.

		MR. TAYLER:  Yeah, we will give that to you post-hearing.

		JUDGE SOLOMON:  Thank you very much.  

		Ms. Ryder, do we want to talk on the record about how we're going to
proceed?  You said something about breaking it down into two panels. 
How do you want to do this?

		MS. RYDER:  We can go off the record and try to figure it out amongst
ourselves.

		JUDGE SOLOMON:  Okay.  Let's go off the record.

		(Off the record.)

		(On the record.)

		JUDGE SOLOMON:  -- the panel, in fact it is already formed of people,
and we'll just go down the panel, and each one of you will introduce
yourselves and state who you are representing, and then we will go from
there.  Go ahead.

		DR. FISCHMAN:  I am Dr. Michael Fischman.

		JUDGE SOLOMON:  Are you close to a microphone, Dr. Fischman?

		DR. FISCHMAN:  Maybe not, sorry.  I'm Dr. Michael Fischman.  I am an
occupational and environmental medicine physician and toxicologist from
the Bay area.  I am here on behalf of ACOEM, the American College of
Occupational and Environmental Medicine.  And, in addition, I am
clinical professor in occupational and environmental medicine at UC San
Francisco.  

		ACOEM, for those of you who don't know, is an organization of about
4,000 occupational physicians and other health professionals.  And our
primary mission is to protect employees and promote health among working
populations.  Did you want me to continue or --

		JUDGE SOLOMON:  No, just -- Dr. Cohen?

		DR. COHEN:  Hi, I am Robert Cohen.  I'm here representing the American
Thoracic Society.  I'm a pulmonary physician and I'm a clinical
professor at the University of Illinois in Chicago, in environmental,
occupational, and health sciences.

		DR. GUIDOTTI:  My name is Tee Guidotti.  I am a medical doctor
specializing in occupational medicine, and I'm a scientist in
occupational environment health.  I am here today representing the
Association of Occupational and Environmental Clinics, AOEC, which I
served as President in 2000.  AOEC was founded in 1987 to represent
primarily clinics and individuals.  And it has since grown to a network
of more than 60 clinics, most of which are at major universities and
training centers for occupational health.

		JUDGE SOLOMON:  And Dr. Sokas?

		DR. SOKAS:  I'm Dr. Rosemary Sokas.  I am an occupational physician. 
I chair the Department of Human Science at Georgetown University.  I am
here to represent the American Public Health Association.

		JUDGE SOLOMON:  Okay.  Each of you will get about 10 minutes. 
Dr. Fischman, you're up first.  Speak into the microphone.  Go ahead.

		DR. FISCHMAN:  Thank you for allowing me to come on behalf of ACOEM. 
I think the general focus of our comments is going to be different than
some of the recent ones that you've heard in that it is going to focus
on some of the medical surveillance aspects and related areas that we
find important to share our thoughts on.  

		First of all, we applaud OSHA's efforts here, renewed efforts to
revise the silica standard, and feel as if this is going to enhance
protection for workers and prevent disease in workers, that the reduced
permissible exposure limit will provide additional protection for
workers, although it will not necessarily be completely protective of
individuals who are exposed close to the permissible exposure limit for
a working lifetime, particularly in terms of the risk for lung cancer.

		We have some recommendations with regard to air sampling and exposure
assessment, but largely as it relates to our needs for information to
take good care of individuals involved.  When I say "our," that's
occupational physicians being able to do so, you know, wanting to ensure
that the sampling that is provided or submitted is representative of the
work activities in which folks are engaged, that they are an adequate
number of samples for determination of the sort of adequate statistical
basis to say that, indeed, the results suggest that levels are below a
certain level and adequate frequency of sampling, especially repeated
sampling, if their process changes.

		And I think most importantly that the information from that sampling
should be made available to the occupational physician or the clinician
who would be doing/conducting the medical surveillance.  They should be
provided with that information either for that individual or for
individuals that have similar exposure who have been monitored.

		The moving into the, well, one other area and I'll limit my comments
about endorsing some of the things that OSHA has indicated in the
standard, but we certainly support the use of alternative materials to
silica when that's feasible and when the toxicology and epidemiology
looking at those materials suggests that they are safe or safer than
silica.

		Moving on into the more specific area of medical surveillance, there
is a number of areas of comment.  We, our team, which consists of a
number of occupational physicians that put the comments together, the
comments then were subsequently reviewed by the ACOEM board.  We
strongly feel that the medical surveillance should be conducted at the
action level, rather than at the permissible exposure limit.  That
provides an additional element of protection for workers, especially if
there is variability in air concentrations present and if that --
sometimes, there may be cases where the air concentrations exceed the
action level or the permissible exposure limit, but they are not, the
person is not being monitored at that time.  So we support that the
trigger would be exposure at or above the action level of 25 µg/m3.

		In terms of the components of the exam, we strongly endorse the
requirement that there be a physical exam conducted by the clinician. 
In addition to the sort of value of the exam itself, it also provides an
occupational physician for a face-to-face interaction between the
employee individual and a clinician to talk about concerns or symptoms,
and other problems.  We support the non-mandatory Appendix A, the
medical surveillance guidelines, in that it provides clinicians, some of
whom may not be as sophisticated in terms of the health effects of
silica, with information that will help guide them in the conduct of the
medical surveillance.

		So then some specific components regarding the imaging procedures. 
OSHA had raised the question about whether or not CT scans or HRCT scans
should be used as sort of the initial screening medical evaluation for
workers.  And based upon our review of the literature and
recommendations from authoritative bodies, our recommendation is they
not be considered as equivalent diagnostic studies in medical
surveillance because the methods for evaluating the images and
determining whether or not there are potential problems on the images
are not so well developed for the CT scan as they are for plain x-ray,
chest x-ray films.  

		There are additional risks or radiation exposure potentially
associated with using the CT scan instead of the x-ray, so there are a
lot of issues there.  We recognize that in the case of individuals who
have abnormal chest x-rays, that there then may be a role for CT scans
in following up on those abnormalities, but not, at least at this point,
recommend it as being the initial imaging procedure.

		Obviously, we support the inclusion of spirometry and support the
inclusion of the baseline testing for latent tuberculosis infection, the
tuberculin skin test or equivalent test because of the increased risk
for tuberculosis among individuals with significant silica exposure.

		Generally, we feel comfortable with and support the recommendation for
the frequency of medical surveillance, but our group felt as if the --
that after the initial evaluation, that a limited surveillance exam be
performed at 18 months, not including the chest x-ray, but as a way of
confirming that individuals are not being massively exposed and
potentially developing more serious, acute forms of silicosis.

		And I think, lastly, we wanted to emphasize that medical surveillance
has more than one purpose, that it, you know, obviously can identify
abnormalities in individuals and allow a determination as to whether
they might be related to excessive silica exposures.  

		A maybe even more important function is that by looking at aggregate
information from those exams and having been reviewed by a qualified
individual with a background or an understanding of epidemiology and
toxicology and occupational medicine, that there is an opportunity to
ensure that the standard itself is adequately protective in that there
is not something that's being missed, problems in terms of the exposure
assessment in a particular worksite. 

		So it is sort of a -- that is, I think, an important role.  And we
actually suggest that for larger employers, that there be a formal
requirement that the aggregate results, the identified results be shared
with the appropriate expert to look for that on a periodic basis, in
addition to the individual assessment of the medical surveillance exam
and the communication of those findings to the worker.

		And I thank you for allowing us to come forward and present our
comments.

		JUDGE SOLOMON:  You can pass the microphone.  Dr. Cohen?

		DR. COHEN:  Thank you, Judge Solomon, and OSHA Panel and peer
reviewers.  I just want to say a quick word about the American Thoracic
Society and the committee that we had that reviewed this proposed rule. 
We are members of the environmental and occupational population health
assembly of the American Thoracic Society, or the ATS, which is an
organization of 15,000 clinician, researchers, educators, and public
health professionals who are dedicated to understand clinical and
scientific understanding of pulmonary disease and improving health
worldwide by advancing research, clinical care, and public health in
respiratory disease.

		Our particular assembly is focused on the contribution of
environmental or occupational factors to the burden of lung disease.

		I'd like to point out that our written comments were also sent out to
our sister professional organizations, and they were reviewed by them
and approved and co-signed by them, and that includes the American
College of Chest Physicians, which is also an international organization
of over 18,700 chest physicians, and the Association of Occupational and
Environmental Clinics, and Dr. Guidotti will speak about that
organization in a moment.  

		And also the Council of State and Territorial Epidemiologists, or
CSTE, and that's an organization that works to advance public health
policy in epidemiologic capacity, an organization of members states and
territories representing public health epidemiologists.  And our
comments were reviewed by that board representing all 50 states and
territories, and signed it as well.

		So we are societies that are deeply concerned with improving
occupational safety and health, and whose members really care for these
estimated 2.2 million workers who have been exposed to respirable silica
and, as a consequence, are at risk for silica-associated diseases.  And
we are here really as advocates for the health of our patients and have
a compelling interest in the policies and the rule that OSHA has
proposed.  

		We really strongly believe that the following three concepts pertain
to this.  One is that diseases related to the inhalation of respirable
silica are still occurring under the current standards.  We also believe
that these diseases are underdiagnosed and underreported, requiring
improved exposure monitoring to really characterize these populations
better, and medical surveillance to detect disease in the populations at
an early stage.  And we believe these diseases are entirely preventable.
 So those three things drive our approach to this.

		Therefore, we are really strong supporters of the OSHA proposed rule
and the reduced permissible exposure limit to 50 µg.  And we think that
will reduce and prevent hundreds of silica-related deaths and more than
thousands of new silica cases each year. 

		I'd like to say that during my 32 years of work at Cook County
Hospital in Chicago, I'm a practicing pulmonologist, we do see these
diseases.  They are not relics of the past.  We see patients who are
coming in from foundries, coming in from stonecutting operations, from
little construction jobs and sites, with silicosis, an aggressive
disease.  

		And I just want to share one case to humanize what we have been sort
of talking about statistically a lot today.  And that was a 39-year-old
landscaper who came to see me with symptoms of cough and shortness of
breath, and really gradually insidious but relentlessly progressive
symptoms.

		We saw him in the early 2000s.  And his chest radiograph showed
fibrotic scars throughout his lungs.  His CT scan showed some alveolar
fillings, air spaces filled with material.  I broncoscoped him, and we
got some kind of milky material and cruddy stuff out that turned out to
be proteinaceous material.  We sent it down to NIOSH, and they did
electronic microscopy, and it showed silicates.

		He had worked as a landscaper for 17 years in the Chicago area and
usually doing yard work.  But it turned out that when we took a real
occupational history, that he had been cutting porcelain brick and
specialized in paving designs, and was cutting this material without
respiratory protection and without -- actually dry-cutting it for at
least half the time, and only over a period of about three or four
years.  At any rate, we diagnosed him with silicosis and
silicoproteinosis.  We tried whole lung lavage on him.  He did not
really improve very much.  We sent him home on oxygen.  He passed away
just a few months later.

		So I'd like to say that we see these cases.  They are still occurring.
 Some of them are very severe.  We believe that they represent really
the tip of the iceberg.  And I think that the proposed rule which
includes provision for increased medical surveillance exams,
identification of hazards, and worker training would/could have
prevented these cases and will prevent cases in the future if they are
passed.

		The ATS really strongly agrees with OSHA's assessment that the
inhalation of respirable silica is strongly associated with disease in
humans and continues under the present standards.  We really believe
they have done a good literature review and that the exposure is related
to the adverse health outcomes that I mentioned.

		We also agree with OSHA's assessment of increased mortality and years
of life lost related to exposure to crystalline silica for both
malignant and nonmalignant respiratory disease at the current PEL of 100
µg.

		The data from the NIOSH work-related lung disease surveillance report
and others show a plateau in silicosis mortality since the 1990s, and we
are concerned that that has been the same without any further reduction
for more than 20 years.  So we think that we still have work to do.

		And I really want to emphasize and we feel very strongly about the
fact that these data are gross underestimates.  And given the long
latency period that we have talked about earlier today, our passive
reporting system where people -- we just wait for them to report it but
we are not actively searching out except for a few states that do active
surveillance.  It's sort of like when I was a medical intern, the lazy
interns had a saying that if you don't take a temperature, you won't
find a fever, so they won't have to go out there and do blood cultures
and work up the patient and take care of the patient.  And sometimes as
a society I feel that we are not taking a temperature at least in terms
of this disease process, that we have to really be doing a much more
active job.  

		I think there are others that will testify in detail about the
malignant respiratory disease association and the strength of the
epidemiologic and toxicologic evidence which formed the basis of the
IARC classification of crystalline silica as a human carcinogen.  But we
believe that that data is strong and that that effect is real, and
further supported by recent studies, which I know you'll be hearing
about later in these hearings.  

		But it is a major concern for our practicing community that care for
patients with this dreaded complication, and people who work in these
jobs often have co-exposures with tobacco smoke that magnifies the risk
of that complication.  We certainly support smoking cessation and other
interventions for them.

		We believe that the proposed rule of 50 µg is reasonable and that
there should be an action level of 25 µg for enhanced exposure
assessment.  And we, like ACOEM, feel that we'll not likely eliminate
the disease, but we concluded that it's probably the best that we could
hope for with our current state of knowledge and with the negotiations
that take place with the industry to try to come up with permissible
exposure limits.

		But we are very encouraged by OSHA's inclusion of medical surveillance
in this new proposed rule, and we think that that will better improve
our state of knowledge and inform our policies in the future as well.

		In terms of the medical surveillance, just to echo some of the
comments of Dr. Fischman, we think that the components that are
specified in the OSHA proposed rule are reasonable and useful and well
justified.  We strongly support including a history, a good medical and
occupational history, which we teach ad nauseam to our residents,
sometimes with success.  A physical exam is important, and spirometry
performed by certified NIOSH technicians would be very important.  We
don't want garbage spirometry that we see out in the industry all the
time.  We want real, not what I call cosmetic or ceremonial spirometry. 

		We want a chest radiograph that's read by NIOSH certified B readers,
and we believe that the NIOSH B reading program can certainly amp up and
train enough certified B readers to handle any potential increased
workload.  

		And we really believe that the examination -- we support the
surveillance examinations being carried out, the full exams every three
years.  And we think it strikes a reasonable balance for early detection
of lung disease with a usually long latency disease and consistent with
recommendations by other organizations.

		We think that OSHA's proposed rule requiring employers to refer
employees for exams if they have had a chest radiograph to someone a bit
more specialized is a good one.  We would augment the rule not just to
pulmonologists, although as a pulmonary supremacist, I think
pulmonologists are probably the best, but we wanted to include our
colleague occupational medicine physicians as well and think that they
are certainly very well qualified and capable of performing those
examinations.

		And we think that OSHA's rule requiring a written medical opinion from
the licensed healthcare practitioner and, if involved, the specialist
occupational medicine physician or pulmonologist, but appropriate
attention should be paid to confidentiality and protected health
information to prevent any unintended consequences of the communication
of abnormal exam results.

		One thing we wanted to raise, and it was in the proposed rule
questions, is the question of medical removal protection.  The ATS and
our signatory organizations thought that that was reasonable.  And it is
not in the proposed rule, but we thought something similar to the Part
90 program under the MSHA program for coal mine health and safety that
miners have available.

		We think if a worker is found to have evidence of clinical silicosis
under the new medical surveillance program, that they should have the
option of removal to a workplace that is no or very low silica in order
to minimize the risk of progressive disease.  It was not feasible before
because there really wasn't a medical surveillance option, but we think
it should be considered now.

		We had a couple of quick ancillary issues, and one is that we thought
that there should be a banning of abrasive silica agents in sandblasting
in the United States.  It is not addressed by OSHA, but we support such
a ban.  And it is one of the greatest risks from crystalline silica. 
And NIOSH has been studying this in a concern since 1974, and there are
bans in many of the armed and uniformed services of the United States,
as well as Great Britain, Germany, Sweden, and other very enlightened
European countries.

		JUDGE SOLOMON:  You're right at the end of your time.

		DR. COHEN:  My conclusion is that we believe that this disease related
to the inhalation of silica should be seen only on the pages of medical
history texts, not in our hospitals or clinics or on our patients' death
certificates.  And the proposed OSHA rule is a significant step in the
right direction of primary prevention.  And where there is documented
difficulty controlling exposures, we think the medical surveillance for
secondary prevention will be very helpful. 

		I just want to thank our ATS committee members: Dr. Bill Beckett from
Harvard; David Christiani from Harvard School of Public Health; Tee
Guidotti; Occupational Medicine Specialist Cecile Rose from National
Jewish Medicine; and our chair, assembly chair, Kerry Rutledge (ph.)
from Yale.  Thank you very much.

		JUDGE SOLOMON:  Okay.  Dr. Guidotti?

		DR. GUIDOTTI:  Thank you, Your Honor.  

		The chief long-term goal of the Association of Occupational
Environmental Clinics is to facilitate the prevention and treatment of
occupational and environmental illnesses and injuries through
collaborative reporting and investigation of health problems.  Our
members have collaborated.  They have investigated health problems.  And
many of them have, in fact, documented cases that demonstrate to us,
and, too, that should demonstrate to OSHA, that silica-related disease
is very much alive.  We see it.  We see it in the real world.  We see it
with real patients.  And we think that after 4,000 years of recognition
that silica kills, that it's high time to make some progress and put an
end to it, because as you know the progress has plateaued and we have
been in a stalemate.

		The Association of Occupational Environmental Clinics is signatory to
the statement prepared by ATS and endorses that statement in all
respects.  That statement strongly supports the proposed rule, and that
is AOEC's position.  AOEC also has some additional remarks.

		AOEC agrees with OSHA's assessment of the health effects, and as I
mentioned earlier, AOEC members have firsthand experience with these
health effects.  We think that it is extremely important to realize that
silica control of exposure is not all about silicosis, that silica
tuberculosis remains a threat particularly where there is a
disadvantaged working population that may still be at a high risk of
exposure not only for tuberculosis, but for other opportunistic
infections that embed themselves in a fibrotic matrix.  Autoimmune
disorders, kidney disease, and lung cancer are all factors that are
specifically identified as related to silica exposure.

		Then there are the nonspecific conditions including the aggravation of
chronic obstructive pulmonary disease, bronchitis, and reduced lung
function, which incidentally does carry its own separate mortality risk
as a risk factor for premature mortality.  That is not specific to the
silica content of the dust, but that it attaches itself to dust
exposure.

		AOEC agrees with OSHA's assessment that exposure to silica leads to
increased mortality and years of life lost.  We think that if all of
these direct silica-related issues and these indirect silica-related
issues such as reduction in lung function were taken into account, that
we would see a multiple effect of mortality and certainly a stunning
effect in terms of person-years of life lost, that silica-related health
outcomes carry a risk of disability from chronic disease.  Loss of
pulmonary function leads to reduced exertional tolerance, less fitness
on the job, and increased risk of death and disability from the
reduction in lung function, which is not a factor that has been taken in
consideration; but in and of itself it is a risk, combined with the
comorbidities of silicate as silica-related disease and other exposures
that occur in a silica exposure situation, and that are also reduced and
controlled in large extent secondarily by the same measures that reduce
silica exposure and therefore enhance the efficiency, all argue, I
think, for a comprehensive approach and for the effectiveness and
efficiency of reducing silica in addressing a wide front of health
threats.

		We think that a fair accounting for all of these outcomes using
measures such as disability adjusted life years lost, as opposed to
crude measures such as mortality, would demonstrate a true increase in
the burden of disease that would be greater than mortality from
silicosis alone by a large multiple.  Those studies are difficult to do.
 They have not been done.  But we think they would show a substantially
greater effect than is estimated in the proposed rule.

		AOEC supports the inclusion of the construction center in the proposed
rule and opposes differentiation among industries in applying
occupational health protection measures.  If there is exposure to
silica, then it should be controlled regardless of the setting in which
it takes place.

		AOEC agrees with OSHA's proposed rule that the PEL should be revised
and would further submit the observation that a substantial body of
scientific evidence suggests that 50 µg/m3 itself is not completely
protective.  However, AOEC understands that although this is not an
ideal, it is realistic and understands that the reason for reducing the
standard to 50, at this time, has a compelling logic.

		AOEC also believes, however, that the surveillance of silica-related
disease and monitoring after the new PEL is established will then inform
us of the adequacy of the reduction and make it possible to get a
clearer picture of what the next step, if any, should involve.  AOEC
also agrees with the action level at 25 and believes that this just
makes good sense.  As you get closer to the PEL, it is only prudent to
monitor more closely.

		AOEC supports the provision in the proposed rule for a program of
medical surveillance that would be triggered as one approaches the PEL
and is supportive of the protocol.  But AOEC is firmly committed to
primary prevention.  The reason to do the surveillance is to ensure that
primary prevention is working.  If you do secondary prevention in order
to do case finding, then that is an admission that the primary
prevention program has failed.  It should only be done in order to
demonstrate conclusively that primary prevention is, in fact, working.

		AOEC has some comments on the cost-benefit analysis, all supportive,
that are in the written comments, so I won't go into that here.  And
AOEC agrees with the recommendation of the ATS calling for the medical
removal provisions under the proposed rule.  Medical removal from
elevated silica exposure or overexposure is also very likely to
contribute to a diminished risk from other respiratory problems such as
bronchitis and the aggravation of chronic obstructive airways disorders.
 AOEC also strongly, strongly supports the prohibition of silica as an
abrasive blasting agent.

		I think that we find it a little odd that what appears to be so
daunting in the United States to control this ancient hazard has, in
fact, already been achieved and achieved quite easily in other developed
industrial countries.  So why it is so difficult to achieve here and not
so difficult in Germany, for example, is a little bit puzzling and, I
think, speaks to technology, motivation strategies, and we think that
these problems can be easily overcome as they have been in other
countries.

		In short, AOEC is proud to stand with ATS, the American Medical
Association, the American Public Health Association, the American
College of Occupational Environmental Medicine, and virtually every
other major American organization in occupational health and
occupational medicine in supporting the OSHA proposed rule.  

		And I would further add as a personal comment that we are talking
about some of the oldest hazards in human society or one of the oldest
hazards.  This is the time now to get it right.  This is the time now to
solve a problem which has been around for far too long because the next
iteration of silica-related issues is going to be much more challenging.
 It is going to involve things like silica fume, aerogels, nanomaterials
which have high cited toxicity, and engineered biomaterials which are on
the horizon as the next generation of silica-related technology.  

		Let's get it right now with bricks, rocks, and stone and get ourselves
in a position where we're a little bit better able to deal with some of
these high-tech problems that are going to be coming up very soon. 
Thank you very much.

		JUDGE SOLOMON:  Right at the end of your time.  Perfect.

		UNIDENTIFIED SPEAKER:  Good timing.

		DR. GUIDOTTI:  Thanks. 

		DR. SOKAS:  I'd like to thank everyone again for the opportunity to
comment on OSHA's proposed silica standard.  The American Public Health
Association champions the health of all people and all communities.  We
strengthen the profession of public health, share the latest research
and information, promote best practices, and advocate for public health
issues and policies ground in research.

		We are the only organization that combines a 140-plus year
perspective, a broad-based member community, and the ability to
influence federal policy to promote the public's health.  APHA and its
53 affiliated state and regional public health associations represent
50,000 public health professionals.

		APHA congratulates OSHA for moving to act decisively to prevent death
and disease from silica exposure.  APHA strongly supports the proposed
silica standard with its reduced exposure limits, options for exposure
control in construction, requirements for medical monitoring including
testing for latent tuberculosis, and the inclusion of important guidance
materials in the appendix. 

		We note the sad history of silicosis causing health disparities among
low-income African American and immigrant workers who have
disproportionately sickened and died from this disease, including from
acute silicosis and from silicotuberculosis.  And to put another face on
the example and to emphasize the impact that silica's effect on
activating tuberculosis has, I actually cared for a 43-year-old man who
was dying from fibrotic end-stage lung disease mostly due to the
tuberculosis that had gone untreated until his two-year-old child died
from disseminated tuberculosis.  So this was an awful sentinel event
that occurred.

		We now have compelling evidence, as you heard and as you know from
your own risk assessment of the other diseases, including cancer and
autoimmune diseases, kidney diseases, and again I think that it is past
time for OSHA to be putting an end to this level of health disparities.

		We support OSHA's risk assessment as sound and demonstrating the
urgent need to reduce the permissible exposure level for respirable
crystalline silica.  We note that the proposed PEL, as others have said,
is a compromise based on feasibility, and OSHA itself recognizes that it
is insufficient to reduce lifetime mortality risk to a range previously
considered to be acceptable for occupational exposures.  

		We have identified additional peer review scientific research
published after OSHA's risk assessment was concluded that is listed in
our written comments that demonstrate, further demonstrate the adverse
health effects at levels below the proposed PEL.  So the proposed PEL,
again, is a compromise.

		I would like to highlight just one of these studies published by Liu
and others in the American Journal of Epidemiology in 2013.  As you
know, they studied over 34,000 workers, who were followed for an average
of 34 years, who had no other known occupational carcinogen exposures
and whose smoking history was documented.  They demonstrated a clear
dose-response relationship between silica exposure and lung cancer. 
Silica exposure at the current PEL for general industry, not even going
to construction, which is huge, was associated with an additional 5 lung
cancer deaths for every 1,000 workers.  Silica exposure at the proposed
PEL still exceeded the traditional 1 lung cancer death per 1,000
workers.  

		And, importantly, in this study, they observed similar lung cancer
outcomes in silica-exposed workers who had no evidence of silicosis.  So
I know you have received arguments that there are threshold levels and
that cancer occurs because of silicosis.  This is not true.  This is
outdated and this fails to reflect current understanding.

		Given this high residual risk even with the implementation of the new
PEL, APHA urges OSHA to modify the proposed standard as follows: to
require posting appropriate warning signs at each regulated area in
languages and at literacy levels that are clearly understandable by the
workers.  

		Include plans to update Table 1 regularly to reflect improvements in
dust control technology.  This is the table that lists exposure control
methods for selective construction operations.  As you heard, prohibit
the use of silica sand in sandblasting operations.

		Clearly prioritize engineering controls to reduce the hazard from
silica with the goal of reducing the need for supplementary respiratory
protection where feasible.

		Develop, distribute, and evaluate appropriate outreach materials for
employers and workers.

		Trigger implementation of medical surveillance requirements at the
proposed action level, rather than at the proposed PEL.  

		The following recommendations are based on public health concerns that
medical surveillance should provide the opportunity to identify sentinel
events and the recognition that workers will be unlikely to participate
fully if they fear job loss as a consequence of surveillance activity.

		Reduce the interval -- so basically, we're in agreement with both
ACOEM and ATS and others to reduce the first interval following the
baseline from three years to one to one and a half years.  I mean just
make that first follow-up closer in time in order to reinforce health
messages and to identify potential failed exposure prevention.  For the
same reason, don't wait -- don't allow a baseline, a previously obtained
baseline exam to be good for three years for a new hire that should be
only for a year.  So that's for the same reason.  Sorry about that.

		We also recommend that OSHA provide -- that OSHA require that the
results of the medical examination be provided to the worker, rather
than the employer, and agree also to offer some form of medical removal
protection, as well as to offer workers the option of requesting interim
medical evaluations if they have symptoms or concerns about respiratory
protection or excessive exposure levels.

		Finally, with respect to the quality of medical monitoring, which has
already been quite substantially addressed, APHA recommends that OSHA
clarify the skills needed for the person who runs the medical
surveillance program.  APHA suggests that OSHA -- again, we agree with
not having the low-dose CT be used as an equivalent procedure for, to
substitute for chest x-rays, but we do believe that it should be used as
a diagnostic option.  And if it has been obtained for diagnostic
purposes, then don't make the person get a chest x-ray; just accept
that.  So it should be accepted.

		We also would like to point out that the use of low-dose CT for cancer
screening has now been solidly established in the general population for
high-risk people with smoking exposure.  And we would like to urge OSHA
to reserve the right to implement requirements for lung cancer screening
using low-dose CT once it has been firmly established what the risk
levels that would warrant, what the combination of risk factors would be
that would warrant the same level of risk that is currently being -- has
been approved by the American Preventive -- public health prevention
services.  And that we would actually call on OSHA to begin that
process, to convene the agencies and the organizations that would be
needed in order to look at what level of risk would warrant low-dose CT,
what the criteria should be so you don't wind up hurting people with
unnecessary procedures. 

		We know that OSHA has been burned in the past by too early jumping on
the bandwagon for cancer surveillance screening.  Arsenic is the prime
example of that.  But this is now different, and this now warrants a
really careful, thoughtful, coordinated look ahead.  And we would ask
OSHA to reserve that right.

		Thank you for your attention.  And we are all happy to answer
questions, I suspect.

		JUDGE SOLOMON:  Thank you.  The peers, the first row, Dr. Ginsberg? 
Dr. Miller, do you want to get in line?  We'll make a line.

		DR. GINSBERG:  I'm Gary Ginsberg.  I'm on the peer review panel.  I'm
from the state of Connecticut, but I don't represent the state of
Connecticut in my comments and questions.  But especially for
Dr. Cohen, but anyone else that cares to chime in on this, there is
some evidence that historically radiographic evidence may underestimate
the rate of silicosis.  I'm wondering how you might think that might
alter the quantitative assessment we might be doing of silicosis risk,
on the one hand, based upon some of that historical data.  

		And, Dr. Cohen, you talked about some of your current cases.  And
much has been made yesterday about current cases really only being where
there is gross exceedances of the PEL, and I'm wondering if you have any
perspective on whether what you are seeing in your practice relates to
exceedances of the PEL or are probably in line with the PEL and still
causing a problem.

		And then I have a more theoretical question if we have time for it,
which is what preexisting conditions in a worker might lead them to be
more sensitive than the average to silica-related diseases?  For
example, there is emerging literature on obesity being an inflammatory
state and increasing response to diesel exhaust particles in the lung,
and whether that or any other conditions may predispose a worker to
being more sensitive than the mean for silicosis.

		JUDGE SOLOMON:  Is this for the whole panel or for just --

		DR. GINSBERG:  Well, the last question more for everybody, but I think
the first two questions may be more for Dr. Cohen.

		DR. COHEN:  Well, I can start and then everyone should chime in as
they -- I should have been taking notes while you were asking your
question.  But I think that certainly chest radiography is insensitive,
to your first question, as an outcome measure.  And I noticed most
people, you're using 1/0.  But there is good radiologic, pathologic
studies that show that people that have negative chest x-rays, certainly
there's great studies that were done on coal miners, a Val Vallyathan
study comes to mind where about two-thirds of them had coal maculism,
fibrotic changes, and normal chest x-rays.  So I think it is a rather
insensitive method for looking as an outcome.

		And I would mention that Dr. Morfeld's  study that was talked about
today, the outcome was 1/1 on his threshold study, so that that was a
very high bar.  So I think that does color it.  And we are probably, I
think what I was trying to stress is that we are underestimating so much
in this and using -- it's a very blunt too, chest radiography.

		DR. GINSBERG:  And in your practice regarding exceedances?

		DR. COHEN:  We don't have exposure data on a lot of these people. 
What we do is we kind of notify OSHA and try to get tele-hazard
evaluations, but we haven't been able to get it.  A couple of cases we
have, and they have been reasonable exposure data.  That may have to do
with the sampling and how the company, you know, performed those
monitoring studies when they were there.  But the exposure data hasn't
been horrible.

		Some of the descriptions are frightening.  And so I think if there was
a surveillance component, that we would pick this up, and then there
could be much more enhanced, you know -- obviously, it's still a
secondary prevention.  But there is some plume effect in some of these
where people are working right behind diamond-tooth saws and they are
getting exposures, as opposed to some area sampling.

		And the third question was?

		DR. GINSBERG:  What might make someone more sensitive?

		DR. COHEN:  I think that we see a lot of people that have
hyper-reactive airways disease, that have, you know, airway and
therefore are more sensitive to respiratory hazards.  I think that would
make them more -- lots and lots of asthma in the inner city, in Chicago,
where the epicenter of increased asthma mortality and airway
hyper-reactivity -- and I don't know as much about obesity and metabolic
syndrome as specific, you know, they are inflammatory systemic diseases.
 But I can say that COPD and these chronic lung diseases themselves are
systemic diseases.  They are not just lung diseases.  People lose
weight.  They are cachectic.  They have a lot of other systemic
complications. 

		DR. GUIDOTTI:  If I can just add to that, we do know that existing
chronic obstructive pulmonary disease and the sense of smoking-related
chronic obstructive airways disease from other causes, even Hnizdo has
very elegantly demonstrated that the superimposition of dust exposures
onto those preexisting acquired lung diseases can in effect tip the
balance and push an individual beyond functional impairment if they are
already at the extreme of pulmonary reserve.  So with this --

		DR. GINSBERG:  What was that reference?

		DR. GUIDOTTI:  What's that?

		DR. GINSBERG:  What was that reference?

		DR. GUIDOTTI:  I didn't hear.

		UNIDENTIFIED SPEAKER:  You have to spell the name.

		UNIDENTIFIED SPEAKER:  Even Hnizdo.

		DR. GUIDOTTI:  Oh, Hnizdo, H-n-i-z-d-o.  And this would be true for
other dust as well as silica.  But with the irreversible fibrosis, the
superimposed by silica, you would expect that to be even worse.  And, of
course, there are a whole variety of conditions, like antiprotease
conditions, like alpha 1-antitrypsin deficiency that would dramatically
increase an individual's problem with handling any inflammatory
condition involving the lung.

		But all of this gets us into a very slippery slope, though.  If we are
too preoccupied with preexisting conditions, then we begin to focus on
the host, as opposed to the exposure.  And these conditions are driven
by the exposure.  So under ADA and other precedent with the Enscold
(ph.) doctrine and in tort liability, and so on and so forth, we can't
go very far down that road, and we shouldn't go very far down that road.
 The real issue is that the workplace should be safe for as close to
everybody as is possible to achieve. 

		DR. GINSBERG:  Yeah, I was bringing up more from the perspective of
understanding dose-response slopes that don't seem to have a threshold
where on an individual level there may be, but on a population level
there may not be.

		DR. SOKAS:  So I just want to comment that I think the Liu paper does
an outstanding job in establishing a dose-response level.  I don't think
-- I think the cancer risk assessment is so slam dunk on this that
everything else is like, is still icing on the cake.  

		I would also like to, you know, kind of in response to some of the
other comments, I think so, so the purpose of the medical surveillance
is to find when stuff is not working.  And we know from a lot of other
OSHA experience with the lead standard which has been in place for
decades, right, sometimes you still find horrendous problems that just
turn up because the lead level that turns up in a lab is high.  And so
for some reason even though they are exposing -- the company is so
dysfunctional that everybody is getting exposed, nevertheless there is
that one piece that's still functional and it captures the problem, and
then you can go back and fix it.

		DR. GINSBERG:  Thank you.

		JUDGE SOLOMON:  Dr. Miller?

		DR. MILLER:  Dr. Ginsberg has already picked up on something that I
wanted to expand a bit on.  Dr. Cohen, your example, a 39-year-old, I
think you said?

		DR. COHEN:  Exactly right.

		DR. MILLER:  Yeah, it seems awfully likely to me that this person has
been exposed way out of control of the existing PEL.  I don't know,
maybe he was self-employed or something like that, if he was a
landscaper.

		DR. COHEN:  No, he was working for a small company.

		DR. MILLER:  He was working for a small company.  I think what my
question is, is do you see aspects of the proposed rule which would
avoid cases like that, because I'm just worried that, you know,
certainly in the construction industry, we see stuff that's out of
control all the time.  And that's my concern, is this going to make
things better?

		DR. COHEN:  Again, I think that that is an extreme case and a tip of
the iceberg.  But I think if there were -- the medical surveillance was
in place, then we would have picked this up, if the worker training,
procedures that are in the new rule were in place that would prevent
this.  So I think that medical surveillance and worker training would
have helped.  The exposure assessments, if they were done appropriate,
probably would have exceeded the current PEL, I would suspect, in that
particular case.

		JUDGE SOLOMON:  Let the record reflect that three out of the four
panelists nodded their heads in affirmation.  Go ahead.

		DR. SALMON:  Hi, I'm Andy Salmon with the state of California, but not
representing the state of California at this point.  I would like to
actually remark on and applaud your bringing to our attention the paper
by Liu, which was I think also mentioned in his written testimony by
Dr. Steenland, who is, of course --

		UNIDENTIFIED SPEAKER:  A co-author.

		DR. SALMON:  -- a co-author, along also with Dr. Hnizdo, another very
well-respected expert in the field.  And my view is that this is a very
influential paper and is of particular interest to me, that I think it
does illustrate the low dose end of the dose-response curve, which was
something which I was concerned about in my initial comments a number of
years ago.  So I am gratified that it is receiving your attention.

		I was hoping that you might also comment on an additional observation
which they made, which was of a near multiplicative relationship to
smoking.  And perhaps you would care to elaborate your views on the
public health significance of this point?

		DR. SOKAS:  So thank you very much.  The Public Health Association is
very much in favor of smoking cessation activity for workers.  And, in
particular, this multiplicative effect, we believe, probably puts
longstanding, high-level exposed silica workers into the range where
they would benefit from the low-dose CT screening, as long as it is
conducted with the appropriate controls to make sure that the radiation
dose is low, that the protocols are followed, and that actually is an
important aspect of that recommendation.  So thank you for commenting on
that.

		DR. CRUMP:  Kenny Crump.  I am on the review panel.  Dr. Sokas, I
wanted to follow up on your statement I believe to the -- I believe you
said something like the threshold is no longer in vogue as a theory and
also that the silicosis as a prerequisite for lung cancer theory does
not seem to be -- to hold water any longer.

		DR. SOKAS:  So, again, this isn't completely laid to rest, but it is
all from the same paper, which is very rich.  I mean they had so many
people and they followed them up so well.  They have virtually the same
response, lung cancer excess response among people without silicosis as
with silicosis in their very large study.

		The workers who had silicosis had had higher levels of cumulative
exposure to silica, so basically silicosis itself is a marker for
higher-level exposure.  But at the lower and lower doses, the
non-silicotic presumably healthy individuals also developed lung cancer.
 

		So the lung cancer, the cancer risk is what really kind of takes, I
think, the lead then in the risk assessment.  And, you know, it is, in
general, we don't use individual thresholds for cancer risk.  In the
population study, there is a threshold risk.  They found that -- but
they wouldn't call it a threshold risk.  They would say if you want to
get the risk to below 1 in 1,000, which is traditionally what OSHA works
towards, then your PEL would need to be around 40 µg/m3, because that's
the -- when they did their lifetime exposure, that was the level that
they found 1 in 1,000 risk.

		DR. CRUMP:  Can you tell me, remind me the name of the paper you are
--

		DR. SOKAS:  Sure.  It's Liu et al. and it is in the American Journal
of Epidemiology in 2013.  L-i-u is the lead author.  And Dr. Steenland
was a co-author, as well as a number of others.

		JUDGE SOLOMON:  Let the record reflect that for three days we have
been talking about that paper.

		DR. FISCHMAN:  Just one additional comment.  It sorts of reflects the
limitations of medical surveillance, including chest x-rays.  Dr. Cohen
pointed out that you may not pick up evidence of silicosis on a chest
x-ray and yet that person may have had a significant exposure.  So the
medical surveillance may not detect it.  But reducing the PEL would tend
to reduce the potential that somebody who has had significant exposures
but doesn't show evidence of silicosis, you know, would protect them
against potential development of lung cancer down the line.

		DR. SOKAS:  And just to add, there are other studies, epidemiologic
studies.  So this is not clinical.  This is large epidemiologic studies
that have, you know, that demonstrate that there is -- and I think
actually you are going to hear from an author on another paper that's
recently been published about autoimmune disease and there is the
studies on renal disease -- don't rely on silicosis.  The people don't
have to have silicosis in order to have abnormalities, that these
abnormalities are found in the absence of silicosis.

		DR. GUIDOTTI:  May I also make an observation?  And that is that we
tend to think of fibrosis and carcinogenesis as being separate
processes.  Actually, they are quite interrelated.  And Dr. Weill was
quite correct when he pointed out that wherever you have an inflammatory
response and fibrosis, you have a potential for an increased burden of
cancer.

		We see this not only across a broad variety of disorders that anyone
would agree are separate pathologies like interstitial pulmonary or
idiopathic pulmonary fibrosis, but we also see it in the laboratory, in
work like the work that was published many years ago by the cancer
investigator, Umberto Saffiotti, who looked at silica exposure and
looked at what he considered to be pre-neoplastic changes in cells that
were around the inflammatory lesions in the lungs long before there was
fibrosis.  So it's a complex, interrelated process.

		DR. SOKAS:  And just to -- again, you don't need the fibrosis in order
to have the adverse effect, so you don't need the silicosis.

		DR. CRUMP:  Thanks.  Thank you very much.

		JUDGE SOLOMON:  Any of the public want to ask some questions?  Okay,
let's start with the people -- you are first, Mr. King, because you are
in the low row.  And you will line up by row.  That's the only equitable
way for me to do this.  I don't want to call on individuals.

		MR. KING:  Good afternoon.  My name is Neil King.  I am representing
the American Chemistry Council's Crystalline Silica Panel.  And I just
have a few questions.  This is a very aggressive panel, so I hope I
don't get my head handed to me.

		JUDGE SOLOMON:  Ask the question, Mr. King.

		MR. KING:  Yeah, I'm going to duck.  I guess first a quick question to
Dr. Guidotti.  You were referencing the success in controlling
silica-related disease in Germany, for example, I think you specified,
as compared to the United States.  Do you know what the occupational
exposure limit happens to be or has been in Germany?

		DR. GUIDOTTI:  Not off the top of my head, but I think that the key in
the German experience has actually been compliance.  Most of the
incident cases that now appear of silicosis in Germany are legacy cases
from the Communist era.  I think that that's partly a function of there
is subscription actually driving, because German MACs actually drove a
lot of the EU-harmonized occupational exposure standards.  It's both the
setting of an appropriate standard and also a careful monitoring and
compliance.

		MR. KING:  I think I agree with that.  I have to say my understanding
is that the occupational exposure limit for crystalline silica in
Germany has been 0.15 mg/m3, so 50 percent higher than what it has been
here for the last 40-some-odd years, which I think emphasizes your point
that it is getting good compliance there that may have made the bigger
difference than what the actual exposure limit was.

		DR. GUIDOTTI:  If you were to look at levels in German workplaces,
actual levels, my suspicion is that they are well below the German MAC
and then the EU standard which may have been nominally above the PEL. 
But, in reality, we are far below ambient or far below extant levels in
the workplace.

		MR. KING:  And do you understand that what the case is in the United
States with respect to both construction and general industry exposures,
whether they are generally below what the existing PEL of 100 µg/m3 is
in general industry, and it is 250 µg/m3 incidentally in construction. 
Do you know whether in the United States, as you suspect may be the case
in Germany, the exposures have been actually below the existing PELs or
above them, or have you no idea one way or the other?

		DR. GUIDOTTI:  Well, I have an idea.  My understanding is that
compliance has actually been rather poor, that there is a great deal of
room for improvement.  I, personally, question whether we will see that
improvement without further pressure.  I do think that we have ample
evidence quite separate and apart from compliance and rather crude
estimates on a population monitoring surveillance basis.  We have much
better data from the very targeted studies where exposure assessment has
been intentional and more refined, that the exposure-response
relationship exists and favors a setting of the PEL at the level that
has been proposed.

		We don't need to look at large population levels and rather, shall we
say, ballpark surveillance figures based on current practices to know
that the exposure-response relationship settles around 50 as a lower and
perhaps more accessible risk threshold.

		MR. KING:  Thank you.  And I do want to come back to that point for
the panel generally in a moment.  But just one question for Dr. Sokas,
I guess.  The Liu study that you mention now, do you know whether or not
there might have been confounders present in that study?

		DR. SOKAS:  They did a pretty good job.  I mean they went through and
they had -- these are waves, you know, where they had established the
cohort from 60 onwards, and had questionnaires that they administered I
believe in '86 to get specific, you know, it's other exposures that
people had.  They excluded 8,000 people because they had potential for
other occupational exposures from some of the different mining
operations.

		MR. KING:  I believe that was the tin mines they excluded, I believe,
where the arsenic was present.

		DR. SOKAS:  You know, I don't remember, but so --

		MR. KING:  But let me ask, but the study included, as I understand it,
a number of mines, mainly tungsten mines and potteries, four potteries.

		DR. SOKAS:  Right.

		MR. KING:  Do you have reason to believe there was not polycyclic
aromatic hydrocarbon exposures in the potteries?

		DR. SOKAS:  Well, the potteries had the same level of silica-related,
clearly silica, you know, the silicosis as the, you know, so they
clearly had silica.  The poly aromatic hydrocarbon exposure, I don't
know.  I'm not sure what the level would have been.

		MR. KING:  I mean there was, as you know, this cohort was taken from a
larger cohort.  This was about --

		DR. SOKAS:  From 74,000, that right.

		MR. KING:  About 74,000.

		DR. SOKAS:  Right.

		MR. KING:  And in a study involving the larger cohort a few years
earlier, where they included I guess eight potteries, these were four
out of the eight, the authors of that study said that there were quite
high polycyclic aromatic hydrocarbon exposures in the potteries.  Do you
know why the authors of this study didn't make any kind of allowance for
that, didn't deal with it?

		DR. SOKAS:  No, I'm not sure.

		MR. KING:  Okay.  I mean if there were such confounding exposures,
that might change the significance of this study, I take it.

		DR. SOKAS:  So if they were uncontrolled, that could be a factor.

		MR. KING:  Okay.  I think, Dr. Cohen, I believe that Dr. Miller has
already touched on the point I was wondering about with your landscape. 
It seemed to me the way you were describing what he was doing, cutting
and sawing in a dry atmosphere with very high dust clouds around him,
that he was exposed to something well above 100 µg/m3 during those
activities.

		DR. COHEN:  Yeah, we talked about that.

		MR. KING:  That's what I thought.  A general question for the panel as
a whole --

		JUDGE SOLOMON:  How much more do you have, Mr. King?

		MR. KING:  Maybe just a couple of minutes, no more than a couple of
minutes, I think.  This may be my last question.

		JUDGE SOLOMON:  Okay.  I'm going to take you to your word.

		MR. KING:  Depending how it is answered.  I presume that each of you
and your organizations have read OSHA's rulemaking and the quantitative
risk assessment that underlies it.  And you all, in one way or another,
in effect, endorse OSHA's findings as to what the risk of death from
nonmalignant risk respiratory disease, lung cancer, renal disease, and
silicosis morbidity, what those would be at the alternative permissible
exposure limits, 150 µg/m3.

		Am I right, you all basically --

		DR. SOKAS:  Yes.

		MR. KING: -- have said something to the effect that, yes, we think
that they did a good job, that their numbers are about right; in fact,
they may have underestimated the number of cases that might be
prevented, etc., things of that sort.

		DR. GUIDOTTI:  Well, actually, in the AOEC written submission, we go
into this in a little bit greater detail that I was able to in the oral
submission.  We think that it is a minimal estimate.

		MR. KING:  Minimal, okay.

		DR. GUIDOTTI:  Yeah.  We think that it rather grossly underestimates
the mortality because of misdiagnosis.  There are ample reasons for the
impact of my own personal experience I've seen cases --

		MR. KING:  A misdiagnosis in the studies that OSHA is relying on to
develop its risk assessment?  Remember, they are not basing their risk
assessment on information about how many cases of silicosis mortality
have been in the United States from 1968 to 2010.

		DR. GUIDOTTI:  You're right, I'm sorry.  I was reflecting on the
overall burden of disease estimates.

		MR. KING:  That's right, it's a different issue.  To get back to my
question then --

		JUDGE SOLOMON:  You've already --

		MR. KING:  I haven't asked the question yet.  I've just set it up.

		JUDGE SOLOMON:  You asked two questions from the time that you said
you had two minutes, and now we're on four minutes.

		MR. KING:  The question is --

		JUDGE SOLOMON:  Mr. King, I don't want to do this to you, okay?  We
have a number of people in line.

		MR. KING:  Just one question, quick question:  Have any of --

		JUDGE SOLOMON:  Tell me what your question is.

		MR. KING:  The question is have any of your, the individuals here or
their organizations done their own quantitative risk assessment for
these disease end points that OSHA has analyzed, or are you basically
relying on OSHA's quantitative risk assessment when you are making
statements about what the risks are at 100 µg/m3, 50 µg/m3, and so on.

		JUDGE SOLOMON:  Is this directed to a specific --

		MR. KING:  To the four of them.  I'm done.  That's the question.

		JUDGE SOLOMON:  Well, they're not NIOSH.  I mean you are there --

		MR. KING:  No, no, I know they're not NIOSH.  That's what I'm just --
just they have all, I'm saying each of their organizations has basically
said we agree with OSHA's quantitative risk assessment results.  And I'm
asking --

		JUDGE SOLOMON:  Let's do it in reverse order.  If you can answer the
question, can you answer the question?

		DR. SOKAS:  We have not redone the entire quantitative risk
assessment.  We have relied on OSHA and NIOSH.

		DR. COHEN:  Many of our members are parts of those research teams and
so that it's not an official project of ATS or APHA or ACOEM or AOEC,
but our members are active scientists and researchers, and so some of
them have been parts of this research that NIOSH and others have
conducted.

		MR. KING:  But haven't done the quantitative risk assessment on their
own?

		DR. GUIDOTTI:  Actually, some member of AOEC, ATS, and I'm sure ACOEM
have performed their own risk assessments, but not as sponsored by the
organizations, which was your question.

		MR. KING:  Thank you, Your Honor.

		JUDGE SOLOMON:  Thank you, Mr. King.

		MS. KRAMER:  Your Honor, I think OSHA has about 15 minutes of
questions for this panel, if there is any way to limit the remaining
people who want to ask questions to about 15 minutes collectively?  And
if people are willing to stay a little bit later tonight, then -- we
want to get everyone's questions answered, but we also have another
group of people that --

		JUDGE SOLOMON:  Okay.  To be fair, I think what I'm going to do is
just limit it to one question, if that's okay.

		DR. WELCH:  From each person or just me?

		JUDGE SOLOMON:  No, each person will get to ask a question.

		DR. WELCH:  Okay.  That sounds good.  Well, my question is for
Dr. Cohen.  In the current, the way OSHA has written the standard, when
a medical surveillance exam is done, the examining provider is supposed
to give the medical results to the employer, who will then inform the
worker.  And I know you have experienced in the mining industry where it
is done differently.  And I was wondering if you could contrast or talk
about your experience among miners and how that information is
transmitted to worker?

		DR. COHEN:  Well, certainly with the Part 90 program and with many
other programs, the information is given to the worker, and the worker
can choose how to handle that information in terms of whether they want
to exercise their rights for medical removal protection or not, the
concern being retribution on the part of the employer, which is illegal.
 But, unfortunately, there are many cases and workers' comp cases that I
see all the time as well where through some method or other, the
employers do carry out some sort of retribution against the worker once
they become aware they have applied for a work-related illness.

		DR. WELCH:  Thank you.

		DR. MONFORTON:  Celeste Monforton.  Dr. Cohen --

		JUDGE SOLOMON:  Please spell your last name?

		DR. MONFORTON:  Oh, Monforton, 

M-o-n-f-o-r-t-o-n.  There have been commenters who assert that there
will not be enough B readers to meet the demand created by the medical
surveillance requirements.  Could you comment on that, please, or
Dr. Fischman, either one?

		DR. COHEN:  We discussed this in our group, and, you know, now that
there are ways of capturing the images digitally and transporting them
to wherever the reader happens to be, that there probably -- you know,
it is not necessary that there be a B reader in your community.  You can
get the image to someone who could, you know, look at those images and
make the evaluation.  

		And somebody already mentioned that there would be an opportunity to
sort of beef up the number of B readers.  And if there were a need,
people would presumably try to take that training and become B readers.

		UNIDENTIFIED SPEAKER:  I'd just add that I think that a lot of these
exams will be normal exams, and as a B reader you can read a normal
x-ray, you know, much more quickly.  It's the complex abnormal ones that
take more time, and I think the market will drive this.  If there is
money to be had, B readers will appear, I believe.  

		JUDGE SOLOMON:  I really shouldn't say this, but I'm afraid I have to.
 You know I do these hearings, and there are board-certified, duly
qualified people in foreign countries.  That's my comment.  Okay, next?

		DR. MIRER:  Frank Mirer, M-i-r-e-r, CUNY School of Public Health.  I
will observe that I once testified and was kept here at the OSHA hearing
for formaldehyde until 11:30 at night, so you people are like -- I mean
give me a break.  But, anyway, and Bob Park was on that panel as well. 
So my question is as practicing physicians, how do you feel about the
idea of disclosing, somebody comes to you with silica exposure, you
diagnose a medical condition, how do you feel about providing that
information direct to the employer rather than having the worker have
the option of whether it goes to the employer or not?

		DR. GUIDOTTI:  I think that --

		DR. MIRER:  And would they come to your clinic if that was the rule of
engagement?

		JUDGE SOLOMON:  That's a second question -- no, go ahead.  And let me
just state for the record that the questioner will be back and he gets
to testify for 10 minutes.  So if you can answer, go ahead.

		DR. GUIDOTTI:  I think that if the notification is directly to the
employer, that that's okay if it's in an aggregate form.  I think that
the real problem is preventing retribution by recognizing the affected
individual.  That kind of goes a little bit beyond the level that we are
prepared to comment on today, but I'd be curious myself to know what the
other panelists would say.

		DR. SOKAS:  In general, you want to give the information to the
individual, so the individual has the ability to make use of that
information.  I think that's generally true.  You do want to make sure
that the employer has the information needed to reduce exposure and to
correct problems in the workplace.  So it's a bit of a balancing act.  

		But from APHA's perspective, our concern is that if the employee knows
that the employer is going to get this information, they're going to
have to get it from the employer.  And their job is not secure since in
this country we don't have real job security without union contracts. 
Then there is every reason to believe that people will avoid the
surveillance if they can possibly avoid it.  And that's even more true
for construction when people are continuously looking to new jobs and
new work because then they would be worried that they have the scarlet
letter, basically, I think.

		JUDGE SOLOMON:  Next?

		DR. SIVIN:  Dr. Darius Sivin, UAW Health and Safety Department.

		JUDGE SOLOMON:  Please, I have to ask you to spell your last name
again.

		DR. SIVIN:  S-i-v-i-n.  Several members of this panel referred to
under-ascertainment and misdiagnosis of silicosis-related disease. 
Earlier in these hearings, we heard arguments related to supposed
declining silica-related mortality.  How would your understanding of
under-ascertainment and misdiagnosis affect your opinion of the
arguments made that the declining mortality that has shown up in
surveillance suggests that there may not be a need for this standard?

		DR. COHEN:  I think we talked quite a bit that we think that this is a
huge problem.  The problem is it is a disease of long latency, so the
relationship between these diseases to the employment and physicians and
practitioners who don't take occupational histories in this country is
huge.  And then workers may not even associate it with it.  We see
people come in with fibrotic lung disease all the time, and we do the
amazing thing of taking the occupational history and we make a
diagnosis.  That's obvious.  So I think that's one of the huge problems,
and passive reporting, and all the things that we have talked about.  So
this is clearly under-estimated, I think.

		DR. GUIDOTTI:  I have personally experienced situations in which
physicians who, by all rights should know better, were absolutely
convinced that a case that they felt or that was clearly silica -- it
was beyond question and was eventually biopsy proven -- was sarcoidosis.
 And since sarcoidosis appears to be increasing in prevalence, I see a
huge potential for that.  And, at the moment, we simply don't know how
much of the true burden of disease of silicosis is obscured by that.

		DR. SIVIN:  Thank you.

		JUDGE SOLOMON:  Mr. Glenn?

		MR. GLENN:  Bob Glenn, G-l-e-n-n.  I'm not a physician, just a poor
country industrial hygienist, so bear with me in this question.  I want
to commend Dr. Fischman and the college for in, I think, 2006 putting
together their comprehensive guidance on medical surveillance, which has
been very helpful to those of us in the field who manage this problem. 
And that recommended occupational and medical history questionnaires, I
suppose smoking as well, physical exam, PPD skin test, and you said or
equivalent, so I'm thinking now the interferon test, chest radiography,
and spirometer.  But you did not recommend HRCT.  You did not recommend
any test for immune-related diseases, such as Rh factor, rheumatoid
factors.  So you didn't recommend any aggressive lung cancer screening
such as sputum cytology, and I don't guess you want to bronch these
people to find out what their cells are like.  And you didn't recommend
creatinine and GFR for kidney.  But you did say that that that was under
consideration.  Has that guidance been updated, and do the other
organizations have that guidance, and what are their thoughts about HRCT
immune-related diseases and kidney disease, which I would put in, by the
way, GFR.

		DR. FISCHMAN:  So interesting question.  I can't take credit for the
2006 guideline because I wasn't involved at that point, but I think, you
know, this is -- medical surveillance is a screening process, and there
is going to be hopefully information provided to the clinician as to
what the exposure levels are and from the individual whether they're
having any symptoms or unusual problems, so that there is an opportunity
in that process to potentially identify some issues like the ones you
mentioned or identify that there might be that.

		And then, of course, one could do additional testing to evaluate that.
 So that would be my sense.  And, no, we haven't updated those
recommendations.

		DR. GUIDOTTI:  I was president of that organization at about that
time.

		MR. GLENN:  Yeah, thank you.

		DR. GUIDOTTI:  And although I don't recall the --

		MR. GLENN:  My congratulations.

		DR. GUIDOTTI:  Well, I guess that's one way to put it.  Although I
don't recall that specific conversation, I think that one very strong
reason why it wouldn't have been put in is that the positive predictive
value of those tests for this particular condition in that population
would make the test performance very poor.

		MR. GLENN:  Yeah, my computer ran out of power, or I'd be able to read
the text from it, but that is what you recommended in that guidance
essentially.

		DR. GUIDOTTI:  I'm sure it is.  But the reason why, as I said earlier,
the performance as a screening test would not be ideal in that
situation.  So I think that the guideline was probably looking forward
to further technical developments.

		MR. GLENN:  Does ATS have --

		JUDGE SOLOMON:  Thank you.  Thank you, Mr. Glenn.  You've already had
your question.

		MR. GLENN:  Dr. Cohen was going to answer, Judge.

		DR. COHEN:  I was just going to say I'll just endorse what Dr. Sokas
said about HRCT.  It's not really ready for prime time as a population
screening, imaging technique, but it is a useful diagnostic technique,
and we would accept it, I think, if it was done.

		MR. GLENN:  Okay.

		JUDGE SOLOMON:  Thank you.

		MR. GLENN:  Occupational histories on a 19-year-old exposed person who
presents with alveolar proteinosis, there should be something in a
recent history of very high exposures.

		JUDGE SOLOMON:  So that's -- you testified again, Mr. Glenn.  

		MR. GLENN:  I have to take what I can get.

		MS. NADEAU:  Elizabeth Nadeau, International Union of Operating
Engineers.

		JUDGE SOLOMON:  You have to spell your name.

		MS. NADEAU:  N-a-d-e-a-u.  

		JUDGE SOLOMON:  Okay. 

		MS. NADEAU:  Could you please comment on the relationship between the
official statistics on silica-related disease and the kind of training
that physicians receive in occupational health?

		JUDGE SOLOMON:  To whom are you --

		MS. NADEAU:  Any.

		DR. GUIDOTTI:  I think that in every medical school I've personally
been associated with, there are then at least three sentences in the
entire medical curriculum.  That I haven't been associated with have
probably got less than that.  I think that there is a tremendous
deficit, and I'd like to think that it's remedied in textbooks like the
American College of Physicians Medicine, which is now Scientific
American Medicine.  But most textbooks don't even mention it.

		DR. SOKAS:  Just a clarifying question.  Were you asking about general
medical education or occupational medicine specific training for
residents?

		MS. NADEAU:  Well, what doctors would generally be trained in and then
both, I mean both circumstances.

		DR. GUIDOTTI:  Ordinary physicians will know about it.  Occupational
physicians will know about it.  Virtually, nobody else.

		DR. COHEN:  There are so few residencies in occupational medicine and
programs that don't -- internal medicine programs that don't have that
really, include very little.  And I would actually say that many
pulmonary programs and very reputable places don't include a lot of it,
unfortunately.  There is a little bit of it, as you said, but it's just
not anywhere near adequate.  So anything that relies on physician
reporting is bound for disaster, if it's history.

		JUDGE SOLOMON:  Thank you very much.

		MS. NADEAU:  Thank you.

		JUDGE SOLOMON:  I probably cut off one of the peers.  Do you still
have a question?  You have to get to the microphone.

		DR. SALMON:  I just had an additional comment in relation to some of
the discussion earlier about the Liu paper.  And I think it's worth just
quoting from the paper that the LFS (ph.) focus on a sub-cohort of
34,018 workers who were unlikely to have been exposed to other
carcinogenic confounders such as radon, polycyclic aromatic
hydrocarbons, and arsenic.  So as a toxicologist, I am not necessarily
one to argue that the epidemiologist always get anything right, but I
think in this case it's fair to observe clearly that that point has been
addressed in this most recent paper relative to the extent to which it
was addressed in some of the previous publications on the same cohort.

		MS. KRAMER:  Thank you.  Really quickly, do you want to just identify
yourself for the record?

		DR. SALMON:  Yeah, Andrew Salmon, peer reviewer.

		JUDGE SOLOMON:  Oh, I'm sorry.  I should have said something.

		MS. KRAMER:  Thank you, Dr. Salmon.  

		JUDGE SOLOMON:  Okay, so now we are on the OSHA questioning.

		MS. KRAMER:  Onto the next, oh, yeah.  

		MR. O'CONNOR:  Yes, Lyn Penniman.

		MS. PENNIMAN:  Yes, hi, everyone.  Thank you for your comments.  I
just had a couple of questions on medical surveillance.  APHA, as well
as I think everyone on the panel, suggested that OSHA consider the
trigger for medical surveillance to be the action level, 25 µg for 30
days or more per year, instead of the proposed PEL.  Could you elaborate
a little bit on the reason for that, anyone?

		DR. SOKAS:  So the reason for APHA's recommendation was really as
recognition that, as OSHA recognizes, the PEL as being proposed is not
protective to the extent that OSHA typically tries to reduce material
impairment to health below a rate of 1 in 1,000 workers, that by OSHA's
estimation, and by pretty much all estimations there is residual risk at
the proposed PEL that is being, again, driven by feasibility.  And in
recognition of that, the medical surveillance would provide attention to
a variety of aspects, including health education, are you wearing your
respirators, how is exposure doing.  

		Just as a comment, I wanted to mention that I actually was involved at
one point in an evaluation of a brick manufacturing facility where they
got a new supervisor who was having trouble with the baghouse, and so
they shut down the baghouse.  And so the individuals working there were
having, obviously, elevated exposures for a number of years.  And the
medical surveillance that took place in that location did not ask what
the exposure was or what the exposure, you know, was.  It was simply
being done for respiratory protection. 

		And so the idea that there needs to be better integration with medical
surveillance serving as a kind of a reminder or a warning, or just a
second check and balance is what's driving the APHA recommendation.

		DR. FISCHMAN:  One of the things that we discussed in our team at
ACOEM was that, you know, you're not sampling 24/7.  And, you know, the
number of samples, hopefully, and the processes during which sampling
was performed are going to be representative of what people experience,
but perhaps they're not always.  So you're providing sort of an extra
margin of safety by having a -- triggering the medical surveillance at a
lower level than at the permissible exposure limit.  So I think that was
one of the things that we considered.

		Also, you know, that provision for trigger at a lower level, at the
action level applies to some of the other OSHA standards, including the
lead standard.  So it's not -- it has sort of precedent at least within
some of the OSHA standards.

		MS. PENNIMAN:  Okay, thank you.  Speaking of the lead standard, my
next question is about medical removal protection.  And I think this is
another item that we had general agreement on as a recommendation that
OSHA should be looking at for the silica standard.

		In the lead standard, when workers are removed, it's because we expect
their lead level to go down.  Silica is different.  And silicosis, as we
know, we've been talking about here is a progressive disease.  How would
you construct medical removal protection in this situation?

		DR. COHEN:  Well, we think that it is a progressive disease in that
the dust is retained in the lungs.  The inflammatory process continues. 
But with continued exposure, we expect worse progressing, you know, and
more severe rates of progression, so we want to prevent that.  So that's
similar to what's done with coal miners.  We think that that is an
important thing to mitigate that ongoing exposure.  And while we cannot
reverse what's there, we would prevent additional injury.

		DR. SOKAS:  And just to sort of pile onto that, so it's not that we're
trying to emulate the lead standard here.  It's that it's already in
effect for coal miners.  And so we would encourage OSHA to explore how
that has work for coal worker pneumoconiosis and see if there is an
equivalent approach that might be useful.

		DR. COHEN:  And the issue of susceptible workers is the other question
so that if it, you know, if everything is in compliance, then this
person is likely more sensitive to have developed disease in a compliant
workplace so that that person likely needs removal because of their
individual host characteristics perhaps.

		DR. GUIDOTTI:  AOEC, in its written testimony, also not only agrees
with the logic of ATS, but also offers another reason, and that's that
although an individual who has developed moderate or advanced silicosis
may be at little risk for that particular outcome with further
exposures, in terms of little risk of making it worse once it's at a
certain level of severity, but additional exposure to respirable
particulates can contribute risk for other outcomes, such as bronchitis
and exacerbation of chronic obstructive airways disease.  So the medical
removal provision both decelerates the potential speed at which
silicosis will develop and also subtracts out the aggravational factor
of the dust exposure for an individual who already has a respiratory
compromise.  

		MS. PENNIMAN:  Thank you for that.

		MR. O'CONNOR:  Stephen Schayer has a few questions.

		MR. SCHAYER:  Oh, good afternoon.  I just have one question actually
for Dr. Cohen.  So you shared that experience with your patient, and I
was wondering if you had any other experience you could share with
patients about how living with silicosis affects quality of life?

		DR. COHEN:  I've had a number, you know, in Chicago, we have the steel
industry and we have a fairly significant -- and small foundries, so we
get people that are chippers and grinders working in that industry.  And
it's like anybody else with chronic advanced lung disease, they are on
home oxygen.  They are, you know, air hunger is a huge part of what
their daily lives are like.

		We try to give them pulmonary rehab, but it's, you know, I see it a
lot in our coal miners as well, but it's just living with that constant
inability to move and to breathe, and it's coughing and nasty.

		MR. SCHAYER:  And this can continue for I mean the rest of their life,
right, or a long time?

		DR. COHEN:  Yeah, these are irreversible diseases, and they are -- you
know, we can palliate them, we vaccinate them, we treat their
exacerbations, and we give them pulmonary rehab and oxygen, but we can't
reverse the process.

		MR. SCHAYER:  Thank you.

		MR. O'CONNOR:  And we'll turn it over to Tiffany DeFoe.

		MS. DeFOE:  Thanks.  I have a few questions.  I'll try to keep them
quick.  Some of them are coming out of individual testimony, but most of
them could be spoken to by anyone on the panel, I'm sure.  

		In Dr. Cohen's test -- written comments, excuse me, you described
several cases of quite severe disease, silicosis that is.  And I'm
wondering do members of your organizations also have experience with
patients who have less severe silicosis?  And if so, can you describe
whether and how their quality of life is affected?

		DR. COHEN:  Well, as many of us are pulmonary specialists and we tend
to see people that are more advanced, so we tend to see the worst of the
worst, but we also, as a B reader, we read x-rays, we see cases of
people that have less severe disease, and their lives are affected to
some degree, but lesser.  They have increased incidence of infections. 
They have increased, you know, the diseases that Dr. Guidotti was
talking about are very important, the obstructive lung diseases,
emphysema, you know, lung function impairment, which impairs your
ability to exercise and to work but not to the degree that you are on
home oxygen.  The cases that we described were people that have died or
near death.  So it's a whole continuum of impairment.

		MS. DeFOE:  So if I understood you correctly, less severe cases can
restrict one's ability to find or retain employment?

		DR. COHEN:  Well, if you're getting a pre-employment chest x-ray and
you have radiologic silicosis, that would be a real problem.  And if
you're doing -- most of these people or most of these workers do manual
labor.  And so even if you are not disabled in the sense that you're
home oxygen, you might be able to work as a pulmonologist, but you could
not work in most of these industries.

		DR. GUIDOTTI:  An individual who has lower lung function to begin
with, whether through an acquired problem like smoking or whether they
are simply born closer to the lower limit of normal in the normal
distribution, is also closer to the tipping point.  It doesn't take much
more for them to have shortness of breath with severe exertion, not
being able to keep up with people, not being able to keep up on the
assembly line.  And, again, as Dr. Cohen points out, most of these
individuals are engaged in rather hard manual labor, and some of them
come from very disadvantaged populations.  So this represents a very
severe restriction on their earning capacity and, therefore, the income
security of their family.

		MS. DeFOE:  Thank you.  Also in Dr. Cohen's written comments, on Page
4, there are a few short paragraphs that reference epidemiologic
studies, for example, showing increased risk of developing emphysema,
showing damaged lung function that has been shown in some studies to be
independent of the scarring effect, evidence that exposure to silica
results in chronic bronchitis, and evidence of increased mortality from
chronic obstructive lung disease.  

		You seem to be referencing specific studies, but I don't see
references.  And I'm wondering if in a post-hearing comment you might be
willing to provide them?

		DR. COHEN:  Yes.

		MS. DeFOE:  Thank you.  Also, in Dr. Cohen's written comments, there
is a statement towards the end that supplied air hoods have been shown
not to be protective.  And I'm wondering if you can elaborate on what
you mean by that?

		DR. COHEN:  This is for sandblasters.  This was really just for
sandblasters that there was -- there is data that people still developed
disease even with external air supplied respirators.  And I can try to
locate that.

		DR. SOKAS:  So that's why you should ban silica sand for sandblasting.

		DR. COHEN:  There is personal protective equipment that will mitigate
that risk entirely in silica sand sandblasting.  The air oscillation and
intense exposures are just hard to overcome.

		MS. DeFOE:  Thank you.  And moving on now to Dr. Guidotti's -- did I
pronounce that correctly?

		DR. GUIDOTTI:  Yes.

		MS. DeFOE:  Yes, thank you.  On Page 4 of your written comments, you
say AOEC observes that a substantial body of scientific evidence
suggests that 50 µg/m3 is not completely protective but understands the
reasons for reducing the standard to 50.

		I am mentioning just to request that in this substantial body of
scientific evidence that you are referring to, if there is any evidence
that you are not aware OSHA to have already seen, would you please
submit that in a post-hearing comment?

		DR. GUIDOTTI:  Sure, I can review that and forward it to you, if I can
identify it, yeah.

		MS. DeFOE:  Thank you.  In the supplement, Exhibit 2, you state
diseases caused by silica are largely untreatable because the scarring
in the lung is irreversible.  Prevention represents the only effective
approach to control.

		I'm wondering are there any medical treatments you would recommend to
help control the symptoms of disease, even if it is not reversible.  And
if so, how effective are they and are there side effects that OSHA
should consider?

		DR. GUIDOTTI:  There is no effective treatment for the underlying
condition, because once the scar tissue is in place, it is in effect
inert to medications.  There have been any number of attempted or
efforts to reverse the fibrosis by various means developed particularly
by the Chinese, at least three or four different treatment options
including a drug called tetrandrine that was in vogue for a short while,
in China, to do this.  They affected the chest film appearance of the
disease, but when it came to altering the actual architecture of the
diseased lung, there was no effect.  So what they were seeing was
something of an illusion.  Once the fibrosis is there, it is there
permanently.

		There are other ways of protecting the individual, for example,
immunization against pneumococcal pneumonia, watching very closely for
superinfection by mycobacteria.  Not just tuberculosis, but a variety of
other opportunistic infections can affect the silica-diseased lung, and
reducing the additional pulmonary impairment from such things as
cigarette-acquired obstructive airways disease that occurs in addition
to the airways irritation that dusts can provoke.  

		But these are all mitigating treatments.  There is no treatment that
affects the actual underlying disease.  And these mitigating treatments,
generally speaking, are very benign.  They don't have much of a side
effect because they are in common use, and, in the case of
immunizations, advocated for the general population.

		MS. DeFOE:  Thank you.  Okay, just a moment while I turn some pages. 
Dr. Sokas, in your written testimony or your written comments, on page
-- well, no page numbers, there is a paragraph where you discuss what
workers have to say about their reasons why respirators should not be
the primary means of protection silica dust.  You say they report that
it is difficult to breathe, especially while engaged in heavy labor
while wearing a respirator, that they are uncomfortable, especially in a
hot environment, and that it is difficult to communicate, which can
reduce safety.  And I'm wondering when workers say these things about
respirators, do they differentiate between different types?  Do they
seem to be --

		DR. SOKAS:  Well, it depends on who you ask.  I mean this is all
fairly common knowledge among, you know, people who have been involved
with workers.  So, obviously, if you've got, you know, the full-face
respirator, the air filtering --

		UNIDENTIFIED SPEAKER:  Air purifying.

		DR. SOKAS:  Air purifying, full-face respirator, that is generally
recognized as being difficult to use.  That is currently the most
protective.  Depending on the kind of work that people are doing, they
will complain about it sooner rather than later.  It depends on how much
they are working.  It also depends on what they are used to.  So you can
go into a healthcare setting, for example, and people complain about a
N95.  So it's not a lot of fun to be in a respirator for prolonged
periods of time.  

		And so the purpose of saying all of this was not to say it's more fun
to have cancer down the road; it's to say, OSHA, if you can encourage as
you do the standard use of the hierarchy of controls that puts
respiratory protection down where you need it because you can't get
there without respiratory protection, that's fine.  But this was sort of
in response to some other comments that I know you've received that say,
oh, yeah, just put them all on respirators, which, you know, this is a
reason not to just put everybody on respirators.  And this is --anybody
will tell you this.  I mean our entire section on occupational health
and safety could get up and give you examples.  So I don't know what
more specific you want me to say about it.

		MS. DeFOE:  You answered my question.  Thank you.  

		JUDGE SOLOMON:  Anybody else?

		MR. O'CONNOR:  OSHA has no more questions.

		JUDGE SOLOMON:  Ms. Ryder, I assume that you want the documents that
they have in front of them?

		MS. RYDER:  Yes, please.  Thank you all for your testimony, and if you
have written remarks that I could enter into the public record, you can
hand them over to me and I will mark them.

		JUDGE SOLOMON:  It's not really my province to ask a lot of questions,
but I do have to -- the other day I brought up, when the NIOSH panel was
here, in the 2000 regulations that became effective in January of 2001
that involve pneumoconiosis, silicosis is a subset of pneumoconiosis and
they addressed something called legal pneumoconiosis.  Is there legal
silicosis?

		DR. COHEN:  I'm very familiar with this because I deal with black lung
cases and those regulations all the time.  And I think that we are
moving away from the terms medical and clinical pneumoconiosis, and
we're calling it coal mine dust lung disease now because of the spectrum
of diseases.  That really just meant obstructive impairments other than
emphysema and chronic bronchitis, which we do see with silica, so there
is --

		JUDGE SOLOMON:  Without getting into the weeds here, I just want to --

		DR. COHEN:  There is.

		JUDGE SOLOMON:  There is a difference between restrictive disorders
and obstructive disorders, and there was some discussion about what
shows up on an x-ray and what doesn't show up on an x-ray.  So is there
some study someplace that would talk about such things?

		DR. COHEN:  That's what I think I was asked by someone to provide the
information on lung function impairment and emphysema associated with
silica, and it can occur absent radiologic silicosis.  And we'll try to
provide those.  I think that there is some of that in the record
already, but we can go --

		JUDGE SOLOMON:  I'm sure that there is.  I saw the usual suspects. 
But this Liu study is relatively new.  It's almost brand new.  So I
assume that that's going to generate a lot of discussion.  Okay.  I'm
sorry that I had to ask those questions.  Do you have any questions
based on what I asked?

		MS. RYDER:  No, I don't think so.

		JUDGE SOLOMON:  All right, thank you very much for this panel.  We're
going to go off the record for a second, and we're going to convene the
last panel of the day.

		(Off the record.)

		(On the record.)

		JUDGE SOLOMON:  Okay, let's go back on the record.  This is the last
panel.  We created this panel.  So starting at the left and going to the
right, please state your name and your organization.

		DR. MONFORTON:  Celeste Monforton, and I am testifying as an
individual.

		DR. ROSENMAN:  Kenneth Rosenman.  I am testifying as an individual.

		DR. GOLDSMITH:  David Goldsmith.  I'm testifying as an individual. 
Although yesterday I said I was affiliated with and I still am with
George Washington University and Georgetown, but I am testifying as an
individual.

		DR. CONE:  James Cone, testifying as an individual.  I work for the
New York City Department of Health.

		JUDGE SOLOMON:  Okay, you can --

		DR. MONFORTON:  Great, thank you.

		JUDGE SOLOMON:  Everybody gets about 10 minutes.

		MS. RYDER:  Judge Solomon, before everyone begins their testimony, I
just wanted to enter Dr. Rosemary Sokas' testimony into the record as
Hearing Exhibit 22.

		JUDGE SOLOMON:  Okay, so that's 22.

		MS. RYDER:  That's 22.  And I am going to reserve Hearing Exhibit 23
for Dr. Cohen's testimony.

		JUDGE SOLOMON:  Okay, so 22 is admitted.

(Whereupon, the document referred to as Hearing Exhibit 22 was marked
and 	 received in evidence.)

		MS. RYDER:  Okay, thank you.  Sorry, go ahead.

		JUDGE SOLOMON:  Okay, sorry.  Go ahead.

		DR. MONFORTON:  Good afternoon.  I'm Celeste Monforton.  I am with
George Washington University, School of Public Health.  I am testifying
here today as an individual of expertise in occupational health and
regulatory policy.  My funding is provided by the Public Welfare
Foundation, and they had no role whatsoever in the preparation of my
testimony.

		Before I begin, I would like to dedicate my participation to Henry
Dixon and J.T. Knuckles.  I consider them friends, both suffered from
silicosis, and died because of it.  They left this world well before
their time.  

		Before he died, Mr. Knuckles was one of the public faces for the
national campaign to eliminate silicosis, coordinated by OSHA, MSHA,
NIOSH, and the American Lung Association.  This is a T-shirt from that
campaign.  I hope the results of this current effort yield more than a
T-shirt.

		On the medical surveillance provisions --

		JUDGE SOLOMON:  Let me just say that she just held up the T-shirt. 
And if you want to enter that into evidence, you can do that also.  Go
ahead.

		DR. MONFORTON:  On the medical surveillance provisions, I concur with
the comments provided by the American Public Health Association on the
type and frequency of screening tests.  This includes the
recommendations that a baseline examination be conducted within one year
of hire, not three years as proposed, and a follow-up physical
examination in 12 to 18 months.

		OSHA's proposed trigger for medical surveillance at the proposed PEL
is inadequate.  The appropriate trigger should be at the action level,
especially given the extraordinary risk of dust from silica-related
disease at the proposed PEL.  A trigger at the action level will give
workers the opportunity to learn about an adverse health condition when
there is still a possibility for some medical intervention or for which
the worker can make a decision about whether they want to continue
working in silica dust.  We must not ignore the fact that the PEL
proposed by OSHA is not a safe level, and it will not prevent workers
from developing occupational illness.

		I disagree with OSHA's assertion that medical removal protection for
workers with silica-related respiratory disease is not useful.  Workers
who have evidence of disease should have the right to remove themselves
from exposure without loss of pay or benefits.  It is appropriate from a
medicals perspective and an ethical one.  Moreover, there is precedent
for this protection.  The opportunity for MRP is a right granted to
underground coal miners who have evidence of coal worker's
pneumoconiosis.

		Workers in general industry and shipyard employment should have the
right to be transferred to a less dusty job at no loss of pay or
benefits.  Like coal miners, workers with silica-related disease should
be given this protection in the rule that allows them to exercise this
right at a time of their choosing.  

		OSHA should explicitly state in the regulatory text that
discriminating against a worker for exercising his or her MRP is a
prohibited practice and deemed a violation of the standard.  Workers
should not have to rely on the OSHA Act's deficient 11(c) provisions to
seek redress from retaliation for having a silica-related disease.

		A number of commenters criticized OSHA for its commitment to the
hierarchy of controls.  Some have called it improper and thoughtless,
counterproductive to employees' health, and illogical and arbitrary. 
Such critiques are out of step with worker health policies across the
globe.  

		For example, Safe Work Australia, the country's tripartite health and
safety body, emphasizes the hierarchy of controls is the best way to
protect workers from hazards.  And I quote, "The ways of controlling
risk are ranked from the highest level of protection and reliability to
the lowest.  The model work Health and Safety Act regulations require
duty holders to work through this hierarchy when managing risk," end
quote.

		The Canadian Province of Ontario's Health and Safety Agency offers a
variety of reasons why PPE is not appropriate when engineering and work
practice controls are available.  These include reduced performance due
to increased difficulty breathing, possible hyperventilation syndrome,
and possible susceptibility to heat stress.  They note that the use of
PPE, quote, "should be considered only the last line of defense, rather
than the first," end quote.

		These factors complement the multitude of reasons OSHA articulates for
the weaknesses and relying on respirators.  These include the employer's
duty to ensure, one, that respirators are individually selected and
fitted for each worker; two, that workers are refitted periodically;
three, the respirators are worn properly each and every time; and four,
that they are maintained precisely as directed by manufacturers and
replaced accordingly.

		I agree with OSHA that in too many work places, employers are unable
to diligently and consistently meet these and other requirements. 
Commenters who disparage the hierarchy of controls suggest that
engineering controls are no different than PPE and that they can fail
over time or be subject to poor selection, design, installation, or
maintenance.  That is a specious argument that doesn't hold water.  It
is illogical to suggest that diligently meeting all the laborious
requirements necessary for an effective respiratory protection program
for a whole crew of employees is easier than ensuring that a handful of
silica-generating pieces of equipment are maintained.

		In the 40-year history of OSHA rulemaking, industry trade associations
have made the predictable complaint that the standard will be too
costly.  But based on retrospective reviews of the actual cost of OSHA
regulations, these assertions have rarely held up.  The Agency has
consistently erred on the side of overestimating the cost.  Researchers
examined the original cost estimates for a variety of OSHA rules.  They
have compared the projections years later to reality and consistently
find significant exaggerations by the Agency of actual costs.

		As I studied the comments in the record from some of the groups who
vehemently oppose this proposal, I feel like I am listening to the rerun
of a bad TV show.  The script is all too familiar.  The litany of
complaints is predictable and largely the same objections raised in
every other OSHA rulemaking.

		We hear that the studies relied on by OSHA to demonstrate risks are
too old to be valuable, that the studies to not reflect conditions in
today's workplaces.  We heard the same thing during the rulemaking on
hexavalent chromium and others.

		We hear that when there are no studies of workers in a particular
industry, there can't be a problem.  We hear employers say we don't have
any workers in our company, so there must not be a problem.  We heard
that whine about bloodborne pathogens and others.

		We hear that lung cancer risk for silica-exposed workers is associated
with smoking.  We heard the same thing during the rulemaking on coke
ovens and others.  We hear that there is a threshold for exposure below
which workers are not at risk of disease.  We heard that one about
benzene and others.

		We hear that silica cannot be accurately measured or analyzed in
laboratories.  The litany of reasons for this one goes on and on, errors
in pump calibration, errors in cyclone calibration, cyclone leakage,
filter cassette leakage, improper flow rate, cyclone particle
distribution, cyclone contamination, and contamination during shipping. 
In every human endeavor, there are a host of potential complications
that may influence the position of results.  

		We do not live in a perfect world where all potential sources of bias
can be eliminated.  Even in immediate life and death settings, such as a
hospital operating room, sophisticated equipment like laser surgical
wants have to be calibrated, and biological samples can be contaminated
if they aren't handled following clear-cut operating procedures.  That
is why we have professions and technical disciplines that establish
procedures and codes of practice.

		Industrial hygienists, company safety personnel, consultants, and
government inspectors have been conducting for decades workplace
sampling for respirable silica.  We should follow the examples of our
neighbors to the north, in British Columbia and Manitoba.  Their silica
samples are collected and analyzed to monitor compliance with their
provinces' 25 µg standard.

		Opponents of worker safety regulations use the existence of
uncertainty, no matter its magnitude or importance, as a tool to counter
imposition of public health protections.  They do so because it may
cause them to spend money to better protect their employees from
injuries and illnesses.

		Consistently, when OSHA final rules are challenged and end up in
court, the Agency has an excellent track record, meeting its legal
burden to use the best available evidence to demonstrate the hazard
posed is a significant risk and to display the regulation is feasible. 
I urge the administration, in particular its political appointees, to
consider this history and the credibility of the opponents' assertions. 
Their economically motivated desire for absolute certainty in science is
counterproductive and futile.

		It is too late for J.T. Knuckles and Henry Dixon and the other
workers lost from a disease that is 100 percent preventable.  Please do
not allow the opponents' claims to distract you from completing this
rulemaking before the end of President Obama's term.

		JUDGE SOLOMON:  Thank you, Dr. Monforton.  Okay, next is
Dr. Rosenman.

		DR. ROSENMAN:  Yes.  So I am Kenneth Rosenman.  I am a professor of
medicine at Michigan State University.  I am a physician and
epidemiologist.  I have been conducting public health surveillance,
interpreting x-rays as a B reader, evaluating patients with silicosis
for over 30 years.  And I note that a number of my publications are
included in the background of the OSHA proposed standard.

		I want to make three points, three points related to the burden of
silica disease.  But before I make those three points, I want to make it
clear I strongly endorse OSHA having a comprehensive standard for
silica, the need to lower the PEL, and I hope that it is promptly
implemented to help the men and women currently exposed to silica.

		So my first point is that mortality from silicosis as collected and
reported by CDC and the national statistics is an inadequate marker of
the burden of silica's toxicity.  And I have six reasons that I am going
to now share with you why I feel confident in my initial -- in this
first point.

		The first is that silicosis is only found on the death certificate of
14 percent of individuals with confirmed silicosis.  So most people who
have been diagnosed with silicosis, you will never see the word
"silicosis" on their death certificate when they die.

		My second point is or my second reason for why mortality is an
inadequate measure is that the overall ratio of individuals with new
onset silicosis who are living is sevenfold times greater than what is
found on death certificates.  The living to dead ratio that we reported
in our published study in 2003 was 6.44.  This ratio has actually
increased in recent years to 15.2.  A similar ratio, an increase in the
ratio of living to dead, were found in the New Jersey surveillance data,
which went from 5.97 to 11.5 times.

		Now, the third reason and consistent with this living to dead ratio
that I just mentioned is that the number of hospitalizations for
silicosis in the country have not been going down.  In 1993, there were
2,028 hospitalizations nationwide with silicosis as one of the discharge
summaries.  In 2011, which is the most recent data available, there were
2,082 hospitalizations with silicosis, actually about 60 more.  This
data is available from the nationwide inpatient sample of the Agency for
Healthcare Research and Quality, on their website.

		So my fourth reason about the inadequacy of the mortality burden is
that the ratio of living to dead people with silicosis is not a function
of silicosis being a benign disease.  Rather, it reflects the lack of
familiarity.  It reflects how we fill out death certificates in the
United States and reflects the lack of familiarity by your general
physician about silicosis.  And it reflects who actually fills out the
death certificates, which many times is not the person who knows the
patient best.

		And to illustrate this point, I want to share with you people who have
confirmed progressive massive fibrosis.  If you look at their death
certificate when they die, only 18 percent mention the word "silicosis."
 I mentioned before the overall was 14 percent.  Now, I am just breaking
it down by severity of disease.  If you look at people with Category 3,
which is clearly obvious advanced silicosis, only 10 percent of have
silicosis mentioned on their death certificate.  

		But why are these people dying?  Well, they're dying from
pneumoconiosis, COPD, lung cancer.  There are lots of them that say
unspecified and interstitial fibrosis or respiratory failure of unknown
origin.  So these are people with aggressive massive fibrosis.  These
are people with Category 3 silicosis.

		So if you actually total up let's say Category 3, what percentage of
people are dying from respiratory disease, 63 percent.  And what
percentage of people with PMF, 53 percent.  What would you expect in the
general population, around 10 percent.  So although silicosis is not
being seen on the death certificate, these people are dying from
respiratory disease.  Silica is a major contributor to these pneumonias,
to these unrecognized respiratory failures.

		My next reason is that silicosis is just one of multiple adverse
outcomes of silica exposure.  And I would contend strongly that
silicosis mortality is a very poor marker of silicosis in general. 
There is actually no evidence whatsoever that silicosis mortality has
anything to do with lung cancer, connective tissue disease, COPD.  So
from our own data, we have reported on 44 individuals with silicosis who
developed rheumatoid arthritis.  We are in the process of showing that
40 percent of our silicotics have renal disease.  

		And, you know, in addition to the surveillance, we did a dose-response
study at a foundry in Indianapolis where we excluded all the workers
with silicosis from the analyses and looked at their breathing, their
pulmonary function test, and found a significant decrease in pulmonary
function at the existing OSHA PEL.

		My final reason for not liking mortality as a measure of burden is
that there are two things that affect disease occurrence.  One is what
are people exposed to.  And the second is, which you will never hear and
people contend, well, the mortality is going down and, therefore, there
is less of a problem, is how many people are being exposed.  

		And actually what has happened is there has been a significant
decrease in the people at risk, not because of the exposure level, but
because they are no longer exposed.  So sharing with you some Michigan
data, the number of workers in Michigan foundries peaked in 1973 and in
1991 the number of workers decreased by 75 percent.  And lo and behold,
if you look at the Michigan surveillance system and lag it by 23, 20
years, the number of cases we are seeing has decreased by 83 percent,
parallel to the decrease in workers at risk.  If you look at the number
of abrasive blasting companies in Michigan using silica, the number went
from 125 to just 36, and that's a 71 percent decrease, again paralleling
the decrease in disease.

		And, finally, you know, let's extrapolate to the country the number of
deaths from 1973 to the most where silica is mentioned -- silicosis is
mentioned on the death certificate, 2008, it went from 765 to 148, which
is an 80 percent decrease, all in that same range of decreased number of
workers at risk.  

		Now, there are increased workers at risk in oil and gas fracking now
and in highway reconstruction, but those workers have not been exposed. 
They haven't had sufficient latency period where we would expect to see
the silicosis showing up on medical record.  So that was my first point
I wanted to make.

		My next two points are much shorter.

		JUDGE SOLOMON:  You have one minute.

		DR. ROSENMAN:  Okay, I can do it.  Dr. Sokas mentioned that silica
disease is a health related disease, is a health disparity issue.  So
the disease is not evenly distributed across the United States
population.  Minority populations are at higher risk.  So, in Michigan,
the incidence of silicosis in African Americans is six-fold greater than
in Caucasians. 

		And my third point is we need to have required medical surveillance. 
OSHA has recommended it.  NIOSH in the past, National Industrial Sand
Association has encouraged silica users since the '70s to provide
medical surveillance for silica.  It is just not happening.  I have
never seen a Michigan abrasive blasting company do medical surveillance.
 I have never seen a construction company.  And we only have two percent
of the foundries in Michigan that provide medical surveillance with an
annual chest x-ray.  So like the representatives from the Acme Brick,
they only do a baseline x-ray.  Well, of course they're not going to see
silicosis.  You know if you don't look for it, it's a self-fulfilling
situation.  You don't look for it, you're not going to find it.  So we
really need medical surveillance.  That's it.

		JUDGE SOLOMON:  Okay, next?

		DR. GOLDSMITH:  Good afternoon.  My name is David Goldsmith.  And I
want to start by thanking OSHA for attempting to revise the silica PEL
and for having this hearing.  I also think that having this hearing and
ultimately making a decision about lowering the PEL for silica will
provide some international leadership on this issue and give people in
America and American industry another way to demonstrate their
leadership.

		A little bit of background.  I received my master's and Ph.D. in
epidemiology from the University of North Carolina.  I am on the
faculties of George Washington and Georgetown University in Washington,
D.C.  I have spent almost my entire academic career addressing
environmental and workplace silica dust problems. 

		In 1982, in collaboration with Dr. Tee Guidotti, I wrote the first
published article linking silica dust exposure with cancer, mostly lung
cancer.  And in 1984, I organized the first of three international
symposia in Chapel Hill, North Carolina, addressing silica dust
exposure, silicosis, cancer, and other diseases.  The other two were
held in San Francisco in 1993, and in Santa Margarita, Italy, in 2002. 
I organized a joint workshop with California EPA and U.S. Environmental
Protection Agency on silica risk assessments in 1992.  I have published
in the peer review literature 26 papers on silica exposure and health
effects and risk assessments.  I have published six book chapters on
silica dust hazards, authored four books or special issues addressing
quartz dust, and I have organized five other publications on this issue.

		I have consulted with the following agencies directly on silica health
effects and risk assessments.  They include the National Institute for
Occupational Safety and Health, Centers for Disease Control, the
California EPA, the U.S. Environment Protection Agency, the
International Agency for Research on Cancer, the U.S. Surgeon General's
Office on Smoking and Health, the Occupational Safety and Health
Administration, the Consumer Products Safety Administration, the
National Cancer Institute, and the Texas Department of Environmental
Quality.

		I was a member of the IARC monograph writing committee for Volume 42,
Silicons and Silicates, published in 1987, where the committee found
that silica dust was a probable human carcinogen.  I am not being paid
for my testimony.  I am speaking on behalf of the medical science
related to silica dust exposure.

		Industry wants the OSHA debate on silica health effects to be on the
uncertainties of whether silica dust is a carcinogen.  It is important
to recognize that evidence for silica's carcinogenicity has been
reviewed three times by the International Agency for Research on Cancer,
once in 1987, 1997, and 2012.  It has been evaluated by California's
Proposition 65 in 1988, by the National Toxicology Program in 2000 and
reaffirmed in 2011, and by the National Institute for Occupational
Safety and Health in 2002.

		According to the last two assessments by IARC in '97 and 2012, silica
is classified as a Type 1 known human carcinogen.  Furthermore, silica
dust is considered carcinogenic in the following EU nations: Belgium,
Denmark, and the Netherlands.  

		Industry wants to argue that silicosis is a required precursor to the
finding of lung cancer and that any lung cancer finding is the result of
fibrotic process, not a function of the silica dust or silica's ability
to produce cancer.  

		That concept was rebutted by this very large Chinese study that we
have been talking about all day.  The author is Liu, published in 2013,
consisting of a cohort of 34,000 tungsten and iron miners and ceramic
workers.  The authors excluded 427 lung cancer cases amongst workers
with silicosis and analyzed the remaining 119 subjects with lung cancer
but who did not have silicosis based on negative x-rays for the absence
of silicosis.

		They found a dose-response relative risk for workers based on
cumulative quartiles of silica exposure that ranged from 1.12, to 1.41,
to 1.58, to 1.70.  In any cohort of silica exposed workers, it is
generally not knowable who has or does not have silicosis when lung
cancer is diagnosed.  However, the Liu et al. study enables the
scientific community to see that workers with silicosis and those
without silicosis both have increased risk for lung cancer.  

		This large Chinese study shows a similar pattern as seen by Steenland
and colleagues from 2001, who examined 10 large silica exposed worker
cohorts from the U.S., Europe, China, and South Africa, all
characterized by very high quality dust measurements and comprehensive
diagnostic determinations.  These authors found an increasing pooled
relative risk for lung cancer for cumulative quintile categories of
silica exposure that went from 1 to 1, to 1.3, to 1.5, to 1.6, the 1.6
being the highest quintile of exposure.

		We also have evidence that silica dust exposure demonstrates
dose-response patterns amongst nonsmokers with lung cancer.  Zika (ph.)
and coworkers in 2006 conducted a multicenter case control study of 223
nonsmokers with pulmonary cancer and 13 -- I'm sorry, 1,039 non-lung
cancer controls from 16 hospital centers in Europe and in the UK.  These
authors showed that exposure to silica dust produced an adjusted odds
ratio from up to 8 years of 1.20, with an odds ratio of 2.39 for
exposure greater than 8 years.  I should say in the latter category that
was statistically significant.

		For cumulative intensity exposure up to 42.1 frequency index years,
the odds ratio from the same study was 1.1, while it was 2.45 and
statistically significant for greater than 42.1 frequency index years. 
In both cases, zero exposure was the referent category.

		Olsen et al., 2011, conducted a case control study in Eastern Europe
and found that women had an odds ratio of 2.69 for silica dust exposure,
and that was adjusted for age, cancer center, pack years, and time since
quitting, with 95 percent confidence intervals, 1.2 to 6.04.

		There have been doubts raised by industry that silica exposure plays a
role in causing anything other than silicosis.  However, the medical and
epidemiology evidence shows that respirable quartz dust is linked with
lung and other cancers, autoimmune diseases such as scleroderma, lupus,
rheumatoid arthritis, and Sjögren's syndrome, chronic kidney disease,
and tuberculosis and other non-silicosis lung diseases such as
emphysema, chronic obstructive pulmonary diseases, and chronic
bronchitis.  

		We recognize that exposure to silica dust places workers at greater
risk for many diseases, especially for those employees lacking
appropriate respiratory protection.  Thus, silica dust must be
considered a plural potential hazard, and in this fashion silica is like
asbestos and cigarette smoking in that exposure clearly increases the
risk of many diseases.  

		There have been literally thousands of research studies on exposure to
crystalline silica in the past 30 years.  Almost every study tells the
occupational research community that workers need better protection to
prevent severe chronic respiratory diseases, including lung cancer and
other diseases in the future.

		What OSHA is proposing to do in revising the workplace standard for
silica seems to be a rational response to the accumulation of published
evidence.  And I want to thank you for your consideration.

		JUDGE SOLOMON:  Thank you, Dr. Goldsmith.  Dr. Cone?

		DR. CONE:  Yes.  My name is James Cone.  I'm an occupational medicine
physician in New York City.  I'm going to speak today, and thank you for
the opportunity, about silicosis and chronic bronchitis in foundry
workers.

		Silicosis is one of those ancient diseases that is unfortunately still
with us.  And I am always amazed when I learn something new about
silicosis.  When I'm at the theater, for example, I was at a play
recently in New York City, an off Broadway play called New Jerusalem,
about the life of Baruch Spinoza, born in 1632.  He died a young man,
unfortunately.  We know him as a philosopher.  And I was surprised to
hear that he, like philosophers today, had to have another job to
support himself.  He actually worked as a lens grinder and produced
lenses for microscopes and glasses and as a result was exposed to
silica.  He is thought to have died actually from silicosis or
complications of silicotuberculosis.  So this is I think again a
historical reference that, you know, it always is surprising how much
silica has affected history.

		Of course, we have heard a lot about the difficulties.  Surveillance
is not an easy method.  Silica is very difficult to actually track.  The
problem is mainly lack of recognition by the workers themselves.  That's
the insidious nature of this disease.  People develop the slow,
progressive symptoms we've heard about.  In some cases, much more
accelerated in the cases where people are massively over-exposed.  

		Those are the pictures of one of the workers that NIOSH was sampling
back in the 1970s and '80s, showing the dramatic nature of potential
silica exposure in the foundry.

		Silicosis has been studied, and we have heard a lot about the more
recent studies.  Phil Landgren (ph.) did a study back in 1986 at NIOSH
showing mid-western steel foundry workers developed silicosis at about a
rate of 10 percent, and 8 out of 10 of those with more than 20 years of
exposure developed silicosis.  There have been other studies in other
countries.  Ken did a nice study; Rosenman did a study published in 1996
about automotive foundry workers of whom about 60 out of 1,000 developed
pneumoconiosis, and of those 28 had silicosis, 3 had progressive massive
fibrosis.  And in a more recent study from China where a 29-year-old
cohort of workers were studied and found a rate of about 2 per 1,000
incidents of silicosis.

		I am presenting a study from 30 years ago.  It was one of my first
studies.  When I was in training, I was an epidemic intelligence service
officer at NIOSH, in Cincinnati, assigned to small-scale studies
investigations.  In this case, it was a request from OSHA or from a UAW
local in Wisconsin for a study of a great iron foundry.  It was delayed.
 The company challenged NIOSH's ability to review medical records,
saying this was a violation of confidentiality.  However, the judge in
this case ruled in the favor of NIOSH, saying it was really appropriate
for a public health agency to have access to important evidence around
the issue of occupational health in this case.  Of course, NIOSH has
regulations to protect that information from public release, and that
includes information from the Freedom of Information Act.  This was
published for the national Tactical Information Service as a health
hazard evaluation available.  It was also distributed to the company and
the workers.

		We did an industrial hygiene evaluation, I and my co-authors from
NIOSH did air sampling from many other substances besides silica were in
issue at this plant.  We did look at silica exposure in all the
different areas of the plant.  We also did a medical evaluation.  I
think that's one of the nice things about NIOSH's Health Hazard
Evaluation program is that it combines those people who are experts in
industrial hygiene, toxicology, medicine, and other specialties.  It's a
unique resource.  We did medical interviews.  We did pulmonary function
testing, pre- and post-shift for those in the core department because
they were exposed to potentially entheogenic substances like
isocyanates.  We did review of company medical records.  I had several B
readers, two B readers read each of the company x-rays and then a third
B reader in case those two disagreed and were not able to come to
consensus.

		And those industrial hygiene results are that in the core area or the
core department, we found that the levels of free crystalline silica
were in the range of between 0 and 130 µg/m3.  Nine out of the eleven
samples were above the NIOSH recommended exposure limit of 50 µg/m3.  	

		The molding and shakeout department had a level between non-detect and
70.  By non-detect, they're able to measure something below 40 µg; 40
was the lowest they were able to actually measure at this time.  About
half of those were above the NIOSH recommended exposure limit.

		In the cleaning and painting and repair department, of course, this is
the chippers and the grinders, these are historically known to have the
highest risk in a foundry for silicosis since the 1930s.  This area had
a level measured of 100 to 550 µg/m3, and all samples were above NIOSH
and OSHA level.  So we had mean crystalline silica levels that were all,
all jobs had greater than NIOSH.  Some jobs had less than the OSHA
standard.  So this study is interesting from that point of view.

		Medical results, we had 67 participate out of a total of 110.  And the
retirees, we had a little trouble getting them to come in, as you might
expect.  But the active workers, we had over 58 percent participate.  Of
those, many or most actually had worked more than 20 years.  It was a
very stable workforce at that time.  And about half of them were current
smokers.  Twelve percent had a history of diagnosed chronic bronchitis. 
And you can see that more than twice as many had a history of symptoms
that suggest potential chronic bronchitis.

		Pulmonary function tests showed that eight of the workers had evidence
of obstructive lung disease.  One had a mixed picture of obstructive and
restrictive disease.  But the company medical records, of course, had
more opportunities to test the workers, found that over half of them had
at least one abnormal pulmonary function test results.

		Chest x-ray results are most relevant for this audience.  And review
of the company medical x-rays by our certified B readers found six cases
consistent with silicosis with small rounded opacities, a prevalence 1/0
or greater.  One had irregular opacities maybe suggesting possible other
occupational, other exposure.  It all had previously been read by
company physicians as normal.  And, in fact, this foundry had been
studied by Carl Zenz in the 1970s, and he declared that silicosis was no
longer problem.

		Years in the foundry ranged from 10 to 36, and five workers were found
to have evidence on chest x-rays of simple silicosis.  One worker had
possible silicotuberculosis.

		So, in summary, I think this is an illustration of why this OSHA
standard is so important.  We have workers in a cleaning department
where silica exceeded the OSHA standard by up to five times, and they
had a prevalence of silicosis in about 24 percent of those workers.  In
a group that were in an area exposed to above the NIOSH REL, but below
the OSHA standard level, the range of silicosis is about four percent,
and this is a statistically significance difference in the rate of
silicosis.

		Certainly, OSHA's risk assessment indicates a lower PEL is indicated,
and I support OSHA's decision to establish a new, more protective
permissible exposure limit of 50.  This is, of course, a compromise
given the need for feasibility.  But the 50 µg level was recommended in
1974, almost 40 years ago, by NIOSH.  So my whole occupational health
career has been living with this recommendation, and it is time for a
change. 

		I really appreciate the opportunity to speak today.  Hopefully, a
further reduction in this exposure will result in a more protective
standard so we don't see further cases or as many cases of silica lung
cancer and other complications in the future.  Thank you.

		JUDGE SOLOMON:  Thank you, Dr. Cone.  Do any of the peer reviewers
have questions?  Dr. Ginsberg?

		MS. RYDER:  Can I just say one thing?  Dr. Ginsberg, if you have
multiple questions, maybe do you want to break them up?

		DR. GINSBERG:  You know my track record.  No, I just have one, I
believe, surprisingly.  Gary Ginsberg on the peer review panel from
Connecticut, and I think my question is mostly geared towards
Dr. Goldsmith.  You talked about the Liu study, and I know we have been
talking about it a lot, but yesterday one of the commenters had a
critique about that study, that because the radiographic evidence of
silicosis, which was I think the basis for the exclusion in their
analysis for the non-silicotic cancer connection, because that is not so
sensitive, that the claim was made I think by Dr. Borak that that study
really is pretty muddy regarding whether or not you really had
non-silicotics, completely non-silicotics that had developed lung
cancer.

		So you made a statement that when you find out somebody has got lung
cancer -- I think your statement was that when you find out somebody has
got lung cancer, you know whether they've got silicosis at the same
time.

		DR. GOLDSMITH:  No, I said exactly the opposite.

		DR. GINSBERG:  Okay.  Can you just clarify whether the Liu study was
reasonable in excluding the silicotics from their cancer statistics?

		DR. GOLDSMITH:  Yep.  I think that it's very eminently reasonable. 
They have x-rays on all of these workers.  They eliminated those that
showed x-ray evidence of silicosis for those who also had lung cancer
and just studied those individuals for which they had a clean x-ray, in
other words no findings of any x-ray abnormalities.

		What I said was that when you are doing studies where you are
evaluating the lung cancer effect of a group of silica exposed workers,
because the focus tends to be on establishing the pulmonary pathology of
cancer, there is much less attention being paid to whether there is or
is not fibrosis or silicosis.  

		The other thing that's true is that you're only going to find the true
findings of the absence of silicosis if you've got data from autopsies. 
And the only study that uses autopsy data to the extent that it does is
from South Africa.  And there you've got a mixed picture where you do
have people with negative chest x-rays, who have autopsies, but who do
show some findings of silicosis, but only on those individuals with
autopsies.  They didn't have universal autopsies in the Liu et al.
studies.  So, by definition, the authors relied on what they could rely
on, which was a negative x-ray. 

		And for that reason I think the study has a great deal of quality to
it, and we should take it at what it's worth.  They used the data that
they could evaluate.  They eliminated the sources of potential
confounding to the extent that they could.  And, therefore, their
findings of a group, I think it was 119 individuals with lung cancer who
didn't have silicosis, but then showed a dose response, that needs to --
that is something brand new.  It needs to be taken seriously.

		DR. GINSBERG:  Okay, but we can't completely rule out that
confounding?

		DR. GOLDSMITH:  Can't rule it out.

		DR. ROSENMAN:  Can I -- am I allowed to respond?

		DR. GINSBERG:  Oh, absolutely.

		DR. ROSENMAN:  You know, to me, the contention is if you don't have
radiographic evidence of silicosis, you're not at risk of lung cancer. 
And whether or not, I mean, because that's how it is spoken because we
don't know what pathologically people have.  And so in the Liu study,
they clearly didn't have radiologic evidence, and so to say if you don't
have silicosis per se, and there are people who are talking about
radiographic evidence, you're not at risk of lung cancer, we're talking
about radiographic evidence.

		DR. GINSBERG:  Understood.

		JUDGE SOLOMON:  How many people from the public have questions?  Okay,
there is at least -- there are several, okay.  So let's start in Row 3.

		DR. MIRER:  Is that me?

		JUDGE SOLOMON:  Yeah, that's you, come forward.  And would the other
people please line up.

		DR. MIRER:  Frank Mirer, CUNY School of Public Health.  Can I get two
questions?

		JUDGE SOLOMON:  Sure.

		DR. MIRER:  Okay.  The first question is for those physicians who see
patients with exposure to silica.  Could you say something about the
progression of disease after exposure has stopped?  Do you see it, I
guess?

		DR. ROSENMAN:  Well, you know, so I do see patients, but the greater
number, I try to present that data, people dying.  And they are dying
from pneumonia and respiratory disease.  And so that's clearly whether
or not their silicosis progresses, I mean they are suffering and they
have the morbidity from respiratory disease.  And so I can see it on
individuals, but I'm overwhelmed more by the data I collect from
surveillance.

		JUDGE SOLOMON:  Next question.

		DR. MIRER:  Okay, the next question is also for -- is for
Dr. Rosenman.  A couple of days ago, there was a review of your work by
Dr. Hessel, and I wondered if you would be interested in commenting on
his comments?

		DR. ROSENMAN:  So I was not here, but I was able to look at his
written report.  I will say overall I don't think his comments make a
difference in my data.  And to be more specific, you know, he talks
about one B reader, and that was me, and I dealt with -- the radiologist
said this person has an abnormal x-ray that looks like silicosis, and I
read those films to confirm the condition.  And, yes, there probably is
inter-reader variability.  But when I'm reading a 3/3, if it's a 3/2 or
even a 2/3, it doesn't make a difference in this situation, so the fact
that there was one B reader.  

		Scientifically, I have all the x-rays, and if NIOSH or OSHA thought --
I never thought it was scientifically important, but we could get a
whole panel to read all those x-rays for about 1,000 people.  

		There was the criticism that the Michigan, since most of our cases
come from foundries, that it somehow would be unique, that you couldn't
use the same living-to-dead ratio in other states.  New Jersey has the
same exact ratio.  Ohio had the same ratio.  Now, Ohio has more
foundries than New Jersey.  New Jersey is not rich in foundries.  Their
exposures are sand mines and making toilet bowls and sinks, and I'm
looking at Dave because we had a classic inspection at a large toilet
bowl manufacturer many years ago.

		So what other critiques did he have?  Oh, then he talks about there
was never any mass silicosis screenings in the state of Michigan.  Our
cases of silicosis that are being identified from the hospital are
people who -- were they admitted with silicosis?  No.  They have the
clinical radiologist seeing abnormalities.  I'm confirming it.  It's not
based on lawyers went out and did screenings.  That did not happen in
Michigan.

		I think he had one other point.  And I think the point, you know --
so, yes, the publication in 2003, you know, we began the system in '87. 
We collected deaths back and cases back to '85.  I don't find anything
inconsistent about that.  And this ratio, as I spoke about in my
testimony, has gotten greater.  And the fact that hospitalizations
across the country have not gone down complements our data that says why
the ratio has gotten greater.  I mean the national data supports us.  So
I don't -- I felt honored that the Chamber reviewed my work, but I don't
feel that it in any way minimizes what I did.

		JUDGE SOLOMON:  Next?  State your name.  I forgot to ask the last
witness to spell.

		DR. WELCH:  Laura Welch, W-e-l-c-h, with the Building Trades. 
Celeste, you had asked that OSHA add to the standard a ban on
discrimination against workers who exercised medical removal protection.
 Do you think that should be for workers who have a medical exam showing
disease, not just medical removal protection but based on any adverse
outcomes from silica on their exam?

		DR. MONFORTON:  Yes.

		DR. WELCH:  Okay, thank you.

		JUDGE SOLOMON:  Next?

		MR. KATRIB:  My name is Rami Katrib, 

K-a-t-r-i-b, and I just had a couple of questions for Dr. Monforton. 
First, you mentioned the Canadian provinces, that they have the 25, the
proposed action level.  Can you tell me a little about how that is
working for them?

		DR. MONFORTON:  Well, when I heard that there were some folks
objecting that you can't measure at 50 and certainly can't measure at
25, I knew that those provinces had that as their standard.  And so I
picked up the phone and I called the health and safety agencies, and I
said, you know, there's people down south of you who don't think you can
measure at 25.  And they were first very surprised to hear that.  But
they said, yeah, that's our standard.

		They have exposure control plan requirements for their employers.  And
they said, you know, the requirement is to make sure that your exposure
control plan is working properly, that that's their sampling that's
required is typically done by consultants, and they said they often send
their samples down here to the States.

		MR. KATRIB:  Great, thank you.  And also --

		DR. MONFORTON:  Oh, the provinces were British Columbia and Manitoba.

		MR. KATRIB:  Okay.  You also mentioned coalminers with regards to the
MRP, medical removal protection.  I was wondering what you can tell me
about how many coalminers actually use the medical removal protection
right under MSHA.

		DR. MONFORTON:  I think Rosie and I inquired with MSHA, some staff
there, and they said I think over the last 10 years, about 2,500 miners
have received the confidential letter saying that they had evidence of
silicosis.  That letter comes from NIOSH and MSHA, I believe.  And at
any given time they said about 70 miners have exercised that right and
are working in less dusty jobs.

		MR. KATRIB:  Oh, thank you.

		JUDGE SOLOMON:  Next?

		MR. MEYERSTEIN:  Hi.

		JUDGE SOLOMON:  State your name and spell your last name, please.

		MR. MEYERSTEIN:  Yes, Your Honor.  Avi Meyerstein.  I'm with Jackson
Lewis on behalf of the Chamber of Commerce.  And I had a couple of
follow-up points to Dr. Rosenman on the two things he just mentioned.

		The first was when we look at the Bang et al. study from 2005, I think
it is, which was looking across 26 states in terms of the silicosis and
they were involving just 6 percent foundry workers, and looking at that
as a comparison point to the Michigan population, doesn't that suggest
that the Michigan population was not a good representative for the rest
of the country?

		DR. ROSENMAN:  I guess I'm not totally sure.  I think you're talking
about a death certificate study done by NIOSH, is that what you're
talking about?

		MR. MEYERSTEIN:  It was Bang et al.  It was a study of the national
occupational respiratory mortality system.

		DR. ROSENMAN:  Right.  So, first of all, New Jersey has the same
ratios as Michigan, and they are a non-foundry state.  And I guess,
second, I am reassured by, I mentioned the hospitalization data, that
there has been no change, and, you know, silica in foundries, I don't
know, silica in other places, it's still silica.  And so I'm not really
clear what you are -- the point.  So, no, I think it's generalizable.  I
mean if other states want to do it, you know, other states that have
done it have gotten the same ratio, Ohio and New Jersey.  And so we're
three for three, at this point.

		MR. MEYERSTEIN:  Contrary to the 26.  But the --

		DR. ROSENMAN:  Well, the 26 is looking at death certificates.  So
you're looking -- you're into apples and, you know, apples and oranges. 
You're looking at death certificates and asking me why only 6 percent of
death certificates that showed silicosis, and I'm telling you you're
missing 95 percent of the people with silicosis.  And so we all, you
know, epidemiologists, when you tell me you've got 14 percent of the
people with this condition and you think that's generalizable, well,
that's just not going to fly.

		MR. MEYERSTEIN:  Okay.  And then the second question is really, well,
I'll leave it at that.  Well, there was one other follow-up point, which
was you had mentioned this I think when you were talking about the legal
sources of the cases, you were referring to the testimony earlier
raising the question about the Judge Jack ruling in Texas with all the
false claims that she found.  I wanted to clarify.  When you were
looking at your cases in the Michigan situation, did you go through
those and determine that they did not have any relation to those mass
silicosis claims?

		DR. ROSENMAN:  Well, first of all, there have been no mass silicosis
claims in Michigan, and there were no mass screenings.  Second of all,
our data is coming from hospitalizations where it is in the medical
record as one of the discharge diagnoses.  So I would say, you know, the
doctors in Michigan, no different than anywhere else, do a poor job in
recognizing silicosis; but when they do recognize it, they generally get
it right.  And there is radiological evidence from the clinical
radiologists in the hospital.  And there's just the mass screening in
Mississippi and Texas, it's just a totally irrelevant point.

		MR. MEYERSTEIN:  And this is the last question.  And do we know, when
we're talking about the hospital records, where that information, you
know, when it says silicosis, where that's coming from?  Do we know that
it is coming from, for example, intake when someone is providing
information, a diagnosis they might have received elsewhere, or is that
from inside the hospital?

		DR. ROSENMAN:  It's a discharge diagnosis.  So to suggest that the
patient doesn't have it, you're suggesting the physicians are committing
Medicare fraud, because generally Medicare is paying for this.  So if
you're very concerned about that, you might want to report it to
Medicare and might want to investigate this, because the physician is
putting this down as a discharge diagnosis.

		MR. MEYERSTEIN:  Okay.

		DR. ROSENMAN:  It's at the time of discharge.

		MR. MEYERSTEIN:  The diagnosis was at the time of discharge.

		DR. ROSENMAN:  Well, the diagnosis could be done any time during the
hospitalization.  It could have been prior.  But the physician is
listing it as a discharge diagnosis.  And to list a diagnosis that isn't
true is fraud.

		MR. MEYERSTEIN:  Okay, thank you.

		JUDGE SOLOMON:  And last?

		DR. COHEN:  Hi, Robert Cohen.  Just a question on you mentioned in the
death certificate, data can -- and I think about people getting
completely wrong diagnoses like pulmonary fibrosis.  Can you comment on
the literature that looks at what's called idiopathic pulmonary
fibrosis, what we sometimes term idiot-pathic pulmonary fibrosis, and
any relationship to epidemiologic evidence or associations to silica or
any other mineral dust exposures, or any other information you might
have about these diseases that are supposedly unknown cause?

		DR. ROSENMAN:  Well, if you look at the definition of idiopathic
pulmonary fibrosis, the healthcare provider is supposed to have taken a
complete occupational environmental history and excluded the possibility
of occupational environmental exposure.  In reality, that doesn't happen
and people get labeled.  

		There is a nice case series, I think it was Dr. King out in National
Jewish, in Denver, where they looked at people referred to them with
idiopathic pulmonary fibrosis or other, you know, and these people had
silicosis, asbestosis, hypersensitivity pneumonitis.  You know, a
minority of them actually had idiopathic fibrosis.  So that's the one
study that immediately came to mind.

		JUDGE SOLOMON:  So I misspoke.  There is one other questioner.  If you
want to come forward, please?

		DR. ANAND:  Hi, my name is Bovnar (ph.) Anand, and I am one of the
occupational --

		JUDGE SOLOMON:  Spell your last name, please?

		DR. ANAND:  It's A-n-a-n-d.  And I am an occupational medicine
resident, PGY-3.  I just had a question for Dr. Rosenman.  So in your
study, did you also do bronchial lavages or biopsies in addition to
x-rays, or was it just x-rays?

		DR. ROSENMAN:  So I think I must have 25 studies, but I think you're
talking about the public health surveillance.

		DR. ANAND:  Yes.

		DR. ROSENMAN:  The public health surveillance is based on the standard
of medical care in the United States, and Michigan practices that way. 
And so this is how physicians are diagnosing silicosis.  So for the most
part, no, people are not getting bronchial lavage. 

		DR. ANAND:  Okay, thank you very much.

		JUDGE SOLOMON:  Okay.  So now we are back to OSHA, Ms. Ryder.

		MS. RYDER:  I think OSHA has another 15 minutes maybe.

		MR. O'CONNOR:  Yes, we have a few questions.  We'll start with Bill
Perry.

		MR. PERRY:  Yes, my thanks out to the panel.  That was very nice
testimony.  We certainly appreciate it.  Let's see, first, we heard
earlier today there was a discussion revolved around a few papers that
dealt with the subject of finding radiologic signs of silicosis in
normal population, presumably non-dust exposed populations.  So I just
wanted to ask Dr. Rosenman if that's ever come up in terms of your
surveillance activities, or is it something that you may have
encountered?  We're trying to just gauge how big an issue is this
really?

		DR. ROSENMAN:  Okay.  So there are a couple of issues.  One, those
data typically are talking about linear changes in the lower lobes.  And
so where we're talking about silicosis, we're talking about a totally
different radiographic picture.  So that's one.

		The second is the surveillance is not surveillance of the general
population.  This is surveillance of people where a healthcare provider
has already diagnosed silicosis and I am confirming it.  And that
confirmation, we follow criteria that the states have developed with
NIOSH and includes not only radiographic or biopsy evidence, but
includes a work history that indicates exposure.  

		So, you know, I guess there could be a few in there, but it's a
totally different population than these random screens of the general
population.

		MR. PERRY:  Okay, thank you.  Dr. Monforton, you talked about various
lines of argument that have appeared in past OSHA rulemakings.  Can you
just describe for the record what your involvement or role in any of
these past rulemakings has been?

		DR. MONFORTON:  I worked at OSHA from 1990 until 1995, and then I was
at the Mine Safety Agency, and I was in what was called the Directorate
of Policy in the Legislative Affairs Office.  And I was not directly
involved.  I was not in the standards office.  You know, I would be
responding to congressional inquiries.  And that's probably where my
interest in this manufacturing uncertainty came from, because you often
saw those in the letters from members of Congress.

		MR. PERRY:  Very good, thank you.  I appreciate that.  Dr. Goldsmith,
I know you said that you participated in, it was the 1996 IARC
committee?

		DR. GOLDSMITH:  '87.

		MR. PERRY:  The '87 committee.

		DR. GOLDSMITH:  '86, published in '87.

		MR. PERRY:  Okay, okay.

		DR. GOLDSMITH:  First one.

		MR. PERRY:  But you are familiar with, of course, the 2012 IAR
findings?

		DR. GOLDSMITH:  Yes.

		MR. PERRY:  There has been quite a bit of discussion at these hearings
and, of course, you've already talked some about the relationship
between, let's say the physiologic relationship between lung fibrosis,
lung inflammation, and lung cancer.  Can I just get your opinion on what
IAR concluded in 2012 with respect to whether lung inflammation, whether
that mechanism is an essential precursor for lung cancer since that has
implications for whether there, in fact, might be a response threshold
for lung cancer?

		DR. GOLDSMITH:  I have two points.  I have read both -- all three IARC
reports on silica very closely.  The one that came out in 1997 omitted
at least two studies from Umberto Saffiotti's laboratory at the National
Cancer Institute that showed a direct mechanistic effect of silica in
pulmonary tissue.  And I will try my best to get the actual citations
and transmit those to you.

		I think part of the reason that there has been, if you will, a
fallback argument that the inflammation that is detected when silica
particles interact with pulmonary tissue is in part because we haven't
got another explanation.  So what appears to be pretty strong evidence
for the particle linked to fibrotic processes is what is assumed to be a
part of or first steps in terms of cancer causation.  

		And I think that this is one of those items that needs actual better
laboratory research certain to confirm the work that Saffiotti's
colleague published, and I apologize for not knowing those dates, but I
think it was '97 or '98, but it was not included -- I take that back. 
It was '96.  It was before the '97 IARC report came out.

		And the simple fact is I don't have a good explanation, but I think
that we are sort of left with that and start with that, so that's the
reason that this argument has been put forward.  I also must say, and
not in defense of anything, but I am not a pathologist, so I'm treading
on thin ice.

		MR. PERRY:  Okay, thank you.  Just a question or two for Dr. Cone.  I
may have missed it, but did you say that the foundry that you were, of
which you were part of the investigation, they had a medical
surveillance program?

		DR. CONE:  They did.  And actually it was fairly state of the art in
the sense they did x-rays and they did pulmonary function tests.  They
did examinations run by a, you know, occupational medicine physician for
many years.  So it was, at the time, relatively state of the art.  

		The thing they didn't do, of course, is have B readers, B reading the
x-rays.  That would have, I think, maybe detected the cases that we
picked up later.

		MR. PERRY:  Okay.  Yeah, actually, we'll need to ask if we could have
a copy of that submitted to the record, because I don't think we have
that study.

		DR. CONE:  Sure.  It was I think Carl Zenz, 1976.

		MR. PERRY:  So these were periodic x-rays taken over time, and that's
what you evaluated?

		DR. CONE:  We evaluated x-rays going back to 1949.  They had a medical
surveillance program including x-rays in as early as 1949.

		MR. PERRY:  Okay.  Have you been involved in other similar foundry
studies?

		DR. CONE:  I have not been involved in specifically a foundry study. 
I've been involved more in evaluating medical surveillance programs for
foundries in Chicago, for example, and other places, San Francisco, just
more as an informal consultant, but I haven't done an actual study.

		MR. PERRY:  Okay.  Is there something you could say then about what is
the state of medical surveillance in the foundries that you have seen? 
Are they generally doing what they should be or not?

		DR. CONE:  I think it's hard to generalize.  I think the larger
foundries tend to do a much better job, and that's to be expected.  They
have more resources.  Small foundries, I think, have difficulty with
arranging some of the medical surveillance as sophisticated as the large
foundries.  And certainly I think there are challenges finding resources
to actually do all the steps that are really required for a proper
medical surveillance program.  But it is possible.  Clearly, some
foundries do it and do it very well.

		MR. PERRY:  Okay, thank you very much.  That's all.

		MR. O'CONNOR:  And we'll turn it over to Stephen Schayer.

		MR. SCHAYER:  Oh, good evening.  So I actually have several
epidemiology questions, so possibly towards Dr. Rosenman or
Dr. Goldsmith.  So they are in reference to testimony that we heard
yesterday.  I'm not sure if you were here, but Dr. Cox had described
multiple biases that can be introduced into models and create
uncontrolled false positive associations.  And he described these biases
to include study selection bias, data selection bias, model selection
bias, model form specification bias, model over fitting bias, model
uncertainty bias, residual confounding bias, exposure measurement error,
and confirmation bias.

		So we were actually wondering in your opinion how likely is it that
all or many of the associations that have been observed in the
peer-reviewed epidemiology literature on respirable crystalline silica
are false positives as a result of these biases.

		DR. GOLDSMITH:  First of all, I don't consider myself an expert on
study bias.  I will say this, that in the 1997 IARC evaluation, there
was a clear statement that the committee evaluating the evidence for
cancer and silica chose I believe the best six studies that were the
least confounded for inability to control for smoking or other kinds of
hazardous exposures like radiation and asbestos and arsenic.

		And what they did was they looked at those studies being the best and
made an argument about whether or not there was evidence that showed
that silica produced or caused cancer.  And their findings were that
when you looked at these six studies, and again I haven't got those from
memory, they produced a body of evidence that was sufficient for the
committee to say that silica was a known human carcinogen.

		All of these things that you are talking about failed to recognize, at
least in my opinion, that the scientists who were conducting these
research studies are in somewhat of an odd situation.  They are trying
to answer a specific question about a specific exposure.  And what they
are doing is to take advantage of absolutely the best evidence they can
lay their hands on.  The best evidence, by the way, also includes the
best industrial hygiene sampling data that they possibly can.  That's
why it is crucial, in my opinion, that we pay attention to those kinds
of studies, that we pay attention to the kinds of studies that were
looked at by the IARC cohort that Steenland did from 2001.  That's where
they had the best evidence to try and find a relationship.

		All of these other things, it seems to me, are smoke screens for an
inability to want to try and see what the body of evidence really shows.
 It doesn't show that exposure to silica is good for you.  It doesn't
show that it lowers your risk of respiratory disease and cancer.  It
doesn't do anything like that.

		JUDGE SOLOMON:  I don't want to break the continuity here, but
Dr. Monforton has to leave.  She has to go to the airport.  So she
wonders if there are any questions that OSHA would put to her, so she
can leave.

		MR. O'CONNOR:  We have no more questions for Dr. Monforton.

		DR. MONFORTON:  Thank you so much.  I appreciate the opportunity.

		MS. RYDER:  Do you have your testimony --

		DR. MONFORTON:  No.  I'll e-mail it to you.

		MS. RYDER:  Okay, thank you.  I'll reserve --

		JUDGE SOLOMON:  What's the next number?

		MS. RYDER:  I will reserve Hearing Exhibit 24 for Dr. Monforton's
testimony.

		UNIDENTIFIED SPEAKER:  Great job, Celeste, safe flight.

		JUDGE SOLOMON:  Okay.  Let's go back to the questioning.

		MR. SCHAYER:  Yes.  So the next question I had, we were wondering if
anyone on the panel has reviewed or is familiar with the study of
Vermont granite workers by Vacek in 2011?

		DR. GOLDSMITH:  Who?  I'm sorry, who is the author?

		MR. SCHAYER:  Vacek, V-a-c-e-k.

		(No response.)

		MR. SCHAYER:  Okay, thank you.  I think that's it for me.  So I will
pass now to Tiffany DeFoe.

		MS. DeFOE:  Hi.  Earlier today, when Dr. Mundt was here, we were
discussing a study of his published in 2011.  It was about 17,600 German
porcelain workers.  And the study was of particular interest to me
because of the low average exposures this population had.  About 70
percent of them had average annual exposures less than the proposed PEL.
 So it's interesting.

		Now, this study, I didn't actually, unfortunately, I didn't get to ask
him the series of questions I wanted to, but I'd like to ask you as
well, if you don't mind.  The study which -- it was a large study.  It
had an average of 19 years follow-up.  The study population was an
average of 35 years old at the beginning of it.  And by the end of the
follow-up, nine percent of the study population had died.  It included
94 lung cancer deaths.  They had smoking status for about 70 percent of
it.

		And the conclusion that Dr. Mundt reached was in this study based on
five categories of cumulative exposure and five categories of average
exposure was that there was no evidence of increasing lung cancer across
exposure at these levels.

		I'm wondering are you familiar with the study?  Have you had a chance
to review it?  And if so, can you comment on it?  If you are not
familiar, I'm just wondering -- well, I'll just start with that
question.

		DR. GOLDSMITH:  I'm familiar with the study.  I don't know if you are
-- okay, Jim.  I'm familiar with the study.  I looked at the study.  I
thought it was very well done.  I don't think I was able to tease out
what the exposure levels were and what the levels in the German
porcelain factories were in comparison to the U.S. OSHA recommended
standards and their existing PELs.  But from what you tell me, it
confirms what I thought was the case, which is that in Germany they are
much more serious about controlling silica dust than we are.  And it is
reflected by the fact that they don't have excess lung cancers.  And
apparently even though they do have some small amount of silicosis based
on x-ray readings, it is not very high.

		So I interpret it as good corporate policy.  I interpret it as good
regulatory policy.  And it is something that we, in the United States,
should try and emulate.  That may not be your answer, but that's what I
thought.

		MS. DeFOE:  No, I'm not looking for any particular answer.  

		JUDGE SOLOMON:  Dr. Ginsberg, you are gesturing.  Is there something
that --

		DR. GINSBERG:  Yes.  Gary Ginsberg, Connecticut.  What I recall
Dr. Mundt saying, and he was here to speak for himself, but what I
recall him saying about that was that a lot of the data came from
pre-Iron Curtain days where the exposures were not only not well
regulated, but not well measured.  And so there may be some
misclassifications in there that would -- you talk about measurement
error weakening, I mean losing your ability to find a threshold, but
measurement error could also work in terms of against you, in terms of
making it difficult to refine the regression slope.

		So I would speculate, but, you know, he's not here to speak for
himself, but I remember him saying that about the measurements from the
old days.

		MS. DeFOE:  And there is one more particular question that I would ask
about it.  Now, I'm not an epidemiologist, so I don't really know if
this is much of a problem.  But in the exposure categories that he
looked at, the final exposure categorization for cumulative exposure, if
I remember correctly, there were about 62 cases in the referent group,
which was up to 3 mg/m3 years of exposure.  And the four groups above
referent in order -- I'm not remembering the exposure cutoffs for them,
I apologize.  But there were 5 cases in the first, 6 in the second, 5 in
the third, and 16 in the top.  

		And I just, just thinking about it, it seems as though
misclassification of a couple of cases here or there could possibly
change the results of the study very much.  But I'm not, as I say, I'm
not an epidemiologist, so I'm asking your opinion on whether there is a
numbers problem here.

		DR. GOLDSMITH:  And my apologies, I haven't looked at the study in
anticipation of your question, so I don't know.  It is possible, but who
is to know?  I think in these cases you have to use what the
investigators classified their subjects into in terms of their exposure
categories.  

		Yes, it would be nice if we could move them around and say we have
definite evidence that these have been misclassified because we know
that there is a bias.  I don't see that.  

		I think if you are going to make those arguments, you have to
demonstrate that that's really true.  And for a lot of the arguments
that are being put forward by industry, they are speculating that there
is the potential for these biases, but they haven't gotten, my
perspective, the actual evidence that this is the case.

		MS. DeFOE:  Thank you.  If you ever do have a chance to look at the
study and you have comments for us post-hearing, we'd be interested.

		DR. GOLDSMITH:  I'll be happy to.

		MR. O'CONNOR:  Lyn Penniman has a question.

		MS. PENNIMAN:  Yes.  I just had one question for Dr. Rosenman.  This
is a question about his study, too, but it's not a mortality study.  It
is a study that you did.  I'm referencing the survey of foundry workers
that you did and was published in 1996.  We have heard a lot about the
problem with silica is overexposure and there really is not very much
risk at the current PEL or certainly below that.

		Do you have -- would there be anything about your study, your
findings, in your experience, that would sort of go to that argument?

		DR. ROSENMAN:  So that study was not part of the public health
surveillance system.  It was a study one in Indiana.  And Dr. Carol
Rice from the University of Cincinnati, a well-respected industrial
hygienist for exposure reconstruction, collected all the exposure data
from that foundry and did a very extensive -- we were able to
characterize everybody's exposure and their average peak cumulative
silica levels.  

		We knew about confounding in terms of asbestos.  And we found a
dose-response with decrements.  And the company did annual spirometry. 
And I spent a long time reviewing those.  And we had specific criteria
to review the quality of spirometry.  And there was a clear
dose-response below the current OSHA standard with decrements in both
FVC, FEV1, and the ratio.  So, yes, that was a long-winded, yes.

		MS. PENNIMAN:  Thank you.

		MR. O'CONNOR:  That concludes our questioning.  I'd like to thank the
panel members.  And on behalf of OSHA, I'd like to extend a special
thanks to our peer reviewers for their work over the past two days.

		JUDGE SOLOMON:  Okay.  So are there any pieces of evidence that you
need to develop?

		MS. RYDER:  Yes.  Before we go off the record, if you all could give
me your written remarks?  Dr. Rosenman, do you have any written
remarks?

		DR. ROSENMAN:  My understanding was we had up to 45 days to do that.

		MS. RYDER:  Yeah, you can send that.

		DR. ROSENMAN:  Okay.  But I will be a little more prompt, so save a
number for me, please.

		MS. RYDER:  Well, that's a little different.  You can submit any
written remarks.  But if you have what you actually read, if you
actually read from something?

		DR. ROSENMAN:  Yes.  But I scribbled all over it, so I'll have to
e-mail you.  If you can give me an e-mail address or somehow --

		MS. RYDER:  Okay.  I can do that off the record.  I'll reserve Hearing
Exhibit 25 for your written remarks.  

		And, Dr. Goldsmith, I have yours.  

		And, Dr. Cone, I have your PowerPoint presentation.  Is this the only
thing that you were reading from?

		DR. CONE:  Yes.  You're going to mark that?

		MS. RYDER:  Yes, okay.  So Dr. Goldsmith's will be Hearing Exhibit
26, and Dr. Cone's PowerPoint presentation will be Hearing Exhibit 27.

		JUDGE SOLOMON:  Okay, so I will admit both into evidence.

(Whereupon, the documents	 referred to as Hearing Exhibits 26 and 27
were marked and received in evidence.)

		JUDGE SOLOMON:  Is there anything else anybody wants to bring up?  

		Not hearing anything else, it is 6:19, and the hearing is over.

		(Whereupon, at 6:19 p.m., the hearing was continued, to resume the
next day, Friday, March 21, 2014, at 9:30 a.m.)

C E R T I F I C A T E

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

INFORMAL PUBLIC HEARINGS FOR THE PROPOSED RULE 

ON OCCUPATIONAL EXPOSURE TO

RESPIRABLE CRYSTALLINE SILICA

March 20, 2014

Washington, D.C. 

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

			      						         					____________________________

			         	ED SCHWEITZER

			         	Official Reporter

		

_________________________

		Continued

 PAGE   905 

 PAGE   637 

  PAGE  637 

Free State Reporting, Inc.

1378 Cape St. Claire Road

Annapolis, MD 21409

(410) 974-0947

			 

Free State Reporting, Inc.

1378 Cape Saint Claire Road

Annapolis, MD 21409

(410) 974-0947

			   PAGE  905